Porcine Model Of Cardiac Arrest Research Articles

Mechanical Ventilation May Not Be Essential for Initial Cardiopulmonary Resuscitation

In a rodent model of cardiac arrest and resuscitation in which the inspired gas mixture was enriched with oxygen, resuscitability and survival were unaffected by positive pressure ventilation. In the present study, in a larger animal model, tidal volumes generated during precordial compression and with spontaneous gasping were quantitated. Domestic pigs with an average weight of 34 kg were anesthetized with pentobarbital. Ventricular fibrillation (VF) was induced electrically. Precordial compression was begun after 4 min of untreated VF. Each of 22 animals received one of two interventions in conjunction with precordial compression: positive pressure ventilation with oxygen or oxygen supplied at the port of a tracheal tube at ambient pressure. After 8 min of precordial compression, defibrillation was attempted. Only very moderate increases in arterial PCO2 were documented during cardiopulmonary resuscitation in the absence of mechanical ventilation but arterial oxygen tension was consistently in excess of 100 mm Hg. Cardiac resuscitability and 48-h survival were approximately the same in animals maintained on inspired oxygen whether or not they were mechanically ventilated (7/11 or 8/11). In the absence of mechanical ventilation, precordial compression and spontaneous gasping yielded minute volumes that exceeded 5 L. Positive pressure mechanical ventilation did not improve resuscitability or postresuscitation outcome in this porcine model of cardiac arrest.

Chest Compression and Ventilation Rates during Cardiopulmonary Resuscitation: The Effects of Audible Tone Guidance

To determine: 1) whether chest compressions during CPR are being performed according to American Heart Association (AHA) guidelines during cardiac arrest; and 2) the effect of an audio prompt to guide chest compressions on compliance with AHA guidelines and hemodynamic parameters associated with successful resuscitation. An observational clinical report and laboratory study was conducted. A research observer responded to a convenience sample of cardiac arrests within a 300-bed hospital and counted the rate of chest compressions and ventilations during CPR. To evaluate the effect of an audio prompt on CPR, health care providers performed chest compression without guidance using a porcine cardiac arrest model for 1 minute, followed by a second minute in which audio guidance was added. Chest compression rates, arterial and venous blood pressures, end-tidal CO2 (ETCO2) levels, and coronary perfusion pressures were measured and compared for the two periods. Twelve in-hospital cardiac arrests were observed in the clinical part of the study. Only two of 12 patients had chest compressions performed within AHA guidelines. No patient had respirations performed within AHA guidelines. In the laboratory, 41 volunteers were tested, with 66% performing chest compressions outside the AHA standards for compression rate without audible tone guidance. With guided chest compressions, the mean (+/- SD) chest compression rate increased from 74 +/- 22 to 100 +/- 3/min (p < 0.01). End-tidal CO2 levels increased from 15 +/- 7 to 17 +/- 7 torr (p < 0.01). Coronary perfusion pressure increased minimally with audible tone-guided chest compressions. The majority of Basic Cardiac Life Support--certified health care professionals did not perform CPR according to AHA-recommended guidelines. The use of audible tones to guide chest compression resulted in significantly higher chest compression rates and ETCO2 levels.

A noninvasive method for monitoring cerebral perfusion during cardiopulmonary resuscitation

Purpose: This study evaluates the use of transcranial Doppler (TCD) ultrasound in assessing the changes experienced by the cerebral circulation during cardiopulmonary resuscitation (CPR) and compares it with measurements of internal carotid artery (ICA) flow rates (ultrasonic flow-meter measurements) and cerebral blood flow (CBF) (radioactive-microsphere measurements) in a porcine cardiac arrest model undergoing closed chest CPR. Methods: Sixteen piglets were anesthetized and subjected to TCD monitoring, ICA flow-rate measurements, and CBF measurements during CPR following induction of ventricular fibrillation. A total of 14 comparisons between TCD and CBF measurements, and 36 comparisons between TCD and ICA flow measurements were performed. Correlations were determined using Pearson's method, and the validity of the correlation was determined using Bonferoni's adjusted probabilities. Results: The correlation between mean cerebral blood flow velocity and mean total ICA flow rate was 0.67 ( P < .01). The correlation between peak systolic blood flow velocity and CBF was 0.76 ( P = .02). Conclusions: TCD can provide on-line information about cerebral perfusion during CPR.

