摘要:

ObjectiveTo assess the value of bioimpedance as a clinical tool by determining the accuracy and bias of single and multiple frequency bioimpedance estimates of total body and extracellular water in comparison with values established by criterion reference techniques.DesignControlled, prospective, single-blind investigation.SettingPrivate, not-for-profit, university-affiliated, acute care hospital.PatientsEight male, post-elective coronary artery bypass graft surgical patients.InterventionsWithin 6 hrs after surgery, estimates of total body and extracellular water volumes were determined using single and multiple frequency bioimpedance techniques. These estimates were then compared with the gold standard volumes measured by deuterium oxide and bromine dilutional space determination, respectively.Measurements and Main ResultsThe mean multiple frequency bioimpedance estimate of total body water of 47.7 +/- 9.4 L was statistically different from the single frequency bioimpedance and deuterium values of 52.5 +/- 9.4 (p < .006) and 53.3 +/- 11.6 L (p < .002), respectively. In comparison, the mean multiple and single frequency bioimpedance estimates of extracellular water, 26.3 +/- 5.4 and 29.2 +/- 5.4 L, respectively, were not statistically different from the bromine value of 27.5 +/- 6.9 L. In addition, the mean errors for multiple and single frequency bioimpedance determinations of extracellular water, -1.2 +/- 2.0 and 1.7 +/- 2.7 L, respectively, were statistically different (p = .001).ConclusionsIn male, post-elective coronary artery bypass graft surgical patients, single frequency bioimpedance was a more accurate and less biased predictor of total body water than multiple frequency bioimpedance. The accuracy and bias of multiple frequency bioimpedance was superior to single frequency bioimpedance for the prediction of extracellular water. Whether this observation remains true for other populations of critically ill patients remains to be investigated.(Crit Care Med 1996; 24:1824-1828)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTriggering a ventilator "ON" at the carinal end of the endotracheal tube decreases imposed work of breathing by bypassing the resistance imposed by the breathing circuit and the endotracheal tube. We compared work of breathing during spontaneous ventilation between three methods of triggering the ventilator "ON": a) conventional pressure triggering from inside the ventilator; b) flow-by triggering; or c) tracheal pressure triggering at the carinal end of the endotracheal tube. We hypothesized that the work of breathing would be substantially decreased with tracheal pressure triggering compared with conventional pressure and flow-by methods in patients receiving continuous positive airway pressure.DesignClinical, prospective study.SettingUniversity teaching hospital.PatientsFourteen adults diagnosed with acute respiratory failure.InterventionsAll patients were breathing spontaneously at an FIO2of 0.30 to 0.40 and received 5 cm H2O of continuous positive airway pressure. Three different methods of triggering the ventilator while set in the continuous positive airway pressure mode were administered in random order.Measurements and Main ResultsReal-time measurements of esophageal pressure and tidal volume were integrated with a respiratory monitor (CP-100, Bicore, Riverside, CA) that uses the Campbell diagram to calculate total work of breathing. Imposed work of breathing was calculated by integrating tidal volume with the pressure at the carinal end of the endotracheal tube. Physiologic work of breathing was calculated by subtracting imposed work of breathing from the total work of breathing. Breathing frequency, the index of rapid shallow breathing (breathing frequency/tidal volume), peak inspiratory flow rate demand, exhaled minute ventilation, and the duration of respiratory muscle contraction assessed by the ratio of inspiratory time to total cycle time were also measured. Data were analyzed by Friedman's repeated-measures analysis of variance on ranks. Alpha was set at .05 for statistical significance.Imposed work of breathing decreased to approximately zero during tracheal pressure triggering. As a result, total work of breathing decreased by approximate 40% compared with the flow-by and conventional methods. During tracheal pressure triggering only, airway pressure increased above baseline pressure to approximate 11 cm H2O, which resembled pressure-support ventilation. Also, during tracheal pressure triggering, tidal volume and peak inspiratory flow rate were significantly increased, while the pressure-time product and the index of rapid shallow breathing were significantly decreased. Hemodynamic status and oxygen saturation were not clinically affected.ConclusionsThe tracheal pressure triggering of a demand-flow continuous positive airway pressure system creates an effect similar to pressure-support ventilation that significantly decreases imposed work of breathing and, thus, total work of breathing. We recommend moving the triggering site of the ventilator to the carinal end of the endotracheal tube.