Clark Blue Book CARDIO

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TABLE of CONTENTS
TABLE of CONTENTS ................................................................................................................................................................... 2

EKG OUTLINE .............................................................................................................................................................................. 4
QRS AXIS QUADRANT METHOD ............................................................................................................................................ 10
CAUSES OF ABNORMAL AXIS ................................................................................................................................................... 11
PERMANENT PACEMAKERS...................................................................................................................................................... 12
EXERCISE TREADMILL TESTS ..................................................................................................................................................... 13
APPROACH TO ARRHYTHMIAS ................................................................................................................................................. 17
SUPRAVENTRICULAR TACHYCARDIA ........................................................................................................................................ 19
ATRIAL FIBRILLATION/ATRIAL FLUTTER ................................................................................................................................... 20
ANTICOAGULATION THERAPY .................................................................................................................................... 23
NOACs (Novel Oral AntiCoagulants) ................................................................................................................................. 24
PREEXCITATION SYNDROME .................................................................................................................................................... 31
ECTOPIC BEATS......................................................................................................................................................................... 32
CHRONIC VENTRICULAR ARRHYTHMIAS .................................................................................................................................. 33
VENTRICULAR TACHYCARDIA / ABERRATION .......................................................................................................................... 34
WIDE QRS TACHYCARDIA ......................................................................................................................................................... 35
NODAL DISEASE ........................................................................................................................................................................ 36
INFRANODAL BLOCK ................................................................................................................................................................ 38
SYNCOPE .................................................................................................................................................................................. 39
HYPERLIPIDEMIA ...................................................................................................................................................................... 40
HYPERTENSION ........................................................................................................................................................................ 54
HYPERTENSIVE EMERGENCY .................................................................................................................................................... 68
HYPERTENSION RX DURING PREGNANCY ................................................................................................................................ 70
CARDIOVASCULAR DISEASE SCREENING .................................................................................................................................. 72
LIFESTYLE / ASA THERAPY ........................................................................................................................................................ 78
STABLE ANGINA PECTORIS ....................................................................................................................................................... 79
CAD in WOMEN ........................................................................................................................................................................ 87
ACUTE CORONARY SYNDROME (UA/NSTEMI) ......................................................................................................................... 90
ACUTE CORONARY SYNDROME (STEMI) .................................................................................................................................. 91
PHYSICAL EXAM...................................................................................................................................................................... 100
INNOCENT HEART MURMUR ................................................................................................................................................. 105
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PROSTHETIC VALVES .............................................................................................................................................................. 109

ENDOCARDITIS ....................................................................................................................................................................... 112
HEART FAILURE ...................................................................................................................................................................... 117
CONGENITAL HEART DISEASE IN ADULTS .............................................................................................................................. 128
TRANSIENT ISCHEMIC ATTACKS ............................................................................................................................................. 132
CEREBROVASCULAR ACCIDENT .............................................................................................................................................. 135
DEEP VENOUS THROMBOSIS ................................................................................................................................................. 142
PREOPERATIVE EVALUATION FOR NONCARDIAC SURGERY .................................................................................................. 151
PERIOPERATIVE MANAGEMENT OF ANTITHROMBOTIC THERAPY ........................................................................................ 164
PERIOPERATIVE TIA/ STROKE ASSESSMENT........................................................................................................................... 166
AORTIC ABDOMINAL ANEURYSM .......................................................................................................................................... 168
AORTIC DISSECTION ............................................................................................................................................................... 170
PERIPHERAL ARTERIAL DISEASE ............................................................................................................................................. 172
PULMONARY HYPERTENSION ................................................................................................................................................ 175
PERICARDITIS.......................................................................................................................................................................... 179
TABLE of CONTENTS
EKG OUTLINE
HEART RATE
Regular Rhythm 1500 divided by # of small boxes (0.04sec) between QRS
Irregular Rhythm # ORS within 6 seconds rhythm strip x 10
RHYTHM
Sinus P wave in front of every QRS, fixed PR interval

P wave upright in Lead 1 and Lead 2
AXIS
Quadrant Method
Lead 1- Tells Rightward axis (negative QRS), Leftward axis (positive QRS)
AVF Tells Upper axis (negative QRS) and Lower axis (positive QRS)
Left Lower Quadrant Always Normal (Lead 1, QRS +, AVF +)
Right Lower Quadrant Always Abnormal (Lead 1 neg, AVF +) > 90
Right Upper Quadrant Always Abnormal (Lead 1 neg, AVF neg)
Left Upper Quadrant (Lead 1 +. AVF neg) Look at QRS in Lead 2
Normal Left Axis is 0 to 30: Positive Wave > Negative

(R > S or R > Q) in Lead 2
Abnormal Left Axis> - 30 : Negative Wave > Positive

(S > R = LAH; Q > R = IWMI) in Lead 2
PWAVE
Normal: Lead 2: rounded, V1 equal initial upward and terminal downward
Left Atrial Abnormality (LAA)
Notched P in Lead 2 0.12 sec wide
Large negative terminal P Wave in V1 0.04 sec wide and 1 mm deep
TABLE of CONTENTS
Right Atrial Abnormality (RAA)
Tall Peaked P in Lead 2 > 2.5 mm tall
Tall peaked initial portion of P wave in V1

P Wave Morphologies
Inverted P wave L2, L3, AVF retrograde activation of atria
Junctional (short PR interval)
Ectopic low atrial (normal PR interval)
Inverted in L1 (left to right atrial activation)
Left atrial rhythm (QRS axis normal)
Lead misplacement (right and left arm QRS axis rightward)
Dextrocardia (P wave axis rightward and reversed R wave progression noted V1-V6)
PR INTERVAL
PR Interval is between 0.12-0.20 sec. Measure the shortest PR interval
PR Segment is isoelectric with the TP interval
If depressed Atrial Injury / Pericarditis / Atrial Infarction
PR > 0.20 sec first degree AV block (atrial, AV nodal or BB conduction)

TABLE of CONTENTS
PR < 0.12 sec Junctional rhythm or bypasses the AV node
Junctional P Wave inverted in Lead 2 (retrograde conduction)
Pre-Excitation P Wave upright in Lead 2
QRS
QRS Duration
0.11 seconds is NORMAL. Measure the longest QRS interval
> 0.12 seconds is ABNORMAL
In Lead V1- if QRS is inverted = LBBB and if QRS is upright = RBBB
In any lead - Initial QRS delay =WPW
- Mid QRS Delay=LBBB
- Terminal QRS Delay=RBBB - Total QRS Delay=Metabolic cause
Secondary ST-T changes (normal for BBB).
ST depression and T waves inversion: In Lead 1, aVL, V5-6 for LBBB

In V1-2 for RBBB
Primary ST-T changes: Absence of secondary changes.

ST isoelectric and T waves upright. Also referred to as pseudonormalization.
Exclude superimposed ischemia, electrolyte disorder or drug effect.
Intraventricular conduction defect (IVCD) - notched or wide QRS not typical for RBBB or LBBB
Incomplete RBBB has QRS duration 0.10-0.11 seconds with rsR configuration, may also
represent RVH with volume overload (ASD) associated with RAA and RAD.
Incomplete LBBB has unexplained left or right axis deviation, or slow R wave progression V1-V6.
Q Waves
In V1 and V2 any Q wave is abnormal (infarction or incomplete LBBB)
In other leads, pathological Q > 0.04 sec wide or > 1/3 the height of R wave
Q waves: Lead 2, 3 aVF = Inferior wall

Lead 1, aVL, V1-6 = Anterior wall
R wave V1 &V2 = True Posterior wall
TABLE of CONTENTS
Q wave in PVC = old MI

RV3 & RV4 (ST-T changes) = RV infarct (with IWMI or trauma)
Hypertrophy
RVH voltage, R atrial abnormality, R axis deviation, strain pattern

Pressure Overload: Pulmonary hypertension (PAH) / Pulmonic stenosis
VOLTAGE: R wave > S wave in V1
STRAIN: ST depression + T wave inversion in V1 & V2
WITH RBBB: RVH is present if R wave in V1 > 15 mm
WITH LBBB: RVH is present if S wave lead 1 or right axis
Volume Overload: Atrial septal defect (ASD)
rSrin lead V1: duration < 0.12 sec mimics IRBBB
LVH voltage, L atrial abnormality, L axis deviation, strain pattern

Pressure Overload: HTN / Aortic Stenosis / IHSS
VOLTAGE: R wave V5 or V6 + S wave V1 or V2 35 mm

R wave limb leads > 20 mm / R wave in aVL> 12mm
R wave L1 + S wave L3 25 mm
STRAIN: ST depression + T wave inversion in L1, aVL, V5, V6
WITH RBBB: Lateral wall voltage decreased less sensitive
WITH LBBB: R wave V6 + S wave V2 > 45 mm
Volume overload: Mitral / Aortic Insufficiency
Low Voltage
QRS voltage < 5 mm in limb leads and < 10mm V leads
Increased QRS voltage + proeminent Q waves and tall upright T waves in leads V5 and V6
Obesity, COPD, pericardial effusion, hypothyroidism, advanced heart disease
Tall R Wave V1 (R > S)
RVH, posterior MI, Lead misplacement, WPW, Dextrocardia, WNL
TABLE of CONTENTS
R Wave Progression
R wave increases from V1 to V6 isoelectric point between V3-4 (over IV septum)
Poor R wave progression is caused by:
Anterior wall infarction
Lead misplacement
Incomplete LBBB (left anterior hemiblock)
Right ventricular enlargement (COPD)
ST SEGMENT
ELEVATION
Localized - Injury, Acute MI, LV Aneurysm
Diffuse - Pericarditis, Early Repolarization
DEPRESSION
Ischemia - if cardiac enzymes are elevated = NSTEMI; localized to coronary distribution
Strain pattern RV in leads V1-2 or LV leads in leads 1, avL, V5-V6
Non-specific response all leads, drug effect, drug effect
PROLONGED
Ischemia, Hypocalcaemia, Hypomagnesaemia, Hypothermia, Drugs
SHORTENED
Hypercalcaemia, Hypermagnesaemia, Drugs (Dilantin-phenytoin, -blockers)
T WAVES
T waves SAME direction as QRS (except V1, V2), height is relative to QRS height (1/3 of QRS),
asymmetrical (slow upstroke rapid down slope)
T waves tall, peaked and symmetrical suggest hyperkalemia (diffuse) or hyperacute Ischemia (localized)
T waves OPPOSITE direction are nonspecific, but may be associated with ischemia (Changes localized in
specific coronary leads)
TABLE of CONTENTS
QT INTERVAL
CORRECTED for heart rate (< 0.46 sec or less than RR interval)
IDIOPATHIC (c/s deafness)
SECONDARY i.e. CAD, CNS Disease, Low K+, Mg++, Ca++, hypothyroidism, Drugs
(Type 1a antiarrhythmic, amiodarone, phenothiazines, tricyclics, antihistamines, Erythromycin,
septra)
Measure from beginning of the QRS to the end of the T wave
To separate a notched T wave from a U wave, note in a notched T wave:
The notch does not reach the baseline
The second portion is usually greater than 50% the height of the first portion of the T wave
U WAVE
May be NORMAL but need to R/O hypokalemia, drugs (pronestyl, quinidine), Hypothermia
If in opposite direction of T wave consider ischemia
TABLE of CONTENTS
QRS AXIS QUADRANT METHOD

- 90
aVF RUQ
LUQ
Abnormal
Normal 0 to 30
Abnormal > - 30
L I QRS inverted
L I - QRS upright
aVF QRS inverted
aVF QRS inverted
L1 - 180
L1 + 0
RLQ
LLQ
Abnormal
Normal
L I QRS inverted
L I QRS upright
aVF QRS upright
aVF QRS upright

aVF +
+ 90
Expanded Left Upper Quadrant
aVF - 90
aVL - 30
ABNORMAL
NORMAL
LI+0
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DETERMINATION OF HEMIBLOCKS
If QRS axis is in the LUQ, the QRS axis is normal, if axis is < - 30 or abnormal if the axis is > - 30
To determine the correct axis in the LUQ:
Lead aVL (-30) separates a normal and abnormal left axis.
Lead 2 is perpendicular to aVL; therefore evaluate the QRS height in Lead 2.
If the QRS height in Lead 2 is more positive (R wave) than Negative (S or Q wave). Then the QRS axis is
Normal LUQ axis.
If the QRS height in Lead 2 is more negative (S or Q wave) than positive (R wave), then the QRS axis is
an Abnormal LUQ axis.
If large S wave is noted in Lead 2, then left anterior hemiblock (LAH). LVH or obesity is present
Iflarge Q wave is noted in Lead 2, then an inferior wall MI is present.
CAUSES OF ABNORMAL AXIS

ABNORMAL LEFT AXIS (> -30)
Marked Obesity
Inferior Wall MI (Q>R wave in Lead 2)
Left Ventricular Hypertrophy
WPW
Left Anterior Hemiblock (S > R wave in Lead 2)
ABNORMAL RIGHT AXIS (> 90)
Tall Slender Phenotype
Extensive Lateral Wall MI
Right Ventricular Hypertrophy
WPW
Dextrocardia
Left Posterior Hemiblock (S > R wave in Lead 1)
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PERMANENT PACEMAKERS
Indications:
Symptomatic sinus node disease // AV node disease // Malignant ventricular arrhythmias

Refractory congestive heart failure
Pacemaker Mode / Code:
DDDR AV sequential demand pacemaker allows AV synchrony
Pace dual / Sense dual / Inhibit dual / Rate responsive
Dual = atrial + ventricular effect
VVIR Ventricular demand pacemaker paces only in RV, use in chronic AF, no AV synchrony
Pace vent / Sense vent / Inhibit vent / Rate responsive
BiV (Biventricular pacing BiV = Cardiac Resynchronization Therapy CRT)

Requires widen QRS and refractory HF - added to DDDR or VVIR pacemaker.
ICD pacemaker inserted for Primary Prevention of sudden death with persistent LVEF 35% on OMT;
Secondary Cardiac Prevention to prevent recurrent cardiac arrest after arrhythmic sudden death.
Lead location and type:
RV (endocardial pacing) most common approach - LV (epicardial pacing via coronary sinus,
employed with BiV pacing or during open heart surgery).
DDD pacing involves RA and RV leads. BiV pacing involves RA, RV and epicardial LV leads.
Bipolar lead results in small pacemaker spike; Unipolar lead results in large pacemaker spike
Pacemaker Evaluation: Failure with capture: Failure to sense
Failure to Capture: Spike without following P or QRS suspect generator failure or lead movement
Failure to Sense: Undersensing pacer not inhibited by spontaneous beat: Oversensing pacer inhibited
in the absence of spontaneous beat due to external electrical stimulation - pectoral muscle stimulation)
Follow Up
Document: Pacemaker company, pacemaker mode, lower pacing heart rate, battery life
F/U VVIR and DDR every 6 months; ICD and BiV every 3 months
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EXERCISE TREADMILL TESTS

INDICATIONS
Evaluation of chest pain (atypical CP)
Risk stratification with CAD (amount of ischemia at risk)
Exercise prescription (METs = Metabolic Equivalent of Task)
Evaluation of exercise induced arrhythmias
Evaluation of effectiveness of medical CAD therapy
Guide the timing of heart valve replacement (NYHA class)
NORMAL RESPONSE TO DYNAMIC EXERCISE
Heart rate increases
Systolic BP increases (< 60 mmHg above the baseline)
Diastolic BP remains the same or decreases
ABNORMAL FINDINGS IN THE TREADMILL
Abnormal BP response or abnormal exam (S4, S3, MR, rales)
ST Segment Changes ( > 1 mm measured at 80msec post J point)
Abnormal J point ST depression
Horizontal ST depression
Downsloping ST depression
ST segment elevation
Exercise parameters: Prognosis / sudden death
Poor exercise capacity, chronotropic incompetence, slow heart rate recovery post
exercise
VALIDITY OF NON-INVASIVE TESTING
Maximal exercise TM: sensitivity 67%, specificity 72%

Lexiscan myoview: sensitivity 83%, specificity 80%
SPECT thallium: sensitivity 88% specificity 77%
Dobutamine Myoview: 80%, specificity 72%
Stress echo sensitivity: 76%, specificity 88%
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HIGH RISK NON-INVASIVE FACTORS (annual mortality rate > 3%)
High-risk Duke treadmill score ( - 11)
Exercise induced LV dysfunction (EF < 35%)
Stress-induced large MPI defect ( >10%)
Stress-induced multiple perfusion defects of moderate size
Exercise induced heart failure (increase lung uptake thallium)
Stress echo wall motion abnormality ( >2 segments) developing at a low dobutamine dose ( <10mg/kg)
or low heart rate ( <120bpm)
Stress echo evidence of extensive ischemia
INTERMEDIATE RISK NON-INVASIVE FACTORS (annual mortality rate 1-3%)
Intermediate-risk Duke treadmill score (score between -10 and +4)
Stress-induced moderate perfusion defect without LV dilation ( <10%)
Stress echo with wall motion abnormality developing at higher dose dobutamine ( >10mg/kg) involving
2 segments.
LOW RISK NON-INVASIVE FACTORS (annual mortality rate < 1%)
Low risk Duke treadmill score (score 5)
Normal or small myocardial perfusion defect with stress and EF > 35%
Normal stress echo wall motion or no change of limited resting wall motion abnormality during stress.
Duke Treadmill Score (DTS)
DTS = EXERCISE TIME (5x ST deviation) (4x exercise angina)
Exercise anginal score 0=no exercise angina
1=nonlimiting angina
2= exercise-limiting angina
Risk prediction (5-year cardiac mortality)

Low-risk + 5 = 5-year mortality rate of 3%
Moderate-risk -10 to + 4 = 5-year mortality rate of 10%
High-risk - 11 = 5-year mortality rate of 35%
Adapted from Shaw LJ; Peterson ED; Shaw LK; et al. Use of a Prognostic Treadmill Score in Identifying Diagnostic Coronary
Disease Subgroups. Circulation. 1998;98:1622-1630. doi:10.1161/01.CIR.98.16.1622
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RISK FACTORS PREDICTING SUDDEN DEATH
Resting HR > 75 bpm
Peak exercise rate increase < 89 bpm
Recovery HR decrease < 25 bpm
ROUTINE TREADMILL TESTING IN WOMEN
Lower sensitivity and specificity
Lower prevalence of multivessel disease
5-20 fold greater incidence of false positive ST-T segment depression
If EKG normal and patient can exercise, routine TM is indicated
DOUBLE PRODUCT
Maximal systolic blood pressure x maximal hear rate > 25,000 [SBP x maxHR > 25,000]
Good measure of myocardial oxygen uptake
Helpful to assess adequacy of exercise when HR increase is limited, but hypertensive BP response is noted
METHODS FOR ORDERING TREADMILL TESTS
ROUTINE TREADMILL TEST

If baseline EKG is normal and patient has good exercise capacity
NUCLEAR TREADMILL TEST or Exercise Echo
If false positive exercise TM suspected, if unable to stop medications before test (digoxin)
Good exercise capacity required
Nuclear Agents: Thallium, Myoview (Technetium 99mTc), Cardiolite (sestamibi - indicated with
morbid obesity, or large A-P chest diameter)
PHARMACOLOGICAL STRESS TESTS
In patients with abnormal resting EKG (LBBB, LVH with strain pattern, digitalis effect)
concomitant stress imaging with echocardiography or MPI (myocardial perfusion imaging) is
indicated.
In patients with LBBB, exercise MPI has an unacceptably low specificity because of septal
perfusion defects that are not related to CAD. In these patients pharmacological stress MPI,
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with adenosine, dipyridamole or regadenoson is suggested over exercise stress imaging.
Intravenous regadenosone should be avoided in patients with significant heart block,

bronchospasm, critical carotid occlusive disease or a condition that prevents their being withdrawn
from theophylline preparations or other adenosine antagonists.
Pharmacological Agents
Regadenosone (LEXISCAN)
0.4mg/5 mL injection for 10 sec for Lexiscan
Produces coronary vasodilation and increases coronary blood flow by activating A2A
adenosine receptor
Regadenosone has a more favorable side-effect profile and appears safe for use in patients
with mild bronchospasm.
To be performed in patients unable to exercise adequately.
Contraindicated: 2nd or 3rd degree heart block, sinus node dysfunction unless these patients
have a functioning pacemaker. Cannot be performed if theophylline usage (patients need to
stop all caffeine use 1 day prior to testing).
Reversed with Aminophylline (50-250 mg) by slow IV (50-100 mg over 60 seconds) to

attenuate severe and/or persistent adverse reactions (chest pain, severe headache)
Caution! In patientswith CKD (stage III, IV, on dialysis) and in patients using Aggrenox
(as it contains dipyridamole) it is best to reverse with Aminophylline in all of these
patients, as adverse reactions can appear later and usually last longer.
Adenosine
149mcg/kg/min IV over 6 minutes
Induces ischemia by producing a coronary steal, short duration of action
All patient unable to exercise adequately unless history of reactive airway disease,
baseline heart block or theophylline usage
Dobutamine Nuclear /Echo
Induces ischemia by increasing cardiac demand (HR and SBP)
To be used if Lexiscan/Adenosine is contraindicated: history of reactive airway disease,

sinus node disease, 2nd or 3rd degree heart block or theophylline usage
Reversed with intravenous Metoprolol by slow IV (5 mg over 60 seconds) to attenuate

severe chest pain or tachyarrhythmias)
All stress agents should be avoided in unstable patients!!!

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APPROACH TO ARRHYTHMIAS
Narrow QRS (SUPRAVENTRICULAR RHYTHM
Regular
Sinus / PSVT (AVNRT/AVRT)/A flutter
Atrial wave
P wave / P wave / F waves
Irregular
A fibrillation/ A flutter/ MAT
Atrial wave
f waves / F waves / P wave
WIDE QRS (VENTRICULAR OR SUPRA RHYTHM WITH ABERRATION)

Regular
V tachy / Sinus / PSVT / A flutter
Atrial wave
AV dissoc / P wave / P wave / F wave
Irregular
A fibrillation / A flutter / MAT
Atrial wave
F wave / F wave / P waves
NARROW QRS TACHYCARDIA

REGULAR
IRREGULAR
Check for patient stability
Check for patient stability
Exclude Sinus Tachycardia
Exclude severe COPD, treat symptoms
If unstable, electrical cardioversion
If unstable, electrical cardioversion
Valsalva procedure / Adenosine Rx
Slow with Diltiazem Rx
Exam for atrial waves (P, afib/flutter waves)
Exam for atrial waves (P, afib/flutter waves)
Evaluate cause (EKG, Echo, Lab, TM)
Evaluate cause (EKG, Echo, Lab, TM)
Long-term therapy, consider ASA
Long-term therapy + ASA
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Types of narrow QRS complex tachycardia

1. Sinus tachycardia
2. Atrioventricular nodal reentrant tachycardia (AVNRT)
3. Atrioventricular reentrant (or reciprocating) tachycardia (AVRT)
4. Atrial tachycardia
5. Inappropriate sinus tachycardia
6. Sinoatrial nodal reentrant tachycardia (SANRT)
7. Intraatrial reentrant tachycardia
8. Junctional ectopic tachycardia
9. Nonparoxysmal junctional tachycardia
10. Atrial fibrillation
11. Atrial flutter
12. Multifocal atrial tachycardia (MAT)
Paroxysmal SVT
-
Incidence 35 per 100.000 person-years
Major causes: AVNRT 60% of cases; AVRT approximately 30% of cases. 10% of cases are caused by AT
or SANRT.
AVNRT is characterized by 2 pathways within the AV node or perinodal atrial tissue
An accessory pathway that connects the atrium to the ventricle characterizes AVRT. EKG shows delta
waves during sinus rhythm if there is antegrade conduction via the accessory pathway, leading to WPW
diagnosis.
SANRT and intraatrial reentrant tachycardia (IART) are 2 major types of paroxysmal reentrants SVT in
which the reentrant circuit does not involve the AV or accessory pathways.
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SUPRAVENTRICULAR TACHYCARDIA
Initial evaluation
Is patient stable or unstable?
Are there serious signs or symptoms that are due to
tachycardia?
Stable
Unstable
Review 12-lead EKG

Regular or Irregular?
Irregular rhythm
Are P waves present?
P waves absent
Atrial fibrillation
Quickly attempt to determine if rhythm is sinus
Regular rhythm
Are P waves detectable?
Multiple P wave
morphologies
MAT
Sinus rhythm
Treat underlying cause
In the presence of significant
cardiac ischemia, IV betablocker may be appropriate
Not sinus rhythm

CARDIOVERSION
Appropriate sinus tachycardia

Treat underlying cause
In the presence of significant cardiac ischemia,
IV beta-blocker may be appropriate
Inappropriate
sinus tachycardia
Treat with IV betablocker
P waves not detectable

P waves detectable
Assess the following:
1.Atrial rate
2.P wave morphology
3.Relationship between
atrial and ventricular
rates
4.Position of P wave in
the cardiac cycle (long
RP vs short RP)
Atrial rate 250 or

greater and flutter
waves
Abnormal P wave
morphology and long
RP interval
Atrial flutter
Atrial tachycardia
Adenosine or carotid massage
Ventricular rate
slows
Rhythm converts
to sinus
AVNRT, AVRT, SANRT,

some atrial tachycardias
Retrograde P wave
and long RP interval
No atrial activity
apparent
Uncommon AVNRT,
AVRT with slow
accessory pathway
Junctional tachycardia,
AVNRT, AVRT, atrial
fibrillation
Retrograde P wave and

short RP interval
P wave identical to sinus

P wave
Abnormal P wave and

short RP interval
Common AVNRT, AVRT,

low atrial tachycardia
SANRT, sinus tachycardia
Atrial tachycardia with AV

nodal delay
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ATRIAL FIBRILLATION/ATRIAL FLUTTER

NARROW QRS, IRREGULAR RATE
RAPID VENTRICULAR RATE

NORMAL / SLOW VENTRICULAR
RATE < 90 bpm
UNSTABLE
NO Rx
AV NODAL DISEASE
STABLE
UNEXPECTED RAPID RATE > 200 bpm
ELECTRICAL
CARDIOVERSION
PREEXCITATION
WPW/LGL
HEPARIN+ AV
NODAL SLOWING
AGENTS
ELECTRICALCARDIOVERSION/
AMIODARONE IV 150 mg over 10 min. /MR x1
DILTIAZEM
BETA-BLOCKER
DIGXIN
AMIODARONE
SPONTANEOUS CARDIOVERSION
CARDIAC CONSULT
PERSISTENT AF
? MEDS
EPISODIC or CONTINUOUS
CONSIDER CARDIOVERSION
AF<6 months, LA< 50 mm, NO Endocardial
Clot, Need for Atrial Kick
CONTROL RATE ONLY

AF> 6 months, LA> 50 mm, Presence of
Endocardial Clot, Persistent Medical Insult
(HF, pneumonia)
SLOW
DURATION <48 hrs or NEG TTE
IMMEDIATE Rx
DURATION >48 hrs or POS TTE

THERAPEUTIC WARFARIN
3 weeks
RESTING RATE (DIGOXIN)

EXERCISE RATE (BETABLOCKER or DILTIAZEM)
LONG-TERM
WARFARIN/NOACs/ASA
ELECTRICAL CARDIOVERSION
PHARMACOLOGICAL CARDIOVERSION
CONTINUE WARFARIN FOR 4 weeks
CONVERTING AGENTS
(FLECAINIDE/AMIODARONE/PROPAFENONE/
SOTALOL)
CONTINUE WARFARIN for AT LEAST 4 weeks
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ATRIAL FIBRILLATION/EMBOLIC RISK

ACC/AHA 2014 recommendsCHA2DS2-VAScrisk score for the assessment of stroke risk for all patients with
non-valvular AF (paroxysmal, persistent or permanent).
CHADS2
C
Congestive heart failure
Hypertension (BP
consistently>140/90mm Hg or treated
HTN on medication)
Points
CHA2DS2-VASc
Points
Congestive heart failure

(or Left ventricular
systolic dysfunction
LVEF 40%)
Age 75 years
Age 75 years
A
Diabetes mellitus
Diabetes mellitus
1
D
S2
Hypertension (BP
consistently>140/90mm
Hg or treated HTN on
medication)
Prior Stroke or TIA
1
Prior Stroke or TIA or
Thromboembolism
Vascular disease (eg.

Coronary artery disease,
Peripheral artery disease,
MI, Aortic plaque)
Age 65-74
1
A
Sex category (i.e. female
gender)
Sc
Max
score
http://www.mdcalc.com/chads2-score-for-atrial-fibrillation-stroke-risk/
http://www.mdcalc.com/cha2ds2-vasc-score-for-atrial-fibrillation-stroke-risk/
Risk factors for stroke and thrombo-embolism in non-valvular AF
Major risk factors
Clinically relevant non-major risk factors
Previous
Heart failure or moderate to severe LV
Stroke
systolic dysfunction (LVEF40%)
TIA
Hypertension
Systemic embolism
Diabetes mellitus
Female sex
Age 75 years
Age 65-74 years
Vascular disease
Information adapted from:
2010 Guidelines for the management of atrial fibrillation European Heart Journal (2010) 31, 2369-2429.
Doi:10.1093/eurheartj/ehq278. Table 8 (a) and Table 8 (b)
Validation of clinical classification schemes for predicting stroke. Results from the national registry of Atrial fibrillation.
JAMA, 2011; 285 (22):2864-2870. Doi:10.1001/jama.285.22.2864
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Patients with non-valvular AF with a history of stroke, TIA, previous embolus or CHA2DS2-VASc 2,
Considered as High Risk and oral anticoagulants are recommended: warfarin (INR: 2-3), dabigatran,
rivaroxaban or apixaban.
In non-valvular AF and a CHA2DS2-VASc = 0, considered Low risk and it is reasonable to omit
antithrombotic therapy.
In non-valvular AF with CHA2DS2-VASc=1, considered Intermittent risk and either no antithrombotic
therapy, or treatment with an OAC or ASA may be considered.
VALVULAR AF
Patients with valvular AF are considered as High Risk and warfarin is recommended at target INR 2.0-3.0
Or 2.5-3.5 should be based upon type and location of the valve.
Considering Anticoagulation TreatmentConsider Embolic vs. Bleeding Risk
HASBLED Risk Score
S
B
Hypertension
Abnormal renal function (creatinine 2,
chronic dialysis, transplant)
Abnormal liver function (cirrhosis, Bili <
2x, AST >3x)
Stroke
Bleeding
L
E
D
Labile INRs
Elderly (age > 65)
Drug/Alcohol abuse
H
A
1
1 for each
1
1
(previous bleed or bleeding diathesis, anemia)
1
1
1 for each
Patients with HASBLED Score > 3 are considered High risk for bleeding and should receive
careful consideration about drug dose or selection of drug agent.
http://www.mdcalc.com/has-bled-score-for-major-bleeding-risk/
TABLE of CONTENTS
22
ANTICOAGULATION THERAPY
ANTIPLATELET AGENTS
In primary prevention, ASA produces absolute risk reduction 0.8% per year; NNT 125 patients.
No significant benefit
In secondary prevention, post TIA or stroke absolute risk reduction 2.5% per year; NNT 40 patients
ASA ineffective in stroke prevention in patients > 75 years. ASA not studied in low risk patients.
Combined ASA plus clopidogrel slightly better than ASA alone with 0.8% reduction in vascular events
and a 0.7% increase in major hemorrhage. The combination was inferior to warfarin (Active A/W Trials).
WARFARIN
In primary prevention, warfarin produces absolute risk reduction 2.7% per year; NNT 37 patients against
no therapy; NNT with prior TIA or stroke NNT 12 patients in 1 year
In secondary prevention, warfarin produces absolute risk reduction 2.6% per year post TIA or stroke; risk
The stroke risk remained 1.7% per year in AF even with warfarin therapy,
In patients treated with Warfarin, INR should be performed weekly until INR stable and at least monthly
when INR is in range and stable (goal 2-3).
For patients with AF who have mechanical heart valves, warfarin is recommended and the target
international normalized ratio (INR) intensity (2.0 - 3.0 or 2.5 - 3.5) should be based on the type and
location of the prosthesis.
For patients with severe or end-stage CKD, warfarin remains the anticoagulant of choice. In patients on
hemodialysis, warfarin has been used with acceptable risks of hemorrhage.
In nonvalvular AF, warfarin should be considered: due to its effectiveness, lesser cost, reversing agents
available and improved tolerance in renal disease. Consider NOAC agents: if INR values poorly
controlled, concern about drug interactions, patient noncompliance with lab draws.
Warfarin risk markers:
Age 75 yo; Intensity of anticoagulation (INR> 4)
History of CVA/TIA; Uncontrolled HTN
Use of antiplatelet agents or 7 medications, History of major bleeding
Recent MI, renal insufficiency, diabetes
CHA2DS2VASc
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23
NOACs (Novel Oral AntiCoagulants)

3 agents approved by FDA: dabigatran, rivaroxaban andapixaban.
Renal function should be evaluated prior to initiation of direct thrombin or factor Xa inhibitors and should
be reevaluated when clinically indicated and at least annually.
Dabigatran etexilate (Pradaxa)
Direct thrombin inhibitor
Dosage: to be taken with a full glass of water

