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Acute Myocardial Infarction:Pathophysiology and Presentation

Thomas C. Smitherman

University of Pittsburgh MedicalCenter

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Acute Myocardial Infarction

750,000 documented acute MIs/year inUSA

Similar number of UAP Half of all deaths occur pre-hospital

Up to 10% die during hospitalization

10% of survivors of initial MI die in yearpost MI, most suddenly, rest with re-MI

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Acute MI

Demographics and Statistics 3:1 to 4:1 male:female ratio in middle age.

Equalizes with aging-in general women

have MI about 20 years later

First MI (men) in 50s, earlier with

prominent risk factors

Accounts for about 50% of all deaths in US

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Thrombus Formation

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Lesions

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Necrosis

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Evolution of Infarction

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Acute Coronary Syndromes (ACS,

Syndromes of Acute Myocardial Ischemia)

Terminology for Use after the first 24-48 h

Q wave MI

Non-Q wave MIUnstable angina

Terminology for use in the first 24-48 h

SAMI with persistent ST-segment elevationSAMI without persistent ST-segment

elevation

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Acute MIElectrical Consequences

Ventricular Tachyarrhythmias

VPBs

Simple

Complex (frequent, multiform, couplets, R on T)

Ventricular Tachycardia

Polymorphic (ischemia)

Monomorphic (re-entrant)

Ventricular Fibrillation

Accelerated Idioventricular Rhythm

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Acute MI

Electrical consequences

BradycardiaSinus bradycardia

AV block

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Acute Myocardial InfarctionElectrical Consequences

Bradycardia

AV Block

At the AV node Usually with inferior/posterior MI Increased vagal tone (common) from Neurocardiac

reflex or AV node damage (rare)

2o

block of Mobitz I (Wenckebach) type 3o block usually slow in onset and heralded by 1o or

2o block

Usually transient (hours or days)

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Acute MI


Bradycardia

AV block

Below AV Node

Damage to His-Purkinje system

Usually with Anterior MI

Often a/w prolonged QRS, BBB, Fasicular blocks

2nd degree block usually Mobitz II type

3rd degree block may occur suddenly

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Acute MI


Atrial tachyarrhythmias

About 10% of cases

Atrial fibrillation, atrial flutter, supraventricular

tachycardia

Usually due to atrial hypertension

a/w higher mortality, because of association with

atrial hypertension, larger MIs, more LV

dysfunction

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Acute MI

Functional consequences

Size of MI important because of effects on LV

function

Global systolic performance (LVEF and C.O.) are the

most easily measured variables

Diastolic LV dysfunction is universal but harder to

measure and usually must be inferred

The larger the MI, the greater the likelihood of CHF

and shock

Regional contraction patterns: hypokinesia, akinesia,

dyskinesia

Stunned myocardium

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Acute MI

Mechanical complications

Myocardial rupture

Free wall, papillary muscle, IV septum

Cardiogenic shock

RV Involvement with inferior MI

LV aneursysm and thrombus

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SHOCK IN ACUTE

CORONARY SYNDROMESHypovolemic

Neurocardiac Reflex

RV Involvement with IMI

Typical Cardiogenic Shock

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SHOCK IN ACUTE

CORONARY SYNDROMESTypical Cardiogenic Shock

> 35-40% of LV involved

Low BP, high PCW, low CO, poor perfusion

RA usually also elevated

Historic death rate ca. 90%, now perhaps 40-60%

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SHOCK IN ACUTE

CORONARY SYNDROMES

RV Involvement with IMI

Proximal RCA occlusion

High RA, CVP

Underfilled LV causes LV stroke volume to

drop

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Acute MI


Left ventricular aneurysm and thrombus

12-15% of MIs

Almost always with Q-wave MI

True aneurysm never ruptures

Soaks up LV contractile energy: worsens CHF

Contributes to stagnant flow: increases risk of LV

thrombus and thromboembolism, especially stroke.

Risk highest in early days, lasts ca. 12 weeks

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Acute MI


Ventricular ruptue

Ca. 10% of all MIs

Risk factors: age, female, hypertension, first MI Dissection at infarct/viable muscle junction

Ca. 90% free wall: hemopericardium, pericardial

tamponade, pulseless electrical activity, worsening

bradycardia, death within minutes. Rare case issubacute and may become a pseudoaneurysm, which

almost always ruptures eventually.

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Acute MI


Ventricular rupture

Papillary muscle rupture (ca. 10% of all ruptures)

Acute mitral regurgitation (MR) Dramatic onset of CHF and new murmur

IV septal rupture (ca. 10% of all ruptures)

Acute ventricular septal defect (VSD)

Dramatic onset of CHF and new murmur Distinguishing acute MR vs. acute VSD

Oxygen run of right heart

Echo/Doppler interrogation

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SHOCK IN ACUTE

CORONARY SYNDROMES

Hypovolemic

Look for cause

LV post-MI functions best with a slightlyoverfilled state: PCW ca. 16-18, PAD ca. 18-20

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Acute MI

Determinants of mortalityLV function

LV size

Status of infarct-related arteryPresence & severity of ventricular rhythm

disorders

Presence of spontaneous or provokable (stresstest-induced) ischemia

Age

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KILLIP CLASSPOST MI

I. Uncomplicated MI, no abnormalities.

II. Rales limited to the lower half of the

lung fields and/or S3.

III. Severe ventricular failure and acute

pulmonary edema.

IV. Typical cardiogenic shock.

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Acute MI

Clinical presentation

Symptoms potentially indicative of MI

New onset of chest discomfort that issuggestive of myocardial ischemia occurring at

rest or with ordinary day-to-day activitiesA change in the angina pattern such that angina

has become more frequent, severe, prolongedor difficult to relieve, or the occurrence of

angina at rest for the first timeChest discomfort suggestive of myocardial

ischemia in patient with known CAD that isunrelieved by rest or nitroglycerin

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Discomfort Associated with the Acute Coronary

Syndromes

Nature of discomfort

Location of discomfort

Duration > 15 - 20 minutes

Associated dyspnea, diaphoresis, palpitations,

nausea/vomiting

History of & risk factors for ASHD

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The Pain of Syndromes of Acute

Myocardial Ischemia

The seven most common categories

A B C D E F G

Pressure Ache Tightness Oppression Bursting Heartburn Burning

Heaviness Soreness Constriction Uncomfortable Fullness Indigestion Searing

Weight Compression Discomfort Swelling

Choking Hard

StrangulationVise-like

Squeezing

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Syndromes





nausea/vomiting


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Discomfort with ACS--Location

Central or substernal

Radiation to neck, jaw, shoulders, arms,

upper back

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Syndromes





nausea/vomiting


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Acute MI

Clinical Presentation

AHA recommends seeking emergency

treatment:

History of angina, known CAD: typical

symptoms not relieved by 3 TNGs within 10

minutesUnrecognized CAD: typical symptoms lasting

more than 2 minutes

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Acute MI

Clinical Presentation

Many are clinically silentca. 25% of all Q-

wave MIs

Physician must be alert to possibility of silentMI

Pulmonary edema and stroke in appropriate

patients should always raise question of acute

MI

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Acute MI

Clinical Presentation and Diagnosis

Electrocardiography

Transmural injury: ST-segment elevation withflattening or concave downwards appearance. Q-waveevolution often follows.

Subendocardial injury: ST-segment depression with flator downgoing appearance. T-wave inversion less

specific. Q-wave evolution unlikely. Fair correlation of leads with LV segments: Anterior:

V1-V4; Inferior: II, III, aVF; Lateral: I, avL, V5-V6.

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Six-Month Mortality

0%

2%

4%

6%

8%

10%

0 30 60 90 120 150 180

Days from Randomization

T-wave inversion

ST-segment depression

ST-segment elevation

T-waveinversion

ST

ST

Baseline ECG and OutcomeGUSTO IIb

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The 12 Lead ECG - Ischemia, injury and infarction

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Inferior Injury

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Anterior Septal Injury with Infarction

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Time Course for Cardiac Markers

Figure

adapted and

modified fromAbbott

a

**

* Recommended

for useLimited use

Not used anylon er

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Non-ischemic Causes of Elevated

Troponin

Direct trauma to the heart and mechanical injury(such as ablation, angioplasty, cardiac surgery,cardioversion (implantable cardioverter defibrillatordischarges)

Myocardial toxins such as adriamycin or 5-fluorouracil

In response to endogenous substances released in

critically ill patients (e.g., patients with septic shock)

Cardiotropic viral infections, pericarditis,

myocarditis Subendocardial injury in patients with increased

wall stress (pulmonary embolism, hypertension,congestive heart failure, acute heart failure withshock, tachycardia, strenuous and prolongedexercise).

acute mi s

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