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Biomedical subjects

E C Rackow

Publications and source records attributed to E C Rackow.

At least 127 records · Page 7Linked to original sources
PubMed1986

Validation of a semi-automated technique for measuring lactate in whole blood.

An electrode-based lactate analyzer was recently developed to facilitate "stat" laboratory measurement of lactate in whole blood. The results obtained with this technique were compared with those of our continuous-flow enzymatic method for 172 analyses of samples from 25 pigs; 88 analyses of samples from 12 normal human volunteers before, during, and after exercise; and 91 analyses of samples from 80 critically ill patients. This comparison revealed strongly significant linear correlations: r = 0.992 for the porcine analyses and r = 0.994 for the combined human analyses. In analytical-recovery studies with pooled porcine plasma with an initial lactate concentration of 3.85 mmol/L, 94.3% of added lactate (1, 5, and 10 mmol/L) was accounted for in the electrode technique, 96% in the reference technique. We conclude that the electrode-based lactate analyzer is rapid, precise, and accurate for measurement of lactate in whole-blood samples.

Animals↗
PubMed1986

Absence of lung edema in nephrotic rats.

The effect of decreases in plasma colloid osmotic pressure (COP) on the development of lung edema was studied in nephrotic rats. Five control animals were compared with five animals with nephrotic syndrome induced by administration of anti-rat glomerular basement membrane antibody. The COP and the left ventricular diastolic pressure (LVDP) were significantly decreased in nephrotic rats. However, no significant differences were seen in the COP - LVDP gradient, weight-to-dry lung weight ratio, or arterial oxygenation between the nephrotic and control animals. These data suggest that decreases in COP during nephrosis are not associated with accumulation of extravascular lung water.

Animals↗
PubMed1986

Oxygen delivery and utilization during rapidly fatal septic shock in rats.

Oxygen delivery and utilization were studied in a rapidly fatal model of rat peritonitis. Cecal ligation and perforation induced peritonitis and septic shock in five animals. Five animals served as sham-operated controls. Arterial pressure, central venous pressure, cardiac index, hemoglobin, plasma colloid osmotic pressure, arterial blood lactate concentration, and arterial and central venous oxygen saturation were sequentially measured over 5 hr. In septic animals, decreases in mean central venous pressure were associated with hemoconcentration and decreases in plasma colloid osmotic pressure from 16.3 +/- 0.8 to 12.2 +/- 0.1 mmHg (P less than 0.05). The cardiac index decreased from 359 +/- 35 to 166 +/- 25 ml/kg/min (P less than 0.001), and arterial lactate increased from 0.2 +/- 0.1 to 2.1 +/- 0.4 mmol (P less than 0.001). However, oxygen consumption was maintained secondary to increases in systemic oxygen extraction. Arterial lactate concentration was inversely correlated with systemic oxygen delivery and central venous oxygen saturation (r = -0.68, P less than 0.05 and r = -0.71, P less than 0.001, respectively). These observations during lethal peritonitis suggest that hypovolemia is associated with increases in microvascular permeability, although the concomitant influence of intravascular pooling cannot be excluded. Decreases in systemic perfusion appear to account for critical oxygen deficits and lactic acidosis. The increases in systemic oxygen extraction imply that cellular oxygen utilization is maintained during lethal septic shock.

Analysis of Variance↗
PubMed1985

Arterial blood gases fail to reflect acid-base status during cardiopulmonary resuscitation: a preliminary report.

The American Heart Association's current standards for CPR indicate that acid-base therapy should be guided by measurements of arterial blood gases. However, we have discovered a striking discrepancy between arterial and venous blood gases during CPR: severe venous hypercarbia and acidosis may coexist with simultaneous arterial alkalosis. Arterial blood gases during CPR, therefore, may not accurately reflect the acid-base status of mixed venous blood and thus may fail to indicate systemic acid-base status.

Acid-Base Equilibrium↗
PubMed1985

Selective acidosis in venous blood during human cardiopulmonary resuscitation: a preliminary report.

During experimental CPR, a marked venoarterial gradient in PCO2 has been reported. This is accompanied by a disproportionate decrease in venous pH and a simultaneous increase in arterial pH. This study includes a case report of human CPR in which simultaneous arterial and mixed venous blood gases were obtained before and after cardiac arrest. Similar venoarterial PCO2 gradients were observed subsequently in six additional patients during arrest. These clinical data indicate that arterial blood gases fail to reflect striking increases in venous PCO2 and decreases in pH due to respiratory acidosis on the venous side of the circulation.

Acidosis↗
PubMed1985

Acid-base determinants of survival after cardiopulmonary resuscitation.

The acid-base and electrolyte conditions which favor survival were examined in 105 patients during and after CPR. There was a sharp decrease in survival when arterial pH exceeded 7.55 during the initial 10 min after initiation of CPR. Measurements made one hour after successful resuscitation also demonstrated an increase in mortality when pH exceeded 7.55. Arterial blood lactate also served as a sensitive quantitative indicator of prognosis, both during and one hour after successful CPR. The adverse effects of alkalemia were largely explained by increases in whole-blood bicarbonate, plasma sodium, and plasma osmolality after administration of sodium bicarbonate.

Acid-Base Equilibrium↗
PubMed1985

Circulatory arrest pressure as a prognostic indicator of cardiopulmonary resuscitation.

In a porcine model of cardiac arrest, the intravascular pressure measured during circulatory standstill was positively correlated with the success of cardiopulmonary resuscitation. When volume was expanded before cardiac arrest, circulatory arrest pressure increased and the success of resuscitation increased. After volume expansion, the hematocrit was reduced and colloid osmotic pressure was decreased. However, neither hematocrit nor colloid osmotic pressure changes were directly related to survival.

