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M H Weil

Publications and source records attributed to M H Weil.

At least 163 records · Page 9Linked to original sources

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↗

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↗

Decreases in mortality on a large urban medical service by facilitating access to critical care. An alternative to rationing.

The admission and case fatality rate (CFR) on a large urban medical service for 12 months before and after the creation of an intermediate care unit were examined. In the year after the intermediate care unit was opened, total admissions to the ICU/CCU decreased by 7.1% as a result of a 14.6% decrease in admission of low-risk patients who did not require critical care services. The CFR of patients on the medical service decreased by 13.3% in the year after implementation of the intermediate care unit. The decrease in mortality was accounted for by a 25.0% decrease in general ward deaths and a 38.8% decrease in ward cardiac arrests. There was no significant difference in the ICU/CCU CFR. The admission of low-risk patients to an intermediate care unit provided greater access to intensive care and was associated with an overall lower medical service CFR.

Chicago↗

Early impairment of oxidative metabolism and energy production in severe sepsis.

We investigated the relationship of systemic blood flow to skeletal muscle tissue oxygenation, lactate production, and energy production during rat peritonitis established by cecal ligation and perforation. The study included five sham rats, five septic rats, and five septic rats infused with 5% albumin. Thermodilution cardiac output and skeletal muscle tissue oxygen tension were sequentially measured over a 6 hr interval. At 6 hr the rectus femoris was biopsied. In sham rats, there was no change in cardiac output or tissue oxygen tension. Skeletal muscle lactate/pyruvate ratio was 10.4 +/- 0.6, ATP was 5.39 +/- 0.23 mumol/g and total tissue adenine nucleotides were 6.41 +/- 0.21 mumol/g. In septic rats, significant decreases in cardiac output and tissue oxygen tension were associated with a lactate/pyruvate ratio of 25.7 +/- 3.7, an ATP level of 4.38 +/- 0.08 mumol/g and tissue adenine nucleotides of 5.59 +/- 0.08 mumol/g (P less than 0.01 vs. sham). In albumin infused septic rats, cardiac output and tissue oxygen tension were maintained at control levels. Skeletal muscle lactate/pyruvate ratio was 14.8 +/- 1.0, ATP was 4.70 +/- 0.12 mumol/g and tissue adenine nucleotides were 5.80 +/- 0.12 mumol/g (P less than 0.05 vs. sham). Despite the maintenance of systemic blood flow and tissue oxygenation in albumin infused septic rats, the increase in lactate/pyruvate ratio and decrease in high energy phosphates suggest impaired oxidative metabolism and energy production early in the course of severe sepsis.

Adenine Nucleotides↗

Oxygen delivery and consumption in patients with hyperdynamic septic shock.

We analyzed the relationship of increases in oxygen delivery to changes in oxygen consumption in ten patients with hyperdynamic septic shock. Increases in oxygen delivery from 413 +/- 14 (SEM) to 535 +/- 19 ml/min X m2 (p less than .01) were associated with increases in oxygen consumption from 136 +/- 10 to 161 +/- 5 ml/min X m2 (p less than .05). Arterial lactate decreased from 4.6 +/- 1.6 to 2.1 +/- 0.3 mmol/L (p less than .05). These observations suggest that oxygen utilization is perfusion-limited in hyperdynamic septic shock.

Aged↗

Hemodynamic effects of digoxin during acute cardiac failure: a comparison in patients with and without acute myocardial infarction.

The hemodynamic effects of digitalis were examined in ten patients with acute cardiac failure. Administration of 10 micrograms/kg of digoxin iv resulted in significant increases in cardiac index, stroke volume index, and left ventricular stroke work index within one hour in five patients with acute myocardial infarction (AMI) and five patients with atherosclerotic heart disease without AMI. These increases were maintained 2 h after digoxin therapy. Indirect assessment of global myocardial oxygen supply (coronary perfusion pressure) and demand (heart rate X systolic arterial pressure X wedge pressure product) did not reveal adverse changes. Digoxin therapy results in rapid improvement in cardiac function during acute cardiac failure in patients with and without AMI.

Cardiac Output↗

Effects of crystalloid and colloid fluids on extravascular lung water in hypoproteinemic dogs.

We compared the effect of crystalloid to colloid fluid infusion on extravascular lung water (EVLW) in hypoproteinemic dogs. Plasmapheresis was used to decrease plasma colloid osmotic pressure (COP) to less than 40% of its base-line level. Five animals were then infused with 0.9% sodium chloride (saline), five with 5% human serum albumin (albumin), and five with 6% hydroxyethyl starch (hetastarch) to increase the pulmonary arterial occlusive pressure by 10 Torr in comparison to the postplasmapheresis level for a 5-h study interval. On completion of the procedure, the lungs were harvested and EVLW measured by the blood-free gravimetric technique. Three to six times the volume of saline compared with albumin or hetastarch (P less than 0.001) was infused. In the saline animals, COP was decreased to 3.3 +/- 1.3 Torr, whereas COP was increased to 18.1 +/- 1.4 Torr in albumin animals (P less than 0.001) and 20.1 +/- 1.6 Torr in the hetastarch group (P less than 0.001). The saline-treated dogs developed gross signs of systemic edema. The EVLW was 8.1 +/- 0.9 ml/kg in saline animals compared with 5.3 +/- 2.1 ml/kg in the albumin (P less than 0.05) and 4.1 +/- 1.4 ml/kg in the hetastarch (P less than 0.01) groups. These data indicate that crystalloid fluid infusion during hypoproteinemia is associated with the development of both systemic and pulmonary edema.

