Porth's Essentials of Pathophysiology, 4e

452

Circulatory Function

U N I T 5

Healthy tissue

Ischemia

Injury

FIGURE 19-6. Zone of myocardial infarction with associated ECG changes. (Adapted from Anatomical Chart Company. Atlas of Pathophysiology. 3rd ed. Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams & Wilkins; 2010:63.)

Necrosis

pain and vagal stimulation. The epigastric distress may be mistaken for indigestion, and the person may seek relief with antacids or other home remedies; this behavior may delay medical interventions. Sudden death from acute MI is death that occurs within 1 hour of symptom onset. 12 It usually is attributed to fatal arrhythmias, which may occur without evidence of infarc- tion. Early hospitalization after onset of symptoms greatly improves the chances of averting sudden death because appropriate resuscitation equipment and personnel are immediately available should a ventricular arrhythmia occur. The recent distribution of automatic external defibril- lators in multiple public arenas highlights the importance of early defibrillation in the survival of patients with STEMI. Diagnosis and Treatment. Because STEMI diagnosis can be challenging before biomarkers and ECG data are available, the immediate management of unstable angina/NSTEMI and STEMI is similar. 12,14 Acute coro- nary syndrome prognosis is associated with the risk of two general complications—arrhythmias and mechani- cal (pump) failure. The majority of deaths from ACS are due to sudden cardiac death related to the development of ventricular fibrillation. Therefore, seeking prompt medical care is a critical element in the effective manage- ment of persons with ACS. The immediate deployment of an emergency medical team capable of resuscitation procedures—specifically defibrillation and expeditious transport to a hospital equipped to initiate reperfusion therapy, manage arrhythmias, and provide advanced cardiac life support—is crucial. 12 The emergency department goals for management of ACS include rapid identification of persons who are can- didates for reperfusion therapy. Evaluation of the person’s chief complaint, typically chest pain, along with other associated symptoms is essential in differentiating ACS from other diagnoses. For any person presenting with symptoms of ACS, providers should perform a 12-lead ECG and continuous ECG monitoring. Treatment regi- mens also include administration of oxygen, aspirin, nitrates, morphine, antiplatelet and anticoagulant ther- apy, β -adrenergic blocking agents (beta blockers), and an angiotensin-converting enzyme (ACE) inhibitor. 12,14

The administration of oxygen augments the oxygen content of inspired air and increases the oxygen satu- ration of hemoglobin. Arterial oxygen levels may fall precipitously after acute MI, and oxygen administra- tion maintains oxygen content of the blood perfusing the myocardial tissue. Platelets play a major role in the thrombotic response to atherosclerotic plaque disruption; therefore, inhibition of platelet aggregation is an impor- tant aspect in the early treatment of both unstable angina/ NSTEMI and STEMI. Aspirin (i.e., acetylsalicylic acid) is the preferred antiplatelet agent for preventing platelet aggregation in persons with ACS. Aspirin, which acts by inhibiting synthesis of the prostaglandin thromboxane A 2 , is thought to promote reperfusion and reduce the likelihood of re-thrombosis. For patients who are aspirin- intolerant, another antiplatelet drug such as clopidogrel may be prescribed. Clopidogrel exerts its effects by inhib- iting the ADP pathway in platelets 18 (see Chapter 12). The severe pain of acute MI gives rise to anxiety and recruitment of autonomic nervous system responses, both of which increase the work demands on the heart. Control of pain in acute MI is accomplished through a combination of nitrates, analgesics (e.g., morphine), and beta-blocking agents. 12 Nitroglycerin is administered because of its vasodilating effect and ability to relieve coronary pain. The vasodilating effects of the drug decrease venous return (i.e., reduce preload) and arterial blood pressure (i.e., reduce afterload), thereby reducing oxygen consumption. Although a number of analgesic agents have been used to treat the pain of acute MI, morphine is usually the drug of choice to be given intra- venously for rapid onset of action. 11 Beta antagonists block β -receptor–mediated functions of the sympathetic nervous system and thus decrease myocardial oxygen demand by reducing heart rate, cardiac contractility (i.e., inotropy), and systemic arterial blood pressure. Immediate reperfusion therapy through use of phar- macologic agents (fibrinolytic therapy), percutaneous coronary intervention, or coronary artery bypass graft- ing is usually indicated for persons with ECG evidence of STEMI. Fibrinolytic drugs degrade blood and plate- let clots, and their use is associated with positive out- comes such as reduced mortality and incidence of lethal