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J Menzies,
L A Magee,
Y C Macnab,
J M Ansermino,
J Li,
M J Douglas,
A Gruslin,
P Kyle,
S K Lee,
M P Moore,
J M Moutquin,
G N Smith,
J J Walker,
K R Walley, J A Russell,
P von Dadelszen
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ABSTRACT: To determine the association between adverse maternal/perinatal outcomes and Canadian and U.S. preeclampsia severity criteria.
Using PIERS data (Preeclampsia Integrated Estimate of RiSk), an international continuous quality improvement project for women hospitalized with preeclampsia, we examined the association between preeclampsia severity criteria and adverse maternal and perinatal outcomes (univariable analysis, Fisher's exact test). Not evaluated were variables performed in <80% of pregnancies (e.g., 24-hour proteinuria).
Few of the evaluated variables were associated with adverse maternal (chest pain/dyspnea, thrombocytopenia, 'elevated liver enzymes', HELLP syndrome, and creatinine >110 microM) or perinatal outcomes (dBP >110 mm Hg and suspected abruption) (at p < 0.01).
In the PIERS cohort, most factors used in the Canadian or American classifications of severe preeclampsia do not predict adverse maternal and/or perinatal outcomes. Future classification systems should take this into account.
Hypertension in Pregnancy 02/2007; 26(4):447-62. · 1.69 Impact Factor
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ABSTRACT: It has previously been postulated that rapid red cell capillary transit through the human lung plays a role in the mechanism of diffusion limitation in some endurance athletes. Methodological limitations currently prevent researchers from directly measuring pulmonary capillary transit times in humans during exercise; however, first pass radionuclide cardiography allows direct measurement of red blood cell (RBC) transit times through the whole lung at various exercise intensities. We examined the relationship between mean whole lung red cell pulmonary transit times (cardiopulmonary transit times or CPTT) and different levels of flow in 88 healthy humans (76 males, 12 females) from several studies (mean age 31 years). The pooled data suggest that the relationship between CPTT and cardiac index (CI), beginning at rest and progressing through to maximum exercise demonstrates that CPTT reaches its minimum value when CI is about 8.1 l m2 x min(-1) (2.5-3 times the CI value at rest), and does not significantly change with further increases in CI. Cardiopulmonary blood volume (CPBV) index also does not change significantly until CI reaches 2.5 to 3 times the CI value at rest and then increases roughly linearly after that point. Consequently, the systematic increase in CPBV index with increasing pulmonary blood flow between 8.1 and 20 l m2 x min(-1) displays an adaptive response of the cardiopulmonary system by augmenting CPBV (and perhaps pulmonary capillary blood volume through distension and recruitment) to offset the reduction in CPTT, as no significant difference in mean CPTT is observed between these levels of flow (P > 0.05). Therefore, these data demonstrate that CPBV does not reach maximum capacity during strenuous or maximum exercise. This does not support the principle of quarter-power allometric scaling for flow when explaining modifications during exercise. Therefore, we speculate that the observed relationships between CPTT, CBPV index and flow may prevent mean CPTT (and perhaps mean pulmonary capillary transit times) from decreasing below the threshold time required for oxygenation.
Experimental Physiology 03/2003; 88(2):191-200. · 3.21 Impact Factor
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ABSTRACT: The purpose was to determine if acute plasma volume expansion (PVE) changed red-cell pulmonary transit time (PTT) during severe exercise. Twelve endurance athletes performed 6.5 min of severe cycling exercise on different days. Pentaspan [(500 ml, infusion condition, I] or placebo [(60 ml saline), non-infusion condition, N] were infused prior to exercise. Blood gas tensions, PTT, multigated acquisition (MUGA) derived cardiac output, and oxygen uptake were measured during exercise. PTT was measured during minute 3 of exercise by radionuclide cardiography. Arterial P(O(2)) (Pa(O(2))), and alveolar-arterial oxygen pressure difference (AaD(O(2))) at minute 3 of exercise did not differ between conditions. Mean PTT at minute 3 of exercise was 0.3 sec longer in the I condition (P=0.002). However, the change in PTT between conditions was not correlated to the change in either Pa(O(2)) or AaD(O(2)). We conclude that PVE slows (lengthens) PTT without affecting pulmonary gas exchange. Therefore, rapid PTT may not be related to hypoxemia during exercise.
