Correspondence
End-Tidal Carbon Dioxide and Outcome of Out-of-Hospital Cardiac Arrest
N Engl J Med 1997; 337:1694-1695December 4, 1997
- Article
To the Editor:
Levine and colleagues (July 31 issue)1 claim that an end-tidal carbon dioxide level of 10 mm Hg or less, measured 20 minutes after the initiation of advanced cardiac life support, accurately predicted death in patients with cardiac arrest who had electrical activity but no pulse. Although not explicitly stated, it appears that all 35 survivors in their study had spontaneous circulation at the time of the measurement of end-tidal carbon dioxide (at 20 minutes) and, conversely, that none of the nonsurvivors had regained spontaneous circulation at this time. This point should be clarified, because if the distinction is accurate, it indicates that the absence of spontaneous circulation at 20 minutes was as sensitive and specific in predicting death as a low level of end-tidal carbon dioxide. Thus, the level of end-tidal carbon dioxide provided no additional prognostic information. Since, in this setting, a low level of end-tidal carbon dioxide was merely a surrogate indicator of the absence of spontaneous circulation, we suggest that placing a finger on the carotid pulse at 20 minutes would have been cheaper, easier, and at least as efficient in predicting the outcome.
End-tidal carbon dioxide, measured after 20 minutes of advanced cardiac life support, may predict the outcome independently of the presence or absence of spontaneous circulation, but this conclusion is not supported by the data presented.
1 ReferencesCharles D. Gomersall, M.B., B.S.
Gavin M. Joynt, M.B., B.Ch.
Andrew P. Morley, M.B., B.S.
Prince of Wales Hospital, Shatin, Hong Kong1
Levine RL ,Wayne MA ,Miller CC . End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med 1997;337:301-306
Full Text | Web of Science | Medline
To the Editor:
There are two groups of patients who deserve specific mention with regard to the study by Levine et al.: patients with pulmonary embolism and patients with obstructive lung disease. In both groups, a low end-tidal carbon dioxide concentration can result from mechanisms other than low cardiac output.1 Neither group was considered in nor excluded from the above study.
A pulmonary embolus reduces blood flow to part of the lung while ventilation to the same area remains normal. This has the effect of increasing the ventilatory dead space, which in turn causes a decrease in the end-tidal carbon dioxide concentration until an equilibrium is reestablished with the arterial carbon dioxide concentration.
Obstructive lung disease (both asthma and chronic obstructive lung disease) may present with a low end-tidal carbon dioxide concentration through either of two mechanisms. First, exacerbations of the disease may entail an acute severe reduction in tidal volume, with the result that the carbon dioxide emitted from the very limited alveolar ventilation is diluted in the relatively large ventilatory dead space. This results in a large arterial–alveolar carbon dioxide gradient and a low end-tidal carbon dioxide concentration. Second, in the presence of airway obstruction, a prolonged expiratory period is required until the emitted carbon dioxide reaches a plateau level representing the true end-tidal carbon dioxide concentration. If the ventilatory rate is sufficiently high, then the next inspiration will begin before the previous expiratory carbon dioxide plateau has been reached, with the effect that the end-tidal carbon dioxide concentration will be artificially low.
Despite these explanations for a low end-tidal carbon dioxide concentration in patients with pulmonary embolus or obstructive lung disease, the outcome of resuscitation in such patients with pulseless electrical activity and an end-tidal carbon dioxide concentration that is persistently less than 10 mm Hg is likely to be as poor as that demonstrated in the study by Levine et al. A low end-tidal carbon dioxide concentration should, however, suggest the possibility of these diagnoses — both as a cause (albeit a partial cause) of the low end-tidal carbon dioxide concentration and so that the specific therapeutic options available for these conditions may be considered.
1 ReferencesPhillip D. Levin, M.B., B.Chir.
Reuven Pizov, M.D.
