Sybil Michaels

Relationship between colloid osmotic pressure and pulmonary artery wedge pressure in patients with acute cardiorespiratory failure

Close relationships between progressive respiratory failure, roentgenographic signs of pulmonary opacification and decreases in the difference between colloid osmotic pressure of plasma and the pulmonary artery wedge pressure (colloid-hydrosatic pressure gradient) were demonstrated in 49 critically ill patients with multisystem failure, in patients in shock. The potential importance of this relationship is underscored by the observation that fatal progression of pulmonary edema was related to a critical reduction in the colloid-hydrostatic pressure gradient to levels of less than 0 mm Hg. More often, reduction in colloid osmotic pressure rather than increases in left ventricular filling pressure (pulmonary artery wedge pressure) accounted for the decline in colloid-hydrostatic pressure gradient. Routine measurement of colloid osmotic pressure, preferably in conjunction with pulmonary artery wedge pressure, is likely to improve understanding of the mechanisms of acute pulmonary edema.

Routine plasma colloid osmotic pressure measurements.

A method for routine determination of colloid osmotic pressure (COP) in the clinical laboratory is described. A transducer membrane system is utilized in which the colloid osmotic pressure (COP) of fresh or refrigerated plasma or albumin is compared to that of isotonic saline. The measurement is completed within an average period of less than four minutes. Duplicate measurements demonstrated high reproducibility (r = >.95) and reference measurements obtained over a period of ten months were consistently within a range of 1 torr. Heparin in excess of 200 units/ml delayed equilibration. Values obtained in normal ambulatory and supine subjects conform closely to those previously reported.

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.

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.

Oxygen delivery, anoxic metabolism and hemoglobin-oxygen affinity (P50) in patients with acute myocardial infarction and shock

Changes in systemic oxygen delivery after acute myocardial infarction were investigated in 21 patients. In seven patients with shock, circulatory failure was characterized by a significant reduction in cardiac index, a decrease in oxygen transport and oxygen consumption and an increase in concentration of blood lactate; a decrease in the affinity of hemoglobin for oxygen (increased P50) was also noted. The P50 averaged 28.8 plus or minus 0.87 (standard error of the mean) torr in patients with shock and 26.0 plus or minus 0.45 torr (P less than 0.05) in patients without circulatory failure. However, there was no significant difference in oxygen extraction from arterial blood between the two groups. The time course of the changes in P50, cardiac index and oxygen consumption was separately examined in 12 patients. In six patients with shock, P50 increased by an average of 4.6 plus or minus 2.05 torr (P less than 0.05) and this augmentation accounted for an estimated 18 percent increase in oxygen release. Maximal P50 values were observed after 24 hours of circulatory failure. In the absence of shock, no consistent changes in P50, cardiac index or oxygen consumption were observed. These data indicate that a reduction in oxygen delivery after acute myocardial infarction is followed by a compensatory increase in P50. This change in P50 accounts for increases in oxygen availability independently of changes in cardiac output.

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

The American Heart Associations 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 acidbase status of mixed venous blood and thus may fail to indicate systemic acid-base status.

A CLOSED-CHEST MODEL FOR THE STUDY OF ELECTROMECHANICAL DISSOCIATION OF THE HEART IN DOGS

A closed chest model in mechanically ventilated dogs is presented for the study of electromechanical dissociation (EMD) after defibrillation for ventricular fibrillation (VF). In seven dogs VF was induced by internal application of an AC current in the right ventricle. Precordial compression was not performed. When VF was continued for either 30 s or 60 s defibrillation typically resulted in complete restoration of electrical and mechanical cardiac activity. Immediately after defibrillation, the mean arterial blood pressure, pulmonary artery pressure, right ventricular filling pressure and cardiac output were markedly elevated; these elevations were accompanied by a slight increase in lactate and a decline in pH of the arterial blood. When VF was continued for 120 s EMD was observed in each instance after defibrillation in association with a regular rhythm. After 5-20 min, the ventricular fibrillation reappeared. The constancy of EMD in this model provides an experimental basis for study of clinical options, by which EMD may be prevented and/or mechanical competence of the heart may be restored.

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.

The “Stat” Laboratory

The critical care environment demands immediate response from the laboratory to aid the physician in the management of the patient who is in a crisis condition and whose immediate survival is threatened by failure of respiratory, cardiac, or metabolic function. These are the circumstances that have prompted the development of the “stat” laboratory.