Archer online USMLE reviews

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Archer Slides are intended for use with Archer USMLE step 3
video lectures. Hence, most slides are very brief summaries of
the concepts which will be addressed in a detailed way with
focus on High-yield concepts in the Video lectures.
These slides are only SAMPLES


Unstable angina
Acute MI
Vaso spastic angina
Lab studies, cxr, ekg, CE, Cardiac cath stat and fix it
if STEMI, If not STEMI f/u with treatment
Aspirin, plavix, heparin/lmwh, beta blocker, statin,
ACEI GP IIb/IIIa inhibitors only if STEMI or
progressive NSTEMI with continuous symps or
progressive EKG changes
Differential diagnosis costochondritis, dissection,
pneumonia, panic attacks
MCC of epigastric pain ACS
Sinus bradycardia ( HR < 60, Sinus)
- No symptoms, HR > 40 observe
- Symptoms, HR < 60 Atropine followed by pacemaker. First
transcutaneous pacer and then transvenos pacer and if you think
its a permanent issue, permanent pacer
- HR < 40 Irrespective of symptoms Atropine and if no response,
then pacemaker.
- Symptoms of bradycardia that needs above approach are
symptoms of poor perfusion ( Shock, altered mental status,
ongoing chestpain, dizziness ) or SOB (CHF)
Heart Blocks
Ventricular fibrillation / Ventricular tachycardia.
Papillary muscle rupture ( Acute MR ) Diagnose, stabilize first
with inotropic support and IABP and then surgery ASAP
Ventricular septal defect Rx similar as with papillary muscle
rupture
Cardiogenic shock
Fibrinous pericarditis ( use ASA, Not NSAIDS)
Dresslers syndrome
Heart Block
First check the EKG to make sure that the bradycardia is secondary to
a heart block not just a simple sinus bradycardia.
If symptomatic bradycardia ( symptoms of poor perfusion) and if EKG
shows sinus bradycardia or First degree or Mobitz type I give
atropine and proceed to Transcutaneous pacemaker ( sedate the
patient before you place it)
If symptomatic bradycardia and the EKG shows Mobitz Type 2 or
Third degree heart block, reach for transcutaneous pacer STAT. No
role for atropine here as it does not work ( severe block) and even
diminishes the ventricular rate further. ( Remember atropine acts at
SA node level)
If a complete heart block even if asymptomatic, place a
transcutaneous pacer. Then Transvenos pacing and once patient is
stable and if heart block is persistent, take him to OR to place a
Permanent pacemaker

Called Intra aortic balloon counterpulsation
Mechanism
Increases cardiac output by reducing afterload
Increases coronary blood flow
Important indications
Cardiogenic shock after anterior wall STEMI as a bridge to coronary
revascularization
Cardiogenic shock from post MI complications such as Acute MR due
to papillary muscle rupture or VSD. As a bridge to surgery
Unstable angina
Post cardiothoracic surgery.
Absolute Contraindications :
Aortic dissection
Severe Aortic regurgitation
Severe peripheral vascular disease ( ballon inflation here may cause further occlusion and
limb ischemia)
Some clinical questions : Remember Athero-embolism complications
can occur after IABP removal

Table 1: Hemodynamic effects of IABP Therapy


Counseling diet, life style changes Stop smoking, cardiac diet
BP control under 140/90. Less than 130/80 if Diabetic.
LDL Cholesterol target < 100
Supervised exercise program.
Physical activity should be slowly increased with a target to return to
normal activity in 6 weeks should perform about 30 minutes of aerobic
activity daily.
Sub maximal stress test 7 days post MI to decide on exercise prescription.
Sex after MI :
Most people may return to sexual activity gradually in 4 weeks. However,
people with severe anginal symptoms post MI will need further evaluation
prior to returning to Sex
Higher levels of erectile dysfunction and decreased levels of sexual contact
has been reported after MI in men. Most of it is related to anxiety ( some
fear sudden death during sex). Also, remember that most post MI patients
are on a beta blocker so, evaluate if it could be the possible etiology
Phoshodiesterase inhibitors can be safely started post MI however,
educate the patients on its dreadful interaction with nitrates.

Diabetes Mellitus
Peripheral Arterial Disease
Abdominal Aorta Aneurysm
Carotid Artery Stenosis
TARGETS For CAD and Its Equivalents
LDL < 100 ( < 70 is preferred target)
Non HDL cholesterol < 150 ( total chol HDL
preferred<130)
Triglycerides < 150
HDL > 40(MEN) and >50(Women)
B.P<130/80 ( Updated Guidelines)
DM nephropathy BP TARGET < 125/75
A 71-year-old woman is hospitalized with an acute inferior wall
myocardial infarction. On physical examination, her heart rate is
100/min, respiration rate is 18/min, and blood pressure is 171/88 mm
Hg. The heart sounds are regular,with normal S1 and S2, an S4, and a
grade 1/6 aortic outflow murmur at the left upper sternal border. The
remainder of the physical examination is unremarkable.
Electrocardiography shows sinus rhythm and inferior ST-segment
elevation. After the administration of aspirin, heparin, metoprolol, and
nitroglycerin, cardiac catheterization shows a mid-right coronary artery
occlusion, which is treated with angioplasty and stent placement. The
remaining coronary arteries are normal.She does well until the second
hospital day when she develops acute dyspnea. On physical examination
her heart rate is 131/min, respiration rate is 40/min, and blood pressure
is 88/58 mm Hg. EKG Sinus tachycardia. There are pulmonary
crackles, a hyperdynamic precordium, a summation gallop, and a short,
early-systolic murmur.
Which of the following is the best course of emergency action for this
patient?
( A ) Right heart catheterization
( B ) Bedside cardioversion
( C ) Bedside echocardiography
( D ) Coronary arteriography


The sudden appearance of pulmonary edema 2 to 7 days following an
acute inferior infarction is characteristic of papillary muscle rupture.
This is a typical presentation of acute, severe mitral regurgitation due to
papillary muscle rupture complicatingmyocardial infarction.
Ischemic papillary muscle rupture most often occurs after inferior wall
myocardial infarction dueto the single vessel blood supply (posterior
descending artery) of the posteromedial papillary muscle, typically 2 to 7
days after acute infarction, and more often after delayed presentation.
Clinical presentation is that of acute pulmonaryedema, variably
associated with hypotension depending on the severity of regurgitation.
The murmur may not be holosystolic due to a nondilated, noncompliant
left atrium.
Transthoracic echocardiography may show the ruptured papillary muscle
and mitral regurgitation, although poor image quality may necessitate
transesophageal imaging.


A 55-year-old man is evaluated in the emergency department for
chest pain of 1-hour duration. The pain is sharp,intense, and radiates
to the back. There is no pleuritic component, and he denies shortness
of breath. He has a 10-year history of hypertension and has smoked
one pack of cigarettes daily for 35 years.On physical examination, his
heart rate is 75/min and blood pressure is 168/92 mm Hg. Oxygen
saturation is 98% on room air. Heart sounds are regular with an S4, a
normal S1 and S2, and a grade 1/6 aortic outflow murmur. The
remainder of the examination is normal. Portable chest radiography
shows a normal cardiac silhouette and clear lungfields. Transthoracic
echocardiography shows left ventricular hypertrophy, normal left
ventricular wall motion during chest pain, and moderate aortic
regurgitation. The EKG shows LVH with strain pattern. Which of
the following is the best test to confirm the diagnosis?
( A ) Serum creatine kinase and troponin
( B ) Computed tomography scan of the thorax
( C ) Ventilation-perfusion scan
( D ) Coronary angiography


Consider aortic dissection in patients with
sharp chest pain, hypertension, and aortic
regurgitation.
Diagnostic tests for aortic dissection include
computed tomography, trans esophageal
echocardiography, and magnetic resonance
imaging.

