Porth's Essentials of Pathophysiology, 4e

450

Circulatory Function

U N I T 5

FIGURE 19-3. (Top) (A) Electrocardiogram tracing showing normal P, Q, R, S, andT waves. (B) ST-segment elevation with acute ischemia. (C) Q wave with acute myocardial infarction. (Bottom) Current- of-injury patterns with acute ischemia. (A) With predominant directed toward the inner layer of the affected ventricle and the ventricular cavity. Overlying leads therefore record ST-segment depression. (B) With ischemia involving the outer ventricular layer (transmural or epicardial injury), the ST vector is directed outward. Overlying leads record ST-segment elevation. (Bottom from Zipes DP, Bonow RO, Mann DL, et al., eds. Heart Disease: ATextbook of Cardiovascular Medicine. 8th ed. Philadelphia, PA: Saunders Elsevier; 2008:174.) subendocardial ischemia, the resultant ST segment is

R

ST elevation

1 mm wide

Almost 4 mm

T

P

U

Q

S

A

B

C

Subendocardial injury: ST depression

Transmural (epicardial) injury: ST elevation

ST

ST

V 5

V 5

ST

ST

A

B

Unstable Angina/Non–ST Elevation Myocardial Infarction

area of infarction is determined by the affected coronary artery and its distribution of blood flow (Fig. 19-4).

Unstable angina/non–ST elevation myocardial infarc- tion (UA/NSTEMI) is a clinical syndrome of myocardial ischemia ranging from angina to myocardial infarc- tion. 14–16 Typically, unstable angina and NSTEMI differ in whether the ischemia is severe enough to cause suf- ficient myocardial damage to release detectable quan- tities of serum cardiac markers. Persons who have no evidence of serum markers for myocardial damage are considered to have unstable angina, whereas a diagnosis of NSTEMI is indicated when there are detectable serum markers of myocardial injury. The pain associated with unstable angina typically has a persistent and severe course and is characterized by at least one of three features: (1) it occurs at rest (or with minimal exertion), usually lasting more than 20 minutes if untreated (i.e., without nitroglycerine); (2) it is severe and described as frank pain and of new onset (i.e., within 1 month); and (3) it is more severe, pro- longed, or frequent than previously experienced. 16 The risk of acute MI in an individual diagnosed with UA/NSTEMI is classified as low, intermediate, or high based upon the clinical history, ECG pattern, and serum biomarkers. The ECG pattern associated with in NSTEMI may display normal or ST-segment depression (or tran- sient ST-segment elevation) and T-wave changes. The degree of ST-segment deviation from baseline is an impor- tant measure of ischemia and indicator of prognosis. ST Elevation Myocardial Infarction Acute ST elevation MI (STEMI) is characterized by the necrosis of myocardial tissue and a consequence of ath- erosclerotic disease of the coronary arteries. The specific

Pathologic Changes. The size and pattern of the infarct depends on the location and extent of occlusion, amount of heart tissue supplied by the vessel, duration of the occlusion, metabolic needs of the affected tissue, extent of collateral circulation, and other factors such as heart rate, blood pressure, and cardiac rhythm. An infarct may involve the endocardium, myocardium, or epicardium, or a combination of these tissue layers. 6 Transmural infarcts involve the full thickness of the ven- tricular wall and most commonly occur when there is obstruction of a single artery (Fig. 19-5). Subendocardial infarcts involve the inner one third to one half of the ventricular wall and occur more frequently in the pres- ence of severely narrowed but still patent arteries. The principal biochemical consequence of MI is the con- version from aerobic to anaerobic metabolism with inad- equate production of energy to sustain normal myocardial function. 18 As a result, a striking loss of contractile function occurs within 60 seconds of onset. 6 Changes in cell struc- ture (i.e., glycogen depletion and mitochondrial swelling) develop within several minutes. These early changes are reversible if blood flow is restored. Although gross tissue changes are not apparent for hours after the onset of MI, the ischemic area ceases to function within a matter of min- utes, and damage to cells occurs in approximately 40 min- utes. Irreversible myocardial cell death (necrosis) occurs after 20 to 40 minutes of severe ischemia 6 (Fig. 19-6). The term reperfusion refers to the reestablishment of blood flow using fibrinolytic therapy or revascular- ization procedures. Early reperfusion after onset of occlusion can prevent necrosis and improve myocar- dial perfusion in the infarct zone. Reperfusion after a