Showing papers on "Hypovolemia published in 1979"

Plasma volume contraction: a significant factor in both pregnancy-associated hypertension (pre-eclampsia) and chronic hypertension in pregnancy.

Abstract: The role of plasma volume in hypertension in pregnancy (pre-eclampsia) was investigated. Significant volume expansion from non-pregnant levels (16.5 +/- 1.60 ml/cm height) was present throughout pregnancy in 189 normal women, reaching 23.1 +/- 1.21 ml/cm at 33-36 weeks amenorrhoea. In another 40 initially normotensive pregnant women who developed hypertension, similar early volume expansion was followed by significant volume contraction in the third trimester, before evaluation of blood pressure in 29 (20.6 +/- 1.26 ml/cm), after it in 11 (18.6 +/- 1.27 ml/cm). Equivalent volume contraction was present in another 44 women studied only after hypertension developed in the third trimester. Oedema had no value as a clinical sign. In another 30 women with chronic hypertension, blood pressure was inversely related to plasma volume (r = 0.822) and to fetal growth (r = -0.710), which was directly related to plasma volume (r = 0.701). Plasma volume depletion plays a significant role in hypertension in pregnancy.

The Dynamics of Vasopressin Release and Blood Volume Regulation During Fetal Hemorrhage in the Lamb Fetus

Abstract: Summary Experiments were performed on 11 long-term fetal lamb prep- arations (103-138 days of gestation) to investigate the sensitivity and relative responsiveness of the fetal volume receptors in mod- ulating fetal plasma arginine vasopressin (pAVP) secretion and plasma renin activity (PRA) secretion during fetal hypovolemia and after fetal blood volume replacement. During fetal hemorrhage there were significant decreases (P < 0.05) in fetal hematocrit (34.7 f 2.58 to 27.0 f 1.64%), plasma proteins (3.14 f 0.15 to 2.78 f 0.19 g/100 ml), mean arterial blood pressure (MABP) (58.1 f 2.59 to 52.2 f 2.60 mmHg) and fetal arterial pH (7.38 f 0.01 to 7.35 f 0.01). A significant increase in fetal pAVP concentration from 0.73 f 0.21 to 34.9 f 10.04 pU/ml (P < 0.01) and fetal PRA from 4.78 2.22 to 40.4 f 18.31 ng/ml/hr (P < 0.05) was demonstrated at the peak of fetal hemorrhage. Two hr after correction of the fetoplacental blood volume, these values were back to base line levels. No change in either maternal pAVP or PRA was seen during fetal hemorrhage. When individual values for log pAVP and log PRA were plotted as a function of percent of fetoplacental blood volume removed the correlation coefficients were 0.82 and 0.60, respectively. A multiple regression analysis showed a high correlation of log pAVP and log PRA with the volume of blood removed and a low partial correlation with the fetal MABP. This suggests the decrease in fetal MABP was not the primary factor explaining the increase in pAVP and PRA during fetoplacental blood volume depletion. The data indicate that the fetal volume receptors for control of arginine vasopressin secretion are fullv functional in the last trimester of gestation and suggests that fetal pAVP and PRA are released as a; exponential function of the wrcent of feto~lacental blood volume de~letion. Finally, an isosmotic water shift from the fetal interstitial space to the fetal vascular space is described during fetal hemorrhage. Speculation It is suggested that a change in the equilibrium between the forces regulating fluid movement through the fetal capillary mem- branes, in accordance with Starling's principle, activates isosmotic water fluxes from the fetal interstitial space to the fetal vascular compartment counteracting the effects of fetal blood volume de- pletion. Therefore, the role of arginine vasopressin (AVP) release during fetal hemorrhage, if any, will be to act as a pressor substance helping to maintain fetal blood pressure. No major effect of AVP on placental membranes was demonstrated in vivo. Available information suggests that the newborn is capable of secreting vasopressin at birth and that both the osmoreceptors and volume control systems are fully functional (14, 21, 22). During fetal life, the increase in concentration of circulating vasopressin has been evoked by either osmolar or volume stimuli, using short-term fetal lamb preparations (exteriorized fetuses) (3, 32). However, the effects of surgical stress and anesthesia on the fetus may themselves have influenced this response (15, 17). Recently, using long-term fetal lamb preparations (chronically catheterized) and avoiding the effects of surgical stress on the fetus, we demonstrated that the fetal osmoreceptor system for control of AVP secretion is fully functional in the last trimester of pregnancy (38). The present protocol was designed to study the responsiveness of the fetal hypothalamic neurohypophyseal system to a hemor- rhagic stimulation under conditions that approximate the usual physiologic situation using long-term fetal lamb preparations. Using a specific and sensitive radioimmunoassay for AVP (34), we were able to assess the sensitivity and relative responsiveness of the fetal volume receptors in modulating fetal AVP secretion during fetal hypovolemia and after fetal blood volume replace- ment. Finally, this model permitted us to investigate the physio- logic mechanisms regulating the fetal blood volume during fetal hemorrhage.