Stress test involves stressing the heart + evaluating
cardiac response to stress.
Indications :
Diagnose CAD ( patients with risk factors and symptoms of
chestpain. Assess pre-test probability)
In a person with known CAD, for assessing the functional
capacity i.e; safety of work/ recreation ( Sub-maximal stress test)
Contraindications :
STEMI less than 4 days
Acute aortic dissection
Myocarditis, Pericarditis
Third degree heartblock
Poorly controlled Heart failure
Severe AS with valve area < 1cm2
For patients presenting with chestpain and CAD risk
factors, rule out Acute MI first with serial cardiac
enzymes before sending for Stress test

Stress Test
Components
Types of Stress
- Tachycardic
-Vasodilator
- Inotropic
Evaluating Response to Stress
- Clinical features
- EKG changes
- Nuclear component/
Myocardial perfusion study
- Echocardiogram ( wall motion
abnormalities)
Exercise Stress Test
Tachycardic type of stress Increase the heart rate by
making the patient walk on a treadmill ( Target Heart Rate
= 220-age) and evaluate response to stress.
Evlauating Cardiac response
Clinical features observe for chestpain, sob during stress
EKG changes ( observe for ST depressions > 2mm during
stress, ventricular arrhythmias)
Specificity of this assessment is lowered ( more false positives) if there are
resting ST-T changes already eg: LVH, LBBB, WPW, Digoxin use)
Adding Myocardial perfusion study ( Nuclear component) -
Thallium or Sestamibi ( Technitium)
Evaluate for the tracer uptake A fixed defect suggests infarcted tissue or
hybernating myocardium. Reversible defect ( tracer uptake on stress and
resolves with rest) suggests ischemia
Echocardiogram ( Exercise Stress Echo) observe wall motion
abnormalities, assesses viability ( viable if myocardial wall is
akinetic at rest and improved with stress)
Exercise Stress Test (treadmill)
most preferred test in anyone who can exercise well as it
allows to assess exercise capacity and symptoms also apart
from evaluating ST segment response.
most sensitive if patients can reach 85% of Target Heart
Rate (220-age)
EKG component alone is sufficient if there is a Low
probability of CAD. EKG component specificity is lower for
patients with resting EKG changes ( LBBB, early
repolarizations, LVH, WPW, pacemaker rhythms)
Combining nuclear component increases sensitivity and
specificity. Nuclear imaging is preferred when patient has
intermediate probability of CAD.
In LBBB, LVH, WPW , Paced LV rhythms, using a
tachycardic stress may produce reversible defects on
myocardial perfusion study in the septal area even in
absence of CAD ( False Positives) so, the solution here is
to use vasodilator stress ( Stress them with out increasing the
heart rate).
Vasodilator Stress: Dipyrimadole (Persantine) or Adenosine Stress test
Mechanism here is by coronary vasodilation and coronary steal phenomenon (
Diseased coronary arteries cannot dilate in response to adenosine where as healthy
arteries dilate well. This leads to more coronary blood flow in healthy arteries as
opposed to diseased arteries. Hence, induces ischemia which can show up as
reversible defect on the Nuclear imaging)
Preferred Choice in
patients who cannot exercise ( osteoarthritis, joint problems, obesity, previous
CVA, Peripheral arterial disease)
patients with LBBB, those already on b-blockers ( prevents achieving target
heart rate in tachycardic stress), paced rhythm, freq PVCs, poorly controlled
hypertension and moderate Aortic Stenosis
Contraindications:
moderate to severe Asthma or COPD ( these agents cause bronchospasm)
high grade heart blocks ( second or third degree
patients already on dipyridamole ( Aggrenox)
patients with recent caffeine ingestion i.e; in last 12 to 24 hours ( caffeine blocks
adenosine receptors and decreases vasodilatory properties of adenosine)
Adverse Effects : Chestpain, Severe headache, Hypotension Reverse with
Aminophylline
In patients who can not walk and who also have contraindications to Vasodilator
stress, use Inotropic stress ( Dobutamine Stress Echo)

Positive Inotropic Stress: Dobutamine Stress Echo
Mechanism :
Dobutamine increases Heart rate as well as contractility of myocardium and
produces ischemia.
Echo is then used to evaluate wall motion abnormailities during dobutamine
infusion. An ischemic myocardial wall is hypokinetic . Also, useful to evaluate
VIABILITY ( when in doubt regarding myocardial stunning vs. Scar) A scar is
Akinetic and does not improve with stress. A stunned myocardium (viable) may
be initially akinetic but improves with stress.
Preferred Choice in
Patients who can not walk and who also have contra indications for Dipyridamole
Stress ( Moderate to severe COPD or asthma, High grade heartblocks)
Post Ischemia patients or Ischemic Mitral regurgitation ( To assess viability)
Not good for
patients with LBBB, on beta blockers, paced rhythm, freq PVCs or atrial
arrhythmias, or poorly controlled hypertension
Prior to Dobutamine stress test, hold AM dose of b-blocker

A 52 y/o man with presents to your office with complaints of exertional
chest pain for the past 4 weeks. The chest pain is usually left sided, occurs
on walking about three blocks and goes away with rest. He has
developed a habit of taking rest when the chest pain comes and he did
not think it needed medical attention until his friend told him yesterday
that it might be a symptom of heart disease. He is concerned and requests
your recommendation. He denies any chest pain or shortness of breath
now. He also reports no change in quality or intensity of his chest pain.
His past medical history is significant for Hypertension and Smoking .
His medications include lisinopril and hydrochlorthiazide. Physical
examination is benign. The next best step in establishing the diagnosis in
this patient is :
Electrocardiogram
2 D -Echocadiogram
Exercise EKG Stress Test
Dobutamine Stress Echocardiogram
Persantin Stress Test
Cardiac Catheterization


Exercise EKG Stress test is the preferred test in evaluating
patients who can walk and are presenting with symptoms
typical of CAD. The patient gives a history of typical
exertional chest pain that improves with rest. This highly
suggestive of stable angina.
The patient has no chest pain now. A resting ECG is useful
to show if there are any baseline changes but it will not
establish the diagnosis. An ECG should be obtained during
stress to establish the diagnosis of ischemic heart disease
In patients who can walk, Exercise stress is the preferred
modality since one can also assess the symptoms, ekg
changes and functional capacity. In patients who cannot
walk, persantin (dipyridamole) stress is preferred
Dobutamine echocardiogram is reserved for patients who
can not walk and have contraindications to dypridamole
stress test.

A 65 y/o man with presents to your office with complaints of exertional
chest pain for the past 4 weeks. The chest pain is usually left sided, occurs
on walking about three blocks and goes away with rest. He has developed
a habit of taking rest when the chest pain comes and he did not think it
needed medical attention until his friend told him yesterday that it might
be a symptom of heart disease. He is concerned and requests your
recommendation. He denies any chest pain now. He also reports no change
in quality or intensity of his chest pain. His past medical history is
significant for pacemaker insertion for a symptomatic second degree heart
block, Hypertension, and Smoking . His medications include lisinopril,
atenolol and hydrochlorthiazide. Physical examination is benign. An EKG
is obtained which reveals pacemaker rhythm with secondary ST-T changes.
The next best step in establishing the diagnosis in this patient is :

2 D -Echocadiogram
Exercise Stress Test ( Treadmill Stress Test)
Dobutamine Stress Echocardiogram
Persantin Stress Test
Cardiac Catheterization

Persantin is the preferred option for stress when Exercise
Stress Test is not useful or can not be done.
Patients with pacemaker rhythms, LBBB and severe LVH,
will have baseline EKG changes that may make EKG
component of the Stress test difficult. However, in these
conditions, Tachycardic stress ( Exercise Stress test) may
also produce false positive defects on nuclear imaging. So,
the solution is to use a different type of stress such as
vasodilator stress ( Persantin). Moreover, this patient was
also on beta blocker which makes it difficult to achieve
target heart rate during the Exercise Stress.
Dobutamine stress test is reserved for patients with
bronchospasm or heartblocks ( in conditions where
persantin is contraindicated)
If stress test revealed ischemia, cardiac catheterization
should be performed.
A 65 y/o man with presents to your office with complaints of
exertional chest pain for the past 4 weeks. The chest pain is
usually left sided, occurs on walking about one block and goes
away with rest. He denies any chest pain now. He also reports no
change in quality or intensity of his chest pain He also reports
having been diagnosed with peripheral arterial disease about 2
months ago for which he was advised exercise therapy. He does
experience leg pain on walking about one block which also
improves with rest. His past medical history is significant for
moderate COPD, Hypertension and a hernia repair about 3 years
ago. His medications include lisinopril, hydrochlorthiazide and
tiotropium inhaler. Physical examination is benign. The next best
step in establishing the diagnosis in this patient is :
2 D -Echocadiogram
Exercise Stress Test ( Treadmill Stress Test)
Dobutamine Stress Echocardiogram
Persantin Stress Test
Cardiac Catheterization

This patient presents with symptoms suggestive of
ischemic heart disease. So, needs a stress test to
establish diagnosis.
He cannot walk to his maximum secondary to
peripheral arterial disease and this will limit the
exercise. So, exercise stress test can not be done.
He has moderate COPD. Using persantin in
patients with COPD/ asthma can exacerbate
bronchospasm .
The preferred choice in this patient is, therefore,
Dobutamine Stress Echo.
Indications
Types
Choice of stress test
Exercise Stress Test
Exercise EKG stress test
Exercise Stress Echocardiogram ( main advantage is in patients
with long standing HTN with LVH and repolarization
abnormalities on EKG and also to demonstrate myocardial
viability)

Pharmacological Stress test ( in patients who cannot walk and in pts
with LBBB, LVH, repolarization abnormalities, electronically paced
ventricular rhythm, preexcitation syndromes (wpw); 1mm ST
segment depressions at rest - that makes EKG less interpretable and
also can have false positive nuclear results with exercise stress test)

Adenosine stress test
Dipyridamole Stress test
Dobutamine Stress Echo ( demonstrates viabile myocardium)

Nuclear Component of stress test ( Thallium)
Would recommend the website :www.ecglibrary.com

Learn some important EKGs:
Delta wave WPW Syndrome treatment in case of WPW with afib
Acute MI
Acute Pericarditis
Electrical alternans pericardial effusion
S1Q3T3 Pattern in PE
Differentiating tachycardias from fibrillation
Ventricular vs. Supraventricular ( atrial ) wide vs. narrow-
complex tachycardias ( exception WPW with afib and LBBB with
tachy are usually wide. But consider a wide complex tachycardia as
a Ventricular tachycardia until proven otherwise!!)


