Porth's Essentials of Pathophysiology, 4e

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Disorders of Cardiac Function

C h a p t e r 1 9

Flow

Coronary artery

Vessel Compression. The large coronary arteries lie on the epicar- dial surface of the heart, with the smaller intramyocardial vessels branching off and moving through the myocardium before merging with a plexus of vessels that sup- ply the subendocardial muscle with blood. During systole, the contract- ing cardiac muscle has a squeezing effect on the intramyocardial ves- sels while at the same time produc- ing an increase in intraventricular pressure that pushes against and compresses the subendocardial ves- sels. As a result, blood flow to the subendocardial muscle is greatest during diastole. Because the time spent in diastole becomes shortened as the heart rate increases, myo- cardial blood flow can be greatly reduced during sustained periods of tachycardia. 3

Systole

Epicardium

Intramyocardial coronary vessels

Muscle contraction

Subendocardial plexus

Endocardium

Diastole

Intramyocardial coronary vessels

Muscle relaxation

Subendocardial plexus

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These currents of injury are represented as a deviation of the ST segment on the ECG. When the acute injury is transmural, the overall ST vector is shifted in the direc- tion of the outer epicardium, resulting in an elevation of the ST segment (see Fig. 19-3). When the injury is con- fined primarily to the subendocardium, the ST vector is shifted toward the inner ventricular layer, resulting in an overall depression of the ST segment. Additional ven- tricular depolarization (QRS) changes may follow the T-wave and ST-segment abnormalities. 11,13 With actual infarction, depolarization (QRS) changes often follow the T-wave and ST-segment abnormalities. Serum Biomarkers Serum biomarkers for ACS, referred to as a cardiac panel, include cardiac-specific troponin I (TnI) and troponin T (TnT), creatine kinase MB (CK-MB), and myoglobin. 12,14 As myocardial cells become necrotic, their intracellular contents diffuse into the surrounding interstitium and into the blood. The rate at which the enzymes appear in the blood depends on their intracellular location, molec- ular weight, and local blood flow. For example, they may appear at an earlier-than-predicted time in patients who have undergone successful reperfusion therapy.

The troponin assays have high specificity for myo- cardial tissue and are the primary biomarker tests for the diagnosis of MI. The troponin complex, which is part of the actin filament, consists of three subunits (i.e., TnC, TnT, and TnI) that regulate the calcium- mediated actin–myosin contractile process in striated muscle (see Chapter 1, Fig. 1-19). Troponin I and tro- ponin T, which are present in cardiac muscle, begin to rise within 3 hours after the onset of myocardial infarc- tion and may remain elevated for 7 to 10 days after the event. This is especially useful in the late diagnosis of MI. 12 Creatine kinase is an intracellular enzyme found in muscle cells. There are three isoenzymes of CK, with the MB isoenzyme being highly specific for injury to myocardial tissue. Serum levels of CK-MB exceed nor- mal ranges within 4 to 8 hours of myocardial injury and decline to normal within 2 to 3 days. 12 Myoglobin is an oxygen-carrying protein, similar to hemoglobin, expressed in cardiac and skeletal muscle. This small molecule is released quickly from infarcted myocardial tissue, and elevated levels can be detected in the blood within 1 hour after myocardial cell death with peak lev- els reached within 4 to 8 hours. 12 Because myoglobin is present in both cardiac and skeletal muscle, this mol- ecule is not specific to cardiac injury.