Showing papers on "Hypovolemia published in 1985"

Thermoregulatory and blood responses during exercise at graded hypohydration levels

Abstract: We studied the effects of graded hypohydration levels on thermoregulatory and blood responses during exercise in the heat. Eight heat-acclimated male subjects attempted four heat-stress tests (HSTs). One HST was attempted during euhydration, and three HSTs were attempted while the subjects were hypohydrated by 3, 5, and 7% of their body weight. Hypohydration was achieved by an exercise-heat regimen on the day prior to each HST. After 30 min of rest in a 20 degrees C antechamber the HST consisted of a 140-min exposure (4 repeats of 10 min rest and 25 min treadmill walking) in a hot-dry (49 degrees C, 20% relative humidity) environment. The following observations were made: 1) a low-to-moderate hypohydration level primarily reduced plasma volume with little effect on plasma osmolality, whereas a more severe hypohydration level resulted in no further plasma volume reduction but a large increment in plasma osmolality; 2) core temperature and heart rate responses increased with severity of hypohydration; 3) sweating rate responses for a given rectal temperature were systematically decreased with severity of hypohydration; and 4) the reduction in sweating rate was more strongly associated with plasma hyperosmolality than hypovolemia. In conclusion, an individual's thermal strain increases linearly with the severity of hypohydration during exercise in the heat, and plasma hyperosmolality influences the reduction in sweating more profoundly than hypovolemia.

Midazolam pharmacodynamics and pharmacokinetics during acute hypovolemia

Abstract: This study was designed to test the hypothesis that acute hypovolemia would compromise the compensatory hemodynamic mechanisms to midazolam and decrease its metabolic clearance. Experiments were performed on seven chronically instrumented female beagle dogs. Animals received a single intravenous dose of midazolam, 10 mg/kg, 4 days apart during normovolemic (N) and hypovolemic (H) states in a random sequence. Hypovolemia was achieved by the withdrawal of 26 ml/kg of blood, equivalent to one-third of the calculated blood volume. Midazolam plasma concentrations were determined at 0.25, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, and 12 h after midazolam injection. Elimination half-life (t 1/2 beta) was significantly longer and total clearance was significantly lower during H than during N. Initial distribution half-life, central compartment volume, total volume of distribution, and plasma protein binding were similar in both N and H states. Midazolam caused a significant decrease in systolic blood pressure (SBP) and an increase in heart rate (HR) during N, and produced significant decreases in SBP, diastolic blood pressure (DBP), and mean arterial pressure (MAP) during H. Midazolam led to similar per cent decreases in blood pressure and cardiac output in states N and H; however, the absolute values of blood pressure and cardiac output were significantly (P less than 0.001) lower in the hypovolemic state than in the normovolemic state. These data suggest that the hypotensive effects of midazolam, like those of other intravenous induction agents, could be potentiated by volume depletion.

Mesenteric ischemia in chronic dialysis patients.

Abstract: 6 chronic dialysis patients with acute mesenteric ischemia are described. 3 had nonocclusive infarctions, and 3 had occlusive disease. 5 of the patients had episodes of severe hypotension or hypovolemia immediately before the onset of abdominal symptoms. All patients had leukocyte counts of greater than 12,000 on admission, and 4 had stools positive for occult blood. The characterisitc features of dialysis-induced hypotenison followed by nonspecific abdominal symptoms and leukocytosis are emphasized.

Rationale for the use of colloids in the treatment of shock and hypovolemia.

Abstract: The question, "Are colloids or crystalloids to be preferred for resuscitation in hypovolemic shock conditions?" is detailed in this review. The effects of these two types of fluid regimes on restitution of circulating blood volume, interstitial rehydration, microvascular blood flow, cellular metabolic recovery and on the incidence of systemic complications such as adult respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC) and multiple organ failure are considered. Colloid containing solutions seem superior to crystalloids due to efficient reexpansion of circulating blood volume and enhancement of capillary blood flow. Resuscitation times and thereby the cellular hypoxic insult are considerable reduced while at the same time the formation of excessive tissue oedema is prevented. Colloids do not seem to adversely affect pulmonary function. Dextran has considerable advantages over other types of colloids for the initial shock treatment due to its antithrombotic properties whereby cell aggregability is prevented and the incidence of systemic complications (microembolism syndromes) is convincingly reduced.

Maintenance of blood volume in snakes: transcapillary shifts of extravascular fluids during acute hemorrhage.

