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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 male postmenopausal
females family history cigarette smoking hypertension
High cholesterol truncal obesity sedentary lifestyle diabetes previous cardiac hx
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 -->
Anterior -->
anterolateral -->
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
Lateral --> inferior --> inferolateral -->
true posterior -->
right ventricular -->
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
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 acute coronary
ischemia inflammatory heart
disease cardiomyopathies circulatory failure &
shock DTs Rhabdomyolysis
Cardiac surgery skeletal m. trauma dermatomyositis,
polymyositis myopathic disorders muscular dystrophy vigorous exercise malignant hyperthermia 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 Complicationsof 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 Complicationsof 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 Complicationsof 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 Complicationsof 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