Effect of hemodialysis on left ventricular function. Dissociation of changes in filling volume and in contractile state.

Nixon, J.V.; Mitchell, Jere H.; McPhaul, John J.; Henrich, William L.

doi:10.1172/jci110779

Cited by 100 publications

(45 citation statements)

References 37 publications

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“…1). A lack of change in mean arterial blood pressure, however, was also noted in a recent study [19] in which intraarterial blood pressure was monitored during regular dialysis. In this study weight loss during dialysis was comparable to that observed in our patients (2.3 and 2.5 kg, respectively).…”

Section: Discussionmentioning

confidence: 63%

Delayed Hypotensive Response to Dialysis in Hypertensive Patients with End-Stage Renal Disease

1986

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This study was designed to determine the ambulatory arterial blood pressure profile in hypertensive patients with end-stage renal disease during and following hemodialysis. Blood pressure was noninvasively monitored at 15-min intervals for 24 h using a fully automatic portable recorder, while the 10 patients studied followed their customary activities and were not receiving any antihypertensive medications. Prior to dialysis, the blood pressure was 179 ± 7.0/101 ± 3.7 mm Hg. After 4 h of dialysis, the systolic blood pressure did not change, while the diastolic blood pressure fell only slightly (178 ± 4.2/94 ± 2.4 mm Hg). After dialysis was completed, a progressive fall in both systolic and diastolic blood pressures was observed reaching the lowest value in the 5th h after dialysis (146 ± 5.5/75 ± 3.2 mm Hg). Thereafter, the fall in blood pressure was sustained during sleep (147 ± 1.7/77 ± 0.9 mm Hg) and during routine daily activities (147 ± 2.0/78 ± 1.0 mm Hg). The delayed fall in blood pressure was observed in patients in whom the plasma renin activity was elevated (8.4 ± 2.4 ng/ml/h) and in patients in whom the plasma renin activity was low or normal (0.9 ± 0.2 ng/ml/h). Our data suggest that during dialysis vasopressor mechanisms are activated to sustain blood pressure and that following dialysis such mechanisms are attenuated allowing the blood pressure to fall towards normal levels. The delayed fall in blood pressure documented by this study indicates that in many hypertensive patients with end-stage renal disease antihypertensive drug therapy is not required the day after dialysis.

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Section: Discussionmentioning

confidence: 63%

Delayed Hypotensive Response to Dialysis in Hypertensive Patients with End-Stage Renal Disease

1986

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“…Previous echocardiographic studies in patients have demonstrated that hemodialysis causes both decreased ventricular chamber size and increased ventricular contractility (40), which are the necessary conditions for triggering paradoxical activation of ventricular mechanoreceptor afferents. Our echocardiographic demonstration that a marked reduction in left ventricular end-systolic dimension (approaching cavity obliteration) during hemodialysis preceded, rather than followed, the onset of vasodepressor syncope is consistent with this ventricular afferent hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Paradoxical withdrawal of reflex vasoconstriction as a cause of hemodialysis-induced hypotension.

et al. 1992

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Acute hypotension is an important complication of hemodialysis, but the underlying mechanisms remain poorly understood. Because hemorrhage-induced hypovolemia can trigger a sudden decrease in sympathetic activity resulting in bradycardia and vasodilation, we hypothesized that hemodialysis-induced hypovolemia also can trigger the same type of vasodepressor reaction, which would exacerbate the volume-dependent fall in blood pressure. We therefore measured blood pressure, vascular resistance, and sympathetic nerve activity (intraneural microelectrodes) during sessions of maintenance hemodialysis in 7 patients with and 16 patients without a history of hemodialysis-induced hypotension. During hemodialysis, blood pressure at first remained unchanged as calf resistance increased in both hypotension-resistant (from 37±4 to 49±5 U, P < 0.05) and hypotension-prone (from 42±6 to 66±12 U, P < 0.05) patients; sympathetic activity increased comparably in the subset of patients in whom it could be measured. With continued hemodialysis, calf resistance and sympathetic activity increased further in the hypotension-resistant patients, but in the hypotensionprone patients the precipitous decrease in blood pressure was accompanied by decreases in sympathetic activity, vascular resistance, and heart rate as well as symptoms of vasodepressor syncope. On an interdialysis day, both groups of patients increased vascular resistance normally during unloading ofcardiopulmonary baroreceptors with lower body negative pressure and increased heart rate normally during unloading of arterial baroreceptors with infusion of nitroprusside. These findings indicate that in a group of hemodialysis patients without diabetes or other conditions known to impair autonomic reflexes, hemodialysis-induced hypotension is not caused by chronic uremic impairment in arterial or cardiopulmonary baroreflexes but rather by acute, paradoxical withdrawal of sympathetic vasoconstrictor drive producing vasodepressor syncope. (J. Clin.

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“…For example, in patients with low ejection fraction, a significant improvement was seen after hemodialysis (28). Henrich and colleagues were able to dissociate changes in cardiac preload and contractile state, and showed that isovolumic hemodialysis produced an upward shift ofthe left ventricular function curve (29). This improvement appeared to be related to increased plasma calcium, rather than to correction of acidosis or removal ofuremic toxins (30).…”

Section: Discussionmentioning

confidence: 99%

Impairment of cardiac function and energetics in experimental renal failure.

Raine¹,

Seymour²,

Roberts³

et al. 1993

J. Clin. Invest.

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Cardiac function and energetics in experimental renal failure in the rat (5/6 nephrectomy) have been investigated by means of an isolated perfused working heart preparation and an isometric Langendorff preparation using 31P nuclear magnetic resonance (31P NMR). 4 wk after nephrectomy cardiac output of isolated hearts perfused with Krebs-Henseleit buffer was significantly lower (P < 0.0001 ) at all levels of preload and afterload in the renal failure groups than in the pair-fed sham operated control group. In control hearts, cardiac output increased with increases in perfusate calcium from 0.73 to 5.61 mmol/ liter whereas uremic hearts failed in high calcium perfusate.Collection of 31p NMR spectra from hearts of renal failure and control animals during 30 min normoxic Langendorff perfusion showed that basal phosphocreatine was reduced by 32% to 4.7 ,mol/g wet wt (P < 0.01) and the phosphocreatine to ATP ratio was reduced by 32% (P < 0.01) in uremic hearts. During low flow ischemia, there was a substantial decrease in phosphocreatine in the uremic hearts and an accompanying marked increase in release of inosine into the coronary effluent (14.9 vs 6.1 jsM, P < 0.01).We conclude that cardiac function is impaired in experimental renal failure, in association with abnormal cardiac energetics and increased susceptibility to ischemic damage. Disordered myocardial calcium utilization may contribute to these derangements. (J. Clin. Invest.

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Effect of hemodialysis on left ventricular function. Dissociation of changes in filling volume and in contractile state.

Cited by 100 publications

References 37 publications

Delayed Hypotensive Response to Dialysis in Hypertensive Patients with End-Stage Renal Disease

Delayed Hypotensive Response to Dialysis in Hypertensive Patients with End-Stage Renal Disease

Paradoxical withdrawal of reflex vasoconstriction as a cause of hemodialysis-induced hypotension.

Impairment of cardiac function and energetics in experimental renal failure.

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