Circulatory shock
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In 16 anesthetized pigs the cardiovascular effects of prostaglandin E1 and methylprednisolone (MPS) during E. coli sepsis were studied. Gated blood pool scans and hemodynamic studies were simultaneously performed. A control group, group I (n = 4), received volume loading alone; groups II, III, and IV received (each n = 4) volume loading after intravenous administration of MPS, prostaglandin E1, and both MPS and prostaglandin E1, respectively. ⋯ The present study indicates that in a porcine model of E. coli septic shock with acute pulmonary hypertension, prostaglandin E1 and MPS treatment decrease pulmonary vascular resistance but also systemic vascular resistance. Prior to and during volume loading right ventricular ejection fraction increased in the prostaglandin E1 group. However, neither prostaglandin E1 nor MPS improved right ventricular performance and forward flow during volume loading.
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Hypertonic saline has been used in the treatment of hypovolemic or burn shock for its rapid volemic effects. Hypertonic solutions could also improve cardiac performance and protect cellular metabolism in acute circulatory failure. We therefore studied the hemodynamic effects of continuous hypertonic saline infusion in the treatment of severe endotoxic shock in the dog. ⋯ Intravascular pressures were similar in the two groups, but cardiac output, stroke volume, and oxygen consumption were significantly higher in the hypertonic group. These results therefore indicate that hypertonic saline can rapidly restore oxygen transport and tissue oxygen consumption in septic shock. The duration of these hemodynamic effects, however, remains to be determined.
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To evaluate potential clinical applications of conjunctival (PcjO2) and mixed venous (SvO2) oximeters in the care of surgical patients, we compared continuous measurements of PcjO2 and SvO2 to conventional invasive hemodynamic and oxygen transport variables during normoxia, hyperoxia, hypoxia, hemorrhagic shock, and resuscitation in dogs. During the normoxic control periods, PcjO2 averaged 76% of the arterial oxygen tension (PaO2). During hyperoxia and hypoxia, PcjO2 correlated well with PaO2 values (r = 0.88) but not with mixed venous oxygen tension (PvO2), whereas the SvO2 correlated well with PvO2 (r = 0.88) but not with PaO2 values. ⋯ Both oximeters had in vivo stabilization and 90% response times of less than 2 min. We conclude that both oximetry systems are potentially useful in high-risk surgical patients to provide better cardiorespiratory surveillance and to signal the need for more intensive assessment of hemodynamic stability. This approach may lead to reduced costs from unnecessary invasive procedures as well as reduced morbidity secondary to earlier warning of cardiorespiratory compromise.
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Radiolabeled microspheres were employed to measure the cerebrovascular response to severe anaphylactic-induced hypotension in pentobarbital-anesthetized dogs. A rapid drop in mean arterial pressure (MAP, 140 to below 50 mm Hg) coincided with total and regional cerebral blood flows (CBF) that were not significantly different from prechallenge values. While blood flow to the occipital region (highest measured region of the brain) was significantly greater than that of brainstem regions prior to and during the shock regimen, no major redistributional phenomena occurred to any cerebral region. ⋯ Similar to our previous findings, CBF was maintained to perfusion pressures of 39 +/- 4 mm Hg. The drop in cerebral vascular resistance during the severe hypotensive period was not associated with a significant decline in arterial PO2, or a significant increase in arterial PCO2, A-V PO2, or V-A PCO2. Our results suggest that the fall in cerebral vascular resistance during anaphylactic-induced hypotension would not be associated with a severely altered cerebral metabolism.