Hemodynamic and metabolic studies on shock associated with bacteremia

Haemodynamic studies in shock associated with infection.

“…The cardiac output in patients with shock associated with infection may be normal (Gilbert et al, 1955), low (Udhoji et al, 1963), or high (Udhoji and Weil, 1965). This disturbing discrepancy has been explained by two mechanisms.…”

“…The hemodynamic alterations occurring in man when infection is associated with shock were investigated originally by Gilbert et al (1955). Similar investigations conducted by Udhoji et al (1963), Udhoji and Weil (1965), Cohn and Luria (1964), and Wilson, Jablonski, and Thal (1964) have contributed to our knowledge of the basic mechanisms producing shock, but further evaluations of the efficacy of therapeutic measures used to combat shock associated with sepsis are necessary.…”

“…had hepatic cirrhosis. Since patients with cirrhosis have increased basal cardiac outputs (Murray, Dawson, and Sherlock, 1958), it is probable that this difference will become recognizable in a larger series of patients and should be taken into account in evaluating other causes for differences in basal cardiac outputs (Udhoji and Weil, 1965).…”

Consequences of acute renal failure relevant to hepatic failure

“…The mechanisms involved include impaired cell-mediated immunity, phagocytic activity and reticulo-endothelial function. Life threatening infections are also a common feature of patients with cirrhosis and fulminant hepatic failure (Udhoji and Weil, 1965;Mummery, Bradley and Jeffries, 1971) so again the effects of hepatic and renal impairment are likely to be additive.…”

Circulatory patterns in clinical shock

“…Hepatic cirrhosis is said to modify the pattern in this way (Udhoji & Weil, 1965), but in my experience most cases of this sort are due to infection and do not have cirrhosis. Alterations in oxygen consumption have led to the suggestion that tissue perfusion is reduced in the hyperdynamic patient, despite the high cardiac output and low peripheral vascular resistance, because of arterio-venous shunts in the micro-circulation (Siegel, Greenspan & del Guercio, 1967).…”