Transcript ACUTE CORONARY SYNDROMES: Acute MI and Unstable Angina

ACUTE CORONARY
SYNDROMES:
Acute MI and Unstable Angina
Tintinalli Chapter 50
September 20, 2005
Acute Coronary Syndrome
(ACS)
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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
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a term used to describe pts with acute
CP and other symptoms of myocardial
ischemia
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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
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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
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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
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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
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Ischemia occurs only when activity
induces O2 demands beyond the supply
restrictions imposed by a partially
occluded coronary vessel
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occurs at a relatively fixed and predictable
point and changes slowly over time
atherosclerotic plaque has not ruptured
thus there is little superimposed thrombus
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ACS
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Atherosclerotic plaque rupture and
platelet-rich thrombus develop
Degree and duration of O2 supplydemand mismatch determines whether
reversible myocardial ischemia w/o
necrosis (unstable angina) or
myocardial ischemia w/ necrosis
(myocardial infarction)
Clinical Features
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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
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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
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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
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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
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Age over 40
male
postmenopausal
females
family history
cigarette smoking
hypertension
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High cholesterol
truncal obesity
sedentary lifestyle
diabetes
previous cardiac hx
Cardiac Risk Factors
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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
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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
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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
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Extremes of blood pressures are
associated with worse prognosis
Heart Sounds
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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
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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
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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
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Only 1-5% of pts with AMI have an
entirely normal initial ECG
ECG criteria and AMI
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Anteroseptal -->
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Anterior -->
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anterolateral -->
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QS deflections in
V1-V3, possibly V4
rS defection in V1, Q
waves V2-4 or decr
in amplitude of initial
R wave in V1-V4
Q waves in V4-6, I,
aVL
ECG Criteria and AMI
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Lateral -->
inferior -->
inferolateral -->
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true posterior -->
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right ventricular -->
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Q waves in I, aVL
Q waves II, III, aVF
Q waves II, III, aVF,
and V5-V6
Initial R waves in
V1-V2 >0,04s and
R/S ratio > 1
Q waves II, III, aVF
& ST elevation rV4
ECG
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In distributions previously described:
– ST elevation suggests acute transmural
injury
– ST depression suggests subendocardial
ischemia
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All inferior wall MI should have right
sided ECG
– ST elevation in rV4 indicates right
ventricular infarction
ECG
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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
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ST elevation in absence of AMI
– early repolarization
– LVH
– pericarditis/myocarditis
– Left ventricular aneurysm
– Hypertropic cardiomyopathy
– hypothermia
– ventricular paced rhythms
– LBBB
Difficult ECG interpretations
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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
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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
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T wave inversion without ischemia
– PE or cor pulmonale
– spontaneous PTX
– myocardial contusion
– LVH
– ventricular paced rhythms
– RBBB
– LBBB
AMI and LBBB
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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
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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
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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
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Unstable angina
acute coronary
ischemia
inflammatory heart
disease
cardiomyopathies
circulatory failure &
shock
DTs
Rhabdomyolysis
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Cardiac surgery
skeletal m. trauma
dermatomyositis,
polymyositis
myopathic disorders
muscular dystrophy
vigorous exercise
malignant
hyperthermia
Ethanol poisoning
Troponin
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Main regulatory protein for the actinmyosin myofibrils
3 subunits:
– inhibitory subunit (Trop I)
– tropomyosin binding subunit (Trop T)
– calcium binding subunit (Trop C)
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Trop I has not been identified in skeletal m.
during any stage of develop therefore
specific to myocardium
Troponin
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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
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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
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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
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1. Dysrhythmias and conduction
disturbances
2. Cardiac failure
3. Mechanical complications
4. Pericarditis
5. Right Ventricular Infarction
6. Other
Dysrhythmias
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Occurs in 72-100% of AMI pts treated in
coronary care unit
PVCs are common in AMI
– occur in >90% of AMI patients
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Atrial premature contractions are also
common
– occur in up to 50% of AMI patients
– not associated with increased mortality
Dysrhythmias
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Early in AMI, pts often show increased
autonomic nervous system activity
– sinus brady, AV block, hypotension
occur from increased vagal tone
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Later, increased sympathetic activity
results in incr catecholamine release
– thus creates electrical instability: PVCs,
Vtach, Vfib, accelerated idioventricular
rhythms, AV junctional tachycardia
Dysrhythmias
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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
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Persistant tachycardia is associated
with poor prognosis
– due increase myocardial oxygen use
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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
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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
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Mobitz II
– usually associated with anterior AMI
– does progress to complete heart block
Conduction Disturbances
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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
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Complete block in setting of anterior MI
results in grave prognosis
Conduction Disturbance
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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
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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
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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
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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
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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
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NSAIDs, steroids, and late
administration of thrombolytics have
been linked to an increased likelihood of
cardiac rupture
– however, studies remain contradictory
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LV hypertrophy appears to be protective
Mechanical Complications
of AMI
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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
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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
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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
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Dressler Syndrome
– post AMI syndrome
– occurs 2 to 10 weeks after AMI
– pts presents with chest pain, fever, and
pleuropericarditis
Right Ventricular Infarction
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Usually seen as a complication of an
inferior infarction
– approximately 30% of inferior wall MI
involve the RV
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Presence of RV infarction is associated
with significant increase in mortality and
cardiovascular complications
Other Complications
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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
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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
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Pts with chest pain syndromes after
CABG
– may have abrupt vessel closure
– symptoms of recurrent ischemia can be
confused with post-AMI pericarditis
Disposition
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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
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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
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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 8090%
If all criteria are not met, stress test
have poor sensitivity
QUESTIONS?
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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?
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2. True or False: Inferior wall MI can
result from occlusion of left circumflex a.
or RCA
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3. True or False: Left ventricular free
wall rupture occurs in 10% of AMI
fatalities usually 3-4 weeks after initial
infarct
QUESTIONS?
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4. True or False: B type natriuretic
peptide has a high specificity in
diagnosing CHF
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5. True or False: Reproducible chest
wall pain rules out ACS.
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Answers: B, true, false, false, false
References
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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.