Abstract: 1. Tracer dilution analysis (D2O,51Cr, and NaS14CN) was used to investigate the steadystate compartmentation of body fluids and the extent of fluid transfer from extravascular to vascular spaces during hemorrhage-induced hypovolemia in two species of snakes,Elaphe obsoleta andCrotalus viridis. 2. Fluid spaces of the two species are not significantly different (means, blood volume 6.1, 5.4; extracellular fluid 42.2, 41.9; total body water 77.2, 77.2% body mass, respectively), but values for extracellular fluid exceed those reported for other reptiles. 3. Both species of snake withstand graded hemorrhage where 4% of the initial blood volume is withdrawn every 10 min until the cumulative deficit is 32%. Some snakes are able to maintain their initial blood volume throughout hemorrhage, while others restore 90% of deficits within 2 h after hemorrhage ceases. Typically, 50–60% of the hemorrhaged deficit is transferred from the interstitium to the circulation throughout hemorrhage (Fig. 2). The source of fluid entering the vascular space is entirely extracellular during hemorrhage, but fluid from the intracellular space may enter the blood within 2 h after hemorrhage ceases. Snakes are able to maintain arterial pressure during these experiments (Fig. 3). 4. The ability of snakes to maintain hemodynamic stability despite substantial losses of blood can be explained in terms of a large interstitial fluid volume that may shift rapidly to the vascula space. Shifts in the opposite direction also occur in response to hemodynamic factors, implying a low resistance to fluid movement across the capillary wall.

Fluid resuscitation of hypovolemia

Abstract: A great deal has been learned about fluid resuscitation in the last several decades. The choice of an appropriate fluid for resuscitation in every given clinical situation has not yet been definitively determined but we can make some conclusions based on currently available data. It should again be emphasized that the goal of resuscitation of hypovolemic shock is quite clear regardless of the choice of fluid; to resuscitate the shock state as quickly as possible while at the same time minimizing the deleterious effects of fluid resuscitation on the pulmonary, renal, immunological and other systems. Animal experimental work reveals that use of colloid solutions to minimize pulmonary edema formation is ineffective, especially in instances where pulmonary capillary permeability is increased. Further, there are suggestions that colloid solutions may actually exacerbate pulmonary dysfunction following resuscitation by changing the characteristics of the pulmonary interstitium and the dynamics of fluid flux in the lung. This is entirely consistent with Starling's theory of a balance of hydrostatic and osmotic pressure, given what we now understand about the “other” or interstitial side of the Starling equation. Aside from the lungs, there are known side effects of various colloid solutions on other organs and body systems. In addition, questions remain about other possible associated short-term and long-term renal, coagulation, and immunological effects. Clinical studies using extravascular lung water as an objective parameter of pulmonary dysfunction show no correlation with fluid balance and no deleterious effects of crystalloid resuscitation. The relative cost of various resuscitation fluids should be a minor point when making therapeutic decisions. These relative costs, however, argue strongly for crystalloid therapy unless advantages for colloid fluids can be proved. Such proof is lacking to date. This is not to say that colloid solutions might never be called for. An occasional situation may arise in which sudden acute hypovolemia is associated with difficulties in obtaining good intravenous access. An example would be the victim of an automobile accident trapped for a prolonged period in a vehicle. Such situations impose practical limits on the amount of volume that can be infused. The use of colloid solutions to provide maximal intravascular volume restoration may be justified in such instances. In the vast majority of cases of hypovolemia, however, the balance of experimental, clinical, and practical considerations convincingly favor the use of a crystalloid solution for resuscitation in association with blood and clotting factors as needed.

Effect of Halothane on Renal Hemodynamics during Normovolemia and Acute Hemorrhagic Hypovolemia