Respiratory Physiology & Neurobiology 09/2002; 131(3):255-68. · 2.24 Impact Factor
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G R Bernard,
E W Ely,
T J Wright,
J Fraiz,
J E Stasek, J A Russell,
I Mayers,
B A Rosenfeld,
P E Morris,
S B Yan,
J D Helterbrand
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ABSTRACT: To assess the safety and effect on coagulopathy of a range of doses of recombinant human activated protein C (rhAPC). To determine an effective dose and duration of rhAPC for use in future clinical trials.
Double-blind, randomized, placebo-controlled, multicenter, dose-ranging (sequential), phase II clinical trial.
Forty community or academic medical institutions in United States and Canada.
One hundred thirty-one adult patients with severe sepsis.
Intravenous infusion of rhAPC (12, 18, 24, or 30 microg/kg/hr) or placebo for 48 or 96 hrs.
No significant differences in incidence of serious bleeding events (4% rhAPC, 5% placebo, p >.999) or incidence of serious adverse events (39% rhAPC, 46% placebo, p = 0.422) between rhAPC- and placebo-treated patients were observed. One of 53 rhAPC-treated patients with suitable immunogenicity samples had a low level, transient, non-neutralizing anti-APC antibody response not associated with any clinical adverse event. Significant dose-dependent decreases in both D-dimer (p <0.001) and end of infusion interleukin 6 levels (p =.021) were demonstrated. No statistically significant effects on fibrinogen or platelet counts were observed. A nonstatistically significant 15% relative risk reduction in 28-day all-cause mortality was observed between rhAPC- and placebo-treated patients.
rhAPC was safe and well-tolerated and demonstrated a dose-dependent reduction in D-dimer and interleukin 6 levels relative to placebo. The dose of 24 microg/kg/hr for 96 hrs was selected for use in future clinical studies.
Critical Care Medicine 11/2001; 29(11):2051-9. · 6.33 Impact Factor
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ABSTRACT: Vasopressin is emerging as a rational therapy for the hemodynamic support of septic shock and vasodilatory shock due to systemic inflammatory response syndrome. The goal of this review is to understand the physiology of vasopressin relevant to septic shock in order to maximize its safety and efficacy in clinical trials and in subsequent therapeutic use. Vasopressin is both a vasopressor and an antidiuretic hormone. It also has hemostatic, GI, and thermoregulatory effects, and is an adrenocorticotropic hormone secretagogue. Vasopressin is released from the axonal terminals of magnocellular neurons in the hypothalamus. Vasopressin mediates vasoconstriction via V1-receptor activation on vascular smooth muscle and mediates its antidiuretic effect via V2-receptor activation in the renal collecting duct system. In addition, vasopressin, at low plasma concentrations, mediates vasodilation in coronary, cerebral, and pulmonary arterial circulations. Septic shock causes first a transient early increase in blood vasopressin concentrations that decrease later in septic shock to very low levels compared to other causes of hypotension. Vasopressin infusion of 0.01 to 0.04 U/min in patients with septic shock increases plasma vasopressin levels to those observed in patients with hypotension from other causes, such as cardiogenic shock. Increased vasopressin levels are associated with a lesser need for other vasopressors. Urinary output may increase, and pulmonary vascular resistance may decrease. Infusions of > 0.04 U/min may lead to adverse, likely vasoconstriction-mediated events. Because clinical studies have been relatively small, focused on physiologic end points, and because of potential adverse effects of vasopressin, clinical use of vasopressin should await a randomized controlled trial of its effects on clinical outcomes such as organ failure and mortality.
Chest 09/2001; 120(3):989-1002. · 5.25 Impact Factor
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ABSTRACT: We examined the pattern of organ system dysfunction, the evolution of this pattern over time, and the relationship of these features to mortality in patients who had sepsis syndrome.
Prospective, multicenter, observational study.
Intensive care units in tertiary referral teaching hospitals.
A total of 287 patients who had sepsis syndrome were prospectively identified in intensive care units. MATERIALS AND MEASUREMENTS: Cardiovascular, pulmonary, neurologic, coagulation, renal, and hepatic dysfunction were assessed at onset and on day 3 of sepsis syndrome. Organ dysfunction was classified as normal, mild, moderate, severe, and extreme dysfunction. We calculated the occurrence rate and associated 30-day mortality rate of organ dysfunction at the onset of sepsis syndrome. We then measured the change in organ dysfunction from onset to day 3 of sepsis syndrome and determined, for individual organ systems, the associated 30-day mortality rate.
