Showing papers on "Hypovolemia published in 1975"

Cardiac contusion: a capricious syndrome.

Abstract: Cardiac contusions are being recognized with frequency. Among 507 patients with non-penetrating chest injuries, 210 had serial electrocardiograms sufficient to evaluate the heart. Forty-five of these 210 patients (21%) had cardiac contusions. These 45 patients and 3 others who were confirmed to have cardiac contusions at necropsy, comprise the 48 patients in this series. Life-indangering cardiac complications occurred in 14 (29%) of the 48 patients, and 4 patients died. The development of cardiac complications following cardiac contusions appears to have a significant relationship to the presence of shock, hypoxia and to factors related to the severity of multiple injuries. These observations have therapeutic implications in management of patients with cardiac contusions through prevention of hypovolemia and hypoxia and avoidance of fluid overload as well as treatment of specific cardiac complications.

Relationship between absolute body-fluid deficits and fluid intake in the rat.

Abstract: Acute absolute body-fluid deficits were induced in rats by injection of the diuretic drug furosemide, which caused up to 20% reduction of extracellular fluid volume and up to 2% reduction of intracellular fluid volume. Water and .3 M NaCl were subsequently made available to allow the rats to replace their body fluids by drinking. The rats increased their intake of both fluids, but replaced less than half of the total deficit, thereby tolerating larger and larger voluntary body-fluid deficits as the size of the diuretic fluid loss increased. Plasma measures showed that the rats sustained hypovolemia after drinking, while intracellular fluid volume was apparently restored. Fluid-depleted rats drank normally in response to intracellular dehydration induced by a sodium chloride load. Incomplete restoration of body-fluid balance after body-fluid depletion is due to a failure to drink in response to extracellular dehydration.

Clinical determinants of survival from postoperative renal failure.

Abstract: In a series of 114 consecutive patients with acute renal failure, the over-all mortality rate was 60 per cent; 62 per cent of the patients had a documented episode of hypotension just prior to the development of acute renal failure. In 11 patients, a second episode of renal failure developed following recovery from the initial episode of acute renal failure; all of these patients died. The urine output rate during the course of acute renal failure was inversely related to the mortality rate in the series as a whole. The mean duration of acute renal failure in survivors of the present series was 11.0 plus or minus 1.4 days. Complications of renal failure in the order of their frequency included hemorrhagic hypotension, sepsis, sepsis with hypotension and consumption coagulopathies; only 12 per cent had no complications. Only six of 51 patients whose clinical course was complicated by sepsis with or without an episode of hypotension survived. By contrast, 30 of 53 patients who had hemorrhagic hypotension without sepsis survived. The date suggest that although acute renal failure has a high mortality rate, it is a benign disease that is potentially reversible. Regardless of age and sex, renal functional recovery will take place if the patient is maintained in good physiologic condition long enough without a continued stress, such as sepsis, hypotension or hypovolemia, all of which prolong renal ischemia. During the course of renal failure, extreme care is essential to maintain adequate circulating volume without extracellular fluid overload; a second hemodynamic insult may result in serious damage to the regenerating renal tubules. We conclude that early recognition of acute renal failure, aggressive management of sepsis, careful titration of fluid and electrolyte therapy, meticulous monitoring, maintenance of the circulation and judicious utilization of dialysis will aid in reduction of mortality in these critically ill patients.

Rattlesnake venom shock in the rat: development of a method.

Abstract: A model in Wistar rats (n = 30, 279-345 g) was developed to study circulatory, respiratory, metabolic, and lethal effects of an intravenous infusion (30 min; 1.25, 1.5, 1.75, and 2.0 mg/kg) of rattlesnake (Crotalus viridis helleri) venom. Venom produced perfusion failure with lactacidemia, hemoconcentration, hypoproteinemia, and death. The severity of poisoning was proportional to the quantity of venom given and to the elevation in lactic acid and hematocrit. Hemorrhages in the diaphragm, intercostal muscles, and intestine were observed at necropsy. In a separate test, rats (n = 12, 311-355 g) received an infusion of 1.5 mg/kg of venom or physiological salt solution. Blood volume was measured 30 min after the end of infusion in both groups with radioiodinated (125I) human serum albumin (RIHSA) and 51Cr-labeled rat red cells. Venom produced a significant reduction in total blood volume index (35%, P less than 0.001), plasma volume index (46%, P less than 0.001), and red cell mass indec (22% P less than 0.005). The slope of the RIHSA-disappearance curve of animals that received venom was more than twice that of the control group. We conclude that perfusion failure following rattlesnake envenomation is associated with hypovolemia due to increases in vascular permeabiltiy and hemorrhage.

