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Altered cardiovascular responsiveness to active tilting in nonalcoholic cirrhosis

1997; Elsevier BV; Volume: 113; Issue: 3 Linguagem: Inglês

10.1016/s0016-5085(97)70184-7

1528-0012

Giacomo Laffi, Giuseppe Barletta, Giulia Villa, Riccarda Del Bene, Donato Riccardi, Piero Ticali, Lorenzo Melani, F Fantini, Paolo Geñtilini,

Hemodynamic Monitoring and Therapy

Background & Aims: The hyperdynamic circulation of hepatosplanchnic compartment, leads to the accumulacirrhosis has been related either to plasma volume tion of ascites.However, recent studies have led to the expansion (increased preload) or peripheral arterial vasuggestion that the increased cardiac output of cirrhosis sodilation (reduced afterload).The aim of this study is mainly caused by plasma volume expansion. 4-8Lewis was to evaluate cardiovascular function in patients et al. 5 showed that patients with cirrhosis and hyperdywith nonalcoholic cirrhosis by echocardiography.Methnamic circulation have higher than normal left ventricuods: Nineteen patients with abnormal sodium handling lar (LV) end-diastolic and end-systolic diameters, a find-(11 sodium excretors and 8 sodium retainers) and 15 ing consistent with an increase in cardiac preload. 9healthy volunteers underwent echocardiographic evalu-Bernardi et al. evaluated systemic hemodynamics of ciration of left ventricular end-diastolic volume index rhotic patients with 8 and without 7 ascites in the supine (LVEDVI) and left ventricular end-systolic volume index and standing positions and found that the hyperdynamic (LVESVI), left ventricular ejection fraction (LVEF), carcirculation of cirrhosis only occurred in the supine posidiac index (CI), mean arterial pressure, and systemic vascular resistance (SVR) during supine resting and tion, suggesting that this syndrome was, at least in part, after 5 minutes of standing.Results: Supine patients caused by the translocation of an expanded blood volume had increased LVEF and CI and reduced LVESVI and from the hepatosplanchnic compartment to the central SVR.LVEDVI was increased only in sodium excretors.area on assumption of the supine position.Standing induced a decrease in LVEDVI in all subjects.The present investigation was aimed at evaluating LV Healthy volunteers maintained cardiovascular homeofunction and systemic hemodynamics in patients with stasis by increasing LVEF and heart rate, whereas circirrhosis, portal hypertension, and different degrees of rhotic patients experienced a decrease in SVI and CI sodium retention during supine rest and after challengdespite marked increments in heart rate, plasma renin ing cardiovascular homeostasis by active tilting.LV volactivity, and plasma norepinephrine level.Conclusions: umes were measured by echocardiography, a reliable In patients with cirrhosis, the increased LVEF and retechnique for this purpose in patients with unaltered LV duced LVESVI while in a supine position point at regeometry, 10,11 as is the case in patients with liver cirrhoduced afterload as an important determinant of the hyperdynamic circulation.Evidence of an increased presis.To better evaluate LV function, we also analyzed load secondary to increased blood volume, indicated by arterial elastance (Ea), an index that describes the interaca high LVEDVI and increased plasma atrial natriuretic tions between LV function and aortic input impedance, peptide levels, was found only in sodium excretors.taking into account the pulsatile nature of pressure andThe altered response to active tilt in cirrhotic patients flow. 12,13 suggests an impaired myocardial contractility.Because alcohol may have a direct toxic effect on cardiac muscle, leading to the so-called alcoholic cardiomyopathy, [14][15][16] the present investigation was performed in P atients with cirrhosis and portal hypertension even- tually develop a hyperdynamic circulation, with in-Abbreviations used in this paper: ANP, atrial natriuretic peptide; creased blood volume and cardiac output and reduced CI, cardiac index; Ea, arterial elastance; LV, left ventricular; LVEDVI, systemic vascular resistance (SVR). 1,2According to the left ventricular end-diastolic volume index; LVEF, left ventricular ejecperipheral arterial vasodilation hypothesis, 3 progressive tion fraction; LVESVI, left ventricular end-systolic volume index; MAP, mean arterial pressure; PRA, plasma renin activity; SVI, stroke vol-arterial vasodilation of unknown cause activates arterial ume index; SVR, systemic vascular resistance; UNaV, urinary sodium baroreceptors, initiating sodium retention, which in turn excretion.increases blood volume and cardiac output and, in the