The Effect of the Preshock Pause on Coronary Perfusion Pressure Decay and Rescue Shock Outcome in Porcine Ventricular Fibrillation

2009 ◽  
Vol 13 (4) ◽  
pp. 487-494 ◽  
Author(s):  
Timothy J. Mader ◽  
Allie T. Paquette ◽  
David D. Salcido ◽  
Brian H. Nathanson ◽  
James J. Menegazzi
Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Tao Yu ◽  
Giuseppe Ritagno ◽  
Jun H Cho ◽  
Shijie Sun ◽  
Max H Weil ◽  
...  

We have previously reported, on the basis of experimental studies, that interruptions of CPR as little as 10 seconds adversely affect the outcomes of CPR. We therefore investigated interruptions of only 5 seconds for delivering ventilation, which corresponds to the current AHA algorithm in which of 30 compressions followed by 2 ventilations are mandated. We hypothesized that even 5 seconds interruption significantly reduces CPP and with significant delay prior to restoring pre-interruption levels. Ventricular fibrillation (VF) was induced and untreated for 15 minutes in 33 male domestic pigs weighting 40±3 Kg. Chest compressions delivered with the aid of mechanical compressor (Thumper, 1000, MI Instruments) with a rate of 100/min. Ventilations were administrated with a compression / ventilation ratio of 30:2 such that 2 ventilations were delivered over a 5 seconds interval. CPP was continuously measured as the difference between comparison diastolic and simultaneous left atrial pressure. CPP significantly decreased during interruptions for ventilation from 20.5±12.8 mmHg to 9.8±6.7 mmHg( P <0.001). After chest compressions were restarted, the CPP increased to 12.5±7.6 mmHg after first compression( P <0.001). A total of 12±7 compressions over a mean interval of 7.2±4.3 seconds was required prior to restoration of CPP to levels corresponding to those that preceded the interruption. As little as the five seconds of interruption in chest compression currently mandated for 30 to 2 ventilations during CPR significantly reduced CPP and delayed restoration of CPP to its pre-interruption level.


Resuscitation ◽  
2001 ◽  
Vol 51 (2) ◽  
pp. 151-158 ◽  
Author(s):  
Ulrich Achleitner ◽  
Volker Wenzel ◽  
Hans-Ulrich Strohmenger ◽  
Karl H Lindner ◽  
Michael A Baubin ◽  
...  

2009 ◽  
Vol 37 (4) ◽  
pp. 369-375 ◽  
Author(s):  
Vassiliki Kitsou ◽  
Theodoros Xanthos ◽  
Konstantinos Stroumpoulis ◽  
George Rokas ◽  
Dimitrios Papadimitriou ◽  
...  

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.


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