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| Photomicrograph of a thrombus showing fibrin (yellow), red blood cells (red) and platelets (blue). |
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Anti-ischemic Therapy
Some of the general care strategies that should be considered during the ED evaluation and initial treatment are dictated by the severity of symptoms. When hospitalized, patients should be resting in bed during an ischemia attack. Subsequent activity should not be inappropriately restrictive; however, the prevention of recurrent symptoms should be the primary focus. Activities can be adjusted appropriately as the patient responds to therapy. Patients exhibiting cyanosis, respiratory distress or other high-risk features should receive supplemental oxygen, and confirmation of adequate arterial oxygen saturation should be obtained.1 |
Also, patients should undergo continuous ECG monitoring during their early hospital phase, because the major preventable cause of death in this early period is sudden, unexpected ventricular fibrillation. Therefore, monitoring of the recurrence of ST-segment shifts provides useful diagnostic and prognostic information.1
In addition, the following treatments may be prescribed:
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Nitrates reduce myocardial oxygen demand while enhancing myocardial oxygen delivery by dilating normal and atherosclerotic epicardial coronary arteries, as well as smaller arteries that constrict by cold, mental or physical exercise and other stressors. With severe atherosclerotic coronary obstruction and with less severely obstructed vessels with endothelial dysfunction, physiological responses to changes in myocardial blood flow are often impaired; therefore, maximal dilation does not occur unless a direct acting vasodilator like nitrates is administered.1 |
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Morphine Sulfate is recommended for patients whose symptoms are not relieved after three serial sublingual nitrate tablets or whose symptoms recur despite adequate anti-ischemic therapy, unless contraindicated by hypotension or intolerance. Morphine sulfate has potent analgesic and anxiolytic effects, as well as potentially beneficial hemodynamic effects. For example, it causes vasodilation and may produce modest reductions in heart rate and systolic blood pressure to further reduce myocardial oxygen demand.1 |
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Beta-Adrenergic Blockers decrease the cardiac workload and myocardial oxygen demand. By blocking the effects of catecholamines on cell membrane beta-receptors, which are primarily located on the myocardium, they lower the heart rate and contractility responses that are triggered by chest pain, exertion and other stimuli. They also decrease systolic blood pressure.1 |
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Calcium Antagonists produce vasodilation and decrease myocardial contractility. All drugs in this class have coronary dilatory properties, although they may have different structures with slightly different mechanisms of action. Calcium antagonists may be used to control ongoing or recurrent ischemia-related symptoms in patients who are receiving adequate doses of nitrates and beta blockers, in patients who are unable to tolerate adequate doses of one or both of these agents, or in patients with variant angina. These drugs are also used for the management of hypertension in patients with recurrent unstable angina.1 |
References
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