Showing papers on "Hypovolemia published in 1992"
TL;DR: In this article, the authors found that during exercise in the heat, sweat output often exceeds water intake, which results in a body water deficit or hypohydration, which causes a hypertonic-hypovolemia of the blood.
Abstract: During exercise in the heat, sweat output often exceeds water intake, which results in a body water deficit or hypohydration. This water deficit occurs from both the intracellular and extracellular fluid compartments, and causes a hypertonic-hypovolemia of the blood. Aerobic exercise tasks are likely to be adversely affected by hypohydration; and the warmer the environment the greater the potential for performance decrements. Hypohydration causes greater heat storage and reduces one's ability to tolerate heat strain. The greater heat storage is mediated by reduced sweating rate (evaporative heat loss) and reduced skin blood flow (dry heat loss) for a given core temperature. Reductions of sweating rate and skin blood flow are most tightly coupled to blood hypertonicity and hypovolemia, respectively. In addition, hypovolemia and the displacement of blood to the skin make it difficult to maintain central venous pressure and thus an adequate cardiac output to simultaneously support metabolism and thermoregulation during exercise-heat stress.
413 citations
TL;DR: In a group of hemodialysis patients without diabetes or other conditions known to impair autonomic reflexes, he modialysis-induced hypotension is not caused by chronic uremic impairment in arterial or cardiopulmonary baroreflexes but rather by acute, paradoxical withdrawal of sympathetic vasoconstrictor drive producing vasodepressor syncope.
Abstract: Acute hypotension is an important complication of hemodialysis, but the underlying mechanisms remain poorly understood. Because hemorrhage-induced hypovolemia can trigger a sudden decrease in sympathetic activity resulting in bradycardia and vasodilation, we hypothesized that hemodialysis-induced hypovolemia also can trigger the same type of vasodepressor reaction, which would exacerbate the volume-dependent fall in blood pressure. We therefore measured blood pressure, vascular resistance, and sympathetic nerve activity (intraneural microelectrodes) during sessions of maintenance hemodialysis in 7 patients with and 16 patients without a history of hemodialysis-induced hypotension. During hemodialysis, blood pressure at first remained unchanged as calf resistance increased in both hypotension-resistant (from 37 +/- 4 to 49 +/- 5 U, P < 0.05) and hypotension-prone (from 42 +/- 6 to 66 +/- 12 U, P < 0.05) patients; sympathetic activity increased comparably in the subset of patients in whom it could be measured. With continued hemodialysis, calf resistance and sympathetic activity increased further in the hypotension-resistant patients, but in the hypotension-prone patients the precipitous decrease in blood pressure was accompanied by decreases in sympathetic activity, vascular resistance, and heart rate as well as symptoms of vasodepressor syncope. On an interdialysis day, both groups of patients increased vascular resistance normally during unloading of cardiopulmonary baroreceptors with lower body negative pressure and increased heart rate normally during unloading of arterial baroreceptors with infusion of nitroprusside. These findings indicate that in a group of hemodialysis patients without diabetes or other conditions known to impair autonomic reflexes, hemodialysis-induced hypotension is not caused by chronic uremic impairment in arterial or cardiopulmonary baroreflexes but rather by acute, paradoxical withdrawal of sympathetic vasoconstrictor drive producing vasodepressor syncope.
255 citations
TL;DR: Data indicate that the reversal of the postoperative extension of the bleeding time is due in part to rewarming and to the release of larger platelets into the circulation, and they suggest that hyperfibrinolysis and complement activation may play an important role in the cardiopulmonary bypass-induced platelet dysfunction.
204 citations
TL;DR: The transfer of fish between hypo- and hyperosmotic environments has been used to examine the effects of ion, volume, or pressure perturbation on the RAS.
Abstract: Publisher Summary This chapter discusses the role of the renin–angiotensin system (RAS), the kallikrein–kinin system (KKS), and atrial natriuretic peptides (ANP) in blood and extracellular fluid volume regulation. The RAS and ANP systems deserve special consideration because of their well-known involvement as antidrop and antirise effectors of pressure and volume in mammals and because of their ubiquity in a variety of fish. The KKS also impacts on fluid balance in mammals and may have similar activities in fish. Hemorrhage, or other perturbations that produce hypotension or hypovolemia, usually activates the teleost RAS. Consecutive l-ml hemorrhages increase drinking and plasma ANG II in FW eels, Anguilla japonica . The transfer of eels to SW after the first hemorrhage, which presumably exacerbates the hypovolemia, enhances drinking and further increases plasma ANG II. The transfer of fish between hypo- and hyperosmotic environments has been used to examine the effects of ion, volume, or pressure perturbation on the RAS.
