摘要:

ObjectiveTo determine whether continuous semiquantitative assessment of end-tidal CO2could provide a highly sensitive predictor of return of spontaneous circulation during cardiopulmonary resuscitation (CPR).DesignProspective, clinical study.SettingPrehospital CPR.PatientsOne hundred twenty patients, during nontraumatic cardiac arrest.InterventionsEnd-tidal CO2values were measured continuously after tracheal intubation, and were categorized as the initial value, and as minimal and maximal values during the first 20 mins.Measurements and Main ResultsPresenting rhythm was asystole in 22 of the first 24 patients. Return of spontaneous circulation occurred in eight patients. Initial, minimal, and maximal end-tidal CO2values were significantly (p less than .01) higher in these patients than in the patients without return of spontaneous circulation. Cutoff values providing a 100% sensitivity and the highest specificity in predicting return of spontaneous circulation were found to be 10 torr for initial and maximal end-tidal CO2values, and 2 torr for the minimal end-tidal CO2value. The number of patients required to reject (with a risk error of less than .05) the hypothesis of an actual sensitivity of less than equals 90% for an observed sensitivity of 100% was found to be 95. In the second part of the study, this hypothesis was prospectively tested for initial and maximal end-tidal CO2values in the subsequent 96 patients. Presenting cardiac rhythm was asystole in 87 patients. Return of spontaneous circulation was obtained in 30 patients. The cutoff value of 10 torr for maximal end-tidal CO2during the first 20 mins after tracheal intubation provided an observed sensitivity of 100% in predicting return of spontaneous circulation with a specificity of 67%. This result allows rejection of the hypothesis of an actual sensitivity of less than equals 90% (p equals .042). By contrast, the observed sensitivity of initial end-tidal CO2was only 87%.ConclusionsEnd-tidal CO2represents a valuable tool for monitoring patients presenting with asystole during prehospital CPR. Fluctuations in end-tidal CO2during CPR and the utility of end-tidal CO2in detecting return of spontaneous circulation justify its continuous measurement. In addition, a high sensitivity (more than 90%) in predicting return of spontaneous circulation is prospectively demonstrated using the maximal end-tidal CO2during the first 20 mins after tracheal intubation, with a cutoff value of 10 torr. Such a prognostic indicator could be used for a more rational approach to prolonged CPR.(Crit Care Med 1996; 24:791-796)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo assess the relevance, both clinical and bacteriologic, of the use of resin-containing blood culture media in blood cultures taken from critically ill patients receiving antibiotics.DesignA prospective, open clinical trial.SettingThe mixed medical surgical intensive care unit (ICU) of a 550-bed urban hospital.PatientsAll ICU patients admitted during a 3-month period (n equals 49) with suspected sepsis requiring blood cultures as part of their laboratory investigations.InterventionsThe use of an aerobic resin-containing blood culture medium, in addition to the regular aerobic and anaerobic media for all blood cultures taken.Measurements and Main ResultsEach blood culture result was classified as to its clinical significance. Changes in patient management were recorded. Culture sets in which the resin-containing bottle provided the information central to the change in patient management were identified. Bacteriologically, the results from the resin-containing medium were compared with the results from the aerobic and anaerobic media. Of 266 blood culture sets, 103 (39%) were positive, growing 278 bacterial and fungal isolates. Clinically, the resin-containing medium alone provided relevant data leading to changes in patient management on three occasions. On two of these occasions, cultures from the regular media provided the same data within 72 hrs. Bacteriologically, 77 (29%) aerobic bottles, 55 (21%) anaerobic bottles, and 89 (33%) resin-containing bottles were positive (statistical comparison of percentages: aerobic vs. resin-containing bottles, nonsignificant; aerobic vs. anaerobic bottles, p less than .046; anaerobic vs. resin-containing bottles, p less than .0027). A similar proportion of pathogens was isolated from the resin-containing bottles only (9%) and aerobic bottles only (6%). A higher proportion of contaminants was isolated from the resin-containing bottles only than the aerobic bottles only in the various sets (17% vs. 7%, p less than .046). The resin-containing bottle showed a trend toward increased detection of Staphylococcus aureus and Pseudomonas aeruginosa bacteremia.ConclusionsThe resin-containing medium offers little clinical benefit to the majority of ICU patients. Bacteriologically, it seems to have a similar overall sensitivity as the regular aerobic medium (with the possible exception of a higher sensitivity for the isolation of S. aureus and P. aeruginosa), but a lower specificity. The wide-spread use of the resin-containing bottle cannot be recommended.