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KEY POINTS
Any acute imbalance between myocardial oxygen supply and demand may result in a syndrome of acute cardiac ischemia. Potential mechanisms include acute changes in coronary anatomy, as in plaque rupture and thrombosis, and acute changes in physiology as in sepsis and hemorrhage.
Acute cardiac ischemia progresses in a typical cascade through perfusion abnormality, metabolic disturbances, diastolic and systolic dysfunction, electrocardiographic changes, symptoms, and ultimately myocardial necrosis, with associated rise in serum biomarkers of myocardial infarction. Therapy to interrupt this cascade is time sensitive in order to prevent irreversible loss of myocytes.
Key elements of initial evaluation of suspected acute cardiac ischemia include a chest pain history, focused examination to exclude alternate diagnoses and assess hemodynamic stability, and a 12-lead electrocardiogram to identify ST-segment elevations. Serum biomarkers of myocardial infarction including troponin creatine kinase and its MB fraction should be measured for diagnostic and prognostic purposes, but should not delay urgent management.
Directed therapy for acute cardiac ischemia should target the suspected mechanism of ischemia. When plaque rupture, thrombosis, and acute obstruction to coronary blood flow are suspected, appropriate treatment includes dual antiplatelet therapy with aspirin and an adenosine diphosphate receptor antagonist, anticoagulation, statin therapy, and consideration of reperfusion therapy. When stable coronary anatomy and an acute change in physiology are suspected, treatment should prioritize correction of the offending physiologic derangements.
Acute cardiac ischemia with ST-segment elevations is a medical emergency requiring immediate cardiology consultation and consideration of reperfusion therapy, including potential primary percutaneous coronary intervention or fibrinolytic therapy.
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Acute cardiac ischemia is defined by new or worsening imbalance between myocardial oxygen supply and demand, most commonly in the setting of coronary artery disease. Despite improvements in medical therapy, the burden of coronary artery disease remains high, affecting over 15 million United States adults.1 Acute cardiac ischemia describes a physiologic disturbance underlying a spectrum of disorders encountered in critical care, from so-called “demand ischemia” in the setting of an acute physiologic insult and stable ischemic heart disease, to acute coronary syndromes (ACS), including unstable angina (UA), non-ST segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).
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Whereas certain physiologic principles of acute cardiac ischemia are common across this spectrum, providing the basis for understanding its natural history and therapy, appropriate management varies importantly with the mechanism of disease. As such, the ability to both identify and discriminate acute cardiac ischemia is fundamental to timely selection and implementation of appropriate therapy. In this chapter, we aim to provide a practical, intuitive review of the spectrum of acute cardiac ischemia for the critical care provider.
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ANATOMIC AND PHYSIOLOGIC CONSIDERATIONS
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Cardiac ischemia results from an imbalance between myocardial oxygen supply and demand. Acute disturbances in supply, demand, or both can precipitate a syndrome of acute cardiac ischemia. Major determinants of myocardial oxygen supply and demand are presented in Table 24–1.
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