A 69-year-old male with past medical history of hyperlipidemia and ascending aortic aneurysm was admitted to the neurology department with a large right hemispheric stroke. Three days after admission his consciousness deteriorated, and he was intubated and ventilated. Transcranial Doppler was performed and showed total circulatory arrest. On physical examination brain stem reflexes were absent. Apnea test was performed. During the test, the patient was disconnected from the ventilator, and oxygen was delivered through a small cannula inserted to the endotracheal tube. Before disconnection, the ventilator was set to a respiratory rate (RR) of 15 breaths per minute and tidal volume of 8 cc/kg of ideal body weight. Arterial carbon dioxide (PCO2) and pH were 55 mm Hg and 7.32, respectively. Twenty-two minutes into the test his PCO2 increased to 65 mm Hg. Breathing efforts were not visually seen during the test. However, an end-tidal CO2 (ETCO2) of 28 mm Hg and an RR of 57/min, which was close to the heart rate, were seen on the monitor (Figure 1). Brain death was declared subsequently.
The concept of brain death was first described in the medical literature in 1959. However, despite more than half a century of general acceptance, clear consensus regarding brain death determination is still lacking. In general, it requires a known, irreversible brain injury, absent signs of brain function, and coma. In some countries, confirmatory tests (eg, transcranial Doppler, cerebral angiography, single-photon emission computed tomography) demonstrating either no cerebral blood flow or lack of brain activity are also required.1
Apnea testing is an essential component in the clinical determination of brain death. Its main purpose is to prove the absence of brain stem respiratory control reflexes in response to a strong breathing stimulus. The test is performed for 8–10 minutes to increase PCO2, which is considered the strongest stimulator for breathing, to 60 mm Hg or 20 mm Hg above the patient’s baseline. When the PCO2 goal is reached and no breathing efforts are seen, the test is considered positive. During apnea, the average rise in PCO2 is 3.7 ± 2.3 mm Hg/min.2 However, in reality, it is variable and depends on factors such as oxygen flow through the endotracheal tube, body temperature, and baseline PCO2. Two studies have suggested transcutaneous CO2 monitoring during the test.3,4 However, comparison to predicting PCO2 rise using the estimated rate mentioned above has not been performed. ETCO2 monitoring has never been examined.
The apnea test can continue as long as the patient remains hemodynamically stable and appropriately oxygenated (saturation >85%). In our case, the patient continued to be stable, and this allowed us to prolong the apnea test to reach the desired PCO2.
We think that cardiac contractions, along with systolic blood flow within the aortic aneurysm (Figure 2), which lies in proximity to the right lung, caused artificial breathing efforts. These were significant enough to cause CO2 washout, illustrated by ETCO2 wave. “Cardiac ventilation” as a cause for prolonged apnea test has been described previously.2,5 However, to our knowledge, this is the first time an ETCO2 has been documented. This can serve as a marker of diminished CO2 rise and alert physicians the apnea test might be prolonged and merit a different approach. Using a mixture of oxygen and CO2 delivered through the cannula during the test to increase CO2 faster or lowering baseline PCO2 by increasing RR before ventilator disconnection to begin with a lower CO2 are some techniques that can be used.
In summary, our article describes a case of cardiac ventilation during an apnea test. We think all medical staff involved in brain death determination should be familiar with this phenomenon. Studies comparing different modalities to monitor PCO2 rise and exploring the best method to overcome the issue of cardiac ventilation should be performed.
1. Wijdicks EF, Varelas PN, Gronseth GS, et al; American Academy of NeurologyEvidence-based guideline update: determining brain death in adults: report of the quality standards subcommittee of the American Academy of Neurology.Neurology2010741911–1918
2. Benzel EC, Gross CD, Hadden TA, et al. The apnea test for the determination of brain death.J Neurosurg198971191–194
3. Lang CJ, Heckmann JG, Erbguth F, et al. Transcutaneous and intra-arterial blood gas monitoring–a comparison during apnoea testing for the determination of brain death.Eur J Emerg Med2002951–56
4. Vivien B, Marmion F, Roche S, et al. An evaluation of transcutaneous carbon dioxide partial pressure monitoring during apnea testing in brain-dead patients.Anesthesiology2006104701–707
5. Nattanmai P, Newey CR, Singh I, et al. Prolonged duration of apnea test during brain death examination in a case of intraparenchymal hemorrhage.SAGE Open Med Case Rep201752050313X17716050