(Crit Care Med 1996; 24:1829-1834)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo determine the clinical variables that affect the prognosis of critically ill patients with sustained unexplained hypotension. A further goal was to develop a prognostic scoring system based on clinical data available at the onset of hypotension.DesignProspective cohort study.SettingThe intensive care units (ICUs) of an academic medical center.Patients60 mins) unexplained hypotension. Using the initial 50 patients (derivation set), a prognostic score was developed that was then tested in the next 51 patients (validation set).InterventionsNone.Measurements and Main Resultsor=to65, mortality 92%, (n = 24). The area under the receiver operating characteristic curve was .85 for the derivation set and .83 for the validation set vs. .76 for the APACHE II score alone.ConclusionsThe prognosis of hypotension in the critical care setting is highly variable, but can be predicted from patient characteristics.(Crit Care Med 1996; 24:1835-1840)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesInhaled nitric oxide has been shown to be a selective pulmonary vasodilator, leading to reduced pulmonary arterial pressure and improved ventilation/perfusion ratio in the acute respiratory distress syndrome. This local pulmonary vasodilation theoretically can be achieved by the airway application of a shortacting vasodilator, such as prostacyclin. We hypothesized that nebulized prostacyclin has the same properties for selective pulmonary vasodilation as inhaled nitric oxide.DesignProspective, experimental study in sheep.SettingInvestigational intensive care unit in a university hospital.SubjectsSix adult ewes of the Merino breed.InterventionsSheep (n = 6) were surgically prepared for chronic study. After 5 days of recovery, the sheep had tracheostomies performed under anesthesia. Intubation with a modified Robert-Shaw tube allowed side-separated ventilation. The entire left lung was ventilated with pure nitrogen, whereas the right lung was ventilated with pure oxygen. Nitric oxide and prostacyclin were added in different concentrations to the nitrogen, with which the left lung was ventilated.Measurements and Main ResultsThe blood flows to the left and right lungs were measured with ultrasonic flow probes on the common and left pulmonary artery. Measurements were taken after each compound had been administered for 10 mins at a predefined dose. Both inhaled nitric oxide and nebulized prostacyclin caused effective, selective, dose-dependent pulmonary vasodilation. Inhaled nitric oxide was able to abolish hypoxic pulmonary vasoconstriction when insufflated into the animals at a concentration of 50 ppm of nitrogen, but 100 ppm of nitric oxide had no further effect. Prostacyclin, at a dosage of 10 micro gram/min, showed maximum pulmonary vasodilation, which could not be further increased by doubling the dosage. However, prostacyclin produced less dilation than high doses of nitric oxide, and its maximum pulmonary vasodilation was comparable with that effect obtained under ventilation with 20 ppm of nitric oxide.ConclusionsBoth drugs selectively dilated the pulmonary vasculature in ventilated alveoli. Prostacyclin nebulization is an excellent tool to reduce pulmonary hypertension and to improve the ventilation/perfusion ratio. Prostacyclin nebulization can be used without the highly sophisticated technical equipment that is needed for controlled nitric oxide inhalation, and may therefore become a new, noninvasive therapeutic approach for treatment of adult respiratory distress syndrome in hospitals that cannot provide nitric oxide inhalation.