176 citations
TL;DR: Improved statistics are derived from experience in burn centers, where there is substantial knowledge of the pathophysiology of burn injury and inadequate volume replacement in major burns is, unfortunately, common when clinicians lack sufficient knowledge in this area.
Abstract: The goal of fluid resuscitation in the burn patient is maintenance of vital organ function at the least immediate or delayed physiological cost. To optimize fluid resuscitation in severely burned patients, the amount of fluid should be just enough to maintain vital organ function without producing iatrogenic pathological changes. The composition of the resuscitation fluid in the first 24 hours postburn probably makes very little difference; however, it should be individualized to the particular patient. The utilization of the advantages of hypertonic, crystalloid, and colloid solutions at various times postburn will minimize the amount of edema formation. The rate of administration of resuscitation fluids should be that necessary to maintain satisfactory organ function, with maintenance of hourly urine outputs of 30 cc to 50 cc in adults and 1-2 cc/kg/% burn in children. When a child reaches 30 kg to 50 kg in weight, the urine output should be maintained at the adult level. With our current knowledge of the massive fluid shifts and vascular changes that occur, mortality related to burn-induced hypovolemia has decreased considerably. The failure rate for adequate initial volume restoration is less than 5% even for patients with burns of more than 85% of the total body surface area. These improved statistics, however, are derived from experience in burn centers, where there is substantial knowledge of the pathophysiology of burn injury. Inadequate volume replacement in major burns is, unfortunately, common when clinicians lack sufficient knowledge in this area.
153 citations
Journal Article•
TL;DR: Infusion of 250 ml hypertonic saline solution in patients with severe hypovolemia was not related to any complications, nor did it affect mortality rates; it improved MAP significantly, acutely expanded plasma volume by 24%, and reduced significantly the volumes of crystalloids and blood required in their resuscitation.
147 citations
TL;DR: The findings suggest that transesophageal echocardiography performed on patients after cardiac operations, at the bedside in the intensive care unit, can readily elucidate the cause of hypotension in the large majority of patients and is a valuable adjunct to hemodynamic evaluation in patient management.
106 citations
TL;DR: Heart rate response to reversible central hypovolaemia can be divided into three stages, and this stage may proceed into irreversible shock with death from cardiac arrest probably related to the formation of free oxygen radicals.
Abstract: 1. Heart rate response to reversible central hypovolaemia can be divided into three stages. In the first stage (corresponding to a reduction of the blood volume by approximately 15%) a modest increase in heart rate ( 120 beats/min) is manifest. This stage may proceed into irreversible shock with death from cardiac arrest probably related to the formation of free oxygen radicals. 2. Recognition of the vasodepressor-cardioinhibitory reaction to a reduced circulating blood volume is important and suggests the need for immediate treatment with volume expansion in critically ill patients.
82 citations
Journal Article•
TL;DR: Cardiopulmonary effects of propofol were studied in hypovolemic dogs from completion of, until 1 hour after administration, and measurements had returned to values similar to those measured prior to prop ofol administration.
Abstract: Cardiopulmonary effects of propofol were studied in hypovolemic dogs from completion of, until 1 hour after administration. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 6 mg of propofol/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to propofol administration, oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after propofol administration, mean pulmonary arterial pressure, pulmonary vascular resistance, oxygen utilization ratio, venous admixture, and arterial and mixed venous carbon dioxide tensions increased, whereas mean arterial pressure, arterial oxygen tension, mixed venous oxygen content, arterial and mixed venous pH decreased from values measured prior to propofol administration. Fifteen minutes after propofol administration, mixed venous carbon dioxide tension was still increased; however by 30 minutes after propofol administration, all measurements had returned to values similar to those measured prior to propofol administration.