(Crit Care Med 1996; 24:797-801)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo investigate the relationship between neurologic outcome and blood glucose concentrations in survivors of cardiopulmonary arrest.DesignRetrospective case series chart review.SettingAdult multidisciplinary intensive care unit (ICU) of a tertiary referral medical center.SubjectsConsecutive patients over a 12-month period surviving cardiopulmonary resuscitation (CPR).InterventionsVariables that were examined that could affect the relationship between the circulating glucose concentration and neurologic outcome included: location of arrest (inhospital/out-of-hospital), age, history of diabetes mellitus, duration of arrest, CPR duration, initial cardiac rhythm, and drugs administered during arrest. Cerebral recovery was evaluated by a 5-point outcome scale (Glasgow Pittsburgh Brain Stem Score) on ICU admission, and 24 and 48 hrs after ICU admission.Measurements and Main ResultsObservations were made on 85 patients, of whom 67% had inpatient CPR and 33% received out-of-hospital CPR. The duration of arrest of 66 (78%) patients was less than 5 mins. Mean CPR duration was 13.7 mins. Twenty-one percent of patients had diabetes. The mean blood glucose concentration post-CPR (n equals 80) was 272 mg/dL (15.1 mmol/L). A statistically significant association was shown between high glucose concentration post-CPR and severe cerebral outcome among a small subset of patients with CPR lasting more than 5 mins.ConclusionsThe present study does not support an association between the concentration of glucose post-CPR and neurologic outcome. The previously reported causal relationship between hyperglycemia and neurologic prognosis may be an epiphenomenon of the severity of global cerebral ischemia in humans.(Crit Care Med 1996; 24:802-806)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveExcessive release of nitric oxide has been implicated as being an important factor contributing to systemic arterial hypotension in septic shock. Hemoglobin is an effective nitric oxide scavenger. The purpose of this study was to test the hypothesis that treatment with cross-linked human hemoglobin can ameliorate systemic arterial hypotension and improve organ perfusion in a porcine model of normodynamic endotoxemic shock.DesignProspective, randomized, controlled trial.SettingLaboratory at a university medical center.SubjectsFourteen, male, random-bred swine.InterventionsAll animals were challenged with Escherichia coli lipopolysaccharide (400 micro gram/kg) infused from t equals 0 to 90 mins. Pigs in group 1 (n equals 7) were infused with cross-linked human hemoglobin (150 mg/kg) at t equals 30 mins. Pigs in group 2 (n equals 7) were infused at t equals 30 mins with 150 mg/kg of dextran (average molecular weight 70,000 daltons) as a 5% (weight per volume) solution.Measurements and Main ResultsAfter infusion of endotoxin, mean arterial pressure decreased significantly (p less than .05) but baseline cardiac index was maintained in both groups. In hemoglobin-treated pigs (group 1), mean arterial pressure was higher than in controls (group 2) from t equals 60 to 120 mins (p less than .05). There were no significant differences between the two groups in systemic vascular resistance index, renal blood flow, mesenteric blood flow, systemic oxygen delivery, or systemic oxygen extraction. Ileal mucosal blood flow was lower (p less than .07) in group 1 than in group 2. Mean pulmonary arterial pressure increased relative to baseline in both groups, but was significantly greater in group 1 as compared with group 2. Compared with controls, infusion of hemoglobin significantly exacerbated endotoxin-induced arterial hypoxemia (p less than .05).ConclusionsTreatment with hemoglobin improved mean arterial pressure in endotoxemic swine without significantly impairing blood flow to the renal or mesenteric vascular beds. Infusion of hemoglobin, however, significantly exacerbated endotoxin-induced pulmonary hypertension and arterial hypoxemia. Additional pharmacologic strategies may be necessary to ameliorate the potential adverse pulmonary effects of administering hemoglobin solutions to patients with sepsis.