Myocardial infarction Prepared by: Dr. Nehad Ahmed
Study objectives • Understand the etiology of myocardial infarction. • Distinguish the types of myocardial infarction that might occur. How do they differ in terms of their myocardial involvement, location and severity? • Understand the sequence of events that accompanies a myocardial infarction. • List the major clinical and physiologic manifestations of myocardial infarction. Why does each occur?
Discuss the role of cardiovascular compensatory mechanisms in myocardial infarction. • Describe the complications that might arise from a myocardial infarction. • Discuss the rationale for the various treatment aspects involved in myocardial infarction.
Introduction • Myocardial infarction or “heart attack” is an irreversible injury to and eventual death of myocardial tissue that results from ischemia and hypoxia. • Myocardial infarction is the leading killer of both men and women in the United States.
Most heart attacks are the direct Result of occlusion of a coronary blood vessel by a lipid deposit. These lipid deposits may accumulate to the point where they completely block a coronary vessel or, more commonly, accumulated lipid plaques may break off from the vascular endothelium and act as a thrombus that blocks a coronary artery at a narrower point downstream. • Prolonged vasospasm might also precipitate a myocardial infarction in certain individuals.
Coronary blood ﬂow and myocardial infarction • The location of a myocardial infarction will be largely determined by which coronary blood vessel is occluded. • The two main coronary arteries supplying the myocardium are the left coronary artery (which subdivides into the left anterior descending and circumﬂex branches) and the right coronary artery
Theleft anteriordescending artery supplies blood to the bulk of the anterior left ventricular wall, while the left circumﬂex artery provides blood to the left atrium and the posterior and lateral walls of the left ventricle. • The right coronary artery provides blood mainly to the right atria and right ventricles. • Nearly 50% of all myocardial infarctions involve the left anterior descending artery that supplies blood to the main pumping mass of the left ventricle.
The next most common site for myocardial infarction is the right coronary artery, followed by the left circumﬂex. • A myocardial infarction may be transmural , meaning it involves the full thickness of the ventricular wall, or subendocardial , in which the inner one third to one half of the ventricular wall is involved. • Transmural infarcts tend to have a greater effect on cardiac function and pumping ability since a greater mass of ventricular muscle is involved.
Manifestations of myocardial infarction 1. Severe chest pain and discomfort — Pressing or crushing sensation often accompanied by nausea, vomiting, sweating and weakness due to hypotension. A signiﬁcant percentage of myocardial infarctions are “silent” and have no symptoms. 2. Irreversible cellular injury — Generally occurs 20 to 30 minutes after the onset of complete ischemia. 3. Release of myocardial enzymes such as creatinephosphokinase (CPK) and lactate dehydrogenase (LDH) into circulation from myocardial damaged cells. 4. Electrocardiogram changes
5. Inﬂammatory response from the injured myocardium — Leukocyte inﬁltration, increased white blood cell counts, fever. • 6. Coagulative necrosis of the area of the myocardium affected by the infarction. • 7. Repair of damaged areas occurs by replacement with scar tissue and not functional muscle tissue; therefore, some alteration in function is inevitable
Complications of myocardial infarction Depending on the extent of the area involved in a myocardial infarction, a number of complications might arise, including: • Rupture of weakened myocardial wall. Bleeding into pericardium may cause cardiac tamponade and further impair cardiac pumping function. This is most likely to occur with a transmural infarction. Rupture of the septum between the ventricles might also occur if the septal wall is involved in the infarction. • Formation of a thromboembolism from pooling of blood in the ventricles.
3. Pericarditis —Often occurs 1 to 2 days after the infarction. 4. Arrhythmia — May be life-threatening and lead to ﬁbrillation 5. Reduced cardiac function
6. Congestive heart failure may result if a large enough area of the myocardium has been damaged such that the heart no longer pumps effectively. 7. Cardiogenic shock — Marked hypotension that can result from extensive damage to the left ventricle. The resulting hypotension will trigger cardiovascular compensatory mechanisms that will further tax the damaged myocardium and exacerbate impaired function. Cardiogenic shock is associated with a mortality rate of 80% or greater.
Key terms Cardiac tamponade — Excessive pressure that develops from the accumulation of ﬂuid in the pericardium. Pericarditis — Inﬂammation of the pericardium. Stroke volume — Volume of blood ejected from each ventricle per beat. End-diastolic volume — Volume of blood remaining in the ventricle at the end of systole (contraction).
Compensatory mechanisms for myocardial infarction • As a result of the hypotension and hemodynamic changes that accompany a myocardial infarction, the cardiovascular system initiates a number of reﬂex compensatory mechanisms designed to maintain cardiac output and adequate tissue perfusion: 1. Catecholamine release — Increases heart rate, force of contraction and peripheral resistance. Catecholamines can, however, be arrhythmogenic.
2. Sodium and water retention. 3. Activation of renin–angiotensin system leading to peripheral vaso- constriction. 4. Ventricular hypertrophy. • Unfortunately, these compensatory changes may increase oxygen demand and workload on the infarcted heart and worsen overall cardiac function.
Rationale for therapy • A main goal of intervention for myocardial infarction is to limit the size of the infarcted area and thus preserve cardiac function. • Early recognition and intervention in a myocardial infarction have been shown to signiﬁcantly improve the outcome and reduce mortality in afﬂicted patients. • If employed in the early stages of myocardial infarction, antiplatelet-aggregating drugs such as aspirin and clot-dissolving agents such as streptokinase and tissue plasminogen activator may be very effective at improving myocardial blood ﬂow and limiting damage to the heart muscle.
Other drugs such as vasodilators, β-adrenergic blockers and ACE inhibitors can also improve blood ﬂow and reduce workload on the injured myocardium and thus reduce the extent of myocardial damage. • The development of potentially life-threatening arrhythmias is also common during myocardial infarction and must be treated with appropriate antiarrhythmia drugs. • Supportive therapies such as oxygen, sedatives and analgesics are also utilized.
Treatment for myocardial infarction 1. Oxygen — Used to maintain blood oxygenation as well as tissue and cardiac O 2 levels. 2. Aspirin — If administered when myocardial infarction is detected, the antiplatelet properties of aspirin may reduce the overall size of the infarction. 3. Thrombolytic therapy — If employed in the ﬁrst 1 to 4 hours following the onset of a myocardial infarction, these drugs may dissolve clots in coronary blood vessels and re-establish blood ﬂow. 4. Vasodilator drugs — Intravenous nitroglycerin can increase blood ﬂow to the myocardium and reduce myocardial work.
5. β-Blockers — Blunt the effect of catecholamine release on the myocardium, Reduce heart rate and myocardial work. 6. Pain management — Sublingual nitroglycerin, morphine if necessary 7. Antiarrhythmia drugs — To treat and prevent a number of potentially life-threatening arrhythmias that might arise following a myocardial infarction. 8. ACE inhibitors — Drugs that block activation of the renin–angiotensin system and thus reduce the negative effects of vasoconstriction and salt and water retention on the myocardium.