Capnography as insight into etiology: A case of cardiac arrest following aortic rupture

Abstract

Our cardiac arrest team was recently activated for a patient who was ambulating when he complained of chest pain and collapsed, unresponsive and pulseless, on the floor. Cardiopulmonary resuscitation (CPR) was started immediately by a witness and the first rhythm analysis showed course ventricular fibrillation, which terminated into pulseless electrical activity following a single biphasic shock of 150 J 1 min into the resuscitation. Given the presentation, acute coronary syndrome was high on the differential. However, the patient had undergone an aortic fenestration for descending aortic dissection five days prior, so other potential etiologies including pulmonary embolus, pneumothorax, and hemorrhage were entertained, but there was no clear evidence to suggest one etiology over another in the first few minutes. Endotracheal intubation was established 6 min into the resuscitation and placement was confirmed with capnography. The end-tidal carbon dioxide (PETCO2) level was initially 12 mm Hg and remained low (5–10 mmHg) throughout the resuscitation despite excellent CPR quality, as demonstrated by a compression fraction of 0.91, an average compression rate of 114/min, and an average compression depth of 51 mm. Fig. 1 shows a 30 s snapshot of the transcript surrounding the second shock for recurrent VF. The team was confused by the seemingly incongruous capnograph and therefore confirmed endotracheal tube placement fiberoptically and replaced the in-line sensor, which yielded no appreciable difference in PETCO2. It was not until hemorrhage was visualized in the patient's left chest tube, 10 min after resuscitative efforts were initiated, that the etiology of the arrest and the low PETCO2 became clear. The patient re-fibrillated 16 min into the resuscitation and received a total of 14 shocks as well as volume resuscitation with several liters of normal saline and multiple units of packed red blood cells. The levels of PETCO2 remained persistently low and the patient's rhythm progressed to asystole. Resuscitative efforts were terminated after nearly 60 min. Autopsy examination revealed disruption of the abdominal aortic mucosa at the site of the patient's recent surgical intervention. Adjacent hemorrhage in the left retroperitoneum extended superiorly into the left hemithorax. Measurement of PETCO2 during cardiopulmonary resuscitation is now officially recommended in the American Heart Association ACLS guidelines.1Neumar R. Otto C. Link M. et al.Part 8: Adult advanced cardiovascular life support: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care.Circulation. 2010; 122: S729-S767Crossref PubMed Scopus (1059) Google Scholar Indications for measuring PETCO2 include confirmation of endotracheal placement of ET tube (Class I, LOE A), optimization of CPR quality (Class II, LOE C), confirmation of return of spontaneous circulation (Class II, LOE C) and collection of data to guide termination of efforts. As capnography becomes more widely utilized and further characterized, PETCO2 levels and capnography profiles may prove helpful in diagnosing the cause of sudden cardiac arrest. Non-traumatic aortic pathology has been estimated to cause 2–4% of acute arrests and is usually not initially suspected.2Kurkciyan I. Meron G. Behringer W. et al.Accuracy and impact of presumed cause in patients with cardiac arrest.Circulation. 1998; 98: 766-771Crossref PubMed Scopus (59) Google Scholar, 3Pierce L. Courtney D. Clinical characteristics of aortic aneurysm and dissection as a cause of sudden death in outpatients.Am J Emerg Med. 2008; 26: 1042-1046Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar, 4Meron G. Kurkciyan I. Sterz F. et al.Non-traumatic aortic dissection or rupture as a cause of cardiac arrest: presentation and outcome.Resuscitation. 2004; 60: 143-150Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar, 5Lee C. Chang W. Fang C. Tsai I. Chen W. Sudden death caused by dissecting thoracic aortic aneurysm in a patient with autosomal dominant polycystic kidney disease.Resuscitation. 2004; 63: 93-96Abstract Full Text Full Text PDF PubMed Scopus (27) Google Scholar Data to suggest this diagnosis early in an arrest could lead to earlier intervention, especially when rupture is not immediately considered. Early in our resuscitative efforts, before significant hemorrhage was evident in our patient, pulmonary embolism and acute coronary syndrome were also high on the differential diagnosis. In a study modeling acute arrest due to massive pulmonary embolism, acute aortic rupture, or ventricular fibrillation, animals with induced massive pulmonary embolism and aortic rupture had lower levels of PETCO2 during the first minute of CPR compared to those with ventricular fibrillation.6Courtney D. Watts J. Klin J. End-tidal CO2 is reduced during hypotension and cardiac arrest in a rat model of massive pulmonary embolism.Resuscitation. 2002; 53: 83-91Abstract Full Text Full Text PDF PubMed Scopus (17) Google Scholar These low levels of PETCO2 are thought to be due to increased dead space and V/Q mismatch.6Courtney D. Watts J. Klin J. End-tidal CO2 is reduced during hypotension and cardiac arrest in a rat model of massive pulmonary embolism.Resuscitation. 2002; 53: 83-91Abstract Full Text Full Text PDF PubMed Scopus (17) Google Scholar Interestingly, areas of V/Q mismatch that develop during hemorrhage have been observed to persist despite volume resuscitation.7Fortune J. Mazzone R. Wagner P. Ventilation–perfusion relationships during hemorrhagic hypoperfusion and reinfusion in the dog.Am J Physiol. 1983; 54: 1071-1082Google Scholar Pneumothorax is also a known cause of acute cardiopulmonary arrest. Compared to a normal capnography profile, in which rapidly increasing PETCO2 levels during expiration are followed by a plateau, PETCO2 levels in the presence of pneumothorax may demonstrate a gradual increase throughout expiration. This is referred to as an obstructive pattern and is due to compression of the airways by the pneumothorax.8Smalhout B. Kalenda Z. An atlas of capnography.2nd ed. Kerckebosche, Zeist, The Netherlands1981Google Scholar PETCO2 levels were low for our patient during resuscitative efforts, but the presence of a normal capnography profile, as well as the presence of a functioning post-operative chest tube, decreased our clinical suspicion of pneumothorax as an etiology for cardiac arrest. Combined with the patient's history and recent surgical intervention, PETCO2 levels and capnography waveforms could have been an early clue of massive internal hemorrhage. In conclusion, persistently low PETCO2 levels with a normal capnography waveform in the setting of correct endotracheal tube placement and adequate CPR quality should prompt consideration of hemorrhage as an etiology of cardiac arrest. No conflicts of interest to declare.