At the onset of sepsis syndrome, clinically significant pulmonary dysfunction was the most common organ failure, but was not related to 30-day mortality. Clinically significant cardiovascular, neurologic, coagulation, renal, and hepatic dysfunction were less common at the onset of sepsis syndrome but were significantly associated with the 30-day mortality rate. Worsening neurologic, coagulation, and renal dysfunction from onset to day 3 of sepsis syndrome were associated with significantly higher 30-day mortality than with improvement or no change in organ dysfunction.
Increased mortality rate in sepsis syndrome is associated with a pattern characterized by failure of nonpulmonary organ systems and, in particular, worsening neurologic, coagulation, and renal dysfunction over the first 3 days. Although initial pulmonary dysfunction is common in patients with sepsis syndrome, it is not associated with an increased mortality rate.
Critical Care Medicine 11/2000; 28(10):3405-11. · 6.33 Impact Factor
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ABSTRACT: Gastric mucosal-arterial PCO2 gradient (P(g-a)CO2) is used to assess splanchnic perfusion and oxygenation. We evaluated whether P(g-a)CO2 reflects whole body (Q) and splanchnic (Qsp) blood flow, oxygen delivery (DO2) and consumption (VO2) after coronary artery by pass graft (CABG) operation. Thirty patients received dobutamine or dopexamine to increase cardiac index, 15 patients enalapril or sodium nitroprusside to lower blood pressure, and 30 patients were controls. We measured Q, Qsp (hepatic vein catheter and indocyanine green), and gastric mucosal PCO2 (nasogastric tonometer) before and after interventions. Multiple linear regression model showed that none of the changes in Q, Qsp, and splanchnic or systemic DO2 and VO2 significantly explained changes in P(g-a)CO2 (deltaP(g-a)CO2). All independent variables together explained only 7% of deltaP(g-a)CO2. Increased splanchnic blood flow (0.65 +/- .19 vs. 0.94 +/- .31 L/min/m2, P < 0.001) and increased splanchnic DO2 (101 +/- 28 vs. 143 +/- 42 mL/min/m2, P < 0.001) during catecholamine infusions were associated with increased P(g-a)CO2 (8 +/- 8 vs. 11 +/- 7 mmHg, P = 0.003). P(g-a)CO2 does not reflect whole body or splanchnic blood flow, DO2 or VO2 after CABG operations. The physiology of P(g-a)CO2 is complex and therefore it is difficult for clinicians to interpret changes in gastric mucosal-arterial PCO2 gradient in individual patients after cardiac surgery.
Shock 08/2000; 14(1):13-7. · 2.85 Impact Factor
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ABSTRACT: Correct early prediction of successful extubation decreases morbidity and mortality. The use of single time point measurements and surrogate markers of true extubation success limits weaning studies. Our aim was to determine whether a "stress test" improves prediction of extubation outcome and to determine the most predictive variables.
Observational study.
Intensive care unit of a teaching hospital.
A convenience sample of 68 patients judged to be ready for extubation.
We decreased pressure support from 5 to 0 cm H2O for 1 hr before extubation (stress test) while patients were on 5 cm H2O continuous positive airway pressure.
We measured respiratory frequency, tidal volume, ratio of respiratory frequency to tidal volume (f/VT), airway occlusion pressure after onset of inspiration (P0.1), and gastric-arterial PCO2 (deltaPg-aCO2 both on 5 cm H2O and 0 cm H2O pressure support. Then all patients were extubated. Failure of extubation was defined as reintubation within 24 hrs. Seventeen patients (25%) failed extubation. With pressure support of 5 cm H2O and continuous positive airway pressure of 5 cm H2O, most predictors were not different between patients who failed and patients who were successfully extubated. After the stress test, deltaPg-aCO2 was 2 (-5; 15) mm Hg (median; quartiles) in successfully extubated patients vs. 28 (-9; 48) in failures (p = .0003), tidal volume was 473 (387; 558) vs. 400 (323; 435) mL (p = .02), and P0.1 was 2.8 (2; 4.1) vs. 4.1 (2.7; 5.3) mm Hg (p = .03), respectively. The stress test increased specificity of deltaPg-aCO2 from 0.45 to 0.94 and positive predictive value from 0.85 to 0.97. The specificity and positive predictive values for f/VT after the stress test were 0.23 and 0.78.
