A Physiologic Analysis of Cardiopulmonary Responses to Ketamine Anesthesia in Noncardiac Patients

Gooding, John M.; Dimick, Alan R.; Tavakoli, Mehrdad; Corssen, Guenter

doi:10.1097/00132586-197810000-00023

Cited by 40 publications

(26 citation statements)

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“…This has been reported in cardiac surgical patients [15]. Pulmonary vascular resistance is increased by ketamine [16], but – in this study – the concomitant ketamine–midazolam infusion does not significantly change the pulmonary vascular resistance.…”

Section: Discussionsupporting

confidence: 49%

Ketamine-midazolam total intravenous anaesthesia for prolonged abdominal surgery

2001

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Section: Discussionsupporting

confidence: 49%

Ketamine-midazolam total intravenous anaesthesia for prolonged abdominal surgery

2001

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“…Meanwhile, several studies about the pharmacology and interaction of ketamine with the cardiocirculatory system have resumed a strong stimulation of sympathomimetic structures in vivo. 29,30 In our study, we observed a reduced necessity for supportive norepinephrine Mean ± standard deviation (SD), each parameter was evaluated hourly and summarized to a daily average value. administration in the S(+)-ketamine group to maintain the CPP >60 mm Hg when compared with the fentanyl group.…”

Section: Discussionmentioning

confidence: 72%

Effects of Fentanyl and S(+)-ketamine on Cerebral Hemodynamics, Gastrointestinal Motility, and Need of Vasopressors in Patients With Intracranial Pathologies

Schmittner¹,

Vajkoczy²,

Horn

et al. 2007

Journal of Neurosurgical Anesthesiology

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In neurosurgical patients, opioids are administered to prevent secondary cerebral damage. Complications often related to the administration of opioids are a decrease in blood pressure affording the use of vasopressors and intestinal atonia. One alternative approach to opioids is the application of S(+)-ketamine. However, owing to a suspected elevation of intracranial pressure (ICP), the administration of S(+)-ketamine has questioned for a long time. The aim of the present study was to evaluate ICP, gastrointestinal motility, and catecholamine consumption in neurosurgical patients undergoing 2 different protocols of anesthesia using fentanyl or S(+)-ketamine. Twenty-four patients sustaining traumatic brain injury or aneurysmal subarachnoid hemorrhage received methohexitone plus either fentanyl or S(+)-ketamine to establish a comparable level of sedation. To reach an adequate cerebral perfusion pressure (CPP), the norepinephrine dosage was adapted successively. Enteral nutrition and gastrointestinal stimulation were started directly after admission on the critical care unit. ICP, CPP, and norepinephrine dosage were recorded over 5 days and also the time intervals to full enteral nutrition and first defecation. There was no difference regarding ICP, CPP, and the time period until full enteral nutrition or first defecation between both groups. Patients who underwent analgesia with S(+)-ketamine showed a trend to a lower demand of norepinephrine compared with the fentanyl group. Our results indicate that S(+)-ketamine does not increase ICP and that its use in neurosurgical patients should not be discouraged on the basis of ICP-related concerns.

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“…As a result, ketamine causes little change in systemic vascular resistance (16). Most studies in adults have shown that ketamine either increases or does not alter PVR (1, 17,18). Studies in infants and children have also demonstrated that ketamine has minimal effects on PVR (19,201.…”

Section: Discussionmentioning

confidence: 99%

Direct Effects of Intravenous Anesthetics on Pulmonary Vascular Resistance in the Isolated Rat Lung

Rich¹,

Roos²,

Anderson³

et al. 1994

Anesthesia & Analgesia

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We determined the direct effects of thiopental, ketamine, midazolam, etomidate, and propofol on pulmonary vascular resistance (PVR), the relationship of the direct effects to the baseline PVR, and the possible interaction with functional endothelium. The intravenous anesthetics were injected randomly into 1) endothelium-intact isolated rat lungs which were either unconstricted or constricted with angiotensin II (n = 10), and 2) lungs with endothelial injury produced by electrolysis (n = 10). In endothelium-intact lungs thiopental (0.5 and 5.0 mg/kg) and etomidate (3.0 mg/kg) significantly (P < 0.05) increased PVR by 3% +/- 1%, 30% +/- 7%, and 29% +/- 5%, respectively. Ketamine (3.0 and 100 mg/kg) and propofol (20 mg/kg) significantly (P < 0.05) decreased the PVR by 6% +/- 1%, 15% +/- 1%, and 8% +/- 1%, respectively. Midazolam (0.3 and 3.0 mg/kg) and smaller doses of etomidate (0.3 mg/kg) and propofol (2.0 mg/kg) did not affect PVR. These responses did not vary with the baseline PVR over a twofold range. The effects of thiopental, ketamine, etomidate, and midazolam were not altered by endothelial injury. In contrast to the vasodilation produced by propofol in normal lungs, propofol (20 mg/kg) significantly (P < 0.05) increased the PVR by 8% +/- 2% after endothelial injury. In conclusion, this study demonstrates that thiopental and etomidate are direct pulmonary vasoconstrictors, ketamine and propofol are direct pulmonary vasodilators, and midazolam has no direct effects in the isolated rat lung. Further, these effects on pulmonary vasculature do not vary with baseline PVR, and only propofol appears to have endothelium-dependent effects.

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A Physiologic Analysis of Cardiopulmonary Responses to Ketamine Anesthesia in Noncardiac Patients

Cited by 40 publications

References 0 publications

Ketamine-midazolam total intravenous anaesthesia for prolonged abdominal surgery

Ketamine-midazolam total intravenous anaesthesia for prolonged abdominal surgery

Effects of Fentanyl and S(+)-ketamine on Cerebral Hemodynamics, Gastrointestinal Motility, and Need of Vasopressors in Patients With Intracranial Pathologies

Direct Effects of Intravenous Anesthetics on Pulmonary Vascular Resistance in the Isolated Rat Lung

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