Kh. Lindner et al., EFFECTS OF ACTIVE COMPRESSION-DECOMPRESSION RESUSCITATION ON MYOCARDIAL AND CEREBRAL BLOOD-FLOW IN PIGS, Circulation, 88(3), 1993, pp. 1254-1263
Background. This study was designed to assess the effects of a modifie
d cardiopulmonary resuscitation (CPR) technique that consists of both
active compression and active decompression of the chest (ACD CPR) ver
sus standard CPR (STD CPR) on myocardial and cerebral blood flow durin
g ventricular fibrillation both before and after epinephrine administr
ation. Methods and Results. During a 30-second period of ventricular f
ibrillation cardiac arrest, 14 pigs were randomized to receive either
STD CPR (n=7) or ACD CPR (n=7), Both STD and ACD CPR were performed us
ing an automated pneumatic piston device applied midsternum, designed
to provide either active chest compression (1.5 to 2.0 in.) and decomp
ression or only active compression of the chest at 80 compressions per
minute and 50% duty cycle. Using radiolabeled microspheres, median to
tal myocardial blood flow after 5 minutes of ventricular fibrillation
was 14 (7 to 30, minimum to maximum) STD CPR versus 30 (9 to 46) mL .
min-1 . 100 g-1 with ACD CPR (P<.05). Median cerebral blood flow was 1
5 (10 to 26) mL . min-1 . 100 g-1 with STD CPR and 30 (21 to 39) with
ACD CPR (P<.01). When comparing STD with ACD CPR, aortic systolic (62
mm Hg [48 to 70] vs 80 [59 to 86]) and diastolic (22 [18 to 28] vs 28
[21 to 36]) pressures, calculated coronary systolic (30 [22 to 361 vs
49 [37 to 56]) and diastolic (18 [16 to 23] vs 26 [21 to 31]) perfusio
n pressures, end-tidal CO2 (1.4% [0.8 to 1.8] vs 2.1 (1.8 to 2.4]), ce
rebral O2 delivery (3.1 mL . min-1 . 100 g-1 [1.5 to 4.5] vs 5.3 [3.8
to 7.5]), and cerebral perfusion pressure (14 mm Hg [4 to 22] vs 26 [6
to 34]) were all significantly higher with ACD CPR. To compare these
parameters before and after vasopressor therapy, a bolus of high-dose
epinephrine (0.2 mg/kg) was given to all animals after 5 minutes of ve
ntricular fibrillation. Organ blood flow and calculated perfusion pres
sures increased significantly in both the STD and ACD groups after epi
nephrine. The differences observed between STD and ACD CPR before epin
ephrine were diminished 90 seconds after epinephrine but were again st
atistically significant when assessed 5 minutes later, once the acute
effects of epinephrine had decreased. No difference in short-term resu
scitation success was found between the two groups. Conclusions. We co
nclude that ACD CPR significantly increases myocardial and cerebral bl
ood flow during cardiac arrest in the absence of vasopressor therapy c
ompared with STD CPR.