Heart transplantation is an established treatment for end stage heart failure. In addition to increased life expectancy, heart transplant recipients report a remarkable improvement in symptoms and functional capacity. Exercise performance following heart transplantation, however, remains impaired even in the absence of exertional symptoms. We have assessed the response to exercise in 47 patients with cardiac failure prior to and then at yearly intervals to five years post transplantation. All patients performed incremental symptom limited exercise tests during which minute ventilation (V'E), oxygen consumption (V'O2) and carbon dioxide production (V'CO2) and heart rate (HR) were measured. Ventilatory response (V'E/V'CO2), anaerobic threshold (V'O2 AT %predicted) and heart rate response (HR/VO2) were calculated. The dead space to tidal volume ratio (VD/VT) and alveolar-arterial oxygen gradient (A-aO2) were computed from transcutaneous monitoring. Despite substantial improvement in subjective functional capacity, heart transplant recipients continue to have limited exercise performance [Maximal V'O2% predicted pre-transplant 41.3 (2.2); 1 year 48.6 (1.7), p <0.001: V'O2 AT% 31.5 (1.1); 1 year 35.6 (1.0); respectively p<0.05]. The maximal oxygen uptake continued to improve at two years post-transplant but, thereafter, there was no further significant change at up to 5 years post transplant [50.9 (1.5)]. At one year post-transplantation peak HR [65.2 (0.9) vs 79.1(1.4)] and the HR/VO2 response [24.0(1.8) vs 79.6(4.2)] were significantly reduced compared to pre-transplant values. The heart rate response remained lower compared to predicted at 5 years post-transplant although there was a significant increase compared to one year post-transplant (32.9 vs 24.0mls/bt). There was a weak but significant relationship between maximal VO2 and peak HR (0.39, p<0.05) and HR/VO2 (r= 0.37, p<0.05) at one year post-transplant. Prior to transplantation the ventilatory response to exercise was elevated [V'E/V'CO2 45.6 (2.5)] and decreased significantly following transplantation [1 yr 34.1 (1.3), respectively p<0.001]. In addition, despite significant improvement in VD/VT after transplantation, it remained higher than normal [Pre VD/VT at maximum exercise 0.35 (0.02); 1 yr 0.31 (0.02); p<0.05]. There was a further fall in the VE/VCO2 and VD/VT at two years post-transplantation with no further change at up to 5 years post transplantation [VE/VCO2 32.0 (1.0); VD/VT 0.29 (0.01)]. Although cardiac output is markedly improved after transplantation, due to chronotropic incompetence associated with denervation, its response remains subnormal and this may explain the residual abnormalities of ventilatory and gas exchange responses to exercise following transplantation.
with bicarbonate fluid (p<005). Mean arterial blood pressure fell at a mean rate of 3 9 (0 90) mm Hg/hour during dialysis with acetate fluid (p<001) and 1-4 (0 52) mm Hg/hour during dialysis with bicarbonate fluid (p<005). The rate of fall was significantly greater during dialysis with acetate than with bicarbonate fluid (p<0 02). The index of venous tone rose at a mean rate of 0-23 (0-05) ml/dl over 40 mm Hg/hour during dialysis with acetate fluid (p<001) and 0-20 (0 05) ml/dl over 40 mm Hg/hour during dialysis with bicarbonate fluid (p<001). Vascular resistance in the forearm increased at a mean rate of [3][4][5][6] (1-12) units/hour during dialysis with acetate fluid (p<002) and 4-5 (1-48) units/hour during dialysis with bicarbonate fluid (p<0 01). There were no significant differences in the changes in venous tone or vascular resistance between dialysis with acetate and bicarbonate fluid. DiscussionThe results of this study point to important abnormalities of the control of the peripheral circulation during dialysis that may contribute to the development of hypotension. The normal responses to a reduction in plasma volume such as that occurring during dialysis are venoconstriction and an increase in peripheral vascular resistance.7 Both of these mechanisms help to prevent a fall in blood pressure. The venoconstriction compensates for the reduced central plasma volume and maintains cardiac filling pressures and thereby cardiac output. The increase in peripheral vascular resistance helps maintain blood pressure despite a fall in cardiac output. Our patients showed a normal increase in peripheral vascular resistance during dialysis, but paradoxically their veins dilated. This venodilatation would accentuate the fall in central blood volume and lead to a fall in cardiac filling pressures and cardiac output and then to hypotension. Evidence supporting this as the mechanism of hypotension during dialysis is that an infusion of fluid often corrects the hypotension.The reason for the abnormal dilatation of the venous bed is unclear. It occurred equally during both types of dialysis and therefore is not due to the vasodilating properties of acetate. It does not seem to be due to autonomic dysfunction as there were appropriate changes in heart rate and peripheral resistance during dialysis, and the veins actively dilated. It is more likely that the correction of the metabolic derangements of renal failure withdrew a stimulus to venoconstriction. Whatever the mechanism, simple measures-for example, wearing support stockings-aimed at reducing pooling of blood in peripheral veins may prevent hypotension induced by dialysis.
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