(Crit Care Med 1996; 24:807-814)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveWe investigated whether ibuprofen could prevent the early decrease in left ventricular contractility that occurs during porcine endotoxemia.DesignProspective, randomized, controlled animal study.SettingUniversity research laboratory.SubjectsAdolescent crossbred pigs (n equals 28).InterventionsAnesthetized pigs were instrumented to measure hemodynamics and left ventricular pressures (using a Millar catheter) and volumes (using a conductance catheter). Pigs were then treated in four groups, according to pretreatment using ibuprofen (15 mg/kg) or saline and subsequent treatment using endotoxin (0111:B4, 50 micro gram/kg) or saline.Measurements and Main ResultsMeasurements of hemodynamics and left ventricular pressures and volumes were repeated after pretreatment with ibuprofen (or saline in controls), and at hourly intervals for 4 hrs after the start of endotoxin or control saline infusions. Left ventricular contractility was primarily assessed using the slope of the end-systolic pressure-volume relationship. Data were analyzed, using a repeated-measures analysis of variance. The slope of the end-systolic pressure-volume relationship was decreased at 4 hrs by 41 plus minus 9% in the saline/endotoxin group (p less than .05) and by 36 plus minus 14% in the ibuprofen/endotoxin group (p less than .05), so that ibuprofen pretreatment had no significant effect on the decrease in left ventricular contractility. Mean arterial pressure decreased in the saline/endotoxin group by 23 plus minus 12% at 1 hr (p less than .05) and by 35 plus minus 12% (p less than .05) at 4 hrs. Ibuprofen significantly reduced the decrease in mean arterial pressure (2 plus minus 6% increased at 1 hr, and 17 plus minus 12% decreased at 4 hrs, both p less than .05 compared with saline/endotoxin). Cardiac output increased by 25% (p less than .05) in the first hour, but then decreased to be slightly (NS) below baseline at 4 hrs in both endotoxin groups. Mean pulmonary arterial pressure was increased in the saline/endotoxin group by 154 plus minus 52% (p less than .05) at 30 mins and by 118 plus minus 40% (p less than .05) at 4 hrs. Ibuprofen prevented the very acute increase in pulmonary arterial pressure (increased by 11 plus minus 33% at 30 mins, p less than .05 compared with saline/endotoxin) and significantly reduced the pulmonary hypertension at 4 hrs (increased by 70 plus minus 25%, p less than .05 compared with both baseline and saline/endotoxin).ConclusionsWe conclude that products of the cyclooxygenase pathway do not play a major role in the early decrease in left ventricular contractility after endotoxin. However, ibuprofen may have a role in reducing the other cardiovascular effects of sepsis.(Crit Care Med 1996; 24:815-819)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo study the therapeutic effect of granulocyte colony-stimulating factor (G-CSF) on the mortality rate and host defense pattern in fulminant intra-abdominal sepsis.DesignProspective, randomized, controlled trial.SettingResearch laboratory in a university hospital.SubjectsAdult male Wistar rats.InterventionsFulminant polymicrobial intra-abdominal sepsis was induced by a 4-mm cecal perforation. Survival experiments were performed with two different doses of G-CSF (20 and 100 micro gram/kg/24 hrs), and therapy was started 7 days or 1 day before, or 4 hrs after sepsis induction (n equals 24). To examine alterations in host response pattern, G-CSF (20 micro gram/kg/24 hrs) was given at sepsis induction, and rats were killed 4, 8, 12, and 24 hrs later (n equals 8-16 per time period). Histologic examination of lung, liver, spleen, and kidney was performed, and blood concentrations of bacteria, endotoxin, tumor necrosis factor (TNF), endothelin-1, packed cell volume, and lactate were determined.Measurements and Main ResultsG-CSF (20 micro gram/kg/24 hrs), given 4 hrs after sepsis induction, reduced the mortality rate from 96% to 42%. Increasing the dose (100 micro gram/kg/24 hrs), or giving G-CSF as prophylaxis (starting 7 days or 1 day before sepsis), gave no further protection. G-CSF attenuated the sepsis-induced enhancement of circulating bacteria, endotoxin, TNF, and endothelin-1, resulting in improved fluid balance and reduced lactate concentration. No histopathologic alterations were observed after G-CSF treatment.ConclusionsG-CSF improves host defense and survival rate in experimentally induced fulminant intra-abdominal sepsis. Clearance of bacteria and endotoxin is improved, concentrations of TNF and endothelin-1 are suppressed, and microvascular flow is improved. G-CSF does not induce neutrophil-mediated tissue damage.(Crit Care Med 1996; 24:820-826)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo determine whether changes in cardiac output, regional blood flow, and intracranial pressure during permissive hypercapnia are blood pH-dependent and can be attenuated by correction of intravascular acidemia.DesignProspective, controlled study.SettingResearch laboratory.SubjectsFemale Marino ewes.InterventionsAnimals were instrumented with a pulmonary artery catheter, femoral arterial and venous catheters, a catheter in the third cerebral ventricle, and ultrasonic flow probes on the left carotid, superior mesenteric, and left renal arteries 1 wk before experimentation. At initiation of the protocol, ewes underwent endotracheal intubation and mechanical ventilation under general anesthesia. Minute ventilation was reduced to induce hypercapnia with a target PaCO2of 80 torr (10.7 kPa). In the pH-uncorrected group (n equals 6), arterial blood pH was allowed to decreased without treatment. In the pH-corrected group (n equals 5), 14.4 mEq/kg of sodium bicarbonate was given intravenously as a bolus to correct arterial blood pH toward a target arterial pH of 7.40 (dose calculated by the Henderson-Hasselbalch equation).Measurements and Main ResultsArterial blood pH, PCO2, cardiac output, intracranial pressure, and carotid, superior mesenteric, and renal artery blood flow rates were measured at normocapnic baseline and at every hour during hypercapnia for 6 hrs. In the pH-uncorrected group, arterial blood pH decreased from 7.41 plus minus 0.03 at normocapnia to 7.14 plus minus 0.01 (p less than .01 vs. normocapnia) as blood PCO2increased to 81.2 plus minus 1.8 torr (10.8 plus minus 0.2 kPa). In the pH-corrected group, arterial blood pH was 7.42 plus minus 0.02 at normocapnia and was maintained at 7.37 plus minus 0.01 while PaCO2was increased to 80.3 plus minus 0.9 torr (10.7 plus minus 0.1 kPa). Significant increases in cardiac output occurred with the initiation of hypercapnia for both groups (pH-uncorrected group: 4.3 plus minus 0.6 L/min at normocapnia vs. 6.8 plus minus 1.0 L/min at 1 hr [p less than .05]; pH-corrected group: 4.1 plus minus 0.4 at normocapnia vs. 5.7 plus minus 0.4 L/min at 1 hr [p less than .05]). However, this increase was sustained only in the uncorrected group. Changes in carotid and mesenteric artery blood flow rates, as a percent of baseline values, showed sustained significant increases in the pH-uncorrected groups (p less than .05) and only transient (carotid at 1 hr) or no (superior mesenteric) significant change in the pH-corrected groups. Conversely, significant increases in renal artery blood flow were seen only in the pH-uncorrected group during the last 2 hrs of the experiment (p less than .05). Organ blood flow, as a percent of cardiac output, did not change significantly in either group. Intracranial pressure increased significantly in the pH-uncorrected group (9.0 plus minus 1.5 mm Hg at normocapnia vs. 26.8 plus minus 5.1 at 1 hr, p less than .05), and remained increased, while showing no significant change in the pH-corrected group (8.5 plus minus 1.6 mm Hg at normocapnia to 7.7 plus minus 4.2 at 1 hr).ConclusionsAcute hypercapnia, induced within 1 hr, is associated with significant increases in cardiac output, organ blood flow, and intracranial pressure. These changes can be significantly attenuated by correction of blood pH with the administration of sodium bicarbonate, without adverse effects on hemodynamics.(Crit Care Med 1996; 24:827-834)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectivesTo investigate the effects of Nomega-mono-methyl-L-arginine (L-NMMA), an inhibitor of nitric oxide synthesis, on hemodynamics, oxygen transport, and regional blood flow in an ovine model of hyperdynamic sepsis and to compare these effects with the responses to norepinephrine.DesignProspective, nonrandomized, controlled experimental study with repeated measures.SettingInvestigational intensive care unit at a university medical center.SubjectsTwenty-five female, healthy, adult sheep of the Merino breed, divided into three groups: nine control sheep; eight sheep treated with L-NMMA; and eight sheep treated with norepinephrine.InterventionsAll sheep were chronically instrumented. After a 5-day recovery period, a continuous infusion of live Pseudomonas aeruginosa (2.5 times 106colony-forming units/min) was started and maintained for the remainder of the experiment. After 24 hrs of sepsis, eight sheep received L-NMMA (7 mg/kg/hr), eight sheep received norepinephrine, and nine sheep received the vehicle alone (0.9% saline). The norepinephrine dosage was continuously and individually adjusted to achieve the same increase in blood pressure as was observed in a matched sheep of the L-NMMA group.Measurements and Main ResultsAfter 24 hrs of sepsis, all sheep developed a hyperdynamic circulatory state with increased cardiac indices and reduced arterial pressures, and systemic vascular resistances. L-NMMA reversed the hyperdynamic circulation, causing an increase in arterial pressure by peripheral vasoconstriction. Norepinephrine led to an increase in blood pressure by augmenting cardiac indices, leaving the systemic vascular resistance unaffected. The norepinephrine dose needed to keep the blood pressure high had to be continuously increased, reflecting the reduced vascular responsiveness to catecholamines during sepsis. Renal blood flow remained unaffected by all treatment forms. Norepinephrine and L-NMMA led to a dramatic increase in urine production. Blocking the nitric oxide synthase with L-NMMA did not interfere with the host's pulmonary ability to clear bacteria, nor did treatment with norepinephrine.ConclusionsBlocking nitric oxide synthase had a marked vasoconstrictive effect. Both norepinephrine and L-NMMA increased arterial pressure without reducing renal blood flow, leading to an improved renal function.(Crit Care Med 1996; 24:835-844)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveThe inhibiting effect of nitric oxide on the aggregation and adhesion of neutrophils and platelets has been well documented in vitro. In vivo evidence, however, is more scant. In this study, we studied the effects of inhaled nitric oxide on pulmonary cellular sequestration in our sham hemodialysis model. Accumulation of neutrophils and platelets in the lungs has been shown to be an early event in this model.DesignProspective, randomized, controlled study.SettingAnimal laboratory at a university medical center.SubjectsTwenty-six anesthetized, mechanically ventilated pigs.Interventions111Indium-oxine was used to selectively label neutrophils or platelets and the activity over the lungs was followed dynamically with a gamma camera. Sham hemodialysis, using a cuprophan hollow-fiber dialyzer, was instituted via catheters in the femoral vessels. The animals were divided into two main groups: a) the nitric oxide recipient group (n equals 12, with platelets labeled in seven animals and neutrophils labeled in five animals); and b) the control group (n equals 14, with platelets labeled in seven animals and neutrophils labeled in seven animals). The animals in the former group were given 50 parts per million of nitric oxide in the inspiratory gas from the beginning of dialysis and for 30 mins onward.Measurements and Main ResultsInhalation of nitric oxide attenuated the increase in activity over the lungs in both the neutrophil and platelet groups during sham hemodialysis. In addition, an inhibiting effect on the increase in pulmonary pressure was noted.ConclusionApart from the effects of nitric oxide on central hemodynamics in this model, the scintigraphic findings indicate an in vivo effect of nitric oxide on the accumulation of platelets and neutrophils in the lungs, probably due to inhibition of the adhesion and/or aggregation of these cells.(Crit Care Med 1996; 24:845-849)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ObjectiveTo determine whether sepsis, with or without thyroid hormonal augmentation, induces myocardial tolerance to an oxidant challenge.DesignA prospective, randomized, controlled animal trial.SettingUniversity research laboratory.SubjectsTwenty male Sprague-Dawley rats.InterventionsAfter anesthesia, animals underwent cecal ligation and puncture, with or without 3,5,3 prime-triiodothyronine replacement (3 ng/hr), or sham surgery. Twenty-four hours later, the heart was rapidly excised for retrograde Langendorff perfusion. Oxyradical challenge consisted of the addition of 200 micro Meter of hydrogen peroxide to the perfusate for 60 mins.Measurements and Main ResultsMyocardial contractility and relaxation were continuously recorded. Perfusate glutathione and lactate dehydrogenase concentrations were determined enzymatically at 30-min intervals for 90 mins. Oxyradical perfusion alone significantly increased glutathione efflux and decreased myocardial contractility when compared with control animals. Prior cecal ligation and puncture decreased oxidant-mediated glutathione efflux and maintained myocardial contractility. 3,5,3 prime-triiodothyronine supplementation appeared to increase late cardiac contractility and cellular integrity during oxidant challenge. However, this increase was not statistically significant.ConclusionsAntecedent septic challenge appears to induce tolerance to further myocardial oxyradical exposure and improves myocardial functional and biochemical integrity. Thyroid hormonal supplementation may provide a modest additional benefit in septic animals.(Crit Care Med 1996; 24:850-854)

ISSN:0090-3493    

出版商:OVID    

年代:1996

数据来源: OVID