Hemodynamic and respiratory effects of negative tracheal pressure during CPR in pigs

Demetris Yannopoulos, Tom P. Aufderheide, Scott McKnite, Kostantinos Kotsifas, Roussos Charris, Vinay Nadkarni, Keith G. Lurie

Research output: Contribution to journalArticlepeer-review

38 Scopus citations


Background: A new device, the intrathoracic pressure regulator (ITPR), was developed to generate continuous negative intrathoracic pressure during cardiopulmonary resuscitation (CPR) and allow for intermittent positive pressure ventilation. Use of the ITPR has been shown to increase vital organ perfusion and short-term survival rates in pigs. The purpose of this study was to investigate the hemodynamic and blood gas effects of more prolonged (15 min) use of the ITPR during CPR in a porcine model of cardiac arrest. Methods: After 8 min of untreated ventricular fibrillation (VF), 16 female pigs were anaesthetized with propofol, intubated, and randomized prospectively to 15 min of either ITPR-CPR or standard (STD) CPR. Compressions were delivered at a rate of 100/min with a compression to ventilation ratio of 15:2. Ventilations were delivered with a resuscitator bag. Tracheal, aortic, right atrial, intracranial pressures (ICP), common carotid blood flow and respiratory variables were recorded continuously. Arterial and venous blood gases were collected at baseline, and after 5, 10, and 15 min of CPR. Coronary perfusion pressure (CPP) was calculated as diastolic aortic pressure-right atrial pressure. Cerebral perfusion pressure (CerPP) was calculated as mean arterial pressure (MAP)-intracranial pressure. Statistical analysis was performed with unpaired t-test and Friedman's Repeated Measures Analysis. Results: ITPR-CPR when compared to STD-CPR resulted in a significant decrease in mean decompression phase (diastolic) tracheal pressure (-9 ± 0.6 mmHg versus -3 ± 0.3 mmHg, p < 0.001), diastolic right atrial pressure (DRAP) (-0.1 ± 0.2 mmHg versus 2.3 ± 0.2 mmHg, p < 0.001) and intracranial pressure (20.8 ± 0.6 mmHg versus 23 ± 0.5 mmHg, respectively, p = 0.04) and a significant increase in total mean aortic pressure, coronary and cerebral perfusion pressures and end tidal carbon dioxide (ETCO2), (p < 0.001). Common carotid artery blood flow was increased by an average of 70%, p < 0.001. ABGs showed progressive metabolic acidosis in the ITPR-CPR group, but PaCO2 remained stable at 34 mmHg for 15 min. In the STD-CPR group, pseudorespiratory alkalosis was observed with PaCO2 values remaining <20 mmHg (p < 0.001). PaO2 was not different between groups. Following 23 min of cardiac arrest (15 min of CPR) ROSC was achieved in 5/8 ITPR-CPR animals versus 2/8 STD-CPR animals p = 0.3. Conclusion: ITPR-CPR significantly improved hemodynamics, vital organ perfusion pressures and common carotid blood flow compared to STD-CPR in a porcine model of prolonged cardiac arrest and basic life support. The beneficial hemodynamic effects of ITPR-CPR were sustained at least 15 min without any compromise in oxygenation.

Original languageEnglish (US)
Pages (from-to)487-494
Number of pages8
Issue number3
StatePublished - Jun 2006

Bibliographical note

Funding Information:
This project was partially supported by an American Heart Assocication Postdoctoral Fellowship grant: 0425714Z.


  • Acid base
  • Blood flow
  • Cardiopulmonary resuscitation
  • Cerebral perfusion pressure
  • Coronary perfusion pressure
  • Intrathoracic pressure


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