Atrial Fibrillation : causes ( structural, metabolic, hypoxic,
hyperthyroid, sudden onset in immobilized pt think PE )
determine whether stable or unstable
Stable Rate control drug therapy ( modify drug rxs
depending on comorbidities available Rxs are CCBs (
diltiazem), Beta blockers, Digoxin, Amiodarone
Unstable Afib Emergent cardioversion
Rate control is enough. Synchronous cardioversion only in
case by case basis rate control is enough usually ( AFFIRM
trial) {The risk of thromboembolic complication increases with
a duration of atrial fibrillation exceeding 48 hours ( TEE
before cardioversion to r/o thrombus if afib duration
exceeded 48hrs) }
AFIB+ CHF use digoxin but it takes time and is not all
that effective in rate control ( 60 mins for onset of action). So,
Metoprolol should be used too here for rate control.
AFIB + Hypotension digoxin, amiodarone after urgent
cardioversion attempts.
Anticoagulation heparin + warfarin overlap untill
therapeutic INR is reached then Cont Warfarin. Stroke risk
increases with age, additional risk factors like hypertension
Urgent cardioversion is indicated only for unstable atrial fibrillation (
Remember if your patient had an afib duration > 48 hours, there is a risk that a
thrombus is already present and cardioversion at this time would increase the
risk of stroke. For this reason, you should do urgent cardioversion ( i.e;
without prior TEE or prior anticoagulation) only when it is extremely needed
meaning in UNSTABLE cases

Recognize what is unstable afib : URGENT cardioversion is indicated
here:
A. symptomatic hypotension ( hemodynamically unstable)
B. ongoing myocardial ischemia ( Angina high rate is not good)
C. CHF resistant to treatment
( In CHF, initially rate control with metoprolol + digoxin, give furosemide to treat
CHF. If acute pulmonary edema, give Morphine also. If all these fail and patient
continues in CHF/sob - cardiovert!)

If patient does not fit above criteria, should not cardiovert with out knowing
the atrial fibrillation duration. As we know Rate control will alone suffice,
non urgent cardioversion is done only in select cases ( in patients where long-
term anticoagulation is risky or unacceptable, patients where atrial kick will
matter advanced chf etc)
For non-urgent cardioversion for afib, following criteria must be met:
Afib < 48 hr duration
For afib > 48 hours TEE showing no clot in left atrium
For afib > 48 hours If TEE cannot be done or TEE showed atrial thrombus,
anticoagulation for 3 weeks prior to and 4 weeks after cardioversion
( i.e; warfarin for 3 weeks, then cardiovert and then continue warfarin for another 4
weeks)



Factors that can increase the Risk of Stroke in
Patients with Atrial Fibrillation
Increasing age
Rheumatic heart disease
Poor left ventricular function or recent
congestive heart failure
Enlarged left atrium
Previous myocardial infarction
Hypertension
History of previous thrombo embolic events
Paroxysmal Atrial fibrillation
No other risk factors for stroke except atrial fibrillation.
Do you anticoagulate these pts with warfarin or would
you just use aspirin?
Remember CHADS2 Score ( CHF, HTN, Age >75, DM,
Previous Stroke/TIA) to predict the risk of stroke in an
Atrial fibrillation patient. Each constituent in CHADS2
gives one point except S which gives 2 points in risk
prediction.
In a case of Atrial Fibrillation, if CHADS2 is 1 or more or if
patient 60 yrs of age or more start A/C with Warfarin
If CHADS2 zero and also, patient less than 60 yrs of age lone
Afib ASA alone!
Remember Even if CHADS2 score is high, some
patients are put only on ASA due to high bleeding risk
( eg: high fall risk in elderly etc.) Weigh risk of
thromboembolism with risk of hemorrhage
A 64-year-old woman with a history of rheumatic fever is
evaluated for a 1-day history of abruptly worsening dyspnea.An
echocardiogram obtained 6-months ago showed left atrial
enlargement and diffuse calcification of the mitral valve and
subvalvular apparatus, with a mean transmitral gradient of 9 mm
Hg. On physical examination, she is sitting upright with labored
breathing. Her heart rate is 144/min, respiration rate is 32/min,
and blood pressure is 138/72 mm Hg. There are pulmonary
crackles and the jugular venous pressure iselevated. Heart sounds
are irregularly irregular with no murmurs. Electrocardiography
shows atrial fibrillation with a ventricular rate of 139/min. Which
of the following is the best immediate management for this
patient?
( A ) Warfarin
( B ) Warfarin plus digoxin
( C ) Percutaneous balloon mitral valvotomy
( D ) Intravenous heparin and esmolol
( E ) Electric cardioversion


In acute heart failure due to atrial fibrillation, initial
therapy must include heart rate control and
anticoagulation.
Initial therapy should be aimed at heart rate control, to
achieve rapid clinical improvement, and
anticoagulation, to prevent left atrial thrombus
formation and to lower thromboembolic risk.
Intravenous heparin achieves therapeutic
anticoagulation rapidly, whereas oral warfarin requires
several days to achieve therapeutic anticoagulation,
during which time there is risk of a thromboembolic
complication.
Although digoxin may be used to help control heart
rate in atrial fibrillation, it takes time to work, and is
often ineffective as a single therapeutic agent.


A 78-year-old woman is scheduled for a right nephrectomy for renal cell
cancer. She underwent aortic and mitral valve replacement 12 years ago
with St. Jude Medical bileaflet mechanical prostheses for rheumatic
valvular disease. She has no other significant medical history. Her only
medications are warfarin (with a target INR of 2.5 to 3.5) andantibiotic
prophylaxis for endocarditis.Which of the following is the best plan for
anticoagulation in the perioperative period?
( A ) Maintain the INR between 2.5 and 3.5 throughout the perioperative
period.
( B ) Stop the warfarin 3 to 5 days before surgery and restart it 1 to 3 days
after surgery.
( C ) Stop the warfarin 3 to 5 days before surgery and start heparin 3 days
before surgery and again 1 day after surgery.
( D ) Maintain the INR between 1.5 and 2.5 throughout the perioperative
period and begin the usual dose ofwarfarin 5 days after surgery.
( E ) Continue warfarin up to the day of surgery; administer vitamin K, 1
mg intravenously on the morning of surgery, and start heparin 1 day after
surgery.

For patients at high risk for thrombosis,
heparin should be substituted for warfarin
before and immediately after surgery.

Polymorphic Ventricular tacycardia
Prolonged QT interval
Drugs prolonging QT interval
Management Principles of TCA toxicity
ICU admission,
Sodium bicarbonate infusion Drug of choice
if EKG changes are present
Antiarrhythmics (Lidocaine)
Magnesium sulfate
Idiopathic degeneration of the conducting system Fibrosis,
sclerosis, or calcification
Ischemic heart disease
Hypertensive heart disease
Valvular heart disease
Drugs -blockers, calcium-channel blockers, digitalis,
amiodarone, adenosine, type IA antiarrhythmic drugs
Infectious diseases Lyme disease, infective endocarditis,
myocarditis (various causes)
Heightened vagal tone Young, healthy subjects (may be normal
variant), Sleeping and Spinal/CNS injuries
Congenital AV block
Electrolyte disturbances Hyperkalemia
Iatrogenic radiofrequency ablations etc
Hypothyroidism
Infiltrative processes Sarcoidosis, amyloidosis
Cardiac tumors Primary or secondary
Neuromuscular diseases Myotonic dystrophy,Erb's (limb-girdle)
dystrophy, peroneal muscular atrophy
Familial
Start with hx Ask about:
Dizziness , Weakness , Fatigue , Effort intolerance , Palpitations ,
Lightheadedness , Loss of consciousness (syncope) symptomatic
bradycardia
Chest pain ( ? MI/ Bradycardia itself)
Fever ( ? IE, myocarditis, Lymes disease )
Rash ( also ask about tick bite, artralgias ? Lyme carditis esply in endemic
zones)
Arthropathy
Medication history ( b-blockers, nondihydropyridine CCBs, digitalis,
clonidine )
History or symptoms of other acute or chronic conditions that can cause heart
block, such as:
Hypertension
Previous/ recent MI (CAD) ( transient AV block common after inferior MI )
Heart murmur
Kidney disease leading to hyperkalemia
Hypothyroidism
Previous heart surgery, catheterization procedure to close a septal defect, or
electrophysiologic ablation procedure
Infective endocarditis complicated by a myocardial abscess or aortic ring
involvement
Myocarditis
Tumors involving the myocardium
Muscular dystrophy ( myotonic dystrophy )
Family history of AV block
Athletes Heart : Athletic participation causes high vagal tone that can reduce
AV nodal conduction!!

