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J Bisera

Publications and source records attributed to J Bisera.

At least 19 recordsLinked to original sources
PubMed1992

Cardiac anaphylaxis in the Sprague-Dawley rat.

Anaphylactic shock was induced in pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats that had been sensitized 21 days earlier to crystallized ovalbumin. The sensitization was confirmed by passive cutaneous anaphylaxis test. Antigen challenge produced an immediate reduction in mean aortic pressure from 168 to 67 mm Hg within 1 minute after intravenous injection of ovalbumin. Plasma histamine increased from 4.5 to 128 ng/ml within 5 minutes after injection of antigen. There were no changes in airway or esophageal pressures after antigen challenge. Left ventricular diastolic pressure was increased, and contractility, as measured by the rate of change of left ventricular pressure (dP/dt), was decreased over an interval exceeding 90 minutes. When isolated, constant flow--perfused hearts from sensitized Sprague-Dawley rats were challenged with antigen, decreases in left ventricular function were observed associated with decreased positive and negative maximum rate of change of left ventricular pressure (dP/dtmax). This experimental model in the rat therefore demonstrated selective myocardial impairment with reduced inotropism and lusitropism after anaphylaxis.

Anaphylaxis↗
PubMed1991

Reversible impairment of myocardial contractility due to hypercarbic acidosis in the isolated perfused rat heart.

BACKGROUND AND METHODS: Striking increases in PCO2 of the myocardium have recently been documented during cardiac arrest. The purpose of the present study was to investigate selective effects of hypercarbia as distinct from acidosis on left ventricular contractile function and oxygen utilization. An isolated, spontaneously beating rat heart preparation was utilized. The perfusate was equilibrated with gases containing 5%, 10%, 20%, and 30% CO2. In a subset of experiments, the [H+] was adjusted independently of PCO2 by decreasing the concentration of HCO3-. RESULTS: When the PCO2 of the perfusate was progressively increased from 36 to 146 torr (4.8 to 29.5 kPa), the left ventricular systolic pressure (LVSP) generated by the isolated heart and the maximum rate of pressure change in the left ventricle (dP/dt) were decreased to 20% of their control values. However, comparable acidosis in the absence of hypercarbia produced only minimal decreases in the LVSP or dP/dt such that contractility remained at greater than or equal to 88%. Increases in the perfusate PCO2 but not in the perfusate H+ were highly correlated with decreases in both myocardial contractility and oxygen consumption (r2 = .88). CONCLUSION: Hypercarbia rather than acidosis accounts for decreased contractility and oxygen utilization in the isolated perfused rat heart.

Acidosis↗
PubMed1991

Pulmonary ventilation/perfusion defects induced by epinephrine during cardiopulmonary resuscitation.

BACKGROUND: Epinephrine has been shown to impair pulmonary excretion of CO2 during resuscitation. This phenomenon was investigated in a rodent model of cardiac arrest and conventional resuscitation. METHODS AND RESULTS: The effects of racemic epinephrine were compared with the selective alpha 1-agonist methoxamine and with saline placebo during cardiac resuscitation in 15 Sprague-Dawley rats mechanically ventilated with gas containing 70% oxygen. Epinephrine and methoxamine but not saline placebo significantly increased coronary perfusion pressure from approximately 32 to 55 mm Hg. Following epinephrine, end-tidal PCO2 decreased from approximately 10 to 5 mm Hg. This was associated with a time-coincident decrease in PaO2 from approximately 130 to 74 mm Hg and an increase in PaCO2 from approximately 26 to 40 mm Hg. These changes indicated increases in alveolar dead space ventilation concomitant with increases in pulmonary arteriovenous admixture. No such effects were observed after administration of either methoxamine or saline placebo. Each of the 15 rats was successfully resuscitated. However, a significantly larger number of transthoracic countershocks were required after epinephrine compared with methoxamine or placebo before return of spontaneous circulation. CONCLUSIONS: Epinephrine induced ventilation/perfusion during cardiopulmonary resuscitation as a result of redistribution of pulmonary blood flow.

Animals↗
PubMed1991

End-tidal carbon dioxide tension as a monitor of native blood flow during resuscitation by extracorporeal circulation.

