Emergency Cardiology

Tongwen Sun
First Affiliated Hospital of Zhengzh
ou University
 Catalog
• Acute myocardial infarction (AMI)
• Heart Failure
• Pulmonary Embolism
• Acute aortic dissection
Nornal Artery of the Heart
A true case
 ECG exam

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6
Inferior MI ,RCA occlusion
Risk factors

Hyperlipemia

Obesity

Hypertension

Smoking etc
Basic Mechanism
 CHD Classification

WHO
• Primary heart sudden stop
• Angina pectoris
• Myocardial Infarction
• Heart Failure of CHD
• Arrhythmia
 Symptom

Presymptoms
• Initial onset angina
• Accelerated angina
• Nausea 、 Vomit 、 Bradycardi
a
• Heart failure 、 Arrhythmia
•
 Symptom

• Acute chest pain 》 30min

dull or sharp burning pain
chest distress
• (gastro-intestinal)GI symptom naus
ea,vomit
• Slight fever
• Arrhythmia
• Hypotension ,Shock ,Heart Failur
e
 Sign

• S1 decreased ， S4
• Pericardial friction rub
• Systolic murmur
• Arrhythmia
ECG evolution
 localization
• Anterior infarction: V3,V4
• Anterolateral infarction: V3-V6,avl,I
• Extensive anterior infarction: I,avl V1-V
6
• Inferior infarction ： II,III,AVF
• Posterior infarction ： V7-V9 ,
reciprocal change in leads V1,V2
• Anterior Septal infarction:V1,V2
 Acute inferior & posterior
infarction

RCA occlusion
Acute anterior septal infarcti
on
LAD
occlusion
Left main occlusion
LCX occlusion
Enzyme changes
 Enzyme changes
Time to
Time to Time to
return to
Initial peak
normal
elevation elevation
range
cTnI 3~12 24hr 5~10d
cTnT 3~12 12hr~2d 3~14d
CK <6H 24h 3~4d
CK-MB 4~6h 16~24h 3~4d
AST 6~12h 24~48h 3~6d
LDH 8~10h 2~3d 1~2w
 Diagnosis
• Typical symptom –chest pain
(position ,duration,feature, relieving
mode)
• Evolution of ECG
• Enzyme changes
• Exclude other diseases
 Differential diagnosis
• Variant Angina pectoris —— transitory ST-T chang
e，
no Q wave , enzyme normal
• Pericarditis —— ST elevation , no Q wave
• Pulmonary Infarction——SⅠQⅢTⅢ ， lung isotope s
can
• Acute abdomen
• Dissection of aorta —— sharp pain ， MRI
 Complication
• Dysfunction or rupture of papill
ary muscle
• Rupture of the heart
• Embolism
• Cardiac aneurysm
• Postinfarction syndrome
rupture of papillary muscle
Emergency therapy

Thrombolysis
Aspirin
Nitrate
β- blocker
 Thrombolytic therepy
Urokinase (UK)——1.0 ～ 1.5 million unit （ 30min ）

Streptokinase (SK)—— 1.5 million unit （ 60min ）

Recombinant tissue plasminogen activator (rt-PA)

Indication for thrombolysis
• Chest pain >30 min ， can’t relieve
by nitroglycerin
• Elevated ST >0.2mv
• Duration < 6h
• Duration >6h ， serious chest pain
,
elevated ST
• Age < 65yr ～ 70yr
 Contraindication
• Recent surgery or hemorrhage
• History of cerebrovascular accident
• Hemorrhage disease
• BP>180mmHg
• Shock , refractory to medicine
 Evaluation of reperfusion
• Indirect index
chest pain relieved in 2h
ST segment declined in 2h >50%
the peak of enzyme advanced （ CK-
MB 《 14h ）
arrhythmia of reperfusion （ PVB,VT)
• Direct index
coronary atery angiography
Intervention therapy

Access
Sketch map
 Left coronary
artery

Right coronary
artery
 Screen

Catheter Injector
Coronary artery angiography

Contrast injection
Intervention therapy

Ballon
Inflation/deflation
 Intervention therapy

After therapy Before therapy

CABG
 CABG
(Coronary artery bypass graft)