Myocardial Hypercarbic Acidosis Reduces Cardiac Resuscitability

The severity of spontaneous myocardial hypercarbic acidosis during cardiac arrest previously has been predictive of the likelihood of restoring spontaneous circulation. The present study investigated whether hypercarbia itself impairs cardiac resuscitation. Since coronary perfusion pressure is the overriding determinant of cardiac resuscitability, we used a porcine model of cardiac arrest in which coronary perfusion pressure was controlled. In 31 domestic pigs anesthetized with pentobarbital, the lungs were mechanically ventilate. Myocardial carbon dioxide tension and hydrogen ion concentration were measured by sensors advanced into the myocardium. After 15 min of untreated ventricular fibrillation, venoarterial extracorporeal circulation was initiated. Animals were randomized to receive a carbon dioxide gas fraction in the extracorporeal perfusate of 0.00, 0.10, 0.30, or 0.50 with oxygen concentration maintained constant at 0.50. Extracorporeal flow was adjusted to maintain a coronary perfusion pressure in the range of 60-80 mmHg, a level of predictive resuscitability. The proportion of animals successfully resuscitated and the proportion of animals maintaining spontaneous circulation for 60 min or longer decreased with increasing perfusate PCO2 and concurrent increases in myocardial CO2 tension in the absence of altered oxygen utilization (P < .01). Hypercarbia, in this experimental setting, was therefore a quantitative determinant of both myocardial resuscitability and the restoration of spontaneous circulation.

Extracorporeal Circulation as an Alternative to Open-Chest Cardiac Compression for Cardiac Resuscitation

Open-chest direct cardiac compression represents a more potent but highly invasive option for cardiac resuscitation when conventional techniques of closed-chest cardiac resuscitation fail after prolonged cardiac arrest. We postulated that venoarterial extracorporeal circulation might be a more effective intervention with less trauma. In the setting of human cardiac resuscitation, however, controlled studies would be limited by strategic constraints. Accordingly, the effectiveness of open-chest cardiac compression was compared with that of extracorporeal circulation after a 15-min interval of untreated ventricular fibrillation in a porcine model of cardiac arrest. Sixteen domestic pigs were randomized to resuscitation by either peripheral venoarterial extracorporeal circulation or open-chest direct cardiac compression. During resuscitation, epinephrine was continuously infused into the right atrium, and defibrillation was attempted by transthoracic countershock at 2-min intervals. Systemic blood flows averaged 198 ml.kg-1.min-1 with extracorporeal circulation. This contrasted with direct cardiac compression, in which flows averaged only 40 ml.kg-1.min-1. Coronary perfusion pressure, the major determinant of resuscitability on the basis of earlier studies, was correspondingly lower (94 vs 29 mm Hg). Extracorporeal circulation, in conjunction with transthoracic DC countershock and epinephrine, successfully reestablished spontaneous circulation in each of eight animals after 15 min of untreated ventricular fibrillation. This contrasted with the outcome after open-chest cardiac compression, in which spontaneous circulation was reestablished in only four of eight animals (p = .038). We conclude that extracorporeal circulation is a more effective alternative to direct cardiac compression for cardiac resuscitation after protracted cardiac arrest.

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.

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.

Calcium-entry blockers during porcine cardiopulmonary resuscitation

1. Calcium-entry blockers increase the intramyocardial pH and decrease the intramyocardial Pco2 of ischaemic canine myocardium. However, the evidence documenting improvements in myocardial acidosis and in myocardial resuscitability after administration of calcium-entry blockers during cardiac arrest is incomplete. We therefore compared the effects of verapamil (0.05 mg/kg) and diltiazem (0.075 mg/kg) with those of saline placebo in an established porcine model of cardiac arrest and cardiopulmonary resuscitation. 2. After verapamil, six of 11 animals were successfully resuscitated; after diltiazem, five of 10; and after saline placebo, six of 10. Coronary perfusion and mean aortic pressures together with end-tidal CO2 concentration during precordial compression were predictive of resuscitation, independently of the drug or placebo. 3. Coronary vein pH decreased to 6.91 +/- 0.06 units (mean +/- SEM) with concurrent increases in PCO2 to levels exceeding 100 mmHg. Coronary vein lactate increased to a maximum of 7.5 +/- 0.6 mmol/l. Coronary vein acidaemia was accompanied by decreases in intramyocardial pH to 6.64 +/- 0.06 units. However, each of these differences between success and failure of resuscitation was unrelated to treatment with calcium-entry blockers. 4. Accordingly, neither verapamil nor diltiazem selectively altered coronary perfusion pressure, attenuated intramyocardial acidosis or improved resuscitability after porcine cardiac arrest and cardiopulmonary resuscitation.