A simple stress test improves prediction of extubation outcome. deltaPg-aCO2 has superior specificity and positive predictive value compared with other variables. The use of true clinical outcome (i.e., extubation) instead of the use of surrogate markers (e.g., tachypnea) distinguishes these results from previous studies.
Critical Care Medicine 08/2000; 28(7):2313-9. · 6.33 Impact Factor
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ABSTRACT: In hypovolemic patients with sepsis syndrome, to determine the effects of colloid volume infusion using 10% pentastarch on abnormal gastric tonometer measurements (gastric intramucosal CO2 tension, gastric intramucosal-arterial PCO2 gradient, and gastric intramucosal pH [pHi]) and on cardiac index, global oxygen delivery, and hemoglobin.
Prospective prepost intervention study.
Tertiary care, university-affiliated 15-bed general systems intensive care unit.
Patients were studied who had sepsis syndrome, who had pulmonary arterial catheters in place, who were hypovolemic (pulmonary arterial occlusion pressure [PAOP] <15 mm Hg), and who had a gastric arterial PCO2 gradient >10 mm Hg.
Baseline measurements of gastric intramucosal CO2 tension, gastric intramucosal-arterial PCO2 gradient, and pHi, as well as arterial lactate, pulmonary arterial occlusion, central venous and systemic arterial pressures, thermodilution cardiac output, and temperature. Boluses of 500 mL pentastarch were administered to a total of 1,000 mL or until PAOP was >18 mm Hg. Measurements were repeated at 30 mins and 120 mins postinfusion of pentastarch.
Volume infusion using pentastarch did not change gastric PCO2, gastric-arterial PCO2 gradient, or pHi. Volume expansion with pentastarch significantly increased cardiac index, global oxygen delivery, and PAOP. Administration of pentastarch decreased hemoglobin and arterial lactate at 30 mins but not at 120 mins.
Volume expansion using a colloidal solution of 10% pentastarch does not change abnormal intramucosal CO2 tension, gastric-arterial PCO2 gradient, or pHi in critically ill hypovolemic patients who have sepsis syndrome despite increasing cardiac index, oxygen delivery, and pulmonary artery occlusion pressure.
Critical Care Medicine 07/2000; 28(7):2254-8. · 6.33 Impact Factor
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ABSTRACT: To evaluate the literature regarding antiinflammatory actions of cytokines, evaluate randomized controlled trials (RCTs) of supranormal oxygen delivery, and suggest alternative mechanism(s) for possible beneficial effects of supranormal oxygen delivery in critically ill surgical patients.
Literature review using Medline and review of selected illustrative studies.
Catecholamines (epinephrine, norepinephrine, isoproterenol, and dopamine) in general inhibit tumor necrosis factor-alpha (TNF) production and may enhance interleukin-6 (IL-6) and IL-10 production. Phosphodiesterase inhibitors also inhibit TNF and may enhance IL-10. All studies used models (cell, animal, or humans infused with endotoxin) of sepsis. RCTs of supranormal oxygen delivery show decreased mortality in high-risk surgical patients; however, prevention or reversal of tissue hypoxia may not be the mechanism of benefit. Antiinflammatory effects of catecholamines are a potential and, to date, unexplored mechanism of the benefit of supranormal oxygen delivery in critically ill surgical patients.
Catecholamines may modulate cytokine response beneficially and could be a mechanism of decreased morbidity and mortality of supranormal oxygen delivery in high-risk surgical patients.
Intensive Care Medicine 04/2000; 26(3):299-304. · 5.40 Impact Factor
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ABSTRACT: Dobutamine infusion is used to increase whole-body oxygen delivery in septic patients to satisfy unmet oxygen demand of hypoxic tissues. However, dobutamine infusion also increases myocardial work and myocardial oxygen consumption. Our goal was to determine the importance of this effect as a fraction of the increase in whole-body oxygen consumption, in a porcine model of septic shock.
Four hours after a 50 microg/kg infusion of Escherichia coli endotoxin (0111: B4, Sigma) in eight anesthetized pigs, whole-body oxygen delivery and myocardial oxygen delivery and consumption were calculated from blood flow and arterial and venous oxygen content measurements. We directly measured whole-body oxygen consumption by analysis of inhaled and exhaled gases using a metabolic cart. Then dobutamine 10 and 20 microg/kg/min was infused and measurements were repeated.
