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Biomedical subjects

E C Rackow

Publications and source records attributed to E C Rackow.

At least 91 records · Page 5Linked to original sources
PubMed1989

Skeletal muscle blood flow and venous capacitance in patients with severe sepsis and systemic hypoperfusion.

Alterations in peripheral vascular tone are presumed to contribute to circulatory failure during severe sepsis. Decreased venous tone with venous pooling may decrease effective circulatory blood volume, while decreased arterial tone with redistribution of systemic blood may compromise tissue nutrient flow. We compared forearm arterial and venous tone and forearm blood flow in ten patients with and ten patients without sepsis. The FVT, MVC, and FBF were measured by air plethysmography. In the septic patients, MCV was 1.4 +/- 0.1 ml compared with 3.1 +/- 0.2 ml in nonseptic patients (p less than 0.01). The FVT was 13.4 +/- 1.0 mm Hg/ml in septic patients versus 7.0 +/- 0.5 mm Hg/ml in nonseptic patients (p less than 0.01). The ratio of FBF to cardiac output was 0.28 +/- 0.07 percent in septic patients and 0.31 +/- 0.07 percent in nonseptic patients. These data suggest that increased peripheral venous capacitance and redistribution of skeletal muscle blood flow are not present in patients with sepsis.

Adult↗
PubMed1989

Improved survival in patients with AIDS, Pneumocystis carinii pneumonia, and severe respiratory failure.

Pneumocystis carinii pneumonia (PCP) causing acute respiratory failure (ARF) in patients with acquired immunodeficiency syndrome (AIDS) has been reported in several studies to have a mortality of 84 to 100 percent. A recent report found a 42 percent survival rate. We followed 58 patients with AIDS who required positive pressure ventilation and identified 33 patients with PCP and ARF who had a PaO2/FIo2 level less than 150 mmHg. We report the survival of 12 of these 33 (36 percent). The mean duration of survival after discharge from the hospital was 7.9 +/- 1.8 months, which is an improvement over previous reports. These data suggest that we should reevaluate the reported recommendations that patients with AIDS, PCP and ARF should not receive intensive care or mechanical ventilation.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Hemodynamic effects of monophosphoryl lipid A compared to endotoxin.

The acute hemodynamic effects of Salmonella minnesota monophosphoryl lipid A (MPL) were compared with Salmonella minnesota lipopolysaccharide (LPS) in rats. Ten animals were randomized to receive either 0.25 mg MPL/100 g or 0.25 mg LPS/100 g intravenously. Arterial pressure (MAP), thermodilution cardiac output (CO), and colloid osmotic pressure (COP) were measured prior to and 30 and 60 min after MPL or LPS administration. In LPS-treated animals, CO decreased from 356 +/- 23 to 229 +/- 24 ml/kg/min at 30 min (P less than .01). MAP decreased from 115 +/- 7 to 89 +/- 2 mm Hg (P less than .05), and COP decreased from 18.4 +/- 0.6 to 15.4 +/- 0.8 mm Hg (P less than .05) at 60 min. In MPL-treated animals, no significant changes were observed in CO, MAP, and COP at 30 and 60 min. Intravenous infusion of MPL does not produce the hemodynamic derangements or increases in capillary permeability observed with endotoxin. These observations are consistent with previous reports demonstrating the limited toxicity of this lipid A derivative.

Animals↗
PubMed1989

Monophosphoryl lipid A blocks the hemodynamic effects of lethal endotoxemia.

Monophosphoryl lipid A (MPL) is a "nontoxic" derivative of lipid A. We hypothesized that, because of the structural similarity between MPL and the lipid A portion of lipopolysaccharide (a "toxic" moiety of endotoxin), hemodynamic events occurring during endotoxemia could be attenuated by administration of MPL. Lipopolysaccharide (LPS) from Salmonella minnesota wild type S and MPL from S. minnesota R595 were used for the study. Fifteen Sprague-Dawley rats were randomized to receive either (1) 0.50 mg LPS per 100 gm body weight intravenously, (2) 0.50 mg MPL per 100 gm body weight intravenously, or (3) 0.5 mg MPL per 100 gm body weight intravenously followed in 15 minutes by 0.50 mg LPS per 100 gm body weight intravenously. Arterial pressure, thermodilution cardiac output, and central venous oxygen saturation were measured before and 30 and 60 minutes after LPS administration. In LPS-treated animals, cardiac output decreased from 448 +/- 28 ml/kg/min to 336 +/- 15 ml/kg/min (p less than 0.02), and central venous oxygen saturation decreased from 71% +/- 1% to 62% +/- 2% (p less than 0.05). Mean arterial pressure decreased from 134 +/- 5 mm Hg to 90 +/- 6 mm Hg (p less than 0.01). In MPL-treated and MPL + LPS-treated animals, no significant changes were observed in cardiac output, central venous oxygen saturation, or arterial pressure. These data indicate that MPL is not associated with the adverse cardiovascular responses observed after LPS administration. Furthermore, administration of MPL blocks the development of acute circulatory failure during endotoxemia.