68 citations
TL;DR: It is suggested that NO production plays an important role in the pathophysiology of hemorrhagic shock and survival rate, survival time, plasma myocardial depressant factor (MDF) activity, MAP, and microscopic gastric alterations were evaluated.
Abstract: Summary: Hypovolemic hemorrhagic shock was induced in rats by intermittently withdrawing blood from an iliac catheter for 20 min until mean arterial blood pressure (MAP) decreased to 30 mm Hg. Survival rate, survival time, plasma myocardial depressant factor (MDF) activity, MAP, and microscopic gastric alterations were then evaluated. NG-nitro-L-arginine methyl-ester (L-NAME), a selective inhibitor of nitric oxide (NO) production from L-arginine, was injected intravenously (i.v.) after the bleeding was discontinued. Untreated hemorrhagic shocked rats died in 27 ± 3.3 min, had enhanced plasma activity of MDF, and exhibited hemorrhagic infiltrates in gastric fundus mucosa. L-NAME (5 and 10 mg/kg) significantly increased survival rate and time, blunted the increase in plasma MDF activity, and protected against the gastric lesions induced by hemorrhagic hypovolemic shock. All these protective effects were reversed by a bolus of L-arginine (30 mg/kg/i.v.), given 2 min after administration of L-NAME. Our findings suggest that NO production plays an important role in the pathophysiology of hemorrhagic shock.
65 citations
TL;DR: Fluid resuscitation from traumatic hemorrhagic shock is a critical component of therapy for the critically injured patient and Identification of hypovolemia and methods to monitor tissue are important aspects of patient care.
TL;DR: BI measured at low frequency can represent a valuable index of acute changes in body water in a group of surgical patients but not in a given individual.
Abstract: Objective: To evaluate the relationship between changes in body bioelectrical impedance (BI) at 0.5, 50 and kHz and the changes in body weight, as an index of total body water changes, in acutely ill surgical patients during the rapid infusion of isotonic saline solution.Design: Prospective clinical study.Setting: Multidisciplinary surgical ICU in a university hospital.Patients: Twelve male patients treated for acute surgical illness (multiple trauman=5, major surgeryn=7). Selection criteria: stable cardiovascular parameters, normal cardiac function, signs of hypovolemia (CVP≤5 mmHg, urine ouput <1 ml/kg×h).Interventions: After baseline measurements, a 60 min fluid challenge test was performed with normal saline solution, 0.25 ml/kg.Measurements and results: Body weight (platform digital scale), total body impedance (four-surface electrode technique; measurements at 0.5, 50 and 100 kHz) and urine output. Fluid retention induced a progressive decrease in BI at 0.5, 50 and 100 kHz, but the changes were significant for BI 0.5 and BI 100 only, from 40 min after the beginning of the fluid therapy onwards. There was a significant negative correlation between changes in water retention and BI 0.5, with individual correlation coefficients ranging from −0.72 to 0.95 (p<0.01–0.0001). The slopes of the regression lines indicated that for each kg of water change, there was a mean decrease in BI of 18 ohm, but a substantial inter-individual variability was noted.Conclusion: BI measured at low frequency can represent a valuable index of acute changes in body water in a group of surgical patients but not in a given individual
TL;DR: It is proposed that, in these episodes, rats are guided by gustatory receptors to obtain the desired NaCl in a palatable solution.
TL;DR: Hypertonic saline-dextran solution resuscitation of intraoperative hypovolemia is performed effectively with smaller fluid and sodium loads, and is devoid of the deleterious effects associated with fluid accumulation induced by a conventional isotonic solution regimen.
Abstract: : We compared a hypertonic solution (7.5% NaCl in 6% Dextran-70, HSD) with isotonic saline (0.9% NaCl, NS) for treatment of intraoperative hypovolemia. Fourteen pigs anesthetized with isofluorane underwent a left thoracotomy, followed by hemorrhage for one hour to reduce mean arterial pressure to 45 mmHg. A continuous infusion of either solution was then initiated and the flow rate adjusted to restore and maintain thoracic descending aortic blood flow at baseline levels during a subsequent two-hour period. Full resuscitation to initial values of aortic blood flow was achieved with both regimens, but the NS group required larger volumes and sodium loads to maintain hemodynamic values. NS resuscitation produced increases in right heart preload (central venous pressure), and afterload (pulmonary artery pressure), resulting in increased right ventricular work.
TL;DR: C cerebral small-vessel vasoconstriction in response to the sympathetic activation unmasked by lower-body negative pressure may interfere with the autoregulatory response to a sudden fall in blood pressure, and may explain the common observation of neurological deficit during hypovolemia even with a normal blood pressure.
Abstract: Although severe hypovolemia can lead to hypotension and neurological decline, many patients with neurosurgical disorders experience a significant hypovolemia while autonomic compensatory mechanisms maintain a normal blood pressure. To assess the effects of normotensive hypovolemia upon cerebral hemodynamics, transcranial Doppler ultrasound monitoring of 13 healthy volunteers was performed during graded lower-body negative pressure of up to -50 mm Hg, an accepted laboratory model for reproducing the physiological effects of hypovolemia. Middle cerebral artery flow velocity declined by 16% +/- 4% (mean +/- standard error of the mean) and the ratio between transcranial Doppler ultrasound pulsatility and systemic pulsatility rose 22% +/- 8%, suggesting cerebral small-vessel vasoconstriction in response to the sympathetic activation unmasked by lower-body negative pressure. This vasoconstriction may interfere with the autoregulatory response to a sudden fall in blood pressure, and may explain the common observation of neurological deficit during hypovolemia even with a normal blood pressure.
TL;DR: This optical method was a means to detect hypovolemia at an early stage and to prevent ultrafiltration induced hypotension by means of an optical reflection method with an optical monitor clipped onto the arterial blood line.
Abstract: A new method is described to noninvasively and continuously measure changes in blood volume (BV) during hemodialysis by means of an optical reflection method with an optical monitor (950 nm) clipped onto the arterial blood line. The amount of reflected light (L) appeared to be linearly proportional to the erythrocyte concentration (r = 0.91). Changes in L correlated well with changes in erythrocyte concentration during hemodialysis (r = 0.94). A study in 10 patients on regular dialysis was done. The BV decrease after 3 hr of treatment was 17.0 +/- 5.2%, and it correlated with the amount of fluid withdrawn by ultrafiltration (mean, 2,519 +/- 589 ml). Five hypotensive episodes were seen that were characterized by a higher rate of BV fall during the preceding 15 min (9.9 +/- 1.9 versus 3.6 +/- 4.3%/hrp; p < 0.05) and by a lower BV value at that moment (78.2 +/- 3.4 versus 84.5 +/- 4.5%; p < 0.025) than in the other five patients at comparable times. It was concluded that this optical method was a means to detect hypovolemia at an early stage and to prevent ultrafiltration induced hypotension.
Journal Article•
TL;DR: Results of this study indicate that etomidate induces minimal changes in cardiopulmonary function when administered to hypovolemic dogs.
Abstract: Cardiopulmonary effects of etomidate administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. One milligram of etomidate/kg of body weight was then administered IV to 7 dogs, and the cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to etomidate administration, heart rate, arterial oxygen tension, and oxygen utilization ratio increased. Compared with baseline values, the following variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, mixed venous oxygen content, and arterial carbon dioxide tension. Three minutes after etomidate administration, central venous pressure, mixed venous and arterial carbon dioxide tension, and venous admixture increased, and heart rate, arterial and venous pH, and arterial oxygen tension decreased, compared with values measured immediately prior to etomidate administration. Fifteen minutes after etomidate injection, arterial pH and heart rate remained decreased. At 30 minutes, only heart rate was decreased, and at 60 minutes, mean arterial pressure was increased, compared with values measured before etomidate administration. Results of this study indicate that etomidate induces minimal changes in cardiopulmonary function when administered to hypovolemic dogs.
TL;DR: It is concluded that hypovolemia induces c-fos expression in hypothalamic neurons known to be associated with blood volume/pressure regulation.
Abstract: Immunoreactivities to Fos proteins were detected in numerous neurons in the supraoptic, paraventricular and accessory neurosecretory nuclei 1 h following withdrawal of 4–5 cc of blood from the rat femoral arteries. Few or no positive cells were observed in the same nuclei in sham-operated or control animals. It is concluded that hypovolemia induces c-fos expression in hypothalamic neurons known to be associated with blood volume/pressure regulation.
TL;DR: It is concluded that a serotonergic mechanism, probably located in the brainstem, may be involved in the decompensatory phase of acute central hypovolemia and partial depletion of neuronal serotonin had no effect on either phase.
Abstract: We tested whether a brainstem serotonergic mechanism influences the hemodynamic response to acute central hypovolemia. An inferior vena caval cuff was gradually inflated so that mean cardiac index (MCI) fell at a constant rate (approximately 8%/min). Under control conditions, mean systemic vascular conductance index (MSVCI) fell progressively until MCI had fallen by approximately 50% (compensatory phase), at which point MSVCI rose abruptly and arterial pressure fell to approximately 40 mm Hg (decompensatory phase). Intravenous methysergide delayed the decompensatory phase and at a critical dose (300-3,000 nmol) abolished it. Methysergide had similar effects when injected into the fourth ventricle, pontomedullary cistern, or lateral ventricle in doses that were 7-10% of the critical i.v. dose, but had no effect when injected into the spinal subarachnoid space. LY53857 was equipotent to methysergide. None of these treatments attenuated the vasoconstriction of the first, compensatory, phase. Partial depletion of neuronal serotonin (after p-chlorophenylalanine or 5,7-dihydroxytryptamine treatment) had no effect on either phase. We conclude that a serotonergic mechanism, probably located in the brainstem, may be involved in the decompensatory phase of acute central hypovolemia.
TL;DR: It is concluded that raising plasma ANP by infusion of the synthetic peptide results in a filtration-independent, tissue-selective increase in albumin transport, which is a potential mechanism for extrarenal fluid shift during circulatory volume overload.
Abstract: Blood-tissue transport of 131I-labeled bovine serum albumin (BSA) during intravenous infusion of synthetic atrial natriuretic peptide (ANP) was examined in anesthetized male Wistar rats. Plasma volumes were maintained at pre-ANP levels by infusion of 2% BSA in lactated Ringer solution (LR) to minimize compensatory responses to ANP-induced hypovolemia. 131I-BSA clearance was measured over 30 min, and 125I-BSA was injected terminally to correct for intravascular volume. Thirty-minute infusion of 20 ng.kg-1.min-1 ANP resulted in a tissue-selective increase in 131I-BSA clearance in jejunum and colon compared with controls given LR only. Smaller but significant increases in tracer clearance also were observed in fat, kidney, left ventricle, and skeletal muscle exposed to 400 ng.kg-1.min-1 ANP. The observed elevation in tracer albumin extravasation was not associated with any measurable increase in tissue extravascular water content. Furthermore, it was shown that coupling of 131I-BSA transport to filtration induced by hindlimb venous congestion was similar in control and ANP-treated rats. In a second series of experiments, plasma ANP levels were determined after 30-min ANP infusions from 0 to 180 ng.kg-1.min-1. Significant linear associations between physiological ANP levels (62-578 pg/ml) and 131I-BSA clearance were demonstrable for small intestine, colon, fat, kidney, and skeletal muscle but not for skin, heart, diaphragm, and lung. We conclude that raising plasma ANP by infusion of the synthetic peptide results in a filtration-independent, tissue-selective increase in albumin transport. Tissue uptake of albumin is a potential mechanism for extrarenal fluid shift during circulatory volume overload.
TL;DR: Pulse rate increase was the most sensitive of the orthostatic vital signs used alone and a pulse rise of greater than 20 beats per minute had a sensitivity of 9% with a specificity of 98%.