Physical Exam :
Look for:
Abnormalities in vital signs, such as:
Hypertension
Bradycardia
Widened pulse pressure and bradycardia in third-degree AV block
Irregular pulse in second-degree AV block
Abnormalities in the jugular venous pulse
Other abnormalities on cardiac exam suggesting structural disease, such as:
Heaves
Thrills
Murmurs
Gallop sounds
Other abnormalities on general physical exam suggesting an underlying
predisposing condition, such as:
Rash
Muscle atrophy
Fasciculations or myotonia
Chest scars from previous cardiac surgery
Peripheral signs of infective endocarditis
Signs of hypothyroidism

Remember with regard to Heart Block after MI
Transient AV block is common after inferior
MI.
AV block associated with anterior MI often
indicates extensive necrosis.
30-day mortality is increased among patients
with MI who develop AV block compared to
those who do not ( prognostic predictor)

The PR interval is 388 ms and constant. Each P wave is followed by a QRS complex.

Note the progressive lengthening of the PR interval until a P
wave is blocked. The PR interval following the blocked P
wave is shorter than the one before the blocked P wave.
Progressive shortening of the R-R interval is best shown in
the 5:4 cycle on the right of the strip
P waves are blocked intermittently. The PR interval does not
change. Note the wide QRS complexes.

No relationship between the atrial and ventricular activity
is present. The atrial rhythm is sinus at 90 beats/min. A
slight sinus arrhythmia is present. The ventricular rhythm
is a wide QRS escape rhythm at 26 beats/min.

Test Notes
ECG with rhythm
strip
Essential to define the type and site of the block.
Echocardiogram Useful to determine the presence and severity of structural heart
disease evidence of previous MI, hypertensive heart disease,
valvular heart disease, and infective endocarditis. Transesophageal
echocardiogram is superior to transthoracic echocardiogram in
identifying aortic root abscesses and infections involving prosthetic
heart valves
Serum electrolytes To evaluate for hyperkalemia, especially in patients with kidney disease
Cardiac enzymes
(creatine kinase,
cardiac troponin)
Can identify ischemia/infarction or myocarditis as potential causes of AV
block
Lyme serology Can identify Lyme disease as a potential cause of AV block
Serum digoxin level Can identify digitalis toxicity as a potential cause of AV block
Thyroid function
tests
To evaluate for hypothyroidism
Blood cultures To evaluate for evidence of bacteremia and possible infective
endocarditis ( ? New onset heart block, bbb)
First step diagnose AV Block. Do not confuse with other sinus
bradycardias or sinus pause, sino atrial exit blocks ( note p will
be absent in sinus types)
Your next step is to look for reversible condition medication/
infection, lymes, increased vagal tone, ischemia etc.
Discontinue the meds that are likely to slow AV nodal conduction.
Reevaluate the patient after d/c of these meds
Hospitalize the pts if they are symptomatic
Hospitalize patients with symptomatic AV block to:
Confirm that syncope, presyncope, or symptoms of heart failure
are due to AV block
Address reversible causes such as electrolyte abnormalities,
hypervagotonia, myocardial ischemia, structural heart disease,
and use of specific medications that can impair AV conduction
Determine the need for:
Electrophysiologic studies
Temporary and/or permanent pacemaker placement

Intravenous atropine, isoproterenol, or theophylline
to facilitate AV conduction in patients with symptomatic
AV block . Do not use in those with infranodal block.
In patients with symptomatic bradycardia, including
those with heart failure, myocardial ischemia, or
hypotension, consider administering atropine to increase
AV conduction
Remember that in
patients with infranodal block ( Mobitz type 2 and Third
degree heart block), atropine can increase the sinus rate
without changing AV conduction the net effect will be
a diminished ventricular rate
In patients without ischemia may use the -agonist
isoproterenol
May use methylxanthine derivative theophylline but
use cautiously in patients with myocardial ischemia.
Do not use isoproterenol or theophylline to treat
bradyarrhythmias in patients with ischemic heart disease
coz they are potentially arrhythmogenic and may
increase myocardial o2 demand.
Drug overdose leading to symptomatic heartblock:
For patients with -blocker or calcium-channel blocker
overdose may use intravenous glucagon to improve
hemodynamic parameters and AV conduction:
For patients with calcium-channel blocker overdose,
administer
Intravenous calcium (calcium chloride, 10 to 20 mL of a 10%
solution, or calcium gluconate, 30 to 60 mL of a 10% solution, over 5
minutes with repeated boluses every 15 minutes for a total of three
to four doses or an infusion of 0.5 mEq of calcium/kgh), which
requires monitoring the serum calcium level and the ECG, or
Infusion of a high dose of insulin along with glucose
For patients with hypotension not responding to above
Rxs, start an infusion of a vasoactive (pressor) drug to
maintain adequate systemic perfusion until pacing can be
initiated.

Rule out reversible causes as discussed earlier
Temporary transcutaneous or transvenous
pacemaker for symptomatic patients who do
not respond to drug therapy
If AV block is not considered to be reversible,
some experts recommend proceeding directly
to permanent pacemaker implantation.
Consult a cardiologist (electrophysiologist) for
implantation of a single- or dual-chamber
permanent pacemaker
Systolic Vs Diastolic
Stages/ NYHA Classes
Management ACEI, Beta blockers, Diuretics,
Spironolactone if indicated ( stage III/ IV)
Cardiac Resynchronization therapy ( CRT) Biventricular
pacemaker for pts with NYHA Class III and widened QRS
complex ( >0.12 sec)
Cardiac transplantation for pts with NYHA Class IV ,
Consider LVAD ( left ventricular assist device) in a pt
waiting for transplantation.
CHF exacerbations
Rx acute episode diuretics, low dose/ no b-block, treat
HTN, Nitroglycerin, natrecor ( Do not use BNP to monitor
response to Natrecor)
? Secondary to what accelerated HTN, MI, ACS, Atrial
Fib, Medication/ diet noncompliance, Missed hemodialysis
Investigate the cause & Rx appropriately underlying
cause for this exacerbation.
Prevent future exacerbations Digoxin reduces
morbidity but not mortality i.e; dig reduces the need for
Heart failure hospitalizations.
Aspirin ( A must in CAD)
Beta Blocker ( A must! reduces mortality by 35 to 65%) (
Contraindications for b-blocker in this setting cardiogenic shock,
2
nd
/3
rd
degree heart block without pacemaker, Severe reactive airway
disease
remember mild to moderate copd/asthma , DM, Peripheral arterial
disease are not a contraindication for beta blockers)
ACEI/ ARBs( reduces mortality by 17-30%) esply if EF<45%, in pts with
Class I IV heart failure, asymptomatic LV dysfunction, Post MI, DM
remember ARBs are not a first line therapy in place of ACEI (ELITE
trial) However, they have equivalent benefits as ACEIs recommended
for use in pts who are intolerant to ACEIs or as an add on therapy to
ACEIs
Aldosterone Antagonists ( Spironolactone/ Eplerenone) reduces
mortality by 15-30% in pts with class III/IV heart failure
Hydralazine + Nitrates ( Bidil) reduces mortality by 43% in African-
Americans with Class III heart Failure when added to standard
care.(The therapeutic role of these agents in HF patients other than
African Americans should be further evaluated, but this represents a
reasonable option for all HF patients who remain Class III or IV,
irrespective of race or ethnicity)
Statin if Hyperlipidemia
Cough is a common side effect.
If ACEI can not be used because of cough,
switch to ARB.
If ACEI or ARB, can not be used because of
angioedema, consider using Hydralazine/
isosorbide combination.

