IN CIRRHOTIC patients, cardiac contractility has been extensively documented to be abnormal.1 When cirrhotic patients are challenged by pharmacological or physiological stress, ventricular hyporesponsiveness is revealed.2 This phenomenon has been termed “cirrhotic cardiomyopathy.” The initial studies in the early 1950s documented the existence of hyperdynamic circulation in cirrhosis, manifested by increased cardiac output and reduced systemic vascular resistance. Some may question the clinical significance of this entity because overt heart failure is not generally a prominent feature of cirrhosis. However, it appears that cirrhotic cardiomyopathy is usually clinically mild or latent. This is likely because the marked peripheral vasodilatation in cirrhosis significantly reduces the afterload of the ventricle, thus in effect “autotreating” the patient and masking any severe manifestation of heart failure. The presence of cirrhotic cardiomyopathy may become unmasked by certain treatment interventions, including liver transplantation, surgical portosystemic shunt, and transjugular intrahepatic portosystemic stent shunts (TIPSS). These procedures induce a significant stress on the heart: the transplantation by multiple mechanisms and the shunts by rapidly shunting a large volume of venous return back to the heart. Studies showing increased left ventricular dimensions in cirrhotic patients were originally interpreted to be secondary to increased circulating blood volume.3 Indeed, whether the central blood volume (ie, blood volume in the heart, lung, and great vessels) is increased in cirrhosis remains controversial, because some investigators have found decreased central blood volume.4 Therefore we analyzed cardiac index (CI), central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), intrathoracic blood volume index (ITBVI), total blood volume index (TBVI), and extravascular lung water (EVLWI) in cirrhotic patients before and after orthotopic liver transplantation (OLT) to evaluate intravascular blood volume status.
Intravascular blood volume in cirrhotic patients / Della Rocca, G.; Costa, M. G.; Coccia, C.; Pompei, L.; Ruberto, F.; Rossi, Massimo; Pietropaoli, Paolo; Cortesini, R.. - In: TRANSPLANTATION PROCEEDINGS. - ISSN 0041-1345. - 33:1-2(2001), pp. 1405-1407. (Intervento presentato al convegno 18th World Congress of the Transplantation-Society tenutosi a ROME, ITALY nel AUG 27-SEP 01, 2000) [10.1016/s0041-1345(00)02529-x].
Intravascular blood volume in cirrhotic patients
F. Ruberto;ROSSI, MASSIMO;PIETROPAOLI, Paolo;
2001
Abstract
IN CIRRHOTIC patients, cardiac contractility has been extensively documented to be abnormal.1 When cirrhotic patients are challenged by pharmacological or physiological stress, ventricular hyporesponsiveness is revealed.2 This phenomenon has been termed “cirrhotic cardiomyopathy.” The initial studies in the early 1950s documented the existence of hyperdynamic circulation in cirrhosis, manifested by increased cardiac output and reduced systemic vascular resistance. Some may question the clinical significance of this entity because overt heart failure is not generally a prominent feature of cirrhosis. However, it appears that cirrhotic cardiomyopathy is usually clinically mild or latent. This is likely because the marked peripheral vasodilatation in cirrhosis significantly reduces the afterload of the ventricle, thus in effect “autotreating” the patient and masking any severe manifestation of heart failure. The presence of cirrhotic cardiomyopathy may become unmasked by certain treatment interventions, including liver transplantation, surgical portosystemic shunt, and transjugular intrahepatic portosystemic stent shunts (TIPSS). These procedures induce a significant stress on the heart: the transplantation by multiple mechanisms and the shunts by rapidly shunting a large volume of venous return back to the heart. Studies showing increased left ventricular dimensions in cirrhotic patients were originally interpreted to be secondary to increased circulating blood volume.3 Indeed, whether the central blood volume (ie, blood volume in the heart, lung, and great vessels) is increased in cirrhosis remains controversial, because some investigators have found decreased central blood volume.4 Therefore we analyzed cardiac index (CI), central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), intrathoracic blood volume index (ITBVI), total blood volume index (TBVI), and extravascular lung water (EVLWI) in cirrhotic patients before and after orthotopic liver transplantation (OLT) to evaluate intravascular blood volume status.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