- 150 mg 1 tab BID (ClCr >50mL/min)
- 75 mg 1 tab BID (ClCr 15-30 mL/min)
- Not recommended in end-stage CKD (dialysis)
Cytochrome P450 metabolism: none; Life: 12-14 hours, Renal elimination: 80%
ACC/AHA recommends it as a useful alternative to warfarin in patients who have non-valvular AF without severe renal and
liver disease
ESC recommends it in patients with non-valvular AF with at least one moderate risk factor.
RE-LY Trial (150 mg BID) superior reduction in stroke and systemic embolism vs. warfarin (2.07% vs 2.78% per year)
and hemorrhage stroke. Increased GI bleeds compared to warfarin, especially in elderly patients 75yo.
Switching patients from warfarin to dabigatran, discontinue warfarin and start dabigatran when the INR is below 2.0.
Switching patients from dabigatran to warfarin, adjust the starting time of warfarin based on creatinine clearance as
follows:
- For CrCl 50 mL/min, start warfarin 3 days before discontinuing dabigatran.
- For CrCl 30-50 mL/min, start warfarin 2 days before discontinuing dabigatran.
- For CrCl 15-30 mL/min, start warfarin 1 day before discontinuing dabigatran.
Converting from/to parenteral anticoagulants:

For patients currently receiving a parenteral anticoagulant, start dabigatran 0-2 hours before the time that the next dose of
parenteral drug was to have been administered or at the time of discontinuation of a continuously administered parenteral
drug (e.g., intravenous unfractionated heparin).
For patients currently taking dabigatran, wait 12 hours (CrCl 30 mL/min) or 24 hours (CrCl <30 mL/min) after the last
dose of dabigatran, before initiating treatment with a parenteral anticoagulant
If possible, discontinue dabigatran 1 to 2 days (CrCl 50 mL/min) or 3 to 5 days (CrCl <50 mL/min) before invasive
or surgical procedures.Consider longer times for patients undergoing major surgery, spinal puncture, or placement of a
spinal or epidural catheter or port, in whom complete hemostasis may be required. Restart as soon as possible.
Discontinuation on Pradaxa without adequate continuous anticoagulation increases the risk of stroke.
To measure adherence for Dabigatran, measure Thrombin level. If low the patient is not taking the medicine.
Contraindications: mechanical prosthetic valve, active pathological bleeding, serious hypersensitivity reaction to Pradaxa.
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24
Rivaroxaban (Xarelto)
Direct factor Xa inhibitor
FDA indication: non-valvular AF, DVT, PE
Dosage in non-valvular AF: to be taken with food

- 20 mg 1 tab qhs with meal (CrCl >50 mL/min
- 15 mg 1 tab qhs with meal (CrCl 15-50 mL/min)
- not recommended in end-stage CKD ( dialysis)
- avoid concomitant use of rivaroxaban with strong CYP3A4 inhibitors.
Cytochrome P450 metabolism: 32%; Life: 9-13 hours; Renal elimination: 33%
ROCKET AF trial: Non-inferior to warfarin regarding prevention of stroke and systemic embolism. No reduction in rates
of mortality or ischemic stroke, but a significant reduction in hemorrhagic stroke and intracranial hemorrhage. Compared to
Warfarin it was non-significantly different in non-major bleeding; had significant reduction in fatal bleeding but increased
GI bleeding and bleeds requiring transfusion)
5 phase III trials dabigatran vs warfarin. Patients with major bleeding on dabigatran required more red cell transfusions but
received less plasma, required a shorter stay in ICU and had a trend to lower mortality compared with those who had major
bleeding on warfarin.
Switching from warfarin to rivaroxaban - discontinue warfarin and start XARELTO as soon as INR < 3
Switching from rivaroxaban to warfarin - No clinical trial data are available to guide converting patients. Manufacturer
recommends stopping rivaroxaban and then begins a parenteral anticoagulant and warfarin at the time the next dose of
rivaroxaban would be taken.
Switching from rivaroxaban to anticoagulants other than warfarin: - if transitioning to an anticoagulant with rapid
onset, discontinue rivaroxaban and give the first dose of the other anticoagulant (oral or parenteral) at the time that the next
rivaroxaban dose would have been taken.
Switching from anticoagulants other than warfarin to rivaroxaban: - start rivaroxaban 0-2 hours prior to the next
scheduled evening administration of the drug (eg low molecular weight heparin or non-warfarin oral anticoagulant) and
omit administration of the other anticoagulant. For unfractionated heparin being administered by continuous infusion, stop
the infusion and start rivaroxaban at the same time.
Rivaroxaban should be stopped at least 24 hours before surgeries or other invasive procedures and should be resumed as
soon as possible. If oral medication cannot be taken consider administering a parenteral anticoagulant.
Premature discontinuation of rivaroxaban increases the risk of stroke
To measure adherence for Rivaroxaban, measure Factor Xa activity. If low the patient is not taking the medicine.
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25
Apixaban (Eliquis )
Direct factor Xa inhibitor
Indications: non-valvular AF, prophylaxis of DVT following hip or knee replacement surgery
Dosage:
-
5 mg 1 tab BID
2.5 mg 1 tab BID on patients 80yo, weight 60 kg, Cr 1.5 mg/dL or patients taking P450
and P-glycoprotein inhibitors
Not recommended in severe or end-stage CKD ( dialysis)
Cytochrome P450 metabolism: 15%; Life: 8-15 hours; Renal elimination: 40%
AVERROES trial: apixaban was superior in preventing stroke vs ASA in patients that couldnt
tolerate/were intolerant to warfarin.
ARISTOTLE trial: apixaban was superior to warfarin in reducing stroke or systemic embolism by 21%.
Also 31% reduction in major bleeding and 11% reduction in all-cause mortality (not CV). Rates of
hemorrhagic stroke and ISH (but not ischemic stroke) were lower in apixaban group. GI bleeding was
similar in both groups. Apixaban was better tolerated than warfarin with slightly fewer discontinuations.
Switching from warfarin to apixaban: warfarin should be discontinued and apixaban started when
INR < 2
Switching from apixaban to warfarin: discontinue apixaban and begin both a parenteral anticoagulant
and warfarin at the time the next dose of apixaban would have been taken, discontinuing the parenteral
anticoagulant when INR reaches an acceptable range.
Switching between apixaban and anticoagulants other than warfarin: discontinue one being taken
and begin the other at the next scheduled dose.
Discontinue apixaban at least 48 hours prior to elective surgeries or invasive procedures with high
risk of bleeding and 24 hours prior to invasive procedures with low risk of bleeding. Bridging is not
generally required. Resume after surgery as soon as possible.
Premature discontinuation of apixaban has increased risk of thrombotic events.
To measure adherence for Apixaban, measure Factor Xa activity. If low the patient is not taking the
medicine.
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26
ATRIAL FIBRILLATION / CARDIOVERSION

ACC/AHA/HRS 2014 Guidelines, JACC 2014 DOI: 10.1016/j.jacc.2014.03.021
FACTS
Most common sustained arrhythmia, 0.4% in general population, and its frequency increases with
advancing age
Mortality risk in atrial fibrillation is increased by 1.5 in men; 1.9in women, peripheral emboli risk is 5%
per year
Initiated by increased vagal tone and is maintained by atrial re-entry
Classification:
o Paroxysmal: AF that terminates spontaneously or with intervention within 7 days of onset
o Persistent: continuous AF that is sustained > 7 days
o Longstanding persistent: continuous AF of > 12 mo duration
o Permanent: joint decision by the patient and clinician to cease further attempts to restore and/or
maintain sinus rhythm. Acceptance of AF may change as symptoms, the efficacy of therapeutic
interventions, and patient and clinician preferences evolve
o Non-valvular AF: AF in the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic
heart valve or mitral valve repair
Hospitalize if: rapid ventricular rate (RVR), hemodynamic symptoms, associated CV disease, high risk
for embolization
Initiation of outpatient anticoagulation with warfarin alone may be considered in patients with a low risk
for embolization despite the warfarin induced-risk of a transient hypercoagulable state
ACUTE THERAPY
ANTICOAGULATIONwith heparin in hospitalized patients as emboli frequently occur within the first
week. Overlap heparin and warfarin 5 days until INR is therapeutic for 2 days in patients with a moderate
or high risk for embolization to prevent a hypercoagulable state.This hypercoagulable state occurs due to
difference in half-life of factor VII, protein C and factor X.
ACUTE RATE CONTROL
o No HF/ normal BP
Diltiazem bolus 0.25 mg/kg, -- infusion 5-15 mg/h
(IV to oral; 3mg/h = 120 mg/d, 5 mg/h = 180 mg/d, 7mg/h = 240 mg/d
TABLE of CONTENTS
27
Metoprolol 5 mg q 5 min x 3, -- 5 mg q 4 h prn

o Uncontrolled HF/ low BP
o Digoxin 0.25 mg IV q 6h for four doses, then maintance dose
o Amiodarone (bolus/drip) - 150 mg IV over 10 min, MR x1, then1mg/min for 6 hours,
then 0.5 mg/min for 18 hours
o Rapid rate > 220 bpm - suspect Preexcitation Syndrome
o See Special Conditions below. Start Procainamide 100 mg IV every 5-10 minutes,
Maximum dose 1.5 g.
CLINICAL ASSESSMENT OF RATE CONTROL:
o
o
o
o
Maximal heart rate mean of resting HR + HR after 50 yards

Minimal hear rate resting HR minus 20 beats
Average heart rate (AHR) HR after one minute of stair climbing
Controlled heart rate AHR 80 bpm and the HR 110 in a Six-minute walk
CARDIOVERSION to NSR
o Rate versus Rhythm Control (AFFIRM, RACE, PIAF, STAF Trials)
If elderly patient, advanced heart disease, no symptoms in AF & can take warfarin long-term, then
survival and QOL is same in AF or NSR. The majority of elderly patients in AF need rate control
only
TIMING OF CARDIOVERSION
o Onset 2 days may cardiovert on heparin if TTE negative for clot
o Onset >2 days or if TTE positive for clot need to anticoagulate with warfarin (INR 23) for at
least 3weeks prior toand 4 weeks after cardioversion, regardless of CHA2DS2-VASc score and the
method (electrical or pharmacological) used restore to sinus rhythm. If TEE negative for clot
may acutely convert on heparin if urgent cardioversion indicated.
EXCLUSIONS
o Giant LA, endocardial clot, acute unstable medical conditions, AF duration > 3-6 months
RISKS OF CARDIOVERSION
o Permanent AF embolic risk = paroxysmal AF = atrial flutter
o Embolic CVA can occur immediately or be delayed up to 30 days due to atrial paralysis.
o Warfarin therapy decreased absolute embolic risk 2.7% per year. NNT for primary prevention of
37 for 1 year to prevent 1 stroke; 12 patients for secondary prevention.
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28
o Post conversion CHF secondary to atrial paralysis and total loss of atrial function resulting in
decreased cardiac output.
o Malignant brady or tachyarrhythmias
o Respiratory distress / pulmonary aspiration
MEDICAL CARDIOVERSION:
o If no contraindication & therapeutic INR 2-3for >3wks.
o Success 47-84% within 24 hours/ 15-30% after 48 hours.
o Lone AF - if normal EF - flecainide, propafenone, sotalol
o Coronary Artery Disease - sotalol, amiodarone
o Hypertension - flecainide, propafenone, amiodarone, sotalol
o Heart failure - amiodarone
ELECTRICAL CARDIOVERSION:
o Anterior - Posterior cardioversion pads
o Biphasic defibrillator - higher success rate, less energy required (100-200 joules), less dermal
injury
o Atropine facilitates electric shock
POST-CONVERSION THERAPY (Electrical or Medical)
o After successful conversion, continue BB or CCB to prevent atrial remodeling & to maintain
sinus rhythm. Stop digoxin.
o Continue converting agent for 2 weeks post conversion.
o Continue anticoagulation for at least 4 weeks or lifelong post conversion.
o For recurrent / high risk AF, consider lifelong warfarin and converting agents (flecainide if lone
AF with normal LV Fx or HTN, amiodarone if HF, sotalol if angina)
o After unsuccessful conversion, continue BB or CCB & warfarin.
o May consider non-invasive LA appendage occlusion still investigational.
o Digoxin may increase the risk of recurrent AF. Continue digoxin only if used to control rate.
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29
INVASIVE THERAPY FOR AF

o AF catheter ablation is useful for symptomatic paroxysmal AF refractory or intolerant to at least 1
Class I or II antiarrhythmic medication, when a rhythm control strategy is desired.
o May be considered in symptomatic long-standing persistent AF refractory or intolerant to at least 1
Class I or II antiarrhythmic medication.
SPECIAL CIRCUMSTANCES
o AF and Hypertrophic cardiomyopathy: anticoagulation is indicated in patients with HCM and
AF independent ofCHA2DS2-VASc score.
o AF and WPW: electric cardioversion is indicated in patients who are hemodynamically
compromised. IV procainamide to restore sinus rhythm and catheter ablation of the accessory
pathway in symptomatic patients with pre-excited AF. Harmful: IV amiodarone, adenosine,
digoxin, nondyhydropiridine and calcium channel antagonists.
o AF and CHF: Harmful: for rate control IV nondyhydropiridine calcium antagonists, IV betablockers and dronedarone (Mulltaq) should not be administered to patients with decompensated
HF.
o AF post-op: Treating patients who develop AF after cardiac surgery with a beta-blocker is
recommended. If contraindicated, use non-dihydropyridine calcium channel blocker. Pre-op use of
amiodarone reduces the incidence of AF in patients undergoing cardiac surgery and is reasonable
to use as prophylactic therapy for patients at high risk for AF.
o
When making the decision to initiate anticoagulation treatment, need to consider risk/benefit
ratio.
TRIPLE ANTICOAGULATION THERAPY (warfarin, ASA, clopidogrel)

o Following coronary revascularization (PCI or surgical) in High-risk patients for embolization with
CHA2DS2-VASc 2, may be reasonable to use Clopidogrel with OAC butwithout ASA to decrease
bleeding risk.
o Triple anticoagulation therapy increases risk of bleeding by 3-6%
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30
PREEXCITATION SYNDROME
WOLFF-PARKINSON-WHITE SYNDROME
Frequency: - 0.2% of general population. 70% unassociated with organic heart disease; Men > women
Mortality: - Sudden death ~ 0-4%
Presentation: - Most common - incidental ECG finding;
-
Less common and may present with tachycardia, chest pain, syncope
Pathological anatomy Kent Fiber connects atrial muscle to ventricular muscle

EKG diagnosis: - Short PRinterval bypass AV node P wave positive in L2
-
Delta wave fusion beat / Prolonged QRS
Symptoms usually none

-
If patient has ectopy likely to have rapid PSVT, rapid atrial fibrillation or flutter.
(90% orthodromic - narrow QRS, 10% antidromic - wide QRS)
Therapy: - Acute therapy

-
For orthodromic PSVT is adenosine, diltiazem, B- blocker.
For antidromic PSVTor atrial fibrillation or flutter is Amiodarone, Flecainide.

Propafenone to blocks both AV node and accessory tract. If hemodynamically unstable,
emergency electrical cardioversion is indicated. Avoid digoxin, diltiazem or b-blocker
as they block only the AV node and could result in increased ventricular rate by
favoring by-pass tract conduction.
- Chronic therapy
- WPW pattern- no symptoms - conduction pathway may disappear with age. Usually
patients do not require therapy.
- If high-risk individuals (high risk occupation or professional athletes) consider EP testing
to see if accessory is associated with rapid conduction
- WPW Syndrome- to prevent recurrent arrhythmias consider ablation > chronic drug
therapy
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31
ECTOPIC BEATS
Narrow QRS
JUNCTIONAL
ATRIAL c ABERRATION
VENTRICULAR*
BEFORE/WITHIN/AFTER
BEFORE
FIXED RELATIONSHIP TO QRS
AV DISSOCIATION
ATRIAL
P/QRS
RELATION
P WAVE
LEAD II
BEFORE
UPRIGHT
or
INVERTED
INVERTED
UPRIGHT
or
INVERTED
0.12
0.12
0.12
PR INTERVAL
Wide QRS
AV DISSOCIATION
NONE
QRS INITIAL
DEFLECTION
SAME AS NORMAL
QRS
SAME AS NORMAL QRS
SAME AS NORMAL QRS
OPPOSITE NORMAL QRS
FILL COMP
PAUSE
RARE
RARE
RARE
COMMON
CONFIG V1
rS
rS
Rsr / RSR
NOT Rsr / RSR
PJC with aberration rare unable to distinguish from PVC
TABLE of CONTENTS
32
CHRONIC VENTRICULAR ARRHYTHMIAS

TABLE of CONTENTS
Identify & Correct: HYPOXIA, CHF, K+, Mg++,

ISCHEMIA, DRUG TOXICITY
HISTORY, PE, EKG, CXR
NSVT
ECHO/TM
NORMAL HEART*
ABNORMAL HEART
HOLTER MONITOR
HOLTER MONITOR
VT
PVCs
CATH
BENIGN
PVCs
BENIGN
NSVT
NSVT
Ischemic
Non-ischemic
-BLOCKER
hx prior MI
Asymptomatic
No Rx
Asymptomatic
No Rx
MADIT I/II
DEFINITE
CATH
Debilitating Sx
Debilitating Sx
SCD-HeFT
SCD-HeFT
-Blocker
-Blocker
? EPS
Flecainide
Flecainide
Propafenone
Propafenone
? EPS
*R/O Brugada (atypical RBBB with ST

elevation in V1, absent deep S wave in I, aVL,
V6) or RVOT Tachy (LBBB configuration
with inferior QRS axis
NSVT = 3 -10 PVCs in a row
VT 20 PVCs in a row
AVID
>9 months
hx prior MI
+
-
Symptomatic
VT/VF
ICD
ECHO
EF 35 %
EF > 35 %
ICD
Ischemic TM
33
CATH
-BLOCKER
VENTRICULAR TACHYCARDIA / ABERRATION

FACTORS FAVORING VENTRICULAR TACHYCARDIA
AV Dissociation
Fusion Beats
Capture Beats
Concordance of precordial QRS
Associated with organic heart disease
Almost regular rhythm
QRS Morphology
Monophasic R, qR, Rsr in lead V1or MCL
R/S ratio in V6 <1
RV outflow tract (children) = RAD, tall R wave in V1
Upright QRS in aVR
QRS duration > 0.14 sec
Marked RUQ axis deviation
FACTORS FAVORING ABERRATION

Supraventricular rhythm with preexisting BBB, functional BBB or preexcitation pathway
Morphology QRS V1or MCL1 (rSR', RSR')
Preceding atrial activity
Initial deflection identical to conducted QRS
Initial beat PAC with normal QRS
Alternating bundle branch block separated by single normal beat
Associated with a normal heart or mild heart disease
TABLE of CONTENTS
34
WIDE QRS TACHYCARDIA
REGULAR
IRREGULAR
ATRIAL FIB /FLUTTER /MAT with ABERRANCY
VENTRICULAR TACHYCARDIA
ABBERANCY with SINUS TACHY
PSVT
ATRIAL FLUTTER
ECTOPIC ATRIAL TACHY
UNSTABLE
ELECTRICAL
CARDIOVERSION
See Atrial fibrillation / flutter chart
STABLE
12 LEAD EKG
FAVORS VT
FAVORS ABERRATION
CAPTURE BEAT/FUSION BEAT/AV

DISSOCIATION
QRS: R/S RATIO IN V6 > 1
QRS ALWAYS UPRIGHT IN aVR
CONCORDANCE OF QRS
MARKED RUQ AXIS
QRS > 0.14 sec
QRS in V1; MCL (rSR, RSR)

ATRIAL ACTIVITY
INITIAL QRS DEFLECTION IDENTICAL TO NARROW QRS
VAGAL PROCEDURE
MEDICAL RX
FIRST TREAT AS VENTRICULAR TACHYCARDIA
LIDOCAINE 0.50-0.75 mg/kg IV q 5-10 minutes (max 3 mg/kg)
AMIODARONE 150 mg IV over 10 minutes (max 2.2 gm/24 hours)
THEN TREAT AS SVT with ABERRANCY
ADENOCARD 6-12 mg IVP. Avoid Verapamil
ELECTRICAL CARDIOVERSION
35
NODAL DISEASE
SINUS NODE DISEASE
Etiology: - congenital, ischemic (RCA), hypothyroid, fibrosis, drugs (B-blockers, CCB, digoxin,
antiarrhythmics, -blocker eye drops)
Presentation: Inappropriate sinus bradycardia or sinus tachycardia, tachy-brady syndrome,
junctional rhythm, sinus arrest or block
The 4 causes for pauses
Therapy: If no Sx - no treatment is necessary. Review medicine list.

Evaluate with a Holter monitor or treadmill. Sinus pause greater than
2 seconds consistent with Sick Sinus Node Syndrome (SSNS).
PAC/PVC
blocked PAC
second degree AV block
sinus arrest or sinus block
Consider adjustment of medications or pacemaker placement, if symptoms are present.
ATRIOVENTRICULAR BLOCK
FIRST DEGREE AV BLOCK
Prolonged PR interval > 0.20 sec no Rx needed, check & adjust drug list.
R/O inferior wall ischemia, increased vagal tone, AV nodal disease, and hypothyroidism.
Delay occurs most often in the AV node, but may occur in atrium, HIS bundle or bundle branches
SECOND DEGREE AV BLOCK
Mobitz I (Wenckebach) - Progressive prolonged PR interval with progressive shortening of the

RR interval before blocked P wave Measure the PR interval before the blocked P wave and after
the blocked P wave to prove progressive delay.
- Block in AV node - QRS usually narrow no Rx needed unless Sx
- If Sx check drug list, R/O inferior wall ischemia, increased vagal tone, conduction disease.
- Treat with atropine, dopamine; pacemaker if symptomatic.
Mobitz II Fixed PR interval on consecutive beats before blocked P wave.
- The QRS is usually wide if block is below AV node.
- R/O anterior wall ischemia, conduction disease, drugs.
- Treat even if no Sx with dopamine, then pacemaker.
2:1 AV Block is either Mobitz I/ II. Need to see progressive conducted beats prior to blocked
beat to determine whether Type I/ II. Look for the company it keeps Type I - IWMI, Type II AWMI.
TABLE of CONTENTS
36
THIRD DEGREE AV BLOCK

AV nodal block with narrow QRS junctional pacer controls the ventricle with rate @ 40-60
bpm. If no sx, then no treatment. If sx use atropine, dopamine, then pacemaker.
Infranodal AV block block is below AV node with a wide QRS (idioventricular pacemaker).
The idioventricular rate is 20-40 bpm. Treat even without sx with dopamine then pacemaker.
TABLE of CONTENTS
37
INFRANODAL BLOCK
BUNDLE BRANCH BLOCK (QRS > 0.12 seconds)
LOCATION of QRS DELAY / CONFIGURATION in V1
INITIAL DELAY Preexcitation Syndrome (WPW) short PR interval
MID DELAY LBBB or ventricular pacer / Inverted QRS in lead V1
TERMINAL DELAY RBBB / Upright QRS in lead V1
TOTAL DELAY Metabolic etiology (high K+, acidosis, hypoxia, drugs)
TRIFASCICULAR SYSTEM
Right bundle branch + left anterior superior hemidivision of LB (LAH) + left posterior inferior
hemidivision of LB (LPH)
MONOFASCICULAR BLOCK
RBBB (does not cause axis shift)
LAH (unexplained abnormal left axis)
LPH (unexplained abnormal right axis)
BIFASCICULAR BLOCK
LBBB
RBBB + LAH
RBBB + LPH
TRIFASCICULAR BLOCK
(BIFASCICULAR block + First degree AV block)
LBBB + first degree AV block
RBBB + LAH + first degree AV block
RBBB + LPH + first degree AV block
THERAPY
Monofascicular block requires no therapy or medicine adjustment.
Bifascicular block requires no therapy unless symptoms. Caution in use of drugs that slow the AV
node such as digoxin, b-blockers, verapamil, diltiazem and antiarrhythmics.
Trifascicular block requires no therapy unless symptoms. Do not use drugs that slow the AV node
such as digoxin, b-blockers, verapamil, diltiazem and antiarrhythmics.
If sx, evaluate with a Holter monitor need to correlate sx with progression to high degree heart block
and need for pacemaker placement.
TABLE of CONTENTS
38
TABLE of CONTENTS
SUDDEN ONSET
SHORT
DURATION
-
Carotid sinus syndrome
Tachy/brady arrhythmias
Orthostatic hypotension 2o
age/drugs
Pulmonary embolus
LAB
-
Carotid massage
Orthostatic BPs
Arrhythmias (QT interval)
Holter /Event monitor

Tilt table
Drug list
EP study
ABGs
EXERCISE
INDUCED
-
IHSS
Vertebral-basilar
insufficiency? Migraine
Pulm HTN
Seizure
Cardiomyopathy
Subclavian steal
Hyperventilation
Bruits
BP both arms
Heart murmur
Arrhythmias (QT)
LAB
-
POSITION
INDUCED
Hyperventilation
Aortic stenosis
PE
GRADUAL
ONSET
LONGER
DURATION
-
PE
SYNCOPE
Hypoglycemia
Glucose
Drug list
EEG
PE
LAB
-
Holter/Event
monitor
Cardiac
echocardiogram
ASSOCIATED
PRODROMATA
Orthostatic
hypotension
vasodepressor postural
1* autonomic insufficiency
2* autonomic insufficiency, drugs,
surgery carotid sinus
-
PE
Atrial myxoma
Hypovolemia
LAB
-
Orthostatic BPs
Orthostatic HRs
Heart murmur/Click
Cardiac echocardiogram
Tilt table
Drug list
PE
Vasodepressor
Valsalva
Post-tussive
Post-micturition
Glossopharyngeal
Arrhythmias
Drugs
Basilar migraine
Dissecting
aneurysm
Arrhythmias (QT)
Drug list
CXR
BP both arms
LAB
-
Holter/Event
monitor
Tilt table
Drug list
EP study
cerebral blood flow to 40% normal / SBP < 50 mmHg

39
HYPERLIPIDEMIA
CHD PATHOLOGY
Endothelial Dysfunction + Plaque formation + Inflammation + Plaque rupture
ENDOTHELIAL DYSFUNCTION (ED)
-
Impaired nitric oxide production in endothelial cells facilitates lipid

deposition in intima, limits coronary dilation, disrupts anticoagulant
surface, increases inflammation and decreases fibrinolysis.
Risk factors cause ED and risk factor treatment reverses ED

dysfunction.
PLAQUE FORMATION
-
Extracellular lipids accumulate and become oxidized. Macrophages

are converted to foam cells. Spontaneous expansion of the arterial
media results in positive remodeling and decreases luminal
obstruction. This asymptomatic phase is detected by IVUS or coronary
CT
INFLAMMATION
-
Oxidized lipids attract inflammatory cells resulting in accumulation of

collagen and calcium with digestion of extracellular matrix. The
plaque enlarges, exceeding the ability of the vessel to dilate leading to
luminal obstruction (negative remodeling). Large plaques result in
angina and infrequently ACS. This symptomatic phase is detected by
treadmill testing and coronary angiography.
PLAQUE RUPTURE
-
Soft, lipid-rich non-obstructive plaques covered by thin fibrous caps

are prone to rupture or erosion, leading to formation of a clot on the
plaque surface that can partially or completely occlude the coronary
artery. This is the most common cause of Acute Coronary Syndrome.
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40
Primary Prevention - Global Risk Assessment

1) Identify higher risk patients with a 10-year ASCVD risk as these are the patients mostly likely
to benefit from Rx. The absolute benefit in ASCVD risk reduction is proportional to the
baseline risk of the individual.
2) However, not all high-risk patients benefit therefore a patient centered approach is required.
The potential of ASCVD risk reduction, adverse effects, drug-drug interaction and patient
preference all must be considered. Age 70 years should not restrict the use of moderatedintensity statin therapy if otherwise indicated.
3) Adults 21 years with primary LDL-C >190 mg/dL should receive high-intensity statin Rx
(10-y risk estimate not required).
4) Diabetes (Type 1 or 2) aged 40-75 years with LDL-C 70-189mg/dL and without clinical
ASCVD. Rx: moderate intensity statin; high-intensity statin Rx if 10-y ASCVD risk 7.5%
5) Without clinical ASCVD or diabetes with LDL-C 70-189 mg/dL and estimated 10-year
ASCVD 7.5%. Rx: moderate to high intensity statin
6) Nontraditional risk factors to consider: LDL-C 160 mg/dL, genetic hyperlipidemia, premature
family history of ASCVD with onset <55 years in first degree male relative or <65 years in first
degree female relative; high-sensitivity CRP 2 mg/L, coronary artery calcium score score>
300 Agatston units or > 75% for age, sex and ethnicity, ankle brachial index < 0.9 or elevated
lifetime risk of ASCVD. These should be considered when:
a) Patients who are not in the 1 of the 4 statin benefit groups
b) Patients in whom the decision to start statin Rx remains unclear.
7) The panel emphasizes that the benefit of statin therapy outweighs the risk of newly diagnosed
diabetes.
8) No RCTs have been identified that demonstrate that titration of the drug dose to specific LDLC level improved ASCVD outcomes in primary or secondary prevention
2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular
Disease Risk in Adults: A Report of the American College of Cardiology/ American Heart Association Task Force
on Practice Guidelines.Neil J Stone, Jennifer Robinson, Alice H. Lichtenstein, et al. Circulation published online
November 12, 2013
http://circ.ahajournals.org/content/early/2013/11/11/01.cir.0000437738.63853.7a.full.pdf+html
TABLE of CONTENTS
41
SECONDARY PREVENTION OF CV DISEASE

BP control: <140/90 mmHg; <130/80 mmHg with diabetes, CADand CKD
Lipid Management
Physical Activity: 30 minutes x 7/week
Weight Management: BMI 18.5-24.9 Kg/m2
Diabetes Melitus: Hgb A1C goal < 7%
Anti-platelet therapy: ASA for CAD; Plavix if ASA allergic; warfarin for atrial
fibrillation or LV clot
RAAS Blockage Rx: ACEI if EF < 40%, DM, CKD; ARB if cannot use ACEI;
Aldactone blocker if EF < 40%
Beta-blocker Rx: If post MI or ACS
Influenza Immunization
Smoking cessation
SECONDARY CAUSES FOR HYPERLIPIDEMIA:

DIABETES MELLITUS Elevated triglycerides and low HDL
NEPHROTIC SYNDROME Elevated cholesterol
CHRONIC RENAL FAILURE Elevated triglycerides
HYPOTHYROIDISM Elevated cholesterol
OBSTRUCTIVE LIVER DISEASE Elevated LDL cholesterol
DRUGS Progestins, Anabolic steroids, Corticosteroids - Elevated LDL cholesterol
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42
STATIN - CHOLESTEROL / PLEIOTROPIC BENEFITS

Plaque Stabilization - removes cholesterol transforming a soft to hard plaque with
decrease risk of plaque rupture. The NNT to reduce cardiac event is = 30.
Above 65 yo NNT = 23
Reduction of luminal obstruction 25-90% reduction within 2-4 yrs
Improves endothelial dysfunction Improves vasomotor tone & decreased thrombosis
via nitric oxide.
Increases thrombolysis & decreases fibrinolysis via platelet nitric oxide
Anti-inflammatory effect - (decreased CRP-hs)
Changes LDL particle size - changes small to large particles
Reduces arteriosclerosis progression in bypass grafts / transplant hearts
Decreases CVA by 32% in secondary prevention @ 4.3year
PHARMACOKINETICS
Cytochrome System
Pravastatin, fluvastatin, rosuvastatin are the statins with little or no P450 metabolism
Solubility
Lipid: simvastatin, atorvastatin, lovastatin
Water: rosuvastatin, pravastatin, fluvastatin
Least muscle symptoms
Pravastatin, fluvastatin (no CYP 3A4 metabolism)
Pravastatin - hydrophilic resulting in less penetration of drug into muscle cell
If symptoms, stop statin until symptoms resolve. Switch to low-intensity statin.
Possible benefit: CoQ10 (150-200mg) or Vitamin D supplement to decrease sx.
Best to use in renal failure: Atorvastatin, Fluvastatin.
Acute liver dysfunction: statin absolutely contraindicated.
Chronic liver dysfunction: statin therapy may be considered but requires careful
monitoring.
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43
2013 ACC/AHA Guidelines on the Treatment of Cholesterol

to Reduce Atherosclerotic CV Risk In Adults
Major Statin Benefit Groups
ALL SHOULD RECEIVE Rx UNLESS CONTRAINDICATED
1) Clinical ASCVD
Rx: High intensity statin unless contraindicated or if age 70 years
(moderate Rx)
2) Primary elevation of LDL-C 190 mg/dl
Rx: High intensity statin unless contraindicated then moderate Rx
3) Diabetes (Type 1 or 2) aged 40-75 years with LDL-C 70-189mg/dL and
without clinical ASCVD
Rx: Moderate intensity statin; high-intensity statin Rx if 10-y ASCVD risk
7.5%
4) Without clinical ASCVD or diabetes with LDL-C 70-189 mg/dL and
estimated 10-year ASCVD 7.5%*
Rx: Moderate to high intensity statin
* The Pooled Cohort Equation

http://tools.cardiosource.org/ASCVD-Risk-Estimator/
http://www.cardiosource.org/~/media/Images/ACC/Miscellaneous/2014/02/Risk App.ashx-
Guidelines_UCM_457698_SubHomePage.jsp
Also available as ASCVD Risk app from iTunes and GooglePlay.
https://itunes.apple.com/us/app/ascvd-risk-estimator/id808875968?mt=8
https://play.google.com/store/apps/details?id=org.acc.cvrisk&hl=en
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44
Intensity Statin Drug Levels

High-Intensity Rx
Atorvastatin 80 mg
(Lowers LDL-C >50%)
Rosuvastatin 40 mg
Atorvastatin10-20 mg
Rosuvastatin 5-10 mg
Simvastatin* 20-40 mg
Pravastatin 40-80 mg
Moderate-Intensity Rx
Lowers LDL-C 30-50%)
Lovastatin 40 mg
Fluvastatin XL 80 mg
Fluvastatin 40 mg bid
Pitavastatin 2-4 mg
*Simvastatin 80 mg should be avoided due to high
risk of drug interactions
Simvastatin 10 mg
Pravastatin 10-20 mg
Low-Intensity Rx
Lovastatin 20 mg
Fluvastatin 20-40 mg
Pitavastatin 1 mg
If unable to tolerate moderate to high intensity statin therapy, consider the use of lowintensity dosages to reduce ASCVD risk.
No RCTs have been identified that demonstrate that titration of the drug dose to
specific LDL-C level improved ASCVD outcomes in primary or secondary prevention.
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45
2014 ADA (American Diabetes Association) Hyperlipidemia Guidelines

