Document Detail


Hemodynamic and respiratory effects of negative tracheal pressure during CPR in pigs.
MedLine Citation:
PMID:  16678959     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 (ETCO(2)), (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 PaCO(2) remained stable at 34 mmHg for 15 min. In the STD-CPR group, pseudorespiratory alkalosis was observed with PaCO(2) values remaining <20 mmHg (p<0.001). PaO(2) 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.
Authors:
Demetris Yannopoulos; Tom P Aufderheide; Scott McKnite; Kostantinos Kotsifas; Roussos Charris; Vinay Nadkarni; Keith G Lurie
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-05-05
Journal Detail:
Title:  Resuscitation     Volume:  69     ISSN:  0300-9572     ISO Abbreviation:  Resuscitation     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-06-05     Completed Date:  2006-11-09     Revised Date:  2009-08-25    
Medline Journal Info:
Nlm Unique ID:  0332173     Medline TA:  Resuscitation     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  487-94     Citation Subset:  IM    
Affiliation:
Department of Cardiology, Cardiac Arrhythmia Center, University of Minnesota, Minneapolis, MN, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Gas Analysis
Cardiopulmonary Resuscitation / methods*
Female
Hemodynamics / physiology*
Pressure
Random Allocation
Regional Blood Flow
Respiration, Artificial / methods*
Survival Rate
Swine
Time Factors
Trachea / physiopathology*
Ventricular Fibrillation / physiopathology

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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