ACUTE CORONARY SYNDROMES: Acute MI and Unstable Angina Tintinalli Chapter 50 September 20, 2005.

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 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

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.