In Acute CHF, Start at very low doses
Start at low dose with careful titration. Increase at intervals of at least 2 weeks until
target dose. The ACC/AHA guidelines recommend using only those beta blockers
and those doses that have been proven to reduce mortality (i.e. mortality reduction is
not a class effect).


Initiation Titration Target
Carvedilol (preferred) 3.125 mg bid. 6.25, 12.5 mg bid 25 mg bid
Metoprolol XL 12.5 mg daily 25, 50, 100, 150 mg daily 200 mg daily
Bisoprolol 1.25 mg daily 2.5, 5 mg daily 10 mg daily

CARVEDILOL is the preferred Beta Blocker has better lipid profile than other beta blockers
COMET demonstrated that carvedilol (beta-1, beta-2,
and alpha-1 blockade) provided a 17% mortality reduction compared to beta-1 selective blockade
with metoprolol tartrate.
The COPERNICUS trial demonstrates survival benefits
with carvedilol in patients with class IV heart failure and that therapy can be initiated during
hospitalization.
IMPACT-HF demonstrates that in-hospital initiation is
safe and improves treatment rates Strongly consider initiation of carvedilol or switching from
other beta blocker to carvedilol prior to heart failure hospital discharge, as this has been shown to
improve patient compliance and treatment utilization.

LVEF < 0.35, Class II / III, all HF etiologies, ICD
therapy reduces mortality by 23% (SCD-HeFT)
LVEF < 0.30, post MI: prophylactic ICD therapy
indicated, reduces mortality by 31% (MADIT II)
Wait > 30 day after acute myocardial infarction before
implanting ICD (DINAMIT)
QRS > 120 ms, LVEF < 0.35, NYHA III or IV: Cardiac
resynchronization therapy plus ICD indicated, reduces
mortality by 43% and death and hospitalization by
22%. (COMPANION)
Prophylactic Placement of an ICD device (with or
without CRT) is recommended in conjunction with
optimal medical treatment in all eligible HF patients
without contraindications, as part of standard
management. Education and counseling of patients
prior to device placement is essential.
Also called Dual chamber pacing (biventricular pacing)
CRT uses uses a specialized pacemaker to re-
coordinate the action of the right and left ventricles in
patients with heart failure.
In approximately 30% of patients with heart failure, an
abnormality in the heart's electrical conducting system
(called an "intraventricular conduction delay" or
bundle branch block as evidenced by widened QRS
>0.12 sec) causes the two ventricles to beat in an
asynchronous fashion. This asynchrony greatly
reduces the efficiency of the ventricles in patients with
heart failure, whose hearts are already damaged.
CRT re-coordinates the beating of the two ventricles by
pacing both ventricles simultaneously. This differs
from typical pacemakers, which pace only the right
ventricle.
Indications
NYHA Functional class III/ IV heart failure despite
optimal medical therapy
QRS greater than 120 msec ( suggesting
intraventricular conduction delay that leads to
cardiac dyssynchrony)
Systolic HF with EF<35%
Left ventricular end diastolic
dimension>55mm(dilated)
Benefits CRT improves quality of life and
reduces re-hospitalizations for worsening heart
failure.
? Does it reduce mortality in HF When
indicated, CRT used along with ICD has been
shown to reduce mortality ( COMPANION
trial). The role of CRT without an ICD in
reducing the mortality is still unresolved
A 64-year-old man is evaluated for a progressive, 3-month history
of dyspnea on exertion and orthopnea. He has a 15-year history of
hypertension, hyperlipidemia, chronic renal insufficiency,
coronary artery disease, and ischemic cardiomyopathy.On
physical examination his heart rate is 92/min and blood pressure
is 144/80 mm Hg. There is elevated jugular venous pressure,
pulmonary crackles, an S3, and dependent edema.The serum
creatinine is 2.8 mg/dL and serum potassium is 4.9 meq/L.
Echocardiography shows dilation of the left atrium, dilation and
extensive scarring of the left ventricle, and an ejection fraction of
25%. In addition to digoxin and furosemide, which of the
following therapies is the optimal initial management for
congestive heart failure in this patient?
( A ) Lisinopril
( B ) Lisinopril and carvedilol
( C ) Carvedilol
( D ) Hydralazine and isosorbide dinitrate
( E ) Hydralazine, isosorbide dinitrate, and carvedilol


Digoxin, diuretics, afterload-reducing therapy,
and -blockers are associated with
symptomatic improvement in patients with
congestive heart failure due to systolic
dysfunction.
Afterload-reducing therapy, -blockers, and in
patients with stage IV left heart failure,
spironolactone are associated with
reduced mortality.

HOCM vs. Aortic Stenosis Murmur
differentiation
Carotid upstroke delayed in AS, brisk in
HOCM
Consider placement of an ICD in patients with HCM at
high risk for sudden death, regardless of whether they
are symptomatic, including those with:
Family history of sudden death at a young age
Young age (<30 years) at diagnosis
Unexplained syncope
Resuscitation from cardiac arrest
Nonsustained or sustained VT during Holter
monitoring
Significant LVH (wall thickness 30 mm)
Abnormal BP response during exercise

A 40-year-old man is evaluated in the office because of a 3-week
history of increasing chest pressure and exertional dyspnea.
Physical examination shows a pulse rate of 65/min and a blood
pressure of 155/90 mm Hg. The carotid arteries have a brisk
upstroke and a bifid contour. There is a grade 4/6 systolic
murmur heard best at the left sternal border in the fourth left
interspace. The murmur increases with the Valsalvas maneuver
and with standing.
Electrocardiography shows left ventricular hypertrophy.
Which of the following drugs will most likely improve the
patients symptoms?
( A ) Digoxin
( B ) Furosemide
( C ) Lisinopril
( D ) Nitroglycerin
( E ) Metoprolol

Bifid carotid pulsation, double apical impulse, a
murmur that increases with Valsalva's maneuver or
with standing, and left ventricular hypertrophy are
typical for hypertrophiccardiomyopathy(Paradoxical
SAM on echo )
-Blockers are indicated in the treatment of
hypertrophiccardiomyopathy.
Vasodilators and other drugs that cause afterload
reduction are hazardous in patients with hypertrophic
cardiomyopathy.
Drugs or maneuvers that decrease left ventricular volume or afterload generally will increase the outflow
tract obstruction, and those drugs that increase volume will decrease the obstruction. Thus, diuretics should
not be used as initial therapy. Nitroglycerin and other vasodilators, and other drugs that cause afterload
reduction, such as angiotensin-converting enzyme inhibitors, are often hazardous to use in patients with this
disease because the associated preload reduction results in diminished left ventricular volume and increased
outflow tract gradient. Digoxin, and other drugs that increase myocardial contractility, should be avoided
because they produce an increase in outflow tract obstruction.

Administer antibiotics to patients with group A streptococcal infections to prevent
rheumatic fever and to patients at risk for endocarditis. ( PRIMARY
PROPHYLAXIS)
Give patients with group A streptococcal infections prompt antibiotic therapy to
reduce the risk of rheumatic fever with either Benzathine penicillin G, 1.2 MU
im once for patients >27 kg, or
Penicillin V, 500 mg po bid-tid for 10 days for adolescents and adults
For patients allergic to penicillin: - erythromycin/ azithromycin
Ensure that patients with a history of rheumatic fever, particularly rheumatic carditis,
receive long-term prophylactic antibiotic therapy to prevent recurrence: (
SECONDARY PROPHYLAXIS)
Administer benzathine penicillin G, 1.2 million units im once a month
Administer every 3 weeks in high-risk patients (e.g., patients with residual carditis or who are poorly
compliant or economically disadvantaged)
As an alternative to benzathine penicillin G, use:
Penicillin V, / Sulfadiazine or Erythromycin
Continue therapy for:
Rheumatic fever prophylaxis for at least 10 years after the last episode and at least until
age 40 in patients with carditis and residual cardiac valve disease
Ten years or into adulthood (whichever is longer) in patients with carditis but no valve
disease
Five years or until age 21 (whichever is longer) in patients who did not have carditis

Jones Criteria*
Major manifestations
Carditis, Polyarthritis, Chorea, Subcutaneous nodules,
Erythema marginatum
Minor manifestations
Clinical findings: Arthralgia, Fever
Laboratory findings: Elevated acute phase reactants
Erythrocyte sedimentation rate, C-reactive protein,
Prolonged PR interval
Supporting evidence of group A streptococcal infection
Positive throat culture of rapid streptococcal antigen
test, Elevated or rising streptococcal antibody titer
Diagnosis + if 2 major or 1major/2minor+ preceding
strep infection
Antibiotics follow with primary/ secondary
prophylaxis regimens as discussed earlier.
Antiinflammatories a must
Use salicylates if polyarthritis
Corticosteroids if severe carditis
Chorea : phenobarbital, lorazepam , haloperidol,
SSRIs
MS
AS
MR
AR