In all patients with hyperlipidemia and DM recommend lifestyle modifications including:
- diet: focusing on the reduction of saturated fat, trans fat, and cholesterol intake;
increase of n-3 fatty acids, viscous fiber and plant stanols/sterols
- Weight loss: if indicated
- Physical activity
- Smoke cessation
Regardless of baseline lipid levels. Statin therapy should be added to lifestyle therapy in
all patients with hyperlipidemia and DM who have overt CVD or who are without CVD,
but are age > 40, 1 CVD risk factors (family history of CVD, hypertension, smoking,
dyslipidemia or albuminuria)
For low-risk patients: without overt CVD, age < 40; consider statin in addition to lifestyle
therapy if LDL-C remains > 100 mg/dL or if > 1 CVD risk factors
LDL-C targeted statin therapy remains the preferred strategy.
LDL-C therapy goals: - Individuals without overt CVD: < 100 mg/dL (2.6 mmol/L)
- Individuals with overt CVD: < 70 mg/dL (1.8 mmol/L) with high
dose of statin is an option.
- If drug-treated patients do not reach the above targets on
maximum tolerated statin therapy, a reduction in LDL-C of 30-40% from baseline is an
alternative therapeutic goal.
First priority treatment if severe hypertriglyceridemia at risk for pancreatitis, then focus
on reducing the LDL-C
Triglyceride levels < 150 mg/dL (1.7 mmol/L) and HDL-C > 40 mg/dL (1 mmol/L) in
men and > 50 mg/dL (1.3 mmol/L) in women are desirable.
Combination therapy has been shown not to provide additional CV benefit above statin
therapy alone and is not generally recommended.
Statin therapy is contraindicated in pregnancy.
Although there is an increased risk of incident diabetes with statin use, the CV rate
reduction with statins outweighed the risk of incident diabetes even for patient a highest
risk for diabetes.
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46
2014 NLA (National Lipid Association) Guidelines

Population: adults > 20 yo
Targets of therapy: Non-HDL-C is more predictive than LDL-C. Both are primary targets.
Apolipoprotein B (apo B) is considered a secondary, optional target for therapy.
If low/moderate ASCVD risk: Trial of lifestyle management prior to initiate drug therapy. Reduction of
saturated fat and cholesterol intake, moderate physical activity, weight loss, consider adding plant
stanols/sterols, increase viscous fiber intake. Evaluate every 6 weeks for atherogenic cholesterol response.
If after 12 weeks, goal is not achieved, consider adding drug therapy/referral to dietician. Once goal
achieved, follow every 4-6 months to monitor adherence to lifestyle therapies.
High/very high ASCVD risk: Lifestyle management concomitant with drug therapy. A moderate or high
intensity statin should be first-line drug therapy for treatment, unless contraindicated. In patients with very
high TG, may consider TG-lowering drug (fibrates, high-dose omega 3 fatty acids, nicotinic acid) for firstline use to prevent pancreatitis. Follow every 6 weeks, increasing the dosage/ intensity if not at goal. If not
at goal after 12 weeks, refer to lipid specialist. Once at goal, follow every 4-6 month for treatment
adherence. Involve patient when making the decision to start statin.
If TG500, may consider TG-lowering drug as first-line therapy.
If TG 500-1000 mg/dL, may start with statin if no history of pancreatitis.
Non-statin therapies (BAS, CAI, fibrate, nicotinic acid) may be considered (alone or in combination) in
those with contraindications to statin therapy.
For patients with statin intolerance, reducing the dose of statin, switching to a different statin or every other
day statin may be considered.
Goals: attain levels below the goal cut points. Non-HDL-C
For patients with ASCVD or DM, consideration should be given to use of moderate or high-intensity statin
therapy irrespective of baseline atherogenic cholesterol levels.
Women with FH of childbearing age should receive pre-pregnancy counseling and instructions to stop:
statins, ezetimibe and niacin at least 4 weeks before discontinuing contraception and should not use these
medications during pregnancy and lactation.
During pregnancy in women with FH: consider LDL-apherisis if there is significant atherosclerotic disease
or if the patient has homozygous FH
Risk category
Low
Moderate
High
Very High
Treatment goal
Non-HDL-C (LDL-C)
< 130 (<100)
< 130 (<100)
< 130 (<100)
<100 (<70)
Consider drug therapy

Non-HDL-C (LDL-C)
190 (160)
160 (130)
130 (100)
100 (70)
Source: NLA Recommendations for Patient-Centered Management of Dyslipidemia available to download at: https://www.lipid.org/
Journal of Clinical Lipidology.2011;5: S1-S8 doi:10.1016/j.jacl.2011.04.003
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47
Lipid and statin monitoring
Initial
Prior to initiating statin, consider fasting lipid panel, ALT, HbA1C (to R/O DM)
Baseline CK levels if patient is at increased risk of adverse muscle events based on personal or
family history of statin intolerance, muscle disease or concomitant drugs which may have
interactions with statins.
Chronic
Routine CK is not indicated unless symptoms.
Follow up hepatic function if symptoms suggesting hepatic toxicity arise.
If confusion or memory impairment occurs while on statin, evaluate for non-statin causes or drug
interactions with statin.
Repeat second lipid panel 4-12 weeks after initiating therapy to determine patients adherence. Then
repeat lipid panel every 3-12 months as clinically indicated.
Clinical muscle syndromes with statin:

Myalgias - muscle ache and/or weakness without CK elevations (1-5% of all patients, up to 25% of
adverse reactions)
Myositis - muscle symptoms with mild CK elevations
Rhabdomyolysis - muscle symptoms with marked CK elevation > 10 times normal (Less than 0.5%
of all patients)
Factors predisposing to myalgias:
High statin dosage, hypothyroidism, advanced age, women > men, small frail body frame, chronic
renal insufficiency, diabetes, trauma, post-op status
Medicines - fibrates, niacin, cyclosporine, antifungals, macrolide antibiotics, verapamil, amiodarone,
alcohol
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48
Non-Statin Cholesterol Lowering Agents

No data has demonstrated that adding a non-statin lipid drug to statin therapy further
reduces ASCVD events.
In high risk patients (clinical ASCVD, age < 75 yo; LDL-C 190 mg/dL; 40-75 yo with
DM) who are intolerant to statins, may consider the use of non-statin cholesterol lowering
drugs.
Niacin: indicated for LDL-C elevation or fasting triglyceride 500 mg/dL;should be
avoided with liver disease, persistent hyperglycemia, acute gout or new onset AF
BAS (bile acid sequestrants): indicated for LDL-C elevation; should be avoided with
tryglicerides 300 mg/dL
Ezetimibe: indicated for LDL-C elevation; when combine with statin monitor
transaminase levels.
Fibrates: indicated for fasting triglycerides 500 mg/dL: should avoid the addition of
Gemfibrozil to statin agent due to increased risk of muscle symptoms. Fenofibrate should
be avoided if moderate/severe renal impairement. If needed, fenofibrate should only be
added to a low- or moderate-intensity statin.
Omega-3 fatty acids: indicated in severe fasting tricglycerides 500 mg/dL
Invasive therapies
LDL-apherisis:
o Non-surgical invasive therapy that is used to acutely remove LDL-C from plasma.
o Can lower LDL-C up to 70-83% after a single treatment.
o Indications: Patients > 14 yo who cannot take/tolerate statins with:
Familial hypercholesterolemia
LDL > 200 mg/dL with CAD despite diet and optimal medical therapy
LDL >300 mg/dL with or without CAD despite optimal medical therapy
Procedure is performed every 2 weeks.
Cannot be performed if patient is on ACEI/ARBs.
Side effects: hypotension, nausea, flushing, and lightheadedness.
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49
Metabolic Syndrome (3 or more risk factors)

Increases CV & all-cause mortality
Hypertension >130/85 mmHg
Fasting hyperglycemia >110 mg/dl
Insulin resistance syndrome
Abdominal obesity
Triglycerides >150 mg/dl, small LDL-C particles
HDL men < 40 mg/dl / women < 50 mg/dl
Prothrombotic & proinflammatory state
Rx - weight loss, exercise, diet, statin, fibric acid, nicotinic acid
Small&Dense LDL-C Particles

Small LDL-C has greater atherogenic potential than large because it filters more readily
into arterial wall
LDL-C particle numbers are measured by Apo A
Associated with increased triglycerides (DM)
Reversed by statins, niacin and fibrate therapy
Therapy for Isolated Low HDL Rx < 40 mg/dl

Increase aerobic physical activity
Stop smoking, treat insulin resistance and DM
Weight loss
Estrogen therapy
Moderate ETOH intake
Drug therapy for secondary prevention
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50
Hypertriglyceridemia Rx
Look for secondary causes: Chronic renal failure, nephrotic syndrome
Drugs: estrogen, bblocker, steroids, retinoids
Weight reduction, diabetes control
Decrease hyperinsulinemia (Glucophage)
ETOH cessation, increase aerobic activity
Diet low carbs, low saturated fats, low cholesterol
Treat with statin therapy. If intolerant to statins and fasting triglycerides 500 mg/dL:
fibrates, Niacin, omega-3 fatty acids.
Natural Medication
Agents that reduce cholesterol: Red yeast rice (natural lovastatin) 3g/day, Stanols &
Stanols (margarine, orange juice), Omega-3fatty acids (DHA, EPA) 3-4 g/day, Soy
Protein, Garlic, Flax seed grain 50 g/day, Pomegranate concentrate
Evidence is not conclusive, although preliminary data promising.
Safety profiles pending long-term trials, some drug interaction identified.
Familial Hypercholesterolemia (FH)

Cholesterol screening should be considered to start at age 2 for children with a family
history of premature CVD, elevated cholesterol, or other major CHD risk factors. (To be
suspected when untreated neither fasting LDL-C nor non-HDL-C is elevated: Adults 20
with LDL-C 190 and non-HDL-C 220; ages 2-20 with LDL 160 and non-HDL-C
190 mg/dL.) Cascade screening: testing lipid levels in all first-degree relatives of
diagnosed FH patients.
Initiate lifestyle management +/- statin therapy
LDL-apherisis if statin therapy does not work, is contraindicated or because of patients
intolerance.
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51
Women with FH of childbearing age: should receive pre-pregnancy counseling and

instructions to stop: statins, ezetimibe and niacin at least 4 weeks before discontinuing
contraception and should not use these medications during pregnancy and lactation.
During pregnancy in women with FH: consider LDL apherisis if there is significant
atherosclerotic disease or if the patient has homozygous FH.
Hyperlipidemia in children (219 years)

AHA /AAP / NLA Policy
Blood levels are not performed before age 2 (more fat calories needed for growth)
NLA 2014: Universal screening at age 9-11 with a fasting lipid panel or non-fasting nonHDL-C. If non-HDL-C 145 m/dL, perform fasting lipid panel. Cholesterol screening
should be considered to start at age 2 for children with a family history of premature
CVD, elevated cholesterol, or other major CHD risk factors. (To be suspected when
untreated fasting LDL-C and non-HDL-C are elevated: Adults 20 with LDL-C 190
and non-HDL-C 220; ages 2-20 with LDL 160 and non-HDL-C 190 mg/dL.)
Stress proper exercise and diet
Secondary causes: diet, obesity, BCP, anabolic steroids
NLA 2011 Children with FH initiate diet and physical activity management, followed by
statin (in children 8 yo or older). Goal 50% reduction of LDL-C or LDL-C < 130
mg/dL. If children with homozygous FH, might need to initiate therapy at an earlier age.
Start drug therapy - only > age 10 if still dyslipidemic despite lifestyle management. Start
with a bile acid sequestrant agent (BAS).
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52
LIPID LEVELS AGES 2-19 yo

TC
LDL
TRIG
HDL
ACCEPTABLE
< 170 mg/dL
< 110 mg/dL
< 150 mg/dL
>35 mg/dL
BORDERLINE
170-199 mg/dL
110-129 mg/dL
----------------
---------------
HIGH
200 mg/dL
130 mg/dL
----------------
Male < 45 mg/dL

Female < 50
mg/dL
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53
HYPERTENSION
TABLE of CONTENTS
LIFESTYLE MODIFICATIONS
Weight reduction
DASH/Mediterranean diet
Dietary sodium restriction
Exercise
Moderate ETOH
Cessation of smoking
K supplementation in diet (ADA, CHEP)
PHARMACOTHERAPY
if BP 140/90 mmHg in the general
population aged < 60 yo
if BP 150/90 mmHg in general population
aged 60 yo
if BP 140/90 mmHg in patients with DM,
CKD, > 60 yo
First line therapy
Second/ third line alternatives
Start with one of:
High doses or Combination of:
Later-line alternatives
eta-blockers
Thiazide type diuretics
Thiazide type diuretics
Alfa-blockers
Calcium channel blockers
Calcium channel blockers
Alfa1/beta-blockers (carvedilol),
vasodilating beta-blockers (nebivolol)
ACE inhibitors
ACE inhibitors
ARBs
ARBs
Central alpha2/-adrenergic agonists

(clonidine)
Direct vasodilators ((hydralazine)
SPECIAL GROUPS
African Americans without CKD: initiate with CCBs and thiazide
Patients with CKD regardless of race: initiate with ACEI or ARBs
DO NOT COMBINE ACEI with ARBs
Loop diuretics (furosemide)

Aldosterone antagonists
(spironolactone)
Peripherally acting adrenergic
antagonists (reserpine)
In patients > 75 yo with CKD, use CCB and thiazide-type diuretic instead of ACEI/ARBs
54
HYPERTENSION
FACTS
65 million (33%) adult Americans have HTN
10% increase in HTN in past decade related to the increase in obesity, elderly population
Early CV markers are often even present before sustained BP elevation.
Such markers include widened pulse pressure, LVH, increased arterial stiffness,
endothelial dysfunction, and microalbuminuria.
70% of patients with HTN are under Rx
50-60% of patients under Rx are controlled
95% of adults with HTN is essential (Idiopathic)
5% of adult HTN is secondary (Sleep Apnea, drug induced, Renal Parenchymal /
Vascular, Endocrine Adrenal / Parathyroid, Pregnancy - related, Coarctation of Aorta)
The risk of CVD begins above 115/75 mmHg, and doubles with each increment of 20/10
mmHg
HTN clusters with other risk factors; 80% will have at least one other risk factors such as
lipid disorder, diabetes, insulin resistance, obesity or LVH.
HTN is a predictor for CV disease:
-
DBP is predictor if age < 50 years
SBP and DBP if age 50-59 years
Pulse pressure if age > 60 years
Circadian Variation in HTN:

-
BP rises during the day & falls during the evening.
Impaired nocturnal dipping or early AM BP surge is associated with

an increased risk of LVH, secondary renal disease and stroke.
DBP rises until age 55 and then decreases, while SBP continues to rise throughout
life.This results in the elderly having isolated systolic hypertension (ISH).
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55
MEASUREMENT
All patients should have their BP assessed at all appropriate clinical visits
BP evaluated on two separate visits, unless end organ damage present.
Patient should be seated, back supported, upper arm bared, legs not crossed
Arm supported at right atrial level (midsternum)
No smoking or caffeine for at least 30 mins
Two or more BP readings should be repeated after at least 2 mins apart
Cuff bladder should nearly encircle the arm (at least 80%)
Mercury column deflated @ 2-3 mm/sec
Record first and last Korotkoff sound, using bell of stethoscope
Report BP to nearest 2 mmHg
Korotkoff sounds produce a lower SBP and a higher DBP than an arterial line
SBP while supine is 8 mmHg higher than while seated
DBP while seated is 5 mmHg higher than while supine
AMBULATORY/ HOME BP MONITORING (ABP):

R/O white-coat HTN (clinic BP > home BP)
R/O white-coat normotension, "Masked" (home BP > clinic BP)
Detects loss of nocturnal dipping or early morning BP surges
SBP & DBP normally dips 10-20% during nights
ABP correlated better with target-organ damage than clinic BPs
ABP helps minimize excess drug Rx decrease symptoms and cost
ABP demonstrates orthostatic hypotension
Average mean ambulatory 24 hour BP = 118/72 mmHg
Average ambulatory daytime BP = 123/76 mmHg
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EVALUATION:
Essential HTN vs Secondary HTN
Evaluate Target Organ disease (25% have CVD @ diagnosis of HTN)
Evaluate for other Risk Factors for CVD (80% have associated RF)
CAUSES TO CONSIDER ADDITIONAL TESTS:

History:
o HTN onset age <30 or > 60 years
o Abdominal trauma
o Sudden onset severe HTN
o Hx abnormal urinalysis, elevated creatinine
o Hypokalemia, hypercalcemia
Resistant HTN
Paroxysmal HTN
Abdominal mass or bruit
Cushing syndrome
ENDOTHELIAL DYSFUNCTION (EF)

EF is impaired in hypertension
EF is improved by hypertensive therapy
TREATMENT - JNC VII

Therapy lowers all cause mortality by 12% and reduces complication rate of CVA, CAD
and all CV events by 18-30%.
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57
JNC 8 2014 - Antihypertensive therapy

Initiate therapy:
-
BP 140/90 mmHg in the general population aged < 60 yo
BP 150/90 mmHg in general population aged 60 yo
Goal therapy:
-
BP < 140/90 mmHg in patients < 60 yo
BP < 150/90 mmHg in patients 60yo
BP < 140/90 mmHg in patients with DM, CKD who are < 60 yo
Antihypertensive therapy:
-
In the general non-black population, including those with DM,initial treatment should
include a thiazide-type diuretic, CCB, ACEI or ARB
In the general black population, including those with DM, initial treatment should include
and thiazide-type diuretic or CCB
In all population aged 18 yo with CKD (+/-DM), treatment should include an

ACEI/ARB to improve kidney outcomes
Patients with CKD regardless of race: initiate with ACEI or ARBs
In patients > 75 yo with CKD, use CCB and thiazide-type diuretic instead of ACEI/ARBs
If BP cannot be reached within 1 month increase the dose of the initial drug or add a
second and then third drug from the recommended classes
Do not use an ACEI and ARB together!
Beta-blockers, alfa-blockers, central alfa2- adrenergic agonists (eg. clonidine), direct

vasodilators (eg. hydralazine), aldosteron receptor antagonists (eg. spironolactone),
peripherally acting adrenergic antagonists (eg. reserpine) and loop diuretics (eg.
furosemide) are not recommended as a first-line therapy.
JNC 8. JAMA. 2014;311(5):507-520. doi:10.1001/jama.2013.2844
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58
ASH 2013 - Antihypertensive therapy

Goal therapy:
- BP< 150/90 mmHg in patients 80 yo
- BP < 140/90 mmHg in patients 60-79 yo
- BP < 140/90 mmHg or < 130/80 mmHg (if tolerated), in patients < 50 yo
In patients with CKD or Diabetes:
- BP < 140/90 mmHg (without proteinuria)
- BP < 130/80 mmHg (with proteinuria) no consensus
- Start lifestyle changes
- In stage I (140-159/90-99) in patients without CV risks,
somemonthsofregularly monitored lifestyle management without drugs can
be considered
- In black patients : initiate with CCB or thiazide. If unable to control BP, add
ACEI/ARB. If needed add Spironolactone, centrally acting agents, blockers.
-
In non-black patients< 60 yo initiate with ACEI/ARB. If uncontrolled, add

CCB, thiazide. If needed add Spironolactone, centrally acting agents, blockers. In non-balck patients 60 yo initiate with CCB or thiazide. If
needed add Spironolactone, centrally acting agents, -blockers.
The Journal of Clinical Hypertension, 2014 Clinical Practice Guidelines for the Management of
Hypertension in the Community A Statement by the American Society of Hypertension and the
International Society of Hypertension. DOI: 10.1111/jch.12237
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59
ADA 2013 - Antihypertensive therapy

Goal therapy:
- BP< 140/80 mmHg in patients with diabetes and HTN
- BP < 130/80 mmHg in young patients, if no side effects
- BP 110-129/65-79 in pregnant patients with diabetes and chronic HTN
(lower than this may be associated with impaired fetal growth).
- Start lifestyle changes
- Initiate with ACEI or ARB
- Administer one or more antihypertensive medications at bedtime. Closely
monitor eGFR, serum K levels if any ACEI/ARB/diuretic is used
- Safe in pregnancy: methyldopa, labetalol, diltiazem, clonidine, and prazosin
Standards of Medical Care in Diabetes Diabetes Care Volume 37, Supplement 1, January 2014
www.care.diabetesjournals.org
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60
CHEP 2014 - Antihypertensive therapy

Initiate therapy:
- BP 160/100 mmHg in patients without macrovascular target organ damage or other CV
risk factors*
- BP 140/90mmHg in patients with macrovascular target organ damage or other
independent CV risk factors
- BP > 130/80 mmHg in patients with diabetes
- SBP > 160 mmHg in very elderly
Goal therapy:
- BP < 140/90 mmHg in the general population, including those with CKD
- BP < 130/80 mmHg in patients with DM
- SBP < 150 mmHg in the very elderly ( 80 yo)
- Caution in elderly patients who are frail and in patients with CAD and have low DBP <
60 mmHg
Antihypertensive agents:
- Combination of both lifestyle modifications and antihypertensive medicines are generally
necessary to achieve target blood pressures.
- Optimum management of the hypertensive patient requires assessment and
communication of overall cardiovascular risk.
- Initial therapy should be monotherapy with a thiazide diuretic, a beta-blocker in patients
< 60 yo, an ACEI in nonblack patients, a long acting CCB or an ARB.
- First-line combinations: thiazide diuretic or CCB with either and ACEI, ARB or betablocker. Combination of ACEI and ARB is not recommended! Caution in
combination of nondihydropyridine and a beta-blocker.
- In patients with diabetes, the combination preferred: ACEI with dihydropyridine CCB
rather than ACEI with HCTZ.
- ISH: initial monotherapy with a thiazide diuretic, a long-acting dihydropyridine CCB or
an ARB. Combination of 2 or more first-line agents or other classes like: alpha-blockers,
ACEI, centrally acting agents or nondihydropyridine CCBs
- Beta-blockers are not recommended as first-line therapy for uncomplicated
hypertension/uncomplicated ISH in patient 60 yo. ACEI are not recommended as firstline therapy for uncomplicated hypertension in black patients. Alfa-blockers are not
recommended as first-line agents for uncomplicated hypertension/uncomplicated ISH.
- Global cardiovascular risk should be assessed in all hypertensive patients.
- Statin therapy is recommended in patients > 40 yo with HTN and 3 CV risk factors and
in all hypertensive patients with atherosclerotic disease regardless of age. Low dose ASA
therapy should be added in hypertensive patients > 50 yo
http://www.hypertension.ca/en/chep*male, >55 yo, smoker, hyperlipidemia, family history of
CVD, LVH, abnormal EKG, microalbuminuria or proteinuria
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61
ESC 2013 - Antihypertensive therapy

Before initiating therapy:
1. Confirm diagnosis of hypertension
2. Detect causes of secondary HTN
3. Assess CV risk using SCORE
4. Assess organ damage, CVD or CKD; and concomitant clinical conditions
5. EKG recommended in all hypertensive patients to detect LVH, LAA, arrhythmias or
concomitant heart disease
6. If positive history of myocardial ischemia, stress EKG is recommended and if positive
and imaging stress test (echo, MPS, MRI)
7. Recommended labs to be performed: creatinine, GFR, urinary protein levels
Initiate therapy:
- For all patients with grade 2 and 3 hypertension (BP 160/100 mmHg)
Goal therapy:
- BP 140/90 mmHg in general population
- SBP < 150 mmHg in patients > 80 yo
Antihypertensive agents:
- Diuretics (including thiazides, chlorthalidone and indapamide), beta-blockers, CCB,
ACEI and ARBs are all suitable for the initiation and maintenance of antihypertensive
treatment.
- Spironolactone/Eplerenone can be used in hypertensive patients as 3-4th line drug or with
heart failure.
- Beta-blockers: vasodilating ones reduce central pulse pressure and aortic stiffness better
than atenolol or metoprolol and affect insulin sensitivity less than metoprolol. Nebivlol
does not worsen glucose tolerance when added to HCTZ. Beta-blockers reduce risk of
exacerbation and mortality in patients with COPD.
- CCB: greater effectiveness than beta-blockers in reducing LVH and slowing down the
progression of carotid atherosclerosis. Some studies suggest that CCB may be slightly
more effective in preventing stroke. Non-dihydropyridine CCB should not be used in
combination with beta-blockers.
- ACEI/ARB: some meta-analysis observe that ACEI may be somewhat inferior to other
classes in preventing stroke. Both ACEI/ARB improve outcome in CHF and reduce
proteinuria. No evidence was found for increased cancer incidence in patients treated
with ARB. ACEI and ARB should not be used together!
- Renin inhibitors: Aliskiren in monotherapy reduces SBP/DBP in younger and elderly
patients; greater antihypertensive effect when given in combination with a thiazide
diuretic, a blocker of RAS at other sites or a calcium antagonist. Prolonged
administration in combination treatment can have a favorable effect on asymptomatic
organ damage (urinary protein excretion) or on prognostic biomarkers for CHF (BPNP).
Centrally active agents and alpha-receptor blockers are often used in multiple drug
combinations and not as a first-line therapy.
- Do not combine Aliskiren with ACEI/ARBs in patients with CKD and DM
Journal of Hypertension 2013;31:1281-1357 http://www.eshonline.org/Guidelines/ArterialHypertension.aspx
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DRUG THERAPY:
Chlorthalidone more effective than HCTZ
Increases risk of new onset diabetes mellitus (NOD) by 3%; benefit outweights the risk
Long-term BP befefit is due to direct vasodilation.
If creatinine > 2 or GFR < 35mL/min/1.73m2 use loop diuretic
All B-Blockers & clonidine cause rebound HTN if suddenly stopped.
Look for compelling indications to assist in drug selection
COMPELLING INDICATIONS:
o Diabetes with proteinuria - BP goal < 130/80 mmHg
o ACEI dilates efferent arteriole and blocks vasoconstriction ANGIOTENSIN II
BLOCKER (ARB) - blocks vasoconstriction
o VERAPAMIL, DILTIAZEM dilate afferent arteriole
o Systolic Cardiac Dysfunction ACEI, ANGIOTENSIN II BLOCKER,
DIURETIC
o Isolated Systolic HTN Elderly DIURETIC, ACEI, BETA BLOCKER,
ISORDIL (arterial), DIHYDROPYRIDINE CCB (improves survival in the
elderly)
o CAD - BETA BLOCKER, ACEI, ALDOSTERONE ANTAGONIST
o Tachyarrhythmias BETA-BLOCKERS, VERAPAMIL, DILTIAZEM
o Preoperative HTN BETA BLOCKER, ALPHA AGONIST
o Diastolic cardiac dysfunction BETA BLOCKER, VERAPAMIL/DILTIAZEM,
ACEI, DIURETIC
o Recurrent stroke prevention DIURETIC, ACEI/ARB, AMLODIPINE. AVOID
BETA BLOCKER as monotherapy
o Migraine headache BETA BLOCKER, CALCIUM BLOCKER (CCB)
o Aortic dissecting aneurysm LABETALOL, BETA BLOCKER, DILTIAZEM
o Erectile Dysfunction ARB/ACEI, CCB. Avoid DIURETIC or BETA
BLOCKER
o Benign prostatic hypertrophy ALPHA BLOCKER - Not monotherapy - less
effective
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o Refractory HTN CCB + ACEI + LOOP DIURETIC +VASODILATING BETA

BLOCKER + SPIROLACTONE + MINOXIDIL
o Athlete ACEI/ARB - AVOID -BLOCKER and DIURETIC
o African-American CALCIUM BLOCKER, thiazide-type DIURETIC. ACEI
decreases proteinuria, rate of decline in GFR (AASK Trial).
o Women of childbearing age / Pregnancy - METHYLDOPA, HYDRALAZINE,
LABETALOL, DILTIAZEM (also reduces uterine contractions), CLONIDINE,
PRAZOSIN. Avoid ACEI/ARB and ATENOLOL in pregnancy.
ACE INHIBITOR IN RENAL INSUFFICIENCY

If the baseline creatinine >1.4 mg/dl and creatinine increases by >30% within 2
months of starting therapy, or if the K increases to >5 mg/mL, then the ACEI must
should be discontinued.
ORTHOSTATIC HYPOTENSION
o Defined as a drop in systolic BP > 20 mmHg or diastolic BP > 10 mmHg.
o Measure BP after 5 minutes supine and at 1and 3minutes after standing
o Hypotension without increase in HR (<10 beats/min) suggests drug effect or
autonomic impairment.
o HR increase > 30 beats/min suggest hypovolemia.
o More common in the elderly
o Results from pooling of 0.5-1liter of blood
NATURAL MEDICATIONS which cause HTN
o Aniseed, mate, St Johns wort, capsicum, cola alkaloids, parsley, blue cohosh,
vervain, agnus cactus, calamus amines, broom alkaloids, bay berry, licorice,
ginseng, guarana, Ma Huang, Pau de Arco, coltsfoot, gentian, ginger
NATURAL MEDICATIONS which cause HYPOTENSION
o Argimony, calamus, celery, corn silk, garlic, ginger, hawthorn, mistletoe, nettle,
sage, wild carrot, yarrow, squill, pokeroot, ginseng, Coenzyme Q10, L- arginine,
goldenseal.
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ISOLATED SYSTOLIC HYPERTENSION (ELDERLY)

o HTN mechanism related to arterial stiffness due to degeneration and hyperplasia
of elastic arteries.
o Elderly patient is greater than 65 years old - BP goal <140/90 mmHg
o Treatment decreases all-cause mortality and reduces stroke incidence.
o Always check BP seated, thenstandingto exclude orthostatic hypotension.
o Avoid lowering DBP < 60-65 mmHg (J shaped curve) in patients with CAD.
o Lifestyle modifications helpful at all ages.
o A decrease in SBP of 20 mmHg or a decrease in DBP of 5 mmHg is beneficial, if
unable to achieve the goal BP, due to either a low DBP or the development of
orthostatic hypotension, or the development of symptoms of weakness or
confusion.
o Start therapy with one drug: Thiazide diuretic, Amlodipine, ACEI / ARB, blocker. Nitrates (reduces arterial stiffness)
ISOLATED SYSTOLIC HYPERTENSION in the VERY ELDERLY

o Very elderly patient is at least 80 years old
o BP goal 150/80 mmHg.- Rx reduces CVA risk. (HYVET Trial)
PSEUDOHYPERTENSION:
o Pseudohypertension is caused by artificial elevation of the Korotoff sounds
above the real SBP due to stiff, non-collapsable arterial walls with aging.
o Suspect Pseudohypertension if:
Symptoms are produced with mild SBP lowering
High SBP is documented but no signs of end-organ damage evident
Demonstration of a non-collapsable, non-pulsilitle radial pulse with
increasing pressure in the BP cuff (Oslers Maneuver)
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CLASSIFICATION: HYPERTENSION FOR AGE < 18 yo

o 1-3% pediatric age patients have HTN
o Prehypertension = average systolic and/or diastolic BP >90th but less than the
95th percentile for gender, age and height on 3evaluations.
o Hypertension = average systolic and/or diastolic BP >95th percentile for gender,
age and height on 3separate occasions.
o Stage 1 is the average BP ranging from >95th to 5 mmHg above the 99th
percentile for gender age and height.
o Stage 2 is the average BP >5 mmHg above the 99th percentile for gender age and
height. These patients require further evaluation within 1week.
o Therapy:
Lifestyle: Low salt diet, DASH diet, exercise, weight loss
Medications: ACEI, ARB, B-blocker, CCB, diuretics.
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Heart, Lung, and Blood Institute The
Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents, 2005
RESISTANT HYPERTENSION:
o Defined: HTN despite 3 or more drugs, including a diuretic and BP still > 140/90
mmHg or controlled on 4 drugs to < 140/90 mmHg
REFRACTORY HYPERTENSION:
o Defined: Uncontrolled HTN on 5 or more antihypertensive drugs with BP still >
140/90 mmHg or controlled on 4 drugs to < 140/90 mmHg
o Etiologies:
Non-adherence: Cost, patient education, drug side effects
Suboptimal therapy: Fluid retention, inadequate drug dosage
Exogenous drugs: Caffeine, cocaine, amphetamine, alcohol, nicotine,
NSAIDS, steroids, oral contraceptives, nasal decongestants, erythropoietin,
herbals (Ginseng, Ma Huang, Bitter Orange)
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66
Secondary HTN: Sleep apnea, renal disease, endocrine disease, obesity,

coarctation of the aorta, pheochromocytoma, renal artery stenosis.
o Prognosis: Higher risk: up to 3 x higher CV Events compared to Non-resistant
HTN
CV events: CVA, MI, CHF, Vascular Dementia
Target organ damage: CAD, LVH, CKD, Albuminuria
2 x Framingham CAD Score vs essential HTN
o Therapy:
Consider volume overload, high catecholamine levels and high aldosterone
levels.
Start with CCB + ACEI or ARB
Change from HCTZ to chlorthalidone or loop diuretics. Furosemide and
Bumetanide as BID drugs, Torsemide can be used daily.
Change to vasodilating beta blockers (carvedilol, labetalol, nebivolol)
Initiate spironolactone - after checking aldosterone/ renin ratio,
Finally consider: hydralazine, clonidine, minoxidil
Renal denervation has not been proven to reduce BP in patients with resistant
HTN (SIMPLICITY HTN-3 trial 2014)
Hypertensive Emergency:
Severe elevations in BP associated with progressive target organ damage.
Hypertensive Urgency:
Severe elevations in BP associated with target organ damage but no evidence of
progressive target organ damage
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67
TABLE of CONTENTS
HYPERTENSIVE EMERGENCY
>210/110 mmHg *
HTN
ENCEPHALOPATHY
UNSTABLE
or
ANGINA
CHF
AORTIC
DISSECTION
ISCHEMIC CVA
ACUTE MENTAL
CHANGES
+
PAPILLEDEMA
LOWER BP TO
CONTROL
SYMPTOMS
LOWER BP TO
CONTROL
SYMPTOMS
LOWER MAP 20%
IV NITRO
NO DIURETICS
or
LOWER SBP TO
90-100 mmHg
IV NITRO
LASIX
LABETOLOL
or
or
or
LABETOLOL
ENALAPRILAT
MITROPRUSSIDE
or
or
IV DILTIAZEM
ESMOLOL
NOTROPRUSSIDE
(if asthma)
IV LABETOLOL
* The patient with BP > 210/120 mmHg without symptoms or abnormal physical findings
with chronic hypertension may be treated with oral agents, observed for 2-3 hours for
effect in the office or ER and then followed closely as outpatient.
68
HYPERTENSIVE EMERGENCIES
CLASS
DRUG
DOSAGE
ONSET
0.25-10
ADVANTAGES
DISADVANTAGES
ENCEPHALOPATHY
NAUSEA
SODIUM
mcg/kg/min
CVA
TWITCH
NITROPRUSSIDE
MAX DOSE
INSTANTANEOUS
CHF
THIOCYANATE TOXICITY
10 min
POST-OP HTN
CYANIDE TOXICITY
RENAL FAILURE with
PARENTERAL
VASODILATORS
ENALAPRILAR
0.625-1.25
15-60 min
ENCEPHALOPATHY
BILATERAL RENAL ARTERY
CHF
STENOSIS
CHF
TACHYCARDIA
mg q 6 hrs
HYPOTENSION
HYDRALAZINE
10-20 mg IV
10 min
BOLUS
ECLAMPSIA
10-40 mg IV
20-30 min
20-80 mg q
5-10 min
HEADACHE
INCREASED ANGINA
AO DISSECTION
LABETOLOL
10 min
PARENTERAL
MI
ENCEPHALOPATHY
HEART BLOCK
CVA
BRONCHOCONSTRICTION
ANGINA
HYPOTENSION
ADRENERGIC
2 mg/min
INHIBITORS
infusion
ECLAMPSIA
PHEOCHROMOCYT
OMA
LABETOLOL
200-400 mg
30-120 min
q 2-3 hrs
ANGINA
ECLAMPSIA
HEART BLOCKE
HYPOTENSION
BRONCHOCONSTRICTION
CHF
RENAL FAILURE
ENCEPHALOPATHY
DRY MOUTH
ORAL AGENTS
CAPTOPRIL
25 mg PRN
CLONIDINE
0.1-0.2 mg
15-30 min
PO q 1 hr
30-60 min
MAX DOSE
DRUG
DROWSY
WITHDRAWAL
HYPOTENSION
0.6 mg
Sublingual captopril and clonidine have some pharmacokinetic and phamacodynamic profile as
oral route. Use with care in patients with coronary or cerebral vascular disease.
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69
HYPERTENSION RX DURING
PREGNANCY
Risk factors of pregnancy-induced hypertension: obesity, age > 40 yo, chronic HTN,
personal or family history of preeclampsia, gestational HTN, nulliparity, multiple
pregnancies, pre-existing vascular disease, collagen vascular disease, diabetes, renal
disease.
Severe hypertension per JNC VII: BP 160/110 mmHg (high risk of stroke and
eclampsia).
BP goal during pregnancy: 130-155/80-105 mmHg.
Prevention of eclampsia recommendations:
o Women with chronic primary or secondary hypertension, or previous pregnancyrelated hypertension, should take low dose aspirin from the 12th week of gestation
until delivery.
o Calcium supplementation (of at least 1g/d, orally) should be considered for
women with low dietary intake of calcium ( <600 mg/d) to prevent preeclampsia.
Treatment of hypertension in pregnancy and postpartum recommendations:
o Severe hypertension in pregnancy should be treated with safe and effective
antihypertensive medications such as methyldopa, labetalol and nifedipine, with
consideration of maternal and fetal side effects.
o Atenolol, ARB's and direct renin inhibitors are contraindicated in pregnancy and
should not be used
o Because of the increased risk of future hypertension and stroke one to 30 years
after delivery in women with a history of preeclampsia it is reasonable to:
-
Consider evaluating all women starting 6 months to the one year

postpartum, as well as those who are past childbearing age, for a history of
preeclampsia/eclampsia,
and
document
their
history
of
preeclampsia/eclampsia as a risk factor