Arterial Pco2 as an indicator of systemic perfusion during cardiopulmonary resuscitation

End-tidal PCO2 (PetCO2) is a quantitative indicator of pulmonary blood flow generated by precordial compression and therefore predicts resuscitability during CPR. A striking increase in PetCO2 follows return of spontaneous circulation. Since PaCO2 is closely related to alveolar PCO2 (PACO2) and therefore PetCO2, we hypothesized that PaCO2 may itself serve as an indicator of the blood flow generated during CPR. In a porcine model of cardiac arrest, PaCO2 during precordial compression was highly correlated with PetCO2 (r = .89), cardiac output (r = .72), and coronary perfusion pressure (CPP) (r = .74). In 14 successfully resuscitated animals, PaCO2, PetCO2, and CPP during precordial compression were significantly higher than in nine nonresuscitated animals. After restoration of spontaneous circulation, there was a marked increase in PaCO2 to levels exceeding control values, which corresponded to the sharp increase in PetCO2 that is characteristic of successful resuscitation. We therefore confirm that both PetCO2 and PaCO2 correspond to the pulmonary blood flow and therefore cardiac output which is generated by precordial compression during CPR. Moreover, both serve as prognosticators of cardiac resuscitability and early indicators that spontaneous circulation has been restored.

Incomplete global myocardial ischemia during cardiac arrest and resuscitation.

During cardiac arrest (no flow) and CPR (low flow), the onset of myocardial ischemia is followed by myocardial respiratory acidosis. Myocardial contractility is more decreased by respiratory than by metabolic acidosis. We demonstrated in a porcine model of cardiac arrest and in human patients increases in mixed venous PCO2 during CPR, whereas PaCO2 was decreased. Consequently, there was a striking increase in the venoarterial gradients for both [H+] and CO2. Both cardiac output (pulmonary blood flow) and the concentration of expired CO2 were simultaneously decreased. In great cardiac vein blood, even more profound respiratory acidosis with only minor decreases in bicarbonate and only moderate increases in lactate were observed. Intramyocardial pH was profoundly decreased. The severity of respiratory acidosis as a determinant of resuscitability and survival should be further investigated.

`Lactate Washout' Following Circulatory Arrest

The measurement of arterial blood lactate concentration for the purpose of estimating the severity and prognosis of acute perfusion failure is suspect because of theoretical errors due to systemic "lactate washout" immediately following restoration of perfusion. If arterial lactate concentrations continue to increase following resuscitation, the assumption that increasing lactate concentrations indicate progression of anaerobiosis due to perfusion failure would be invalidated. Lactate washout was therefore investigated in a porcine model of cardiac arrest due to electromechanical dissociation. Cardiopulmonary resuscitation was initiated and maintained for intervals of 30 minutes or until spontaneous circulation was restored. In 25 trials on 14 successfully resuscitated animals, the arterial blood lactate concentration decreased within four minutes after resuscitation from cardiac arrest. In 24 animals in whom resuscitation efforts failed, arterial lactate concentrations increased throughout the observation period. Lactate washout occurred during an interval of only 2.6 +/- 0.3 minutes (mean +/- SEM). These results indicate that lactate measurements are not invalidated because of a washout phenomenon under the extreme conditions of cardiac arrest.

'Lactate washout' following circulatory arrest

The measurement of arterial blood lactate concentration for the purpose of estimating the severity and prognosis of acute perfusion failure is suspect because of theoretical errors due to systemic "lactate washout" immediately following restoration of perfusion. If arterial lactate concentrations continue to increase following resuscitation, the assumption that increasing lactate concentrations indicate progression of anaerobiosis due to perfusion failure would be invalidated. Lactate washout was therefore investigated in a porcine model of cardiac arrest due to electromechanical dissociation. Cardiopulmonary resuscitation was initiated and maintained for intervals of 30 minutes or until spontaneous circulation was restored. In 25 trials on 14 successfully resuscitated animals, the arterial blood lactate concentration decreased within four minutes after resuscitation from cardiac arrest. In 24 animals in whom resuscitation efforts failed, arterial lactate concentrations increased throughout the observation period. Lactate washout occurred during an interval of only 2.6 +/- 0.3 minutes (mean +/- SEM). These results indicate that lactate measurements are not invalidated because of a washout phenomenon under the extreme conditions of cardiac arrest.

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.

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.

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.

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.

Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation.

Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation.