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Another important consideration is the role of ventilation during chest compressions. The need for ventilation with bystander CPR for patients with short‐duration VF has been questioned [745–49]. The theoretical bases for this approach include: 1) the distractions posed by multiple interventions; 2) the subsequent reduction in number of chest compressions; 3) the adverse effect of hyperventilation on CPP; and 4) bystander reluctance to perform mouth‐to‐mouth ventilation [38,50–52]. Although “no ventilation” has practical value for bystander care, it is not clear how or if these principles should be applied to EMS care. There is some evidence that prearrival instruction for compression‐only CPR by emergency medical dispatchers results in delivery of earlier and more chest compressions, but not to an increase in survival [53, 54]. Some EMS systems have adopted protocols making active ventilation optional during the initial resuscitation, instead placing an oral airway and oxygen mask until sufficient rescuers are on scene. This allows the first‐arriving crew to focus on compressions and defibrillation. However, recent studies support that chest compressions alone do not provide clinically significant ventilation, and that outcomes are improved with adequate ventilation during resuscitation [55, 56].

Considerable scientific data have highlighted the importance of controlled ventilation during resuscitation. During cardiac arrest resuscitation, hyperventilation increases intrathoracic pressure, resulting in decreased preload and CPP [38]. Furthermore, inadvertent hyperventilation occurs frequently during resuscitation efforts, despite specific training to avoid this phenomenon. Ventilation during cardiac arrest should consist of tidal volumes of 500‐600 mL at a respiratory rate of 8‐10 breaths/min.

The impedance threshold device (ITD) is a ventilation adjunct that may be attached to either a facemask or an endotracheal tube. It contains a one‐way valve that permits exhalation during the downstroke of chest compression but prevents passive inhalation during the upstroke of chest compression. As a result, the ITD generates increased negative intrathoracic pressure during chest recoil, increasing cardiac preload and CPP. While preclinical and small trial data were favorable, a large randomized trial of the ITD versus sham device yielded similar rates of survival with good neurologic outcome between groups (ITD 5.8% vs. sham device 6.0%; p = 0.71) [57–62].