Effect of dopamine on intrapulmonary shunt fraction and oxygen transport in severe sepsis with circulatory and respiratory failure.

Abstract: The hemodynamic response to a dopamine HCl infusion (10 microgram/kg per min) was measured in 25 adult patients with severe sepsis: there were 6 patients with circulatory hyperdynamic states, 9 patients with myocardial failure, and 10 with hypovolemia. Each patient also had acute respiratory failure. Changes of intrapulmonary shunt fraction (Qs/Qt), arterial and mixed venous oxygen tension (PaO2 and PvO2), oxygen transport, and oxygen consumption (VO2) were evaluated before and after dopamine infusion. Dopamine infusion produced clinical improvement and increased cardiac output. The hemodynamic response seemed to differ slightly according to the pattern of circulatory failure: chronotropic effect appeared to be predominant in hyperdynamic states, whereas inotropic effect appeared to be predominant in myocardial failure or hypovolemia. Moreover, in hypovolemic patients we noted a rise in pulmonary capillary wedge pressure suggesting an additional increase in venous return. During this treatment, we also noted a worsening of the Qs/Qt despite the increase in pulmonary blood flow; this worsening did not prevent significant improvements in VO2, but the improvement in PVO2 was offset by increased Qs/Qt and PaO2 remained unchanged.

Renin and aldosterone secretions during hypovolemia in rats: relation to NaCl intake.

Abstract: Plasma renin activities (PRA) and aldosterone concentrations increased in parallel over a wide range of plasma volume deficits produced in unanesthetized rats by extravascular administration of polyethylene glycol (PEG) solution. When PEG-treated rats were given water to drink, their intakes were proportional to PRA; when given water and 0.5 M NaCl, PRA and the steroid concentrations diminished concurrently in association with sodium consumption. Aldosterone concentrations and NaCl intakes were markedly enhanced after PEG treatment in rats maintained on a sodium-deficient diet for 4 days. On the other hand, a clear relation between PRA and water intake, and between circulating aldosterone levels and sodium intake, was not suggested by other experiments in this series. For example, bilateral nephrectomy abolished the rise in PRA during hypovolemia yet rats drank water normally. Moreover, aldosterone concentrations were substantially elevated by PEG treatment in the nephrectomized rats yet sodium appetite was abolished. These and other findings suggest that neither angiotensin nor aldosterone plays a prominent role in stimulating water and saline intakes during hypovolemia.

Measurement of toe temperature for assessing the severity of acute circulatory failure.

Abstract: The temperature gradient between the ventral surface of the first toe and the ambient temperature was measured and compared with established hemodynamic measurements in 71 critically ill patients Thirty-two patients had acute myocardial infarctions, 21 patients had primary bacteremia and 18 patients had primary hypovolemia which followed acute blood loss The temperature gradient served as a more predictable indicator of survival or fatality than either arterial pressure or cardiac index in each group of patients Patients who improved after treatment and survived had increases in the toe minus ambient temperature gradient to more than 4 degrees C, whereas a gradient of less than 3 degrees over an interval of 12 hours was typically observed in patients who subsequently died These observations indicate that the toe minus ambient temperature gradient provides a valuable, inexpensive and noninvasive monitor of tissue perfusion in critically ill patients

Treatment of Circulatory Shock With Dopamine: Studies on Survival

Abstract: Therapeutic effects of dopamine hydrochloride on the peripheral and metabolic defects of shock were investigated in 34 patients with circulatory shock associated with myocardial infarction, bacteremia, or hypovolemia. Severity of the circulatory defect characterized by hypotension, reduced cardiac output, oliguria, and notably reduced skin (toe) temperature before treatment with dopamine was not directly related to survival. However, the arterial blood concentration of lactate before treatment with dopamine indicated the likelihood of survival. Patients who ultimately survived following treatment with dopamine had normal or only mildly elevated levels of arterial blood lactate before therapy. No patients with established shock states in whom perfusion failure was associated with substantial increases in the level of arterial blood lactate survived regardless of treatment with dopamine. Increases in toe temperature during dopamine treatment also emerged as a uniquely good indicator of favorable outcome during therapy.