-
Evaluate and treat for cardiovascular risk factors including hypertension,

obesity, smoking and dyslipidemia.
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70
o After giving birth, women with chronic hypertension should be continued on

their antihypertensive regime, with dosage adjustments to reflect the decrease in
volume of distribution and glomerular filtration rate that occurs following
delivery, They should also be
monitored carefully for the development of
postpartum preeclampsia.
Adapted from: Guidelines for the Prevention of Stroke in Women A Statement for Healthcare
Professionals From the American Heart Association/American Stroke Association.C Bushnell,
LD McCullough, IA Awad et al. Stroke. 2014; 45.
DOI: 10.1161/01.str.0000442009.06663.48
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71
CARDIOVASCULAR DISEASE
SCREENING
The Framingham Risk Score
-
Intended for Adults 20 yo without history of heart disease or diabetes.
Framingham 10 year risk score for developing CAD events

HIGH RISK
>20% 10 year absolute risk
INTERMEDIATE RISK
10-20% 10 year absolute risk
LOW RISK
<10% 10 year absolute risk
http://cvdrisk.nhlbi.nih.gov/calculator.asp
Determine Framingham Risk Score

Risk factor Age men/women
Age (years)
Men
Women
20-34
-9
-7
35-39
-4
-3
40-44
45-49
50-54
55-59
60-64
10
10
65-69
11
12
70-74
12
14
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72
Risk factor Total Cholesterol (mg/dL) men/women

TC
Age 20-39
40-49
50-59
60-69
70-79
<160
0/0
0/0
0/0
0/0
0/0
160-199
4/4
3/3
2/2
1/1
0/1
200-239
7/8
5/6
3/4
1/2
0/1
240-279
9/11
6/8
4/5
2/3
>280
11/13
8/10
5/7
3/4
1/2
Risk factor Systolic Blood Pressure (mmHg) men/women

SBP
No Rx
Rx
< 120
0/0
0/0
120-129
0/1
1/3
130-139
1/2
2/4
140-159
1/3
2/5
>160
2/4
3/6
Risk factor Smoking men/women

Age 20-39
40-49
50-59
60-69
70-79
NO
0/0
0/0
0/0
0/0
0/0
YES
8/9
5/7
3/4
1/2
1/1
Risk factor HDL-C (mg/dL) men/women

HDL-C
Men
Women
<40
41-49
50-59
>60
-1
-1
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73
Determine your patients 10-year absolute risk of CHD

Risk level
Men
Women
High (>20%)
>15 points
>20 points
Intermediate (10-20%)
12-14 points
20-22 points
Low (<10%)
0-11 points
-9-19 points
The greater the Absolute 10 year CHD Risk, the more aggressive therapy should be.
Severity of angina does not correlate with anatomic severity, therefore need to risk
stratify angina patients
2013 10-Year ASCVD* Risk Estimator

Determine the 10-year risk estimates for individuals 40-79 years of age
Male
Gender
20-79 yo
Age
Race
Female
White
African-American
HDL-C (mg/dL)
20-100
Total-C (mg/dL)
130-320
Diabetes
Yes
Other
No
90-200
Systolic BP (mmHg)
Treatment for HTN
Yes
No
Smoker
Yes
No
*10-year and lifetime risks for AtheroScleroticCardioVascular Disease using the pooled Cohort Equations
Available at:
http://tools.cardiosource.org/ASCVD-Risk-Estimator/ or as
ASCVD Risk App from iTunes or GooglePlay
https://itunes.apple.com/us/app/ascvd-risk-estimator/id808875968?mt=8
https://play.google.com/store/apps/details?id=org.acc.cvrisk&hl=en
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74
Pretest Probability of CHD patients with chest pain according to age, gender
and symptoms
Age
30-39 yo
40-49
50-59
60-69
Nonanginal pain
Atypical angina
Typical angina
Men
4
13
20
27
Men
34
51
65
72
Men
76
87
93
94
Women
2
3
7
14
Women
12
22
31
51
Women
26
55
73
86
UpToDate Adapted from Diamond GA, Forrester JS N - Engl J Med 1979; 300:1350 and Weiner DA, Ryan TJ - N Engl J Med 1979
Traditional Risk Factors

Hypertension
Hyperlipidemia
Hyperlipidemia
Obesity
Smoking
Physical inactivity
Psychological stress (anxiety, depression, socioeconomic disadvantages)
Novel Risk Factors

The US Preventive Services Task Force and the American College of Preventive
Medicine (ACPM) do not recommend the use of the following non-traditional risk factor
for routine screening of asymptomatic adults with no history of CHD
o
Hs-CRP (high-sensitivity C-reactive protein)
ABI (ankle-brachial index)
Leukocyte count
Fasting blood glucose level
Carotid intima-media thickening
Coronary artery calcium score
Homocysteine level
Lipoprotein (a) level

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75
Non-Invasive Testing
EKG: US Preventive Services recommend against routine screening using resting or
exercise EKG in asymptomatic adults. However if symptoms of CP, perform EKG.
Exercise stress test: ACC/AHA 2002 recommends it as the initial stress test of choice in
patients undergoing evaluation for suspected or known CAD. Patients need to have a
normal baseline EKG and can exercise to the maximum predicted HR (220 minus
patients age). A negative test rules out proximal large vessel CAD.
Exercise stress test with imaging (exercise-echo, exercise-MPI)
Electron-Beam Computed Tomography Scan Coronary Artery Calcium Score:
measure of coronary artery burden hat correlates with the presence of atherosclerosis.
EBCT does not predict the degree of plaque obstruction or risk of plaque rupture.
Not a good screening test, except possibly in the intermediate risk primary
prevention group who has a CHD event risk in he 10-20% by the Framingham Risk
profile. CAC score>300 = high risk for future CHD events.
Computed Tomography Angiography: CTA identifies coronary anatomy with the
highest sensitivity (83-99%) and specificity (93-98%). CTA can identify plaque type as
well as the degree of stenosis. It defines calcified obstructive plaques and smaller noncalcified plaques. Beta-blockers are often needed to maintain a slow heart rate.CTA is
limited by the presence of coronary calcium, renal insufficiency, marked obesity and
metallic interference from coronary stents. CTA delivers twice the radiation dose as
invasive angiography. It outperforms MRI with higher sensitivity with comparable
sensitivity. CTA has a high negative predictive value (95-100%) and in stable patients
with low pretest likelihood of CAD can be used to exclude coronary stenosis. In higher
risk patients, CTA should not replace invasive angiography. Often used to screen patients
with a borderline exercise stress test or MPS study to decide if invasive therapy is
required.
Cardiac Magnetic Resonance Imaging Study: measures myocardial perfusion, cardiac
function and myocardial viability. It has superior resolution compared with myocardial
nuclear scanning and echocardiography. Study limitations: tortuosity and small diameter
of coronary arteries, constant cardiac motion surrounding adjacent signal artifact.
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76
Invasive testing
Coronary angiography (2014 ACC/AHA Guidelines)
-
Patients with presumed SIHD who have unacceptable ischemic symptoms despite GDMT
and who are amenable to, and candidates for, coronary revascularization.
To define the extent and severity of coronary artery disease (CAD) in patients with
suspected SIHD whose clinical characteristics and results of non-invasive testing indicate
a high likelihood of severe IHD and who are amenable to angioplasty or coronary
revascularization
Patients with suspected symptomatic SIHD who cannotundergo diagnostic stress testing,
or have indeterminate or nondiagnostic stress tests, when there is a high likelihood that
the findings will result in important changes to therapy.
Patients with stress test results of acceptable qualitythat do not suggest the presence of
CAD when clinical suspicion of CAD remains high and there is ahigh likelihood that the
findings will result in important changes to therapy.
COURAGE Trial (2007) demonstrates no advantage to undergo angiography and

angioplasty if ischemic chest pain can be contolled with medications - similar infarction
and death rates. (N Engl J Med 2007; 356:1503-1516April 12, 2007DOI: 10.1056/NEJMoa070829)
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77
LIFESTYLE / ASA THERAPY

Control all risk factors (see chapters on HTN, hyperlipidemia).
Lifestyle modifications are EFFECTIVE in all age groups
ACC/AHA 2013 guideline on lifestyle management to reduce CV risk
o Diet
Follow: DASH dietary pattern / USDA Food pattern / AHA diet
Reduce percent of calories from saturated fat (goal 5-6% of calories from
saturated fat)
Reduce percent of calories from trans-fat.
Lower sodium intake < 2400 mg sodium/day, desirable < 1500 mg/day in
patients with HTN.
o Physical activity (engage in moderate-to-vigorous intensity aerobic activity,
lasting on average 40 minutes/session, 3-4 times a week; cardiac rehabilitation
programs)
o Weigh management (goal BMI 18.5-24.9 kg.m2, waist circumference < 40 inches
in men and < 35 inches in women)
o Limit alcohol consumption
o Smoking cessation counseling (including exposure to environmental tobacco
smoke)
Pharmacotherapy or psychotherapy for patients suffering from depression, anxiety.
ASA:
o Most current clinical guidelines consider that routine use of aspirin for primary
prevenetion is not recommended.
o FDA 2014 recommends against use of ASA for primary prevention in patients
without history of CVD (CAD, stroke, PAD)
o AAFP (2011): ASA 81 mg daily should be considered for primary prevention in
men 45-59 yo with a 10-year risk score > 4%, men 60-60 yo with 10-year risk
score >9% and in men 70-79 yo with a 10-year risk score > 12%.
o AAFP (2011): ASA 81 mg daily should be considered for primary prevention in
women ages 50-59 with a 10-year stroke risk >3%, women ages 60-69 with a 10year stroke risk>8% and in women ages 70-79 with a 10-year stroke risk >11%.
o USPSTF (2009) recommends the use of ASA 81 mg daily for primary prevention
in women ages 55-79 with increased 10-year stroke risk score. No ASA in women
< 50 yo.
o USPSTF (2009) recommends the use of ASA 81 mg daily for primary prevention
in men ages 45-79 with increased 10-year CVD-risk score.
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78
STABLE ANGINA PECTORIS

2014 ACC/AHA/AATS/PCNA/SCAI/STS Guidelines
J Am Coll Cardiol 2014: 64:18;1929-1944
ISCHEMIC HEART DISEASE
o Chronic Coronary Syndrome (CCS)
o Acute Coronary Syndrome (ACS)
o Unstable angina
o STEMI - ST segment elevation MI
o NSTEMI - Non ST segment elevation MI
PREDICTORS OF SURVIVAL
o Plaque anatomy (Cholesterol / Fibrous cap / Inflammation)
o Ischemic potential
o LV function (EF < 35%)
o Malignant ventricular arrhythmias
DIAGNOSIS / HISTORY
o Define typical / atypical / noncardiac pain
o Predictable anginal onset (Obstructive Angina) ST depression
o Rest anginal onset (Spasm angina) ST elevation
o Variable anginal onset (Obstructive/spasm angina) ST depression
o Evaluate anginal aggravating factors, frequency, severity and duration of attacks.
o Aggravating factors: mental stress, anemia, fever, pain, increased physical
activity, medicine nonadherance
o Arm exercise produces anginal events more than leg exercise, especially if
activity done above the shoulder level.
o Anginal duration > with mental stress than with physical exercise.
o Anginal equivalents: unexplained fatigue, shortness of breath, dizziness, presyncope, nausea
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79
TREATMENT (2013-2014 ACC/AHA Guidelines)

Patient education
o Lifestyle modifications is EFFECTIVE in all age groups
o Diet
- (DASH dietary pattern/ USDA Food pattern / AHA diet)

- Reduce percent of calories from saturated fat (goal 5-6% of
calories from saturated fat)
- Reduce percent of calories from trans-fat.
- Lower sodium intake< 2400 mg sodium/day, desirable < 1500
mg/day in patients with HTN, reduce intake by at least 1000
mg/daily even if the esired daily sodium intake is not yet achieved.
o Physical activity (average 40 minutes of moderate-to-vigorous intensity

aerobic activity at least 4 times a week; cardiac rehabilitation programs)
o Weigh management (goal BMI 18.5-24.9 kg.m2, waist circumference < 40
inches in men and < 35 inches in women)
o Limit alcohol consumption
o Smoking cessation counseling (including exposure to environmental
tobacco smoke)
o Risk factors management:
o Lipid management: all patients should receive high-intensity statins
unless contraindicated (see 2013 ACC/AHA hyperlipidemia guidelines)
o BP management (in patients with CAD and BP> 140/90, antihypertensive
therapy should be instituted in addition to or after a trial of lifestyle
modifications)
o Diabetes management
o Management for psychological factors: depression
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80
Medical therapy
o Primary survival advantage:
o ASA 75-162 mg daily indefinitely unless contraindicated. Decreases CAD
events in men; decreases CVA in women.
o Clopidogrel 75 mg daily, if ASA is contraindicated.
o ASA + Clopidogrel 75 mg daily/Ticagrelor 90mg BID up to 12 months
post MI or stent placement.
o Secondary survival advantage medications:
o ASA; if warfarin required and high bleeding risk withhold ASA
o Beta-blocker - Class effect, at least 1 year after MI, should be continued for
3 years. Should be used in all patients with systolic dysfunction (LVEF
40%), with systolic heart failure or prior MI, unless contraindicated. Use
limited only to carvedilol, metoprolol succinate, and bisoprolol: have been
shown to reduce risk of death.
o Statin: high-intensity level in all patients unless contraindicated or unable to

tolerate.
o ACEI in CAD patients, especially in patients with HTN, systolic dysfunction

(LVEF 40%) with or without symptoms, CKD and diabetics with
proteinuria). If ACEI cannot be tolerated use ARBs.
o Calcium channel blockers: Diltiazem, verapamil do not improve survival

- use if cannot tolerate beta-blocker due to severe depression, brittle
diabetes, asthma. Do not combine with beta-blocker, as both are negative
inotropic and slow AV conduction. Avoid with significant systolic heart
failure.
- Long-term dihydropyridine (amlodipine, nifedipine) do not improve
survival. Nifedipine increases mortality post MI. Use only in stable
angina, if cannot tolerate beta-blocker (acute HF, SA or AV node disease).
These agents combine well with beta-blockers in stable angina if need
extra anginal or BP control.
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81
o If SA or AV nodal disease use amlodipine, nifedipine or nitrates. The

height of the systolic BP will determine the best agent to use. (nifedipine >
amlodipine > nitrates lowers SBP).
o Other medications:
o Estrogen therapy is not recommended in postmenopausal women with
SIHD with the intent of reducing CV risk or improving clinical outcomes.
o Vitamin C, vitamin E, beta-caroten supplementation are not recommended
in patients with SIHD to reduce CV risk of improving clinical outcomes.
o Treatment of elevated homocysteine with folate or vitamins B6 and B 12
is not recommended with the intent of reducing CV risk or improving
clinical outcomes.
o Other therapies:
Chelation therapy: series of intravenous infusions of disodium ethylene
diaminetetraacetic acid (EDTA) in combination with other substances to
improve blood flow in atherosclerotic vessels, treating angina and
preventing cardiac events. Per 2014 ACC/AHA guidelines, the usefulness
of chelation therapy is uncertain for reducing cardiovascular events in
patients with SIHD.
Indications for Heart Catheterization:

o Stable angina pectoris:
Failed medical therapy (patient needs to be on OMT (optimal
medical therapy)
High-risk history or high-risk treadmill markers
History of near sudden death, malignant ventricular arrhythmias
Unclear medical diagnosis of chest pain or heart failure.
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82
INTERVENTIONAL THERAPY IN STABLE ANGINA

PCI
o Does not prevent MI or improve survival compared to medical therapy in stable
angina. It does improve the frequency of angina.
o An average of 20 lesions are noted in each coronary vessel by intravascular
ultrasound (IVUS).
o Treatment of choice for single vessel disease.
o Good Rx for 2-3vessel coronary disease in non-diabetics. (PCI = CABG in
survival, but more repeat procedures required with PCI. CABG > PCI in symptom
control.)
o In diabetics, CABG more effective than PCI in multi-vessel disease
STENT
o Decreases early thrombosis by 30% (decreases acute recoil, but increases
neointimal hyperplasia)
o MRIis safe @ 8 weeks post insertion.
o Bare metal stents require dual ASA + Clopidogrel 75 mg daily/Prasugrel 10 mg
daily/Ticagrelor 90 mg BID for at least 1 year with DES and up to 12 months
with BMS. May be beneficial up to 18 months.
o Drug eluting stents (DES) require dual Rx for at least 1 year. Mat be beneficial
up to 18 months.
o DES
decreases
thrombosis
potential
but
also
delays
spontaneous
endothelialization requiring prolonged dual antiplatelet therapy.

o Transient distal embolic microvascular disease & vasospasm are produced by
PCI. It is clinically benign but causes an abnormal thallium study in first few
months post PCI. Perform thallium post stent placement only if recurrent angina
or CHF.
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83
CABG: - for symptom control, survival but not to decrease MI

o Symptom control:
o Failed medical therapy with coronary obstruction > 75%.
o Diabetes mellitus with double or triple vessel disease.
o Unsuitable anatomy for PCI.
o Increased survival:
o Left main disease >50% disease.
o Left main equivalent.
o 3vessel disease >70%.
o 2 vessel disease >95% with proximal LAD and poor LV function.
o Outcome:
o 15% occlusion of vein grafts @ 1yr.
o 60% patency of SVG grafts @ 10 yrs: LAD > RCA = CIRC.
o 85% patency of IMA grafts @ 10 yrs.
o Survival still increased @ 15 yrs but recurrent angina is common.
o 2014 ACC/AHA guidelines recommendations:
o A Heart Team approach to revascularization is recommended in patients
with diabetes mellitus and complex multivessel CAD.
o CABG is generally recommended in preference to PCI to improve survival
in patients with diabetes mellitus and multivessel CAD for which
revascularization is likely to improve survival (3- vessel CAD or complex
2-vessel CAD involving the proximal LAD), particularly if a LIMA graft
can be anastomosed to the LAD artery, provided the patient is a good
candidate for surgery.
HYBRID CORONARY REVASCULARIZATION
o Planned combination of LIMA-to-LAD artery grafting and PCI of 1 non-LAD
coronary arteries is reasonable if: poor target vessels for CABG, lack of suitable
grafts, unfavorable LAD for PCI (vessel tortuosity or chronic total occlusion).
o Planned combination of LIMA-to-LAD and PCI non-LAD coronary arteries
may be reasonable as an alternative to multivessel PCI or CABG.
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84
ALTERNATIVE THERAPIES - Intractable Angina 5-15% patients

o Ranolazine (Ranexa): A sustained-release selective inhibitor of the late
sodium current that is approved for refractory angina. Can be useful in
combination with beta-blockers to relieve symptoms in patients in whom initial
treatment with beta-blockers is unsuccessful. It decreases left ventricular end
diastolic pressure and increases ejection fraction with no effect on heart rate or
blood pressure. It is contraindicated with a prolonged QT interval, in patients
taking drugs that prolong QT interval and with hepatic impairment. It is
extensively metabolized by the CYP3A4 system. It interacts with diltiazem,
verapamil, macrolide antibiotics, digoxin and simvastatin. The starting dose is
500 mg twice daily.
o Enhanced external counterpulsation (EECP): EECP consists of application of
pneumatic cuffs applied to the lower extremities that sequentially inflate during
diastole and deflate during systole to augment coronary filling and reduce LV
afterload. This improves angina, QOL, exercise capacity. Benefit persists up to 3
years. An outpatient procedure consisting of daily 1hour sessions for 7weeks. Per
2014 ACC/AHA Guidelines, EECP may be considered for relief of refractory
angina in patients with SIHD.
ANTI-ANGINAL THERAPY
Drug
Anti-anginal
Cardio
SA/AV nodal
Negative
protective
delay
inotrope
Beta-blocker #
++
Verapamil
No
Diltiazem
No
Nifedipine XL*
No
No
+/-
Amlodipine
No
No
No
Nitrates
No
No
No
# Improves survival in patients with angina post MI

*Indication: SPASM ANGINA or FIXED ANGINA ASSOCIATED WITH SA / AV NODAL DISEASE or acute
CHF. SHORT ACTING Nifedipine SHOULD BE AVOIDED.
NIFEDIPINE > AMLODIPINE > NITRATES LOWER SBP
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85
TRIPLE ANTICOAGULATION THERAPY - (STENT + Atrial fibrillation)

o Warfarin therapy is an alternative option to ASA in CAD, but does not prevent
coronary stent thrombosis.
o Clopidogrel/Prasugrel/Ticagrelorare more effective than ASA in preventing stent
thrombosis.
o Triple therapy increases the bleeding risk by 3-6%.
o Double or triple therapy requires H2 blocker therapy.
o The prudent use of triple therapy remains a balance between the risks of embolism
versus the risks of bleeding.
o If low risk of bleeding, continue triple therapy for 1-3-6 months depending upon
which type of stent (BMS, sirolimus or paclitaxel).
o During triple therapy INR goal for AF should be limited to 2.0-2.5.
o If
high
risk
of
bleeding
but
low
AF
embolic
risk,
use
ASA
clopidogrel/Prasugrel/Ticagrelor for 1-3-6 months. Avoid warfarin.

o If high risk of bleeding and high AF embolic risk, employ bare stent. Use triple
therapy for 1month and continue warfarin longterm.
o Consider bare metal stents (BMS) if: early surgery required (pospone at least 1month
post stent placement), coagulopathy present, cost prohibitive, medicine nonadherance.
o If high risk of bleeding, high AF embolic risk and drug eluting stent was placed use
triple therapy for 1 month, then continue warfarin + clopidogrel/Effient for 3-6
months depending upon type of DES placed. High bleeding risk include prior GI
bleeding, advanced age, concurrent anticoagulants, NSAIDS, positive H pylori.
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86
CAD in WOMEN
CVD is the leading cause of mortality in women.
AHA recommends for the risk assessment of CVD (10-years FRS) in women to begin at
age 20, classifying women in 3 categories:
o 1. Ideal cardiovascular health
o 2. At risk
o 3. At high risk.
There are racial/ethnic differences in risk factors, with black and Hispanic women
having a higher prevalence of hypertension and diabetes. The highest CVD morbidity and
mortality occurs in black women.
Autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis) and
preeclampsia are significant risk factors for CVD in women.
Psychological stress (anxiety, depression) and socioeconomic disadvantages are
associated with a higher CVD risk in women.
Microvascular disease with endothelial dysfunction also known as female pattern disease
or cardiac syndrome X, is the etiology of ischemia in more women than men. Cardiac
catheterization is normal with persistent CAD symptoms.
Women are more likely to have atypical cardiovascular symptoms such as: sudden or
extreme fatigue, dyspnea of unclear etiology, sleep disturbances, anxiety, nausea,
vomiting, indigestion.
ACC/AHA guidelines recommend a routine exercise stress test as the initial evaluation in
symptomatic women who have a good exercise capacity and a normal baseline ECG.
Exercise stress perfusion study (MPS) or exercise echo should be reserved for
symptomatic women with higher pretest likelihood for CAD or indeterminate routine
testing.
Women often receive less medical therapy and lifestyle counseling than men.
After PCI procedure, women experience higher rate of complications and mortality than
men.
Management of stable CAD in women should be the same as in men and should include:
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87
ASA, beta-blocker, high-intensity statin, ACE inhibitor (EF<40%); nitrates, and calcium
channel blocker (CCB) for angina management.
In microvascular disease, beta-blockers have been shown to be superior to CCB for
angina management. Statins, ACE inhibitors, ranolazine, and exercise can improve
angina scores and endothelial dysfunction in female pattern disease. Short term trials ( <
6 months) have shown that L-arginine can also improve small vessel endothelial function
and angina class.
Takotsubo cardiomyopathy
Also known as the broken heart syndrome, apical ballooning syndrome or transient
left ventricular dysfunction syndrome
Occurs infrequently, < 0.02% of all hospital admissions in USA (2008)
Occurs mostly in older, postmenopausal women after a stressful event: emotional or
physical
Presentation mimics STEMI: chest pain, DOE, ST-segment elevation, T wave inversion
and Q waves, mildly elevated troponins, marked elevation of serum cathecolamines and
P-BNP
Initial management should be the same as an acute MI (follow code STEMI) until a
coronary angiogram is obtained
Coronary angiogram is usually normal or shows minimally obstructed coronary arteries
and regional wall motion dyskinesis or akinesis that extends beyond any single coronary
artery. LV outflow obstruction and systolic dysfunction are common.
Echocardiogram should be obtained for all patients with Takotsubo cardiomyopathy
Treatment: No specific guidelines. Beta-blockers should be started and continued longterm. ACEI/ARBs can be considered and continued until LV systolic dysfunction is
resolved. If suspicion of thrombus consider anticoagulation. If significant hypotension
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88
with outflow tract obstruction, phenylephrine may be effective. If cardiogenic shock:

inotropes and intra-aortic balloon counterpulsation.
Both systolic dysfunction and wall motion abnormalities are transient and should resolve
within 4-8 weeks. F/U with echocardiogram in 8-10 weeks.
Mortality rate < 2%, recurrence rate 10% in the first 4 years.
Complications: shock, thrombus, heart failure, CVA, VT, LV rupture, ventricular septal
rupture
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89
ACUTE CORONARY SYNDROME (UA/NSTEMI)

Initial Evaluation
Focused history/exam
EKG, CXR, Troponin I pending
(If EKG is non-diagnostic, repeat in 5 minutes)
VCMC Protocol
Initiate Therapy
ASA 325 mg chewed
NTG SL or IV if persistent or recurrent pain (usual
dose 5-200 micrograms/min)
Morphine
Beta-blocker (Metoprolol 5 mg IV every 5 min x 3)
Statin (Atorvastatin 80 mg)
*Discuss with Invasive Cardiologist if OK to initiate
Clopidogrel 300 mg / Ticagrelor 180 mg or
Enoxaparin 1 mg/kg q 12 hours- max dose 100
mg/dose
Low Clinical Risk
Low clinical pretest likelihood of CAD
New onset angina > 2 weeks
Crescendo angina @ high workload
Atypical chest pain
Normal EKG
Normal Troponin I > 6 hr
ED or Outpatient Rx
Exercise/Rest MPS
Higher Clinical Risk

Refractory ischemic chest pain
Recurrent or persistent ST deviation
Ventricular tachycardia
Hemodynamic instability
Heart failure or EF < 40%
Cardiogenic shock
H/o CABG or PCI
Age > 65 yo
Intermediate Risk
Ischemic pain resolved
No arrhythmias
Stable hemodynamics
No acute ST-T changes
DOU admission
HighRisk
Refractory ischemic pain
Persistent ST deviation
Ventricular tachycardia
Hemodynamic instability
HF/Cardiogenic shock
Call invasive cardiology for PCI (ask which
anticoagulant and antiplatelet agent to start)or
ICU admit
Continue drug therapy

ASA 81-160 mg daily indefinitely
NTG 0.4 mg SL every 5 min x 3 PRN for chest pain or IV if persistent or
recurrent pain (usual dose 5-200 micrograms/min)
Metoprolol 25-50 mg PO every 6 hr
High-intensity statin therapy
90 or
Clopidogrel 75 mg daily/Ticagrelor 90 mg BID/Prasugrel 10 mg daily
Enoxaparin 1 mg/kg q 12 hours max dose 100 mg/dose)
Add ACEI if HTN, HF, DM or EF < 40% day 2
ACUTE CORONARY SYNDROME (STEMI)

Initial Evaluation
Focused history/exam
EKG, CXR, Troponin I pending
(if EKG is non-diagnostic, repeat in 5 minutes)
Initiate Therapy
ASA 325 mg chewed
NTG SL or IV if persistent or recurrent pain (usual
dose 5-200 micrograms/min)
Morphine
Beta-blocker (Metoprolol 5 mg IV every 5 min x 3)
Statin (Atorvastatin 80 mg)
*Discuss with Invasive Cardiologist if OK to
initiateClopidogrel 300 mg / Prasugrel 60 mg /
Ticagrelor 180 mg or Enoxaparin 1 mg/kg q 12
hours- max dose 100 mg/dose
Add ACEI in the first 24 hrs in patients with anterior
wall location, HF or EF 40%
PCI-capable hospital
Initiate
Code STEMI
Send to cath lab for Primary
PCI if DTB time 90 min
Non-PCI capable hospital
Transfer for primary PCI

if DTB time 120mins
(Class I)
Administer fibrinolytic agent

within 30 mins of arrival if
DTB time > 120 mins
(Class I)
Post MI Therapy
Treadmill test prior to discharge if PCI is not performed
High risk TM-consider early PCI and medical therapy
Low risk TM-continue medical therapy
Long term medical therapy
ASA 81-325 mg daily
NTG 0.4mg SL every 5 min X 3PRN
Metoprolol 25-50 mg PO every 6 hrs
High-intensity statin
Clopidogrel 75 mg daily/Ticagrelor 90 mg BID/Prasugrel 10
mg daily
Continue ACEI in patients with anterior wall location, HF or
EF 40%. Switch to ARB if patient is intolerant to ACEI.
91
Risk Factor Management
ACUTE CORONARY SYNDROME