In a porcine model of cardiac arrest, we investigated end-tidal carbon dioxide tension as a monitor of native blood flow during resuscitation by extracorporeal circulation. After 15 minutes of cardiac arrest and after precordial compression and transthoracic countershocks had failed, extracorporeal circulation consistently restored spontaneous circulation. Native end-tidal carbon dioxide tension, which averaged 29.8 +/- 1.0 mm Hg before arrest, was only 5.2 +/- 0.8 mm Hg during precordial compression. After the start of extracorporeal circulation, native end-tidal carbon dioxide tension was measured during 15-second interruptions of pump flow. End-tidal carbon dioxide tension progressively increased with a corresponding increase in native cardiac index. The correlation coefficients between end-tidal carbon dioxide tension and native cardiac index averaged 0.92 +/- 0.03 (mean +/- standard error of the mean). When end-tidal carbon dioxide tension exceeded 15 mm Hg, mean aortic pressure in each instance was 60 mm Hg or greater, and the animal was successfully weaned from extracorporeal support. We conclude that end-tidal carbon dioxide tension serves as a reliable monitor of blood flow through the lung and therefore of native cardiac output during weaning from extracorporeal circulation. It therefore indicates when native cardiac output is likely to be adequate to sustain spontaneous circulation.

Animals↗
PubMed1990

[Determinants of survival in cardiopulmonary resuscitation].

Prognostic indices for survival after cardiopulmonary resuscitation (CPR) were investigated in 14 male Sprague-Dawley rats (500 +/- 50 g) and in 16 domestic pigs (25 +/- 4 kg). Arterial and venous blood gas and lactate measurements in association with the coronary perfusion pressure (CPP) and the end-expiratory CO2 concentration (ETCO2) were evaluated. Additional parameters in the porcine studies were coronary venous blood gas measurements and intramyocardial pH. Volume controlled ventilation was established and catheters were placed in the thoracic aorta and in the right atrium in both animal species. Additionally in the pigs, the pulmonary artery and the great cardiac vein were catheterized and intramyocardial pH was measured with a glass pH electrode placed in the diaphragmatic left ventricular myocardium. Ventricular fibrillation was induced with a direct current and external chest compression was initiated after four minutes in the rats and after three minutes in the pigs. Transthoracic DC defibrillation was attempted with 10J after two minutes of compression in the rats and with 300J after eight minutes of compression in the pigs. Eight of 14 rats and eight of 16 pigs were successfully resuscitated. Significant veno-arterial gradients for pH and pCO2 but not for lactate were observed during CPR in both animal species. With the exception of arterial pH in the pigs (p less than 0.05), neither arterial nor venous blood gas measurements nor intramyocardial pH separated resuscitated from non-resuscitated animals. However, CPP and ETCO2 significantly separated resuscitated from non-resuscitated animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1990

Increases in coronary vein CO2 during cardiac resuscitation.

We investigated the aortic, mixed venous, and great cardiac vein acid-base changes in eight domestic pigs during cardiac arrest produced by ventricular fibrillation and during cardiopulmonary resuscitation (CPR). The great cardiac vein PCO2 increased from a control value of 52 +/- 2 to 132 +/- 28 (SD) Torr during CPR, whereas the arterial PCO2 was unchanged (39 +/- 4 vs. 38 +/- 4). The coronary venoarterial PCO2 gradient, therefore, increased remarkably from 13 +/- 2 to 94 +/- 29 Torr. The simultaneously measured great cardiac vein lactate concentrations increased from 0.24 +/- 0.06 to 7.3 +/- 2.34 mmol/l. Much more moderate increases in the lactate content of aortic blood from 0.64 +/- 0.25 to 2.56 +/- 0.27 mmol/l were observed. Increases in great cardiac vein PCO2 and lactate were highly correlated during CPR (r = 0.91). After successful CPR, the coronary venoarterial PCO2 gradient returned to normal levels within 2 min after restoration of spontaneous circulation. Lactate content was rapidly reduced and lactate extraction was reestablished within 30 min after CPR. These studies demonstrate marked but reversible acidosis predominantly as the result of myocardial CO2 production during CPR.

Animals↗
PubMed1989

End tidal carbon dioxide as an haemodynamic determinant of cardiopulmonary resuscitation in the rat.

