Resuscitation
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In 54 patients with circulatory arrest mainly due to ischaemic heart disease cerebral functions were tested longitudinally during primary cardiopulmonary resuscitation or basic life support. Cerebral recovery was characterized by the appearance of functions in caudorostral sequence. ⋯ If circulation was re-established it usually happened within less than 20 min of basic life support. Prolongation of the resuscitation attempt beyond this time occasionally resulted in a selective reestablishment of circulation (brain death) but most often resulted in a dissociated recovery of cerebral functions (cardiac death).
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Comparative Study
Plasma volume changes after infusion of various plasma expanders.
In the immediate post-operative period after moderate surgical procedures, 1 litre of a colloid solution or saline was given intravenously. The plasma volume expansion after infusion of dextran 70 (Macrodex), hydroxyethylstarch (Volex), polygelatin (Haemaccel), albumin and saline was found to be between 790 and 180 ml. The most efficent plasma expander was dextran, followed by hydroxyethylstarch. ⋯ As the metabolic pathways of hydroxyethylstarch have not yet been further explored, dextran is preferred when using artificial colloids. Judged by its secondary effects alone, including the influence on plasma protein patterns, albumin seems to be the compound of choice. Polygelatin and saline are not efficient expanders when hypovolaemia is to be corrected rapidly.
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Fifty grams of albumin were infused into patients in the immediate post-operative period as either 5, 20 or 25% solutions. With all three solutions the increase in plasma volume was 500 ml or 11 ml/g of retained albumin, which is less than the normal water-binding capacity of albumin found in studies in vitro and in some clinical studies. ⋯ Since albumin is a good plasma expander and a drug with a few secondary effects it is recommended in the treatment of shock. We prefer the 5% solution, which contains an electrolyte solution and is more easily infused, because of its low viscosity.
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The effects of hyperbaric oxygenation with 2 atm. pressure and 100 percent oxygen on cerebrovascular tone were assessed by the reactivity of the cerebral vessels to CO2 and vasomotor capacitance index (the cranial pressure divided by the mean arterial pressure) in 50 anaesthetized artifically ventilated dogs, in which intracranial pressure was raised by slow inflation of an extradural balloon. Hyperbaric oxygenation reduced the intracranial pressure only at the stage when the cerebral vessels were still responsive to CO2, as indicated by a rise in intracranial pressure of 30-70 mmHg; under these circumstances, both the reactivity of CO2 and the vasoconstrictor tone of cerebral vessels were improved by hyperbaric oxygenation. ⋯ In extreme intracranial hypertension (above 100 mmHg) when there was reactivity to CO2 and the electroencephalogram was flat, rapid balloon deflation was followed by a further gradual increase of intracranial pressure and hyperbaric oxygenation did not restore the cerebrovascular tone. The effect of hyperbaric oxygenation in experimental intracranial hypertension appeared to be dependent upon the vasoconstrictor tone of the cerebral vessels, which would be indicated by a vasodilator response to CO2.