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At least 19 recordsLinked to original sources
PubMed2003

Early multiple organ failure after recurrent endotoxemia in the presence of vasoconstrictor-masked hypovolemia.

OBJECTIVE: Critically ill patients who develop multiple organ failure during systemic inflammatory states are often predisposed to hypovolemia and vasoconstrictor therapy. Although numerous investigations have evaluated the sequelae of systemic inflammation, no data are available on the contribution of chronic vasoconstrictor-masked hypovolemia to organ dysfunction and morphology. DESIGN: Prospective, randomized laboratory investigation. SETTING: University research laboratory. SUBJECTS: Eighteen adult chronically instrumented sheep. INTERVENTIONS: The animals were randomly assigned to one of three groups. In the norfenefrine-masked hypovolemia plus endotoxemia (NMH+ENDO) group, mean arterial pressures of 80 mm Hg were maintained by using the alpha1-adrenergic catecholamine norfenefrine for 52 hrs during hypovolemia. Hypovolemia was induced by hemorrhage (about 23 mL x kg(-1)) until mean arterial pressures reached 40 mm Hg. Endotoxin (0.5 microg x k(-1)) was then injected after 4, 16, 28, and 40 hrs. The NMH group received norfenefrine-masked hypovolemia but no endotoxin. In the ENDO group, recurrent endotoxemia was induced during normovolemia. MEASUREMENTS AND MAIN RESULTS: Despite profound differences in fluid management, cardiovascular filling pressures were not statistically different between groups. Endotoxemia induced norfenefrine-refractory shock (p < .05 vs. the other groups) and contributed to renal dysfunction only during vasoconstrictor-masked hypovolemia. Norfenefrine-masked hypovolemia caused disseminated cardiac cell necrosis independent of endotoxemia (p < .05 vs. ENDO). CONCLUSIONS: Hypovolemia can be masked when volume status is monitored by filling pressures. In this new model of endotoxemia-associated multiple organ failure, chronic vasoconstrictor-masked hypovolemia turned systemic inflammation into a life-threatening condition with renal and cardiovascular failure. Cardiomyocyte necroses were caused by vasoconstrictor-masked hypovolemia but were unrelated to cardiovascular failure.

Adrenergic alpha-Agonists↗
PubMed2001

Deterioration of left ventricular chamber performance after bed rest : "cardiovascular deconditioning" or hypovolemia?

BACKGROUND: Orthostatic intolerance after bed rest is characterized by hypovolemia and an excessive reduction in stroke volume (SV) in the upright position. We studied whether the reduction in SV is due to a specific adaptation of the heart to head-down tilt bed rest (HDTBR) or acute hypovolemia alone. METHODS AND RESULTS: We constructed left ventricular (LV) pressure-volume curves from pulmonary capillary wedge pressure and LV end-diastolic volume and Starling curves from pulmonary capillary wedge pressure and SV during lower body negative pressure and saline loading in 7 men (25+/-2 years) before and after 2 weeks of -6 degrees HDTBR and after the acute administration of intravenous furosemide. Both HDTBR and hypovolemia led to a similar reduction in plasma volume. However, baseline LV end-diastolic volume decreased by 20+/-4% after HDTBR and by 7+/-2% after hypovolemia (interaction P<0.001). Moreover, SV was reduced more and the Starling curve was steeper during orthostatic stress after HDTBR than after hypovolemia. The pressure-volume curve showed a leftward shift and the equilibrium volume of the left ventricle was decreased after HDTBR; however, after hypovolemia alone, the curve was identical, with no change in equilibrium volume. Lower body negative pressure tolerance was reduced after both conditions; it decreased by 27+/-7% (P<0.05) after HDTBR and by 18+/-8% (P<0.05) after hypovolemia. CONCLUSIONS: Chronic HDTBR leads to ventricular remodeling, which is not seen with equivalent degrees of acute hypovolemia. This remodeling leads to a greater decrease in SV during orthostatic stress after bed rest than hypovolemia alone, potentially contributing to orthostatic intolerance.

Adult↗
PubMed2000

Specific angiotensin II receptor blockage improves intestinal perfusion during graded hypovolemia in pigs.

OBJECTIVE: To investigate the potential of specific angiotensin II subtype 1 (AT1) receptor blockade to modify the mesenteric hemodynamic response to acute hypovolemia and retransfusion. DESIGN: Prospective, randomized, controlled experimental study. SETTING: University-affiliated animal research laboratory. SUBJECTS: Fasted, anesthetized, ventilated, juvenile domestic pigs of both sexes. INTERVENTIONS: Acute, graded hypovolemia by 20% and 40% of the total estimated blood volume followed by retransfusion in control animals (CTRL; n = 10) and animals pretreated with the AT1 receptor blocker candesartan (CAND; n = 10). MEASUREMENTS AND MAIN RESULTS: Invasive monitoring of arterial and central venous blood pressures, cardiac output, portal venous blood flow, and jejunal mucosal blood flow. Blood gases were repeatedly analyzed to calculate oxygen delivery and consumption. Thirty minutes after each level of hypovolemia at 20% and 40%, cardiac output was decreased in CTRL animals from a baseline of 2.9 +/- 0.1 to 1.8 +/- 0.2 and 1.1 +/- 0.2 L/min, with no differences compared with CAND animals. Cardiac output was restored to 3.0 +/- 0.3 L/min 30 mins after retransfusion in CTRL animals, with no significant intergroup differences. Baseline portal venous blood flow (Q(MES)) and jejunal mucosal perfusion (PU(JEJ)) were greater in CAND animals compared with CTRL animals. During graded hypovolemia, CAND animals maintained Q(MES) and PU(JEJ) at significantly higher levels compared with CTRL animals, particularly after 40% hemorrhage (+221% and + 244%, respectively, relative to the mean values in CTRL animals). The same pattern was observed after retransfusion. Moreover, the calculated mesenteric critical oxygen delivery was significantly greater in CTRL animals (74 mL/min) compared with CAND animals (34 mL/min). No animals died in the CAND group, whereas four animals died during 40% hypovolemia or retransfusion in the CTRL group. CONCLUSIONS: Specific AT1 blockade before acute hypovolemia significantly ameliorated mesenteric and, in particular, jejunal mucosal hypoperfusion. In addition, cardiovascular stability was improved, and mortality in conjunction with acute hypovolemia and retransfusion could be completely avoided. These findings support a fundamental role of the renin-angiotensin system in the mesenteric response to acute hypovolemia and indicate a substantial interventional potential for candesartan in conjunction with circulatory stress.

Acid-Base Equilibrium↗
PubMed2006

Critical postcraniotomy cerebrospinal fluid hypovolemia: risk factors and outcome analysis.

OBJECTIVE: Critical cerebrospinal fluid (CSF) hypovolemia may cause acute postoperative clinical deterioration in aneurysmal subarachnoid hemorrhage patients after craniotomy for microsurgical aneurysm clipping. We sought to identify risk factors for critical CSF hypovolemia and determine this syndrome's effect on clinical outcome. METHODS: Between April 2001 and June 2004 at Columbia University Medical Center, 16 aneurysmal subarachnoid hemorrhage patients were diagnosed with postoperative critical CSF hypovolemia, whereas 151 patients who underwent craniotomy for clipping were not. The demographics, as well as the presenting radiographic and clinical characteristics, of these groups were evaluated. In addition, a 2:1 matched case-control comparison of patients with and without critical CSF hypovolemia was completed using clinical data, operative variables, and outcome data. Outcome analysis was performed with a battery of tests designed to assess global outcome, cognitive function, independence, and quality of life. RESULTS: There was no difference in clinical grade, Fisher score, age, and sex distribution between patients diagnosed with critical CSF hypovolemia and the general aneurysmal subarachnoid hemorrhage population at Columbia University Medical Center. Subsequent 2:1 matched case-control comparison demonstrated a higher incidence of global cerebral edema on admission computed tomographic scans (75 versus 31%; P < 0.01) and a significantly longer operative time for patients with critical CSF hypovolemia (5 h 18 min versus 4 h 22 min; P < 0.03). No significant differences were observed between groups in outcome assessments at the time of hospital discharge or the 3-month follow-up examination. CONCLUSION: Risk factors associated with an increased incidence of critical CSF hypovolemia after aneurysm surgery include the presence of global cerebral edema on admission head computed tomographic scans and prolonged operative time. In such patients, heightened suspicion of CSF hypovolemia is crucial because rapid and appropriate management obviates excess morbidity and mortality.

