Comparison of Hemodynamic and Regional Blood Flow Changes at Equivalent Stages of Endotoxin and Hemorrhagic Shock

Rutherford, Robert B.; Balis, John V.; Trow, Richard S.; Graves, Glenn M.

doi:10.1097/00005373-197611000-00007

Cited by 27 publications

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“…skin and skeletal muscle. This pattern of redistribution was also seen in aggregate anaphylaxis (Smedeg5rd et al 1979) and has been reported to occur in hemorrhagic and endotoxin shock in the monkey (Forsyth et al 1970. Rutherford et al 1976).…”

Section: Discussionsupporting

confidence: 57%

Anaphylactic shock in monkeys passively sensitized with human reaginic serum

Smedegård

Revenäs²,

Lundberg

et al. 1981

Acta Physiologica Scandinavica

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Mechanisms inducing a low cardiac output (CO) state in IgE-mediated (cytotropic) anaphylactic shock in anesthetized Macaca irus monkeys were studied. 7 monkeys were sensitized by 2 i.v. injections of a human reaginic serum containing a high concentration of IgE antibodies against dog albumin. Anaphylactic shock was elicited 48 h after the last sensitization dose, by an i.v. injection of dog albumin. The severe anaphylactic shock which developed was characterized by an initial phase consisting of increased CO (+16%, mean value, 1 min after challenge), pulmonary hypertension and systemic vasodilatation followed by a phase consisting of decreased CO (-67%), a fall in mean arterial pressure from 113 to 45 mmHg, decreases in left and right arterial pressures (-5.3 and -3.2 mmHg, respectively) and increases in pulmonary vascular (+364%) and total peripheral (+30%) resistances. These changes were recorded 5 min after challenge and the values then remained essentially unaltered during the rest of the 30-min observation period. Pulmonary vascular resistance was only increased by 140% at the end of that period. Myocardial blood flow was maintained during shock at the expense of flow to other organs. However, initially there was a redistribution of blood flow within the left ventricular myocardium, resulting in a relative decrease in subendocardial flow. This finding was not related either to occasional S-T changes in the electrocardiograms or to the level of decreased CO. The oxygen supply to the myocardium was reduced in shock but the reduction was always smaller than the corresponding decrease in heart work. Two additional monkeys sensitized with an IgE fraction from the human serum showed a smaller amount of specific IgG in their serum prior to challenge than the other monkeys. The response to challenge was milder, but resembled the initial vasodilatory reaction in monkeys sensitized with serum. These data on cytotropic anaphylaxis in the monkey show that the main cause of decreased CO and thus of the shock state is a decreased venous return, primarily due to peripheral blood pooling and, to a smaller extent, extravasation of plasma. No appreciable involvement of the heart in the induction of shock was detected.

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Section: Discussionsupporting

confidence: 57%

Anaphylactic shock in monkeys passively sensitized with human reaginic serum

Smedegård

Revenäs²,

Lundberg

et al. 1981

Acta Physiologica Scandinavica

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“…Irreversible shocks in the end will enter a predeath agonic stage and exhibit universal hypodynamic features of unresponsiveness to catecholamines, reduced metabolism, hypothermia, and reduced oxygen consumption independently on shock etiology. [12] Coagulopathy as DIC kills by occluding the microcirculation (arterioles, capillaries, venulae) and causing generalized hypoxia; hypothermia and acidosis kill by freezing and impairing life-indispensable enzymatic processes and by dampening life-saving responses. Terminal primary hypothermia cannot be reversed, is accompanied by terminal coagulopathy and indicates energy-production failure; terminal coagulopathy manifests with bleeding distant to any possible injury or tissue damage site, for example, mouth gush; and irreversible acidosis impairs endogenous and exogenous catecholamines response.…”

Section: Introductionmentioning

confidence: 99%

Shock - A reappraisal: The holistic approach

Bonanno

2012

J Emerg Trauma Shock

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Shock as reaction to life-threatening condition needs to be reclassified in a timely and more scientific synopsis. It is not possible or beneficial any longer to avoid a holistic approach in critical illness. Semantics of critical illness has often been unfriendly in the literature and a simplification with the elimination of conceptual pleonasms and misnomers under the exclusive light of physiology and physiopathology would be advantageous. Speaking one language to describe the same phenomenon worldwide is essential for understanding; moreover, it increases focus on characterization and significance of the phenomena.

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“…No or inadequate intervention during the stage of decompensation leads to the so called ‘no-return point’ (NRP), where all shocks enter a predeath agonic stage and exhibit universal hypodynamic features of unresponsiveness to catecholamines, reduced metabolism, hypothermia, and reduced oxygen consumption with SvO 2 independently on shock etiology . Irreversible shocks in the end will enter a predeath agonic stage and exhibit universal hypodynamic features of unresponsiveness to catecholamines, reduced metabolism, hypothermia, and reduced oxygen consumption independently on shock etiology[99–100] [Figure 1]. Coagulopathy kills by occluding the microcirculation (arterioles, capillaries, venulae) and causing generalized hypoxia, hypothermia and acidosis by freezing and impairing life indispensable enzymatic processes and by dampening life-saving responses.…”

Section: Introductionmentioning

confidence: 99%

Clinical pathology of the shock syndromes

Bonanno

2011

J Emerg Trauma Shock

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The clinical aspects of shock syndromes are described from their inception as compensated physiology to a stage of decompensation. The clinical significance of hypotension, fluid-responsive and non fluid-responsive hypotension, is discussed. Untimely or inadequate treatment leads to persistent subclinical shock despite adjustments of the macrohemodynamic variables, which evolves in a second hit of physiological deterioration if not aggressively managed. Irreversible shock ensues as consequence of direct hit or as result of inadequate or delayed treatment and is characterized by drug-resistant hypotension.

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Comparison of Hemodynamic and Regional Blood Flow Changes at Equivalent Stages of Endotoxin and Hemorrhagic Shock

Cited by 27 publications

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Anaphylactic shock in monkeys passively sensitized with human reaginic serum

Anaphylactic shock in monkeys passively sensitized with human reaginic serum

Shock - A reappraisal: The holistic approach

Clinical pathology of the shock syndromes

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