ACUTE CORONARY
SYNDROMES:
Acute MI and Unstable Angina
Tintinalli Chapter 50
September 20, 2005
Acute Coronary Syndrome
(ACS)
Ischemic heart disease accounts for
500,000 deaths annually in the U.S.
CAD and myocardial ischemia contribute
to > 5 million ER visits yearly for chest
pain
15% of pts with chest pain will have
acute MI and 25-30% will have unstable
angina
ACS
a term used to describe pts with acute CP
and other symptoms of myocardial
ischemia
During the initial exam, often not possible to
determine whether permanent damage to
the myocardium has occurred
– Only in retrospect after serial ECGs or cardiac
markers can the distinction b/w AMI or UA be
made
Pathophysiology
ACS is caused by secondary reduction
in myocardial blood flow due to
– coronary arterial spasm
– disruption of atherosclerotic plaques
– platelet aggregation or thrombus formation
at site of atherosclerotic lesion
Thrombus formation
Atherosclerotic plaque formation occurs
through repetitive injury to vessel wall
When plaque ruptures, potent
thrombogenic substances are exposed to
platelets
These platelets respond by adhesion,
activation, and aggregation thus initiating
thrombus formation in the coronary vessels
The extent of O2 deprivation and thus
clinical presentation of ACS depend on
the limitation of O2 delivery by thrombus
adhering to fixed, fissured, or eroded
plaques
Stable Angina
Ischemia occurs only when activity
induces O2 demands beyond the supply
restrictions imposed by a partially
occluded coronary vessel
occurs at a relatively fixed and predictable
point and changes slowly over time
atherosclerotic plaque has not ruptured
thus there is little superimposed thrombus
ACS
Atherosclerotic plaque rupture and
platelet-rich thrombus develop
Degree and duration of O2 supply-
demand mismatch determines whether
reversible myocardial ischemia w/o
necrosis (unstable angina) or
myocardial ischemia w/ necrosis
(myocardial infarction)
Clinical Features
Main symptom of ischemic heart
disease is chest pain
– need to characterize its severity, location,
radiation, duration, and quality
– ask about associated symptoms: N/V,
diaphoresis, dyspnea, lightheadedness,
syncope, palpitations
Reproducible chest wall tenderness is
not uncommon
Patients with ACS may complain of easy
fatigability
Usually an AMI is accompanied by more
prolonged and severe chest discomfort
and more prominent associated
symptoms
Angina Pectoris
Exercise, stress, or cold environment
classically precipitates angina
duration of symptoms typically < 10
minutes, occasionally lasting up to 20
minutes
usually improves within 2-5 minutes
after rest or nitroglycerin
ACS
Up to 30% of patients with AMI are
clinically unrecognized
– Some of these patients have had atypical
symptoms for which they didn’t pursue
medical advice
– Worse prognosis for pts who have atypical
symptoms at the time of their infarction
– women and elderly most likely to have
atypical symptoms
Cardiac Risk Factors
Age over 40 High cholesterol
male truncal obesity
postmenopausal sedentary lifestyle
females diabetes
family history previous cardiac hx
cigarette smoking
hypertension
Cardiac Risk Factors
Risk factors are modestly predictive of
CAD is asymptomatic patients
In the ER, risk factors are poor predictors
of cardiac risk for MI or other ACS
– In males, only DM and family history are
weakly predictive
– Cardiac risk factors are not predictive of ACS
in female ER chest pain pts
Physical Examination
Not helpful in distinguishing pts with
ACS from those with non cardiac
etiologies
Pts may appear deceptively will without
distress or be uncomfortable, pale,
cyanotic, and in respiratory distress.