Animals↗
PubMed1989

Lung and muscle water after crystalloid and colloid infusion in septic rats: effect on oxygen delivery and metabolism.

We compared the effect of crystalloid infusion with that of colloid infusion on extravascular lung water and muscle water in septic rats. We also examined the relationship of lung and muscle edema to arterial oxygenation and muscle energy metabolism during sepsis. Cecal ligation and perforation were used to induce sepsis. Five animals served as sham-operated controls. Five animals were infused with 0.9% saline solution and five with 10% low molecular weight hydroxyethyl starch (hetastarch). Thermodilution cardiac output, plasma colloid osmotic pressure, and arterial blood gases were sequentially measured over a 6-hour interval. At 6 hours, a biopsy specimen was taken from the rectus femoris and the lungs and adductor magnus muscle harvested for gravimetric analysis (wet-dry/dry weight ratio). The colloid osmotic pressure was 16.1 +/- 1.2 mm Hg in the control animals, 9.3 +/- 0.5 mm Hg in the saline solution-infused animals, and 21.6 +/- 0.5 mm Hg in the hetastarch-infused animals at 6 hours (p less than 0.05 saline vs control, hetastarch). The lung wet-dry/dry weight ratio was 3.46 +/- 0.11 in the control animals, 3.74 +/- 0.13 in the saline group, and 3.64 +/- 0.11 in the hetastarch group (difference not significant). Arterial oxygenation was not significantly different in the three groups. Muscle wet-dry/dry weight ratio was 3.11 +/- 0.16 in the control animals, 2.75 +/- 0.12 in the hetastarch-infused animals, and 3.06 +/- 0.08 in the saline-infused group (not significant). There were no significant differences in skeletal muscle energy production or lactate/pyruvate ratio between the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

'Lactate washout' following circulatory arrest.

The measurement of arterial blood lactate concentration for the purpose of estimating the severity and prognosis of acute perfusion failure is suspect because of theoretical errors due to systemic "lactate washout" immediately following restoration of perfusion. If arterial lactate concentrations continue to increase following resuscitation, the assumption that increasing lactate concentrations indicate progression of anaerobiosis due to perfusion failure would be invalidated. Lactate washout was therefore investigated in a porcine model of cardiac arrest due to electromechanical dissociation. Cardiopulmonary resuscitation was initiated and maintained for intervals of 30 minutes or until spontaneous circulation was restored. In 25 trials on 14 successfully resuscitated animals, the arterial blood lactate concentration decreased within four minutes after resuscitation from cardiac arrest. In 24 animals in whom resuscitation efforts failed, arterial lactate concentrations increased throughout the observation period. Lactate washout occurred during an interval of only 2.6 +/- 0.3 minutes (mean +/- SEM). These results indicate that lactate measurements are not invalidated because of a washout phenomenon under the extreme conditions of cardiac arrest.

Animals↗
PubMed1988

End-tidal carbon dioxide concentration during cardiopulmonary resuscitation.

We prospectively measured the end-tidal carbon dioxide concentration during 13 episodes of cardiac arrest in 10 critically ill patients receiving mechanical ventilation, to evaluate its usefulness as an indicator of circulatory status during cardiac arrest and resuscitation. The end-tidal carbon dioxide concentration decreased from a mean (+/- SD) of 1.4 +/- 0.9 to 0.4 +/- 0.4 percent after the onset of cardiac arrest. During precordial compression, it increased to 1.0 +/- 0.5 percent. The decreases in the end-tidal carbon dioxide concentration were associated with increases in systemic oxygen extraction (r = 0.79). Spontaneous circulation was restored on seven occasions. This was heralded by a rapid increase in the end-tidal carbon dioxide concentration, from 1.3 +/- 0.5 percent to an overshoot value of 3.7 +/- 2.1 percent, within approximately 30 seconds. The concentration then declined to a stable value of 2.4 +/- 1.8 percent four minutes after resuscitation. However, it remained 0.7 +/- 0.4 percent in six patients in whom resuscitative efforts failed to restore spontaneous circulation. These observations are consistent with experimental studies of cardiopulmonary resuscitation in pigs, in which the end-tidal carbon dioxide concentration varied directly with the cardiac output produced by precordial compression. We therefore propose that measurement of the end-tidal carbon dioxide concentration may be a practical, non-invasive method for monitoring blood flow generated by precordial compression during cardiopulmonary resuscitation and an almost immediate indicator of successful resuscitation.

Aged↗
PubMed1988

Effects of tromethamine and sodium bicarbonate buffers during cardiac resuscitation.

The effects on cardiac resuscitability of iso-osmolal solutions of tris-hydroxymethyl-aminomethane (tromethamine), sodium bicarbonate (NaHCO3) and sodium chloride placebo were compared in 30 domestic pigs using a well-established model of electrically induced cardiac arrest and resuscitation. We hypothesized that a carbon dioxide (CO2) consuming buffer like tromethamine would reduce and sodium bicarbonate would increase the respiratory acidosis of mixed venous blood, which had recently been demonstrated in our laboratory, Tromethamine did decrease and sodium bicarbonate did increase both arterial and mixed venous CO2 during cardiopulmonary resuscitation (CPR). Both concentrations of end-tidal CO2 and coronary venous PCO2 were significantly lower after tromethamine than after bicarbonate. However, tromethamine produced an unexpected vasodilator effect with reduction of mean aortic and coronary perfusion pressures to levels that are known to reduce resuscitability and survival independently of its buffer action. Neither resuscitability nor survival was altered by bicarbonate therapy in comparison with sodium chloride placebo.

Acid-Base Equilibrium↗
PubMed1988

Effects of hetastarch and albumin on coagulation in patients with septic shock.

The effect of 6% hydroxyethyl starch (hetastarch) and 5% human serum albumin (albumin) infusion on coagulation in 12 patients with septic shock was evaluated. Patients were randomly assigned to receive either albumin (N = 6) or hetastarch (N = 6) infusion over a 24-hour study interval. The prothrombin time (PT), partial thromboplastin time (PTT), and quantitative platelet count (PC) were obtained prior to and following 24 hours of fluid infusion. Hetastarch patients received 4934 +/- 1354 mL and albumin patients received 3067 +/- 256 mL over the study interval. After hetastarch infusion, the PT increased 2.2 +/- 0.7 seconds, PTT increased 20.0 +/- 4.1 seconds (P less than .01), and PC decreased 158 +/- 36 X 10(3)/mm3 (P less than .02). After albumin administration, the PT decreased 1.2 +/- 1.7 seconds, PTT increased 20.5 +/- 10.6 seconds and PC decreased 100 +/- 34 X 10(3)/mm3. There were no significant differences in the changes in PT, PTT, or PC between the groups. The authors conclude that hetastarch infusion does not result in increased bleeding in patients with septic shock compared with albumin infusion, despite moderate effects on the hemostatic coagulation profile.

Aged↗
PubMed1988

Guide to ethical decision-making for the critically ill: the three R's and Q.C.

Ethical decision-making for the care of the critically ill and injured has never been more difficult than it is today. Major technologic advances prolong life but often provide questionable benefit in human terms. Both the ethical commitment to the individual patient and the competition for access to expensive and scarce health resources prompt the search for clinically useful and operationally appropriate criteria for decision-making. The mnemonic 3 R's and Q.C. was evolved as a practical tool by which the ethical basis for interventions may be tested. The first tier, the 3 R's, is likely to resolve the vast majority of ethical issues. These are appropriately addressed at the bedside by clinicians who determine whether a proposed intervention is Rational, Redeeming, and Respectful. When the ethical issues cannot be resolved at the bedside on the basis of the 3 R's, a second tier of testing of Quality of Life and Cost (Q.C.) is triggered. This addresses decision-making which is not exclusively or even primarily in the skill domain or authority of most physicians. It calls for assistance by those who represent a broader base of societal involvement including multidisciplinary experts in ethics and law who serve as consultants or who are organized into medical center-wide ethics committees.

