Discriminating the effect of accelerated compression from accelerated decompression during high-impulse CPR in a porcine model of cardiac arrest☆
Received 28 September 2009; received in revised form 4 December 2009; accepted 20 December 2009. published online 01 February 2010.
Abstract
Aim of the study
Piston based mechanical chest compression devices deliver compressions and decompressions in an accelerated pattern, resulting in superior haemodynamics compared to manual compression in animal studies. The present animal study compares haemodynamics during two different hybrid compression patterns to a standard compression pattern resembling that of modern mechanical chest compression devices.
Method
In 12 anaesthetized domestic pigs in ventricular fibrillation, coronary perfusion pressures (CPP) and cerebral cortical blood flow (CCBF) was measured, and transesophageal echocardiography (TEE) was performed. Two hybrid compression patterns, one with accelerated trapezoid compression and slower sinusoid decompression (TrS), and one with slower sinusoid compression and accelerated trapezoid decompression (STr), were tested against a standard accelerated trapezoid compression–decompression pattern (TrTr) in a cross-over randomised setup.
Results
There were 7% (1, 14, p=0.046) lower CCBF and 3mmHg (1, 5, p=0.017) lower CPP with the TrS compared to TrTr pattern. No significant difference between STr and TrTr pattern in either CCBF, 6% (−3, 15, p=0.176) or CPP, 0mmHg (−2, 3, p=0.703) was present. Our TEE recordings were insufficient for haemodynamic comparison between the different compression–decompression patterns. Despite standardized sternal piston position and placement of the pigs, TEE revealed varying degree of asymmetrical heart chamber compression in the animals.
Conclusion
Both cardiac and cerebral perfusion benefited from accelerated decompression, while accelerated compression did not improve haemodynamics. The evolution of mechanical CPR is dependent on further research on mechanisms generating forward blood flow during external chest compressions.
aInstitute for Experimental Medical Research and Centre for Heart Failure Research, Oslo University Hospital - Ullevål, Norway
bDepartment of Anaesthesiology, Oslo University Hospital - Ullevål, Oslo, Norway
cDepartment of Cardiology, Oslo University Hospital - Ullevål, Oslo, Norway
dNational Competence Centre of Emergency Medicine, Oslo University Hospital - Ullevål, Oslo, Norway
eResearch Institute of General Reanimatology RAMS, Moscow, Russia
fSurgical Intensive Care Unit, Oslo University Hospital - Ullevål, Oslo, Norway
Corresponding author at: Institute for Experimental Medical Research, Oslo University Hospital, N-0407 Oslo, Norway. Tel.: +47 23016837; fax: +47 23016799.
ABSTRACT