Vital Signs
Bradycardic rhythms are more common
with inferior wall MI
– in the setting of anterior wall MI,
bradycardia or heart block is very poor
prognostic sign
Extremes of blood pressures are
associated with worse prognosis
Heart Sounds
S1 and S2 are often diminished due to poor
myocardial contractility
S3 is present in 15-20% of pts with AMI
– implies a failing myocardium
S4 is common in pts with long standing HTN or
myocardial dysfunction
Presence of new systolic murmur is an ominous sign
– signifies papillary m. dysfunction, flail leaflet of mitral
valve, or VSD
ECG
12 lead is single best test to identify pts
with AMI upon presentation to ER
Current guidelines state that the initial 12
lead ECG must be obtained and
interpreted within 10 minutes of patient
presentation
Yet ECG has a relatively low sensitivity
for detection of AMI
ECG
ST segment is elevated on the initial
ECG in approximately 50% of pts with
AMI
– most other AMI pts will have ST depression
and/or T wave inversions
Only 1-5% of pts with AMI have an
entirely normal initial ECG
ECG criteria and AMI
Anteroseptal --> QS deflections in V1-
V3, possibly V4
Anterior -->
rS defection in V1, Q
waves V2-4 or decr
in amplitude of initial
R wave in V1-V4
anterolateral --> Q waves in V4-6, I,
aVL
ECG Criteria and AMI
Lateral --> Q waves in I, aVL
inferior --> Q waves II, III, aVF
inferolateral --> Q waves II, III, aVF,
and V5-V6
true posterior -->
Initial R waves in V1-
V2 >0,04s and R/S
ratio > 1
Q waves II, III, aVF &
right ventricular --> ST elevation rV4
ECG
In distributions previously described:
– ST elevation suggests acute transmural injury
– ST depression suggests subendocardial
ischemia
All inferior wall MI should have right sided
ECG
– ST elevation in rV4 indicates right ventricular
infarction
ECG
Reciprocal ST segment changes
predict:
– a larger infarct distribution
– an increased severity of underlying CAD
– more severe pump failure
– a higher likelihood of cardiovascular
complications
– increased mortality
Difficult ECG interpretations
ST elevation in absence of AMI
– early repolarization
– LVH
– pericarditis/myocarditis
– Left ventricular aneurysm
– Hypertropic cardiomyopathy
– hypothermia
– ventricular paced rhythms
– LBBB
Difficult ECG interpretations
ST depression in absence of ischemia
– hypokalemia
– digoxin effect
– cor pulmonale and right heart strain
– early repolarization
– LVH
– ventricular paced rhythms
– LBBB
Difficult ECG interpretations
T wave inversions without ischemia
– persistent juvenile pattern
– seizures or Stokes Adams syncope
– post-tachycardia T wave inversion
– post-pacemaker T wave inversion
– Intracranial pathology (CNS hemorrhage)
– Mitral valve prolapse
– pericarditis
– primary or secondary myocardial disease
T wave inversion without ischemia
– PE or cor pulmonale
– spontaneous PTX
– myocardial contusion
– LVH
– ventricular paced rhythms
– RBBB
– LBBB
AMI and LBBB
In the setting of LBBB, the following are
indicative of AMI
– 1. ST elevation 1mm or greater and
concordant with the QRS complex
– 2. ST depression 1mm or more in leads
V1, V2, or V3
– 3. ST elevation 5mm or greater and
discordant with the QRS complex
Cardiac Enzymes
Serial measurements are more
sensitive and accurate than initial single
measurement
serum markers have less utility in the
diagnosis of UA, only about 50% will
have elevated troponins
CK-MB
Most commonly used marker in ACS
a serial rise to above 5 times baseline followed
by fall back to baseline is considered diagnostic
for AMI
peaks at 12-24 hours, with fall back to baseline
in 2-3 days
useful in detecting recurrent infarction after the
initial 24-48 hours by noting a repeat elevation
in the level
Conditions Associated
with Elevated CK-MB
Unstable angina Cardiac surgery
acute coronary ischemia skeletal m. trauma
inflammatory heart dermatomyositis,
disease polymyositis
cardiomyopathies
myopathic disorders
circulatory failure &
muscular dystrophy
shock vigorous exercise
DTs malignant hyperthermia
Rhabdomyolysis
Ethanol poisoning
(chronic)
Troponin
Main regulatory protein for the actin-myosin
myofibrils
3 subunits:
– inhibitory subunit (Trop I)
– tropomyosin binding subunit (Trop T)
– calcium binding subunit (Trop C)
Trop I has not been identified in skeletal m.