Adult↗
PubMed2000

Hypovolemia in rats increases mortality rates following endotoxin administration.

The aim of the present study was to examine whether acute or chronic hypovolemia increase the mortality rates of rats following endotoxin injection. Another aim of this study was to examine whether this increase in sensitivity can be explained by increased leakage of endotoxin from the digestive tract to the blood stream. Chronic hypovolemia was caused by water deprivation for 8 days. Acute hypovolemia was caused by injection of sucrose (300mg/100g) or by hemorrhage of a volume of up to 2.1 ml/100g. The hypovolemia was examined by measuring the plasma volume using Evans Blue (EB). Endotoxin at various doses was injected to the hypovolemic rats and the lethality of the various treatments was examined. Acute and chronic hypovolemia caused a significant increase inthe mortality rates of rats injected IP with a dose of 1-1.5 mg/100g endotoxin. Endotoxin administration (6mg/100g) by drinking to hypovolemic rats did not cause death at all. In contradistinction, injection of galactoseamine to rats that underwent similar treatments caused 100% mortality. Endotoxin tolerance reduced the mortality rates following galactoseamine injection to the control level of administration of endotoxin without hypovolemia (p < 0.001). Injection of the antibiotic polymixin B following the galactoseamine injection also decreased mortality rates to 40% (p < 0.05). Examination of plasma endotoxin concentration exhibited a significant increase following administration of endotoxin by drinking to hypovolemic rats (p < 0.001) compared to rats that received the same amount of endotoxin but without hypovolemia. These results indicate that one possible explanation for the increased mortality rate of the hypovolemic rats after endotoxin injection is due to leakage of endotoxin from the digestive tract.

Animals↗
PubMed2000

Angiotensin II blockade in existing hypovolemia: effects of candesartan in the porcine splanchnic and renal circulation.

Angiotensin II (AngII) is an important vasoconstrictor during hypovolemia. This study focused on the effects of the AngII receptor blocker candesartan on intestinal, hepatic, and renal hemodynamics during severe hypovolemia when administered in preexisting moderate hypovolemia. It was hypothesized that specific AngII receptor blockade might enhance splanchnic perfusion during hypovolemia. Fasted, anesthetized, ventilated, juvenile pigs were hemorrhaged by 20% of the blood volume for 30 min. Animals were then randomized to receive candesartan (CAND, n = 11) or the vehicle (CTRL, n = 10) prior to further hemorrhage to 40% of the blood volume for 30 min. The shed blood was then retransfused. Systemic and splanchnic hemodynamics were recorded including intestinal mucosal, superficial and parenchymal hepatic, and cortical and medullary renal microcirculation by laser-Doppler flowmetry. Arterial blood gases were analysed. Candesartan-treated animals maintained mesenteric and jejunal mucosal perfusion during 40% hypovolemia compared to CTRL animals, while no differences were observed in the hepatic and renal circulation. Retransfusion restored mesenteric and renal blood flows despite persistent hypotension and reduced cardiac output in both CAND and CTRL animals. Renal medullary and hepatic parenchymal microcirculation failed to recover during retransfusion in both CAND and CTRL animals. Arterial acidosis, hypercarbia, and a negative base excess were observed in CTRL animals following retransfusion whereas those parameters were normalised in CAND animals. Administration of candesartan in moderate hypovolemia ameliorated the reduction and consequences of mesenteric and intestinal, but not hepatic perfusion during severe hypovolemia. No adverse effects were observed in the renal circulation.

Acid-Base Equilibrium↗
PubMed1999

Physiological and ventral medullary surface activity during hypovolemia.

The objective was to determine ventral medullary surface responses to blood loss sufficient to induce shock. We examined changes in scattered light from rostral and intermediate areas of the ventral medullary surface in four intact, drug-free cats during acute hypovolemia. Scattered light images, collected during 660 and 560 nm illumination to measure cellular activity and hemodynamic aspects, respectively, were digitized at 50 frames/s during baseline, and during withdrawal of 20-30% blood volume. Hypovolemia elicited a profound hypotension and eventual bradycardia. In all cats, a modest increase in ventral medullary surface reflectance (activity decline) accompanied initial blood loss; as hypovolemia continued, and blood pressure declined, reflectance switched to a decline (activity increase), with the lowest reflectance occurring at maximal blood loss. Hypovolemia elicited multiple transient physiologic behaviors, including tachycardia, tachypnea, intermittent isolated and sustained bursts of enhanced inspiratory efforts, and extensor activation of the somatic musculature. The phasic physiological behaviors during hypovolemia were accompanied by partial recovery of medullary surface reflectance and blood pressure towards baseline values; however, reflectance continued to decrease as blood pressure progressively fell after these recovery efforts. Patterns of reflectance were not uniform over areas examined; isolated regions of enhanced or diminished reflectance appeared upon the overall images. Optical signals indicating hemodynamic changes followed the neural activity patterns, but not precisely. Regions within the ventral surface are responsive to hypovolemia, and to transient behaviors associated with momentary restoration of blood pressure; these ventral surface areas may assume essential roles in the systemic response to hypovolemic-induced shock.

Animals↗
PubMed2002

Hypovolemia and neurovascular control during orthostatic stress.

Humans exposed to real or simulated microgravity experience decrements in blood pressure regulation during orthostatic stress that may be related to autonomic dysregulation and/or hypovolemia. We examined the hypothesis that hypovolemia, without the deconditioning effects of bed rest or spaceflight, would augment the sympathoneural and vasomotor response to graded orthostatic stress. Radial artery blood pressure (tonometry), stroke volume (SV), brachial blood flow (Doppler ultrasound), heart rate (electrocardiogram), peroneal muscle sympathetic nerve activity (MSNA; microneurography), and estimated central venous pressure (CVP) were recorded during five levels (-5, -10, -15, -20 and -40 mmHg) of randomly assigned lower body negative pressure (LBNP) (n = 8). Forearm (FVR) and total peripheral vascular resistance (TPR) were calculated. The test was repeated under randomly assigned placebo (normovolemia) or diuretic (spironolactone: 100 mg/day, 3 days) (hypovolemia) conditions. The diuretic produced an approximately 16% reduction in plasma volume. Compared with normovolemia, SV and cardiac output were reduced by approximately 12% and approximately 10% at baseline and during LBNP after the diuretic. During hypovolemia, there was an upward shift in the %DeltaMSNA/DeltaCVP, DeltaFVR/DeltaCVP, and DeltaTPR/DeltaCVP relationships during 0 to -20 mmHg LBNP. In contrast to normovolemia, blood pressure increased at -40 mmHg LBNP during hypovolemia due to larger gains in the %DeltaMSNA/DeltaCVP and DeltaTPR/DeltaCVP relationships. It was concluded that acute hypovolemia augmented the neurovascular component of blood pressure control during moderate orthostasis, effectively compensating for decrements in SV and cardiac output.

Adult↗
PubMed1997

Sympathetic and renin-angiotensin activation during graded hypovolemia in pigs: impact on mesenteric perfusion and duodenal mucosal function.

Sympathetic and angiotensinergic activation reduce splanchnic oxygen delivery during hypovolemia, which may lead to failure of the intestinal mucosal barrier and eventually multiple organ dysfunction. This study integrates sympathetic and angiotensinergic responses with splanchnic hemodynamics and duodenal mucosal function during hypovolemia and evaluates pharmacologic blockade of either system to ameliorate the impact of acute hypovolemia. Chloralose-anesthetized pigs subjected to 20 and 40% blood volume reductions were randomized to controls or administered guanethidine or enalaprilate to block sympathetic and angiotensinergic activation, as assessed by plasma norepinephrine spillover and angiotensin II levels, respectively. Mesenteric and hepatic oxygen delivery/consumption as well as duodenal mucosal alkaline secretion and potential difference were determined. Hypovolemia preferentially increased mesenteric sympathetic outflow and caused a vigorous angiotensinergic activation. Guanethidine and enalaprilate blocked effectively the sympathetic and angiotensinergic responses. Treatment with enalaprilate, but not guanethidine, prevented the reduction of mesenteric oxygenation and duodenal mucosal alkaline secretion and potential difference observed in control animals. The down-regulation of mesenteric oxygenation and duodenal mucosal function during hypovolemia can be prevented by administration of enalaprilate, whereas guanethidine is uneffective in this respect. Interference with the reninangiotensin system might be of clinical interest to support mesenteric perfusion and organ function in hypovolemia.

Angiotensin II↗
PubMed2006

Central hemodynamics during lung recruitment maneuvers at hypovolemia, normovolemia and hypervolemia. A study by echocardiography and continuous pulmonary artery flow measurements in lung-injured pigs.

OBJECTIVE: The impact of lung-recruitment maneuvers on heart function at different volemic levels has not been studied in detail. We therefore investigated the effect on central hemodynamics of lung recruitment maneuvers at hypovolemia, normovolemia and hypervolemia in experimental lung injury. DESIGN: Randomized, controlled, cross-over experimental study. SETTING: Animal laboratory at a university hospital. PARTICIPANTS: Eleven anesthetized and lung-lavaged pigs. INTERVENTION: The animals were randomized to 10-s lung recruitment maneuvers followed by 30-s maneuvers (40 cm H(2)O airway pressure) or vice versa, performed under hypovolemia, normovolemia and hypervolemia. MEASUREMENTS AND MAIN RESULTS: Left-ventricular end-diastolic diameter and cardiac output were measured before, during, and 1 min and 5 min after the lung recruitment maneuver and left-ventricular eccentricity index was calculated for before and during the maneuver. Cardiac output and left-ventricular end-diastolic diameter (within parentheses) decreased significantly during both the 10-s and 30-s lung recruitment maneuvers at hypovolemia, by a mean of 89% (35) and 92% (33), at normovolemia by 75% (33) and 86% (32), and at hypervolemia by 56% (32) and 64% (43), respectively. At hypovolemia, cardiac output was increased above baseline 1-5 min following the 30-s maneuver. Left-ventricular eccentricity index increased significantly during the maneuver, indicating right ventricular dysfunction. CONCLUSIONS: In this animal lung injury model, lung recruitment maneuvers significantly decreased left-ventricular end-diastolic volume and cardiac output at hypovolemia. Hypervolemia did partly counteract this compromise. In addition, a marked right-ventricular dysfunction during the maneuver was found.

Animals↗
PubMed2000

Influence of hypovolemia on the pharmacokinetics and the electroencephalographic effect of propofol in the rat.