Animals↗

Comparison of blood lactate concentrations in central venous, pulmonary artery, and arterial blood.

Arterial blood lactate is regarded as a very good indicator of the severity and prognosis of circulatory shock. Accordingly, the practical issue of whether such measurements might be equally valid on blood sampled from the right atrium or superior vena cava or from the pulmonary artery was investigated. In blood sampled prospectively on 50 occasions in 12 patients (group 1), arterial blood lactate ranged from 0.39 to 9.71 mmol/L. A very high correlation (r = .995) was observed between blood sampled simultaneously from an arterial and central venous catheter. The maximum absolute difference was 0.5, and mean difference 0.029 mmol/L. Comparable correlations were obtained between arterial and simultaneously sampled pulmonary artery blood (r = .994). We analyzed retrospectively the results of lactate analyses on 104 paired blood samples from the pulmonary artery and peripheral artery in 23 critically ill and injured patients (group 2) whose arterial blood lactates ranged from 0.46 to 12.99 mmol/L. We also found a high correlation (r = .998) between arterial and simultaneously sampled pulmonary artery blood lactate. The maximum absolute difference was 0.82, and the mean difference 0.03 mmol/L. These data demonstrate that lactate measurements in venous blood sampled either from a pulmonary artery or from a central venous catheter yield lactate concentrations essentially equivalent to those in arterial blood.

Adult↗

Increases in oxygen extraction during rapidly fatal septic shock in rats.

Oxygen utilization was studied in a lethal model of rat peritonitis. Cecal ligation and perforation induced rapidly fatal septic shock in five animals. Five animals served as sham-operated controls. Arterial pressure, cardiac output, arterial blood lactate concentration, and arterial and central venous blood gases were sequentially measured over a period of 3 hours. In septic animals, systemic oxygen extraction increased from 33% +/- 5% to 70% +/- 5% (P less than 0.01) to maintain total body oxygen consumption. However, arterial lactate level increased from 0.5 +/- 0.1 mmol/L to 4.9 +/- 0.5 mmol/L (P less than 0.01) over the same study interval. Cardiac output was correlated with central venous oxygen desaturation (r = 0.66, P less than 0.001). Central venous oxygen saturation was inversely correlated with lactate concentration (r = -0.87, P less than 0.001). These data suggest that cellular oxygen utilization is largely maintained during rapidly fatal septic shock.

Animals↗

Hemodynamic response to fluid repletion in patients with septic shock: evidence for early depression of cardiac performance.

We prospectively studied 18 patients with septic shock prior to and during volume infusion in order to evaluate their hemodynamic response to fluid repletion. Fluid challenge increased left heart filling pressure from 7.7 +/- 0.5 to 15.4 +/- 0.6 mm Hg (P less than .01). The increases in left ventricular filling were associated with significant increases in stroke volume index from 25.4 +/- 2.5 to 35.7 +/- 2.5 ml/min/M2 and cardiac index from 2.49 +/- 0.19 to 3.32 +/- 0.16 L/min/M2. However, at the end of fluid challenge, the patients exhibited depressed left ventricular performance as evidenced by a left ventricular stroke work index of 29.5 +/- 2.6 g X m/M2. Over the next 24 hours of maintenance fluid infusion, the left ventricular stroke work index increased to 36.8 +/- 4.2 g X m/M2 (not significant). These data suggest that volume infusion restores ventricular filling in patients with sepsis. Although fluid repletion increases stroke and cardiac output, depressed left ventricular performance appears to be an early finding in septic shock.

Aged↗

Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation.

We investigated the acid-base condition of arterial and mixed venous blood during cardiopulmonary resuscitation in 16 critically ill patients who had arterial and pulmonary arterial catheters in place at the time of cardiac arrest. During cardiopulmonary resuscitation, the arterial blood pH averaged 7.41, whereas the average mixed venous blood pH was 7.15 (P less than 0.001). The mean arterial partial pressure of carbon dioxide (PCO2) was 32 mm Hg, whereas the mixed venous PCO2 was 74 mm Hg (P less than 0.001). In a subgroup of 13 patients in whom blood gases were measured before, as well as during, cardiac arrest, arterial pH, PCO2, and bicarbonate were not significantly changed during arrest. However, mixed venous blood demonstrated striking decreases in pH (P less than 0.001) and increases in PCO2 (P less than 0.004). We conclude that mixed venous blood most accurately reflects the acid-base state during cardiopulmonary resuscitation, especially the rapid increase in PCO2. Arterial blood does not reflect the marked reduction in mixed venous (and therefore tissue) pH, and thus arterial blood gases may fail as appropriate guides for acid-base management in this emergency.

Acid-Base Equilibrium↗

Arteriovenous carbon dioxide and pH gradients during cardiac arrest.

In a porcine preparation of cardiac arrest, we demonstrated that there is a marked paradox of venous acidemia and arterial alkalemia. This paradox is related to decreased clearance of CO2 from the lungs when pulmonary blood flow is critically reduced. Accordingly, increased venous PCO2 rather than metabolic acidosis due to lactic acidosis predominates during the initial 8 min of cardiopulmonary resuscitation. Arterial blood gases fail as indicators of systemic acid-base status and therefore as indicators of tissue acidosis.

Acid-Base Equilibrium↗