Abstract: The authors conducted this study to: (1) determine the effect of age on orthostatic vital signs; and (2) to define the sensitivity and specificity of alternative definitions of "abnormal" orthostatic vital signs in blood donors sustaining an acute 450-mL blood loss. The population studied were 100 healthy adult volunteer blood donors and 100 self-sufficient ambulatory citizens attending a senior citizens daytime activity center. Subjects with a history of orthostatic hypotension were excluded. Subjects were first placed in the recumbent position and their rate pulse and blood pressure were determined after 1 minute; these same parameters were measured in the same arm beginning 30 seconds after standing. In blood donors measurement of orthostatic vital signs was repeated immediately after blood donation. Blood donors served as their own controls in the determination of sensitivities and specificities. Mean orthostatic vital sign changes were as follows: pulse rate, 2 +/- 7 beats per minute; systolic blood pressure, -3 +/- 9 mm Hg; and diastolic blood pressure, 1 +/- 7 mm Hg. There was no clinically meaningful variance in orthostatic blood pressure changes with age. For a given specificity, pulse rate increase was the most sensitive of the orthostatic vital signs used alone; a pulse rise of greater than 20 beats per minute had a sensitivity of 9% with a specificity of 98%.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: Changes in abdominal pressure may affect the patterns of QSVC and QIVC during respiration, depending on blood volume status, and a prolonged inspiration with hypovolemia may decrease QivC because of the development of a vascular waterfall.
Abstract: Respiratory induced changes in superior (QSVC) and inferior (QIVC) vena caval flows and abdominal pressures were evaluated in anesthetized closed-chest dogs. QSVC and QIVC were measured with ultrasound transit time flow probes (n = 5), and general (Pab) and regional subdiaphragmatic (Pd) abdominal pressures were measured by air-filled balloons (n = 5), during two respiratory maneuvers produced by phrenic nerve stimulation, i.e., simulated spontaneous inspiration (SSI), and Mueller maneuver (MM), with the airway occluded to minimize diaphragmatic descent. With hypervolemia: during SSI, QSVC decreased, QIVC increased, and right atrial pressure increased (P less than 0.05) despite a decrease in esophageal pressure (Pes), i.e., Kussmaul's sign; during MM, both QSVC and QIVC increased (P less than 0.05) without Kussmaul's sign. The ratios delta Pab/delta Pes and delta Pd/Pes were larger during SSI than MM (P less than 0.01). With hypovolemia: during SSI and MM, QSVC increased and QIVC decreased with a venous pressure gradient across the diaphragm (P less than 0.05), consistent with development of a vascular waterfall. These results suggest that 1) changes in abdominal pressure may affect the patterns of QSVC and QIVC during respiration, depending on blood volume status; 2) a prolonged inspiration with hypovolemia may decrease QIVC because of the development of a vascular waterfall; 3) QSVC and QIVC may be interdependent during respiration; and 4) the essential mechanism of Kussmaul's sign is a substantially larger inspiratory increase in abdominal pressures produced by diaphragmatic descent compared with the decrease in intrathoracic pressure under hypervolemic conditions, rather than the presence of pericardial pathology or right heart dysfunction.
TL;DR: The results indicate that blood flow to bone marrow is highly variable and hormonally and/or locally regulated, which may have practical consequences for marrow transplantation technology and for administration of drug therapy to patients with insufficient bone marrow hematopoiesis.
TL;DR: Using models of exercise, inactivity and confinement, integrated and redundant roles for vascular volume and cardiovascular baroreflexes have been demonstrated as probable underlying mechanisms that contribute independently to the development of orthostatic hypotension following spaceflight, and data suggest that loading of arterial baroreceptors may be necessary to maintain barore Flex function.
TL;DR: Cardiovascular responses to phlebotomy and postural change were evaluated using a large database developed in a study designed to establish the safety of blood donation by older individuals to indicate that the ability to respond to hypovolemia andPostural change remains relatively intact in healthy elderly individuals.
Abstract: Background.— Responding appropriately to hypotensive challenges is an important determinant of health and functional independence in elderly individuals. Cardiovascular responses to phlebotomy and postural change were evaluated using a large database developed in a study designed to establish the safety of blood donation by older individuals. Methods.— The groups studied included 464 subjects aged 65 years and younger (range, 52 to 65 years) and 532 subjects more than 65 years old (range, 66 to 78 years old). Blood pressure and pulse rate measurements were followed by the withdrawal of 500 mL of blood. These measurements were repeated, first in the supine and then in the sitting position. Results.— Nearly all individuals studied remained hemodynamically stable after these two challenges. Age was not an independent predictor of blood pressure change after either phlebotomy or postural change. Large decreases in diastolic blood pressure were equally rare in both age groups. However, more older subjects (15.2%) exhibited a decline of 20 mm Hg or more in systolic blood pressure following phlebotomy, compared with the middle-aged group (6.9%). These age-related differences did not persist after controlling for the higher initial systolic blood pressures observed in the older subjects. Postphlebotomy postural change to the sitting position had little additional effect. Conclusions.— These results indicate that the ability to respond to hypovolemia and postural change remains relatively intact in healthy elderly individuals. The higher prevalence of a significant drop in systolic blood pressure after phlebotomy, orthostasis, and possibly other homeostatic challenges in older subjects is probably due to the presence of higher basal blood pressure readings, including hypertension. In spite of these differences, blood donation is appropriate and should be encouraged in healthy elderly individuals in this age group. (Arch Intern Med.1992;152:366-370)
TL;DR: The results make worthwhile further investigations on HHS in the presence of a focal brain lesion causing brain edema to find out whether the HHS are useful also for the treatment of intracranial hypertension.