during any stage of develop therefore specific to
myocardium
Troponin
Peak level in 12 hours
prolonged elevation for 7 to 10 days before
returning to baseline
– thus making trop of no use in detecting recurrent
infarctions during this time
Rise in serum Trop I or T is considered diagnostic
for AMI
Low level elevations in Trop correlate with risk for
CV complications in UA, CAD, and renal failure
Myoglobin
Rises within 2-3 hours of symptoms
onset
peaks within 4 to 24 hours
more sensitive than CK and CK-MB but
not specific for cardiac muscle
there is a high false-positive rate due to
its presence in all muscle tissue
Complications of MI
1. Dysrhythmias and conduction
disturbances
2. Cardiac failure
3. Mechanical complications
4. Pericarditis
5. Right Ventricular Infarction
6. Other
Dysrhythmias
Occurs in 72-100% of AMI pts treated in
coronary care unit
PVCs are common in AMI
– occur in >90% of AMI patients
Atrial premature contractions are also
common
– occur in up to 50% of AMI patients
– not associated with increased mortality
Dysrhythmias
Early in AMI, pts often show increased
autonomic nervous system activity
– sinus brady, AV block, hypotension occur
from increased vagal tone
Later, increased sympathetic activity results
in incr catecholamine release
– thus creates electrical instability: PVCs, Vtach,
Vfib, accelerated idioventricular rhythms, AV
junctional tachycardia
Dysrhythmias
Hemodynamic consequences of
dysrhythmias are dependent on
ventricular function
– Normal hearts have a loss of 10-20% of left
ventricular output when atrial kick is
eliminated
– Reduced left ventricular compliance can
result in 35% reduction in stroke volume when
the atrial systole is eliminated
Dysrhythmias
Persistant tachycardia is associated with
poor prognosis
– due increase myocardial oxygen use
When Vtach occurs late in AMI course,
usually associated with transmural
infarct and left ventricular dysfunction
– induces hemodynamic deterioration
– mortality rate approaches 50%
Conduction Disturbances
First degree and Mobitz I (Wenckebach)
– more common with inferior AMI
– intermittent during the first 72 hrs after infarction
– rarely progresses to complete block or
pathologic rhythm
Mobitz II
– usually associated with anterior AMI
– does progress to complete heart block
Conduction Disturbances
Complete Heart Block
– occurs in setting of inferior MI
– usually progresses from less AV blocks
– this form is usually stable & should resolve
– Mortality is 15% in absence of RV involvement
& increases to 30% when RV is affected
Complete block in setting of anterior MI
results in grave prognosis
Conduction Disturbance
New RBBB
– occurs in approximately 2% of AMI pts
– associated with anteroseptal AMI
– associated with increased mortality
because often leads to complete AV block
Conduction Disturbance
New LBBB
– occurs in 5% of pts with AMI
– associated with high mortality
– Left posterior hemiblock associated with
higher mortality than isolated anterior
hemiblock
• represents larger area of infarction
Cardiac Failure
15-20% of AMI pts present in some
degree of CHF
More severe the degree of left ventricular
dysfunction, the higher the mortality
– dependent on the net effect of prior
myocardial dysfunction, baseline myocardial
hypertrophy, acute myocardial necrosis, &
acute reversible dysfunction (“stunned
myocardium”)
Cardiac Failure
B-type natriuretic peptide
– useful for risk stratification of pts with non
ST elevation MI and UA
– elevated levels of BNP early in the hospital
course predict a worse outcome at 30 days
Mechanical Complications
of AMI
Sudden decompensation of previously
stable AMI pt should raise concern of the
“mechanical” complication
Free wall rupture
– occurs in 10% of AMI fatalities, usually 1 to 5
days after infarction
– rupture of LV free wall usually leads to
pericardial tamponade and death (>90% of
cases)
Mechanical Complications
of AMI
NSAIDs, steroids, and late
administration of thrombolytics have
been linked to an increased likelihood of
cardiac rupture
– however, studies remain contradictory
LV hypertrophy appears to be protective
Mechanical Complications
of AMI
Rupture of interventricular septum
– is more often detected clinically than
ventricular wall rupture
– pts have chest pain, dyspnea, sudden
appearance of new holosystolic murmur
• murmur often associated with palpable thrill and
best heard at lower left sternal border
– more common in pts with anterior wall MI
and pts with extensive (3 vessel) CAD
Mechanical Complications
of AMI
Papillary Muscle Rupture
– occurs in 1% of pts with AMI
– more common with inferior wall MI
– usually occurs 3 to 5 days after AMI
– occurs with a small to modest sized MI
– posteromedial m. commonly ruptured
• receives blood from only one coronary a.
