Therapeutic hypercapnia after cardiac arrest: a pilot feasibility and safety randomized controlled trial

None listed

Cardiac arrest is a relatively common and devastating event in Australia and New Zealand (ANZ). It is associated with extremely high mortality. A large proportion of those who survive are left with serious neurological disability. Such disability includes memory loss, paralysis and difficulty in thinking and speaking. These deficits often lead to a loss of independence and the need to be admitted to aged-care facilities. Immediate cardio-pulmonary resuscitation and defibrillation by bystanders has only partly improved the outcome of these patients. For those who survive the immediate phase and are admitted to the intensive care unit, actively decreasing the body temperature to 33-34 degrees C has been shown to protect the brain. Although limited, these results suggest that some interventions after cardiac arrest can improve brain outcome. Perhaps other interventions could lead to similar results and further improve patient’s recovery and quality of life after cardiac arrest. In a recent observational study in 12,000 ANZ patients who were admitted in ICU after a cardiac arrest, we found that those who had an elevated partial pressure of carbon dioxide (PaCO2) in the 24 hours following the cardiac arrest had a higher chance of having a satisfactory neurological recovery. These patients were 20% more likely to be able to go back home at the end of their hospital stay as compared with those whose PaCO2 was either in the normal or low range. These findings are similar to those seen in previous animal studies. They also make physiological sense: a higher PaCO2 is known to trigger an increase in the amount of blood directed towards the brain. An increase in brain blood flow after a cardiac arrest (a state of no flow) should be logically associated with a higher chance of recovery. However, these findings need to be confirmed by prospective trials before they can be applied to all patients with a cardiac arrest. PaCO2 is normally controlled by the lungs and its arterial partial pressure is directly related to the rate and amplitude of the breathing process. After a cardiac arrest, patients typically are unconscious or heavily sedated by medication and their breathing process is almost entirely taken care of by a ventilator (breathing machine). In such circumstances, the PaCO2 is determined by the medical team. Currently, a “normal” value for PaCO2 (35-45 mmHg) is targeted by clinicians. However, changing this target value to 50-55 mmHg, would be technically easy to implement and carry no extra cost. Based on the findings of our retrospective study (Schneider et al, Resuscitation 2013), on animal studies and logic, we hypothesize that a higher PaCO2 in the first 24 hours after cardiac arrest will be associated with less neurological injury and be feasible and safe. To test this hypothesis, we plan to randomly allocate 75 patients admitted to ICU after cardiac arrest to either “High PaCO2” or “Control” group. The pan to enrol 75 participants is purposeful. This approahc willl provide the means to obtain a complete set of brain biomarker samples (those being baseline, 24 hour, 36 hour and 72 hour) for a total of 50 participants. The key outcomes of interest would be whether such trial can be done, whether this therapy appears safe and whether it decreases blood test-based markers of brain injury (brain proteins like neuron specific enolase and S100 protein), indicating that a biological benefit is taking place.