Abstract: Hypertonic/hyperoncotic solutions (e.g. HHS: 7.2 % NaCl/10% dextran-60) are highly effective to normalize cardiovascular function in hemorrhagic shock due to rapid mobilization of fluid from the extravascular compartment. Since experiences are limited with regard to potential side effects of this treatment on the central nervous system, the present studies were carried out under particular consideration of the cerebral blood flow and O2 supply. HHS was administered in albino rabbits subjected to α-chloralose anesthesia and artificial ventilation with and without hemorrhagic hypovolemia. Hemorrhagic hypovolemia of 30 min duration was induced by withdrawal of approximately one third of the circulating blood volume resulting in a decrease in arterial blood pressure to 40 mm Hg. HHS was studied in addition in normovolemic animals. Cardiac output was rapidly normalized by infusion of HHS in animals with hypovolemia, while it increased intermittently in normovolemic animals. In animals with hemorrhagic shock arterial blood pressure recovered by treatment to approximately 70% of normal, whereas blood pressure remained unchanged after infusion of HHS in normovolemic controls. Cerebral blood flow, which was assessed by H2 clearance at the brain surface, had a range of 43.0–50.3 ml/100 g/min under control conditions. It remained virtually unchanged during hemorrhagic hypovolemia and also after infusion of HHS in normovolemic animals. Treatment of shock by HHS was followed 90 or 120 min later by a moderate increase in regional cerebral blood flow to 61 ml/100 g/min. Local tissue PO2 at the brain surface was obtained by an O2 multiwire electrode in the vicinity of the H2 clearance measurements using a weightless suspension system to avoid compression of the brain surface. Infusion of HHS in normovolemic animals did not affect the O2 supply of the brain. Hemorrhagic hypovolemia which led to a left shift of the cerebral PO2, histogram was followed by gradual normalization after fluid resuscitation. The current findings taken together do not indicate adverse side effects of this efficient method of fluid resuscitation with regard to the cerebral blood and O2 supply. The results make worthwhile further investigations on HHS in the presence of a focal brain lesion causing brain edema to find out whether the HHS are useful also for the treatment of intracranial hypertension.
TL;DR: Dxtran infusion is a safe, effective, and low-cost replacement therapy in patients with cirrhotic ascites treated by LVP and dextran and there was no deterioration of these functions in the nonedematous patients treated byLVP even though the protective effect of edema against LVP was lacking in them.
Abstract: Surgicalorty patients with cirrhosis of the liver and tense ascites were randomized to receive either aldactone 400 mg/day and furosemid 80 mg/day (n = 20) or repeated large volume paracentesis (LVP) and infusion of low molecular weight dextran (n = 20). Both treatment groups were similar in clinical and laboratory parameters. Complete mobilization of the ascitic fluid was achieved in all receiving LVP and dextran therapy within 1 week of the treatment, in contrast to the minimal mobilization of the ascitic fluid in patients receiving diuretics even after 2 weeks of therapy. Renal function, the clinical parameters of systemic hemodynamics, serum electrolytes, and hepatic function remained stable in patients receiving LVP and dextran and were similar to those in the diuretictreated patients. We found no deterioration of these functions in the nonedematous patients treated by LVP and dextran even though the protective effect of edema against LVP was lacking in them. Plasma volume estimation in six nonedematous cirrhotic patients treated by LVP and dextran did not reveal any hypovolemia after complete mobilization of ascites. The frequency of complications and death were similar in the two groups. Dextran infusion is a safe, effective, and low-cost replacement therapy in patients with cirrhotic ascites treated by LVP.
