Page 149 - Cardiac Nursing

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C HAPTER 5 / Atherosclerosis, Inflammation, and Acute Coronary Syndrome 125
production. The infarcted area is further complicated by coronary necrotic wall is very thin during this phase. Cardiac rupture can
vasoconstriction and thrombi embolization. Cardiac myocyte cell occur at any time after an infarction but most commonly within
death may activate the production of free radicals that plug the this first week. Rupture of the myocardial wall causes massive
coronary capillaries causing the “no flow” phenomenon. 237,238 hemorrhage into the pericardial space, resulting in cardiac tam-
The location of the infarction correlates with disease in a particu- ponade and pump failure. In the second week of the repair
lar area of the coronary circulation. For example, disease in the process, insulin secretion increases to mobilize glucose from the
proximal left anterior descending artery may cause wall motion wound repairs. The initial phase of the collagen matrix is weak
22
abnormalities in the anterior or anterior–septal walls of the my- and vulnerable to reinjury. By the third week, scar formation has
ocardium. Other common designated infarct areas include infe- begun. Postinfarct remodeling of the noninfarcted myocardium
rior, lateral, posterior, or septal sites. also begins. 253 The surviving myocytes hypertrophy because they
Reperfusion of the infarcted area is necessary to alter the cannot divide to make up for the loss of pump function of the
necrotic process. Re-establishment of coronary blood flow can be dead myocytes. Fibrous connective tissue replaces necrotic tissue.
achieved by thrombolytics or catheter-based procedures. 18 Strep- There may be excessive deposition of collagen in the hypertro-
tokinase, anistreplase, and tissue plasminogen activator are fibri- phied myocardium. Collagen is not a contractile protein and
nolytic agents that act as “clot busters.” 257 Percutaneous coronary fibrosis may lead to a stiff or noncompliant ventricle and impaired
interventions are performed to place a wire across the blocked or contractility of the surviving myocardium. Current research has
stenosed coronary artery and inflate a balloon within the stenotic focused on early metalloproteases activation and decreasing extra-
portion of the artery. This procedure is called percutaneous trans- cellular matrix degradation. 261 After 6 weeks, the necrotic area is
luminal coronary angioplasty (PTCA). More often, a stent is completely replaced by scar tissue, which is strong but ineffective
placed in the coronary artery to ensure effective coronary artery in contributing to overall contractility of the myocardium. My-
blood flow to the myocardium. Some patients may have sponta- ocardial infarction can result in abnormal wall motion abnormal-
neous reperfusion when a thrombus disperses naturally. See Chap- ity, decreased myocardial function, reduced stroke volume,
ter 23 for details outlining these interventional cardiology proce- diminished ejection fraction, elevated ventricular filling pressures,
dures. If patients are not amenable to these interventions, then and sinoatrial node dysfunction.
they may undergo surgical revascularization with coronary artery The degree of left ventricular functional impairment after a
bypass surgery (see Chapter 25). myocardial infarction depends on the size and location of the in-
farct, function of noninfarcted myocardium, collateral circulation,
Evolution of Myocardial Infarction and compensatory mechanisms. 258 These compensatory mecha-
and Postinfarct Remodeling nisms operate to optimize cardiac output and peripheral perfu-
sion. Impairment of left ventricular function with subsequent de-
The immediate and long-term consequences of acute myocardial creased cardiac output activates arterial vasoconstriction, which
infarction are determined by the size of the infarct zone and posi- increases vascular resistance and mean arterial pressure. Venocon-
tion of the infarct. 1,258 A large myocardial infarct, more than 40% striction increases venous return to the heart and ventricular fill-
damage of the myocardium, can cause markedly reduced left ven- ing. Higher diastolic filling pressures are necessary to maintain ad-
tricular failure and circulatory failure. Cardiogenic shock will equate stroke volume to a point. Increased ventricular pressure
eventually occur if blood perfusion to the myocardium is not re- and volume stretches myocardial fibers to increase the force of
stored. The infarcted segment undergoes a series of changes dur- contraction, according to the Starling law. Aldosterone is released
ing the process of healing and wound repair. Some of these to stimulate renal retention of sodium and water, thereby further
changes can pose further risks to the patients. Initially, the infarct increasing circulatory filling pressures. The depressed my-
area is bruised and cyanotic from lack of nutrients and blood flow. ocardium develops temporary left ventricular enlargement caused
Cardiac enzymes are released from the cells and can be detected in by cardiac dilatation from these compensatory mechanisms at-
the blood stream. 22 These biochemical markers of cellular injury tempting to sustain cardiac output.
include creatinine kinase and creatinine kinase-MB, which are the The hemodynamic effects of a myocardial infarction depend
cardiac muscle enzymes sometimes present in skeletal muscle. on the extensiveness and location of myocardial damage and
They increase within 4 to 6 hours of cellular injury, peak in 18 to restoration of coronary blood flow. 1,3,250,253,257,258 Heart rate
24 hours, and last approximately 2 to 3 days. 249 The cardiac- may be normal or borderline normal with mild myocardial de-
specific troponins are regulatory proteins that control the calcium- pression. Tachycardia is observed in some patients with more ex-
mediated interaction of actin and myosin. Cardiac-specific tro- tensive myocardial damage and is considered a poor clinical cor-
ponin T and cardiac-specific troponin I elevate 4 to 6 hours after relate. Blood pressure may be hypertensive in the initial phases of
cellular injury, peak at 18 to 24 hours, and persist for at least 10 a myocardial ischemia. As myocardial depression worsens, hy-
days. 248 In addition, cardiotrophin-1, a member of the IL-6 fam- potension ensues. Reflex sympathetic stimulation increases heart
ily of cytokines, is elevated in ischemic heart disease and thought rate and contractility. Conversely, inferior wall myocardial infarc-
to have a role in postmyocardial infarction wound healing. Occa- tions may stimulate parasympathetic response of reduced heart
sionally, elevated troponins are seen in chronic dialysis patients rate and blood pressure, further compromising the depressed my-
and postcardiac bypass patients. 259 Biomarkers of myocardial in- ocardium. As myocardial function worsens, contractility is re-
jury can be measured and are discussed in Chapter 14. One of the duced, wall compliance is altered, stroke volume is reduced, and
most promising biomarkers is CRP, manufactured in the liver, filling pressures including left ventricular end-systolic and end-
which increases during inflammatory response to tissue injury. 260 diastolic volumes are elevated resulting in pulmonary edema and
By the second or third day after myocardial infarction, leuko- circulatory failure. If the cycle is not reversed with restoration of
cytes infiltrate the necrotic area and scavenger neutrophils release coronary blood flow, then cardiogenic shock, cardiac rupture, and
proteolytic enzymes to break down the necrotic tissue. The death ensue.