Progressive hypovolemia leading to shock after continuous hemorrhage and 3:1 crystalloid replacement.

Abstract: Dogs subjected to arterial hemorrhage and infused with 3:1 volumes of lactated Ringer's solution became progressively hypovolemic, to the point of frank shock. Stability and normovolemia were restored only after additional fluid delivery, in a net ratio of 8:1. These were the mathematically predicted values that satisfied Starling's hypothesis.

Bartter syndrome. Typical facies and normal plasma volume.

Abstract: • Two girls with hypokalemic and hypochloremic metabolic alkalosis and failure to thrive were found to have Bartter syndrome at ages 9 and 6 months. Both had normal blood pressures despite substantial elevation of plasma renin activity and evidence of secondary hyperaldosteronism. A similarity in facial features, including prominent forehead, a large head, triangular facies with drooping mouth, and large eyes and pinnae, was noted in these two infants and in published pictures of other infants with the syndrome. Although the normotension associated with substantial elevation of plasma renin activity and hyperaldosteronism in Bartter syndrome has been considered the effect of hypovolemia, a normal or slightly elevated plasma volume was found in these infants, suggesting that in certain cases an alternate mechanism for the depressed response to renin may be present. (Am J Dis Child129:1205-1207, 1975)

Development and treatment of post-traumatic pulmonary platelet trapping.

Abstract: In anesthetized dogs soft tissue trauma resulting in hypovolemia was associated with pulmonary trapping of 51Cr tagged platelets. The efficacy of various forms of therapy aimed at preventing pulmonary trapping of platelets following trauma was evaluated. Lung biopsies were assayed before trauma and at hourly intervals for accumulation of autologous 51Cr tagged platelets reinfused 24 hours prior to the experiment. The study showed that pulmonary platelet trapping secondary to soft tissue trauma could be prevented by treatment with Dextran 40, Dextran 70 and methyl-prednisolone administered one hour after trauma and by pretreatment with aspirin.

The influence of diet on response to hemorrhagic shock.

Abstract: Prior nutrition is known to influence tolerance to hypovolemic shock. This study was undertaken to determine the influence of dietary composition on the response of animals subjected to hypovolemic shock. Particular attention was directed to the role of high and low protein diet content with a proportionate change in carbohydrate content to yield isocaloric diets. Rats were placed on one of three diets and were subsequently subjected to shock either by 1) hemorrhage to a pre-determined mean arterial blood pressure, or by 2) hemorrhage of a pre-determined volume of blood based on per cent of body weight. Serial measurements were made of blood pressure, blood volume removed, survival time,hematocrit, blood glucose, pH and blood gases. The results indicate that a high protein diet does not prolong tolerance to recurrent blood loss but there is a greatly reduced tolerance to hemorrhage shock in rats whose body weight was maintained on a low protein/high carbohydrate diet. The latter animals also exhibited impaired refill of plasma volume and a paradoxical, continuing hyperglycemic response during hypovolemia. This study suggests that although an abundant supply of blood glucose is available as an energy source, glucose uptake in the peripheral tissues is inhibited during hypovolemia by unknown mechanisms and thus homeostasis is curtailed. The protein content of the diet may be a critical factor in carbohydrate use during shock.

Ventricular function in experimental hemorrhagic shock.

Abstract: Hemorrhagic shock was induced in 20 spontaneously breathing adult greyhounds by lowering the mean arterial pressure to 40 millimeters of mercury. In the first group of six dogs, reinfusion was carried out without delay; in a second group of six dogs, hypovolemia was continued for two hours, during which time the arterial pressure was permitted to rise in response to intact cardiovascular reflexes; in a third group of eight dogs, the mean arterial pressure was artificially maintained at 40 millimeters of mercury for two hours, initially by further bleeding. In all dogs in the latter group, take-up of blood from the reservoir was required during the second hour to maintain the arterial pressure, this being indicative of irreversible shock. In two of this group, fatal arrhythmias developed during reinfusion. All three groups showed evidence of ventricular dysfunction during and immediately after reinfusion, as indicated by disproportion between left ventricular stroke work and left ventricular end diastolic pressure, these data being used to construct ventricular function curves. Measurement of dP/dt maximum suggested that this dysfunction was due to impairment of myocardial contractility. The first two groups recovered normal function within one hour; the third group failed to have such a recovery. Evidence indicates that generalized tissue hypoxia, in addition to myocardial hypoxia, is important in the cause of cardiac dysfunction in irreversible shock.

