Hemodynamic Measurements in Septic Shock

Wilson, Robert F.; Thal, Alan P.; Kindling, Paul H.; Grifka, Thomas J.; Ackerman, Edward S.

doi:10.1001/archsurg.1965.01320130123014

Cited by 134 publications

(30 citation statements)

References 12 publications

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“…Because canine endotoxin models produced a low cardiac output, this animal model was felt to be characteristic of the low output syndrome (4). However, subsequent studies demonstrated unequivocally that most patients had a normal or high cardiac output in the initial phases ofseptic shock (7)(8)(9)(10)(11)(12)(13)(14)(15). Thus, ifmyocardial depression was indeed a part of septic shock in humans, a low cardiac output was not a sensitive reflection of cardiac dysfunction.…”

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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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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“…Recent studies of human septic shock have shown clearly that the most common initial cardiovascular pattern consists of a high cardiac index (CI),' a decreased systemic vascular resistance index (SVRI), and a normal or low measure of preload, most commonly expressed clinically as a decreased pulmonary capillary wedge pressure (PCWP) (7)(8)(9)(10)(11)(12)(13)(14)(15). In a recent evaluation of septic shock patients (16), these hemodynamic parameters were further defined by performing simultaneous measurements of radionuclide-gated blood pool scans along with the intravascular catheter-derived hemodynamic parameters.…”

Section: Introductionmentioning

confidence: 99%

Gram-negative bacteremia produces both severe systolic and diastolic cardiac dysfunction in a canine model that simulates human septic shock.

Natanson¹,

Fink²,

Ballantyne³

et al. 1986

J. Clin. Invest.

243

111

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A canine sepsis model that simulates the human cardiovascular response to septic shock was produced in 10 conscious unsedated dogs by implanting an Eschichia coli-infected clot into the peritoneum, resulting in bacteremia. By employing serial, simultaneous measurements of radionuclide scan-determined left ventricular (LV) ejection fraction (EF) and thermodilution cardiac index (CI), the end-diastolic volume index (EDVI) was calculated (EDVI = stroke volume index + EF). By using three different methods of quantifying serial ventricular performance (EF, shifts in the Starling ventricular function curve using EDVI vs. stroke work index, and the ventricular function curve response to volume infusion), this study provides evidence (P < 0.01) that septic shock produces a profound, but reversible, decrease in systolic ventricular performance. This decreased performance was not seen in controls and was associated with ventricular dilatation (P < 0.01); the latter response was dependent on an adequate volume infusion. Further studies of EDVI and pulmonary capillary wedge pressure during diastole revealed a significant, though reversible, shift (P < 0.001) in the diastolic volume/ pressure (or compliance) relationship during septic shock.

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“…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%

“…Many workers came to the view that the hyperdynamic circulation was a feature of early shock that became hypodynamic with time and hypovolaemia [107±109, 116,117,119,120]. This view was supported by clinical observations and the fact that many hypodynamic patients would respond to a fluid challenge by a decrease in SVR and an increase in CI [115,121], and that death appeared to be associated with metabolic acidaemia [108,116,120,122,123] and a low cardiac output [110,111,116,120].`The confusion in the literature over sepsis presenting as a hyperdynamic or hypodynamic cardiac state and as a low or high resistance vascular state may result from comparing patients who were at different points in their septic episode' [124]. McLean et al described a further two patterns.…”

Section: Clinical Haemodynamicsmentioning

confidence: 99%