Abstract: The effects of halothane on renal hemodynamics under both normovolemic and hypovolemic conditions were investigated in chronically instrumented conscious dogs whose homeostatic mechanisms were not altered by the presence of preexisting drugs. Renal blood flow and aortic pressure were assessed by prior implantation of Doppler ultrasonic flow probes on the renal artery and a catheter in the descending aorta. Administration of halothane to conscious normovolemic dogs (Group HN) resulted in 11-26% decreases in renal vascular resistance with no significant changes occurring in renal blood flow. In a second group of animals made hypovolemic while awake (Group AH), 30% of the blood volume was removed over one-half hour. In response to hemorrhage, these conscious animals' renal blood flow did not significantly change from the normovolemic control, and renal vascular resistance significantly decreased. With no further intervention, renal vascular resistance and renal blood flow remained unchanged from the level achieved after the 30% hemorrhage. A third group of animals (Group HH) was hemorrhaged in a manner similar to that of Group AH. They also showed no significant changes in renal blood flow and a significant decrease in renal vascular resistance in response to hemorrhage. Thereafter, administration of halothane, as in Group HN, to this group produced 11-23% decreases in renal vascular resistance with no significant decline in renal blood flow from the hypovolemic control levels established after hemorrhage. The author concludes the following: administration of halothane to normovolemic conscious dogs does not decrease renal blood flow; a moderate degree of acute hemorrhagic hypovolemia does not decrease renal blood flow in conscious dogs; and administration of halothane to acutely hypovolemic conscious dogs does not impair renal perfusion.

Hemodynamic effects of naloxone in early canine hypovolemic shock.

Abstract: The contribution of endorphins (endogenous opiates) to the pathophysiology of shock was evaluated by the administration of naloxone (NAL) at different time intervals after inducing hypovolemia. Forty-four dogs were bled into a reservoir to a mean arterial pressure (MAP) of 40-45 mmHg and maintained at this pressure for 30, 45, or 60 minutes. The animals were then given either intravenous 0.9% NaCl (S) or NAL. Animals treated after 30 minutes of hypovolemia at a fixed MAP had similar hemodynamic responses to both NAL or S. After 45 minutes, the NAL-treated animals showed significant improvement in MAP, cardiac output (CO), and survival (P less than 0.05) when compared with S-treated animals. Animals treated with NAL after 60 minutes showed little significant hemodynamic difference from animals treated with S but all S-treated animals died during the 60-minute treatment period. Plasma endorphinlike activity (PELA) rose with hypovolemia and then returned toward control levels in all NAL treated animals before reinfusion of shed blood while it remained elevated in S-treated animals until after reinfusion.

Fluid replacement during hypothermia.

Abstract: Hypothermia produces acidosis, depressed cardiac function, hypovolemia and hypotension. This study was designed to examine the cardiovascular dynamics involved with restoration of the hypovolemia before rewarming. Mixed breed splenectomized adult dogs (n = 16) were anesthetized with pentobarbital and cooled to a right atrial temperature of 25 degrees C at a rate of 3 degrees C X h-1. The animals were maintained at 25 degrees C for 6 h and rewarmed at 3 degrees C X h-1. Group 1 was given no fluid, Group 2 was given saline (20% of plasma volume infused in 10 min). 2 h after reaching 25 degrees C and Group 3 received saline just prior to rewarming. The hematocrit was elevated in all groups (p less than 0.05) upon cooling, but did not differ between groups even after saline was given. Cardiac output (Co) at 25 degrees C was 35% of precooled values. Group 2 increased their Q by 15% with fluid and this Q was maintained at higher levels than Groups 1 or 3 for the next 4 h. Plasma volume, heart rate, and cardiac contractility returned to control levels upon rewarming, but Q remained low (less than 10%). The level of Q at the start of rewarming did not affect the final level of Q.

Cardiovascular actions of nitrous oxide or halothane in hypovolemic swine.

Abstract: During normovolemia, nitrous oxide causes mild sympathetic stimulation and direct myocardial depression; these effects offset each other, resulting in only minimal cardiovascular changes. To test the hypothesis that during hypovolemia this balance would change and depression predominate, 10 swine were made hypovolemic (30% blood loss) and then were given 70% N2O (0.25 MAC in swine) or an equipotent concentration of halothane, an agent that does not cause sympathetic stimulation. The alternate anesthetic was given to the same hypovolemic swine on another day. Five minutes after induction of anesthesia during hypovolemia, both N2O and halothane caused significant, physiologically important deterioration of compensation for hemorrhage. Halothane decreased systemic vascular resistance (SVR); N2O was more variable in its action, and SVR did not decrease significantly. Both agents caused similar decreases in cardiac output, mean aortic blood pressure, stroke volume, oxygen consumption, and left ventricular minute work, despite increases in plasma epinephrine concentration and plasma renin activity. No differences were found between groups for any of these variables (P greater than 0.05). Plasma norepinephrine concentration increased only in the N2O group and was greater in that group than in the halothane group. The deterioration of cardiovascular compensation for hemorrhage was expressed metabolically by similar decreases in the two groups in partial pressure of oxygen of mixed venous blood and by increases in blood lactate concentration. Thirty minutes after induction of anesthesia, with stable end-tidal anesthetic concentrations, both groups had some cardiovascular, but no metabolic, recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of acute alcohol intoxication on the outcome of severe non-neurologic trauma.