BACKGROUND: Hypovolemia decreases the dose requirement for anesthetics, but no data are available for propofol. As it is impossible to study this in patients, a rat model was used in which the influence of hypovolemia on the pharmacokinetics and pharmacodynamics of propofol was investigated. METHODS: Animals were randomly allocated to either a control (n = 9) or a hypovolemia (n = 9) group, and propofol was infused (150 mg x kg(-1) x h(-1)) until isoelectric periods of 5 s or longer were observed in the electroencephalogram. The changes observed in the electroencephalogram were quantified using aperiodic analysis and used as a surrogate measure of hypnosis. The righting reflex served as a clinical measure of hypnosis. RESULTS: The propofol dose needed to reach the electroencephalographic end point in the hypovolemic rats was reduced by 60% (P < 0.01). This could be attributed to a decrease in propofol clearance and in distribution volume. Protein binding was similar in both groups. To investigate changes in end organ sensitivity during hypovolemia, the electroencephalographic effect versus effect-site concentration relation was studied. The effect-blood concentration relation was biphasic, exhibiting profound hysteresis in both hypovolemic and control animals. Semiparametric minimization of this hysteresis revealed similar equilibration half-lives in both groups. The biphasic effect-concentration relation was characterized by descriptors showing an increased potency of propofol during hemorrhage. The effect-site concentration at the return of righting reflex was 23% (P < 0.01) lower in the hypovolemic animals, also suggesting an increased end organ sensitivity. CONCLUSIONS: An increased hypnotic effect of propofol occurs during hypovolemia in the rat and can be attributed to changes in both pharmacokinetics and end organ sensitivity.

Anesthesia, Intravenous↗
PubMed2005

Influence of hypovolemia on the electroencephalographic effect of isoflurane in a swine model.

BACKGROUND: Hypovolemia alters the effect of several intravenous anesthetics by influencing pharmacokinetics and end-organ sensitivity. The authors investigated the influence of hypovolemia on the effect of an inhalation anesthetic, isoflurane, in a swine hemorrhage model. METHODS: Eleven swine were studied. After animal preparation with inhalation of 2% isoflurane anesthesia, the inhalation concentration was decreased to 0.5% and maintained at this level for 25 min before being returned to 2% (control). After 25 min, hypovolemia was induced by removing 14 ml/kg of the initial blood volume via an arterial catheter. After a 25-min stabilization period, the inhalation concentration was decreased to 0.5%, maintained at this level for 25 min, and then returned to 2% (20% bleeding). After another 25 min, a further 7 ml/kg blood was collected, and the inhalation concentration was altered as before (30% bleeding). End-tidal isoflurane concentrations and an electroencephalogram were recorded throughout the study. Spectral edge frequency was used as a measure of the isoflurane effect, and pharmacodynamics were characterized using a sigmoidal inhibitory maximal effect model for the spectral edge frequency versus end-tidal concentration. RESULTS: There was no significant difference in the effect of isoflurane among the conditions used. Hypovolemia did not shift the concentration-effect relation (the effect site concentration that produced 50% of the maximal effect was 1.2 +/- 0.2% under control conditions, 1.2 +/- 0.2% with 20% bleeding, and 1.1 +/- 0.2% with 30% bleeding). CONCLUSIONS: Hypovolemia does not alter the electroencephalographic effect of isoflurane, in contrast to several intravenous anesthetics.

Anesthetics, Inhalation↗
PubMed2004

A comparison of changes in cardiac preload variables during graded hypovolemia and hypervolemia in mechanically ventilated dogs.

We developed an online monitoring system to measure systolic blood pressure variation (SPV) and its down (dDown) and up components, along with pulse pressure variation (dPP). Using the system, we compared different cardiac preload indicators-such as stroke volume variation (SVV) and corrected flow time (FTc)-along with central venous pressure and pulmonary artery occlusion pressure in mechanically-ventilated dogs during normovolemia, graded hypovolemia (-200 and -350 mL), and hypervolemia (+200 and +350 mL). We simultaneously measured these preload indicators along with global hemodynamic variables and investigated their validity and limitations to access preload changes. SPV increased from 4.8 +/- 1.4 mm Hg at baseline to 11.2 +/- 1.8 mm Hg during hypovolemia (-350 mL), but it did not change significantly during hypervolemia. Similar changes were observed with dDown, dPP, and SVV. FTc, conversely, increased during hypervolemia but remained unchanged during hypovolemia. The results of this study indicate that SPV, dDown, dPP, and SVV are useful indicators of hypovolemia, but not of hypervolemia. Conversely, hypovolemia could not be detected reliably by FTc, but it does reflect blood volume changes during hypervolemia. Although SPV, dDown, and dPP measurements require no additional invasion and cost beyond arterial cannulation, their limits must be kept in mind for the monitoring of blood volume status in mechanically-ventilated patients.