(Crit Care Med 1996; 24:1841-1848)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesThe present study was undertaken to assess the fluid balance and hemodynamic effects during the first 8 hrs of resuscitation in animals with a large body surface area burn, using lactated Ringer's solution, 6% hetastarch, and hypertonic saline dextran.DesignA prospective, blinded, controlled, terminal study, using anesthetized animals. The initial baseline period was followed by scald injury, and three different treatment regimens were administered from coded bags to achieve a physiologic end point.SettingUniversity laboratory.SubjectsEighteen female sheep (35 to 45 kg) were anesthetized with isoflurane.InterventionsTest solutions (10 mL/kg of either lactated Ringer's solution, hetastarch, or hypertonic saline dextran) were infused 30 mins after the scald injury at a rate to restore and maintain the baseline oxygen delivery (DO2) value.Measurements and Main ResultsCardiovascular hemodynamics, plasma sodium concentration, plasma colloid osmotic pressure, and fluid balance were measured before and after scalding and resuscitation. After the initial 10-mL/kg test solution dose was given, lactated Ringer's solution was infused to achieve the same end point of baseline DO2for the remainder of the 8 hrs.The scald caused an initial 30% reduction in cardiac output, a 20% reduction in mean arterial pressure, and 10% to 15% increase in hematocrit. All three test solutions restored and maintained baseline DO2within 1 hr. However, hetastarch and hypertonic saline dextran reduced the net fluid volume over 8 hrs by 48% and 74%, respectively, compared with lactated Ringer's solution. Edema in the burn wound was not affected by treatment, while hypertonic saline dextran reduced edema in nonburned skin compared with both lactated Ringer's solution and hypertonic saline dextran. Plasma colloid osmotic pressure was significantly higher in the hetastarch and hypertonic saline dextran groups. A continuous decrease in plasma sodium concentrations from baseline values (140 to 145 mmol/L) was measured in the lactated Ringer's solution and hetastarch groups (130 to 133 mmol/L) over 8 hrs. Plasma sodium concentrations in the group receiving hypertonic saline dextran were increased (150 to 155 mmol/L) at 4 hrs, but returned toward baseline by 8 hrs.ConclusionsNet volume loading can be reduced markedly by initial resuscitation of large body surface area burn injury using a colloid (hetastarch), and can be further reduced by use of hypertonic saline colloid. Hyponatremia was apparent in the isotonic crystalloid- and colloid-treated animals, but not in those animals treated with hypertonic saline colloid.(Crit Care Med 1996; 24:1849-1857)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Objectives1) The investigation of fiberoptic PO2, PCO2, and pH sensor technology as a monitor of brain parenchyma during and after brain injury, and 2) the comparison of brain parenchyma PO2, PCO2, and pH with intracranial pressure during and after hypoxic, ischemic brain insult.DesignProspective, controlled, animal study in an acute experimental preparation.SettingPhysiology laboratory in a university medical school.SubjectsFourteen mongrel dogs (20 to 35 kg), anesthetized, room-air ventilated.InterventionsAnesthesia was induced with thiopental and maintained after intubation using 1% to 1.5% halothane in room air (FIO20.21). Mechanical ventilation was established to maintain end-tidal PCO2approximate 35 torr (approximate 4.7 kPa). Intravenous, femoral artery, and pulmonary artery catheters were placed. The common carotid arteries were surgically exposed, and ultrasonic blood flow probes were applied. A calibrated intracranial pressure probe was placed through a right-side transcranial bolt, and a calibrated intracranial chemistry probe with optical sensors for PO2, PCO2, and pH was placed through a left-side bolt into brain parenchyma. Brain insult was induced in the experimental group (n = 6) by hypoxia (FIO20.1), ischemia (bilateral carotid artery occlusion), and hypotension (mean arterial pressure [MAP] approximate 40 mm Hg produced with isoflurane approximate 4%). After 45 mins, carotid artery occlusion was released, FIO2was reset to 0.21, and anesthetic was returned to halothane (approximate 1.25%). The control group (n = 5) had the same surgical preparation and sequence of anesthetic agent exposure but no brain insult.Measurements and Main ResultsMonitored variables included brain parenchyma PO2, PCO2, and pH, which were monitored at 1-min intervals, and intracranial