Dobutamine infusion increased whole-body oxygen delivery but did not increase metabolic cart measured whole-body oxygen consumption. Dobutamine infusion of 10 and 20 microg/kg/min increased myocardial oxygen consumption by 7.0 +/- 0.6 (80 +/-10%) and 12.0 +/- 2.0 mL O2/min (142 +/- 30%), respectively (P < .01).
In this porcine model of sepsis, dobutamine infusion significantly increases myocardial oxygen consumption. Because whole-body oxygen consumption does not change, dobutamine infusion may fail to increase and may decrease oxygen consumption by other organs.
Journal of Critical Care 10/1999; 14(3):125-32. · 2.13 Impact Factor
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ABSTRACT: To determine (1) predictors of in-hospital mortality and long-term survival in patients with acute respiratory failure (ARF) caused by acquired immunodeficiency syndrome-related Pneumocystis carinii pneumonia (PCP) and (2) long-term survival for patients with ARF relative to those without ARF.
A retrospective medical chart review was conducted of all cases of PCP-related ARF for which the patient was admitted to the intensive care unit of a single tertiary care institution between 1991 and 1996. Data were extracted regarding physiologic scores, relevant laboratory values, and duration of previous maximal therapy with combined anti-PCP agents and corticosteroids at entry to the intensive care unit. Duration of survival was determined by Kaplan-Meier methods from date of first hospital admission and compared for patients with and without ARF.
There were 41 admissions to the intensive care unit among 39 patients, with 56.4% in-hospital mortality. Higher physiologic scores (Acute Physiology and Chronic Health Evaluation II [APACHE II], Acute Lung Injury, and modified Multisystem Organ Failure scores) were predictive of in-hospital mortality. Duration of previous maximal therapy also predicted in-hospital mortality (45% for patients with <5 days of previous maximal therapy vs 88% for those with > or =5 days of previous maximal therapy; P = .03). Combining physiologic scores and duration of previous maximal therapy enhanced prediction of in-hospital mortality. There was no difference in long-term survival between patients with PCP with ARF and those without ARF (P = .80), and baseline characteristics did not predict long-term survival.
In-hospital mortality of patients with acquired immunodeficiency syndrome-related PCP and ARF is predicted by duration of previous maximal therapy and physiologic scores, and their combination enhances predictive accuracy. Long-term survival of patients with ARF caused by PCP is comparable to that of patients with PCP who do not develop ARF, and determinants of in-hospital mortality do not predict long-term survival.
Archives of Internal Medicine 05/1999; 159(7):741-7. · 11.46 Impact Factor
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M M Arons,
A P Wheeler,
G R Bernard,
B W Christman, J A Russell,
R Schein,
W R Summer,
K P Steinberg,
W Fulkerson,
P Wright,
W D Dupont,
B B Swindell
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ABSTRACT: The objective was to compare the clinical and physiologic characteristics of febrile septic patients with hypothermic septic patients; and to examine plasma levels of cytokines tumor necrosis factor alpha (TNF-alpha and interleukin 6 (IL-6) and the lipid mediators thromboxane B2 (TxB2) and prostacyclin in hypothermic septic patients in comparison with febrile patients. Most importantly, we wanted to report the effect of ibuprofen treatment on vital signs, organ failure, and mortality in hypothermic sepsis.
The study was performed in the intensive care units (ICUs) of seven clinical centers in the United States and Canada.
Four hundred fifty-five patients admitted to the ICU who met defined criteria for severe sepsis and were suspected of having a serious infection.
Ibuprofen at a dose of 10 mg/kg (maximum 800 mg) was administered intravenously over 30 to 60 mins every 6 hrs for eight doses vs. placebo (glycine buffer vehicle).
Forty-four (10%) septic patients met criteria for hypothermia and 409 were febrile. The mortality rate was significantly higher in hypothermic patients, 70% vs. 35% for febrile patients. At study entry, urinary metabolites of TxB2, prostacyclin, and serum levels of TNF-alpha and IL-6 were significantly elevated in hypothermic patients compared with febrile patients. In hypothermic patients treated with ibuprofen, there was a trend toward an increased number of days free of major organ system failures and a significant reduction in the 30-day mortality rate from 90% (18/20 placebo-treated patients) to 54% (13/24 ibuprofen-treated patients).