Abstract: The influence of acute alcohol intoxication on the outcome of severe non-neurologic trauma was investigated in a prospective study. Alcohol was found in the blood in 35 of the 69 patients, with mean level 136 +/- 13 mg/100 ml. The patients were admitted to hospital 29.5 +/- 2 min after the injury and had mean ISS 25 +/- 2. In the patients with alcohol in the blood, the blood pressure and PCO2 on arrival were lower than in the other patients. When the alcohol level exceeded 100 mg/100 ml, the blood pressure and PCO2 were lower than in the sober patients despite significantly shorter time between injury and admission to hospital. The hospital stay and mortality were similar in the alcohol and the control group. The greater hypovolemia in the patients with alcohol in the blood indicates that alcohol may be a negative factor for the traumatized patient if resuscitation is delayed, and it underlines the need for rapid and adequate fluid resuscitation of these patients. Language: en

Influences of fasting and water intake on plasma refill during hemorrhagic shock.

Abstract: The hyperglycemic response to hypovolemia has been regarded as an essential osmotic force for promoting the early phase of the internal restoration of plasma volume. Our previous studies of rats fasted 24 hours revealed that they did not develop the hyperglycemic response to hemorrhage observed in fed animals but they had a similar hyperosmotic response. The solutes responsible for the hyperosmolality in the fasted animals were primarily products of anaerobic glycolysis, rather than glucose which accounted for most of the hyperosmolality in fed animals. Plasma refill as reflected by a fall in the hematocrit (Hct) and survival time was significantly reduced in the fasted animals. This study was undertaken to test the hypothesis that the failure of fasted rats to exhibit a normal restoration of plasma volume after hemorrhage may reflect the detrimental effects of fasting on the state of hydration and on the plasma oncotic pressure of the fasted animals rather than the absence of a hyperglycemic response. Four groups of anesthetized rats (280-380 gm) were bled acutely and maintained at an arterial pressure of 40 mm Hg. Before hemorrhage animals in Group A were well fed, those in Groups B, C, and D were fasted for 24 hours. Rats in Group B were induced to drink by addition of sodium chloride in their water, rats in Group C spontaneously had a normal fluid intake, and rats in Group D had a significant reduction in their 24-hour fluid intake. The results demonstrated that 24 hours of fasting led to a loss of body weight of 7 to 10% and a fall in the concentration of plasma total protein of 12 to 17% in all rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Naloxone on Regional Blood Flow Distribution in Canine Hemorrhagic Shock

Abstract: The opiate antagonist naloxone increases arterial pressure, maximal left ventricular dp/dt and cardiac output when administered to dogs subjected to hemorrhagic shock. The purpose of this study was to investigate regional blood flow changes associated with naloxone treatment in anesthetized hypovolemic and normovolemic dogs. Hypovolemic dogs (n = 10) were bled over 30 min (t = -30 to t = 0) to a pressure of 45 mm Hg which was maintained for 1 hr. At t = 60, five dogs received naloxone (2 mg/kg + 2 mg/kg X hr), and five received an equal volume of saline. Regional blood flows were determined at t = -30, 45, and 90 min using 15-micron microspheres. Normovolemic dogs (n = 10) were subjected to the same protocol except they were not bled. During hypovolemia, naloxone produced significant increases in myocardial, intestinal, hepatic, and adrenal blood flows whereas saline treatment did not. No significant changes in skin, muscle, fat, pancreatic, renal, or brain flows were detected. The increases in blood flow were not associated with significant changes in vascular resistance. Naloxone had no significant effects on any hemodynamic parameter during normovolemia. The beneficial effects of naloxone in hemorrhagic shock include increased blood flow to vital organs due to increased perfusion pressure which is secondary to improved cardiac performance.

Scrotal and abdominal skin necrosis complicating intravenous vasopressin therapy for bleeding esophageal varices.

Abstract: Two patients with severe liver disease developed scrotal necrosis after intravenous vasopressin infusion for bleeding esophageal varices. One of these patients also developed anterior abdominal wall skin necrosis. Although ischemic complications secondary to vasopressin are probably not totally avoidable, attention to hypovolemia, concomitantly administered pressor drugs, patient position, and points of local pressure may decrease the likelihood of these previously unreported complications.

