Venous return in hemorrhagic shock after application of military anti-shock trousers.

UNLABELLED: The effect of Military Anti-Shock Trousers (MAST) on inferior vena cava blood flow was studied during graded hypovolemia using a pump reservoir system and an in-line electromagnetic flowprobe. During hemorrhagic shock MAST inflation increased cardiac output 25.4% ( CONTROL: 0.92 +/- 0.09 l/min) and arterial pressure 50% ( CONTROL: 60 +/- 2 mmHg). The so-called "autotransfusion" effect due to blood displacement from the lower part of the body into the central circulation was found to be only 4.3 +/- 0.6 ml/kg, a volume much less than previously estimated in the literature. We conclude that MAST inflation reliably improves cardiac output and systemic blood pressure above the diaphragm in dogs subjected to hemorrhagic shock. This effect is mainly due to a diversion of the cardiac output to the upper half of the body due to impedance of flow to the abdomen and lower extremities, rather than to a significant volume shift constituting an autotransfusion of blood from the lower part of the body.

MAST augmentation of external cardiac compression: role of changing intrapleural pressure.

Ventricular fibrillation was induced in nine dogs weighing 18 to 22 kg. CPR was performed with a mechanical chest compressor. Mean carotid flow during CPR was 7.9 +/- 1.5 ml/min. After MAST inflation to 100 mm Hg, the flow increased to 15.7 +/- 3.7 ml/min. Intrathoracic aortic systolic pressure was also significantly increased from 65 +/- 7 to 73 +/- 8 mm Hg. When the thorax was vented with chest tubes bilaterally, no change in carotid flow or arterial pressure was noted on closing or opening the chest tubes. One liver laceration and two gallbladder contusions were noted at autopsy. MAST inflation apparently augments carotid flow an systolic pressure. Variations in intrapleural pressure do not seem to have a significant influence on CPR.

The kinetics of extracellular potassium changes during hypoxia and anoxia in the cat cerebral cortex.

Extracellular potassium activity, [K+]0, was continuously measured using potassium specific microelectrodes in the cerebral cortex of cats before and after hypoxic or anoxic insults. Two patterns of [K+]0 increase were seen. A slow, linear rise occurred during hypoxia and hypothermia and was correlated with changes in mean blood pressure (B/P). A fast, complex, exponential rise resembling spreading depression occurred during anoxia and was unassociated with B/P changes. The fall of [K+]0 after reversal of the insult was described by a single exponential function with rate constants from 0.009 to 0.0194 sec-1. It is suggested that the linear rise is primarily a result of sodium pump inhibition and that the exponential rise is due to a superimposed sudden increase in cell membrane permeability perhaps secondary to transmitter release. The kinetics of the fall of [K+[0 is consistent with the normalization of the sodium and potassium gradients across the cell membranes secondary to Na+-K+ATPase activity.

Changes in cortical subarachnoid fluid potassium concentrations during hypoxia.

Seventeen rhesus monkeys underwent 20-minute episodes of hypoxia (mean Po2, 18 to 28 mm Hg). In 14 animals that maintained mean blood pressures greater than 60 mm Hg, increases in potassium concentration averaging greater than 1 mEq/liter were observed in the cortical subarachnoid fluid. These changes were reversible with oxygen administration and were usually not associated with morphologic evidence of brain injury. Cisterna magna fluid, sampled in five animals, showed smaller increases in potassium concentration (mean, 0.3 +/- 0.4 mEq/liter). The arteriovenous difference in potassium concentration was consistently positive, suggesting movement of potassium from blood to brain during hypoxia. The amount of potassium accumulation in the cortical subarachnoid fluid was closely related to the severity of the hypoxia. Threshold Po2 levels, below which potassium changes occurred, were estimated at 29 mm Hg for the arterial blood and 20 mm Hg for the jugular venous blood. Massive potassium accumulations in the cortical subarachnoid fluid (greater than 10 mEq/liter) developed in three animals that sustained severe arterial hypotension during hypoxia.

Brain extracellular potassium activity during hypoxia in the cat.

Brain extracellular potassium activity, recorded by a potassium-selective microelectrode technique, was studied in 27 anesthetized, paralyzed cats during hypoxia. Potassium activity remained essentially constant until the arterial pO2 decreased to 20 to 23 mm Hg. If the blood pressure was allowed to decrease during hypoxia, even to the 70 to 100 mm Hg range, the associated increases in potassium activity were accentuated, often to levels greater than 20 mEq per liter. The electrocorticogram regularly became isoelectric by the time the potassium activity reached 6 to 10 mEq per liter. Elevations of the blood pressure with epinephrine injections reversed both the increases in potassium activity and the electrocorticogram flattening. Extracellular potassium homeostasis during hypoxia appears to depend on the maintenance of a normal arterial perfusion pressure.