Animals↗
PubMed1985

Observations on colloid osmotic pressure, hematocrit, and plasma osmolality during cardiac arrest.

A porcine model of cardiac arrest with irreversible electromechanical dissociation was associated with highly significant decreases in colloid osmotic pressure in the absence of increases in hematocrit during the initial half hour of CPR. Pulmonary edema was typically observed. These observations are best explained by increases in capillary permeability to plasma proteins. The progression of acidemia was remarkably slow; arterial blood pH remained normal for more than 16 min. Even though there was significant lactic acidosis, concurrent respiratory alkalosis during CPR accounted for the greatly delayed onset of acidemia. There was also an as-yet unexplained increase in plasma osmolality.

Animals↗
PubMed1985

Echocardiographic observations during cardiopulmonary resuscitation: a preliminary report.

Echocardiographic studies were conducted during CPR to establish whether blood flow through the heart was passive or whether cardiac compression accounted for forward blood flow. M-mode and two-dimensional echocardiographic studies were performed on anesthetized minipigs during external CPR and open-chest cardiac massage. With external compression, mitral valve closure was observed during compression systole and valve opening during compression diastole. The aortic valve opened during compression systole and closed during compression diastole. Identical observations were made during open-chest cardiac compression. Left ventricular area was computed during compression systole. A 24% reduction in the area of the left ventricle during precordial compression confirmed left ventricular ejection of blood. Saline tracer was injected into the right and left ventricles. Echocardiographic observation of the tracer demonstrated forward blood flow across the pulmonic and aortic outflow tracts during compression. There was minimal valvular regurgitation. These findings support the concept of cardiac compression as a mechanism for forward blood flow during open- and closed-chest CPR.

Animals↗
PubMed1985

Cardiac output and end-tidal carbon dioxide.

Previous studies demonstrated selective increases in mixed venous carbon dioxide tension (PvCO2) during CPR in a porcine model of cardiac arrest. This was associated with a decrease in end-tidal carbon dioxide concentration (ETCO2), possibly due to a critical reduction in cardiac output and therefore pulmonary blood flow during CPR. We investigated the relationship between ETco2 and cardiac output before cardiac arrest and during CPR. Observations in 19 minipigs confirmed a high linear correlation between ETco2 and cardiac output. We conclude that the increase in Pvco2 and the concurrent decrease in ETco2 reflect a critical reduction in cardiac output, which reduces alveolar blood flow to the extent that carbon dioxide clearance by the lung fails to keep pace with systemic CO2 production.

Animals↗
PubMed1985

End-tidal CO2 as a guide to successful cardiopulmonary resuscitation: a preliminary report.

Utilizing a well-established porcine model of cardiac arrest, we found that end-tidal CO2 concentration (ETCO2) strikingly decreased to approximately 24% of control levels, immediately after cardiac arrest and before precordial compression. During precordial compression, ETCO2 progressively increased to 46% of control values in successfully resuscitated animals but only to 26% in animals which failed to respond to resuscitation efforts. After successful resuscitation, ETCO2 rapidly returned to baseline values. These data indicate that ETCO2 may be a useful monitor for assessing the adequacy of CPR.

Animals↗
PubMed1984

The relationship between oxygen delivery and consumption during fluid resuscitation of hypovolemic and septic shock.

The effects of increasing oxygen delivery (DO2) on oxygen consumption (VO2) in eight patients with septic shock and five patients with hypovolemic shock were studied during fluid resuscitation. In the septic shock group, DO2 increased from 315 +/- 29 to 424 +/- 25 ml/min/m2 (p less than 0.01) and VO2 increased from 134 +/- 8 to 151 +/- 7 ml/min/m2 (p less than 0.01). In the hypovolemic shock group, DO2 increased from 239 +/- 26 to 386 +/- 48 ml/min/m2 (p less than 0.01) and VO2 increased from 96 +/- 9 to 135 +/- 6 ml/min/m2 (p less than 0.01). There was no significant difference in either the increase in DO2 or VO2 between the septic shock and hypovolemic shock patients. We conclude that increasing DO2 by fluid resuscitation increases VO2 during both hypovolemic and septic shock.

Aged↗
PubMed1983

Adverse effects of febrile state on cardiac performance.

The hemodynamic characteristics of 36 febrile patients were studied when temperature was greater than 100 degrees F and after resolution of fever (temperature less than or equal to 100 degrees F). The patients were divided into those with bacterial infection (group I, n = 26) and those whose fever was noninfectious in etiology (group II, n = 10). Analysis of patients likely to have coronary artery disease (CAD) (subset A, n = 12) and those unlikely to have CAD (subset B, n = 7) was carried out. To maintain constant preload, pulmonary artery wedge pressure varied by not more than 2 mm Hg in all patients. Resolution of fever was associated with a 23% increase in stroke volume index (SVI) and 37% increase in left ventricular stroke work index (LVSWI) for group I (p less than 0.01). Group II showed a 27% increase in SVI and a 38% increase in LVSWI (p less than 0.05). Both subsets A and B showed significant increases in LVSWI after resolution of fever. We found evidence of decreased left ventricular performance during the febrile state in patients with and without infections. Since all groups and subsets maintained a normal or high cardiac index associated with increased heart rate during the febrile state, the tachycardic response of the febrile patient may serve to maintain cardiac output when myocardial performance is impaired.

Adolescent↗