pressure, MAP, arterial hemoglobin oxygen saturation (by pulse oximetry), end-tidal PCO2, and carotid artery blood flow rate, for which data were collected at 15-min intervals for 7 hrs. Arterial and mixed venous blood gas analyses were done at approximate 1-hr intervals.Baseline data agreed closely with other published results: brain parenchyma PO2of 27 +/- 7 (SD) torr (3.6 +/- 0.9 kPa); brain parenchyma PCO2of 69 +/- 12 torr (9.2 +/- 1.6 kPa); and brain parenchyma pH of 7.13 +/- 0.09. Postcalibration data were accurate, indicating stability and durability over several hours. In six experiments, during the brain insult, brain parenchyma PO2decreased to 16 +/- 2 torr (2.1 +/- 0.3 kPa), brain parenchyma PCO2increased to 105 +/- 44 torr (14 +/- 5.9 kPa) (p < .05), and brain parenchyma pH decreased to 6.75 +/- 0.08 (p < .05). Intracranial pressure (ICP) remained nearly constant (baseline 16 +/- 6 to 14 +/- 5 mm Hg at the end of the brain insult). Cerebral perfusion pressure (CPP = MAP - ICP) decreased (baseline 95 +/- 15 to 28 +/- 8 mm Hg; p < .05). On release of brain insult stresses, ICP increased to 30 +/- 9 mm Hg and CPP increased to 71 +/- 19 mm Hg (p < .05). A biphasic recovery was observed for brain parenchyma pH, which had the slowest recovery of the monitored variables. On average, brain parenchyma pH gradually returned toward baseline, and was no longer significantly different from baseline 3 hrs after release of insult stresses. Brain parenchyma PCO2continued to decrease rapidly after brain insult and then remained approximate 52 +/- 10 torr (approximate 6.9 +/- 1.3 kPa) (p < .05). Brain parenchyma PO2increased from a minimum at the end of brain insult to a maximum of 43 +/- 17 torr (5.7 +/- 2.3 kPa) within 1.25 hrs (p < .05), and then gradually decreased to approximate 35 +/- 10 torr (approximate 4.7 +/- 1.3 kPa). Cerebral perfusion pressure gradually decreased as ICP increased 3 to 5 hrs after insult.ConclusionsIntracranial chemistry probes with optical sensors demonstrated stable, reproducible monitoring of brain parenchyma PO2, PCO28 hrs. Significant changes in brain parenchyma PO2, PCO2, and pH occurred without corresponding changes in intracranial pressure. Placement of intracranial chemistry probes can be accomplished with techniques similar to those used for standard intracranial pressure probes.(Crit Care Med 1996; 24:1858-1868)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo evaluate the oxygen transporting capabilities of hemoglobin vesicles by studying the physiologic responses to exchange transfusion with hemoglobin vesicles in anesthetized rats. Exchange transfusions with phosphate buffered saline, hemoglobin vesicles containing methemoglobin (and therefore, deprived of oxygen transporting capabilities), and washed rat red blood cells were used as controls.DesignProspective, randomized, controlled trial.SettingDepartment of Surgery, School of Medicine, Keio University.SubjectsTwenty-seven male Wistar rats.InterventionsThe rats were anesthetized with an intraperitoneal injection of sodium pentobarbital (50 mg/kg). Catheters (PE-20 tubing, outer diameter 0.8 mm, inner diameter 0.5 mm) were introduced into the right jugular vein for infusion and the right common carotid artery for blood withdrawal and mean arterial pressure measurements. The left kidney was exposed by median abdominal incision, and a needle-type polarographic oxygen electrode was placed in the left renal cortex for renal cortical tissue oxygen tension measurements.Measurements and Main ResultsPhosphate buffered saline and methemoglobin vesicles were administered as nonoxygen-carrying fluids, and rat red blood cells as oxygen-carrying fluid. Measurements included mean arterial pressure, arterial blood gas analysis, and renal cortical tissue oxygen tension as an indicator of systemic oxygen transport. In the rat red blood cell and hemoglobin vesicles groups, mean arterial pressure was sustained at the end of the exchange transfusion (82.3 +/- 27.5% and 73.5 +/- 11.5%, respectively, from the basal values). However, in the phosphate buffered saline and methemoglobin vesicles groups, mean arterial pressure decreased significantly (p < .05) (33.9 +/- 13.8% and 35.7 +/- 8.2%, respectively). Renal cortical tissue oxygen tension in the rat red blood cell and hemoglobin vesicles groups was sustained at a significantly higher level (p < .05) (83.5 +/- 9.3% and 75.0 +/- 11.9%, respectively) compared with the phosphate buffered saline and methemoglobin vesicles groups (44.9 +/- 12.8% and 58.3 +/- 6.2%, respectively) at the end of the exchange transfusion. Metabolic acidosis was more progressive in the phosphate buffered saline and methemoglobin vesicles groups, manifested as lower pH and base excess values. Platelet counts tended to decrease slightly in the hemoglobin vesicles and methemoglobin vesicles groups, but the changes were not significant.ConclusionsHemoglobin vesicles have an oxygen transporting capability almost equivalent to rat red blood cells and can be considered as a potential artificial oxygen carrier.