DX: HISTORY, PHYSICAL EXAM (S4, S3, rales)
TROPONIN I
In ACS is highly specific and sensitive.
If measured in non-ACS, patient sensitivity and specificity is low.
Troponin increased with pericarditis, myocarditis, HF, sepsis, exercise, tachyarrhythmias,
EP ablation, AICD discharge, cardioversion, renal failure, or Heterophilic antibodies.
Troponin levels are a poor marker of re-infarction due to long half-life.
CPK-MB levels are a better marker for re-infarction due to shorter half -life.
MARKER
SPECIFIC
INITIAL (hr)
PEAK (hr)
NORMALIZE
MYOGLOBIN
CPK-MB
TROPONIN I
+/+
++
2
6
6
6
18
18
10 hr
72hr
10 days
N-terminal BNP ELEVATION

Ischemia mildly elevates NT-BNP.
Flash pulmonary edema will produce slightly higher but still only mild elevations (only
small amounts stored in ventricular myocytes).
Shortness of breath with NT-BNP < 300pg/ml HF unlikely
Chronic systolic dysfunction produces levels NT-BNP:
Age < 50 yo HF likely if > 450 pg/ml
Age > 50 yo HF likely if > 900 pg/ml
NT-BNP is a powerful predictor of 30 days and 10-month mortality in ACS.
MI Classification (J AM Coll Cardiol 2012)
Type 1: Acute MI secondary to plaque disruption - most frequent
Type 2: Acute MI realted to increased demand or decreased supply (coronary spasm,
coronary embolus, profound anemia, arrhythmias, HTN, hypovolemia).
Type 3: Sudden unexpected cardiac death
Type 4a: MI related to PCI
Type 4b: MI related to coronary stent thrombosis
Type 5: MI related to CABG
Unstable angina or non-ST segment elevation MI(NSTEMI)
Clot is platelet rich and subtotally obstructive lesion.
ST segment elevation MI (STEMI)
Clot is fibrin rich and totally obstructive lesion.
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92
ACUTE CORONARY SYNDROME: 2009/2013 Guidelines

o Unstable angina (UA): - Chest pain + localized ST depression or T wave changes or
no EKG changes + negative cardiac enzymes. Subsets: New onset angina, crescendo
angina, angina at low workload, prolonged angina, spasm angina, post-MI angina.
TIMI High Risk Factors (7 RF): Age > 65 years, > 3CAD risk factors, coronary
stenosis >50%, ST segment deviation, 2 angnal episodes within 24 hours, use of ASA
in prior 7days, elevated troponin I levels. 14 Day Risk (mortality, MI and ischemia)
0/1= 4.7%; 2 = 8%; 3= 13%; 4 = 20%; 5 = 26%; 6/7= 40%
High risk: Medical therapy + Urgent Invasive Rx
Low risk: Medical therapy + Myocardial perfusion study (MPS)
o Acute Non-ST segment elevation MI(NSTEMI): - Chest pain + localized ST
depression or T wave changes+ abnormal cardiac enzymes.
High Risk: See TIMI High Risk Factors above. High risk Rx: Medical therapy +
urgent invasive Rx
Low risk Rx: Medical therapy + Delayed Invasive Rx (~48 hrs)
o Acute ST segment elevation MI (STEMI): - Chest pain, localized ST elevation +
abnormal cardiac enzymes. All STEMIpatients, if presenting within 12 hours,
should be considered for Urgent Invasive Rx. If it can be performed within 90
minutes + Medical therapy; if PCI unavailable consider thrombolysis + Medical Rx.
MEDICAL Rx TO STABILIZE PLAQUE - (UA, NSTEMI, STEMI)
o ANTI-PLATELET AGENTS
ASA 162-325 mg Chew STAT then 81-325 mg daily indefinite.
If allergic use Clopidogrel 75 mg daily
If stent employed extend, ASA 162-325 mg for 1-6 months.
P2Y12 Receptor inhibitors: CLOPIDOGREL/PRASUGREL/TICAGRELOR
-
Clopidogrel 300-600 mg, then 75 mg daily for at least12 months, longer therapy in DES
and high risk patients with DM or prior stent thrombosis ~ 18 months
Indicated: High-risk UA, NSTEMI, post stent placement, STEMI
Clopidogrel & ASA improves the combined endpoint of CV death rate, nonfatal MI and
stroke rate (CURE Trial)
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93
Clopidogrel is a pro-drug whoseactivation may be prevented by some PPI agents. Use

H2 blockers or possible Protonix.
Stop clopidogrel 7days before CABG or non-cardiac surgery.
-
Prasugrel 60 mg is the initial dose, then 10 mg daily for 1 year with DES, BMS.
Faster onset, a 2.2% absolute risk reduction in mortality, MI and stroke but a higher risk
of bleedingin patients with STEMI and prior stroke, TIA or ICH. Should not be
administered to patients with a history of prior stroke or TIA.
Special dosing (5 mg daily) for patients < 60 kg, or 75yo (generally not recommended)
Stop 7 days before surgery.
Ticagrelor180 mg, then 90 mg BID for at least 1 year with BMS more if DES.
ASA 81 mg is the preferred maintenance dose with Ticagrelor.
Stop 5 days before surgery.
GP IIb/IIIa INHIBITORS Glycoprotein platelet inhibitor (combine
with heparin)
PCI - If not adequately pre-loaded with clopidogrel
MI - high risk patient without pre-loaded with clopidogrel, patients having
thrombic complications (side branch closure) or if large thrombin burden
Renal dosed, eliminate infusion and safer in radial artery approach.
Abciximab 0.25mg/kg IV bolus, then 0.125mcg/kg/min (max 10mcg/min)
Tirofiban high-bolus dose 25mcg/kg IV bolus, then 0.15mcg/kg/mim; in
patients with CrCl<50mL/min reduce infusion by 50%.
o ANTI-THROMBIN AGENTS
Heparin (UFH) Recommended if renal failure or urgent CABG expected. Dose is
weight-adjusted at 60 U/kg (maximum 4,000 U), followed by infusion 12 U/ kg. Goal is
PTT 50-70 seconds. Continue for 48 hours.
Enoxaparin (Lovenox) - Decreases recurrent MI, ischemic events, revascularizations,
thrombocytopenia compared to UFH. Continue until hospital discharge.
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94
Fondaparinux - Less bleeding in UA/ NSTEMI patients compared with LMWH. Avoid
if creatinine > 3mg/dL or early PCI considered. Dosage: 2.5 mg IV, then 2.5 mg SQ
daily. Continue until hospital discharge. No advantage with STEMI.
THROMBOLYSIS: STEMI only (See VCMC ED Thrombolysis protocol)
Reteplase - variant of t-PA (rPA: 10 U repeat 10 U bolus in 30 minutes) + UFH (given
first) + ASA
Altaplase - recombinant t-PA (front loaded drip) + UFH + ASA
CLOPIDOGREL with thrombolysis is beneficial (CLARITY Trial).
Clinical Markers:
Sudden relief of pain
Reperfusion ventricular arrhythmias slow VT / PVCs
Early and peak CPK enzyme rise
Resolution of ST segment elevation
Complications:
Hypotension; Bleeding (minor 3% / major 0.3%); Death
Contraindications:
Previous hemorrhagic stroke; Ischemic or embolic CVA within one year,
Intracranial neoplasm, Active internal bleeding (not menses)
Aortic dissection
Relative contraindications:
Uncontrolled HTN >180/110 mmHg
Use of anticoagulation with INR >2; Coagulopathy
Recent trauma within 2-4 weeks; Major surgery <3weeks
Prolonged CPR >10 mins; Pregnancy
Active peptic ulcer; Recent history of internal bleeding within 2-4 weeks
Noncompressible vascular punctures
Prior streptokinase Rx (5 days to 2 year)
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95
MEDICAL Rx TO PREVENT REMODELING - UA, NSTEMI, STEMI

BETA-BLOCKER
Metoprolol 5 mg IV q 5 min X 3, if ongoing pain; PO if pain resolved, then 50 mg bid to
achieve beta blockade (HF 55 bpm).
Start only when patient is clinically stable.
Reduces HF, ventricular arrhythmias, sudden death, recurrent MI, cardiac rupture and
reduces mortality.
START UNLESS: HR< 60 bpm, SBP <100 mmHg, CHF, PR interval >0.24 secs., 2o or 3o
A-V block, asthma, severe peripheral vascular disease
Beta-blockers give additional benefit with diabetics.
ACE INHIBITOR
Start in the first 24 hours in all patients with STEMI with anterior location, HF, or
EF40%. Add if persistent HTN is present.
Very beneficial if systolic dysfunction, HF, DM is present.
ACE inhibitor may be beneficial in all CAD patients. (HOPE)
Improves overall survival, risk of HF, recurrent MI
USE UNLESS: SBP < 100 mmHg, or renal failure
ACE inhibitor can replaced with ARBs if patient is intolerant to ACEI.
STATIN
Started before discharge, optimally within first 24 hrs of admission
Employ Atorvastatin 80 mg stat & daily - (MIRACL Trial). Continue indefinitely with
high-intensity statin, unless contraindicated see Cholesterol chapter.
Statins decrease recurrent ischemic events, improve endothelial function, stabilize plaque,
decrease thrombogenicity, and reduce inflammation.
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96
PERCUTANEOUS CORONARY INTERVENTION FOR ACS - (PCI)

2013 ACC/AHA/ACAI Guidelines
Indications: All STEMI and high-risk ACS
First choice over thrombolysis if done within 90 mins, and if operator performs >75
PCIs /yr & if hospital >200 PCIs /yr
Treat culprit coronary lesion only (causing ischemia/infarction).
Stent reduces clinical and angiographic spasm and restenosis
Bare metal stent: continue P2Y12 Receptor inhibitors + ASA for 12 month
Drug eluding stent: (delayed risk of thrombosis) Sirolimus or Paclitaxel (Taxus).
Continue P2Y12 Receptor inhibitors + ASA for at least 12 months. DES have a decreased
need for repeat PCI compared to BMS.
Extend higher dose ASA at 162-325 mg/day for 1 month with BMS, 3 months with
sirolimus BMS and 6 month for paclitaxel BMS. ASA 81 mg is the preferred dose in
combination with Ticagrelor.
PCI-CURE & CREDO Trials recommend continuing clopidogrel for at least 12 months.
If atrial fibrillation present, triple therapy (warfarin, ASA, P2Y12 Receptor inhibitors)
should be continued in patients at low bleeding risk for 12 months; in patients at high
bleeding risk remain on triple therapy for the first month and continue P2Y12 Receptor
inhibitors and warfarin for the remaining 11 months (stop ASA).
OTHER MEDICAL THERAPY: (UA/NSTEMI/STEMI)
NITRATES SL / IV / Cutaneous
Indication: Angina, CHF, HTN.Small survival improvement by 5%.
GLYCEMIC CONTROL
-
Benefit only in a complicated AMI.
Hyperglycemia is associated with increased levels of inflammatory markers and is an

independent predictor of mortality in AMI. . Intensive glycemic control (BS goal < 150
mg/dL) in complicated AMI provides benefit and avoids hypoglycemic events.
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97
CALCIUM BLOCKER AGENTS:

-
Long-lasting verapamil and diltiazem Employ if unable to use B-blocker for recurrent
angina.
Nifedipine contraindicated post MI due to increased mortality.

EPLERENONE (INSPRA)
Reduces mortality & morbidity in addition to optimal post MI HF Rx
Benefit in NYHA #2-4 patients. NNT is 50 patients to prevent one death.

POST MI DEPRESSION:
20% frequency post AMI and is associated with higher rate of cardiac death and all-cause
mortality.
Sertraline (Zoloft) safe and effective drug in initial and recurrent depression.
SSRIs inhibit metabolism of B-blockers, warfarin, CCB, statins, losartan, and lidocaine
via the CYP 450 system.
Increased risk of bleeding when SSRI are added to GBIIb/IIIa agents, ASA, Plavix and
anti-thrombin agents due to a serotonin induced platelet dysfunction.
ACUTE MI WITH NORMAL CORONARY ANGIOGRAM
7% of MIs have normal coronaries; 7% have non-obstructive disease
Patients tend to be younger, women > men / Prognosis better / Rx same
Etiologies: rapid clot lysis, coronary spasm, methamphetamines or cocaine use, small
vessel disease, demand MI, Tako-tsubo Syndrome (Post menopausal women with chest
pain, ST changes, transient ballooning of distal LV, related to emotional stress and
increased sympathetic stimulation).
DISCHARGE:
Discharge 3 days post PCI, 5 days post conservative MI therapy, 7-10 days post
complicated MI (3 days post last complication)
Consider MPS - Prior to discharge if no PCI or CABG.
Beta Blocker / ACE Inhibitor Continue lifelong - prevents LV remodeling
ASA 81-325 mg/d avoid NSAID use post MI
If warfarin required in a patient with high bleeding risk, may withhold ASA.
TABLE of CONTENTS
98
Clopidogrel 75 mg daily/Ticagrelor 90 mg BID/Prasugrel 10 mg daily for at least 12

months.
Statin Agent High-intensity statin therapy continued lifelong regardless of LDL level
Warfarin If atrial fibrillation, endocardial clot, large AWMI
ICD for symptomatic sustained VT at least 1 month post MI with EF < 35%. Wearable
cardioverter defibrillator (vest) is designed to bridge a temporary risk of sudden
arrhythmic death until ICD implantation or when the risk can not be determined yet
(newly diagnosed cardiomyopathy).
Risk Factor Therapy: Exercised-based multidiscipline cardiac rehabilitation for secondary

prevention.
MI CHART / COMPLICATION / THERAPY CHART

MI
Mech Cardiac
Location defect
Shock
RV
Infarct
Conduction Ventricular TPWMI

Defect
Post MI
Arrhythmia
Blood
Vessel
B-
Inferior
Wall
VSD
MI
MR
No
Yes
SA Node
Slow VT
Yes
AV Node
Blocker
RCA
ASA
ACEI
STATIN
BBlocker
Anterior
Wall
VSD
MI
MR
Yes
No
Bundle
Fast VT
Branch
Block
No
ASA
L-Main
ACEI
LAD
STATIN Circumflex
Heparin
Warfarin
3-6 mo
Slow VT 3PVCs in a row WITH RATE < 100 bpmFast

VT 3PVCs in a row WITH RATE > 100 bpm
TPWMI = True posterior wall MI
RV Infarct = RV infarction (HYPOTENSION with DRY LUNGS)
Right-sided EKG - reverse V leads, check R-V4
Proximal RCA occlusion = ST elevation + upright T wave
Circumflex occlusion = ST depression + inverted T wave ACEI = ACE Inhibitor
VSD = Acute Ventricular septal rupture (IWMI > AWMI)
MR = Acute Mitral Regurgitation secondary to papillary muscle dysfunction
TABLE of CONTENTS
99
POST-DISCHARGE FOLLOW-UP
Consider disability for 6-8 weeks depending upon work effort.
Symptom - limited treadmill prior to returning to work for exercise Rx.
Resume sexual activity, with usual partner, after day 10 or when can walk one block or
climb a flight of stairs.
Resume driving after one week at home.
Patient may travel by plane after 2 weeks if clinically stable.
PHYSICAL EXAM
PALPATION:
o POINT OF MAXIMAL IMPULSE (PMI):
Left Ventricular PMI three characteristics
1) Sizeof a quarter
2) Locationis 5th ICS in the MCL
3) Durationis short 1/3of systole
There are two adjustments to disease process:
LV dilation enlarged PMI, displaced laterally but of normal duration, caused by
volume overload
LV hypertrophy normal size PMI, not displaced but sustained, caused by
pressure overload
Right Ventricular PMI:
1) Location is at the mid left sternal border, noted best in expiration, in the left lateral
decubitus position
2) Size of a silver dollar
3) Duration is brief tapping quality
There are two adjustments to disease process:
RV dilation increased size but normal duration - volume overload
RV hypertrophy sustained duration but a normal size and location pressure
overload
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100
o ECTOPIC IMPULSE:
LV aneurysm located between LSB and the LV apex best appreciated in the left
lateral decubitus position. Impulse is out of sequence with PMI (anterior wall).
o THRILL:
Vibratory sensation appreciated with bony prominences of hand.
Helps to localize site of murmur associated with grade 4/6 murmur
Aortic stenosis @ 2nd RICS, pulmonic stenosis @ 2nd LICS, VSD @ 3rd LICS,
mitral insufficiency @ LV apex
AUSCULTATION:
o S1 Louder than S2 at LLSB. S1is heard best with diaphragm.
Increased by increased contractility, short PR interval, mild to moderate mitral
stenosis
Decreased by decreased contractility, first degree AV block, mitral insufficiency or
severe mitral stenosis
S1is usually single but may be split with inspiration with a RBBB.
o S2 - Louder than S1@ 2nd LICS. S2 is heard best with diaphragm.
S2 is increased by aortic or pulmonary hypertension or PA dilation.
S2 is decreased by severe aortic or pulmonic stenosis.
Normally splits with inspiration (S2A-S2P). S2A moves earlier due to pooling of
blood in the lung and S2P moves later due to increased venous return to the RV.
If S2P split is heard at the LV apex, pulmonary HTN is present.
Widely split S2 occurs with atrial septal defect, total anomalous pulmonary venous
return, RBBB.
Fixed split S2 occurs with atrial septal defect, total anomalous pulmonary venous
return.
Paradoxical split S2 occurs with severe aortic stenosis, acute ischemia, LBBB, RV
pacemaker rhythm, CHF and HTN (S2P-S2A).With inspiration S2 then becomes
single due to delayed S2P.
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101
o S4 - is noted at LLSB (RV) or at the LV apex (LV). RV S4 increases with

inspiration. S4 is only heard with bell and transmits poorly in tissue, being very
localized. If press bell firmly against the skin, the bell becomes a diaphragm and S4
disappears. S4 indicates abnormal diastolic function of the ventricle (severe AS,
HTN, CAD, PS, HCM).
S4 is caused by vigorous atrial contraction with blood hitting stiff, non-compliant
ventricular wall. S4 is not present in atrial fibrillation. S4 may be noted in first degree
AV block alone.
o S3 Is noted at LLSB (RV) or at the LV apex (LV). LV S3 increases with expiration.
S3 is only heard with the bell and transmits poorly in tissues, being very localized. If
press bell firmly against the skin, the bell becomes a diaphragm and the S3disappears.
S3indicates abnormal systolic function of the ventricle (EF < 30%) due to HF
(sensitivity 50%, specificity 92%), severe MR, AI, or VSD in adults. S3 is normal in
children & pregnancy. The S3 increases with coughing, exercise, extrasystoles, and
leg elevation (by increasing ventricular filling and stroke volume).
o EC Ejection clicks are high frequency and best heard with the diaphragm.
Aortic EC is heard @ 2nd RICS or LLSB. It does not vary with respiration and
follows S1.
Pulmonic EC is heard @ 2nd LICS or LLSB. It decreases with inspiration and
follows S1. This is the only right -ided event that decreases with inspiration.
o Mitral Valve Opening Snap
The opening sound of the mitral valve is heard at the LLSB or LV apex. It is best
heard with diaphragm. It follows S2. The OS-S2 interval is inversely proportional to
the severity of mitral stenosis (isovolumetric period).
o Non Ejection Click (NEC)
Non-ejection clicks occur with mitral valve prolapse. They are heard in mid to late
systole. They may be single or multiple and may be associated with mitral
TABLE of CONTENTS
102
insufficiency. They are associated with billowing or prolapse of the mitral valve
leaflets.
o Grading Heart Murmur: related to intensity of heart sounds.
Grade 1/6 faint murmur heard only with prompting in a quiet room.
Grade 2/6 a soft murmur heard without prompting.
Grade 3/6 a loud murmur heard across precordium.
Grade 4/6 a loud murmur associated with a thrill always pathologic.
Grade 5/6 a loud murmur heard with the stethoscope on its side.
Grade 6/6 a loud murmur heard with the stethoscope off chest.
HEART SOUNDS
Around S1
Low frequency sounds heard only with the bell.
They transmit poorly in tissue and are localized.
LLSB right ventricular S4 occurs with pulmonary hypertension, RV infarct or
pulmonic stenosis
LV Apex - left ventricular S4 occurs with HTN, ischemia, or LVH.
High frequency sounds heard with both the diaphragm and the bell.
They transmit well in tissue and are heard widely.
LLSB split S1 moves with inspiration, and may disappear with expiration.
2nd RICS Aortic ejection click is associated with a short ejection murmur of mild AS.
2nd LICS Pulmonic ejection click is associated with a short ejection murmur of mild
PS. The click is the only right-sided event that decreases with inspiration.
LV Apex Mitral non-ejection click is associated with mitral valve prolapse, and often
a murmur of MR. Best heard upon sitting or standing (decrease heart size).
Around S2
Low frequency sounds heard only with the bell.
They transmit poorly in tissue and are localized.
LLSB right ventricular S3 is associated with systolic dysfunction of the RV.
TABLE of CONTENTS
103
LV Apex left ventricular S3 is associated with systolic dysfunction of the LV, severe
MR, may be normal < 20 yo.
LV Apex summation gallop (S3+S4) is associated with systolic dysfunction, atrial
dysfunction and sinus tachycardia.
High frequency sounds heard with both the diaphragm and the bell.
They transmit well in tissue and are heard widely.
2nd RICS split S2 widens with inspiration.
LV Apex split S2 widens with inspiration and is associated with pulmonary HTN.
LLSB mitral opening snap associated with murmur of mitral stenosis.
LV Apex pericardial knock associated with constrictive pericarditis.
HEART MURMUR EVALUATION

1. Murmur frequency
Harsh frequency: Flow from high to high pressure areas
Aortic stenosis - Left ventricle to aorta in systole
Pulmonic stenosis - Right ventricle to pulmonary artery in systole
High frequency: Flow from high to low-pressure areas
Mitral insufficiency - Left ventricle to left atrium in systole
Tricuspid insufficiency - Right ventricle to right atrium in systole
Aortic insufficiency - Aorta to left ventricle in diastole
Ventricular septal defect - LV to RV in systole
Pulmonary insufficiency with pulmonary HTN - PA to RV in diastole
Low frequency: Flow from low to low pressure areas
Mitral stenosis - LA to LV in diastole
Tricuspid stenosis - RA to RV in diastole
Pulmonic insufficiency with normal PA pressure - PA to RV in diastole
Musical: Innocent murmur
2. Murmur timing:
Systolic - AS / PS / MR / TR / VSD / Innocent murmur
Diastolic - AI / PI / MS / TS
TABLE of CONTENTS
104
3. Murmur location:
2nd RICS - AS
2nd LICS - PS / ASD / CoA / innocent murmur
3rd LICS - IHSS / VSD / AI
4th LICS - TR / TS
LV apex - MR / MS
INNOCENT HEART MURMUR

An innocent murmur is always systolic, usually grade 1-2/6, unassociated with a thrill, is
musical in quality and changes intensity with change in body position.
It is associated with a normal S1, S2, PMI, and carotid pulse. BP is normal in both arms.
The differential diagnosis of an innocent heart murmur is not related to the murmur itself but
rather the presence of clicks, abnormal pulses, BP obtained in both arms and LV apex
abnormalities.
Aortic stenosis, mild: 2nd RICS // grade 2-3/6 SEM
Normal S1and S2
Aortic ejection click at 2nd RICS (like split S1)
Pulmonic stenosis, mild: 2nd LICS // grade 2-3/6 SEM
Normal S1and S2
Pulmonic ejection click at 2nd LICS (like split S1) that decreases with
inspiration
Atrial septal defect: 2nd LICS // grade 2-3/6 SEM
Murmur represents a flow murmur via pulmonary artery.
Normal S1, fixed split S2 (increased flow to RV with inspiration and
expiration delaying pulmonary valve closure)
EKG: incomplete RBBB (ostium secundum)
Left axis deviation (ostium primum)
TABLE of CONTENTS
105
Coarctation of the Aorta: 2nd LICS // grade 2-3/6 SEM more laterally located
Normal S1and S2
BPs different in both arms
Pulse delay between radial and femoral pulse
BP decreased in thigh. Thigh BP normally > arm
Idiopathic hypertrophic subaortic stenosis: 4th LICS at LSB // grade 2-3/6 SEM
Normal S1and S2
Apex bisferiens quality (double impulse)
Carotid pulse bisferiens quality (double impulse)
Mitral insufficiency if LV outflow obstruction present
Murmur louder with standing, softer when supine
Mitral valve prolapse: LV apex // grade 3/6 mid /late /holo systolic murmur
Normal S1and S2 // mid systolic click or clicks
Murmur louder with standing, softer when supine
TABLE of CONTENTS
106
TABLE of CONTENTS
107
TABLE of CONTENTS
108
PROSTHETIC VALVES
2009/2006 ACC/AHA Guidelines: Update. Rahimtoola 2010;55(22):2413-26
The choice between mechanical and stented bioprosthesis depends upon age, risk of long-term
anticoagulation and longevity of the valve.
MECHANICAL VALVES: 55% of all prosthetic heart valves.
ST JUDE / BILEAFLET
Durability: ~ at least 20 years
Advantage: Helpful in small valve annulus / Less structural breakdown
Embolic risk: =1%/year on warfarin; 2.2%/year on ASA; 4%/year with no anticoagulation
The risk is 2x if valve in the mitral versus aortic position. Long term warfarin / twice the risk
of bleeding than bioprosthetic valves due to higher INR goal
Hemolysis establish an LDH baseline level
Valve failure change in click loudness or new murmur
Mitral valve murmur MR // OC (S2) >CC (S1) abnormal Doppler gradient >7mmHg
Aortic valve murmur AI // OC (S1) >CC (S2) abnormal Doppler gradient >15 mmHg
increased hemolysis
Valve obstruction: Sx: HF, embolus. Frequency: ~ 1-5% per year; mitral > aortic
Dx: Echo // Rx either surgery or thrombolysis (Alteplase 10 mg bolus, then 90 mg over 90
minutes)
BIOPROSTHETIC VALVES: 45% of all prosthetic heart valves
Type: Porcine, bovine pericardium, homografts, autograft mounted on metal stent
Durability: 10-15% of the valves fail within 15 years
Related to patient age, valve type and valve location
Age:
Breakdown @ 15 years < age 65 years = 26%

Breakdown @ 15 years > 65 years only 9%
Valve type:
Homografts @ 15 years = 20% breakdown

Heterograft @ 15 years = 35% breakdown
Valve position: Porcine mitral valve > breakdown than aortic position
TABLE of CONTENTS
109
Advantage:
Does not require long term warfarin in the aortic position

Valve may require long term warfarin in the mitral position if high risk factors
present- see chart on page 68.
Valve of choice in patients> 65 years if high risk for warfarin Rx
All TV replacements
Embolic risk: similar to mechanical valve ~ 1% per year

Valve failure
Mitral valve = MR / MS, abnormal Doppler gradient >9 mmHg, increased
hemolysis
Aortic valve = AI / AS, abnormal Doppler gradient >20 mmHg
Valve Surgery Mortality Rates:
Aortic valve = 4% // Mitral valve = 6%
Aortic valve + CABG = 6.8% // Mitral valve + CABG = 13.3%
Significant complication rate: ~ 3% per year // Death rate ~ 1% per year.
TABLE of CONTENTS
110
ANTICOAGULATION FOR PROSTHETIC VALVES+

MECHANICAL VALVES
INR
Anti-platelet Rx
ALL
2.5-3.5
ASA 75-100 mg
2-3
ASA 75-100 mg
2-3
ASA 75-100 mg
2.5-3.5
ASA 75-100 mg
Aortic valve plus risk factors*
2.5-3.5
ASA 75-100 mg
Mitral valve risk factors*
2.5-3.5
ASA 75-100 mg
BIOPROSTHETIC VALVES
INR
Anti-platelet Rx
Aortic valve, Mitral valve
2-3
ASA 75-100 mg
2.5-3.5
ASA 75-100 mg
ASA 75-100 mg
Aortic valve + risk factors*
2-3
ASA 75-100 mg
Mitral valve + risk factors*
2.5-3.5
ASA 75-100 mg
First 3 months
After 3 months
Aortic valve low thrombogenicity

St. Jude; Medtronic-Hall
Aortic
valve
medium
thrombogenicity
Bjork-Shiley
Aortic valve high thrombogenicity
Lillehei-Kaster; Omniscence; StarrEdwards
First 3 months
Aortic valve + risk factors*

Mitral valve + risk factors*
After 3 months
Aortic valve, Mitral valve
* Risk factors include Atrial fibrillation, LV dysfhunctione with LVEF35%), left atrial dilation 50 mm, previous
thromboembolism, spontaneous echocardiographic contrast and hypercoagulable condition.
ESC guidelines recommend higher INR target for prostheses with medium and high thrombogenicity (AVR and no
risk factors: 3.0 for medium and 3.5 for high; MVR and/or risk factors: 3.5 for medium and 4.0 for high).
ACC/AHA Prosthetic heart valves: selection of the optimal prosthesis and long-term management.
Circulation.2009; 119:1034-1048
TABLE of CONTENTS
111
ENDOCARDITIS
NATIVE
VALVES
Organism
Streptococcus
>
Enterococcus
>
Staphylococcus
DRUG
ABUSER
Staphylococcus
>
Strep+Entero
>
Fungi+Gramneg
>
Mixed organisms
PROSTHETIC
VALVE
Early < 60 days
Staph epi
>
Staph aureus
>
Gram neg
>
Candida
Late > 60 days
Streptococcus
Gender
M>F
M>F
M>F
Age
>50 yo
20-30 yo
>60 yo
Normal/Abnormal
Valve
20% / 80%
80% / 20%
0% / 100%
Clinical
Onset
Chronic/Acute
Acute
Early Acute
Late Chronic >Acute
Valve
Involved
A > M > Congenital
TV > AV > MV
AV > MV
Suture line
Emboli
Systemic
Pulmonary
Systemic
Heart
Murmur
80%
Infrequent
100%
Mortality
Staph 40%
(TV) Staph 10%
Early 40-80%
Late 20-40%
TABLE of CONTENTS
112
ENDOCARDITIS
May involve valves, endocardium, endothelium
Vegetations occur at high pressure areas (L >R), and downstream in blood flow
Virulent organisms attack normal and abnormal valves (Staphylococcus)
Less virulent organisms attack only abnormal valves
Clinical picture of IE related to vegetation and immune response.
Bulky vegetations obstruct valves Virulent organisms perforate valves Immune
complement mediated cause glomerulonephritis and arthritis
If IE on native valves, avoid anticoagulation. If IE on prosthetic valves continue warfarin.
If CVA hold warfarin 2 week to allow time for the thrombus to organize and avoid
hemorrhagic conversion.
Subacute IE onset more likely to have peripheral signs.
Splenomegaly, petechiae 30%, Roth spots 5%, Osler nodes (tender) 25%, clubbing, +
rheumatoid factor 50%
Neurological sx 30% - greater with left sided infections meningitis, abscess, mycotic
aneurysms, CVA. 65% emboli to CNS (MCA).
Endocarditis can occur without fever (renal failure, immunosuppressed), and without a
heart murmur
Negative culture endocarditis Fastidious organisms, prior antibiotic therapy,
nonbacterial source, poorly timed blood cultures
Cardiac echo TTE (sensitivity 65%, specificity 98%) routine screening test, abnormal
findings depend upon size of vegetation (staph & candida-large), duration of infection,
patients body size, pulmonary status. Consider TEE (sensitivity 85%, specificity 98%)
if: unclear Dx, to Dx abscess (continued fever), to evaluate valvular insufficiency,
prosthetic valve & CHF.
TEE less good for right-sided vegetations.
Indications for surgery: non-treatable organism (fungus), no response to antibiotic Rx
(continued fever & positive blood cultures), myocardial abscess, valve ring abscess, valve
dehiscence or perforation, acute CHF, hemodynamic instability, recurrent emboli, large
vegetation > 10 mm.
TABLE of CONTENTS
113
DUKE DIAGNOSTIC CLINICAL CRITERIA FOR ENDOCARDITIS

MAJOR CLINICAL CRITERIA
POSITIVE BLOOD CULTURES:
o TYPICAL MICROORGANISM FOR ENDOCARDITIS FROM 2 SEPARATE
BLOOD
o CULTURES STREP VIRIDANS, STREP BOVIS, HAEK GROUP, STAPH
AUREUS, OR ENTEROCOCCUS
ABSENCE OF PRIMARY FOCUS
PERSISTENT POSITIVE BLOOD CULTURES FROM BLOOD CULTURES DRAWN
> 12 HRS APART
SINGLE POSITIVE BLOOD CULTURE FOR COXIELLA BURNETII
EVIDENCE OF ENDOCARDIAL INVOLVEMENT
o POSITIVE ECHO: PEDUNCULATED VEGETATION, VALVE DISRUPTION,
ABSCESS DEHISCENCE OF PROSTHETIC VALVE.
o NEW OR INCREASING VALVULAR INSUFFICIENCY
MINOR CLINICAL CRITERIA
PREDISPOSITION
o KNOWN HEART LESION
o IV DRUG USAGE
TEMPERATURE > 100.4 F
VASCULAR EVENTS:
o EMBOLI (SYSTEMIC/PULMONARY), MYCOTIC
o ANEURYSM
o INTRACRANIAL/CONJUNCTIVAL HEMORRHAGES
o JANEWAY LESIONS
IMMUNOLOGIC EVENTS:
o GLOMERULONEPHRITIS
o OSLER NODES
o ROTH SPOTS
o RHEUMATOID FACTOR
POSITIVE BLOOD CULTURES
o ATYPICAL ORGANISM
DEFINITE I.E.:
PATHOLOGY (VEGETATION OR ABSCESS WITH MICROORGANISM_
2 MAJOR CRITERIA
1 MAJOR, 3 MINOR CRITERIA
5 MINOR CRITERIA
POSSIBLE I.E.:
1 MAJOR, 1 MINOR CRITERION
3 MINOR CRITERIA
DIAGNOSIS of I.E. REJECTED:
FIRM ALTERNATIVE Dx NOTED
RESOLUTION OF MANIFESTATIONS OF IE WITH ANTIBIOTICS IN 4 DAYS OR LESS\NO PATHOLOGIC
EVIDENCE OF IE AT SURGERY OR AUTOPSY AFTER LESS THAN 4 DAYS OF ANTIBIOTIC Rx
SPECIFICITY = 99%//NEGATIVE PREDICTIVE VALUE = 92%
TABLE of CONTENTS
114
CARDIAC CONDITIONS ASSOCIATED WITH IE RISK
Circulation 2007; 115:1-19
http://www.heart.org/idc/groups/heartpublic/@wcm/@hcm/documents/downloadable/ucm_307684.pdf
PROSTHETIC CARDIAC VALVES

o (TISSUE & MECHANICAL)
PRIOR BACTERIAL ENDOCARDITIS*
CYANOTIC CONGENITAL HEART DISEASE (CHD)
o UNREPAIRED CYANOTIC CHD
o PALLIATIVE SHUNTS / CONDUITS
o COMPLETELY REPAIRED CHD WITH PROSTHETIC MATERIAL /
DEVICE PLACED BY SURGERY OR CATHETER FOR THE FIRST 6
MONTHS#
o REPAIRED CHD WITH RESIDUAL DEFECTS AT THE SITE OR
ADJACENT TO THE SITE OF A PROSTHETIC PATCH OR PROSTHETIC
DEVICE (WHICH INHIBIT ENDOTHELIALIZATION)
CARDIAC TRANSPLANTATION RECIPIENTS WHO DEVELOP CARDIAC
VALVULOPATHY (Leaflet thickening or reguritation)
* Except for these conditions, antibiotic prophylaxis is no longer recommended for any other
form of CHD.
#
Prophylaxis is recommended because endothelialization of prosthetic material occurs within 6
months after the procedure.
RECOMMENDATIONS FOR IE PROPHYLAXIS

ALL DENTAL PROCEDURES THAT INVOLVE MANIPULATION OF GINGIVAL
TISSUE OR THE PERIAPICAL REGION OF TEETH OR PERFORATION OF THE ORAL
MUCOSA*
PROCEDURES OF UPPER RESPIRATORY TRACT INVOLVING INCISION or
BIOPSY OF THE MUCOSA INCLUDING T&A
BRONCHOSCOPY ONLY WITH BIOPSY
DRAINAGE OF RESPIRATORY ABSCESS OR EMPYEMA
SURGERY INVOLVING INFECTED SKIN, MUSCULOSKELETAL SYSTEM
GI/GU PROCEDURES ONLY WITH ONGOING INFECTION
SURGERY TO PLACE PROSTHETIC HEART VALVES or PROSTHETIC
INTRAVASCULAR OR INTRACARDIAC MATERIALS
* The following do not need prophylaxis: routine anesthetic injections through noninfected tissue, taking dental
radiographs, placement of removable prosthodontic or orthodontic
appliances, adjustment of orthodontic appliances, placement of orthodontic brackets, and bleeding from trauma to
the lips or oral mucosa.
TABLE of CONTENTS
115
RECOMMENDATIONS FOR IE PROPHYLAXIS

PREVENTION OF BACTERIAL ENDOCARDITIS
RECOMMENDATIONS BY AMERICAN HEART ASSOCIATION

Circulation 2007;115:1-19
REGIMENS FOR DENTAL, ORAL, RESPIRATORY OR ESOPHAGEAL PROCEDURES

AMOXICILLIN
Adults: 2 gm
STANDARD PROPHYLAXIS
Children: 50 mg/kg
30-60 minutes before procedure
AMPICILLIN
Adults: 2 gm IM or IV
Children: 50 mg/kg IM or IV
UNABLE TO TAKE
ORAL MEDICATIONS
Or
CEFAZOLIN or CEFTRIAXONE
Adults: 1 g IM or IV
ALLERGIC TO PENICILLIN
ALLERGIC TO PENICILLIN
AND UNABLE TO TAKE
ORAL MEDICATIONS
CEPHALEXIN
Adults: 2 gm
Children: 50 mg/kg
Or
CLINDAMYCIN
Adults: 600 mg
Children: 20 mg/kg
Or
AZITHRO or CLARITHROMYACIN
Adults: 500 mg
Children: 15 mg/kg
CEFAZOLIN or CEFTRIAXONE
Adults: 1 gm IM or IV
Or
CLINDAMYCIN
Adults: 600 mg
Children: 20 mg/kg
TABLE of CONTENTS
116
HEART FAILURE
2013 ACCF/AHA Guideline
J Am Coll Cardiol 62:e147-239
PRESENTATION
o SYMPTOMATIC
o Left Heart:
Congestive (DOE, Orthopnea, PND)
Low Output (fatigue with exercise)
o Right Heart (JVD, Hepatomegaly, Ascites, Edema)
o Systolic Dysfunction (Poor Contractility)
o Diastolic Dysfunction (Inadequate Relaxation)
o {Heart Failure with Preserved Systolic Dysfunction
o ASYMPTOMATIC
o Low EF without symptoms (Inactive/Elderly)
EVALUATION
o CXR: Heart Size:
Enlarged Chronic Systolic Dysfunction
Normal Acute CHF, Diastolic Dysfunction,
Constrictive Pericardial Disease, COPD,
Mitral Stenosis, Addisons disease
Blood Flow:
Venous Redistribution to Upper Lobes (CHF)
Arterial Redistribution to Mid Lobes (Shunt)
o EKG: Q Waves (MI), Low voltage, LVH, Arrhythmias
o ECHO: Systolic (EF < 40%) vs Diastolic Dysfunction
Muscular vs Valvular vs Pericardial Etiology
o NT-BNP Test:
The RV and LV secrete brain-type natriuretic peptides in response to
change in volume or pressure stressors.
Elevated in RV, LV, systolic or diastolic HF
TABLE of CONTENTS
117
Diagnostic levels: BNP = N-terminal proBNP (NT proBNP)

Less than 300pg/ml HF unlikely:
If< 50 yo HF likely if > 450 pg/ml; if > 50 yo HF likely if> 900 pg/ml
Chronic HF - obtain baseline BNP when best compensated; 50% increase
above baseline predicts acute on chronic HF
Prognostic: High levels after therapy are strongly predictive of poor
prognosis and readmission to the hospital
In chronic HF therapy BNP guided therapy improves long-term mortality
Causes for elevated NT-BNP:
HF, LVH, Myocarditis, Cirrhosis with ascites
Primary pulmonary hypertension, Atrial fibrillation
Renal failure, levels fall post dialysis
Primary Hyperaldosteronism, Cushings syndrome
Levels increase with age; decrease with obesity
NYHA CLASSIFICATION OF HEART FAILURE*
o NYHA #I - no symptoms
o NYHA #II - symptoms with moderate activity
o NYHA #III - symptoms with mild activity (activities of daily living)
o NYHA #IV - symptoms at rest
* Classification represents present clinical status
STAGES OF HEART FAILURE: * AHA/ACC
o Stage A - asymptomatic / risk factors for heart failure present
o Stage B - asymptomatic / systolic dysfunction is present
o Stage C - symptomatic / heart failure present
o Stage D symptomatic / end stage heart failure (refractory HF)
* Stage represents worst clinical status
2013 ACCF/AHA Definitions of HF:
o I HF with reduced EF(HFrEF) when LVEF 40%, aka Systolic dysfunction
o II HF with preserved EF (HFpEF) when LVEF 50% aka Diastolic HF
HFpEF borderline when LVEF 41-49%
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EXCESSIVE NEUROHORMONAL RESPONSE:

o Heart failure is caused by an acute or chronic insult but is perpetuated by
induced neurohormal imbalance. The imbalance causes early myocyte death.
Therapy for HF is based upon excessive neurohormonal response to low cardiac
output resulting in over stimulation of:
Sympathetic system
Renin-angiotensin-aldosterone system
Arginine vasopressin system
Endothelin system
Cytokine system
SYSTOLIC HF THERAPY:
1) PRELOAD RX:
First Line Therapy IMPROVES SHOR-TERM SURVIVAL
o Loop diuretics:
Furosemide 20-40 mg oral or IV; duration of action 6 hours; poorly absorbed by
GI tract (50%)
Bumetanide 2-4 mg oral or IV; shorter duration of action; well absorbed by GI
tract (100%)
Torsemide 10-20 mg oral or IV; longest duration of action; best absorbed by the
GI tract especially with ascites
o Combination Therapy:
IV / po Furosemide + po Metolazone (5-10 mg)
IV / po Furosemide + IV Chlorothiazide (500 mg)
IV Furosemide drip (10-20 mg/ h) + IV bolus Furosemide
o Elevated BUN / Creatinine ratio may represent: Volume depletion / poor cardiac
output / blood in gut / catabolic state
o Spironolactone (target dose 25 mg QD) / Eplerenone (50-100 mg)
Blocks aldosterone system beyond ACEI & Angiotensin blocker II 30%
decrease in all cause mortality - NYHA class # 2-4 / EF <35%
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o Diuretic Rx mayDECREASES LONG-TERM SURVIVAL due tocontinued

activation of the RAAS system therefore always use the lowest effective dosage.
Non-potassium sparing > potassium-sparing diuretics increases mortality. This effect
is dose related.
o High Dose Nitrates in heart failure (180-240 mg) improves symptoms, decrease
hospitalizations in systolic HF, and decrease remodeling with or without ischemia,
decreases LV afterload. Combines well with diuretics.
2) AFTER-LOAD RX: DECREASES SVR and IMPROVES LONG-TERM
SURVIVIAL (22-37%)
o Effective Agents (NNT=77)
ACE Inhibitor - blocks AT1& AT2 receptors - Blocks vasoconstriction but also
causes vasodilation via increased bradykinin
Angiotensin II Blockers (ARB) cause additive renin suppression to ACEI increases survival & morbidity in HF alone or with ACEI or B-blocker
(CHARM). ARB agents block vasoconstriction by blocking AT 1 receptor only.
Hydralazine + Nitrates (BiDil)induces benefit via nitric oxide production.
Highly effective in African Americans additive to ACEI or ARB and beta-blocker
o Initiate After-load Rx:
Start after isovolumic state achieved with diuretics
Acutely if HTN persists after dyspnea improves
o Target dosage*/Maximal dosage:
Captopril 50 mg TID / 100 mg TID, Enalapril 10 mg BID / 20 mg BID,
Ramipril 10 mg QD / 20 mg QD, Lisinopril 20 mg QD / 40 mg QD,
Quinapril 20 mg BID / 20 mg BID, Benazepril 20 BID / 40 mg BID,
Fosinopril 20 mg QD / 40 mg QD, Hydralazine 75 mg TID / 100 mg QID
+ Isordil 40 mg TID / 80 mg TID, Losarten 50 mg BID / 100 mg BID, Valsartan
160 mg QD / 320 mg QD
* Unclear whether target dose improves morbidity or mortality more than
standard dosage, but it does increase endurance & decreases hospitalizations.
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o ACEI Classes if cutaneous rash occurs change class of drug

Captopril (Sulfhydryl)
Enalapril, Lisonopril and Benazepril (Carboxyl)
Fosinopril (Phosphynyl)
o ACEI are first agents of choice in HF
Benefit is a class effect (all ACEIs helpful) reduce mortality and morbidity.
If baseline creatinine >1.4 mg & it increases > 30% in two months, or if persistent
hyperkalemia need to stop ACEI.
Then use hydralazine + nitrates.
GFR is a better marker of renal function than serum creatinine in elderly.
o ACEI cough
Cough is related to elevated bradykinin level.
Need to R/O continued CHF.
If no or mild symptoms, do not discontinue ACEI.
If needed may switch to Angiotensin II Blocking Agent.
If cough persists, stop ACEI & ARB and use hydralazine + nitrates.
o Angioedema - ACEI >ARB, women & AAs; Related to increased bradykinin
(Rx with antihistamines, steroid, epinephrine), may cross-react with ARBs.
o Hyponatremia (< 135 mEq/l) may be related to depletion or dilutional mechanism.
Depletion: related negative Na balance and seen with hypokalemia and
hypomagnesium due to potent diutetic and corrected if needed by isotonic saline
Dilutional: related to impaired water exection and seen with edema, ascites and
pleural effusions. Corrected by loop diuretic, acetazolamide and arginine
vasopressin (AVP) antagonists (Tolvaptan, Conivapan) at least short-term.
o Persistent HTN:
Consider the combination of ACEI or ARB with hydralazine to get additive HTN
and afterload benefit.
o Benefit of ACEI/ ARB
Prevents ventricular remodeling, decreases LV afterload (arteriolar resistance),
especially helpful in diabetic patients.
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3) DIGOXIN RX
POSITIVE INOTROPIC THERAPY or NEUROHORMONAL THERAPY?
o D.I.G. Study Digoxin improves sx and decreases hospitalizations but no effect on
survival (May improve survival if level < 1.1ng/ml).
Need to watch dose in frail or small-framed individuals.
Digoxin does inhibit Sympathetic & Angiotensin System.
o INITIATE DIGOXIN THERAPY:
After patient is isovolumic and afterload Rx is achieved. Only digitalize acutely
for control of rapid supraventricular arrhythmias.
INOTROPIC AGENTS INCREASE SUDDEN DEATH (Dobutamine, Milrinone,
high dose Vesnarione)
4) NEGATIVE INOTROPIC THERAPY (Beta-blocker therapy):
CHRONIC Rx IMPROVES LONG TERM SURVIVAL (30- 65%)
o More beneficial than ACEIs in outcome of HF
o Benefit is a drug specific effect, not a beta-blocker class effect.
o Carvedilol improves the mortality and morbidity more than intermediate acting
metoprolol despite the fact that both agents achieved equal heart rate reduction.
o Start BB once the patient is isovolumic and stable (NYHA #2-4) usually after patient
is on PRELOAD Rx & AFTERLOAD Rx.
o Beta-blocker may be given before afterload Rx, if low BP limits use of both agents.
o May produce temporary deterioration in the clinical status.
o EFFECTIVE AGENTS: Stage CHF
Goal to achieve heart rate 55-60 bpm
DOSAGE: Initiation / Titration (2-8 weeks) / Target
Carvedilol - Coreg - (nonselective 3rd generation beta blocker);
3.125 mg BID / 6.25 mg BID, to 25 mg BID
Metoprolol succinate (selective 2nd generation beta blocker)
6.25 mg BID / 12.5 BID, 25 mg BID, 50 mg BID
Bisoprolol - Zebeta - 2.5-20 mg daily
o Beta-blockers benefit patients with mild, moderate and severe systolic heart failure.
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5) HMG-CoA Reductase Inhibitor STATIN

o ACC/AHA 2013 In all patients with a recent or remote hx of MI or ACS, statins
should be used to prevent symptomatic HF and cardiovascular events. Otherwise, in
the absence of other indications, statins are not beneficial as adjunctive therapy when
prescribed solely for the diagnosis of HF.
o Observational trials, small prospective studies
o Lipophilic agents (atorvastatin) 2004-2007 better muscle penetration
o Hydrophilic agents (rosuvastatin) not beneficial (CORONA, GISSI-HF Trials)
o More benefit in the earlier stages of the disease
o May be more beneficial with elevated C-reactive protein
6) ALDOSTERON ANTAGONIST Rx:
o Improves survival in systolic HF NYHA II-IV
o Spironolactone dosage 25 mg/day
o Eplerenone dosage 25-50 mg/day
o Avoid if creatinine > 2.5mg/dL in men, > 2mg/dL in women and K > 5mEq/L.
o HEART FAILURE RISK PREDICTOR
Seattle Heart Failure Model
http://depts.washington.edu/shfm/app.php?accept=1&enter=ENTER
REVIEW OF THERAPY FOR SYSTOLIC HEART FAILURE

1) Preload therapy: improves short-term survival but may decrease long-term survival
2) Afterload therapy: improves long-term survival.
3) Digoxin therapy: improves symptoms, but no effect on survival
4) Beta-blocker therapy: improves survival
5) HMG-CoA Reductase Inhibitors: may improve survival if CAD present
6) Aldosterone antagonist Rx: improves survival
7) Decrease or remove diuretic therapy used for preload reduction
8) RCT data extensive with Level 1A evidence
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RIGHT VENTRICULAR FAILURE:

o Causes: LV failure > cor pulmonale > R sided valve disease (IE)
o If secondary to LV failure - treat as LV failure.
o If secondary to lungs - therapy limited to preload therapy + O2 - digoxin only for
arrhythmias, ACEI Rx not helpful.
o If secondary to right sided valve disease - use preload Rx + digoxin.
ANTICOAGULATION RX: HEPARIN / WARFARIN / ASA
o Hx of embolic events
o Atrial fibrillation - chronic or paroxysmal
o Anticoagulation of no benefit in HF in NSR
DIASTOLIC FAILURE - HEART FAILURE WITH NORMAL EF - (HFNEF)
o Abnormalities in diastolic > systolic function, decreased exercise reserve, mild
compromise in systolic function (twisting and untwisting)
o Volume sensitive to Pre-Load Rx
o Normal Heart Size on CXR with HF
o Hx of HTN, Aortic Stenosis, HCM, CAD, Elderly
o ECHO Marked atrial filling wave A > E wave
REVIEW OF THERAPY FOR DIASTOLIC HEART FAILURE
1) Decrease preload and pulmonary congestion
2) Slow heart rate in atrial fibrillation/flutter
3) Control systolic and diastolic hypertension
4) Control ischemia
ACUTE DECOMPENSATED HEART FAILURE (ADHF)
50% Systolic dysfunction // 50% Diastolic dysfunction
o Acute heart failure results in decreased cardiac output that activates of the RAAS
reducing the GFR and increasing release of aldosterone. This results in volume
overload and increased SVR.
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o Diuretics attempt to correct the volume status but are often hampered by the
RAAS induced decrease GFR. In addition diuretics may increase angiotensin II
levels.
o The addition of vasodilator agents that increase GFR and lower the SVR are often
needed in addition to diuretics. (NTG, nitroprusside, nesiritide).
o Three Clinical Syndomes have been reconized in ADHF related to peripheral
perfusion (warm or cold) and the presence of pulmonary congestion (wet or dry):
WARM and WET: most common presentation with the best prognosis. The skin
is warm and pulmonary rales or wheezes are noted.
Rx - diuretic, then ACEI when euvolumic
COLD and WET: The skin is cold (very high SVR) and pulmonary rales or
wheezes are noted. Admit to ICU.
Rx consists of diuretic + vasodilators.
COLD and DRY: The skin is cold but no pulmonary rales or wheezes are noted
Rx consists of dobutamine + careful fluid challange. Poor prognosis
CART Risk Analysis: (BUN > 43mg/dL, serum creatinine > 2.7mg/dL,
SBP < 115 mmHg) - All three factors 22% mortality; No risk factors; 2%
mortality. (CHF 2008; 14:127-34).
NON-PHARACOLOGICAL THERAPIES:
BIVENTRICULAR PACING (CRT) - Improves mortality & Sxs.
Indicated: If refractory systolic dysfunction NYHA II,III,IV despite GDMT (Guideline
Determined Medical Therapy), sinus rhythm, LBBB or QRS 150 msec, EF 35%. BiV
pacing
improves
synchronization,
exercise
endurance,
QOL
and
survival.
(Circulation.2013;128:e240-e327)
ICD Therapy: for primary prevention of SCD sudden cardiac death - to reduce total
mortality in patients with nonischemic dilated cardiomyopathy or ischemic heart disease
at least 40 dayspost-MI with LVEF 35% and have NYHA II,III symptoms on chronic
GDMT. Wearable cardioverter defibrillator (vest) is designed to bridge a temporary risk
of sudden arrhythmic death until ICD implantation or when the risk cannot be determined
yet (newly diagnosed cardiomyopathy).
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CARDIOPULMONARY ASSIST DEVICE: Percutaneous (IABP)

Stabilize patient with hemodynamic comprise to allow further diagnostic
evaluation, PCI or surgery.
Contraindications: Severe AI; severe PAD; bleeding diathesis; recent CVA, head
trauma; uncontrolled sepsis. CHF 2008;14:141-8.
VENTRICULAR ASSIST DEVICE: (LVAD) To allow bridge to cardiac transplant or
short-term stabilization of jeopardized myocardium.
Complications: non-pulsatile flow (renal dysfunction), hemolysis, infection
(blood, local), ventricular arrhythmias, LV clot, thrombocytopenia.
Contraindications: Severe AS, prosthetic AV, aortic aneurysm, severe PAD,
intracardiac clot, bleedong diathesis, uncontrolled sepsis.
Survival to hospital discharge in LVAD therapy is 40-60%.
HEART TRANSPLANT: 2007 ISHLT Registry

INDICATIONS: REFRACTORY CHF or ISCHEMIA/ARRHYTHMIAS
(45% nonischemic cariomyopathy; 38% CAD)
Frequency: 5,000 cardiac transplants per year
United Network for Organ Sharing - has established national priority rules
CRITERIA:
Severe reduction in exercise capacity (peak VO2 < 10 mL/kg)
Prognosis scores (HFSS, Seattle HF Model)
EXCLUSIONS:
Increased pulmonary vascular resistance
Infection
Malignancy
RELATIVE EXCLUSIONS:
Age > 60 years
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DM with end-organ damage

Advanced lung disease
Cirrhosis or renal disease
Inadequate financial resource
Non-adherence to medical follow-up
Recent improved survival is realted to better immunosuppression & infection

control.
MORTALITY: 80% two-year survival, then 70% five-year survival.
COMPLICATIONS OF TRANSPLANT:
Cause of death after transplant:
Allograft rejection; CMV infection; Allograft Vasculopathy; Lymphoma
or other solid malignancies, non-CMV infection, multiple organ failure
Long-term co-morbidities post transplant:
HTN, Hyperlipidemia, DM, CKD, transplant vasculopathy.
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CONGENITAL HEART DISEASE IN

ADULTS
ACC/AHA Guidelines.
Circulation 2008; 118:e714-e833
GUCH (Grown Up Congenital Heart Disease) represents 6% of an adult cardiology
UNDIAGNOSED ASYMPTOMATIC
Bicuspid aortic valve
Atrial septal defect (ASD)
Mitral valve prolapse (MVP)
Coarctation of aorta (COA)
Pulmonic stenosis (PS)
IHSS
PREVIOUSLY DIAGNOSED UNDER MEDICAL Rx / PRIOR SURGERY
Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Tetralogy of Fallot (TOF)
Complex congenital heart disease
DIAGNOSTIC APPROACH TO CHD:

Cyanotic vs Acyanotic Disease
Increased pulmonary blood flow vs decreased pulmonary blood flow
COMMON ADULT ACYANOTIC LESIONS:

Secundum Atrial Septal Defect
Sx increased pulmonary infections, DOE, fatigue
PE systolic ejection murmur 2nd LICS + fixed split S2. The murmur results
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from increased blood flow across pulmonary valve murmur is not due to flow
across septal defect if large shunt, develop RV lift + flow murmur of tricuspid
stenosis
EKG IRBBB (hypertrophy of RV outflow tract)
CXR increased pulmonary flow, PA & RV size, small aortic knob
ECHO increased RV size, paradoxical IV septal motion
DOPPLER L to R shunt (QP/QS > 2 = significant)
SURGERY in adult if QP/QS shunt > 2
POST-OP Long term atrial arrhythmias
Primum Atrial Septal Defect

Sx same
PE same
EKG IRBBB + left anterior hemiblock (notched S wave in lead 2)
Sinus Venosus Atrial Septal Defect

Sx same
PE same
EKG ectopic atrial rhythm
ECHO may not see shunt by doppler study
CXR Scimitar sign / Snowman sign
Ventricular Septal Defect Membranous / Muscular
Sx SOB, orthopnea, PND
PE harsh systolic ejection or pansystolic murmur at the 4th LICS + a thrill
@LLSB - If large shunt, will develop a flow murmur of mitral stenosis
EKG biventricular hypertrophy
CXR increased pulmonary flow and PA size, increased
RV & LV size, small aorta
ECHO increased RV size + shunt noted by doppler study
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SURGERY in adults with sx or if QP/QS shunt > 1.5

POST-OP RBBB if corrected due to ventriculotomy, CHF
Patent Ductus Arteriosus

Sx SOB, orthopnea, PND, no sx, differential cyanosis
PE machinery continuous murmur at 2nd LICS may be only systolic if
pulmonary HTN
EKG LVH
CXR increased pulmonary blood flow and LV size, calcified ductus
ECHO increased flow in pulmonary artery
SURGERY symptoms or shunt with flow QP/QS shunt > 2
Coarctation of Aorta Pre or post ductal
Sx Claudication, HTN, CHF, no sx, differential BP in arms
PE systolic ejection murmur at the 2nd LICS, decreased femoral pulses, pulse
delay femoral to radial artery, decreased BP in femoral artery, associated with
bicuspid AV valve
EKG LVH
CXR upper rib notching on the inferior surface, aorta reversed 3 sign
ECHO TEE / MRI
SURGERY significant HTN, pressure gradient across > 20 mmHg
POST-OP aneurysm at surgical site (watch for rupture), long term HTN despite
good repair
COMMON CYANOTIC ADULT LESIONS: CO-MANAGE WITH CONSULT

Eisenmengers Complex
Reversed L to R shunt is secondary to progressive pulmonary HTN. Common in VSD,
ASD, PDA, usually not amenable to correction
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Tetralogy of Fallot partial or total correction

Transposition of Great Arteries
Single ventricle (single ventricle with a large VSD, tricuspid atresia)
S/P cardiac shunts (Rastelli, Fontan, Glen procedures)
COMPLICATIONS OF CONGENITAL HEART DISEASE

CHF RV systolic and diastolic dysfunction
(1) RV unable to function as the systemic ventricle
(2) Tricuspid valve does not function well with systemic pressures
(3) Development of pulmonary HTN
(4) Development of significant pulmonary valve or tricuspid insufficiency
(5) Infective endocarditis
Cerebral abscess (left to right shunt)
Sudden death cardiomyopathy, IHSS, TOF ventricular tachycardia
Atrial flutter cyanotic heart disease early electrical cardioversion, avoid negative inotropic
drugs, and need to anticoagulate.
WPW associated with Ebsteins anomaly & TGA
Thrombosis Pulmonary artery or surgical shunts
Cerebral hemorrhage
High-risk patients for procedures cardiac or noncardiac surgery, pregnancy
Erythrocytosis no phlebotomy unless Hyperviscosity Sypmtoms (headache, blurred vision,
dizziness, fatigue, myalgias, paresthesias), Rx with low dose iron until MCV improves
Aortic aneurysms s/p CoA repair, increased risk with pregnancy
CHD OUTLOOK
90% CHD patients are employable (Acyanotic > Cyanotic)
If parent with CHD (risk greater if male parent has CHD) there is a 5-7% risk of having a child
with CHD
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TRANSIENT ISCHEMIC ATTACKS

SUPORTIVE MEASURES
Oxygen, Glucose, control Fever
Keep SBP < 160 mmHg, DBP < 90 mmHg
Adequate hydration
HIGH RISK
LOW RISK
ABCD2 Risk Score

4-7
4-8% CVA Risk @ 2 days
Admit for Evaluation
ABCD2 Risk Score

0-3
1% CVA Risk @ 2 days
Outpatient Evaluation
Diffusion weighted MRI - STAT
Carotid Duplex
If sx carotid distribution, if sm or no neurological defect
If otherwise surgical candidate
SURGICAL THERAPY
Carotid site only
Sm or no neurologic defect
Surgical candidate
Carotid lesion > 70% obstruction
Surgical mortality/morbidity < 6%
MEDICAL THERAPY
Carotid or vertebral site
Anti-platelet agent for ischemic events
Warfarin for cardiac embolic ischemic events
Statin, ACEI, Diuretic, Risk Factor Rx
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TRANSIENT ISCHEMIC DISEASE

AHA/ASA: Stroke / TIA Guidelines. STROKE 2014
500,000 TIAs per year, 15% TIA proceed to CVA @ 3month, gretest risk in the first 48
hours.
TIA = Transient neurologic deficit with abrupt onset without evidence of infarction on
brain imaging (diffusion-weighted MRI), usually lasting less than 1hour.
Carotid distribution resolves usually within 14 mins / Vertebral within 8 mins, if
symptoms persist for greater than 1hour only 14% will resolve.
TIA may be a precursor for ischemic strokes in 50%, cardioembolic disease stroke in
30%, lacunar stroke in 15%.
Need to R/O Todds paralysis, complicated migraine, hypoglycemia, subdural bleed,
drugs, hypercoagulable states, vasculitis
ABCD2 Risk Score: 1point (Age >60: sBp >140, dBp >90: Clinical signs; speech
impairment: Duration 10-59 minutes: Diabetes); 2 points (unilateral weakness:
Duration 60 minutes. Stroke risk @ 48 hours: Score 0-3- 1% (low risk);
Score 4-5 - 4.1% (moderate risk), 6-7- 8.1% (high risk) Admit patient if Score >4.
If Rx started <1day, CVA rate decreased by 80% @ 3months.(EXPRESS Trial 2007)
Evaluation and therapy:

Determine carotid vs. vertebral distribution by history & exam.
Carotid: monocular vision loss, aphasia, personality changes, neglect
Vertebral: cranial nerve involvement, ataxia, bilateral weakness or sensory loss,
Diplopia, dysarthria, vertigo, altered consciousness
STAT diffusion-weighted MRI scan of head to exclude small CVA or bleed.
Carotid duplex: if sx in carotid distribution, if either no or small residual neurologic
defect and if patient otherwise a surgical candidate
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Ischemic etiology:
First choice is ASA @325 mg then, 81mg daily (RR reduction =18%).
Alternative to ASA: Aggrenox (ASA + dipyridamole) BID - (RR reduction over
ASA = 23%) or Clopidogrel 75 mg/d, an ADP blocker (RR reduction over ASA =
10%)
Statin + risk factor therapy
2014 AHA/ASA recommendations: The combination of aspirin and clopidogrel
might be considered for initiation within 24 hours of a minor ischemic stroke or
TIA and for continuation for 90 days.
Cardioembolic etiology: multiple stroke sites, presence of atrial fibrillation, mitral
stenosis, mechanical heart valve, recent MI/ LV aneurysm or cardiac clot, patent
foramen ovale
IV heparin / warfarin, and risk factor therapy
Endarterectomy: carotid site, small or no neurologic defect, significant carotid
obstruction >70%
Low surgical morbidity and mortality < 6%
Angioplasty + stent - high risk surgical patient, s/p carotid surgery
Medical therapy: carotid or vertebral site, risk factor therapy, anticoagulant depending on
mechanism of TIA, Statin, and ACE inhibitor.
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CEREBROVASCULAR ACCIDENT
Etiology:
85% ischemic {thrombotic or embolic (cardiac-to-artery or artery-to-artery)}
15% hemorrhagic (intracerebral, subarachnoid, subdural, epidural)
Onset of stroke:
750,000 strokes in USA per year resulting in >150,000 deaths
Thrombotic etiology: 80% present as completed defects and 20% progress.
Lacunar strokes represent 20% of all strokes and results from thrombosis of penetrating
branches of cerebrum & brainstem related to systemic hypertension
Embolic etiology: sudden onset of completed sx without loss of consciousness.
Hemorrhagic etiology: sudden onset of severe headache.
Hemorrhagic or brain stem etiology: sudden loss of consciousness
Young Age: suggest AV malformation, cerebral aneurysm, endocarditis, vasculitis,
traumatic carotid disease, hypercoagulability, neoplasm, patent foramen ovale,
vasoactive drug (cocaine).
Evaluation:
Stat CT of head without contrast to R/O bleed or tumorMay remain normal for 6-24 hrs post ischemic stroke and may miss events in the
posterior fossa or cortical surface
MRI head scan- more reliable early (1hr) and with lesions involving the cortical white
matter, or posterior fossa.
MR Angiogram tend to overestimate degree of vascular stenosis, leless helpful with
lesions in the carotid siphon or middle cerebral artery.
Four Vessel Selective Angiography gold standard benefit must be weighed against
the risk 0.5 3%
Transesophageal echocardiogram if young age or unclear etiology (aortic arch atheroma,
atrial septal defect, cardiac clot, valvular disease)
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Hypercoagulable State:
Test at least 2 months post stroke
5% likelihood in general adult CVA population
Hereditary: < 45 years old, recurrent thrombosis, thrombosis during pregnancy, +
FH, skin necrosis - Protein C and S, antithrombin III
Acquired:
<
45
years
old,
anticardiolipin,
lupus
anticoagulant,
and
myleoproliferative syndromes.
Clinical Syndromes:
Internal Carotid Artery: ipsilateral monocular blindness, contralateral weakness or sensory
loss
Middle Cerebral Artery: contralateral weakness or sensory loss, deficit face & arm > leg,
visual field defect, aphasia (dominant), neglect (non-dominant)
Anterior Cerebral Artery: contralateral weakness or sensory loss, deficit leg > arm & face,
personality changes
Posterior Circulation: cortical blindness, ataxia, ipsilateral cranial nerve involvement,
diplopia, dysarthria, altered LOC
Medical Therapy:
ANTI-PLATELET agents:
Primary CVA Prevention: ASA 81mg daily -only if 10 year risk for CHD events >6-10%,
in men 45-79 years, women 55-79. (USPSTF 09)
Acute CVA therapy: ASA 160-325 mg within 48 hours of a CVA, decreases nonfatal
CVAs with only slight increase of hemorrhage
Secondary CVA Prevention:
-
ASA 50-325 mg daily - ASA produces an 18% relative risk reduction (2.5% AAR) over
placebo. ASA is cheap and well tolerated.
Aggrenox (Dipyridamole SR200 mg + ASA25 mg) BID. ESPS-2 and ESPRIT trials
show a slight absolute risk reduction over ASA (23% relative risk reduction over ASA).
More side effects and more expensive.
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Clopidogrel (Plavix) 75 mg/d - if TIA or CVA on ASA or if unable to take ASA

(CAPRIE Trial 10% RRR over ASA).
2014 AHA/ASA recommendation: If CVA/TIA is attributable to severe stenosis
(70-99%) of a major intracranial artery, Clopidogrel 75 daily + ASA 81 mg daily
for 90 days may be reasonable.
PRoFESS Trial - Aggrenox = Clopidogrel in rate of recurrent CVA. MATCH Trial - no

advantage of adding ASA to clopidogrel to prevent second CVA or TIA and increased risk of
serious bleeding.
HEPARIN
Stroke in evolution - no evidence that helpful - if used, avoid heparin bolus, use heparin
drip @ 12 units/kg/hr
Cardioembolic strokes indicated - wait for CT to R/O bleed on admission; if stroke
large by exam or by CT - hold heparin for two weeks, (only 2-3% recurrent emboli per
week - risk higher for hemorrhagic conversion of CVA than risk of repeat emboli), then
start warfarin at maintenance dose.
Native valves endocarditis - no role for anticoagulation.
Prosthetic mechanical valve endocarditis: stop anticoagulation for at least two weeks to
allow time for the thrombus to organize. Restart warfarin watching for hemorrhagic
conversion to a hemorrhagic stroke.
THROMBOLYSIS: r-tPA (narrow therapeutic window)
Results: Therapy increases acute intracerebral hemorrhage but results in a 30% less
disability @ 3 months, no change in mortality @ 1year.
Recombinant tissue plasminogen activator: Front-loaded (0.9 mg/kg; maximum 90 mg;
10% as bolus, remainder infused over 1hr)
Stroke management team required
Inclusion criteria:
-
Age >18 yrs, onset less than 4.5 hours before treatment,
Baseline CT showing no bleed,

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Clinically meaningful neurological defect (ECASS III, SITS-ISTR Trials)
Help to Harm Ratio 33:1 @ 3 hours; 6:1 @ 4.5 hours

Exclusion criteria:
Minor or rapid improving signs or symptoms / bleed on CT
Seizure at onset of CVA,
Prior CVA or serious injury within 3months,
Major surgery or trauma within 2 weeks,
GI / GU hemorrhage within 3weeks, SBP >185 mmHg
DBP >110 mmHg,
Symptoms of subarachnoid hemorrhage,
Arterial puncture or lumbar puncture within 1week
Platelet count < 100,000 / mm3, warfarin (INR > 1.7)
Heparin therapy within 48 hrs.with elevated aPTT
Clinical pericarditis,
Pregnancy or lactation
If initiated between 3-4.5 hours additional exclusions: age >80 years, combination of CVA
and diabetes, NIH Stroke Score > 25, use of warfarin independent of INR level
STATINS: (even if LDL-C < 100 mg/dl)
High-intensity statins according to 2013 ACC/AHA guidelines
Lower CVA risk 20% for primary prevention
Lower CVA risk by 32% for secondary prevention
Trials with significant decreased relative CVA reduction: 4S - 30% / CARE - 31% /
LIPID 19% / HPS - 30%
Benefit in the absence of CAD (SPARCL Trial) - 16% RRR.
ACE Inhibitor Therapy:
Start chronic BP therapy 2 days - 2 weeks post CVA, ~ once cerebral edema has resolves
Hope Trial (Ramipril 10 mg/d)
Lowered risk of death, MI, CVA, CABG, heart failure in high risk group with
preexisting vascular disease 23% reduction in MI, CVA, death from CVD
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Progress Trial (ACEI + diuretic)

ACEI reduced ischemic and hemorrhagic CVA by 28% even in normotensive
patients.
Consider ACEI plus diuretic as initial HTN therapy. Beta-blocker are less effective (do
not lower Central aortic BP).
SURGICAL THERAPY: Carotid distribution only
Carotid Endarterectomy (CEA):
Symptomatic patients with > 70% stenosis
Benefit is noted if surgical mortality and morbidity < 6% (NASCET & ECST) & if life
expectancy at least 5 years. With surgery the absolute risk reduction (ARR) 17%.
NNT requires 6 surgeries to prevent 1 stroke in 5 years.
Consider surgery within 2 weeks post- ischemic event.
Symptomatic patients with 50-69% stenosis
If surgical mortality and morbidity <3% & if life expectancy at least 5 years
Less benefit (men > women)
22 surgeries to prevent 1 stroke in 5 years
Symptomatic patients with < 50% stenosis
No surgical benefit over medical rx
Asymptomatic patient with > 60-99% stenosis (SPACE trial)
If surgical mortality and morbidity < 3%
Absolute risk reduction only 1.2% (ACAS)
Benefit only noted after 5 years postop / less benefit in women
200 surgeries to prevent 1 stroke after 5 years
Angioplasty & Stent (CAS): (ICSS, CREST, SAPPHIRE trials)
If the carotid lesion is not amenable to surgery, if co-morbid medical conditions preclude
CEA, or if post-CEA stenosis is present.
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CEA compared to CAS has a lower stroke and death rate 4.4 versus 2.3% but has a
higher MI rate 2.3versus 1.1%.
Results vary depending upon type of cerebral protection, patient selection and age. Still
await the further studies.
Complications:
Seizures: evaluate Na and glucose levels
SIADH: low serum Na+ with high urine Na+
Cerebral Edema: maximal on day 3-5 but may persist for 10 days. Hyperventilate to
pCO2 = 35, Mannitol & surgical consult
Hypertension:
-
Ischemic CVA: lower SBP 220 /DBP 120mmHg by 15% in 24 hrs. BP goal < 140/90
mmHg. For recent lacunar stroke reasonable SBP target < 130 mmHg.
Hemorrhagic CVA:
o If known HTN, lower MAP <130 mmHg,
o If no prior HTN, lower MAP <110 mmHg
o Post aneurysm clipping raise SBP to maintain CPP - CPP (70 mmHg) = MAP (90
mmHg) ICP (20 mmHg) with fluids and/or vasopressors to prevent spasm + use
nimodipine.
o After 7days start to lower BP toward goal of < 140/90 mmHg
Infection: Pneumonia > urinary
Pulmonary Emboli
Secondary prevention
PFO:
-
antiplatelet therapy if none used prior
if both PFO and a venous source of embolism are present, anticoagulation is

recommended. If contraindicated, IVC filter is reasonable.
available data (RESPECT, PC Trial) do not support a benefit for PFO closure compared
to medical treatment.
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in the setting of PFO and DVT, PFO closure by a transcatheter device might be
considered, depending on the risk of recurrent DVT.
Intracranial atherosclerosis:
-
if attributable to severe stenosis (70-99%) add Clopidogrel 75 mg daily with ASA for
first 3 months
if attributable to 50-99% stenosis, maintain SBP < 140 mmHg, high intensity statins
if attributable to 50-99% stenosis, stenting is not recommended and considered

investigational
AF:
-
oral anticoagulation (NOAC only for non-valvular AF or Warfarin)
if Warfarin/NOAC are contraindicated, may consider ASA + Copidogrel
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DEEP VENOUS THROMBOSIS

ACCP GUIDELINES 2012; Chest 2012;41(2):e419S-e94S
PATHOGENESIS: 7th ACCP Conference Chest 2004; 126: 401S

Location: at any point along the vein but most originate in the valve pockets
Lower limbs (calf veins) > upper limb or right heart
Involvement of superficial veins is usually benign and self-limited, but may extend to deep
venous system
Involvement of deep veins higher risk for embolization, proximal > distal; 30% of deep calf
vein clots may extend to proximal veins.
Most significant and fatal emboli arise in the proximal thigh veins.
Complete resolution of large clots rare < 10%, while resolution of small calf veins clots are
often complete.
Deep venous thrombosis closely related to pulmonary emboli:
-
50% patients with DVT will have pulmonary emboli by lung scan.
70% patients with pulmonary emboli will have DVT.
Recurrent DVT 30% within eight years despite therapy.

RISK FACTORS: (LITE Trial Am J Med 2004; 117:119)
o Activation of coagulation (surgery, anesthesia, malignancy, HRT, BCP, pregnancy,
shock, burns, hypercoagulable states, hyperhomocysteinemia, erythropoietin,
chemotherapy)
o Venous stasis (surgery, obesity, immobilization, CHF, prior DVT, varicose veins,
age, hospitalization, acute MI, CVA)
o Vascular injury (surgery, trauma, central venous catheters)
PHYSICAL EXAMINATION:
Clinical signs and symptoms not reliable

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Predictive accuracy of physical examination to predict DVT is only 40-50%.

o Unilateral peripheral edema
o Leg pain (Homan's sign)
o Warmth
o Venous dilation
o Palpable cord
o Ascites
Clinically exclude:
o Cellulitis
o Lymphangitis
o Drug induced (CCB)
o Baker's cyst
o Muscle tear/injury
OBJECTIVE TESTING: 2007 AAFP / ACP GUIDELINES (Ann Int Med 5(1))
1) Evaluate pretest probability with Wells Criteria - see page **
2) D-dimer Test by Elisa ot turbidimetric method. If test negative (< 500 mcg/L) with a
low or intermediate pre-test probability excludes DVT or pulmonary embolus. If
positive (> 500 mcg/L) results are not specific.
3) Venous Ultrasound proximal > distal vein accuracy. Positive predictive value 94% for
first episode for proximal clot but may miss iliac, femoral clots. If negative with high
clinical suspecion, repeat study in 5 days. Sensitivity only 75% for calf clots.
4) Venography used when venous ultrasound equivocal, may cause phlebitis.
Accuracy better with proximal > distal vein disease. Test is able to detect only 50% calf
clot.
MRI venography is more sensitive than Doppler in detecting DVT but inferior to
contrast venography.
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TREATMENT OF PROXIMAL DEEP VEIN THROMBOSIS: Medical / Mechanical

If untreated 50% result in PE
Low-Molecular Heparin (LMWH) Enoxaparin (Lovenox)
First choice over UFH becauses reduces mortality and major bleeding.
ACP/AAFP 2007Guidelines (Ann Int Med 146 (3))
Dosage = 1mg/kg q 12 hrs. (up to 150 mg) SQ bid or
1.5 mg/kg (up to 180 mg.) S.Q. daily. Continue for 5-7days.
Use actual body weight.
In an obese patient when a dose of enoxaparin > 100 mg is given, measure anti
Factor X activity at 6-8 hours after the first dose to allow optimal dosage
adjustment.
If GFR <30 decrease dose to 0.5 mg/kg.
There is only incomplete protamine reversal (50%) with enoxaparin..
Unfractionated Heparin (UFH) weight-adjusted therapy
Goal aPTT > 1.5-2.5 X control; IV: 80 units/kg bolus with infusion 18 units/kg
per hour; aPTT measured @ 6 hrs.post bolus and at least daily.
Alternative therapy: SQ dosage of 17,500 U every 12 hours.
Fondaparinux (Arixtra)
Dosage = 5 mg SQ daily if weight <50 kg; 10 mg SQ if weight >100 kg.
Continue for 5 days. There is only incomplete protamine reversal (50%).
To measure effect can measure anti factor Xa activity if needed.
Start therapy with UFH / LMWH/ Fondaparinux for at least 5 days with warfarin until
INR therapeutic for 2 days. Start with warfarin @ 10 mg/day to decrease risk of induced
hypercoagulable state due to a rapid drop in Protein C. Factor VII also quickly drops
prolonging the INR, but not providing antithrombotic benefit until factor II decreases
over 5-7days.
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DURATION of WARFARIN THERAPY: PT/INR goal is 2-3

Chest 2008; 133(6):454S-545S ; Chest 2012;41(2):e419S-e94S
o 3 months Rx: for first DVT event with reversible causes - {recurrent DVT risk <3%}
o 6-12 months Rx: idiopathic DVT, DVT at unusual site, isolated calf DVT {recurrent
DVT risk <10%}
o 12 month Rx: for DVT associated with Protein C or S levels > 90%
o VTE peripartum: continue at least 6 weeks postpartum; enoxaparin 40 SQ/d
o Morbid obesity: UFH titrate aPTT 1.5-2.5 upper normal/ bridge for 5 days (J Thromb
Haemost 2007; 5;119.)
o Renal failure: Enoxaprin contraindicated if CrCL <15 mg/min; 1mg/kg if CrCl 15-30
mL/min: UFH 80 U/kg load, then 18 U/kg/hr
o Post therapy do venous Doppler & D dimer - if negative - stop therapy if positive,
then continue for 6 more months and then restudy.
**** Continue warfarin as long as tests are positive ****
o Indefinite Rx: if recurrent or life-threatening VTE, antiphosolipid antibodies,
Antithrombin III deficiency, HomozygousV Leiden, long-term risk (cancer) {recurrent DVT risk >10%}
o Active cancer patients with DVT or PE should recieve LMWH for 3-6 months
followed by indefinite warfarin Rx.
o If recurrent DVT with malignancy or hypercoagulable state may have warfarin
resistance - switch to lifelong Lovenox therapy
(Chest 2008; 133:454 // Ann Intern Med 2008; 149:481)
New Oral Anticoagulants (NOACs) see pages 25-27:

o Dabigatran (Pradaxa) = direct thrombin inhibitor
Treatment of DVT and PE in patients who have been treated with a
parenteral anticoagulant for 5-10 days
Used to reduce the risk of recurrence of DVT and PE in patients who have
been previously treated
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Dosage: use only with CrCl>30mL/min 150 mg orally BID after 5-10 days
of parenteral anticoagulation
When CrCl<50 mL/min avoid concomitant use of P-gp inhibitors
o Rivaroxaban (Xarelto) = factor Xa inhibitor
o Treatment of DVT and PE
o Used to reduce the risk of recurrence of DVT and PE following initial 6
month treatment for DVT and/or PE
o Used as prophylaxis of DVT following hip or knee replacement surgery
o Dosage:
For treatment of acute DVT and PE: 15 mg BID with food for the
first 21 days. After 21 days change to 20 mg once daily with food
at the same time each day.
For reduction of recurrence of DVT and PE: 20 mg once daily with
food at the same time each day.
For prophylaxis of DVT following hip or knee replacement
surgery: 10 mg once daily with/without food. The initial dose
should be taken 6-10 hours after surgery provided that hemostasis
has been established. Duration of treatment: 35 days after hip
replacement surgery and 12 days after knee replacement suregery.
o Not recommended in prosthetic valves.
o Apixaban (Eliquis) = factor Xa inhibitor
Used as prophylaxis of DVT following hip or knee replacement surgery
Dosage:
2.5 mg BID, intial dose should be taken 12-24 hours after surgery
Duration of treatment: 35 days after hip replacement surgery,
12 days after knee replacement surgery
At 2.5 mg BID, co-adminisration with strong dual inhibitors of
CYP3A4 and P-gp should be avoided.
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THROMBOLYTIC THERAPY:
Indicated only for massive ileofemoral thrombosis DVT with gangrene risk
May be indicated for extensive proximal vein thrombosis in patients with a low risk of
bleeding
Does decrease venous clot faster that UFH or LMWH and therefore may decrease
postphlebitic syndrome but only at a higher risk of bleeding
Rx: Altaplase 100 mg over 2 hrs.; Streptokinase 250,000 U over 30 min. then 100,000 U
over 24 hrs.; Urokinase 4,400 U/kg over 10 min, then 2,200 U/kg over 12 hr.
TREATMENT OF DISTAL (calf) DVT:

If untreated 5-20% result in PE; If untreated up to 30% progress to DVT.Followup
venous Dopplers are recommended looking for extension.
Therefore treatment identical to that of proximal deep vein thrombosis
TREATMENT OF UPPER EXTREMITY DVT:

Axillary vein or Subclavian vein
Classified as: Primary: effort thrombosis
Secondary: due to indwelling IV devices, tumor, hypercoagulopathy
Dx: ultrasound or venogram
Rx: UFH / warfarin for 6-12 months; if marked swelling & low-bleeding risk may
consider Urokinase 250,000 IU over 1hr, then 1000 IU for 24 hr.
TREATMENT OF SUPERFICIAL THROMBOPHEBLITIS (SP):

Rx for infusion-related thrombophlebitis is topical or oral diclofenac. Rx for
uncomplicated SP is heat, elevation and NSAIDS for 7-10 days, if extension small < 5
cm and location distant to saphenofemoral or saphenopopliteal junctions.
Rx to prevent progression to DVT: enoxaprin 40 mg sqqd X 5 days followed by warfarin
for 1month (ACCP 2008).
If symptoms persist or additional risk factors are present, repeat initial ultrasound in 5
days to r/o proximal vein progression.
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NONPHARMACOLOGICAL INFERIOR VENA Caval Interruptions:

Permanent - therapeutic
Retrievable - used for prevention of PE in high-risk patients (trauma) - remove in
2-3weeks
Therapeutic indications:
1) Anticoagulation bleeding
2) Inability to use anticoagulation (VTE within 7days of brain surgery, high-risk
patients undergoing urgent major surgery)
3) Pulmonary emboli despite therapeutic anticoagulation
4) Major PE with severe cardiovascular instability
When possible use anticoagulation with Cava interruptions
HYPERCOAGULABLE STATE:
o High risk patients:
Life threatening DVT, FH of DVT, unusual site of DVT, unprovoked
DVT, recurrent DVT, h/o warfarin induced skin necrosis.
Screening panel:
Activated Protein C resistance assay, if + then Factor V Leiden by PCR,
Prothrombin gene mutation (PCR), Antithrombin activity, Protein C & S
activity, Factor VIII activity
Homocysteine level, Anticardiolipin antibodies (IgG, IgM)
Lupus anticoagulant panel antibodies (IgG, IgM), Lupus anticoagulant
panel
o Lower risk patient:
Provoked clot, negative or minimal FH, non-life threatening clot
Screening panel:
Activated Protein C resistance assay, if + then Factor V Leiden by PCR
Prothrombin gene mutation (PCR), Homocysteine level, Anticardiolipin
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Measure screening panels after full course of anticoagulation for 3-6 months.
Need to be off warfarin for 2 weeks.
If high - risk patient convert to Lovenox and stop 24 hours before testing.
Homocysteine &antiphospholipid antibodies can be checked on heparin or
warfarin.
COMPLICATIONS OF THERAPY:
Heparin: 5-10% bleeding
Natural/ herbal agents with additional antiplatelet activity: cat's claw, dong quai, evening
primrose, feverfew, garlic, ginger, ginkgo, red clover, horse chestnut, green tea, ginseng
Protamine 1mg per 100 units heparin if needed right after heparin given:
50% dose if given greater than 1hour after heparin,
25% dose if given greater than 2 hours after heparin
Thrombocytopenia - HAT / HIT - 2-3% (CHEST 2008; 133:340S-380S)
Type I - early onset,(onset day 1-4). Observe; no thrombosis.
Type II - late onset, IgG mediate (usual onset day 5-14 up to 4 weeks), thrombotic
sequelae occur, rare hemorrhagic sequelae
Evaluate with Heparin antibody (ELISA) or Serotonin Release Assay. If platelets
fall >50%, d/c the heparin and add lepirudin (renal clearance) 0.4 mg/kg, then
0.15 mg/kg/h or argatroban (hepatic clearance) 2 mcg/kg/min with subsequent
dose to keep, after 2 hrs, aPTT 1.5-3x control (not to exceed 100). Fondaparinux
(Arixtra) may also be used but supporting data considered weak (ACCP 2012).
Do not start warfarin until platelet count >150,000 - Check for DVT, even if no
symptoms. Rx for least 6 weeks if no thrombosis, continue 3-6 mo if thrombosis.
Overcoagulation:
INR <5 ----hold warfarin 2 days
INR 5-9 --- hold warfarin & vitamin K 1-2.5 mg po
INR >9 ---- hold warfarin & vitamin K 2.5-5 mg po
INR >20 -- hold warfarin & admit for IV vitamin K 10 mg
Serious bleeding -- FFP + vitamin K 10 mg slow IV (anaphylaxis)
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Warfarin resistance = INR < 2 with stable warfarin dose >15 g/day
Can be acquired or hereditary (genetic polymorphism VKORC1, CYP2C9)
Review medicine compliance, diet and drug interactions.
Warfarin drug interactions: http://www.coumadin.com/pdf/Interactions_With_COUMADIN.pdf
Check warfarin level:
- if therapeutic = pharmacodynamic resistance
- if level is subtherapeutic either non-compliance or resistance
Increase warfarin dose or switch to LMWH or fondaparinux.
Warfarin pharmacokinetic resistance (diminished absorption or increased elimination
of the drug):
- genetic factors (duplication or multiplication of cytochrome P450 enzyme
genes : CYP2D6, CYP2A6)
- hypoalbuminemia may increase the free fraction of warfarn resulting in
enhaced rates of clearance and a shorter plasma half-life
- hyperalbuminemia may paradoxically also contribute to warfarin resistance via
drug binding
- hyperlipidemia: several observers have found that lowering TG increases the
sensitivity to warfarin irrespective of the means used to achieve this decrease.
- diuretics: may decrease the response to warfarin by reducing the plasma volume
with a subsequent increase in clotting factor activity.
Warfarin failure = a new thrombotic event despite a therapeutic prothrombin time and INR.
Most commonly seen in patients with malignant diseases or lupus anticoagulant/antiphospholipid
antibody (APLA) syndrome.
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PREOPERATIVE EVALUATION FOR

NONCARDIAC SURGERY
2014 ACC/AHA Guidelines
Approach to Preoperative Evaluation

1.
2.
3.
4.
Determine temporal necessity of operation

Determine the combined surgical and patient risk of major adverse cardiac events
(MACE) Lee/ Gupta Risk Index
Evaluate for ACS or clinical risk factors
Determine activity status (DASI)
Less < 4 METS requires further testing
Determine need for preoperative cardiac testing and therapy
5.
Temporal necessity of operations:

-
Emergency procedure: life or limb is threatened if not in OR within < 6 hours

Urgent procedure: life or limb is threatened if not in OR between 6-24 hours
Time-sensitive procedure: when a delay of > 1-6 weeks to allow for an evaluation and
significant changes in management will negatively affect outcome (e.g.: oncologic
procedures)
Elective procedure: can be delayed up to 1 year.
Risk of surgical procedures:

-
Low risk: when the combined surgical and patient characteristic predict a risk of a major
adverse cardiac event (MACE) of death or MI of < 1% (e.g.: cataract and plastic surgery)
Elevated risk: when risk of MACE 1%
Calculation of Risk to Predict Perioperative Cardiac Morbidity

RCRI (Revised Cardiac Risk Index) calculator assesses perioperative risk of major
cardiac complications (MI, pulmonary edema, ventricular fibrillation or primary cardiac
arrest and complete heart block)
o http://www.mdcalc.com/revised-cardiac-risk-index-for-pre-operative-risk/
Qx Cal App (Lee Criteria) - Free
o For patients with a low risk of perioperative MACE, further testing is not
recommended before the planned operation
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Tools have been created by the American Colelge of Surgeons:
o http://www.riskcalculator.facs.org/
o http://www.surgicalriskcalculator.com/miorcardiacarrest
o http://www.qxmd.com/calculate-online/cardiology/gupta-perioperative-cardiacrisk (Gupta risk calculator)
o Qx Calculate App (Gupta Risk) free
Clinical Risk Factors
CAD (history of MI, history of positive exercise stress test, current chest pain considered
fue to myocardial ischemia, use of nitrate therapy, ECG with pathological Q waves)
Heart failure with preserved or reduced LV function (presence or history of PE,
bilateral rales or S3 gallop / PND / CXR showing pulmonary vascular redistribution)
NTP levels independently predict cardiovascular events in the first 30 days after vascular
surgery.
Valvular heart disease
Recommended for patients with clinically suspected moderate or greater degree of
valvular stenosis or regurgitation undergo perioperative echocardiography. If no prior
echocardiograph within 1 year or if there is a significant change in clinical status or
physical examination since last evaluation, echocardiogram is indicated.
For adults who meet standard indications for valvular intervention (replacement and
repair) onthe basis of symptoms and severity of stenosis or regurgitation, valvular
intervention beforeelective non-cardiac surgery is effective in reducing perioperative risk.
Aortic stenosis: Elevated-risk elective noncardiac surgery with appropriate intraoperative

and postoperative hemodynamic monitoring is reasonable to perform in patients with
asymptomatic severe aortic stenosis. (2015 J Am Coll Cardiol 65(3): 295-302).
Mitral
stenosis:
Elevated-risk
elective
noncardiac
surgery
using
appropriate
intraoperative and postoperative hemodynamic monitoring may be reasonable in

asymptomatic patients with severe mitral stenosis if valve morphology is not favorable
for percutaneous mitral balloon commissurotomy.
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Arrhythmias and conduction disorders

-
AF: if clinically stable no changes in therapy, except for adjustment of anticoagulation
Ventricular arrhythmias (single PVCs or non-sustained VT): no therapy unless it results

in hemodynamic compromise or are associated with significant structural heart disease or
inherited electrical disorders
Pre-existing conduction disorders: sinus node dysfunction, atrioventricular block require

caution if peroperative beta-blocker therapy is being considered. Isolated bundle branch
block and bifascicular block generally do not contraindicate use of beta-blockers.
High-grade conduction abnormalities (complete AV block), if unanticipated, require

temporary or permanent pacing.
Cardiovascular implantable electronic devices (ICD): before elective surgery in a
patient with an ICD, the surgical/procedure team and clinician following the ICD should
communicate in advance to plan perioperative management of the ICD.
Pulmonary vascular disease:
Chronic pulmonary vascular-targeted therapy (i.e., phosphodiesterase type 5 inhibitors,

solubleguanylatecyclase stimulators, endothelin receptor antagonists, and prostanoids)
should be continued unless contraindicated or not tolerated in patients with pulmonary
hypertension who are undergoing noncardiac surgery.
Unless the risks of delay outweigh the potential benefits, preoperative evaluation by a
pulmonaryhypertension specialist before noncardiac surgery can be beneficial for patients
with pulmonaryhypertension, particularly for those with features of increased
perioperative risk.
Adult congenital heart disease (ACHD):
These patients should have their preoperative evaluation in a regional center specializing
in congenital cardiology
High-risk include: prior Fontan procedure, cyanotic ACHD, pulmonary arterial

hypertension, clinical HF, significant dysrhythmia.
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Activity Status (Exercise and Functional Capacity)

-
Good functional status = low risk
Reduced functional status = increased risk
If no recent exercise stress test, functional status can be estimated from activities of daily
living, expressed in terms of metabolic equivalents (METs):
1 MET = resting or basal oxygen consumption of a 40yo, 70 kg man
>10 METs = excellent functional capacity
7-10 METs = good functional capacity
4-6 METs = moderate functional capacity
<4 METs = poor or unknown functional capacity Requires further CV testing
DASI (Duke Activity Status Index) scale

Activity
METS
Can you
1. take care of yourself, that is, eating, dressing, bathing, or using the toilet?
2.75
2. walk indoors, such as around your house?
1.75
3. walk a block or 2 on level ground?
2.75
4. climb a flight of stairs or walk up a hill?
5.50
5. run a short distance?
8.00
6. do light work around the house like dusting or washing dishes?
2.70
7. do moderate work around the house like vacuuming, sweeping floors, or carrying in groceries?
3.50
8. do heavy work around the house like scrubbing floors or lifting or moving heavy furniture?
8.00
9. doyardwork like raking leaves, weeding, or pushing a power mower?
4.50
10. have sexual relations?
5.25
11. participate in moderate recreational activities like golf, bowling, dancing, doubles tennis, or
throwing a baseball or football?
12. participate in strenuous sports like swimming, singles tennis, football, basketball, or skiing?
6.00
7.50
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Preoperative Cardiac Testing

-
12-lead EKG
Preoperative resting 12-lead electrocardiogram (ECG) is reasonable for patients with
knowncoronary heart disease, significant arrhythmia, peripheral arterial disease,
cerebrovasculardisease, or other significant structural heart disease, except for those
undergoing a low-risk surgery.
Preoperative resting 12-lead ECG may be considered for asymptomatic patients without
knowncoronary heart disease, except for those undergoing low-risk surgery
Routine preoperative resting 12-lead ECG is not useful for asymptomatic patients
undergoinglow-risk surgical procedures
Assessment of LV function
-
It is reasonable for patients with dyspnea of unknown origin to undergo preoperative

evaluation of LV function.
It is reasonable for patients with HF with worsening dyspnea or other change in clinical
status toundergo preoperative evaluation of LV function.
Reassessment of LV function in clinically stable patients with previously documented LV

dysfunction may be considered if there has been no assessment within a year.
Routine preoperative evaluation of LV function is not recommended
Exercise stress testing for myocardial ischemia and functional capacity

-
For patients with elevated risk and excellent (>10 METs) functional capacity, it is
reasonable to forgo further exercise testing with cardiac imaging and proceed to surgery.
For patients with elevated risk and unknown functional capacity, it may be reasonable to
performexercise testing to assess for functional capacity if it will change management.
For patients with elevated risk and moderate to good (4 METs to 10 METs) functional
capacity, it may be reasonable to forgo further exercise testing with cardiac imaging and
proceed to surgery.
For patients with elevated risk and poor (<4 METs) or unknown functional capacity, it
may bereasonable to perform exercise testing with cardiac imaging to assess for
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myocardial ischemia if it will change management.

-
Routine screening with noninvasive stress testing is not useful for patients at low risk for
noncardiac surgery.
Cardiopulmonary exercise testing

-
Cardiopulmonary exercise testing may be considered for patients undergoing elevated

riskprocedures in whom functional capacity is unknown
Non-invasive Pharmacological stress testing

-
It is reasonable for patients who are at an elevated risk for noncardiac surgery and have
poor functional capacity (<4 METs) to undergo noninvasive pharmacological stress
testing (either pharmacological stress MPI or dobutamine stress echocardiogram) if
it will change management.
Routine screening with noninvasive stress testing is not useful for patients undergoing
low-risk noncardiac surgery.
Special situations:
In patients with abnormal resting EKG (LBBB, LVH with strain pattern, digitalis
effect) concomitant stress imaging with echocardiography or MPI may be an
appropriate alternative.
In patients with LBBB, exercise MPI has an unacceptably low specificity because
of septal perfusion defects that are not related to CAD. In these patients
pharmacological stress MPI, particularly with regadenoson is suggested over
exercise stress imaging.
Regadenosone has a more favorable side-effect profile and appears safe for use in
patients with bronchospasm.
Dobutamine should be avoided in patients with serious arrhythmias or severe
hypertension.
All stress agents should be avoided in unstable patients!!!
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In patients in whom echocardiographic image quality is inadequate for wall

motion assessment (morbid obesity, severe COPD), alternative methoods such as
MPI may be appropriate.
Coronary Angiography
-
Routine preoperative coronary angiography is not recommended.
Evidence does not support the use of an ambulatory EKG as the only diagnostic test to
refer patients for coronary angiography, but it may be appropriate in rare circumstances
to direct medical therapy.
Perioperative Cardiac Therapy

Coronary revascularization before noncardiac surgery
-
Revascularization before noncardiac surgery is recommended in circumstances in which

revascularization is indicated according to existing clinical practice guidelines (CPGs).
It is not recommended that routine coronary revascularization be performed before

noncardiacsurgery exclusively to reduce perioperative cardiac events.
Timing of elective noncardiac surgery in patients with previous PCI

-
Elective noncardiac surgery should be delayed 14 days after balloon angioplasty and 30
days after BMS implantation.
Elective noncardiac surgery should optimally be delayed 365 days after drug-eluting stent
(DES) implantation.
In patients in whom noncardiac surgery is required, a consensus decision among

treatingclinicians as to the relative risks of surgery and discontinuation or continuation of
antiplatelettherapy can be useful.
Elective noncardiac surgery after DES implantation may be considered after 180 days if
the risk of further delay is greater than the expected risks of ischemia and stent.
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Elective noncardiac surgery should not be performed within 30 days after BMS
implantation orwithin 12 months after DES implantation in patients in whom dual
antiplatelet therapy (DAPT) will need to be discontinued perioperatively.
Elective noncardiac surgery should not be performed within 14 days of balloon

angioplasty in patients in whom aspirin will need to be discontinued perioperatively.
Perioperative Medical Therapy

Beta-blockers therapy:
-
Beta-blockers should be continued in patients undergoing surgery who have been on

beta-blockerschronically.
It is reasonable for the management of beta-blockers after surgery to be guided by clinical

circumstances (e.g.: hypotension, bradycardia, bleeding), independent of when the agent
was started.
In patients with intermediate- or high-risk myocardial ischemia noted in preoperative risk

stratification tests, it may be reasonable to begin perioperative beta-blockers.
In patients with 3 or more RCRI risk factors (e.g., diabetes mellitus, HF, CAD, renal
insufficiency, cerebrovascular accident), it may be reasonable to begin beta-blockers
before surgery.
In patients with a compelling long-term indication for beta-blocker therapy but no other
RCRI risk factors, initiating beta-blockers in the perioperative setting as an approach to
reduce perioperative risk is of uncertain benefit.
In patients in whom beta-blocker therapy is initiated, it may be reasonable to begin

perioperative beta-blockers long enough in advance to assess safety and tolerability,
preferably more than 1 day before surgery.
Beta-blocker therapy should not be started on the day of surgery!!!
Abrupt withdrawal of long-term beta-blockers is harmful.

Statin therapy:
Statins should be continued in patients currently taking statins and scheduled for
noncardiacsurgery.
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Perioperative initiation of statin use is reasonable in patients undergoing vascular surgery.
Perioperative initiation of statins may be considered in patients with clinical indications

according to GDMT who are undergoing elevated-risk procedures.
Alpha-2 agonists therapy:

-
Alpha-2 agonists for prevention of cardiac events are not recommended in patients who
are undergoing noncardiac surgery.
Calcium channel blockers therapy:

-
Shown to reduce ischemia and supraventricular tachycardia (SVT), reduced death/MI

(Diltiazem). Dihydropyridines and verapamil did not decrease the incidence of
myocardial ischemia, although verapamil decreased the incidence of SVT.
Calcium channel blockers with substantial negative inotropic effects (diltiazem,

verapamil) may precipitate or worsen HF in patients with depressed EF and clinical HF.
Angiotensin-converting enzyme inhibitors therapy:

-
Continuation of angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor

blockers(ARBs) perioperatively is reasonable.
If ACE inhibitors or ARBs are held before surgery, it is reasonable to restart as soon as
clinicallyfeasible postoperatively.
Nitroglycerin:
-
Prophylactic intravenous nitroglycerin is not effective in reducing myocardial ischemia in

patients undergoing noncardiac surgery.
Antiplatelet therapy:
-
In patients undergoing urgent noncardiac surgery during the first 4 to 6 weeks after BMS
or DESimplantation, dual antiplatelet therapy (DAPT) should be continued unless the
relative risk of bleeding outweighs the benefitof the prevention of stent thrombosis.
In patients who have received coronary stents and must undergo surgical procedures
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That mandate the discontinuation of P2Y12 platelet receptorinhibitor therapy, it is

recommended that aspirin be continued if possible and the P2Y12 platelet receptor
inhibitor be restarted as soon as possible after surgery.
-
Management of the perioperative antiplatelet therapy should be determined by a

consensus of thesurgeon, anesthesiologist, cardiologist, and patient, who should weigh
the relative risk of bleedingversus prevention of stent thrombosis.
In patients undergoing nonemergency/nonurgent noncardiac surgery who have not had

previouscoronary stenting, it may be reasonable to continue aspirin when the risk of
potential increasedcardiac events outweighs the risk of increased bleeding.
Initiation or continuation of aspirin is not beneficial in patients undergoing elective

noncardiacnoncarotid surgery who have not had previous coronary stenting unless the
risk of ischemic events outweighs the risk of surgical bleeding.
Anticoagulation therapy:
-
The role of anticoagulants (warfarin, NOAC agents) other than platelet inhibitors in the
secondary preventon of myocardial ischemia or MI has not been elucidated.
The risk of bleeding for any surgical procedure must be weighed against the benefit of
remaining on anticoagulants on a case-by-case basis.
In minor procedures (cataract, minor dermatologic procedures) it may be reasonable to

continue anticoagulation perioperatively.
NOAC agents do not appear to be acutely reversible, no reversible agent available at this
time.
Patients with prosthetic valves taking vitamin K antagonists may require bridging therapy
(see protocol for warfarin bridging).
Management of postoperative arrhythmias and conduction disorders:
AF and atrial flutter are the most common sustained arrhythmias that occur in the
postoperative setting.
Rate control with beta-blockers or calcium channel blockers (diltiazem,
verapamil), digoxin (if systolic HF or with contraindications or inadequate
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response to other agents).

Beta-blockers and calcium channel blockers with substantial negative inotropic
effects may precipitate or worsen HF in patients with depressed EF or clinical HF.
Beta-blockers compared to diltiazem may accelerate the conversion of
postoperative supraventricular arrhythmias to sinus rhythm.
Cardioversion of minimally symptomatic AF/atrial flutter is generally not
required until correction of the underlying problem has occurred. Should perform
cardioversion when hemodynamic compromise is present.
IV amiodarone may be used to aid in restoring or maintain sinus rhythm if its
benefits outweigh the risk of hypotension and other side effects.
Digoxin and calcium channel blockers should be avoided in the setting of preexcited AF.
-
Narrow-complex tachycardia (SVT):

Perform vagal maneuvers, IV adenosine or verapamil.
Most antiarrhythmis agents (beta-blockers, calcium channel blockers, class IC
antiarrhythmic agents) can be used to prevent further recurrences in the
postoperative setting.
For recurrent SVT consider outpatient ablation.
Asymptomatic PVCs:
Do not require perioperative therapy or further evaluation
Very frequent ventricular ectopy or runs of nonsustained ventricular tachycardia:

May require antiarrhythmic therapy if they become symptomatic or result in
hemodynamic compromise.
New-onset of postoperative complex ventricular ectopy, particularly polymorphic
ventricular tachycardia, should be evaluated for myocardial ischemia, electrolyte
abnormalities, or drug effects.
Give IV beta-blockers, lidocaine, procainamide or amiodarone.
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Perioperative management of patients with ICDs:

Patients with ICDs who have preoperative reprogramming to inactivate shocking
component should be on cardiac monitoring continuously during the entire period
of inactivation, and external defibrillation equipment should be readily available.
Systems should be in place to ensure that ICDs are reprogrammed to active
therapy before discontinuation of cardiac monitoring and discharge from the
facility. A magnet may be applied/ taped over the pacemaker generator to
inactivate the shocking mechanism in lieu turning off the shocking component.
Perioperative anemia management:
Anemia can contribute to myocardial ischemia, especially in patients with CAD
2012 American Association of Blood Banks CPG recommends a restricted
transfusion strategy (Hgb< 7 g/dL to 8 g/dL) in asymptomatic, hemodynamically
stable patients without CAD.
It also recommends adherence to a restrictivetransfusion strategy in hospitalized
patients with cardiovascular disease and consideration of transfusion for patients
with symptoms (e.g., chest pain, orthostasis, congestive HF) or hemoglobin <8
g/dL (21).
In
postoperative
patients,
the
recommended
maintenance
hemoglobin
concentration is 8 g/dL, unless the patient exhibits symptoms.

Surveillance and management for perioperative MI:
Measurement of troponin levels is recommended in the setting of signs or
symptoms suggestive of myocardial ischemia or MI.
Obtaining an ECG is recommended in the setting of signs or symptoms suggestive
of myocardialischemia, MI, or arrhythmia.
The usefulness of postoperative screening with troponin levels in patients at highrisk forperioperative MI, but without signs or symptoms suggestive of myocardial
ischemia or MI, isuncertain in the absence of established risks and benefits of a
defined management strategy.
The usefulness of postoperative screening with ECGs in patients at high-risk for
perioperative MI, but without signs or symptoms suggestive of myocardial
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ischemia, MI, or arrhythmia, is uncertainin the absence of established risks and

benefits of a defined management strategy.
Routine postoperative screening with troponin levels in unselected patients
without signs or symptoms suggestive of myocardial ischemia or MI is not useful
for guiding perioperative management.
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PERIOPERATIVE MANAGEMENT OF
ANTITHROMBOTIC THERAPY
(AHA 2012)
(Bridging Warfarin Therapy)
High risk annual risk >10% (consider Bridging Therapy)

o AF (CHADS2 score 5 or 6; <3 months stroke/TIA, CHADS2 5-6, rheumatic heart
disease)
o Mechanical heart valve (ball/tilting disc valve, mitral valve, < 6 months
stroke/TIA
o Venous thromboembolism (<3 months VTE; severe thrombophilia)
Moderate risk (case by case)

o AF (CHADS2 3-4)
o Mechanical heart valve (bileaflet aortic valve + > 1 risk factors)
o Venous thromboembolism (VTE 3-12 months prior or cancer)
Low risk (no Bridging Therapy required)

o AF (CHADS2 0-2)
o Mechanical heart valve (bileaflet aortic valve without risks)
o Venous thromboembolism (VTE > 12 months ago)
THERAPEUTIC OPTIONS
o A) Stop clopidogrel 7 days before surgery
o B) Stop warfarin 5 days before surgery without bridging therapy.
Check PT the day before surgery.
If INR <1.5 proceed with surgery.
If INR >1.8 give Vitamin K 1mg SQ.
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o C) Stop NOAC:
Dabigatran 1-2 days before when CrC l 50 ml/min, 3-5 days
when CrCl> 50 ml/min. If high risk of surgery (spinal): even > 5
days
Rivaroxaban 24 hours before surgery
Apixaban 48 hrs before high risk surgeries and 24 hrs before low
risk surgeries
o C) Bridging therapy protocol - Consider in High Risk Group
o Before surgery
If preop INR 2-3, stop warfarin 5 days before surgery, If INR 3-4.5
stop warfarin 6 days before surgery.
36 hrs after last warfarin dose, start enoxaparin 1mg/kg SQ BID.
Stop enoxaparin 24 hours before procedure.
o After surgery
Restart enoxaparin 24 hrs following procedure
Restart warfarin at preoperative dosage on first postop day
Monitor daily INR
Stop enoxaparin when INR 2-3for two days
CBC & Platelet count on day 3 & 7to screen for HIT
Resume NOACs as soon as possible.
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PERIOPERATIVE TIA/ STROKE

ASSESSMENT
EVALUATION OF TIA / STROKE PATIENT FOR SURGERY
o POST-TIA - Start ASA, perform Carotid Ultrasound
If non-obstructive (< 70%), proceed with surgery
If carotid obstruction >70%, perform carotid surgery first.
o POST CVA
Semi-elective surgery, need to WAIT 4 WEEKS.
Elective surgery, need to WAIT 8 WEEKS.
EVALUATION OF HIGH RISK PULMONARY PATIENT FOR SURGERY
o Cessation of smoking for > 8 weeks
o Consider Nebulized therapy PREOP IF REACTIVE AIRWAY DISEASE present
o Continue inhaled and systemic glucocorticoids. Consider increasing the steroid
dose if Cushinoid, therapy longer than 3weeks or doses > 20 mg daily.
o Avoid PANCURONIUM
o Consider EPIDURAL ANALGESIA OR INTERCOSTAL NERVE BLOCK
HERBAL PRODUCTS AND SURGERY
o Echinacea
Allergic reaction, immune suppression,
Hepatoxic
HOLD as early as possible
o Ephedra
MI, CVA, HTN, ARRHYTHMIAS - HOLD at least 24 hours
o Garlic
Bleeding, Lowers PRELOAD - HOLD at least 7days
o Ginkgo
Bleeding - HOLD at least 36 hours
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o Ginseng
Low blood sugar & bleeding
HOLD for at least 7days
o Kava
Prolong anesthesia - HOLD for at least 24 hours
o St JohnSWort
Decreases effect of cyclosporin, warfarin, steroids - hold 5 days
o Valerian
Prolongs anesthesia.
Needs a SLOW TAPER weeks before surgery.
Withdraw with benzodiazepines.
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AORTIC ABDOMINAL ANEURYSM

(ACC/AHA Guidelines 2013. Circulation)
ETIOLOGY
o Common - atherosclerosis, M > F, smoking hx, advanced age, + FH, HTN
o Rare - cystic medial necrosis (Marfans, Ehlers-Danlos), mycotic, trauma
TYPE Aneurysm defined > 3 cm: Clinically important > 4 cm
o Fusiform involve entire circumference of aorta
o Saccular involve only a portion of the circumference of aorta
LOCATION
o 75% below renal artery
SYMPTOMS
o Asymptomatic
o Compression / erosion into adjacent tissues, peripheral emboli from thrombus in
AAA, painful leak, sudden rupture, back pain
FINDINGS
o Palpable, pulsatile, non tender mass, Incidental X-ray finding (75% calcified)
EVALUATION
o Abd X-ray / Abd ultrasound / Abd spiral CT / Abd MRI
o Aortogram may underestimate true size of aneurysm due to thrombus
SCREENING - USPSTF recommends one time ultrasound screen (sensitivity 95%
Specificity 100%) only in men 65-75 who have ever smoked.
ACC recommends screening in men 60 or older with + FH of AAA
PROGNOSIS (related to size, rate of expansion)
o Risk of rupture related to size of aneurysm:
< 4 cm very low risk of rupture @ 5 years
> 5.5 cm markedly increased risk of rupture @ 5 years > 25%
> 0.5 cm interval increase within 6 months high risk of rupture (large
aneurysms expansion 0.3-0.4 cm per year)
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Related to associated CAD (CAD equivalent conditions) and the presence of

cerebrovascular disease
MEDICAL
o Smoking cessation, control HTN and lipids, and B-blocker therapy
SURGERY
o Elective AAA 2.7% mortality
o Expanding AAA 15% mortality: Rupturing AAA 50% mortality
o Indications size > 5.5 cm in men, > 4.5 in women / symptomatic AAA / rapidly
expanding AAA (1 cm expansion over 6 months), consider if size 5-6 cm in
otherwise good candidate
o Endovascular EVAR grafts, lower operative mortality but similiar long-term
mortality, more costly, more repeat proceedures. NEJM 2010; 362
Follow-up
o Serial abdominal ultrasound or CT every six months for aneurysm 4 - 5.4 cm
o Testing every 2 years, if AAA is 3 - 4 cm , no further testing if <3 cm
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AORTIC DISSECTION
2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines
(J Am Coll Cardiol 2010; 55:1509-1544)
ETIOLOGY
o Risk factors: M > F, age > 50 year old, HTN ~ 80%, pregnancy, connective tissue
disease, bicuspid aortic valve, coarctation of aorta
TYPE
o DAILY Classification (STANFORD)
Type A Involves the ascending aorta 72% (IRAD)
Type B Distal dissection starting distal to L subclavian artery 28%
Acute < 14 days of sx / Chronic > 14 days of sx
o DeBAKEY Classification (DB)
Type 1 Originates in ascending aorta & continues at least to aortic arch
Type 2 Limited to ascending aorta
Type 3 Originates in the descending aorta
Symptoms:Painless /tearing pain, anterior, interscapular, syncope,dyspnea, weakness
Physical exam:
o Hyper-hypotension, loss of pulse (right carotid, left femoral), Aortic
insufficiency, CVA, anterior spinal artery ischemia (paraplegia), MI (right > left
coronary)
FINDINGS
o Wide mediastinium, left pleural effusion, normal EKG unless dissection involves
the right coronary ostium
DIAGNOSIS
o TEE poor for descending aorta (98% sens/ 91% spec)
o CT with contrast (95% sens/ 90% spec)
o MRI with contrast (98% sens/ 98% spec)
o Aortogram (90% sens/ 95% spec)
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TREATMENT - if untreated the mortality is 50% in the first 2 days

o Therapy determined by the type and acuity of dissection
ACUTE Rx
o Type A mortality with surgery Rx = 32% @ 5 years (DB type I & II)
(Risk factors for surgery: Advanced age, abrupt onset chest pain, hypotension,
shock, tamponade, and kidney failure before surgery)
o Type B mortality with medical Rx = 20% @ 5 years (unless complicated by
leak, continued expansion, or end organ injury)
May combine with EV stent if disease is infra renal.
Reevaluate in 1-2 mo. continue medical Rx unless size > 5-6 cm or
new complication (DB TYPE III)
MEDICAL Rx Lower SBP and decrease LV contractility
o Labetalol IV or B-blocker IV + ACE inhibitors or Nipride // Diltiazem IV + ACE
inhibitor or Nipride - if asthma
o Avoid beta-blockers if aortic insufficiency present increase regurgitation time
o Acute SBP goal 100-120 mmHg // Chronic SBP goal < 120/80 mmHg
o Follow-up CT/MRI scan @ 3, 6, 12 months, then every 12 to 24 months
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PERIPHERAL ARTERIAL DISEASE

2013 ACCF/AHA Guidelines
(Circulation 2013; 127:1425-1443.)
ETIOLOGY
o Atherosclerosis medium to large blood vessels, age >70 yo, M> F, HTN /
hypercholesterolemia / diabetes / smoking / elevated homocysteine
o Fibromuscular medium to small blood vessels, age> 30 yo, F> M
o Patients with PAD are at triple the risk of all-cause mortality.
o 30% people over the age70 years have PAD
o PAD represents a Coronary Artery Equivalent Disease; 90% with PAD by heart
catheterization have CAD, 50% will have cerebrovascular disease,
o 50% will have renal artery stenosis
LOCATION
o Buttock & hip pain - aortoiliac disease
o Thigh pain - common femoral artery / aortoiliac disease
o Upper 2/3 calf - superficial femoral artery
o Lower 1/3 calf - popliteal artery
o Foot - tibial or peroneal artery
SYMPTOMS one joint distal to level of occlusion
o 20-50% - Silent disease (ankle-brachial index < 0.9) - under diagnosed
o 40-50% - Claudication with exercise (ankle-brachial index < 0.7)
o 1-2% - Claudication at rest with critical ischemia (ankle-brachial index < 0.5)
o 5 P's (pain, pallor, pulselessness, parathesias, paralysis) - severe disease
o Symptoms not relieved by leaning forward (lumbar stenosis)
PHYSICAL EXAM
o Examination of pulses alone will miss 50% of patients with PAD (best indicator
is absence of posterior tibial pulse)
o Decreased pulses (dorsal pedis pulse may be absent in 10% of normal people)
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o Leriche Syndrome (buttock pain, impotence), bruits, muscle atrophy, hair loss,
thickened nails, decreased temperature, peripheral cyanosis, ulcers, gangrene,
pallor, and dependent rubor.
EVALUATION
o Ankle-brachial index (< 0.9 occlusive disease, < 0.5 severe disease)
o Doppler / Duplex ultrasound /Aortogram with peripheral runoff
o CT angiogram / MRI angiogram
PROGNOSIS
o Mortality rates from all causes are 3x higher for patients with PAD
o Treated claudication: Symptoms slowly progress:
At 10 yrs, 70% improve or remain unchanged, only 20% worsen.
The five and ten year survival is 70% and 50%.
Less than 20% of patients with PAD require vascular surgery,
Less than 10% require amputation.
ACC/AHA 2005 Practice Guidelines Circulation 2006; 113: 1476-1537;
o TASC II 2007 Consensus Report J Vasc Surgery 2007; 45 (S 55)
MEDICAL THERAPY
o SUPPORTIVE RX
Meticulous foot care
Exercise - improves endothelial function, vascular angiogenesis,
decreases red cell aggregation
o RISK FACTOR RX
Smoking cessation (decreases disease progression, decreases sx)
Diabetes mellitus (microvascular disease only), HTN (+/- benefit)
o DRUG RX
ASA - (81-325mg daily) Class IA recommendation - decreases surgical
need, increases graft patency, but does not improve symptoms.
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Cilostazol (Pletal) - Class IA recommendation -vasodilator, inhibit

platelet aggregation, decreases symptoms, increase walking. Cannot use
with HF (inhibits phosphodiesterase III). Improves claudication,
functional status, QOL and ABI - >Trental
Pentoxifylline (Trental) Class IIb recommendation - alternative choice
to Pletal - improves RBC flexibility, reduces plasma viscosity, reduces
platelet reactivity, reduces increased clotting) increased walking ability,
modest benefit (12% increase)
ACE Inhibitor - Class IIa recommendation -with or without hyper tension
(HOPE Trial)
Statin - high-dose required, decreases new or worsening claudication by
38% by improving endothelial function, but benefit takes weeks to months
to be achieved, decreases disease progression (Simvastatin)
HTN lower BP<140/90 mmHg. Beta-blockers are not contraindicated
Clopidogrel (75mg daily) - Class IB recommendation - alternative to
aspirin - relieves ischemic events but not claudication.
Thrombolysis for acute occlusion only < 7 days (Urokinase> TPA)
Heparin & Warfarin Embolic etiology
SURGICAL RX
o INDICATIONS:
Rest pain, salvage of extremity, unacceptable symptoms
o TYPES:
Angioplasty- Class 1A
Local disease (<10 cm) // Poor surgical risk
Long-term success related to extent of disease
More successful in larger, proximal vessels
Stent therapy is of benefit with iliac artery stenosis.
Graft Aortobifemoral - 80% success at 10 years
-Autogenous saphenous graft femoral popliteal
80% success at 5 years
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- Autogenous saphenous graft - infrapopliteal

60% success at 5 years
- Long term success of graft related to: 1) Site of distal suture line (F > P >
T) and 2) Run off of distal vessel.
PULMONARY HYPERTENSION
ACCF/AHA 2009 Expert Consensus on Pulmonary HTN
(J Am CollCardiol 2009 53(17))
DEFINITION:
o Mean pulmonary artery pressure > 25 mmHg at rest
WHO ANATOMIC CLASSIFICATION OF PH:
o 1) Pulmonary Arterial Hypertension
Idiopathic PAH
Intimal fibrosis & medial hypertrophy of small pulmonary
arterioles -- leading to vascular obstruction, increased PVR,
PHTN, RV overload
Collagen
Vascular
Disease,
Congenital
shunts,
Portal
Hypertension, HIV infection, Drug induced, Pulmonary venoocclusive disease

o 2) PH associated with systolic/diastolic dysfunction &valvular disease
o 3) PH associated with lung disease or hypoxia (COPD, ILD, OSA)
o 4) Chronic thromboembolic disease
o 5) Multifactorial: sarcoid, myeloproliferativedosorders, tumor
WHO FUNCTION CLASSIFICATION:
o CLASS 1: pulmonary hypertension but without symptoms with ordinary activity
(dyspnea, fatigue, chest pain, near syncope)
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o CLASS II: pulmonary hypertension with slight limitations with ordinary physical
activity (dyspnea, fatigue, chest pain, near syncope)
o CLASS III: pulmonary hypertension resulting in marked limitation. No
symptoms at rest but symptoms with less than ordinary activity (dyspnea, fatigue,
chest pain, near syncope): a = early stable / b = late
o CLASS IV: pulmonary hypertension with symptoms with rest or any physical
activity. Signs of right heart failure noted. (dyspnea, fatigue, chest pain, near
syncope).
PROGNOSIS:
o Related to PH class > II, EKG with RVH, or RV / RA enlargement, decreased RV
function, Six minute walk endurance (<300 meters or arterial desaturation > 10
units), elevated BNP, increased mean RA pressure > 10mmHg, mixed venous
saturation < 60%, CI < 2 L/min/m2, failure to improve with therapy in 3months
PAH - 15% mortality @ 1year. PH associated with congenital heart disease has a
better prognosis, PH associated with other disease have worse prognosis.
STEPS IN INITIAL EVALUATION:

o 1. ECHOCARDIOGRAM - left heart + right heart disease or right heart disease
only, Bubble study with agitated saline to detect intra-atrial shunts. PH is likely if
PASP > 50 mmHg (TRV > 3.4 cm); PH is unlikely if PASP <36 mmHg. Moderate
PH>50mmHg, Severe PH > 100 mmHg. May not exclude PH.
EKG demonstrates right atrial abnormality, RVH, right axis deviation.
ChestX-ray- prominent main PA with pruning of peripheral pulmonary arteries in
the lateral 1/3 of lung fields, enlarged RV
o 2.If PH identified with significant left heart disease - treat left heart condition
o 3. If PH not identified with low clinical suspicion seek alternative dx; if high
clinical suspicion for PH despite normal echo - further tests.
o 4. If PH identified in the absence of significant left leart disease - further tests.
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FURTHER TESTING: Order of testing should be based upon suspected WHO group
expected.
o PULMONARY FUNCTION TEST
o OXIMETRY overnight
o SLEEP APNEA STUDY
o LUNG SCAN - ventilation / perfusion or CT pulmonary angiogram
o SIX MINUTE WALK TEST - looks for other causes, establish WHO Class
o LABORATORY -screening for rheumatic disorders SCL-70, ANA, sed rate,
CRP liver function tests, hepatic ultrasound/doppler to evaluate portal
hypertension, HIV testing.
o RIGHT HEART CATHETERIZATION - normal pulmonary wedge
THERAPY:
o Treatment improves hemodynamic measures
o Improves WHO functional class
o Improves the six minute walking test
o Appears to improve survival. No large randomized controlled trial has
demonstrated improved survival.
PRIMARY THERAPY: Treat the cause of the PH
o Group 1: No specific primary therapy effective for idiopathic PH.
o Group 2: Treat left heart disease. Advanced Rx usually not indicated.
o Group 3: Oxygen therapy improves survival. Advanced Rx not indicated.
o Group 4: Anticoagulation / surgical thromboendarterectomy.
o Group 5: Dependant upon cause identified.
o All Groups should be considered for: Oxygen, WARFARIN (decrease insitu
thrombus), DIURETICS, and DIGOXIN - for rate control, EXERCISE.
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ADVANCED THERAPY: WHO class II-IV with PH despite primary therapy

WHO class II-IIIa (stable) 10-15% are responders
Right Heart Catheterization needed to confirm the Dx
VASOREACTIVE WITH RIGHT HEART CATH

Decrease in PAP by at least 10 mmHg to < 40 mmHg with an
increased or unchanged CO and stable SBP .
Agents IV Epoprostenol {Flolan} @ 1-2 ng/kg/min & increase by 2
ng/kg/min q10 min until fall in SBP or increase in HR or Sx (N, V,
HA) or IV Adenosine @ 50 mcg/kg/min & increase q 2 min until Sx
or goal of 350 mcg/kg/min) or inhaled Nitric oxide @ 10-20 ppm
CCB-LA - nifedipine (30-420 mg/d) or diltiazem (120-900
mg/d)
No randomized controleed trial showing benefit!
If fail CCB or CLASS IIIa
- Oral Bosentan- (Tracleer @125-250 mg bid)
NOT VASOACTIVE WTH WITH RIGHT HEART CATH

Bosentan (Tracleer); ambrisentan (Letairis @ 5-10 mg)
Epoprostenol (Flolan) - first line for Group 1class IV vasodilation / inhibits platelet aggregation / inhibits vascular
remodeling -- IV or subcutaneous pump
Iloprost (Ventavis @ 2.5 mcg inhaled 6-9 doses daily)
Sildenafil - reduces hypoxia-induced vasoconstriction
Atrial septostomy (unload right sided increased pressure)
COMBINATION THERAY
Epoprostenol + Bosentan
Bosentan + Sildenafil
Sildenafil + Epoprostenol
Sildenafil + Iloprost
Bosentan + Iloprost
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DRUG SELECTION
o WHO Class II: Ambrisentan, Bosentan or Sildenafil (or Tadalafil)
o WHO Class III: Ambrisentan, Bosentan, IV Epoprostenol (or Treprostinil),
inhaled Iloprost, Sildenafil
o WHO Class IV: IV Epoprostenol
PERICARDITIS
ACUTE PERICARDITIS
o History - sharp, pleuritic chest pain, worse with lying down & swallowing, better
with sitting up, associated with fever. Patient often notes recent viral infection.
o Physical Exam
RUB: harsh scratching high frequency rub heard at left lower sternal
border, best heard with the diaphragm. Rub may have1to 3components
(ventricular systole, ventricular diastole, atrial systole). The rub may
soften with decreased inflammation or by the development of pericardial
effusion.
VENOUS PRESSURE elevated
HEART SOUNDS may be soft with large epicardial effusion.
PULSUS PARADOXUS is highly diagnostic of pericardial tamponade. It
is best measured with the patient supine. Measure above the systolic blood
pressure by 20 mmHg and slowly lower until initial systolic sound first
heard intermittently. Then proceed downward until systolic sound is heard
with every beat. If this spread is greater than 10 mmHg, tamponade is
present. The heart rhythm needs to be regular to be accurate. The most
common cause forpulsus PARADOXUS is status asthmaticus
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EKG
STAGE 1 Diffuse concave ST segment elevation is noted in all
leads except in aVR where ST depression is noted. This represents
ventricular epicardial injury. Diffuse PR segment depression is
noted in all leads except in aVR where PR elevation is noted. This
represents atrial epicardial injury.
STAGE 2 The ST and PR segments return to baseline.
STAGE 3 After the ST & PR segment return to baseline, diffuse T
wave inversion occurs. Chronic pericarditis is marked by persistent
Stage 3 findings.
STAGE 4 The T waves return to baseline.
ELECTRICAL ALTERNANS occurs with a large epicardial
effusion but not necessarily tamponade. The QRS height alternates
every other beat demonstrating excessive motion of the heart
within a large effusion.
ECHO
The echo determines the size of the effusion. Systolic compression of the
right atrium or right ventricle by the effusion produces hemodynamic
compression. The diagnosis of tamponade however is clinical, based upon
pulsusparadoxus, equalization of intracardiac pressure readings by a
pulmonary artery catheter (RA mean = RV diastolic = PA mean =
pulmonary wedge pressure), or clinical signs of low systolic BP, narrow
pulse pressure, and sinus tachycardia. Inspiratory disappearance of the
femoral artery pulse is a late clinical finding of tamponade.
Right and left ventricular function is also determined by the echo to
exclude associated transmural myocarditis. All pericarditis is associated
with a mild epicarditis that does not affect the global or regional systolic
function (normal ejection fraction).
TABLE of CONTENTS
180
LABORATORY
o Cardiac enzymes are usually slightly elevated due to associated
epicarditis. The signs of inflammation are often elevated (ESR /
hsCRP).
DIFFERENTIAL DIAGNOSIS
o Viral (coxsackie, echo)
o Autoimmune (SLE, rheumatoid, scleroderma)
o TB (after pulmonary involvement)
o Metastatic cancer breast or lung, lymphoma or melanoma.
o Melanoma, lymphoma, leukemia - predilection
o AIDS (infection /malignancies)
o Post-MI (acute /delayed - Dresslers Syndrome)
o Trauma (acute /delayed - Dresslers Syndrome)
o Post radiation
o Uremic
o Myxedema
TREATMENT
o Depends upon etiology of pericarditis
o ASA, COLCHICINE, NSAIDS or steroids for inflammation
o Tamponade - emergency (IV saline + dopamine)
o Needle aspiration of fluid by EKG or echocardiogram guidance
TABLE of CONTENTS
181

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1

TABLE of CONTENTS ................................................................................................................................................................... 2

PROSTHETIC VALVES .............................................................................................................................................................. 109

Regular Rhythm 1500 divided by # of small boxes (0.04sec) between QRS

Irregular Rhythm # ORS within 6 seconds rhythm strip x 10

Sinus P wave in front of every QRS, fixed PR interval

Left Lower Quadrant Always Normal (Lead 1, QRS +, AVF +)

Right Lower Quadrant Always Abnormal (Lead 1 neg, AVF +) > 90

Right Upper Quadrant Always Abnormal (Lead 1 neg, AVF neg)

Left Upper Quadrant (Lead 1 +. AVF neg) Look at QRS in Lead 2

Normal Left Axis is 0 to 30: Positive Wave > Negative

Abnormal Left Axis> - 30 : Negative Wave > Positive

Normal: Lead 2: rounded, V1 equal initial upward and terminal downward

Left Atrial Abnormality (LAA)

Notched P in Lead 2 0.12 sec wide

Large negative terminal P Wave in V1 0.04 sec wide and 1 mm deep

Right Atrial Abnormality (RAA)

Tall Peaked P in Lead 2 > 2.5 mm tall

Tall peaked initial portion of P wave in V1

Inverted P wave L2, L3, AVF retrograde activation of atria

Junctional (short PR interval)

Ectopic low atrial (normal PR interval)

Inverted in L1 (left to right atrial activation)

Left atrial rhythm (QRS axis normal)

Lead misplacement (right and left arm QRS axis rightward)

PR Interval is between 0.12-0.20 sec. Measure the shortest PR interval

PR Segment is isoelectric with the TP interval

If depressed Atrial Injury / Pericarditis / Atrial Infarction

PR > 0.20 sec first degree AV block (atrial, AV nodal or BB conduction)

PR < 0.12 sec Junctional rhythm or bypasses the AV node

Junctional P Wave inverted in Lead 2 (retrograde conduction)

Pre-Excitation P Wave upright in Lead 2

0.11 seconds is NORMAL. Measure the longest QRS interval

> 0.12 seconds is ABNORMAL

In Lead V1- if QRS is inverted = LBBB and if QRS is upright = RBBB

In any lead - Initial QRS delay =WPW

- Mid QRS Delay=LBBB

- Terminal QRS Delay=RBBB - Total QRS Delay=Metabolic cause

Secondary ST-T changes (normal for BBB).

ST depression and T waves inversion: In Lead 1, aVL, V5-6 for LBBB

Primary ST-T changes: Absence of secondary changes.

In V1 and V2 any Q wave is abnormal (infarction or incomplete LBBB)

Q waves: Lead 2, 3 aVF = Inferior wall

Q wave in PVC = old MI

RVH voltage, R atrial abnormality, R axis deviation, strain pattern

VOLTAGE: R wave > S wave in V1

STRAIN: ST depression + T wave inversion in V1 & V2

WITH RBBB: RVH is present if R wave in V1 > 15 mm

WITH LBBB: RVH is present if S wave lead 1 or right axis

Volume Overload: Atrial septal defect (ASD)

rSrin lead V1: duration < 0.12 sec mimics IRBBB

LVH voltage, L atrial abnormality, L axis deviation, strain pattern

VOLTAGE: R wave V5 or V6 + S wave V1 or V2 35 mm

STRAIN: ST depression + T wave inversion in L1, aVL, V5, V6

WITH RBBB: Lateral wall voltage decreased less sensitive

WITH LBBB: R wave V6 + S wave V2 > 45 mm

Volume overload: Mitral / Aortic Insufficiency

QRS voltage < 5 mm in limb leads and < 10mm V leads

Obesity, COPD, pericardial effusion, hypothyroidism, advanced heart disease

Tall R Wave V1 (R > S)

RVH, posterior MI, Lead misplacement, WPW, Dextrocardia, WNL

R wave increases from V1 to V6 isoelectric point between V3-4 (over IV septum)

Poor R wave progression is caused by:

Anterior wall infarction