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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 14 patients undergoing major abdominal surgery, epidural analgesia was performed and cardiovascular changes were examined by insertion of Swan-Ganz catheters. To counteract the hypotensive episodes associated with epidural block, Dobutamine (1-3 micrograms/kg body wt min-1) and Metaraminol (0.5-1.5 micrograms/kg body wt min-1) in various doses were infused and the effects of these vasoactive agents were examined. Epidural analgesia decreased arterial pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure and central venous pressure associated with marked decrease in cardiac index, stroke volume index, left ventricular and right ventricular stroke work without changes in systematic vascular resistance, pulmonary vascular resistance or heart rate. The infusion of Metaraminol caused a marked increase in arterial pressure, pulmonary arterial pressure, wedge pressure and central venous pressure. Calculated variables of stroke volume, systemic vascular resistance, left and right stroke work and cardiac work increased significantly. The infusion of Dobutamine caused a marked increase in arterial and pulmonary arterial pressure, wedge pressure, central venous pressure and cardiac index associated with those calculated changes of left and right stroke work and cardiac work, which were increased markedly. On the other hand, heart rate, stroke volume and pulmonary vascular resistance did not show any remarkable changes. Our study indicates that the fall in arterial blood pressure associated with epidural block may be due to marked decrease in cardiac output, and the infusion of Dobutamine is one of the desirable methods to counteract the hypotensive episode.
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PMID:Metaraminol and dobutamine for the treatment of hypotension associated with epidural block. 633 Aug 25

The cardiovascular effects of oral and intravenous administration of 0.05 and 0.1 mg/kg of the isosterically modified prostaglandin (PG) analog, (+)- 4-(3-[3-[2-(1-hydroxycyclohexyl)ethyl]-4-oxo-thiazolidinyl] propyl) benzoic acid were ascertained in conscious mongrels. After 0.05 mg/kg p.o., mean arterial pressure (MAP), obtained from indwelling catheters, fell from 105 +/- 1 to 100 +/- 4 mm Hg and total peripheral resistance (TPR) decreased from 0.062 +/- 0.006 to 0.039 +/- 0.002 mm Hg/ml/min. Cardiac output (CO), measured via electromagnetic flow probes, rose from 1.8 +/- 0.2 to 2.6 +/- 0.1 l/min and heart rate from 109 +/- 13 to 128 +/- 8 beats/min. The 0.1 mg/kg p.o. dose produced similar results. Intravenous injection of 0.1 mg/kg immediately dropped MAP from 103 +/- 6 to 58 +/- 3 mm Hg and TPR from 0.049 +/- .006 to .014 +/- .002 mm Hg/ml/min. CO climbed from 2.3 +/- 0.2 to 5.3 +/- 0.5 l/min and HR increased from 126 +/- 9 to 254 +/- 14 beats/min. Stroke volume was not affected by either oral or intravenous administration of the PG analog. Pretreatment with 100 micrograms/kg timolol blunted the CO and HR responses to 0.1 mg/kg iv of the PG analog without affecting the depressor response. Metaraminol infused during injection of 0.1 mg/kg iv of the PG analog diminished all responses. When compared to the cardiovascular effects of hydralazine and nitroprusside, the profile of the PG analog activity closely resembled that produced by the arterial vasodilator, hydralazine; in contrast, nitroprusside (which also dilates veins) reduced stroke volume, but did not significantly affect HR. In conclusion, dilation of the resistance vessels by the PG analog decreased MAP and TPR and reflexly elevated CO and HR in conscious dogs.
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PMID:Cardiovascular responses to an isosterically modified prostaglandin analog in conscious dogs. 652 20

We have compared three methods of preventing hypotension during subarachnoid anaesthesia. We attempted to maintain systolic arterial pressure (SAP) greater than 75% of baseline by use of i.v. fluids (preloading with normal saline 16 ml kg-1 and, if necessary, three subsequent boluses of 2.5 ml kg-1), an infusion of metaraminol titrated as necessary between 0 and 5 mg h-1 and an infusion of ephedrine titrated as necessary between 0 and 120 mg h-1. SAP and mean arterial pressure (MAP) were measured by automated oscillotonometry, central venous pressure (CVP) by a manometer and cardiac index (CI), stroke index (SI) and heart rate (HR) by transthoracic electrical bioimpedance. Systemic vascular resistance index (SVRI) was derived. Fluids alone failed to maintain SAP in five of 10 patients. Although CI and CVP were maintained, SVRI decreased (25 (SD 15)%; P = 0.02). Metaraminol maintained SAP in all 12 patients. The main cardiovascular change was decreased HR (15 (8)%; P = 0.0001). Ephedrine failed to maintain SAP in two of 12 patients and was accompanied by several cardiovascular changes: HR (21 (12)%; P = 0.001) increased and SI (16 (10)%; P = 0.0001), CVP (3.8 (1.5) cm H2O; P = 0.0001) and SVRI (24 (6)%; P = 0.0001) decreased. Treatment failures resulted from failures to maintain SVRI in the fluid group and CVP and SVRI in the ephedrine group.
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PMID:Hypotension during subarachnoid anaesthesia: haemodynamic analysis of three treatments. 811 May 64