Hemodynamic and Metabolic Studies on Shock Associated with Bacteremia

Udhoji, Vasant N.; Weil, Max Harry

doi:10.7326/0003-4819-62-5-966

Cited by 83 publications

(16 citation statements)

References 35 publications

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“…Gram-negative bacteriemia produces multiorgan dysfunction, septic shock, and frequently death (1)(2)(3)(4)(5)(6)(7). The pathogenic factors and mechanisms involved in septic shock are still unclear.…”

Section: Introductionmentioning

confidence: 99%

Endotoxin-induced pulmonary dysfunction is prevented by C1-esterase inhibitor.

Guerrero

Velasco²,

Rodriguez³

et al. 1993

J. Clin. Invest.

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In septic shock, hypotension, disseminated intravascular coagulation, and neutrophil activation are related to the activation of the blood coagulation contact system. This study evaluates in dogs the effect of the Cl-esterase inhibitor (C1-INH), a main inhibitor of the blood coagulation contact system, on the cardiovascular and respiratory dysfunction associated with endotoxic shock. Two groups were included: controls, which received Escherichia coli endotoxin, and a C1-INH group in which Cl-INH was infused before E. coli endotoxin administration.In both groups, endotoxin produced hypodynamic shock; however, the decrease in the systolic index and the ventricular systolic work indexes were greater in controls than the C1-INH group. In controls, the arterial 02 partial pressure decreased by 30% and the alveolo-arterial 02 difference increased by 625%, these parameters remained unchanged in the C1-INH group. Hypoxemia was associated with increased intrapulmonary shunt, decreased blood coagulation contact factors, and decreased C3c. In contrast, C1-INH administration prevented endotoxin-induced hypoxemia, the increase in intrapulmonary shunt, and the decrease in blood coagulation contact factors.This study shows that, in dogs with endotoxic shock, pulmonary dysfunction is associated with an activation of the blood coagulation contact phase system. An inhibition of this system by C1-INH prevented the hypoxemia induced by endotoxic shock. (J. Clin. Invest. 1993.91:2754-2760

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Section: Introductionmentioning

confidence: 99%

Endotoxin-induced pulmonary dysfunction is prevented by C1-esterase inhibitor.

Guerrero

Velasco²,

Rodriguez³

et al. 1993

J. Clin. Invest.

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“…One type had a bounding pulse ascribed to a high cardiac output; a second syndrome was characterized by "cold, clammy" skin and a faint pulse and this syndrome was postulated to result from a low cardiac output. This low cardiac output was equated with inadequate heart function and was designated the heart failure or myocardial depression ofseptic shock (4)(5)(6). Because canine endotoxin models produced a low cardiac output, this animal model was felt to be characteristic of the low output syndrome (4).…”

Section: Introductionmentioning

confidence: 99%

A circulating myocardial depressant substance in humans with septic shock. Septic shock patients with a reduced ejection fraction have a circulating factor that depresses in vitro myocardial cell performance.

Parrillo¹,

Burch²,

Shelhamer³

et al. 1985

J. Clin. Invest.

554

180

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We have previously described a subpopulation of patients with septic shock who had a reversible depression of radionuclidedetermined left ventricular ejection fraction (EF). To investigate the mechanism of this myocardial depression, an in vitro model of mammalian myocardial cell performance was established employing primary spontaneously beating rat myocardial cells. The contraction of a single cardiac cell was quantitated by recording the changes in area occupied by the cell during contraction and relaxation. In 20 septic shock patients during the acute phase, the mean left ventricular EF was decreased (mean = 033, normal mean = 0.50), and serum obtained during this acute phase induced a mean (±standard error of the mean) 33±4% decrease in extent and 25±4% decrease in velocity of myocardial cell shortening during contraction (P < 0.001). In contrast, serum obtained from 11 of these same patients before shock (n = 2) or after recovery (n = 9) of the left ventricular EF (mean = 0.50) showed a return toward normal in extent and velocity of shortening (P < 0.001). Sera from 17 critically ill nonseptic patients, from 10 patients with structural heart disease as a cause for a depressed EF, and from 12 healthy laboratory personnel, induced no significant changes in in vitro myocardial cell performance. In 20 patients during the acute phase of septic shock, the decreased EF in vivo demonstrated a significant correlation (r = +0.52, P < 0.01) with a deerease in the extent of myocardial cell shortening in vitro. The quantitative and temporal correlation between the decreased left ventricular EF and this serum myocardial depressant substance argues for a pathophysiologic role for this depressant substance in producing the reversible cardiomyopathy seen during septic shock in humans.

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“…In contrast, the`hyperdynamic' group had larger circulating volumes, had been in shock for shorter periods of time [105], and had tended to survive [116]. This was the pattern seen in prospectively studied patients who became bacteraemic immediately following urological procedures [117,118].…”

Section: Clinical Haemodynamicsmentioning

confidence: 84%

“…However, in 1965, Weil's group described a second group of patients with increased CI and low SVR [105], as did other investigators [106±115].…”

Section: Clinical Haemodynamicsmentioning

confidence: 90%

“…The first group tended to have reduced circulating volumes [105], which as early as 1965 one group attributed to the combination of sepsis and hypovolaemia: in the combined form of hypovolaemia and sepsis, the usual low total peripheral resistance of pure septic shock often may be raised by the added stimulus of hypovolaemia' [110]. This pattern was also associated with acidaemia and death [116].…”

Section: Clinical Haemodynamicsmentioning

confidence: 99%

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