Animals↗
PubMed2004

[Ketamine for subarachnoid anesthesia during hypovolemia: preliminary study in pigs].

OBJECTIVES: To assess whether subarachnoid ketamine has fewer hemodynamic effects than lidocaine in normal and hypovolemic pigs and to determine whether or not the effects of ketamine are dose-dependent. METHODS: Thirty pigs were randomly allocated to receive subarachnoid administration of lidocaine 2 mg x kg(-1), ketamine 1 mg x kg(-1) or ketamine 2 mg x kg(-1), in a situation of either normal or reduced blood volume. The pigs were assigned to six groups: group L2 (2% lidocaine 2 mg x kg(-1), normovolemia), group L2H (2% lidocaine 2 mg x kg(-1), hypovolemia), group K1 (ketamine 1 mg x kg(-1), normovolemia), group K1H (ketamine 1 mg x kg(-1), hypovolemia), group K2 (ketamine 2 mg.kg(-', normovolemia), and group K2H (ketamine 2 mg x kg(-1), hypovolemia). To induce hypovolemia 30% of the calculated blood volume was withdrawn from each pig. The subarachnoid space was catheterized, and invasive measurements of hemodynamic variables (derived from arterial, central venous and pulmonary artery catheter monitoring) were obtained. Variables were recorded at baseline and 5 and 15 min after drug injection in the normovolemic groups, and at baseline after inducing hypovolemia and 5 and 15 min after drug injection in the hypovolemic groups. RESULTS: In the normovolemic pigs no significant differences were detected between groups. In hypovolemic pigs differences were observed in heart rate and arterial pressure between the ketamine 1 mg x kg(-1) and lidocaine 2 mg x kg(-1) groups (P < 0.05). The decreases in heart rate and arterial pressure were less marked in the ketamine group. Mixed venous oxygen saturation and cardiac index deteriorated to a lesser degree in both ketamine groups than in the lidocaine groups (P < 0.05). CONCLUSIONS: Racemic ketamine administered by subarachnoid injection in hypovolemic pigs produces less deterioration in hemodynamic variables than does lidocaine. Hemodynamic changes caused by ketamine were not dose-dependent. These findings may be of interest, given the increased use of ketamine in neuroaxial anesthesia and analgesia and perhaps the possible use of neuroaxial ketamine in hypovolemic patients.

Anesthesia, Spinal↗
PubMed1991

Hemodynamic effects of high frequency jet ventilation during acute hypovolemia.

The hemodynamic effects of high frequency jet ventilation (HFJV) at three different rates (60, 100, 200/min) and at rate 200/min combined with jet sighs 12/min (HFJV-200 + 12S) during two degrees of hemorrhagic hypovolemia were investigated in dogs. Also, the results were compared with those of intermittent positive pressure ventilation (IPPV). Two degrees of hypovolemia were produced by bleeding dogs until mean arterial pressure was 25% or 50% lower than basic value respectively. At both periods of hypovolemia, HFJV at rate 60 or 100 were found to have better hemodynamic effects than IPPV due to their lower airway pressures. However, HFJV at rate 200 or HFJV-200 + 12S did not demonstrate the same superiority because of their higher airway pressure, the latter even represented a tendency of worse hemodynamic effect than IPPV. The best cardiovascular effect was seen during HFJV at rate 100. Our study indicated that the hemodynamic effect of HFJV better than that of IPPV during acute hypovolemia can be seen only when proper ventilatory settings are chosen. Jet sighs at 12/min added to usual HFJV are not beneficial to circulatory function. It is recommended that HFJV at a rate below 200/min without jet sighs be used in patients who need respiratory support during acute hypovolemia or shock.

