Porth's Essentials of Pathophysiology, 4e

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Circulatory Function

U N I T 5

Pericardium

LA

Thrombus

LV

RA

LV

Pseudoaneurysm

RV

Transmural infarct with rupture

RV

A

B

C

FIGURE 19-9. Acute mechanical complications of myocardial infarction. (A) Papillary muscle rupture. (B) Interventricular septum rupture. (C) Rupture of the free wall of the left ventricle with pseudoaneurysm formation. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Mechanical defects result from changes that occur in the necrotic and subsequently inflamed myocardium and include rupture of the ventricular septum, papillary muscle, or free ventricular wall (Fig. 19-9). 6,12 Partial or complete rupture of a papillary muscle is a rare but often fatal complication of transmural myocardial infarction. It is detected by the presence of a new systolic murmur and clinical deterioration, often with pulmo- nary edema. Ventricular septal rupture occurs less fre- quently than in the past because of reperfusion therapy. Previously thought to require surgical intervention only in symptomatic patients, surgical repair is now recom- mended for all patients with ventricular septal rupture. Complete rupture of the free wall of the infarcted ventri- cle occurs in up to 10% of patients and usually results in immediate death. 12 It usually occurs 3 to 7 days postin- farction, usually involves the anterior wall, and is more frequent in older women. 6 A more common mechanical postinfarction complication is mitral valve regurgita- tion, which results from early ischemic dysfunction of the papillary muscle and underlying myocardium. A left ventricular aneurysm is a sharply delineated area of scar tissue that bulges paradoxically during sys- tole 6,12 (Fig. 19-10). This section of the myocardium does not contract with the rest of the ventricle during systole. Instead, it diminishes the pumping efficiency of the heart and increases the work of the left ventricle, predisposing the patient to heart failure. Ischemia in the surrounding area predisposes the patient to develop- ment of arrhythmias, and stasis of blood in the aneu- rysm can lead to thrombus formation. Surgical resection may be performed to prevent these complications when other treatment measures fail. 12 Chronic Ischemic Heart Disease Myocardial ischemia is defined as the inability of the coronary arteries to supply blood to meet the metabolic demands of the heart. Most often limitations in coro- nary blood flow are the result of atherosclerosis, but vasospasm may serve as an initiating or contributing factor. 20,21 Coronary artery disease is divided into three

heart and extends through the myocardium to involve more of the transmural thickness of the ischemic zone. Myocardial cells that undergo necrosis are gradu- ally replaced with scar tissue. An acute inflammatory response develops in the area of necrosis approximately 2 to 3 days after infarction. 6 Thereafter, macrophages begin phagocytizing the damaged necrotic tissue; the infarcted area is gradually replaced with an ingrowth of highly vascularized granulation tissue, which in turn becomes less vascular and more fibrous in composition. At approximately 3 to 7 days, the center of the infarcted area remains soft and yellow; therefore, if rupture of the ventricle, interventricular septum, or valve structures occurs, it will usually happen at this time. Replacement of the necrotic myocardial tissue usually is complete by the 7th week. Importantly, areas of the myocardium that have been replaced with scar tissue lack the ability to contract and initiate or conduct action potentials. The stages of recovery from MI are closely related to the size of the infarct. Fibrous scar tissue lacks the contractile, elastic, and conductive properties of normal myocardial cells; the residual effects and the complica- tions of the MI are determined essentially by the extent and location of the injury. Among the numerous com- plications of MI are life-threatening arrhythmias, peri- carditis, stroke, thromboemboli, and mechanical defects (e.g., mitral valve regurgitation, ventricular septal rup- ture, left ventricular wall rupture, and left ventricular aneurysm). Depending on its severity, MI has the poten- tial for compromising cardiac contractility resulting in cardiogenic shock or heart failure (see Chapter 20). These serious complications are discussed later. Pericarditis tends to occur in patients with large infarcts, a lower ejection fraction, and a higher occur- rence of heart failure. It may appear as early as the 2nd or 3rd day postinfarction or up to several weeks later. 12 Pericarditis that occurs weeks to months after MI or Dessler syndrome is thought to be mediated by autoim- mune mechanisms. In contrast to the pain associated with MI, the pain with pericarditis is sharp and stabbing, and this pain increases with inspiration. The pain may be relieved by positional changes. Because of reperfusion therapy, this complication has been greatly reduced.