This effect is difficult to evaluate because of the complex interactions between the forces generated by elevated intrathoracic pressure and the autoregulatory responses of the hepatic vasculature. Although understanding of hepatic circulatory physiology has considerably increased, mechanisms involved in the regulation of liver blood flow have yet to be fully elucidated.
Mechanical ventilation with positive end-expiratory pressure (PEEP) decreases cardiac output by reducing venous return. The liver, which is an important regulator of venous return, plays an essential role in this reponse. Early studies reported that continuous positive-pressure ventilation decreased total hepatic blood flow mainly by reductions in portal venous flow. Recent experimental studies in different animal models ( M.§tu,s.9h§k...,§.0.d P.!D§ky..,198Z, M..at,u.s.c,h..a..k,.a..n.d P.,!0§kY...1989; .§.d.e..QZ.a...,§L§L.
1995) have contributed to the understanding of the mechanisms by which positive-pressure ventilation and PEEP alter the characteristics of hepatic pressures and flows (Fig 1).
Fig. 1 Schematic representation of the forces interacting to determine the characteristics of hepatic blood flow (Q L) during phasic increases in intrathoracic pressure during positive-pressure ventilation. Positive-pressure ventilation can alter Q L and its distribution by (a) decreasing cardiac output and thus hepatic arterial flow (Q ha) and portal venous flow (Qpv), (b) diaphragmatic compression, which increases intrahepatic closing pressure ( Pc) and creates a postsinusoidal flow-limiting segment, (c) transmission of a peak-inspiratory right atrial pressure wave ( Pra) towards the liver, decreasing the pressure gradient for Q L, and (d) increasing abdominal pressure (Pab), which influences transmural portal venous pressure ( Ppv) and Pc. Pha, hepatic arterial pressure; Rha, hepatic arterial resistance; Rpv, portal venous resistance; Ps, sinusoidal pressure; Phv, hepatic venous pressure; Qvc, inferior vena caval flow. (Reproduced with permission from M.§iu§cha.k..,§nd..,PiD.s.ky..,il989)..)
PEEP decreases both hepatic arterial and portal flow in parallel with the reduction in cardiac output ( Brienza ef a/ 1995). Increased intra-abdominal pressure will decrease transmural pressure in the portal vein and the upstream driving pressure for portal inflow. An increase in right atrial pressure, which represents the effective back-pressure to portal vein flow when the portosinusoidal waterfall is exceeded, decreases the downstream pressure gradient for hepatic venous outflow. Moreover, diaphragmatic descent, which occurs during mechanical ventilation with PEEP, produces mechanical compression of the liver surface, reduction in the diameter and number of perfused sinusoids, and alterations in filtration rate. This explains the significant increase in liver venous resistance observed during ventilation with PEEP, which results in a further decrease in portal flow and total venous return.
The fall in hepatic artery flow is also associated with an increase in back-pressure, consistent with an increase in surrounding tissue pressure. Arterial resistance is not significantly increased, probably because of an intact compensatory hepatic arterial buffer response ( Brienza.efa/: 1995).
Volume expansion, which is commonly used to attenuate the hemodynamic effects of PEEP, restores total cardiac output and liver blood flow to pre-PEEP levels
(Matuschak and Pin.s.ky„.19§Z, 1989). BlieDZaeLa/ (1995) reported that volume expansion during ventilation with PEEP significantly decreased portal venous resistance (owing to the distension of the portal vein by transmural pressure) and restored portal vein flow. However, hepatic artery flow was incompletely restored.
Altered hepatic function, producing a decrease in hepatocyte extraction and intrinsic clearance abilities, impairment of hepatic storage, and reduced biliary excretion, has been observed during mechanical ventilation with and without PEEP. This was not confirmed by Matuschak etal, (1987) who showed that addition of PEEP did not influence indocyanide green extraction and clearance. They postulated that despite a decrease in hepatic blood flow, the increase in hepatic back-pressure may increase trans-sinusoidal passage of diffusable substances into the space of Disse and enhance their uptake. However, it is conceivable that the hemodynamic consequences of PEEP could induce liver dysfunction in the presence of hypoxemia, hypotension, or any other condition in which the hepatic arterial buffer response is abolished and oxygen supply to the liver is compromised.
Significant falls in mesenteric blood flow may occur during use of PEEP; this is independent of raised intra-abdominal pressure and cannot be reversed by volume expansion, although it may be reversible by early gut feeding. The role of drugs with b-adrenergic properties, particularly dopexamine, which may compensate for the decrease in splanchnic and portal inflow induced by PEEP should be further investigated. The effect of PEEP-induced hemodynamic changes on the intrinsic metabolic regulation of hepatic circulation by endothelial and Kuppfer cells in steady state, shock, sepsis, and multiple organ dysfunction also remains to be evaluated.
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