Journal Article•
TL;DR: It is concluded that LBNP and intravenous saline loading produce major changes in pulmonary blood-flow and minor effects on pulmonary gas exchange, and that the response to acute changes in fluid distribution is not significantly altered during simulated microgravity.
Abstract: Exposure to microgravity redistributes body fluids with important secondary effects on cardiovascular function. We tested the hypothesis that the fluid shifts also affect pulmonary gas exchange. Microgravity was simulated in six male volunteers by a 10-day period of bedrest at 6 degrees head-down tilt (HDT). Lower body negative pressure (LBNP) and intravenous saline loading superimposed acute changes in fluid distribution on the prolonged effects of HDT. HDT produced relative dehydration and hypovolemia with decreased pulmonary blood flow and diffusing capacity. Before bedrest, pulmonary blood flow decreased by 24% during LBNP and diffusing capacity by 7%, while functional residual capacity increased by 14% (p<0.05). Intravenous saline loading caused a 24% increase in pulmonary blood-flow (p<0.05). Functional residual capacity decreasedby 10% and diffusing capacity by 6% (p<0.05). Lung tissue volume did not change significantly. Head-down tilt had only minor effects on the responses to LBNP and saline loading. We conclude that LBNP and intravenous saline loading produce major changes in pulmonary blood flow and minor effects on pulmonary gas exchange, and that the response to acute changes in fluid distribution is not significantly altered during simulated microgravity.
TL;DR: It is concluded that high-dose vitamin C must be given until 8 hours after burn injury to maintain adequate hemodynamic stability in the presence of a reduced resuscitation fluid volume.
Abstract: Twenty-four guinea pigs with third-degree burns over 70% of the body surface area were divided equally into four groups. All animals received Ringer's lactate (R/L) beginning 30 minutes after burn injury. Group 1 received R/L without vitamin C beginning 2 hours after burn injury. Groups 2, 3, and 4 received R/L with vitamin C until 4, 8, and 24 hours after burn injury, respectively. Beginning 3 1/2 hours after burn injury the hourly fluid volume was reduced to 25% of the Parkland formula calculation. The hourly sodium and fluid intake in each group was the same. Groups 1 and 2 demonstrated higher hematocrit and lower cardiac output values as compared with those values for group 3, indicating hypovolemia and hemoconcentration in these groups. Group 3 showed hematocrit and cardiac output values equivalent to those values for group 4. We conclude that high-dose vitamin C must be given until 8 hours after burn injury to maintain adequate hemodynamic stability in the presence of a reduced resuscitation fluid volume.
TL;DR: The data suggest that the described process of fluid gain into the circulation may be capable of increasing plasma volume by as much as 600 ml within only 10 min, suggesting that such plasma volume control might be much more potent than previously believed.
Abstract: Compensatory, net fluid transfer across the capillaries was studied in the arm of man with plethysmographic technique during experimental hypovolaemia induced by lower body negative pressure (LBNP). Thirty, 60, and 110 cmH2O LBNP evoked rapid transfer of fluid from tissue to blood at average rates of 0.053, 0.088 and 0.147 ml min-1 100 ml-1 soft tissue, i.e. graded responses typical for a true homeostatic regulation. Other experiments demonstrated a net fluid absorption not only from the arm but also from a wide range of skeletal muscle and skin regions in the body during experimental hypovolaemia, i.e. the more or less generalized response required if the absorption process is to contribute importantly to plasma volume regulation. In a third series of experiments it was shown that gradually applied LBNP was a much less efficient stimulus for fluid gain into the circulation than rapidly instituted LBNP, tentatively explaining the fairly slow plasma volume refill in main in previous literature after experimental, true and necessarily slow blood loss. Taken together, the findings described warrant the conclusion that the described process of fluid gain into the circulation may be a very important component in the overall homeostatic circulatory regulation in states of hypovolaemia. The data in fact suggest that the process might be capable of increasing plasma volume by as much as 600 ml within only 10 min, suggesting that such plasma volume control might be much more potent than previously believed.