Baroreflex function in a patient with Bartter' s syndrome

Abstract: There is little information regarding circulatory re. sponses in Bartter's syndrome, with the exception of marked resistance to vasopressors. We investigated baroreflex function in a 40-year-old woman with this syndrome. The patient showed oscillation of heart rate even with a small increase in blood pressure after administration of vasopressor agents. Variations in heart rate and blood pressure were exaggerated during halothane, nitrous oxide and oxygen anaesthesia. Although the mechanism of the unstable baroreflex in this syndrome remains to be proved, the instability may be attributable to many factors such as prostaglandins, hypovolemia, hypokalemia, halothane, nitrous oxide and positive pressure ventilation. Bartter's syndrome is rare, although the exact incidence is not known, t The syndrome is characterized by hypokalemic hypochloremic alkalosis, hyperreninemia, hypcraldosteronism and hyperplasia of the juxtaglomerular apparatus of the kidneys. Patients with this syndrome have normal blood pressure and show marked resistance to the pressor actions of angiotension II and norepinephrine. 1-7 Because treatment with prostaglandin synthetase

Effects of bleeding on mitochondrial ultrastructure in the avian kidney.

Abstract: SUMMARY Three levels of hypovolemia were produced in awake and anesthetized domestic chickens by withdrawing 2.5, 5.0, or 10.0 ml blood per kg body weight. A commercial indirect bloodpressure monitor was unable to detect significant differences between hemorrhaged birds and age-matched controls. Perfusion-fixed kidney samples from unanesthetized birds had mitochondrial low-amplitude swelling in proximal tubular epithelial cells. This response was slight at the lowest bleeding level but was definite at the middle and marked at the highest bleeding levels. RESUMEN

Orthostatic heart rate and arterial blood pressure changes in normovolemic children

Abstract: Orthostatic heart rate and blood pressure changes were determined in 112 normovolemic children from two to 12 years of age. In normal children, two to eight years of age, and nine to 12 years of age, the heart rate may increase as much as 30 and 40 beats per minute, respectively, upon standing. The orthostatic systolic blood pressure change is independent of age and may, in normal children, fall as much as 27 mm Hg. The orthostatic diastolic blood pressure change, as determined by the fourth or fifth Korotkoff sounds, showed great variability, and probably will not be useful in the assessment of a child's intravascular volume status. Orthostatic changes in heart rate and blood pressure, within the above limits, cannot be used as evidence of hypovolemia, since these changes can occur in normovolemic children.

Changes in plasminogen activator activity and plasmin inhibition in the pig during experimental hypovolaemia.

Abstract: A markedly decreased plasminogen activator activity (PAA) was seen in lung, heart and kidney after experimental hypovolemia in the pig. In 2 of 12 cases, an increased PAA was found in liver and spleen. In skeletal muscle, skin, sciatic nerve and in 10 of 12 cases in liver and spleen PAA was unchanged. A slightly increased plasmin inhibition was noted only in the lung. These changes in tissue PAA were reflected by an increase in the PAA of euglobulin fractions concomitant with a decrease in antiplasmin activity in the blood samples obtained during the bleeding experiments.

Continuous measurement of fluid mobilization from ICF space following acute dehydration by dialyzation in dogs.

Abstract: The changes of the distribution of body fluid following acute isotonic dialyzation were studied from the results of continuous monitoring of extracellular fluid volume and physiological parameters. An indicator of extracellular space, 51Cr-EDTA, was injected into splenonephrectomized dogs. After the equilibrium of tracer dilution was attained, 10 ml/kg of plasma water was isotonically withdrawn by means of a dialyzer of hollow fiber type. The volumes of extracellular fluid (ECF) and plasma (PV) were continuously monitored for 80 min and plasma osmolality was measured at 10 min intervals. At the 50-60th min after the fluid modification, the reduction of PV was only 3.8 ml/kg and that of ECF was 4.2 ml/kg. The continuous profile of ECF change showed a significant mobilization of water from intracellular fluid (ICF) soon after the dialyzation. It is concluded that, in the state of hypovolemia, plasma fluid is replenished with the transvascular fluid absorption from interstitial space and that, concomitantly, the reduction of ISF is restituted with the fluid mobilization from ICF into extracellular space within the early stage of 1 hr. Good linear correlation was found between the amount of mobilized water from ICF and the increment of plasma osmolality. An increase in osmotic force was considered the mechanism which caused the fluid shift. These findings suggest that the change in plasma osmolality is a good predictor of mobilized volume from ICF in hypovolemia. The effects of inverse fluid modification, i.e., isotonic infusion, were also compared.

