Furthermore, routine interruptions in chest compressions― such as for positive pressure ventilations in non-intubated patients―likely further hinder survival rather than contribute meaningfully to outcome. For example, medical students performing traditional CPR took an average of 14 seconds to administer two mouth-to-mouth ventilations after each group of 15 compressions. This effectively reduced the number of compressions to a mere 43 per minute, or less than half the guideline-mandated 100 per minute, thus theoretically reducing circulation to the heart and brain by a similar percentage (29). Yu et al demonstrated that swine receiving more than 80 compressions per minute during CPR had a 100% survival at 24 hours compared with a dismal 10% survival in animals that had less than 80 compressions per minute (30). Kern et al found statistically significantly higher coronary artery perfusion pressures and markedly higher neurological normal 24 hour survival in swine receiving continuous chest compressions compared with controls receiving traditional CPR (31).
Increasingly data such as these do raise the question of what―if any―benefit rescue breathing has in adult resuscitation. Human data show that a strategy of continuous chest compressions―without rescue breathing―is equally efficacious to traditional CPR in terms of outcome (32). Two physiologic theories prevail: 1) the mechanics of chest wall compression may be sufficient to provide a limited minute ventilation independent of supplemental ventilation (author’s speculation); and 2) the improved oxygenation that occurs in those receiving artificial ventilation is offset by the deleterious impact on hemodynamics that occur when chest compressions are interrupted for ventilation (34).
Second Effective Stratagem: Until an adult inpatient can be defibrillated, the focus of resuscitation should be on proper continuous chest compression depth and rate, not on ventilation.
Ventilations are Harmful
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Cardiopulmonary collapse has immediate consequences on cellular physiology. Both due to a lack of expiration of carbon dioxide and the development of lactatemia due to the shift to anaerobic metabolism, blood pH drops precipitously. As the pH shifts out of the physiologic range, drugs begin to perform in unexpected ways or fail altogether; ion trapping occurs; and many electrolytes begin to shift in or out of cells affecting their serum concentration. Diminished or absent cardiac output accelerates these derangements in a relentless positive feedback loop. Logic, therefore, dictates that anything that can improve oxygenation and ventilation would be helpful at slowing or reversing this pathophysiology. Surprisingly, however, clinicians’ lack of knowledge of both equipment and technique often promotes, rather than mitigates, the physiologic derangements.
The bag-valve-mask (BVM) is one of the least understood resuscitation devices. For example, clinicians occasionally place a BVM over spontaneously breathing patients who are exceptionally ill with the goal of augmenting patients’ meager ventilations. However, the BVM is constructed only for positive pressure ventilation and thus, unless the clinician squeezes the bag in perfect coordination with the patient’s ventilatory effort, the BVM will paradoxically smother the patient.
The bag portion of the BVM is designed for a one-handed squeeze to deliver a tidal volume that is roughly 750cc; this volume is in keeping with guideline recommendations of positive pressure ventilation volumes of roughly 10cc/kg/ventilation (29). Yet, clinicians commonly use two hands to compress the BVM maximally during resuscitation (theoretically delivering upwards of double the recommended volume).
In addition to excessive volume, clinicians also deliver ventilations too rapidly. Abella et al. showed that during human resuscitations, ventilation rate exceeded the recommended goal of 20 ventilations/minute 60.9% of the time (27). Theoretically, high minute ventilations lead to an increased incidence of gastric insufflation, regurgitation, and post-resuscitation aspiration.
Though no studies have ever been performed to understand why clinicians hyperventilate patients during resuscitation, it is interesting to speculate that clinicians are not only trying to raise blood oxygen levels rapidly, but also to reverse the profound metabolic and respiratory acidosis that occur during CA. While seemingly mechanistically sound, the logic that supraphysiologic minute ventilations will profoundly change blood pH without other physiologic costs is specious at best. Aufderheide et al. Demonstrated that hyperventilation during resuscitation in swine resulted in increased intrathoracic pressures, markedly reduced coronary artery perfusion pressures, and resultant proportional reductions in survival rates as hyperventilation increased (35). Clinically these findings are known as auto-PEEP, a known complication of artificial ventilation that results in systemic arterial hypotension. Thus the paradox: aggressive attempts to overcorrect systemic acidoses via higher minute ventilations leads to worsening systemic blood pressures and thus worsening lactic acidosis. I believe that iatrogenic hypotension is one of the most common problems to complicate an otherwise successful resuscitation and that more research is urgently needed on this issue.