Cardiac contusion: A capricious syndrome

Abstract: Cardiac contusions are being recognized with frequency. Among 507 patients with non-penetrating chest injuries, 210 had serial electrocardiograms sufficient to evaluate the heart. Forty-five of these 210 patients (21%) had cardiac contusions. These 45 patients and 3 others who were confirmed to have cardiac contusions at necropsy, comprise the 48 patients in this series. Life-indangering cardiac complications occurred in 14 (29%) of the 48 patients, and 4 patients died. The development of cardiac complications following cardiac contusions appears to have a significant relationship to the presence of shock, hypoxia and to factors related to the severity of multiple injuries. These observations have therapeutic implications in management of patients with cardiac contusions through prevention of hypovolemia and hypoxia and avoidance of fluid overload as well as treatment of specific cardiac complications.

Physiopathology of accidental drowning

Abstract: The first phase of accidental drowning begins with asphyxia, due to either laryngospasm (10-15 percent of cases) or water aspiration. The second phase is characterized by water and electrolyte changes in the blood. The physiopathological modifications caused by drowning in fresh water differ from those of drowning in sea water. The hypotonic fresh water quickly diffuses in the bloodstream. The consequences are, in many cases, hypervolemia with pulmonary edema, hemolysis, hyperkalemia with risk of ventricular fibrillation, diminution of hemoglobin, and a relative decrease in plasma concentration of Na, Cl, Ca, and albumin. Further, inactivation and washing out of the anti-atelectasis factor from the alveoli by fresh water facilitate the formation of atelectasis. In cases of accidental drowing in sea water the osmotic gradient is in inverse: the electrolytes of aspirated salt water diffuse in the circulation, whereas the blood serum and the plasma albumin pass into the alveoli. Acute pulmonary edema often follows these pathological changes. Hypovolemia with circulatory collapse, hemoconcentration with rise in hemoglobin, hematocrit, sodium, potassium and albumin, and, finally, an elevated risk of thromboembolism due to increased blood viscosity, represent further complications. On the other hand, ventricular fibrillation is rare, hemolysis is absent and atelectasis usually does not occur.

[Pulmonary microembolism: pulmonary hemodynamics following trauma and hemorrhage (author's transl].

Abstract: Standardized bone trauma by means of open osteotomy is performed on both hind legs of 16 out of 24 anaesthetised mongrels. During the following 6 hours the most important parameters of blood coagulation and the serum lipids are estimated at regular intervals. Subsequently in a number of the animals 50% of the total blood volume is withdrawn continuously over a period of one hour. All animals without the preceding trauma survive the hemorrhage. The animals in the trauma group die on the average 42 minutes after the beginning of the hemorrhage. The trauma causes an acute decrease in total platelet count (GTZ) to 40% of the pretraumatic value. During an initial phase of hypercoagulability there is a formation of reversible microaggregations containing platelets and fibrin, caused by an increased turnover of coagulation factors. Secondary fibrinolysis develops in the traumatised animals. A further increase in coagulation is caused by the following hemorrhage. In combination with decreased and inhibited fibrinolysis, a disseminated intravascular coagulation state is found and results in irreversible pulmonary microthrombosis. Massive pulmonary fat deposits cannot be found histologically in spite of an increase in serum triglycerid levels to 35% above the pretraumatic values. In dogs great amounts of fat are filtered by the glomeruli and are demonstrable in the tubular epithelium. Histological examinations show a marked disseminated pulmonary microthrombosis of platelets, fibrin and fat in those animals with trauma and hemorrhage. Only the accompanying hypovolemia produces the characteristic histologic changes of the so-called Pulmonary Microembolism Syndrome.

Metabolic management of the horse with acute abdominal crisis

Abstract: SUMMARY The horse with an abdominal crisis caused by acute gastro-intestinal tract obstruction develops hypovolemia, hemoconcentration, electrolyte depletion, metabolic acidosis and shock. During preparation for operation, treatment with fluids, antibiotics and bicarbonate will impede metabolic imbalance. Stomach decompression may slow the passage of sodium, water and potassium to the gut lumen, reduce pain and minimize the risk of stomach rupture. Selected laboratory determinations and the monitoring of arterial and venous pressures will provide a measure of severity and serve as a guide to replacement therapy. In the post surgical period, vigilance must be directed towards potassium and bicarbonate imbalanc and adequate hydration.