(Crit Care Med 1996; 24:1869-1873)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo investigate the benefit of the hyperosmolar agent, mannitol, and the xanthine oxidase inhibitor, allopurinol, in experimental pneumococcal meningitis in the rat.DesignA prospective, randomized, controlled experimental study.SettingExperimental animal laboratory in a university hospital.SubjectsSixty-five anesthetized and artificially ventilated adult male Wistar rats, weighing 250 to 300 g.InterventionsMeningitis was induced by intracisternal injection of live pneumococci. Infected rats were randomized to receive mannitol or allopurinol.Measurements and Main ResultsThere were marked increases in regional cerebral blood flow (measured by laser-Doppler flowmetry), intracranial pressure, brain water content, and cerebrospinal fluid white blood cell count in infected rats within 6 hrs after infection (p < .05, compared with uninfected controls). Continuous infusion of mannitol (0.6 g/kg/hr iv), started just before infection, attenuated the increases of regional cerebral blood flow, intracranial pressure, and brain water content (p < .05, compared with untreated infected rats 6 hrs after infection). When continuous mannitol treatment was started 4 hrs after infection, intracranial pressure at 6 hrs was significantly lower than in untreated infected rats. When mannitol was given by a bolus injection (1.5 g/kg iv) at 4 hrs after infection, intracranial pressure measured 0.5 hr thereafter was consistently reduced in all animals (intracranial pressure reduction by 21.3 +/- 5.1 [SEM] %). Pretreatment with allopurinol (150 mg/kg iv) did not significantly influence regional cerebral blood flow, intracranial pressure, and brain water content in pneumococci-injected rats. Both agents, mannitol and allopurinol, did not inhibit cerebrospinal fluid pleocytosis in infected rats. In uninfected rats, mannitol significantly increased regional cerebral blood flow by a nitric oxide-independent mechanism, whereas allopurinol slightly decreased blood flow.ConclusionsMannitol attenuated pathophysiologic changes in experimental pneumococcal meningitis. One possible mechanism of the mannitol effect might be scavenging of hydroxyl radicals which have been shown to be involved in the pathophysiology of pneumococcal meningitis. The failure of allopurinol to modulate pathophysiologic parameters may suggest that during early experimental pneumococcal meningitis in the rat, the xanthine oxidase pathway seems not to be a major source of reactive oxygen species.(Crit Care Med 1996; 24:1874-1880)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo determine whether peptic activity in bronchoalveolar fluid, due to the presence of the gastric proteolytic enzyme pepsin, could serve as a biochemical marker for pulmonary aspiration of gastric contents.DesignProspective, experimental trial.SettingA university animal research laboratory.SubjectsThirty-six New Zealand rabbits, weighing 2 to 4 kg.InterventionsNew Zealand rabbits were anesthetized, intubated via tracheostomy, and mechanically ventilated. Pulmonary aspiration was induced by the intratracheal instillation of 2 mL/kg human gastric juice (pH 1.2 +/- 0.2; pepsin activity 0.02 +/- 0.006 micro gram/mL; human gastric juice group, n = 24) or normal saline solution (pH 5.2 +/- 0.2; normal saline solution group; n = 12). Mechanical ventilation was continued. Bronchoalveolar lavage was performed at 15 mins (human gastric juice group, n = 8; normal saline solution group, n = 4), 30 mins (human gastric juice group, n = 8; normal saline solution group, n = 4), or 60 mins (human gastric juice group, n = 8; normal saline solution group, n = 4) postaspiration.Measurements and Main ResultsPeak airway pressure and PaO2values were measured at baseline and 15 and 30 mins after aspiration. The pH of retrieved