Hypothermic sepsis has an incidence of approximately 10% and an untreated mortality twice that of severe sepsis presenting with fever. When compared with febrile patients, the hypothermic group has an amplified response with respect to cytokines TNF-alpha and IL-6 and lipid mediators TxB2 and prostacyclin. Treatment with ibuprofen may decrease mortality in this select group of septic patients.
Critical Care Medicine 05/1999; 27(4):699-707. · 6.33 Impact Factor
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ABSTRACT: We tested the hypothesis that treatment with the glutathione repleting agent, L-2-oxothiazolidine-4-carboxylic acid (OTZ), could prevent endotoxin-induced ventricular dysfunction. Rabbits were treated with OTZ 2.4 g/kg (10% solution subcutaneously), or an equal volume and osmolality of saline, 24 h prior to, and again (intravenously) just prior to, infusion of 1 mg/kg E. coli endotoxin (or vehicle control). Ventricular contractility was measured in isolated hearts perfused by support rabbits. Contractility did not change in control groups (Saline/Control [n = 7] or OTZ/Control [n = 7]) over 6 h. However, Emax decreased in the Saline/Endotoxin group (-16.1 +/- 4.5% from baseline, n = 7, p < 0.05) and this was prevented by pretreatment with OTZ in the OTZ/ Endotoxin group (+6.3 +/- 4.1%, n = 7, p < 0.05 by analysis of variance). To better understand the mechanism of this effect we measured myocardial glutathione concentration and found it to be greater in OTZ/Endotoxin animals (104 +/- 4 ng/g) than in the Saline/Endotoxin animals (80 +/- 3 ng/g, p < 0.05). OTZ did not appreciably alter the endotoxin-induced increase in serum concentration of tumor necrosis factor (TNF) or the endotoxin-induced increase in myocardial leukocyte content. We conclude that oxygen radicals contribute to the early decrease in left ventricular contractility after endotoxin infusion and this decrease may be prevented by OTZ.
American Journal of Respiratory and Critical Care Medicine 10/1998; 158(4):1109-13. · 11.08 Impact Factor
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ABSTRACT: To validate a previously developed multisystem organ failure (MSOF) score with and without the addition of the lactate dehydrogenase (LDH) level as a predictor of survival to hospital discharge in patients with AIDS-related Pneumocystis carinii pneumonia (PCP) and acute respiratory failure (ARF).
Retrospective chart review between April 1, 1991, and September 30, 1996.
University-affiliated tertiary care center in downtown Vancouver, British Columbia, Canada.
All patients with PCP-related ARF admitted to the ICU of St. Paul's Hospital during the study period.
As putative prognostic instruments, data were extracted regarding the APACHE II (acute physiology and chronic health evaluation II), acute lung injury (ALI), AIDS, and modified MSOF scores, as well as LDH levels, at entry to the ICU. Patients were stratified based on an LDH level of < or > or = 2,000 U/L and this threshold was assessed in its predictability of outcome when added to each of the above scores. For APACHE II, the score was categorized in six groups and evaluated with and without inclusion of the LDH. Receiver operating characteristic curves were constructed for LDH and for each score with and without the LDH level to assess accuracy of prediction. The area under each curve was calculated and compared to estimate the statistical significance of observed differences.
There were 40 admissions to the ICU of 38 patients with 52.5% mortality. The ALI and AIDS scores were not predictive of outcome. The modified MSOF and APACHE II scores were significant predictors of survival and the performance of both was enhanced by the addition of LDH.
Both the APACHE II and the modified MSOF scores were significant predictors of outcome in the patient population studied. These results validate the modified MSOF score as an effective predictor of survival to hospital discharge among patients with AIDS-related PCP who develop ARF and the performance of the score is enhanced by the addition of the LDH level.
Chest 07/1998; 114(1):199-206. · 5.25 Impact Factor
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ABSTRACT: To determine if oxygen consumption/oxygen delivery (VO2/DO2) relationships derived using calorimetry (which are not influenced by shared measurement error) agreed with those obtained using the pulmonary artery (PA) catheter alone. To evaluate three strategies to reduce the influence of shared measurement error to determine if agreement between the two methods could be improved.
Twenty-seven patients were studied following coronary artery bypass surgery. Calorimetric VO2, six thermodilution cardiac outputs (COs), and arterial and mixed venous oxygen content measurements were made at baseline and were repeated 30 min following dobutamine administrations of 3 microg/kg/min and 5 microg/kg/min.