Symptoms
Syncope during exertion
Exertional angina
Exercise intolerance
Heart failure symptoms
Consider aortic valve replacement in patients with
symptomatic AS.
Consider aortic valve replacement in patients with:
Symptomatic severe AS ( ?? SEVERE AS of <1cm2 without
symptoms)
Severe AS who are undergoing coronary bypass surgery
Severe AS who are undergoing surgery on the aorta or other heart
valves
Consider valve replacement in patients with moderate AS
who:
Are undergoing other cardiac or aortic surgery
Have left ventricular dysfunction
Develop hypotension on an exercise stress test
Aortic valvuloplasty reserved for symptomatic adult
patients who are not candidates for aortic valve
replacement due to comorbid conditions or in patients who
do not desire surgical intervention
Evaluate patients with AS at least annually.
For patients with mild AS:
Perform a careful history and physical examination annually
For patients with moderate to severe AS:
Perform an interim history and physical examination every 6
months or more frequently if symptoms occur
Reinforce the need for prophylaxis against endocarditis
Use serial echocardiograms to evaluate left ventricular
hypertrophy and function in addition to the aortic
valve area:
Annually in patients with severe AS
Every 2 years in patients with moderate AS
Every 5 years in patients with mild AS


A 71-year-old woman is evaluated for fatigue and a
gradual decrease in stamina during the past 3 years.
Her physical examination shows a grade 2/6
crescendo-decrescendo systolic murmur heard loudest
at the right upper sternal border. Which of the
following features suggest that the murmur is caused
by hemodynamically significant
aortic stenosis?
( A ) The murmur encompasses S1
( B ) The first component of S2 is accentuated
( C ) The murmur peaks in the latter half of systole
( D ) There is an associated diastolic murmur
( E ) The murmur is associated with a widened pulse
pressure


Remember murmur only occurs when there is flow
across this narrow valve. Murmur cant occur early if
there is severe stenosis coz no flow occurs until left
ventricle contracts enough to build a gradient in
pressures.
Clinical features that are associated with the murmur
of hemodynamically significant aortic stenosis include
a late-peaking murmur that encompasses S2, a
diminished aortic component, and a diminished and
delayed carotid pulse.
These also suggest Aortic stenosis rather than just a
sclerosis
A 41-year-old man with a history of a bicuspid aortic valve comes
to the office for a routine follow-up examination. He runs 20 miles
per week and swims 1000 yards twice weekly. He denies
exertional dyspnea or declining exercise tolerance. His only
medication is antibiotic prophylaxis for endocarditis. On physical
examination, his heart rate is 68/min and blood pressure is 142/56
mm Hg. The cardiac apex is enlarged. The heart sounds are
regular with a normal S1 and S2 and a grade 2/4 decrescendo
diastolic murmur heard best at the right upper sternal border.
Echocardiography shows mild left ventricular dilation; the left
ventricular ejection
fraction is 70%. Which of the following is the best management
for this patient?
( A ) An angiotensin-converting enzyme inhibitor
( B ) Rest and exercise radionuclide vetriculography
( C ) Exercise thallium scintigraphy
( D ) Heart catheterization with left ventriculography
( E ) Aortic valve replacement


Use vasodilators in patients with aortic regurgitation and
hypertension, left ventricular dilation, or in symptomatic
patients.
This is an asymptomatic man with severe aortic regurgitation, mild left
ventricular dilation, and normal left ventricular systolic function.
Vasodilator therapy is indicated in patients with any degree of aortic
regurgitation and systolic hypertension, in asymptomatic patients with
severe regurgitation and left ventricular dilation (as with this patient), or
in patients with severe regurgitation and symptoms of left ventricular
systolic dysfunction but a contraindication for surgery. Data show that
angiotensin-converting enzyme inhibitors increase exercise capacity and
that nifedipine may delay the needfor surgery. In the absence of direct
comparisons between the two, present recommendations suggest that
either agent is acceptable


Aortic valve replacement is indicated for severe aortic regurgitation plus
symptoms, left ventricular systolic dysfunction, or substantial left
ventricular dilation (>70 to 75mm in diastole or >50 to 55 mm in systole).
Assessment of left ventricular systolic function using radionuclide
ventriculography or invasive left ventriculography is indicated only if the
information is not available using echocardiography.


In case of Infective Endocarditis, most often questions are on
Prophylaxis where to give it? How do you decide? What advise will
you give patient etc!!
In case of IE prophylaxis First determine if the patient has a cardiac
condition that puts him at HIGH risk for IE or not and then determine
whether the planned procedure presents a significant risk of
bacteremia with organisms known to cause IE.
As per AHA (2007) guidelines, IE prophylaxis is recommended only
in HIGH RISK cardiac conditions prior to high risk dental procedures
alone. No prophylaxis is recommended for Moderate risk cardiac
conditions (i.e; Rheumatic Heart Disease, MS, MR, MVP with MR,
VSD, AS are no longer an indication for IE prophylaxis prior to ANY
procedure!)
As per AHA-2007 guidelines, No prophylaxis is recommended in
ANY cardiac condition prior to GI/ GU procedures
If USMLE Step3 has not updated their questions so as to meet the
above guidelines, you will most likely receive a credit for such a
question.

Cardiac Conditions Associated with Endocarditis
Endocarditis prophylaxis recommended
High-risk category
Prosthetic cardiac valves,bioprosthetic and homograft valves
Previous bacterial endocarditis
Complex cyanotic congenital heart disease (e.g., single ventricle states, transposition
of the great arteries, tetralogy of Fallot)
Surgically constructed systemic pulmonary shunts or conduits
Endocarditis prophylaxis not recommended
Moderate-risk category
Most other congenital cardiac malformations (other than above and below)
Acquired valvar dysfunction (e.g., rheumatic heart disease)
Hypertrophic cardiomyopathy
Mitral valve prolapse with valvar regurgitation and/or thickened leaflets
Negligible-risk category (no greater risk than the general population)
Isolated secundum atrial septal defect
Surgical repair of atrial septal defect
ventricular septal defect, or patent ductus arteriosus (without residua beyond
6 months)
Previous coronary artery bypass graft surgery
Mitral valve prolapse without valvar regurgitation
Physiologic, functional, or innocent heart murmurs
Previous Kawasaki disease without valvar dysfunction
Previous rheumatic fever without valvar dysfunction
Cardiac pacemakers (intravascular and epicardial) and implanted
defibrillators
IE prophylaxis recommended only for patients at
highest risk for IE - prosthetic heart valves,
previous IE, cyanotic congenital heart
malformations, and surgically constructed
systemic pulmonary shunts and injection drug
users.
Patients at moderate risk for IE ( those with non
cyanotic congenital heart disease, HOCM, MVP
with regurgitation and acquired valvular
dysfunction i.e; rheumatic valvular disease) are no
longer a candidates for prophylaxis prior to any
procedure.
Although IE occurs rarely, its high mortality ( 20
40% mortality rate) prompts experts to recommend
antibiotic prophylaxis among high-risk patients for IE.
Procedures associated with high rates of
bacteremia
most dental procedures;

some upper respiratory tract procedures


Dental procedures associated with high rates
of bacteremia (>10%) with organisms known to
cause IE
Tooth extraction,
Routine cleaning and scaling
Any procedure involving gingival
manipulation.
Low risk for bacteremia (No prophylaxis)
Fluoride treatment, Placement of removable
orthodontic or prosthodontic appliances,
Placement of rubber dam and Postoperative
suture removal

Gastrointestinal procedures
Tonsillectomy,
Esophageal stricture dilation
Endoscopic retrograde cholangiography
variceal sclerotherapy.
Routine gastrointestinal procedures, including
upper endoscopy or colonoscopy (with or
without biopsy)
Transrectal biopsy of the prostate,
Cystoscopy
Urethral dilation.
Insertion of a Foley catheter into an infected
bladder.
Uncomplicated Vaginal delivery
Caesarian section
Uterine D&C
Insertion/ removal of IUDs.
Rigid bronchoscopy is
associated with high rates of
bacteremia, whereas flexible
bronchoscopy is not.
Give prophylaxis prior to rigid
bronchoscopy
Class Procedures High Risk Antibiotic regimens
Dental Routine cleaning
Tooth extraction
Periodontal procedures
Dental implant placement
Reimplantation of avulsed teeth
Endodontic instrumentation (root
canal)

Preferred oral regimen:
Amoxicillin, 2 gm po

Oral alternative regimens:
Clindamycin 600 mg po, Cephalexin, 2 gm
po,Cefadroxil, 2 gm po,Azithromycin, 500
mg po, Clarithromycin, 500 mg po

Preferred intravenous regimen:
Ampicillin, 2 gm iv

Intravenous alternative regimen:
Cefazolin, 1 gm iv, Clindamycin, 600 mg iv
Pulmonary
Rigid bronchoscopy, Surgical
operations that involve respiratory
mucosa


Same as for dental procedures
Oral medications should be taken 60 minutes before
the procedure; intravenous medications should be
administered 30 minutes before the procedure. Only a
single dose is recommended.


Azithromycin has been recommended as an alternative
to clindamycin in children.
An IV drug abuser who recently survived an
infective endocarditis episode come to you and says
that she cannot give up IVDA but requests you for
prophylaxis because she is a high risk for IE as she
continues to inject herself putting herself at a risk
for bacteremia what would you do??
For injection drug users, there
is no preventive strategy that
could be effective other than
discontinuing injection drug
use.
Look for fever, new murmur, look for heart blocks on
EKG, Blood cultures, TEE.
TEE shows vegetations and if pt has other criteria for IE
but negative blood cx think about previous partial
Rx vs. HACEK organisms.
If TEE shows vegetations, cultures ve, no other
suspicion of atypical bugs or partial Rx reconsider
ur diagnosis ( most likely not IE )
Antibiotics nafcillin + gentamicin. In IVDA
Vancomycin + gentamycin ( S.viridans, Enterococci are
most common bugs that cause SBE. In IVDA, S.aureus
should be strongly suspected. Gentamicin is added for
synergism)
Recognizing and managing complications aortic
valve abscess, acute AR, Acute renal failure, Septic
Embolism ( a new LBBB on EKG can indicate an
abscess)
You should not anticoagulate IE patients!
A 58-year-old man is evaluated for acute dyspnea and hypotension of 1-
hours duration. He was hospitalized for fevers, chills, and weight loss after
a routine dental cleaning 2 weeks ago. Blood cultures were positive for
gram-positive cocci. Echocardiography showed a mobile, soft-tissue density
mass on the aortic valve. Therapy with intravenous vancomycin and
gentamicin was begun, and the patient was doing well until this
morning.On physical examination, his heart rate is 108/min, respiration
rate is 52/min, and blood pressure is 84/54 mm Hg.The cardiac apex is not
displaced, murmurs are not heard, but diffuse crackles are present. After
initiation of mechanical ventilation, portable chest radiography shows a
normal cardiac silhouette and interstitial edema. Repeat
electrocardiography shows sinus tachycardia and T-wave inversion in the
inferior and lateral leads. Echocardiography shows severe aortic
regurgitation. Which of the following is the best immediate therapy for
this patient?
( A ) Intravenous heparin and a ventilation-perfusion scan
( B ) Intravenous -blockers and an angiotensin-converting enzyme
inhibitor
( C ) Intravenous isoproterenol and nitroprusside
( D ) Intravenous furosemide and an aortic balloon pump
( E ) Left heart catheterization


Treat acute severe aortic regurgitation with nitroprusside, isoproterenol,
and chronotropic agents (or temporary pacing).
An intra-aortic balloon pump is contraindicated in the setting of severe
aortic regurgitation.
-Blockers should be avoided in acute aortic regurgitation. Slowing the
heart rate increases the diastolic interval and exacebates AR
The patient presents with aortic valve endocarditis, but quickly
develops acute, severe aortic regurgitation with hemodynamic collapse.
The physical findings of aortic regurgitation are often subtle or absent
when aortic regurgitation occurs abruptly. Without time for
compensatory left ventricular dilation, increased stroke volume and
widened pulse pressure are absent, and the diastolic murmur may be brief
or absent due to rapid equilibration of aortic and left ventricular
pressures. Echocardiography confirms the clinical suspicion of acute,
severe aortic regurgitation, and immediate therapy should be aimed at
hemodynamic stabilization before surgery.

The medical management of acute, severe aortic regurgitation is aimed at
afterload reduction to decrease the severity of regurgitation, inotropic
agents to support blood pressure, and chronotropic agents (or temporary
pacing) to increase heart rate and thereby decrease the diastolic interval
and the severity of regurgitation. Nitroprusside and isoproterenol are
appropriate first-line therapeutic interventions.

Symptoms differentiate the pain from neuropathy,
pseudocluadication ( lumbar canal stenosis) and Thromboangitis
Obliterans (Bergers disease)
Differentiate Pseudoclaudication ( claudication pain does not occur
with standing. But pseudoclaudication appears with standing)
Relief time : 5 mins of rest ( conversely, relief in pseudoclaudication
occurs 30 mins after sitting or changing position)
Investigations ABI, Arterial doppler, MRA (only if surgery is
planned)
Management : 2 goals Deal with PAD symps and then also deal
with increased CAD/CVD/Mortality risk
Exercise therapy, supervised best to improve walking distance
Cilostozol ( phosphodiesterase inhibitor) causes 40 -50%
improvement in walking distance over 6 month period. (
contraindicated in Heart failure)
clopidogrel to deal with CAD/ mortality risk. Preferred
antiplatelet therapy over aspirin in PAD pts ( CAPRIE study)
Surgery in select cases ( not responsive to medical Rx; Severe symps
causing occupational/ life disability; risk vs.benefit ratio)
Cardiovascular stress test
Primary/ essential follow ups, stages of HTN (
JNC VII criteria ), Lifestyle modifications, Drug
Rx, choice of antihypertensive, Caution with ACEI
in pregnant/ reproductive age group females

Secondary whom to suspect and whom to
screen ( not obese, < 30yr age group, no family hx,
metabolic abnormalities on labs, ? episodic)
coarctation of aorta ( Rx Sx),
hyperaldosteronism, hyperthroidism,
hypercalcemia, Renal artery stenosis,
Phaeochromocytoma, liddles syndrome, licorice
abuse, medication induced (OCPills, NSAIDs)
Lifestyle Modification Approximate SBP Reduction
Weight Reduction 5 to 10 mm Hg for every 10kg weight
reduction
DASH Diet 8 to 14 mm Hg
Dietary Sodium Restriction 2 to 8 mm Hg
Physical activity 4 to 9 mm hg
Moderation of alcohol use 2 to 4 mm hg
BP Classification SBP DBP
Normal <120 and <80
Prehypertension 120-139 or 80-89
Stage 1 hypertension 140-159 or 90-99
Stage 2 hypertension =/>160 or =/>100

In adults (>18 years), note that classification is based on
an average of 2 or more readings obtained at 2 or more
separate visits.
When white coat HTN is suspected or if the diagnosis
of sustained HTN is not certain, consider ambulatory
BP monitoring or self-recorded (home) BP
measurements.
SBP is more important Cardiovascular risk factor.
Cardiovascular disease risk doubles with each
20/10mmHg increment over 115/75.
Targets
140/90
130/80 if diabetic or CKD
125/75 if Diabetic Nephropathy ( microalbuminuria)
Consider 2 agents if BP >20/10 above goal. One agent
should usually be Thiazide diuretic. Second agent can
be ACEI, ARB, Beta blocker or Calcium channel
blockers.
Two or more agents usually required for effective
control of blood pressure
Thiazides are first choice and first line agents in most
cases. ( ALLHAT Trial)

The Antihypertensive and Lipid-Lowering Treatment
to Prevent Heart Attack Trial.
ALLHAT reiterated the importance of Diuretic as an
initial therapy in Hypertension
Diuretics are more effective than ACEIs and CCBs in reducing the
complications of HTN such as heart failure and angina in all
races.
Diuretics reduced the incidence of stroke in african american
population more than ACEI.
Diuretics are inexpensive agents.
For these reasons, Thiazide-type diuretics should be preferred for
first-step antihypertensive drug therapy.
In diabetics with HTN, Thiazides should be considered as a first-
line therapy, despite the fact that they may adversely affect
insulin resistance and potassium balance in some individuals
because the advantage is that they reduced cardiovascular events
better than ACEIs or CCBs ( unless there is a compelling
indication for ACEI such as microalbuminuria or Chronic Kidney
Disease)