– present with acute dyspnea, increasing CHF, and new
holosystolic murmur consistent with mitral
regurgitation
Pericarditis
Occurs in 10-20% of post-AMI pts
more common with transmural MI
usually occurs 2-4 days after AMI
Pericardial friction rubs detected more
often with inferior wall and right ventricular
infarcts
Pericardial effusions may also be present;
may take months to resorb
Dressler Syndrome
– post AMI syndrome
– occurs 2 to 10 weeks after AMI
– pts presents with chest pain, fever, and
pleuropericarditis
Right Ventricular Infarction
Usually seen as a complication of an
inferior infarction
– approximately 30% of inferior wall MI
involve the RV
Presence of RV infarction is associated
with significant increase in mortality and
cardiovascular complications
Other Complications
Left ventricular thrombus formation
arterial embolization
venous thrombus
pulmonary embolism
postinfarction angina
infarct extension
– **these are diagnoses to think about when a pt
presents to the ER after recent discharge from the
hospital
Postprocedure Chest Pain
Pts who present with symptoms of ACS
shortly after angioplasty or stent placement
should be assumed to have abrupt vessel
closure
Subacute thrombotic occlusion after stent
placement occurs in approximately 4% of
pts 2 to 14 days after procedure
– this less common than closure after angioplasty
Pts with chest pain syndromes after
CABG
– may have abrupt vessel closure
– symptoms of recurrent ischemia can be
confused with post-AMI pericarditis
Disposition
All patients with acute chest pain need
to be evaluated for the possibility of
ACS
– pts are admitted to appropriate level of
care depending on their risks
Results of prior cardiac catheterization
are very useful for risk stratification
Cardiac Cath Results
– pts with previously documented minimal stenosis
(<25%) or normal coronary arteriograms have
excellent long-term prognosis
• more than 90% of these pts are free from MI 10
yrs later
– a recent cardiac cath (within last 2 yrs) with
normal or minimally diseased vessels almost
eliminates the possibility of ACS due to
atherosclerosis
• doesn’t eliminate vasospasm or small vessel dz
Stress Tests Results
When pts complete all stages of the
stess protocol, have no ECG changes
and normal imaging studies, exercise
testing can r/o acute ischemic
syndromes with sensitivities b/w 80-
90%
If all criteria are not met, stress test
have poor sensitivity
QUESTIONS?
1. Which of the following is false about
new RBBB?
– a. Occurs in 2% of AMI pts
– b. Occurs most commonly with inferior
wall MI
– c. Often leads to complete AV block
– d. Associated with increased mortality
QUESTIONS?
2. True or False: Inferior wall MI can
result from occlusion of left circumflex a.
or RCA
3. True or False: Left ventricular free
wall rupture occurs in 10% of AMI
fatalities usually 3-4 weeks after initial
infarct
QUESTIONS?
4. True or False: B type natriuretic
peptide has a high specificity in
diagnosing CHF
5. True or False: Reproducible chest
wall pain rules out ACS.
Answers: B, true, false, false, false
References
Tintinalli, J. “Emergency Medicine: A
Comprehensive Study Guide.” 6th edition.
pg. 343-351.
Ma, O.J. and David Cline. “Emergency
Medicine: Just the facts.” 2nd edition. pg.
91-97.
Rivers, C. “Preparing for the Written Board
Exam in Emergency Medicine.” 4th edition.
pg. 60-76.
