Circulatory shock
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Serial measurements of arterial blood lactate were compared with established hemodynamic, respiratory, and metabolic measurements as prognostic indicators of survival or fatality in 28 patients with acute myocardial infarction complicated by heart failure and/or cardiogenic shock. Measurements were compared at the time of admission, at the time of maximal response to therapy, and 4 h prior to discharge or the onset of the agonal period. ⋯ No patient survived in whom the arterial blood lactate was greater than 4 mmol/L for more than 12 h, regardless of the magnitude of the stroke volume, the left ventricular filling pressure, or the cardiac work. We regard the measurement of arterial blood lactate as a consistently useful prognostic indicator of survival or fatality in patients with acute myocardial infarction and myocardial failure.
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The purpose of this study was to evaluate during hemorrhagic hypotension and shock the effect of angiotensin II on renal blood flow, glomerular filtration rate, and sodium and potassium excretions, and to determine its role in the development of irreversible hemorrhagic shock. Anesthetized dogs were subjected to a hemorrhagic shock protocol. Angiotensin II was infused at 100 ng/kg/min i.v. from 50 mm Hg initial hemorrhage until the experiment was terminated. ⋯ However, once shock had developed, the survival time from reinfusion to 50 mm Hg normovolemic hemorrhagic shock was not affected by exogenous angiotensin II (4.4 +/- 1.4 to 3.6 +/- 0.7 h.) During hemorrhagic shock, exogenous angiotensin II significantly increased sodium excretion and total renal blood flow. Glomerular filtration rate, potassium excretion, and arterial sodium and potassium concentrations were not affected. These data indicate that angiotensin II prolonged the development of irreversible hemorrhagic shock and selectively increased sodium excretion and total renal blood flow.
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Sepsis and septic shock were induced in fifteen awake rabbits by the infusion of live Escherichia coli. Sodium K+, and adenosine triphosphate (ATP) concentrations in red blood cells (RBC) and plasma were measured during the control, septic, and septic shock periods. The significant elevations of Na+ content in RBC during sepsis appeared to be primarily a function of increased cell membrane permeability. ⋯ Hyponatremia and hyperkalemia were apparent in the late stages of sepsis, these alterations reached statistically significant levels in the shock period. The electrolyte derangements associated with sepsis and septic shock could not be related to energy depletion. The continuous significant accumulations of ATP, observed in RBC and plasma, were interpreted as a result of decreased energy utilization and attributed to the diminished active ion transport by the impaired Na+-K+ pump.