Hypovolemia and hypotension complicating management of acute cardiogenic pulmonary edema

Abstract: After the acute onset of heart failure and in the absence of acute myocardial infarction, plasma volume may occasionally be depleted to the extent that the patient presents with clinical signs of circulatory shock. In five patients, the acute onset of clinical and radiographic signs of cardiogenic pulmonary edema were associated with reduction in arterial blood pressure and cardiac output. The pulmonary arterial wedge pressure was within normal limits but a reduction in plasma volume was demonstrated, which is best explained by the rapid translocation of plasma water that represented pulmonary (and most likely also peripheral) edema fluid. The infusion of 5 percent albumin solution significantly increased cardiac output, mean arterial pressure and cardiac work, reversed lactic acidosis, enhanced furosemide-induced diuresis and was followed by a decrease in both clinical and radiographic signs of pulmonary edema. These observations confirm that volume expansion may constitute appropriate treatment for some patients with cardiogenic pulmonary edema who may present with hypotension and who are unresponsive to conventional therapy.

Shock and resuscitation III accurate refractometric COP determinations in hypovolemia treated with HALFD

Abstract: In 38 critically burned patients with symptomatic hypovolemia being treated by intravenous fluids, the accuracy of colloid oncotic pressure (COP) calculated from the refractometrically-determined serum total protein (TP RI ) was compared with COP values determined by a commercially-available clinical oncometer. Sera were obtained randomly from seven patients receiving Ringer's lactate solution, five receiving a hypertonic solution (240 mOsm Na + ) and 26 receiving a hypertonic solution containing albumin (12.5 gm/liter, HALFD method). There was poor correlation between COP measure and that calculated from RI in patients receiving colloid-free fluid, but high correlation (r=0.925) in patients receiving HALFD. There was high correlation (r=0.951) between measured COP and values calculated from TP RI in patients receiving hypertonic fluid, colloid-containing hypertonic fluid, or no fluid:COP = 4.08 (TP RI ) − 4.61.

Reversal of ethanol induced body dehydration with prolonged consumption in rats

Abstract: Ethanol induced negative water balance has been previously inferred from fluid turnover rates upon initial exposure followed by restored normal fluid balance with prolonged exposure. The first two experiments of the present investigation noted hypovolemia and carcass dehydration during the initial few days of forced choice maintenance on 10% ethanol with recovery to near normal levels of intravascular volume and carcass water after 2 months of forced consumption. A third experiment attempted to test whether the alcohol induced dehydration could be corrected with the administration of exogenous ADH.

Effect of vasopressin on portal pressure during volume replacement after acute hemorrhage.

Abstract: This study evaluated both the isolated and combined effects of intravenous vasopressin and volume replacement on cardiac output and portal pressure in hypovolemic dogs. Following acute hemorrhage and sustained hypotension (60 mm Hg for 45 min), 20 anesthetized dogs received either: no treatment; intravenous vasopressin (20 units/30 min); Ringer's lactate (volume equal to shed blood/30 min); or intravenous vasopressin and Ringer's lactate. At 30 minutes after hypotension, cardiac output decreased 52% and portal pressure decreased 61% in control animals. Hypovolemia plus intravenous vasopressin resulted in significant reductions in cardiac output (41%) and portal pressure (62%) compared to baseline recordings, but not compared to control animals. Following hypovolemia and Ringer's lactate, cardiac output and portal pressure increased to prehemorrhage levels. With vasopressin and Ringer's lactate, portal pressure remained decreased (39%), while cardiac output returned to prehemorrhage levels. This study demonstrates that administration of intravenous vasopressin during hypovolemia does not cause an added reduction in cardiac output and does not prevent restoration of the normal cardiac output by volume replacement. Moreover, administration of vasopressin during volume replacement prevented a return of portal venous pressure to prehemorrhage levels.

Circulatory defects during phenformin lactic acidosis

Abstract: Detailed hemodynamic and metabolic studies were performed during the course of phenformin related lactic acidosis in two patients. Arterial blood lactate was increased to 11.5 and 26.1 mM/L and arterial blood pH was reduced to 7.05 and 6.80 units, respectively. A marked reduction in cardiac indices (0.94 and 1.15 L/min/m2), stroke volume, and stroke work were observed, with either normal or increased arterial resistance. Mild increases in pulmonary artery systolic pressure (50/11), 45/25 mmHg) were observed, but necropsy in both cases disclosed no evidence of pulmonary vascular obstruction. In the absence of increases in central venous and pulmonary artery wedge pressure, a cardiac failure was excluded as primary cause of the low output state. Hypovolemia was excluded on the basis of radioisotope dilution measurements of plasma volume and red cell mass and no increase in cardiac output followed volume expansion. Oxygen extraction from blood was not grossly impaired. These observations indicate that phenformin-related lactic acidosis may evolve as a circulatory defect characteristic of shock in which oxygen delivery rather than oxygen utilization is impaired. The hemodynamic defect is best explained by a defect in the intravascular distribution of blood volume.

Effects of acute lactic acidosis on some hemodynamic and hematologic values in three cows.