Ovarian hyperstimulation syndrome. Notes on the physiopathology and treatment apropos of 3 cases

Abstract: Hyperstimulation appeared in one case on the 10th 11th day after ovulation, allowing by its presence the very precocious diagnosis of successful fecondation. The study of blood coagulation revealed that hypercoagulability was mainly related to hyperactivity of the thrombocytes and of the coagulation proteins. The pathogenesis of the syndrome is discussed. Increase in the permeability of the capillary vessels and hypovolemia seem to be responsible for the main accidents. Unfortunately as we have no real mean of decreasing the permeability of the capillary vessels, the treatment can be directed only against hypovolemia and its results. The infusion of macromolecular fluids, the restriction of sodium and water intake, together with the prescription of spironolactone have been successfully employed in those three cases.

Diuretics and Nonocclusive Infarcts

Abstract: To the Editor.— The article, "Diuretic Agents: Inciting Factor in Nonocclusive Mesenteric Infarction?" (229: 1451, 1974), by John B. Sharefkin, MD, and William Silen, MD, describes three cases of nonocclusive mesenteric infarctions following diuretic and digitalis therapy and suggests hypovolemia, diuretic-induced, together with vasospasm, possibly digitalis-induced, as the mechanism for the infarction. Although some hypovolemia seems to have occurred, the slight elevation in blood urea nitrogen level of two of the patients renders the hypovolemia theory not too impressive. Another more likely explanation may be the hypothesis forwarded by Alexander Leaf, MD, 1,2 suggesting cell swelling as the possible cause of nonocclusive infarcts. The cell swelling is caused by potassium efflux coupled with sodium chloride and water influx across the cellular semipermeable membrane, and thus interference with cell metabolism and possibly impingement on micro-circulation. The current knowledge of the mechanisms of adenosine triphosphate (ATP)-dependent active sodium-potassium transport involving the specific

Arterial-venous magnesium gradients in hypovolemic shock: an indication of the irreversible state.

Abstract: SummaryArterial-venous magnesium differences were examined in mongrel dogs stressed with reversible and lethal hypovolemia. Increases in serum Mg with hemorrhage have long been known to occur in both humans and animals, yet, increased blood Mg levels have not been viewed as an indicator of the irreversible shock state. The magnesium gradient was shown to be a good indicator of cell destruction which is consistent with lethal shock.This research was aided in part by support from the Steroid Research Fund, Cleveland, Ohio.

[Circulatory and metabolic disturbances in accidental hypothermia (author's transl)].

Abstract: This work sums up several studies: clinical observation (electrocardiogram, cardiac rhythm, circulatory state), and biology (glycemia, blood oxygenation, acid-base balance) in 24 cases of accidental hypothermia, not related to poisoning by central nervous system depressive agents; haemodynamics in 18 of these cases; pathology of the myocardium in 11 cases; haemodynamics and microscopy of the myocardium in dogs with slowly induced or prolonged hypothermia; finally an electron microscope study in hypothermic rats Electrocardiographic study and continuous monitoring of cardiac rhythm and tracing show, in addition to well known manifestations (bradycardia, lenghtening of QT, J wave), acute dysrhythmias, particularly circulatory arrests by asystole during or even 72 hours after rewarming The clinical haemodynamic changes, measurable (cardiac output, mean arterial pressure, central venous pressure), or computable (stroke volume, peripheral resistances) are observed during rewarming Several haemodynamic developments can be distinguished: --favourable evolution when the initial disturbances (decrease in cardiac output and in stroke volume, increase in peripheral resistances) disappear without any therapeutic support: --haemodynamic developments showing at a certain time evidence of hypovolemia requiring only moderate vascular replacement; --haemodynamic developments showing myocardial damage In some cases, only hypothermia accounts for these In circulatory arrests during or after rewarming, these haemodynamic disturbances raise the hypothesis of severe cardiac changes due to hypothermia itself

Effect of glucagon on changes of carbohydrate metabolism in experimental hemorrhagic shock

Abstract: The behaviour of venous blood glucose, lactate and pyruvate concentration was tested in experimental shock, caused by bleeding in rabbits. The animals of one group were retransfused after 1.5 hours hypotension of 40 mm Hg. The animals of another group were left with a total blood removal of 2% body weight. We found a significantly higher blood sugar reaction in the longer surviving animals of the group in comparison to the ones, which died early. A single or repeated intravenous application of 70/1000 mg glucagon was not followed by a statistically visible change of blood sugar-, lactate- and pyruvate values in shock versus the control group. In spite of pronounced hypovolemia 20 of 22 animals, treated with glucagon, showed an increase of blood pressure by 20 mm Hg and of cardial frequency, especially after the first injection over a period of 10 minutes with decreasing tendency in the further course of shock.