ACEI must be used in Diabetic patients with evidence of
nephropathy ( microalbuminuria) unless there are
contraindications.
Beta blockers reduce mortality in post MI patients and must
be used Post MI
ACEI must be used in post MI patients if the EF is less than
45%
CKD is a compelling indication for ACEI
In patients with history of TIA/ CVA ACEI and Diuretics
have been shown to reduce the risk of recurrent stroke (
PROGRESS trial).
In CHF, use antihypertensives depending on the class of heart
failure ( as discussed in previous slides). Betablockers and
ACEIs are must in all classes of CHF unless contraindicated.
Spironolactone must be added in Class III/ IV heart failure.
Hydralazine/ Isosorbide combination is useful in african
americans with Class III heart failure
Resistant or Refractory hypertension is defined
as failure of concomitant use of three or more
different antihypertensive agents ( one of
which is a diuretic) to lower blood pressure to
less than 140/90 mmHg in all age groups.
Uncontrolled blood pressure increases the risk
of stroke, CHF, Aortic dissection, MI and Renal
failure.
If response to maximal therapy is inadequate,
consider the following possibilities.
White coat HTN
Suboptimal adherence to therapy
Volume overload
Concomitant drug-related causes, such as use of
NSAIDs , Oral contraceptives , black licorice,
Erythropoetin and Psychotropic drugs.
Alcohol use.
Recreational drugs
Associated conditions, such as smoking or Sleep
apnea ( early morning headaches and excessive day
time sleepiness, Obesity are some clues to OSA)
Secondary HTN

Medication non compliance is a major barrier in
adequately controlling the blood pressure
Side effects and cost can reduce the adherence.
Some Important Side Effects:
Beta blockers : Erectile Dysfunction, Fatigue, Depression
CCBs: Ankle Edema
ACEIs : Cough, angioedema ( rare)
Thiazides : hypokalemia, gout (hyperuricemia),
hypercalcemia ( low dose thiazide is not contraindicated
in gout)
Direct vasodilators ( Hydralazine, minoxidil ) fluid
retention, headache.
Spironolactone gynecomastia, impotence
Hydralazine drug induced lupus 9 anti histone +ve, anti
dsdna negative)

Before searching for causes of secondary hypertension
which involves expensive testing, more common issues
like appropriateness of the regimen, possible drug
interactions, associated conditions like alcohol or drug use,
poor adherence to treatment, white coat/office hypertension,
volume overload, obesity and sleep apnea should be
carefully evaluated and investigated!
After eliminating and reversal of these reversible
contributing factors, if the BP is still not controlled,
consider and rule out secondary HTN.
However, if there are any clues that point to secondary
HTN ( hypokalemia on labs, episodic HTN and
headaches, Abdominal bruit, rib notching on chest x-
ray, Radio-femoral delay on physical exam ), that
particular entity should be promptly investigated and
treated.
NSAIDS reduce vasodilatory prostaglandins and cause
afferent renal vasoconstriction and reduced renal blood
flow.
What NSAIDS can do to your patients?
Worsen Renal insufficiency ( vasomotor component or allergic
interstitial nephritis)
Cause Refractory Hypertension
Cause CHF exacerbation by causing fluid retention ( activates
Renin-angiotensin axis)
Increase the risk of cardiovascular events.
Can lead to NSAID induced gastritis or Peptic ulcer
Avoid NSAIDS in
Renal Insufficiency
Very Elderly due to risk of renal insufficiency
Acute Coronary Syndrome scenarios
Difficult to control Hypertension
Congestive Heart Failure
NSAIDs are common over the counter drugs.
People often self medicate with NSAIDs for
pain eg: osteoarthritis , low backache etc
Whenever a patient was previously stabilized
on a given antihypertensive regimen becomes
resistant to the therapy, first question to be
asked is if the patient started using NSAIDs.
NSAIDs interfere with actions of beta blockers,
thiazide diuretics, loop diuretics and ACEI.
Patients taking these drugs should be warned
against the use of NSAIDs.

Oral contraceptive pills can lead to worsening
of pre-existent Hypertension in some women.
OCPs can also cause new onset overt HTN in
women who were previously normotensive.
Malignant HTN can also occur in rare cases
after starting OCPills
Management :
Discontinue OC pills in the above scenarios.
Return to baseline blood pressure may take 2 to 12
months after cessation of therapy.
Do not start OC Pills in women greater than 35 years
and who also smoke since it can cause additive
cardiovascular risk.
Consider it as a cause of refractory
hypertension if there are clues such as obesity,
neck circumference > 17 cm, snoring at night
and excessive day time sleepiness.
Get a Sleep study ( Polysomnogram)
Weight reduction strategies and address
secondary causes of obesity ( hypothyroidism)
If diagnosis confirmed, treat with CPAP at
nights ( CPAP has improved BP in some
studies in patients with OSA)
When to evaluate?
Causes
Work up
Treatment
Under age 16 or new onset diastolic Hypertension
(>100 mm hg) above age 55 .
Under age 30 - if resistant to two or more drugs or if
does not have any risk factors like morbod obesity or
family history of essential HTN.
Any time when there is a clue on the physical exam (
cushingoid facies, central obesity, delayed femoral
pulses, low blood pressure in lower extremities ) or lab
values ( unexplained hypokalemia) that may suggest
secondary cause.
Refractory hypertension after the contributory causes
have been ruled out or treated.
Hospitalization for Hypertensive Crises ( although
most common cause for crises is medication non
compliance)



Delayed femoral pulses or low BP in lower
extremities or hypertension in upper extremities
Coarctation of aorta
Abdominal bruit Renal artery stenosis
Cushingoid facies, central obesity, ecchymoses,
striae cushing syndrome
Triad of pounding headache, palpitations and
sweating associated with elevated BP or
paroxysmal elevations of BP in a patient with
otherwise stable HTN Pheochromocytoma
Neck circumference > 17cm, smoring at nights,
excessive day time sleepiness Obstructive sleep
apnea

PAC/ PRA ratio r/o primary hyperaldosteronism (
ratio > 20 is suggestive, greater than 60 more specific).
Confirm with 24 hr urinary aldosterone
Plasma metanephrines or 24 hr urinary metanephrines
r/o pheochromocytoma ( 24 hr urinary is more
specific as well as very sensitive)
Dexamethasone suppression test ( Start with low dose
Dexa - give 1mg Dexa and check early morning
cortisol should be less than 2.5 mcg%) r/o cushings
syndrome.
Renal Artery MRA ( r/o renal artery stenosis)
Coarctation of aorta : CXR and then, MRA/ Echo
TSH r/o hyperthyroidism
Calcium r/o hypercalcemia ( hyperparathyroidism)


Clinical clues for diagnosing Renovascular HTN:
History and clinical findings ( abdominal bruit)
Sudden onset of HTN above age 55
Sudden resistant HTN in previously well controlled BP.
Worsening renal function after starting ACEI or ARB
( define ACEI induced ARF)
Malignant HTN ( Hypertensive emergency i.e. with target organ
dysfunction)
Recurrent flash pulmonary edema
Low K on lab values ( remember renovascular HTN leads to secondary
Hyperaldosteronism)
Causes: Atherosclerosis of Renal artery in the elderly,
fibromuscular hyperplasia in the Young
Diagnosis : Renal MRA ( MRA is the preferred screening test
now for patients with atherosclerotic renovascular disease.
Renal Doppler ultrasound was the first screening test earlier but
where available, MRA is better since Doppler requires techinical
expertise and requires longer time to perform )
Therapy : Medical ( use diuretic, add spironolactone, consider
alpha blockers, consider minoxidil or hydralazine), Rx
Percutaneous transluminal angioplasty with or with out stent
Vasculopathy involving medium and large arteries.
Renal arteries are most commonly involved and the
second most affected arteries are the carotids.
Seen commonly in Young and middle aged women.
Most often it is asymptomatic but can lead to
Refractory hypertension.
Diagnostic tests involve ultrasound, MRA and
angiography. Ultrasound may have a low sensitivity in
asymptomatic patients. MRA is the preferred test of
choice. Angiogram is the gold standard and should be
used when treatment is considered.
Therapy :
Asymptomatic patients Observe
Refractory Hypertension Angiogram and Percutaneous
transluminal angioplasty of the renal artery. Stenting may be
needed in complicated cases.
Other causes and work up for secondary
Hypertension please refer Endocrinology
section
Resistant Hypertension : after addressing the issues discussed in
previous slides, add following agents in refractory HTN for better
control :
Nifedepine ( Procardia XL)
Minoxidil
Hydralazine
Add Spironolactone
Hypertensive Urgencies
Captopril is preferred choice ( short acting and can be titrated )
Labetalol
Fenoldapam ( preferred in patients with severe asthma/ copd where beta blocker is
contraindicated)

Hypertensive Emergencies ( associated with target organ
dysfunction CHF, Flash pulmonary edema, Papilledema,
Blindness, Encephalopathy, Acute Renal Failure)
Put an Arterial line for monitoring MAP adequately
Sodium Nitroprusside
Labetalol drip
Nitroglycerin drip if patient has concomitant CHF ( reduces preload ) .

NSAID related
OSA related/ identifying and treating
OCP related/ worsening HTN after starting
OCP
Choosing initial therapy in HTN
Treating HTN urgency and Emergency
Fenoldapam use

END!