Hadassah University Hospital, Ein Karem, Jerusalem 91120, Israel1
Hatle L ,Rokseth R . The arterial to end-expiratory carbon dioxide tension gradient in acute pulmonary embolism and other cardiopulmonary diseases. Chest 1974;66:352-357
CrossRef | Web of Science | Medline
Author/Editor Response
The authors reply:
To the Editor: Gomersall and colleagues correctly point out that all surviving patients in our series had a restoration of spontaneous circulation within 20 minutes after resuscitative measures had been initiated. Their inference that placing a finger on the carotid pulse would be equally efficient in predicting the outcome, however, is an oversimplification. This method would have been effective in identifying resuscitated patients; spontaneously breathing people with a pulse are easily identified. But at the bedside, identifying resuscitated patients is one thing, and distinguishing between patients who might be resuscitated and those who are irreversibly dead is another.1 Although we did not have enough data to say so in our article, we noted that the survivors had an end-tidal carbon dioxide level that was higher than 10 mm Hg from the start or rapidly reached this threshold; the nonsurvivors did not. A persistently low level of end-tidal carbon dioxide may identify patients with a very high risk of death, allowing even earlier discontinuation of advanced cardiac life support than in our study. Conversely, an end-tidal carbon dioxide level higher than 10 mm Hg may identify patients in whom advanced cardiac life support should be continued. Whether a finger placed on the carotid pulse while the patient was in the back of an ambulance would provide a physician with adequate evidence of futility at 20 minutes is questionable. Some physiologic evidence of futility is essential at this early stage, and we have reported a highly discriminating criterion.
Levin and Pizov point out that obstructive lung disease and pulmonary emboli cause abnormal excretion of carbon dioxide, information that can be used to diagnose bronchospasm and pulmonary embolism.2 Although it is possible that massive ventilation–perfusion abnormalities would mask a rising end-tidal carbon dioxide level, we find it difficult to imagine that out-of-hospital cardiac arrest in combination with such abnormalities would be survivable, regardless of resuscitative efforts. Our series has now been expanded to include more than 500 patients, so it is likely that some patients with such abnormalities have been included. We have not had any survivors with major ventilation–perfusion abnormalities. Levin and Pizov's suggestion is provocative, however, especially in the light of a study suggesting that thrombolytic therapy may help improve survival in this group.3
3 ReferencesRobert L. Levine, M.D.
Baylor College of Medicine, Houston, TX 77030Marvin A. Wayne, M.D.
City of Bellingham Emergency Medical Services, Bellingham, WA 98225Charles C. Miller, Ph.D.
Baylor College of Medicine, Houston, TX 770301
Pepe PE ,Levine RL ,Fromm RE Jr ,Curka PA ,Clark PS ,Zachariah BS . Cardiac arrest presenting with rhythms other than ventricular fibrillation: contribution of resuscitative efforts toward total survivorship. Crit Care Med 1993;21:1838-1843
CrossRef | Web of Science | Medline2
Kline JA ,Meek S ,Boudrow D ,Warner D ,Colucciello S . Use of the alveolar dead space fraction (Vd/Vt) and plasma D-dimers to exclude acute pulmonary embolism in ambulatory patients. Acad Emerg Med 1997;4:856-863
CrossRef | Web of Science | Medline3
Bottiger BW ,Reim SM ,Diezel G ,Bohrer H ,Martin E . High-dose bolus injection of urokinase: use during cardiopulmonary resuscitation for massive pulmonary embolism. Chest 1994;106:1281-1283
CrossRef | Web of Science | Medline
- Citing Articles (3)
Citing Articles
1
Allan R. de Caen, Monica E. Kleinman, Leon Chameides, Dianne L. Atkins, Robert A. Berg, Marc D. Berg, Farhan Bhanji, Dominique Biarent, Robert Bingham, Ashraf H. Coovadia, Mary Fran Hazinski, Robert W. Hickey, Vinay M. Nadkarni, Amelia G. Reis, Antonio Rodriguez-Nunez, James Tibballs, Arno L. Zaritsky, David Zideman. (2010) Part 10: Paediatric basic and advanced life support. Resuscitation 81:1, e213-e259
CrossRef2
D.Mark Courtney, John A. Watts, Jeffrey A. Kline. (2002) End tidal CO2 is reduced during hypotension and cardiac arrest in a rat model of massive pulmonary embolism. Resuscitation 53:1, 83-91
CrossRef3
Yuji Morimoto, Osamu Kemmotsu, Yoshiko Morimoto, Satoshi Gando. (1999) End-tidal carbon dioxide and resuscitation. Current Opinion in Anaesthesiology 12:2, 173-177
CrossRef