bronchoalveolar lavage fluid was measured and pepsin activity in sample fluid was determined.Changes from baseline in peak airway pressure and Pao sub 2 were significant in human gastric juice animals at 15 and 30 mins when compared with normal saline solution animals (PaO sub 2 -4% vs. -44%, peak airway pressure 20% vs. 36% at 15 mins; PaO2-16% vs. -79%, peak airway pressure 28% vs. 69% at 30 mins; normal saline solution group vs. human gastric juice group, p < .02). Bronchoalveolar lavage fluid pH was not significantly different between groups at any time postaspiration (6.6 +/- 0.7 vs. 6.0 +/- 0.4 at 15 mins; 7.4 +/- 0.9 vs. 6.5 +/- 0.4 at 30 mins; 7.2 +/ 0.5 vs. 6.4 +/- 0.4 at 60 mins, normal saline solution group vs. human gastric juice group, p = NS). No peptic activity was present in bronchoalveolar lavage fluid from normal saline solution animals at any time. In the human gastric juice group, peptic activity was detected in postaspiration bronchoalveolar lavage fluid in eight of eight animals at 15 mins, six of eight animals at 30 mins, and five of eight animals at 60 mins (normal saline solution group vs. human gastric juice group; p < .001 at 15 mins, p < .01 at 30 mins, p = NS at 60 mins). Peptic activity of bronchoalveolar lavage fluid varied; mean values were greater at 15 mins than at 30 or 60 mins (pepsin activity: 0.004 +/- 0.002 micro gram/mL vs. 0.002 +/- 0.001 micro gram/mL vs. 0.0006 +/- 0.0001 micro gram/mL, respectively, p < .05).ConclusionsThe results of this study suggest that peptic activity in bronchoalveolar lavage fluid can be detected up to 60 mins after induced, experimental gastric juice aspiration and may prove a clinically useful biochemical marker for episodes of occult pulmonary aspiration of gastric contents.(Crit Care Med 1996; 24:1881-1885)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo determine the hemodynamic responses to a wide range of specific, controlled, graded levels of hypoxic hypoxia over 120 mins in a neonatal porcine model and to identify the PaO2threshold for altered hemodynamic homeostasis.DesignProspective, experimental, animal study.SettingUniversity cardiovascular research laboratory.SubjectsThree-day-old domestic swine.InterventionsAnesthetized, intubated, and ventilated 3-day-old pigs (n = 88) were assigned to one of five predetermined graded PaO2groups: Group I (normoxia, PaO2= 80 torr [10.7 kPa]); group II (PaO2= 60 torr [8.0 kPa]); group III (PaO2= 40 torr [5.3 kPa]); group IV (PaO2= 30 torr [4.0 kPa]); or group V (PaO2= 20 torr [2.7 kPa]).Measurements and Main ResultsHemodynamic parameters including heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP), and pulse pressure were evaluated. Acid-base status (arterial pH and lactate) was monitored in each experimental group over the 120-min study period. Hemodynamic and acid-base parameters were unaltered in animals in groups I and II. In group III animals, blood pressure was maintained (partly by increased heart rate), and acid-base balance was unaltered. In contrast, group IV animals had a gradual and progressive decrease in systolic blood pressure, diastolic blood pressure, and MAP, and slightly decreased pulse pressure, despite sustained tachycardia. Group IV animals also developed mild lactic acidosis. Group V animals exhibited a biphasic hemodynamic response, while the heart rate response was characterized by tachycardia at the induction of hypoxia, which was reduced in magnitude by 120 mins. The biphasic hemodynamic response in this group of animals included an initial increase in systolic and pulse pressures, followed by a gradual and progressive decrease in systolic and diastolic blood pressures, MAP, and pulse pressure. In addition, group V animals also developed profound progressive lactic acidosis.ConclusionsIn anesthetized neonatal pigs, tachycardia occurred in response to a PaO2of 40 torr (5.3 kPa), and thus marked the threshold for altered hemodynamic homeostasis. Beyond this threshold, both the 30 torr (4.0 kPa) and 20 torr (2.7 kPa) groups had a PaO2-dependent "late" hypotension, while only the 20 torr (2.7 kPa) group had a significant biphasic hemodynamic response characterized by "early" hypertension. The "late" hypotension which occurred in these two profound hypoxia groups indicates an inability to adequately adjust hemodynamics during prolonged hypoxic hypoxia.(Crit Care Med 1996; 24:1886-1892)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID