High quality chest compressions are the foundation of the resuscitation – this includes proper rate of compressions, proper depth, and limiting “no-flow” times. Technological advances in real-time CPR feedback have improved the quality of CPR, and novel approaches to keep the compression fraction above 90 percent are implemented in many systems. Two of the biggest improvements to increase the compression fraction are to limit the peri-shock pause and to de-emphasize airway management. As an example, intubation should be performed without interrupting compressions, or the provider can utilize a blind insertion airway device. The execution of the resuscitation bundle can vary; however, the key is to limit any interruption in compressions. Although compressions precede airway management in a cardiac arrest, we have to remember that ventilation plays a very important role to compliment these compressions and other interventions.
As an example, Idris et al shows that ventilating in cardiac arrest favorably affects hypoxia, hypercarbic acidosis, and acidemia. This has a direct influence on the efficacy of drugs and defibrillation. Lurie et al also showed “that periodic lung inflation maintains the structural integrity of the lungs and lowers pulmonary vascular resistance,” thereby improving blood flow through the lungs.
On the other hand, hypoventilating during cardiac arrest causes detrimental consequences. Lurie et al showed that giving only 2 breaths per minute versus 10 breaths per minute causes the lungs become more atelectatic. The atelectasis is believed to cause a “reduction in the transmission of the energy from the elastic chest-wall recoil during CPR” which decreases blood flow. In addition, pulmonary vascular resistance increases causing trans-pulmonary blood flow to decrease.
Not ventilating also affects medication administration. Idris et al showed that CPP responded better to epinephrine in ventilated animals versus non-ventilated animals. This would suggests that “ventilation may play an important role in regulating CPP and ROSC through the vascular response to catecholamines,” making it more likely to achieve ROSC in a ventilated patient.
Another consequence of improper ventilation in cardiac arrest is hypercarbic acidosis, which causes peripheral vasodilation and “blunts the vasoconstriction response to exogenous epinephrine.” Higher PACO2 also effects cerebral blood flow by increasing cerebral vasodilation secondary to cerebral autoregulatory mechanisms. In addition, if ROSC is achieved, the hypoxia and hypercarbia “profoundly decreases the myocardial force of contraction.” This would make a re-arrest more likely.
In summary, not ventilating has profound and potentially harmful effect on the resuscitation process. When deploying the “silver chain” of resuscitation, we should also follow the “goldilocks rule” of performing interventions correctly. Whether we perform compressions or ventilate the patient, rates that are too fast or too slow are detrimental. We have to do things “just right!”
How about that!
Trouble is, while there are numerous physiological arguments for ventilating, by and large outcome-based research (meaning the actual "does it work?" data) suggests that it either has no benefit or is harmful. That doesn't mean it's never helpful for anyone, or that with the right approach to minimizing the harms we can't still glean the benefit, but that's pretty much where we're at right now...
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