Abstract
Patients who have been restricted to bed rest following myocardial infarction or cardiac artery bypass grafting routinely develop orthostatic hypotension or frank syncope during their initial attempt at ambulation. Orthostatic intolerance and reduced exercise capacity secondary to bed rest is accompanied by reduced circulating blood volume, lower cardiac output, attenuated cardiac baroreflex responses, and limited baroreflex-mediated vasoconstrictive reserve. Data from the literature provides compelling evidence that the deconditioning effects of bed rest are independent of the disease state and associated with the absence of regular exposure to orthostatic stress. When orthostatic stress is repeatedly increased during bed rest by application of reverse gradient garments, lower body negative pressure, or standing upright, improved orthostatic and exercise performances are associated with restoration of circulating blood volume, maintenance of cardiac output, accentuated cardiac baroreflex responsiveness, and enhanced baroreflex-mediated vasoconstrictive reserve. The available data indicate that the inability of cardiovascular mechanisms to adequately compensate for the orthostatic stress induced by the upright posture is the most important factor limiting functional performance after bed rest, particularly in middle-aged men. Intermittent exposure to orthostatic stress during the bed rest stage of hospital convalescence and recovery phase at home may obviate much of the deterioration in cardiovascular performance that follows myocardial infarction.