Abstract: Some hemodynamic and hematologic effects of acute experimental lactic acidemia in 3 healthy cows are presented. Lactic acidemia was induced by intravenous infusion of a 10% solution of racemic lactic acid. The prominent features of the acidification of the blood were increases in carotid artery blood pressure and responses to intravenously injected norepinephrine, slight bradycardia and slight hyperventilation. Intravascular hemolysis with hemoglobinuria was a constant finding. Otherwise, no adverse effects of the acidemia were noted. These changes were paralleled by a progressive fall in arterial blood pH, base excess and PCO2 and increasing venous blood L (+)-lactate concentrations A reasonable explanation for the hemodynamic effects of the acidemia is peripheral vasoconstriction elicited by either stimulation of the sympathetic nervous system or increased sensitivity of vasoconstrictive receptors. The results are discussed with special reference to primary lactic acidosis encountered in grain engorgement in ruminants and to the secondary lactic acidosis of shock. These conditions are characterized by hemoconcentration and hypovolemia. Therefore, the results of this study of healthy normovolemic cows may not be valid in the severely dehydrated, hemoconcentrated and acidemic cow as hypotension is reported in the literature in connection with ruminal acidosis in sheep.

Regional gastric mucosal blood flow in hypovolemic shock.

Abstract: The effect of hypovolemia on the mucosal blood flow of the gastric corpus and antrum were tested with the microsphere method 30 and 60 min after induction of hemorrhagic shock in the rat. The results demonstrate a marked reduction after 30 and 60 min without any significant differences between the corpus and the antrum. This reduction is largely dependent on cardiac and circulatory function. It is concluded that the differences in energy metabolism, which have been implicated as explanation for the different susceptibility to develop stress lesions by Menguy and Masters, cannot be attributed to different degrees of ischemia.

Variations of catecholamines in mixed shock. Therapeutic implications. Experimental and clinical investigations.

Abstract: The variations of catecholamines, cortisol and aldosterone in mixed shock (traumatic, hemorrhagic and septic) were studied experimentally and clinically. In the stage of collapse adrenaline decreased by 81.4% and noradrenaline by 62.6% as compared with the preoperative values. These decreases were found to be directly proportional to the decrease of arterial blood pressure, pulse amplitude and diuresis as well as to the slowing down or even stop of microcirculation. The value of plasma cortisol increased in the stage of collapse by 98.3% and that of aldosterone by 66.27% as compared with the preoperative values. Treatment with a pharmacodynamic sympatheticolytic-vasopressor-adrenocortical mixture is recommanded when the blood pressure remains below 50--60 mm Hg for 1--2 hrs and when the treatment for the correction of hypovolemia with fluids and sympatheticolytics has failed. Clinically, this treatment gave good results in 34 of the 58 cases studied (58.6%).

Monitoring the critically ill surgical patient.

Abstract: Critically ill surgical patients account for approximately half the patients in an active multidisciplinary critical care unit. Hypovolemia and sepsis are common in such patients and affect a number of organ systems. Monitoring these systems provides therapeutically relevant information that may decrease morbidity and improve patient survival. Circulatory hemodynamics may be assessed by direct measurement of the arterial blood pressure, central venous and pulmonary artery pressure monitoring and cardiac output determination; the data thus obtained are valuable in guiding fluid replacement in the hypovolemic individual. The respiratory status may be assessed by bedside spirometry and measurement of arterial blood gas tensions to gauge pulmonary function and the need for assisted ventilation. Renal dysfunction is common in such patients; careful analysis of both urine and blood may identify prerenal as opposed to renal and postrenal factors. Monitoring of the gastrointestinal tract, especially for hemorrhage, is important. Finally, careful attention to nutritional status and provision of adequate protein and energy intake by mouth or by vein is a vital component of the optimal care of these patients.

Predictive Value of Core — Toe Temperature and Mixed Venous Oxygen Saturation After Cardiac Surgery

Abstract: Some of the patients returning to the surgical intensive care unit resemble a shock like condition. They are pale, cold, have a clammy skin and a low mixed venous oxygen saturation. All their signs point to hypovolemia and require intravenous fluidloading. The hypothesis that a-blockade is useful in such patients was tested in a randomly selected group of patients. Group 1, 43 patients with severe cardiac deformities, received a-blockade (largactil 2.5 to 5 mg i. v.) while group II, 25 patients undergoing similar cardiac surgery did not receive any a-blockade drug. Fluid replacement was similar in both groups.

Prognosis of Acute Pancreatitis

Abstract: The overall mortality in acute pancreatitis is approximately 13% to 15%.1,2The mortality of hemorrhagic pancreatitis is far greater than edematous pancreatitis, at least 20%3 and in some series greater than 50%.4 Fatalities do occur on the basis of edematous pancreatitis,4–6 usually from hypovolemia leading to shock and renal shutdown.2