End tidal PCO2 (PETCO2) has been found to be a good prognostic indicator of successful resuscitation from cardiac arrest. To explore the value of this measurement further, we carried out a series of experiments during cardiac arrest and closed chest resuscitation in 14 mechanically ventilated Sprague-Dawley rats. Ventricular fibrillation (VF) was induced by a 10 mA current delivered to the right ventricular endocardium. After 4 min of VF, precordial compression was begun with a mechanical thumper and defibrillation was attempted 2 min later. PETCO2 decreased abruptly during cardiac arrest to 0.3 mm Hg (0.04 kPa). With precordial compression, it increased to 11 mm Hg (1.5 kPa). Within 3 min of successful defibrillation, there was an overshoot in the PETCO2 to 44 mm Hg (5.8 kPa) with return to baseline levels approximating those of the pre-arrest control measurements over the 60 min that followed restoration of spontaneous circulation. The PETCO2 measurement during precordial compression predicted the success of defibrillation with return of spontaneous circulation. When PETCO2 exceeded 9 mm Hg (1.2 kpA), 7 of 8 animals were successfully resuscitated. When PETCO2 was less than 9 mm Hg during precordial compression, none of six animals were successfully resuscitated. The PETCO2 correlated with the mean aortic (r = 0.71) and coronary perfusion pressure (r = 0.80) generated during precordial compression. In corroboration of previously reported observations on pigs, dogs, and human patients, PETCO2 served as a non-invasive monitor of the effectiveness of precordial compression for maintaining coronary perfusion and therefore cardiac viability during CPR. The PETCO2 was also useful in that it promptly signalled restoration of spontaneous circulation.

Animals↗
PubMed1989

Myocardial acidosis associated with CO2 production during cardiac arrest and resuscitation.

Previous studies from our institution demonstrated significant hypercarbic acidosis in the mixed venous (pulmonary artery) blood in animals and human patients during cardiac arrest and cardiopulmonary resuscitation (CPR). In the present study, the acid-base state of the myocardium during cardiac arrest was investigated. Cardiac arrest was electrically induced in 11 pentobarbital-anesthetized and mechanically ventilated domestic pigs. Precordial compression was begun 3 minutes after onset of ventricular fibrillation and continued for 8 minutes. During CPR, there was rapid onset of profound myocardial acidosis with an increase in intramyocardial [H+] from 54 +/- 5 to 146 +/- 20 nmol/l (7.27 +/- 0.04 to 6.88 +/- 0.20 pH units). Great cardiac vein PCO2 increased from 57 +/- 2 to 158 +/- 12 mm Hg. Profound hypercarbic acidosis in great cardiac vein blood was associated with myocardial lactate production to levels of 8.1 +/- 0.7 mmol/l. Only moderate decreases in cardiac vein bicarbonate concentrations from 31 +/- 1 to 23 +/- 1 mmol/l were observed. These acid-base changes were almost completely reversed over an interval of 60 minutes after the animals were successfully resuscitated by DC countershock. The PCO2 in cardiac vein blood was significantly greater than that of mixed venous blood, demonstrating disproportionate myocardial production of CO2 during CPR. Accordingly, it is CO2 production during ischemia that is implicated as the predominant mechanism accounting for myocardial [H+] increases during cardiac arrest. Important clinical implications for buffer therapy during CPR and, in particular, treatment with bicarbonate emerge from these observations.

Acidosis↗
PubMed1989

Mechanism of blood flow generated by precordial compression during CPR. I. Studies on closed chest precordial compression.

The mechanism of forward flow produced by precordial compression during CPR was investigated with the aid of echocardiographic and hemodynamic measurements in anesthetized, mechanically ventilated domestic pigs. Both mitral and tricuspid valves opened during compression diastole and closed during compression systole. Valve motion persisted throughout resuscitation in 17 of 22 animals which were hemodynamically resuscitated. There was a 25 percent reduction in left ventricular area during compression systole. Maximum pressure generated during compression systole in the aorta exceeded that of the right atrium throughout the 12-min interval of precordial compression in successfully resuscitated animals. These observations provide evidence of direct cardiac compression as the mechanism accounting for effective forward blood flow during CPR. The persistence of valve function, chamber compression, and pressure gradients during precordial compression was predictive of successful resuscitation. The absence of these factors prognosticates failure of resuscitation and explains, in part, the inconsistency of prior reports.

Adult↗
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↗
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↗