Dobutamine produced a dose-dependent increase in DO2, from 378+/-65 mL/min/m2 to 446+/-78 mL/min/m2 (p<0.01) and in both PA catheter and calorimetric-derived VO2, from 104+/-18 mL/min/Mi2 to 114+/-22 mL/min/m2 (p<0.05) and from 117+/-15 mL/min/m2 to 126+/-19 mL/min/m2 (p<0.01), respectively. Agreement was poor (bias=12%, SD=21%) between the calorimetric and PA catheter methods of determining VO2/DO2 slope. When three CO measurements were used to calculate VO2, and three separate CO measurements were used to calculate DO2, the level of agreement between the two methods improved (bias=2%, SD=15%). Increasing the number of COs resulted in a similar improvement in the level of agreement between the two methods. Weighting the slope to the observed change in DO2 was the best method to improve the level of agreement (bias=2%, SD=6% for three COs).
To reduce the influence of shared measurement error, the best strategy to improve the measurement of VO2/DO2 slope is to maximize the change in DO2 (optimally over 100 mL/min/m2).
Chest 06/1998; 113(5):1347-55. · 5.25 Impact Factor
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ABSTRACT: To determine the levels of glutathione and cysteine in patients with ARDS and examine the effect of treatment with N-acetylcysteine (NAC) and L-2-oxothiazolidine-4-carboxylate (Procysteine; Clintec Technologies Inc; Chicago [OTZ]) on these levels and on common physiologic abnormalities, and organ dysfunction associated with ARDS.
Randomized, double-blind, placebo-controlled, prospective clinical trial.
ICUs in five clinical centers in the United States and Canada.
Patients meeting a predetermined definition of ARDS and requiring mechanical ventilation.
Standard care for ARDS and I.V. infusion, every 8 h for 10 days, of one of the following: NAC (70 mg/kg, n=14), OTZ (63 mg/kg, n=17), or placebo (n=15).
Both antioxidants effectively repleted RBC glutathione gradually over the 10-day treatment period (47% and 49% increases from baseline values for NAC and OTZ, respectively). There was no difference in mortality among groups (placebo, 40%; NAC, 36%; OTZ, 35%). However, the number of days of acute lung injury was decreased and there was also a significant increase in cardiac index in both treatment groups (NAC/OTZ [+]14%; placebo [-]6%).
Our findings suggest that repletion of glutathione may safely be accomplished with NAC or OTZ in patients with acute lung injury/ARDS. Such treatment may shorten the duration of acute lung injury, but larger studies are needed to confirm this.
Chest 08/1997; 112(1):164-72. · 5.25 Impact Factor
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ABSTRACT: To determine what volumes are commonly used for rapid volume infusions in critically ill patients admitted to the intensive care unit (ICU) for > 12 hrs; and to determine the effectiveness of a typical rapid volume infusion in producing hemodynamic change and increasing left ventricular end-diastolic volume.
A prospective survey of clinical practice (part 1) and a prospective clinical investigation (part 2).
Two hospital ICUs (11 and six beds) of which one is university affiliated.
Critically ill patients admitted to the ICU for > 12 hrs.
Infusion of 500 mL of normal saline over 5 to 10 mins.
For 1 month, we recorded the volume and composition of all volume infusions given as a rapid bolus in patients admitted to the ICU for > 12 hrs. We then measured the effected the median rapid volume infusion in a subset of 13 patients by measuring hemodynamics (using arterial and pulmonary artery flotation catheters) and left ventricular end-diastolic area (using transgastric short-axis views from transesophageal echocardiograms). During 470 patient days, 159 rapid volume infusions were administered. The average rapid volume infusion administered was 390 +/- 160 mL (median 500; interquartile range 250 to 500). Crystalloid solutions were used for two thirds of the rapid volume infusions and colloid solutions were used for one third of the rapid volume infusions. The rapid volume infusion of 500 mL of saline did not significantly increase mean arterial pressure (78.0 +/- 11.9 to 79.3 +/- 14.6 mm Hg), cardiac index (4.3 +/- 1.7 to 4.6 +/- 1.8 L/min/m2), right atrial pressure (11.1 +/- 3.8 to 12.4 +/- 3.3 mm Hg), left ventricular end-diastolic area (8.6 +/- 1.7 to 9.1 +/- 1.8 cm2/m2), or left ventricular end-systolic area (3.5 +/- 1.5 to 3.6 +/- 1.5 cm2/m2). Pulmonary artery occlusion pressure increased slightly but significantly from 12.9 +/- 3.4 to 14.7 +/- 3.3 mm Hg (p < .05).
After patients are admitted to the ICU for > 12 hrs, rapid volume infusions are common therapeutic interventions but the rapid volume infusions are typically small. The effect of a typical rapid volume infusion on hemodynamics and left ventricular areas in these patients is surprisingly small.
Critical Care Medicine 07/1997; 25(6):965-70. · 6.33 Impact Factor
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G R Bernard,
A P Wheeler, J A Russell,
R Schein,
W R Summer,
K P Steinberg,
W J Fulkerson,
P E Wright,
B W Christman,
W D Dupont,
S B Higgins,
B B Swindell
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ABSTRACT: In patients with sepsis the production of arachidonic acid metabolites by cyclooxygenase increases, but the pathophysiologic role of these prostaglandins is unclear. In animal models, inhibition of cyclooxygenase by treatment with ibuprofen before the onset of sepsis reduces physiologic abnormalities and improves survival. In pilot studies of patients with sepsis, treatment with ibuprofen led to improvements in gas exchange and airway mechanics.
From October 1989 to March 1995, we conducted a randomized, double-blind, placebo-controlled trial of intravenous ibuprofen (10 mg per kilogram of body weight [maximal dose, 800 mg], given every six hours for eight doses) in 455 patients who had sepsis, defined as fever, tachycardia, tachypnea, and acute failure of at least one organ system.
In the ibuprofen group, but not the placebo group, there were significant declines in urinary levels of prostacyclin and thromboxane, temperature, heart rate, oxygen consumption, and lactic acidosis. With ibuprofen therapy there was no increased incidence of renal dysfunction, gastrointestinal bleeding, or other adverse events. However, treatment with ibuprofen did not reduce the incidence or duration of shock or the acute respiratory distress syndrome and did not significantly improve the rate of survival at 30 days (mortality, 37 percent with ibuprofen vs 40 percent with placebo).
In patients with sepsis, treatment with ibuprofen reduces levels of prostacyclin and thromboxane and decreases fever, tachycardia, oxygen consumption, and lactic acidosis, but it does not prevent the development of shock or the acute respiratory distress syndrome and does not improve survival.
New England Journal of Medicine 04/1997; 336(13):912-8. · 53.30 Impact Factor
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ABSTRACT: Recent observations have highlighted errors in the thermodilution technique of measuring cardiac output. Thus, cardiac output measurements using transesophageal echocardiography and the Fick method were compared with simultaneous thermodilution measurements.
In 13 mechanically ventilated critically ill patients, cardiac output was determined simultaneously using (1) transesophageal echocardiography (COTEE, (2) the Fick method (COFICK, and (3) thermodilution (COTD immediately before and after a rapid infusion of 500 mL of saline. Left ventricular end-diastolic and end-systolic areas were measured using the transesophageal echocardiographic transgastric short axis view, and COTEE was calculated from the corresponding volumes. Absolute cardiac output values and the changes from before to after saline infusion (delta CO) were compared using analysis of variance, linear regression, and the Bland and Altman method.
There were no significant differences between COTEE (8.0 +/- 3.4), COFICK (8.4 +/- 3.3), and COTD (8.3 +/- 3.0) or between delta COTEE, delta COFICK, and delta COTD using analysis of variance. However, correlations between COTEE and COTD (r2 = 0.46; P < .00001), COFICK and COTD (r2 = 0.46; P < .0001), and COTEE and COFICK (r2 = 0.42; P < .0001) were only moderately good. Using the method of Bland and Altman, the mean difference (+/-2 standard deviations) between COTEE and COTD was 0.3 +/- 4.3 L/min, between COFICK and COTD was -1.0 +/- 3.8 L/min, and between COTEE and COFICK was 0.6 +/- 5.6 L/min, whereas the difference between delta COTEE and delta COTD was 0% +/- 26%, between delta COFICK and delta COTD was 9% +/- 46%, and between delta COTEE and delta COFICK was 8% +/- 39%.
There are substantial differences in cardiac output as measured by these three methods, best demonstrated using the method of Bland and Altman. The variability of cardiac output and its derivatives (eg, oxygen delivery) should be borne in mind when making clinical decisions on individual patients.
Journal of Critical Care 10/1996; 11(3):109-16. · 2.13 Impact Factor