Bypass

Bypass

Bypass
Heart Failure
 Objectives
Understand the cornerstones of therapy
• angiotensin-converting enzyme inhibito
rs, diuretics, and digitalis
• review the role of other therapies: phar
macotherapeutic as well as nonpharma
cotherapeutic approaches
 Definition
• HF is the inability of the heart to adeq
uately perfuse metabolizing tissues.
The most common cause of this is my
ocardial failure ,which can be caused
a wide variety of disease states.It ma
y affect the left and right ventricles ind
ividually or both together .
 Epidemiology

• 4.7 million patients in the United States

are estimated to have heart failure
• 470,000 new cases recognized annually
• Each year, 875,000 hospitalized
patients have a primary diagnosis of
heart failure. It is the major hospital
discharge diagnosis for patients in the
Medicare age group.
 Epidemiology
• heart failure increases with age
• half of all heart failure hospitalizations
occur in individuals > age 65 years.
• In the United States, the estimated cost
s for the management of patients with h
eart failure exceed $10 billion annually.
 Treatment objectives
• Decrease symptoms
• Improve exercise capacity
• Enhance quality of life
• Decrease morbidity
• Retard the progression of heart failure
• Improve survival
 Cornerstones of Therapy
• Angiotensin converting enzyme (ACE) i
nhibitors
• diuretics
• digitalis
• guidelines for the severity-based therap
y of heart failure.
 Asymptomatic Patients
For asymptomatic patients with left ven
tricular dysfunction (NYHA class I), typi
cally those with an ejection fraction bel
ow 40%,

ACE inhibitors are recommended

 Symptomatic Patients
• NYHA class II
– ACE inhibitors, mild diuretics, and digoxin,
with or without the use of B-blocker therapy
• NYHA class III
– add loop diuretics
• NYHA class IV
– consider positive inotropic agents
– surgical therapies may also be applied
A, B, C, D, Es of Heart Failure Therapy

A angiotensin converting enzyme inhibitors

anticoagulants, amiodarone, AICD, assist
devices
B beta blocking drugs
C calcium channel blocking drugs, coronary
revascularization, cardiac transplant,
cardiomyoplasty, cardiac reduction surgery
D diet, diuretics, digitalis, dobutamine
E exercise
Angiotensin Converting Inhibitors p
hysiologic benefits
Arteriovenous Vasodilatation
  pulmonary arterial diastolic pressure
  pulmonary capillary wedge pressure
  left ventricular end-diastolic pressure
  systemic vascular resistance
  systemic blood pressure
  maximal oxygen uptake (MVO2)
 Angiotensin Converting Inhibitors
physiologic benefits
  LV function and cardiac output
  renal, coronary, cerebral blood flow

• No change in heart rate or myocardial contra

ctility
• no neurohormonal activation
• resultant diuresis and natriuresis
 Angiotensin Converting Inhibitors
clinical benefits
• Increases exercise capacity
• improves functional class
• attenuation of LV remodeling post MI
• decrease in the progression of chronic HF
• decreased hospitalization
• enhanced quality of life
• improved survival
 Asymptomatic Patients
Enalopril
SOLVD Prevention Trial
EF<35%
 HF progression,  hospitalization
Captopril
SAVE, GISSI-3, ISIS-4
Post MI, EF <40%
 overall mortality,  re-infarction
 hospitalization,  HF progression
 Symptomatic Patients
Hydralazine + Isosorbide dinitrate

VHeFT-I
 mortality, improved functional class
as compared with use of digoxin and diuretics
VHeFT-II
proved less effective than enalopril
 Symptomatic Patients
Enalopril + digoxin + diuretics

SOLVD Treatment Trial

EF<35%, FC III-IV
 mortality,  hospitalization
CONSENSUS-II
FC IV
 mortality (40%),  symptoms,  hospitalization
improved functional class
 Symptomatic Patients
Losartan (AT-II inhibitor)

ELITE Trial

losartan improved the survival of elderly heart failure

patients treated compared with captopril therapy
Guidelines to ACE Inhibitor Therapy

• Contraindications
– Renal artery stenosis
– Renal insufficiency (relative)
– Hyperkalemia
– Arterial hypotension
– Cough
– Angioedema
• Alternatives
– Hydralazine + ISDN, AT-II inhibitor
Guidelines to ACE Inhibitor Therapy

• It is important to titrate to the dosage regi

men used in the clinical trials … in the abs
ence of symptoms or adverse effects on e
nd-organ perfusion
• in very severe heart failure, hydralazine an
d nitrates added to ACE inhibitor therapy c
an further improve cardiac output
 Anticoagulant Therapy

• Recommended for
– patients with NYHA III-IV and EF <30% or ventri
cular aneurysm or very dilated LV
• Indicated for
– patients with heart failure who have atrial fibrill
ation, a prior embolic episode, identified intrac
ardiac thrombus, left ventricular aneurysm, thr
ombophlebitis, or prolonged bed rest
– titrate INR to 2 to 3
 Arrhythmias

Sudden death occurs in about

50% of patients with heart failure
 Amiodarone

• Randomized clinical trials

– CHF-STAT
NYHA II-III patients with ischemic cardio
myopathy - amiodarone had no affect on
survival
– GESICA
NYHA III-IV patients with more non-ische
mic cardiomyopathy - open labeled amio
darone decreased mortality
 AICD

• Randomized clinical trials

– AVID
amiodarone vs implantable defibrillator
showed the AICD group had lower mortality
• AICD should be considered for patients with
ventricular fibrillation or prior sudden death
• Beta-blockers or amiodarone may be approp
riate for patients with sustained VT, with or
without symptoms
 Assist Devices

• a bridge to cardiac transplantation

• candidates must meet the inclusion and
exclusion criteria for cardiac
transplantation
 -blocking Drugs
• Physiologic benefits
– increase the density of -1 receptors
– inhibit catecholamine toxicity
– decrease neurohormonal activation
– decrease heart rate
– provide antihypertensive, antianginal, and
antiarrhythmic effects
– antioxidant and antiproliferative effects
 -blocking Drugs
• Clinical benefits
– decrease symptoms of HF
– improve left ventricular function
– improve exercise tolerance
 -blocking Drugs - Clinical Trials

• BHAT ( -Blocker Heart Attack Trial)

– propranolol decreased cardiovascular mor
tality, sudden death, and reinfarction in po
st-MI patients
– benefit is greatest in patients who also had
left ventricular dysfunction
 -blocking Drugs - Clinical Trials

• SAVE (Survival and Ventricular Enlarge

ment)
– post-MI patients with an EF <40%
 - blockers reduced mortality both in the A
CE inhibitor and the placebo group
– lowest mortality occurred in patients recei
ving both ACE and -blocking therapy
 -blocking Drugs - Clinical Trials

• MDC (Metoprolol in Dilated Cardiomyop

athy)
– NYHA II-III with dilated cardiomyopathy
– no decrease in mortality
– significant decrease in symptoms
– significant increase in exercise tolerance,
LV ejection fraction, quality of life
 -blocking Drugs - Clinical Trials

• MOCHA (Multicenter Oral Carvedilol He

art Failure Assessment Trial)
– NYHA II-III heart failure
– quadruple therapy (+ACE, diuretic, digoxi
n)
– 49% decrease in the combined endpoints o
f mortality and hospitalization
– no improvements in exercise tolerance
 -blocking Drugs - Clinical Trials

• PRECISE
(Prospective Randomized Evaluation of
Carvedilol on Symptoms and Exercise)
– decrease in mortality from 8% to 3%
– 40% decrease in hospitalization
– decrease in symptoms
– improvement in LV ejection fraction
– no affect on exercise tolerance
 Calcium Channel Blocking Drugs

• Potential benefit:
– anti-ischemic and vasodilatory effects
• Adverse effect:
– negative inotropic properties
• MDPIT / SPRINT trials
– diltiazem, verapamil, and nifedipine are not
recommended for patients with HF
 Calcium Channel Blocking Drugs

• PRAISE-1 (Prospective Randomized Am

lodipine Survival Evaluation)
– NYHA III-IV heart failure
– ACE, digoxin, diuretics ± amlodipine
– no change in total mortality
no survival benefit in ischemics
improved survival in non-ischemics
– no change in exercise tolerance
 Coronary Revascularization
• 80% of patients with heart failure have coron
ary disease
• Patients should be evaluated for the presenc
e of myocardial ischemia and the potential b
enefit of revacularization
• Survival was improved by revascularization c
ompared with medical therapy, even in the ab
sence of angina pectoris (Duke database)
 Cardiac Transplantation
• Survival of 60%-90% at 1-yr, 70% at 5-yr
• Inclusion Criteria:
– must first exclude remediable myocardial ischemia
– heart failure refractory to optimal medical Rx
– left ventricular ejection fraction <20%
– VO2 max  14 mL/kg/min
• Problems:
– rejection, graft atherosclerosis, neoplasia, cost/av
ailability
 Cardiomyoplasty
Cardiac Reduction Surgery

• currently considered experimental

 Diet
• Traditional approach non-pharmacologic
management is sodium and water restricti
on
• Sodium excess is the main reason for hear
t failure exacerbation
• Restrict sodium to 2 to 3 grams / day
 Diuretics
  sodium and water retention
  symptoms of volume overload
• thiazide diuretics are not active with GFR
<30 mL/min
• in resistant edema, loop diuretics, K+-spari
ng diuretics, and metolazone are indicated
 Digitalis
• Beneficial hemodynamic effects
  cardiac output
  left ventricular ejection fraction
  left ventricular diastolic pressure
  exercise tolerance
  natriuresis
  neurohormonal activation
 Digitalis - Clinical Trials
• DIG (Digitalis Investigation Group)
– NYHA class I-IV heart failure
– no change in mortality compared with
placebo therapy
  combined endpoint of hospitalizations
and death
  serious arrhythmia and MI
 Digitalis - Clinical Trials
• RADIANCE (Randomized Assessment of th
e effect of Digoxin on Inhibitors of ACE)
– ejection fraction <35%
– ACE, diuretics, digoxin
– associated with  exercise tolerance in pa
tients with normal sinus rhythm
– withdrawal of digoxin resulted in  exercis
e tolerance, and  in hospitalization
 Digitalis - Clinical Trials

• PROVED (Prospective Randomized Study

of Ventricular Function and Efficacy of Digo
xin)
– mild-to-moderate HF with EF <35%
– in NSR and not on ACE inhibitor therapy
– withdrawal of digoxin resulted in  exerci
se tolerance and  in hospitalization
 Dobutamine
• ß-1 receptor agonist
• low-dose dobutamine (2-3 ug/kg/min)
–  myocardial contractility and cardiac outp
ut, arteriovenous dilatation
• high-dose dobutamine (5-15 ug/kg/min)
– tachycardia, arrhythmia, splanchnic and ren
al vasoconstriction
– associated with symptomatic benefit
• continuous home pump infusion
 Exercise Training
AHCPR
Cardiac Rehabilitation Guidelines
Exercise training in patients with HF
– decrease symptoms
– improves exercise tolerance
– benefit additive to that attained with ACEI
– no worsening of left ventricular function
 Exercise Training
Clinical Trials on exercise following MI
• EAMI (Exercise and Anterior MI)
• ELVD (Exercise in LV Dysfunction)
• both interventional groups showed improvement
in functional capacity and decrease in symptoms
• ELVD also showed an improvement in ejection fr
action
 Conclusion
Effects of Heart Failure Therapies
• Improve in survival
– ACE inhibitors
– ß-blocking drugs (selective)
• Increased mortality
– positive inotropic agents
– calcium channel blocking drugs (?)
• Neutral on survival
– digitalis
 Conclusion
Effects of Heart Failure Therapies
• Prevention of ischemia
– ß-blocking drugs (selective)
– coronary revascularization
– anticoagulant therapy
• Hemodynamic improvement
– ACEI, digitalis, diuretics, hydralazine/ISDN
• Prevention of sudden death
– amiodarone and AICD
 Causes of HF exacerbation
noncompliance with salt restriction 22%
infectious pulmonary process 20%
use of antiarrhythnic medication (48hr) 15%
use of metoprolol 15%
arrhythmia
calcium channel blockers
inappropriate reduction in therapy

Arch Int Med 2001;161:2337-2342

5/02 medslides.com 101
 Acute left ventricular failure
• Acute left ventricular failure(LVF) is a very
common condition and is also a medical e
mergency . It is therefore important that yo
u know all the management steps includin
g druges and dose
 Management of Acute LVF
• Sit the patient up
• Administer 100%oxygen via a facial mask
• Estabilish periperal intravenous access and adm
inister:
• IV diamorphine 2.5-5mg
• IV frusemide 80-100mg
• Intravenous nitrates
• strophantin K 0.2mg +NS 20ml IV > 15min
• Intravenous amminophylline
 Acute right ventricular failure
• Patients who have an inferior or posterior
MI may present with predominantly RVF. T
his is not commom , but it is important to r
ecoginse the signs and know how to treat
it. Basically it is often possible to imposive
function by increasing heart volume .
• You must aware that hypotension afte
r inferior MImay be secondary to the c
ombination of RVF and relative underf
illing of the RV . The treatmentof this i
s careful fluid challenge with CVP mo
nitoring.
 Difference
• Treatment of acute RVF can be oppo
site to that of acute LVF.Fluid adminis
tration may be needed in RVF. In LVF
the fluid needs to be removed.
Pulmonary Embolism
 Pulmonary Embolism
• Pulmonary embolism (PE) and deep veno
us thrombosis (DVT) afflict millions of indiv
iduals worldwide and account for several h
undred thousand deaths annually in the U
nited States. Few health care providers re
alize that the case fatality rate for PE, appr
oximately 15 percent, exceeds the mortalit
y rate for acute myocardial infarction.
Most Common Symptoms or Sig
ns of PE

• Symptoms
• Otherwise unexplained dyspnea,Chest pain, eith
er pleuritic or “atypical”
• Signs
• Tachypnea ,Tachycardia, Low-grade fever,Tricu
spid regurgitation murmur, Accentuated P2
• ECG :S1Q3T3
    
 
Clinical Decision Rule
• >4 score points = high probability
•  ≤4 score points = non–high probability
•  DVT symptoms or signs=3
• An alternative diagnosis is less likely than PE=3
• HR > 100/min=1.5
• Immobilization or surgery within 4 wk=1.5
• Prior DVT or PE1.5
• Hemoptysis=1
• Cancer treated within 6 mo or metastatic=1
 Diagnosis
• Diagnosis of PE is more difficult than treatment o
r prevention. The most useful approach is the cli
nical assessment of likelihood, based on present
ing symptoms and signs, in conjunction with diag
nostic testing. When PE is not highly suspected,
a normal plasma d-dimer usually suffices to rule
out this condition. When PE is highly suspected,
especially with an elevated d-dimer, chest CT sc
anning is the best imaging test. Of note is that ac
ute respiratory failure caused by other illnesses
such as asthma or pneumonia may mimic PE.
 Differential Diagnosis of PE
• Anxiety, pleurisy, costochondritis
• Pneumonia, bronchitis
• Myocardial infarction
• Pericarditis
• Congestive heart failure
• Idiopathic pulmonary
 Classification of Acute PE
• Massive PE:
• Systolic BP ≤ 90 mm Hg or poor tissue
perfusion or multisystem organ failure
• + left main pulmonary artery thrombus
or “high clot burden”
• Treatment :Thrombolys or IVC filter or
embolectomy + anticoagulation
 Submassive PE

Hemodynamically stable but moderate or s

evere right ventricular dysfunction or enlarg
ement
Addition of thrombolysis, embolectomy, or fi
lter remains controversial
 Small to moderate PE

• Normal hemodynamics and norm

al right ventricular size and functio
n
• Treatment: Anticoagulation
 ECG Signs of PE
• Sinus tachycardia
• Incomplete or complete RBBB
• Right axis deviation
• T wave inversions in leads III and aVF or i
n leads V1-V4
• S wave in lead I and a Q wave and T wave
inversion in lead III (S1Q3T3)
• QRS axis greater than 90 degrees or an in
determinate axis
• Atrial fibrillation or atrial flutter
 Management
• Low risk: Anticoagulation alone
• High risk : Thrombolys or embolectomy +
anticoagulation
• Drugs : Low-Molecular-Weight Heparins , Warf
arin
• Fibrinolysis :
• The FDA has approved alteplase for massive PE
. The dose is 100 mg as a continuous infusion o
ver 2 hours, without concomitant heparin.
Acute aortic dissection
 Acute aortic dissection
• Acute aortic dissection is an uncommon but pot
entially life-threatening illness that occurs with a
n incidence of approximately 2.9/100,000/yr wit
h at least 7000 cases per year in the United Sta
tes.Early mortality is as high as 1 percent per h
our if untreated, but survival may be improved s
ubstantially by the timely institution of appropria
te medical and/or surgical therapy. Prompt clini
cal recognition and definitive diagnostic testing
are essential in the management of patients
Commonly Used Classification of A
ortic Dissection
• DeBakey
• Type I: Originates in the ascending aorta, propa
gates at least to the aortic arch and often beyon
d it distally
• Type II: Originates in and is confined to the asce
nding aorta
• Type III: Originates in the descending aorta and
extends distally down the aorta or, rarely, retrogr
ade into the aortic arch and ascending aorta
• Stanford
• Type A: All dissections involving the a
scending aorta, regardless of the site
of origin
• Type B: All dissections not involving t
he ascending aorta
 Clinical Manifestations
• Symptoms: the most common initial sympt
om of acute aortic dissection is pain, which
is found in up to 96 percent of cases, where
as the large majority of those without pain a
re found to have chronic dissections. The p
ain is typically severe and of sudden onset a
nd is as severe at its inception as it ever bec
omes, in contrast to the pain of myocardial i
nfarction, which usually has a crescendo-lik
e onset and is not as intense
• Less common symptoms at initial evaluati
on, occurring with or without associated ch
est pain, include congestive heart failure
(7 percent), syncope (13 percent), cerebro
vascular accident (6 percent), ischemic pe
ripheral neuropathy, paraplegia, and cardi
ac arrest or sudden death.
Diagnosis
Dessection in the descending part
of aortic arch
descending aorta dissection
• aortic dissection is diagnosed by t
he presence of two distinct aortic l
umina, either visibly separated by
an intimal flap
 Therapy
• Therapy for aortic dissection aims to halt progression
of the dissecting hematoma because lethal complicati
ons arise not from the intimal tear itself but rather from
the subsequent course taken by the dissecting aorta, s
uch as vascular compromise or aortic rupture. Without
treatment, aortic dissection has a high mortality rate. I
n a collective review of long-term survival in patients w
ith untreated aortic dissection, more than 25 percent of
all patients died within the first 24 hours after the onset
of dissection, more than 50 percent died within the first
week, more than 75 percent died within 1 month, and
more than 90 percent died within 1 year
• Initial therapeutic goals include the elimination
of pain and reduction of systolic blood pressur
e to 100 to 120 mm Hg (mean of 60 to 75 mm
Hg) or the lowest level commensurate with ad
equate vital organ (cardiac, cerebral, renal) pe
rfusion. Beta-blocking agents should be admin
istered simultaneously, regardless of whether
pain or systolic hypertension is present. Pain,
which may itself exacerbate hypertension and
tachycardia, should be promptly treated with in
travenous morphine sulfate.
 For the acute reduction of arterial pressure,
the potent vasodilator sodium nitroprusside i
s effective. It is initially infused at 20 µg/min
with the dosage titrated upward, as high as
800 µg/min, according to the blood pressure
response. When used alone, however, sodi
um nitroprusside can actually cause an incr
ease in dP/dt, which in turn may potentially
contribute to propagation of the dissection.
Therefore, concomitant beta-blocking treat
ment is essential.
Management
 Question
• 1. What’s the definition of cardiac arrest?
• 2. What’s the cause of cardiac arrest?
• 3.How to recognise cardiac arrest?
• 4.Explain basic life support and advanced l
ife support
• 5.Give some drugs for CPR use
 Question
• 1. coronary artery consistes of
• 2.How to diagnose AMI?
• 3.Differential diagnosis of AMI
• 4. What’s the Indication and contraindication for t
hrombolysis in patients with AMI? How to judge t
he resultes thrombolysis?
• 5. What’s the complication of AMI ?
• 6. Explain the therapy methods for AMI.
• 7. Explain the risk factors of AMI?
 Question
• 1. What’s the definition of HF?
• 2.What’s A, B, C, D, Eof HF Therapy?
• 3.How to deal with acute LVF and acute RVF? What’s th
e difference?
• 4. What’s the symptoms or signs of PE?
• 5.Explain the classification and management of acute P
E.
• 6.Give the classification of aortic dissection and c
linical used therapy ways .