Critical Care↗
PubMed1988

Relationship of oxygen delivery and mixed venous oxygenation to lactic acidosis in patients with sepsis and acute myocardial infarction.

Critical decreases in oxygen delivery (DO2) and mixed venous oxygen saturation (SvO2) are associated with anaerobic metabolism and, therefore, lactic acidosis. We studied 50 consecutive patients with sepsis and 50 consecutive patients with acute myocardial infarction (AMI) in whom the arterial blood lactate was greater than 1 mmol/L in order to determine critical thresholds of DO2 and SvO2. In both groups, critical values of DO2 or SvO2 associated with lactic acidosis could not be identified. The DO2 ranged from 136 to 811 ml/min.m2 and SvO2 ranged from 28% to 73% in the patients with sepsis. The DO2 ranged from 115 to 434 ml/min.m2 and SvO2 from 17% to 72% in patients with AMI. The absence of threshold values for DO2 and SvO2 probably reflects the influence of distributive flow abnormalities as well as differences in metabolic requirements in these critically ill patients.

Acidosis, Lactic↗
PubMed1988

Incomplete global myocardial ischemia during cardiac arrest and resuscitation.

During cardiac arrest (no flow) and CPR (low flow), the onset of myocardial ischemia is followed by myocardial respiratory acidosis. Myocardial contractility is more decreased by respiratory than by metabolic acidosis. We demonstrated in a porcine model of cardiac arrest and in human patients increases in mixed venous PCO2 during CPR, whereas PaCO2 was decreased. Consequently, there was a striking increase in the venoarterial gradients for both [H+] and CO2. Both cardiac output (pulmonary blood flow) and the concentration of expired CO2 were simultaneously decreased. In great cardiac vein blood, even more profound respiratory acidosis with only minor decreases in bicarbonate and only moderate increases in lactate were observed. Intramyocardial pH was profoundly decreased. The severity of respiratory acidosis as a determinant of resuscitability and survival should be further investigated.

Animals↗
PubMed1988

Cardiopulmonary resuscitation in the rat.

A standardized method of cardiopulmonary resuscitation in rodents has been developed for anesthetized, mechanically ventilated rats. Ventricular fibrillation was induced and maintained by an alternating current delivered to the right ventricular endocardium. After 4 min of ventricular fibrillation, the chest was compressed with a pneumatic piston device. Eight of 14 animals were successfully resuscitated with DC countershock after 6 min of cardiac arrest. In confirmation of earlier studies from our laboratories in dogs, pigs, and human patients, this rodent model of cardiopulmonary resuscitation demonstrated large venoarterial [H+] and PCO2 gradients associated with reduced pulmonary excretion of CO2 during the low-flow state. Mean aortic pressure, coronary perfusion pressure, and end-tidal CO2 during chest compression were predictive of successful resuscitation.

Acid-Base Equilibrium↗
PubMed1988

Expired carbon dioxide: a noninvasive monitor of cardiopulmonary resuscitation.

End-tidal CO2 concentration (ETCO2) may serve as a simple noninvasive measurement of the blood flow generated by precordial compression during cardiopulmonary resuscitation (CPR). In a mechanically ventilated porcine preparation of ventricular fibrillation, onset of fibrillation was associated with a rapid decrease in ETCO2 from 4.0 +/- 0.2% to less than 0.7 +/- 0.2%. With precordial compression, it increased to 1.9 +/- 0.3%. Animals that were successfully defibrillated after 12 min of CPR demonstrated an immediate increase in ETCO2. The ETCO2 increased from 1.9 +/- 0.3% to 4.9 +/- 0.3% over an interval of between 30 and 60 sec. These changes in ETCO2 were closely related to proportionally similar decreases and increases in cardiac output (CO), and a close correlation between ETCO2 and CO was demonstrated (r = .92). A similar highly significant correlation between ETCO2 and CO was also demonstrated during open-chest cardiac massage (r = .95). ETCO2 therefore serves as a noninvasive measure of pulmonary blood flow and therefore CO. In 17 successfully resuscitated animals. ETCO2 during precordial compression averaged 1.7 +/- 0.2%, whereas it was only 0.5 +/- 0.1% in five animals in whom resuscitation procedures were unsuccessful (p less than .001). Accordingly, ETCO2 prognosticates outcome during CPR and immediately identifies restoration of spontaneous circulation.

Animals↗