1817 hyperinflation (airtrapping) as a stimulant of adh response in children with chronic asthma

Abstract: Elevation of plasma antidiuretic hormone (ADH) levels during status asthmaticus is well documented. The physiologic mechanisms responsible for the hormone release include hypovolemia, diminished left atrial filling due to hypoxemia and vasoconstriction from bronchospasm, stress and the role of adrenergic agents. We postulated that hyperinflation (airtrapping) in a chronic asthmatic child could reduce left atrial filling by mechanical forces and so increase the ADH response. The study included 12 chronic asthmatic children (age range:10–15 years, Sex:m:f::8:4). All bronchodilators were discontinued at least 24 hours before the study which consisted of measurement of lung functions including airway resistance and total lung capacities by body plethysmography. In addition, blood was collected for plasma ADH levels, serum and urine osmolalities. 9/12 children had 6–8 fold increase in plasma ADH levels (N-up to 1.7 mU/ml) with normal airway resistance and >120% of predicted normals for total lung capacities. 4/12 had normal lung functions with normal levels of plasma ADH levels. 4/9 children with elevated ADH levels were given furosemide to induce diuresis and this had no effect on either the plasma ADH levels nor the lung functions. In conclusion, 1. hyperinflation in itself produces ADH response 2. whether the hormone causes a negative effect on the lungs by shift in the water balance remains to be studied and 3. diuresis appears to have no effect on either the hormonal response or improving the lung functions.

518 is prolapse of umbilical cord a cause of neonatal hypovolemic shock

Abstract: Prolapse of the umbilical cord (PUC) has been considered a cause of stillbirth and neonatal hypovolemic shock. Traditional theory held that, during labor, a significant portion of blood volume leaves the fetus between contractions, while placental blood does not reach the fetus because of cord compression. This theory antedated modern management of PUC. The objectives of this study were to determine the impact of current management of PUC with tocolysis, maternal position changes, cord reposition and prompt C-section, on fetal/neonatal mortality and on incidence of neonatal hypovolemic shock. 38,585 deliveries occuring during 2½ yrs. were reviewed, and there were 103 (0.37%) cases of PUC identified. Hypovolemia was evaluated by clinical signs of hypoperfusion, heart rate, blood pressure and Hct changes during the first 5 hours of life. Stillbirth rate in PUC was 8 times that without PUC. Infants born after PUC did not have low Apgar scores. There were no neonates with clinical evidence of hypovolemia or shock. Heart rate, blood pressure, and Hct from those born with PUC were not significantly different from normal. This study shows: a)high incidence of stillbirths associated with PUC, b)virtual absence of cardiovascular and clinical signs of hypovolemia in neonates born after PUC. We conclude that with current perinatal management, PUC is not a cause of neonatal hypovolemic shock; however, further early diagnostic efforts are required if the high incidence of stillbirths associated with PUC is to be reduced.

The Role of Small-Molecule Removal in the Control of Treatment Morbidity with Hemodialysis and Hemofiltration

Abstract: In 1976, it was suggested that the critical factor in maintaining the blood pressure during isolated ultrafiltration (UF) was the stability of the serum osmolality, and that by inference the high incidence of symptomatic hypotension seen with efficient dialysis was due primarily to large drops in the serum osmolality.(1) A consequence of this ingenious study, limited to one series of acute experiments in only six selected patients, was the birth of the “shifters” school. The “shifters” believe that dialysis hypotension is due to hypovolemia during UF. The hypovolemia is exaggerated by the passage of extracellular fluid into the cells at the same time as it is removed from the body. Their conclusions are based on imprecise space measurements, and their results are often dubious.(2,3) I have never believed in the “shifter” school and feel that Bergstrom and associates’ conclusions(1) could not apply in a chronic situation. To study this matter in more detail we selected six patients(4) with a high incidence of symptomatic hypotension (drop in mean arterial pressure of more than 20% together with a requirement for nursing attention ± fluid replacement) during conventional hemodialysis lasting 4 hr and employing a 1-m2 cuprophane dialyzer. The study was divided into three parts. Each part lasted for 1 month. During part 1, the dialysate flow rate (single pass) was 500 ml/min; in part 2, the dialysate flow rate was 300 ml/min; and in part 3, the dialysate flow rate was 100 ml/min. All other parameters were kept as near constant during all parts of the study.