In healthy patients, post-ECT changes of blood pressure or heart rate and rhythm are transient and safely managed. In the general population, the estimated mortality with ECT is about 1 in 10 000 patients or 3 to 4 in 100 000 treatments (150), mostly due to cardiac complications. Anesthesia effects, muscle relaxants, and hypoxia often contribute to the risk factors for mortality.

ECT has a biphasic effect on the cardiovascular system. Initially, coincident with the tonic phase, apnea, and a forced expiration-induced Valsalva effect, there is a marked parasympathetic discharge. The increased vagal tone may cause profound bradycardia, hypotension, and risk for sinus arrest or arrythmias. This vagal effect, including excessive oral secretions, may be attenuated or blocked by atropine or glycopyrrolate pretreatment. Subconvulsive stimuli (missed attempts at inducing seizures) may result in excess vagal outflow, which if not countered by seizure-induced sympathetic activation, may precipitate severe and life-threatening bradyarrythmias and hypotension. Using suprathreshold stimuli and pretreatment with anticholinergic medication to prevent such complications should be considered in high-risk patients (147).

This initial phase is followed by sympathetic discharge, causing a 15-fold increase in plasma epinephrine within seconds of the electrical stimulus (151), with the opposite effect. It leads to increase in cardiac output, systemic vascular resistance, hypertension, and tachyarrythmias, thus increasing myocardial oxygen demand. Administering short-acting beta blockers, such as esmolol or labetolol, may attenuate this sympathetic effect. The “rate-pressure product index” (the product of the heart rate and systolic blood pressure) (152) can be used to predict cardiac ischemia, which may occur when the index is over 20 000 (153). Fortunately, the plasma half-life of norepinephrine is brief, and its effects are transient during ECT, but it can lead to myocardial infarction (MI) or intracerebral hemorrhage in vulnerable, often elderly, patients with known risk factors (154).

A controlled study (155) found that preexisting disease predicted the type of cardiac complication. The severe cardiac patients were defined by an ejection fraction less than 50%, a QRS interval of greater than 100 ms, or 10 or more extrasystoles. Patients with preexisting ischemic disease and conduction disorders were at risk for ischemia and arrhythmias, respectively. Despite having 8 major and 14 minor cardiac complications among 40 patients, there were no deaths, and 38 of the 40 were able to complete the ECT course. Authors concluded that with close monitoring, ECT could be given with relative safety to patients with severe cardiovascular disease. A retrospective study of 80 patients who were divided according to their degree of cardiac risk found the cardiac group to be more prone to developing minor but not major complications, compared with case-control subjects, with no deaths or permanent cardiac morbidity during ECT (156). Although these studies suggest a higher cardiac risk associated with ECT in patients with cardiovascular disease, ECT should not be dismissed as an option, because most patients in both trials were able to complete the course of treatment (157).

Recent MI is a risk for reinfarction during ECT (158). Although not studied objectively, it is suggested that after an MI, a 3-month interval be allowed to lapse prior to ECT (147). The clinical decision when to administer ECT after an MI, however, is based on its severity and the time lapsed since its occurrence, as well as on other effective treatment options available for the psychiatric condition. Other significant cardiovascular risk factors that must be assessed include uncompensated congestive heart failure, severe valvular disease, unstable angina, uncontrolled hypertension, fragile vascular aneurysms, and clinically significant cardiac arrythmias (7).

A thorough medical evaluation is critical prior to considering ECT for high-risk cardiac patients (158).