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J Bisera

Publications and source records attributed to J Bisera.

49 records · Page 3Linked to original sources
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

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↗
PubMed1978

An "oncometer" of clinical measurement of colloid osmotic pressure of plasma.

Measurement of colloid osmotic pressure complements measurements of pulmonary artery wedge pressure for assessing the risks of pulmonary edema and constitutes an increasingly important reference for purposes of guiding selection of colloid or crystalloid fluids in patients with acute cardiac disease. We describe a simple device for its routine clinical measurement. A membrane, selectively impermeable to molecules of relative molecular mass (Mr) greater than 30000, is rigidly mounted between a sample chamber and a reference chamber filled with isotonic saline. A pressure transducer measures the negative pressure developed in the reference chamber and displays it on a digital panel meter. The sensor chamber accommodates samples of 50 to 300 microliter. Equilibration is completed within 2 min. A control solution of human serum albumin (50 g/liter) is measured to confirm the accuracy of calibration of the system, with reproducible readings of 25.9 g/cm2 within one SD (equivalent to 0.4 g/cm2). Technical simplicity of operation and modest costs of disposables have made feasible the routine measurement of colloid osmotic pressure.

Colloids↗