Chapter 21 Marini Acute Coronary Syndromes

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SECTION II • Medical and Surgical Crises

pain of coronary thrombosis, calcium channel antagonists have not improved survival in sev- eral clinical trials; in at least one study, short- acting nifedipine adversely affected survival. Therefore, the routine use of calcium channel antagonists cannot be advocated. In the event of severe hypertension complicating AMI or UA, however, diltiazem or amlodipine may be used along with the use of ACEI agents and β -blockers. 9. Oral Anticoagulants: Chronic systemic anti- coagulation is indicated in those at risk for sys- temic or venous thromboembolism, like those with large anterior MI with akinetic apex, severely reduced LV function, AF, and pres- ence of LV thrombus on echocardiography (see Chapter 30). In patients with large anterior MI, oral anticoagulants (warfarin or newer alterna- tives) may be continued for 3 to 6 months. General Support of the ACS Patient Close monitoring for electrical and mechanical complications and direct control of pain and stress are basic measures applied to all MI victims. A liq- uid diet usually is provided for 24 hours after infarc- tion. Temperature extremes of foods are avoided in an attempt to minimize the risk of arrhythmias. Sedation and stool softeners to prevent anxiety and straining also may decrease the risk of arrhythmias. When systemic anticoagulation is not performed, subcutaneous heparin (7,500 units SQ b.i.d.) or enoxaparin (40 mg SQ, once daily) is indicated for the prevention of deep venous thrombosis for patients with MI on strict bed rest. Bed rest is mandatory during the initial day of management. However, once adequate reperfusion and stability are assured, early ambulation is advisable. Cardiac rehabilitation personnel should make an initial eval- uation, preferably soon after reperfusion therapies. Despite numerous large-scale clinical trials, several commonly used therapies remain of unproven ben- efit (Tables 21-6 and 21-7).

Outcome of Myocardial Infarction Overall, MI carries a mortality risk of approximately 15% to 20%. Most deaths occur within the first hour or two of infarction and are the result of pre- hospital ventricular arrhythmias, which, to a large degree, cannot be prevented. The in-hospital death rate is around 5% to 9%, which has improved signifi- cantly over the last 4 decades, because of advances in reperfusion therapies. In contrast to prehospital mortality, most deaths in patients reaching the hos- pital occur from refractory pump failure. Therefore, survival is maximized by limiting infarct size and by promptly treating mechanical and electrical compli- cations. Survival is best predicted by the patient’s age, preinfarction physical fitness, degree of left ventricular impairment (a reflection of the mass of lost myocardium), and comorbid conditions. COMPLICATIONS OF MYOCARDIAL INFARCTION Half of all patients sustaining MI have no signifi- cant complications. Of those with a complicated course, most serious events occur within the first Oral ACEI for high-risk patients Begin risk factor modification DURING HOSPITALIZATION Consider starting ACEI and β -blocker if not started on admission 6 WEEKS POST-DISCHARGE Discontinue ACEI for low-risk patients with ejection fraction >40%, without CHF 1-YEAR POST-DISCHARGE Discontinue β -blocker if low risk and no other indications exist for its use INDEFINITELY Continue aspirin and risk factor modification Table 21-7.  Therapy of Acute MI ACUTE THERAPY Aspirin, 325 mg p.o. Sublingual TNG p.r.n. for pain Morphine sulfate, 2–10 mg IV p.r.n. for pain Oxygen 2–3 L by nasal cannula IV β -blocker Consider thrombolytic therapy, PTCA Continue ECG monitoring, daily aspirin, and β -blocker DAY 1

Table 21-6.  Unproven Interventions in Acute MI Antiarrhythmic agents

Calcium channel antagonists Magnesium sulfate therapy