The hemodynamic status of preascitic cirrhosis: An evaluation under steady-state conditions and after postural change
✍ Scribed by Prof. Mauro Bernardi; Claudio de Marco; Franco Trevisani; Carlo de Collibus; Lorenzo Fornalé; Mario Baraldini; Pietro Andreone; Carmela Cursaro; Fabio Zacá; Amedeo Ligabue; Giovanni Gasbarrini
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 732 KB
- Volume
- 16
- Category
- Article
- ISSN
- 0270-9139
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✦ Synopsis
To assew the hemodynamic status of patients with compensated cirrhosis, mean arterial pressure, cardiac index and peripheral vascular resistance and markers of central (plasma concentrations of atrial natriuretic factor) and arterial volemia (plasma norepinephrine concentration, plasma renin activity) were studied in 10 patients and 10 healthy control subjects under steady-state conditions (after 2 hr of standing) and after assumption of the supine position (30,60, and 120 min). After standing, neither hemodynamice nor markers of effective volemia differed sigd h a n t l y between controls and patients. By evaluating the areas under the curve during the 2 hr of supine poeture, the increase in cardiac output and plasma natriumtic factor and the decrease in peripheral vaacular resistance were greater in patients (2.69 f 0.43 [SX.M.] I J m W , 32.8 f 7.2 pg/ml/hr -1,103 * 248.4 dyn sec/cm6/hr, respectively) than in controle (0.53 f 0.24 L/min/hr, p = 0.005; 17.4 f 4.7
pg/ml/hr, p = 0.006; -266.5 2 206.2 dynsec/cm5/hr, p = 0.02). The declines in heart rate, p!asma norepinephrine concentration and plasma re-activity did not differ significantly. Mean arterial pressure did not significantly change. Our results suggest that during periods of upright posture, cirrhotic patients in the preascitic stage, who are known to have espanded blood volume, compensate for dilatation of the splanchuic vascular bed through total hypervolemia. The latter becomes excessive during recumbency, leading to supernormal increases in venous return, central volemia and cardiac index. The decline in peripheral vascular resistance appears to be a compensatory mechanism to maintain steady arterial blood pressure. Thus increased cardiac index and reduced peripheral vascular resistance in recumbent compen-