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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

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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
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
  • 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
  • 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
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
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
  • 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
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
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
  • 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


postmenopausal females

family history

cigarette smoking


High cholesterol

truncal obesity

sedentary lifestyle


previous cardiac hx

Cardiac Risk Factors
cardiac risk factors14
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
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
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
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
  • 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
  • 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
ecg criteria and ami21
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 Criteria and AMI
  • 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
  • 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
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 interpretations25
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 interpretations26
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
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


circulatory failure & shock



Cardiac surgery

skeletal m. trauma

dermatomyositis, polymyositis

myopathic disorders

muscular dystrophy

vigorous exercise

malignant hyperthermia

Ethanol poisoning (chronic)

Conditions Associated with Elevated CK-MB
  • 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
  • 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
  • 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
Complications of MI
  • 1. Dysrhythmias and conduction disturbances
  • 2. Cardiac failure
  • 3. Mechanical complications
  • 4. Pericarditis
  • 5. Right Ventricular Infarction
  • 6. Other
  • 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
  • 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
  • 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
  • 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
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 disturbances41
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
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 disturbance43
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
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 failure45
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
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 complications of ami47
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 complications of ami48
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 complications of ami49
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
  • 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
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
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
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
  • 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
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
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
  • 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
  • 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
  • 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
  • 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.