OPTImizing Ventilation to Improve Survival From Out-of-Hospital Cardiac Arrest: The OPTIVO Randomized Controlled Trial

Rationale Chest compressions and ventilations are the two primary components of cardiopulmonary resuscitation (CPR); one of the few treatments to get a Class 1 recommendation from the American Heart Association (AHA) guidelines for the treatment of patients in cardiac arrest. While there is a significant body of literature examining chest compression quality the evidence regarding optimal ventilation quality is limited.

Current guidelines recommend providing ventilations of 500-600ml, or enough for chest rise, to adult patients in cardiac arrest in either a 30:2 ventilation to chest compression ratio without an advanced airway or one breath every six seconds (10 per minute) with an advanced airway. Little has changed in these recommendations over the last 10 years. It is recognized, however, that the evidence informing these recommendations is based on limited, low-quality evidence from non-cardiac arrest populations. Both the International Liaison Committee on Resuscitation (ILCOR) and the AHA have identified that there remains a significant knowledge gap with respect to optimal ventilation strategies during out-of-hospital cardiac arrest (OHCA) resuscitation.

Hyperventilation and Hypoventilation Proper ventilation during cardiac arrest is important to provide oxygenation to vital organs, such as the brain, and remove harmful metabolism by-products (e.g. carbon dioxide). Improper ventilation, both hypoventilation (too little) and hyperventilation (too much) can be detrimental to patient survival and neurological outcomes. What constitutes optimal ventilation, however, is unknown.

Hypoventilation can lead to increased ischemic injury from reduced oxygen delivery to the brain during cardiac arrest. It can also cause a build-up of CO2 resulting in a respiratory acidosis which can have detrimental consequences to the heart and cardiovascular function. The amount of ventilation that is required during cardiac arrest though is not known. Research examining passive oxygenation (no active ventilation) demonstrates mixed results with respect to cardiac arrest outcomes. While outcomes have been mixed, in general passive oxygenation may not provide sufficient tidal volumes (often under 20mL) generated with chest compressions for adequate gas exchange.

Hyperventilation can lead to air-trapping and an increase in intrathoracic pressure, leading to increased right atrial pressure, decreased coronary perfusion pressure, and decreased venous return and cardiac output.9 During positive pressure ventilation, the increase in intrathoracic pressure during inspiration leads to a decrease in right ventricular preload, ultimately decreasing cardiac output. Decreased cardiac output and coronary perfusion lead to reduced rates of return of spontaneous circulation, which ultimately leads to reduced survival. Aggressive ventilations can also cause gastric insufflation and gastric regurgitation leading to pneumonia and other associated airway complications. Previous research has shown that ventilation with lower volumes (365mL) is associated with lower airway pressures, and reduced incidence of gastric insufflation without changes in oxygen saturation. Similarly, ventilations with 6mL/kg result in same CO2 clearance as larger tidal volumes. Furthermore, research examining end-tidal CO2 tracings has hypothesized that hyperinflation is a common phenomenon during cardiac arrest.