Animals↗
PubMed1998

Hemodynamic changes in patients developing effective hypovolemia after total paracentesis.

BACKGROUND/AIMS: In many centers paracentesis is considered the treatment of choice for tense ascites. However, the mechanism of effective hypovolemia after paracentesis, the main complication associated with this procedure, remains unknown. In the current study, systemic hemodynamics was sequentially studied before and after total paracentesis in 46 patients with cirrhosis and tense ascites. The aim of the study was to assess the mechanism of effective hypovolemia after paracentesis. METHODS: Plasma renin activity and aldosterone, mean arterial pressure, cardiac output (ECO-Doppler) and systemic vascular resistance were measured before, and 3 h, 6 h and 6 days after total paracentesis associated with plasma volume expansion. RESULTS: Effective hypovolemia after paracentesis (defined as 50% increase in plasma renin activity up to a level over 4 ng x m(-1) x h(-1) at the 6th day after paracentesis) occurred in 20 cases [plasma renin activity increased from 8+/-17 to 19+/-2.7 ng x m(-1) x h(-1)]. In the remaining 26 cases no changes in plasma renin activity [8.5+/-2.4 vs. 8.7+/-2.2 ng x m(-1) x h(-1)] were observed. The amounts of ascitic fluid volume removed were similar. Effective hypovolemia after paracentesis was associated with a significant decrease in mean arterial pressure (89+/-2 vs. 81+/-3 mmHg) and systemic vascular resistance [1263+/-67 vs. 1014+/-80 dyn x s(-1) x cm(-5)] 6 days after treatment. In contrast, no significant changes in these parameters were observed in patients not developing this complication. In the whole group of patients a significant inverse relation was observed between changes in plasma renin activity and in systemic vascular resistance (r=0.74;p< 0.001). CONCLUSIONS: These results indicate that effective hypovolemia after paracentesis in cirrhosis is predominantly due to an accentuation of the arteriolar vasodilation already present in these patients.

Adult↗
PubMed1992

The cerebral hemodynamics of normotensive hypovolemia during lower-body negative pressure.

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.

Adult↗
PubMed1988

Kinetics of drug action in disease states. XXV. Effect of experimental hypovolemia on the pharmacodynamics and pharmacokinetics of desmethyldiazepam.

It has been reported that hypovolemia secondary to extensive blood loss alters the functionality of the central nervous system and is associated with changes in the dose requirements or intensity of action of various central nervous system depressants, including a benzodiazepine. To investigate the mechanism(s) of this effect, the influence of experimental hypovolemia on the pharmacodynamics, receptor binding and pharmacokinetics of a benzodiazepine drug was determined. Adult male Sprague-Dawley rats were made hypovolemic by removal of about 30% of their blood over 30 min. An i.v. infusion of desmethyldiazepam (DDZP) was started 30 min later and continued until the animals lost their righting reflex. Compared to results obtained with normal controls, the hypovolemic rats required about one-half the dose of DDZP to produce loss of righting reflex and had significantly lower DDZP concentrations in serum and cerebrospinal fluid at that time. This effect of substantial blood removal could not be reversed by prompt return of the removed blood to the animals. Experimental hypovolemia had no apparent effect on the in vitro binding of tritiated diazepam to benzodiazepine receptor sites in the cerebral cortex of rats. The plasma clearance of DDZP was decreased significantly and the biological half-life was increased in hypovolemic rats compared to normal animals when both received a 30-mg/kg dose by i.v. infusion over 10 min. It is concluded that acute hemorrhagic hypovolemia increases the sensitivity of the central nervous system to the depressant effect of DDZP and decreases the body clearance of that drug in rats. Thus, the pharmacodynamics as well as the pharmacokinetics of a benzodiazepine are altered by hypovolemia.

Animals↗