Introduction:
The American Heart Association (AHA) recommends the use of end-tidal CO
2
(ETCO
2
) to evaluate the quality of chest compression delivery during CPR. In a pediatric model of asphyxial cardiac arrest, ETCO
2
-guided chest compression delivery improved survival over standard CPR. Since the most common cause of pediatric cardiac arrest is respiratory failure, we investigated whether this observed survival benefit persisted in a model of respiratory failure preceding cardiac arrest.
Methods:
Prior to a 17-min asphyxial cardiac arrest, peak inspiratory pressures were adjusted to a goal PaCO
2
of 80 torr to mimic pre-arrest respiratory failure. Male swine (3-4 kg) were randomized to receive either ETCO
2
-guided or standard CPR for 10 min of BLS followed by 10 min of ALS. In the ETCO
2
-guided group, chest compression rate and depth were adjusted to obtain a maximal ETCO
2
level. In the standard group, chest compressions were delivered per AHA guidelines. Hemodynamic parameters were recorded every 30 seconds, and resuscitation was continued for 20 min or until ROSC.
Results:
Twenty swine underwent asphyxial cardiac arrest. After adjustment of ventilation prior to asphyxia, pH and PaCO
2
were 7.15 and 79 torr in the ETCO
2
-guided group and 7.14 and 78 torr in the standard group. Survival was greater in the ETCO
2
-guided group than in the standard group (7/10 versus 1/10; p=0.02). During resuscitation, mean ETCO
2
and chest compression rate were higher in the ETCO
2
-guided group (38.6 ± 1.2 versus 22.9 ± 1.2, p=0.01; 154.4 ± 1.2 versus 100.5 ± 0.1, p<0.001, respectively). During resuscitation, diastolic blood pressure, myocardial perfusion pressure, systemic perfusion pressure, and cerebral perfusion pressure were higher in the ETCO
2
-guided group (
Figure 1
)
Conclusions:
ETCO
2
-guided chest compression delivery improves survival and resuscitation hemodynamics over standard CPR in a pediatric model of respiratory failure and cardiac arrest.
End-Tidal CO2–Guided Chest Compression Delivery Improves Survival in a Neonatal Asphyxial Cardiac Arrest Model*