Cardiovascular and neuroendocrine responses to water immersion in compensated heart failure

The hypothesis was tested that cardiovascular and neuroendocrine (norepinep hrine, renin, and vasopressin) responses to central blood volume expansion are blunted in compensated heart failure (HF). Nine HF patients [New York H eart Association class II-III, ejection fraction 5 0.28 +/- 0.02 (SE)] and 10 age-matched controls (ejection fraction = 0.68 +/- 0.03) underwent 30 mi n of thermoneutral (34.7 +/- 0.02 degrees C) water immersion (WI) to the xi phoid process. WI increased (P < 0.05) central venous pressure by 3.7 +/- 0 .6 and 3.2 +/- 0.4 mmHg and stroke volume index by 12.2 +/- 2.1 and 7.2 +/- 2.1 ml.beat(-1).m(-2) in controls and HF patients, respectively. During WI , systemic vascular resistance decreased (P < 0.05) similarly by 365 +/- 66 and 582 +/- 227 dyn.s(-1).cm(-5) in controls and HF patients, respectively . Forearm subcutaneous vascular resistance decreased by 19 +/- 7% (P < 0.05 ) in controls but did not change in HF patients. Heart rate decreased less during WI in HF patients, whereas release of norepinephrine, renin, and vas opressin was suppressed similarly in the two groups. We suggest that reflex control of forearm vascular beds and heart rate is blunted in compensated HF but that baroreflex-mediated systemic vasodilatation and neuroendocrine responses to central blood volume expansion are preserved.