Neurology -- Correspondence for Dyken et al., 62 (3) 491-493

Correspondence published:

Reply to Stevens et al: Mark E. Dyken, Mark Eric Dyken, M.D., F.A.H.A., A.B.S.M., Herbert A. Berger, M.D., F.C.C.P., F.A.C.P., A.B.S.M., Thoru Yamada, M.D., A.B.S.M., and Christine L. Glenn, RPSGT, R EEG T. (23 June 2004)

Obstructive sleep apnea associated with cerebral hypoxemia and death: Damien Stevens, Suzanne Stevens (23 June 2004)

Reply to Stevens et al 23 June 2004

Mark E. Dyken,
The Roy J. and Lucille A. Carver College of Medicine
200 Hawkins Drive, 2107 RCE Iowa City, Iowa 52242-1053,
Mark Eric Dyken, M.D., F.A.H.A., A.B.S.M., Herbert A. Berger, M.D., F.C.C.P., F.A.C.P., A.B.S.M., Thoru Yamada, M.D., A.B.S.M., and Christine L. Glenn, RPSGT, R EEG T.
Send Correspondence to journal:
Re: Reply to Stevens et al

mark-dyken{at}uiowa.edu Mark E. Dyken, et al.

We thank Stevens et al for their interest in the important issue of CO2 retention following the implementation of supplemental oxygen therapy in critically ill patients.
Our original manuscript was in the format of Neurology's Brief Communication. [1] The comments provide strong support for our routine monitoring of oxygen saturation (SaO2), arterial blood gas (ABG) and end-tidal CO2 (PETCO2). In some patients with chronic obstructive lung disease or neuromuscular disorders, supplemental oxygen can lead to hypoventilation and hypercapnea after a relatively brief period of time.
When analyzing sleep, and the placement of an arterial line is denied (or is not otherwise possible), serial ABGs are not practical as they disrupt sleep, and as such, provide data that is suspect. Nevertheless, a single ABG can provide a baseline from which PETCO2 trends can be followed with confidence (circumventing inaccuracies intrinsic to the concomitant use of supplemental oxygen delivery systems). [2] Using such methodology, worsening hypercapnea with hypoventilation and respiratory arrest might logically imply iatrogenic death resulting from the use of supplemental oxygen.
Our patient was admitted with congestive heart failure, on 5 liters of supplemental oxygen, with a PaO2 of 60 mm Hg. An increase to 9 liters of oxygen resulted in a sustained SaO2 greater than or equal to 90%, without evidence of respiratory compromise for over 6 hours. During polysomnography (PSG), PETCO2 and SaO2 were monitored, with respective waking baseline values of 23 mm Hg and 92%. The PETCO2 ranged from 32 mm Hg (in association with an SaO2 of 95%), to a low of 19 mm Hg with an SaO2 of 94% (noted just prior to the terminal event).
Prior to the terminal event, our subject demonstrated only obstructive respiratory abnormalities. Our original submission included the PSG tracing that documented the temporal, cause-and-effect, association between a prolonged obstructive apnea and an acute myocardial infarction. All subsequent respiratory abnormalities were agonal. [3]
The current literature has addressed cause-and-effect relationships between OSA and acute cardiovascular catastrophe and death as matters of speculation. [4] The critical analysis demanded of our research allows us to confidently report upon such relationships as matters of fact. [1,5] Hopefully, this important information will justify large, detailed population studies that may rationalize the routine aggressive analysis of OSA in critically ill patients.
References
1. Dyken ME, Yamada T, Glenn CL, Berger HA. Obstructive sleep apnea associated with cerebral hypoxemia and death. Neurology 2004;62:491-3.
2. Sanders MH, Kern NB, Costantino JP, Stiller RA, Strollo Jr PJ, Studnicki KA, Coates JA, Richards TJ. Accuracy of end-tidal and transcutaneous PCO2 monitoring during sleep. Chest 1994;106:472-83.
3. Plum F, Posner JB. The pathologic physiology of signs and symptoms of coma. In: The diagnosis of stupor and coma (Edition 3). Philadelphia: F.A. Davis Company, 1982;32-41.
4. Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995;96:1897-1904.
5. Dyken ME, Yamada T, Berger HA. Transient obstructive sleep apnea and asystole in association with presumed viral encephalopathy. Neurology 2003;60:1692-1694.

Obstructive sleep apnea associated with cerebral hypoxemia and death 23 June 2004

Damien Stevens,
Kansas City, MO
4321 Washinton St., Suite 5100, Kansas City, MO 64111,
Suzanne Stevens
Send Correspondence to journal:
Re: Obstructive sleep apnea associated with cerebral hypoxemia and death

damienstevens{at}sbcglobal.net Damien Stevens, et al.

We have some comments regarding one of the cases recently reported by Dyken et al. [1] Case 2 involves a patient with �severe chronic obstructive pulmonary disease.� During the polysomnogram, which was performed on supplemental oxygen at 9 liters per minute, obstructive sleep apnea was noted as well as �new onset central apneas.� Respiratory arrest was followed by cardiac arrest. No data was supplied regarding arterial blood gases and whether hypercapnia was present prior to or developed during the study.
The well-known phenomena of acute respiratory failure induced by supplemental oxygen may have precipitated this respiratory arrest in this patient. [2-4] Oxygen at the level provided was certainly sufficient to induce hypoventilation in patients with chronic obstructive lung disease and the typical polysomnogram findings would be hypopneas as well as central apneas, which were reported. Based upon the information provided, it appears more likely the respiratory arrest in this individual was due to supplemental oxygen inducing respiratory acidosis and eventual arrest rather than obstructive sleep apnea playing a direct role.
References
1. Dyken ME, Yamada T, Glenn CL, Berger HA. Obstructive sleep apnea associated with cerebral hypoxemia and death. Neurology 2004;62:491-493.
2. Gay PC, Edmonds LC. Severe hypercapnia after low-flow oxygen therapy in patients with neuromuscular disease and diaphragmatic dysfunction. Mayo Clin Proc 1995;70:327-330.
3. Moloney ED, Kiely JL, McNicholas WT. Controlled oxygen therapy and carbon dioxide retention during exacerbations of chronic obstructive pulmonary disease. Lancet 2001;357(9255):526-8.
4. Robinson TD, Freiberg DB, Regnis JA, Young IH. The role of hypoventilation and ventilation-perfusion redistribution in oxygen-induced hypercapnia during acute exacerations of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000;161:1524-9.