A Case of Complex Sleep Apnea?

Case Editor - Jeremy Falk

Reviewed By Sleep and Respiratory Neurobiology Assembly

Submitted by

Dai Yumino, MD, PhD

Fellow

Sleep Research Laboratory of the Toronto Rehabilitation

Toronto General Hospital of the University Health

Centre for Sleep Medicine and Circadian Biology

T. Douglas Bradley, MD

Professor

Sleep Research Laboratory of the Toronto Rehabilitation

Toronto General Hospital of the University Health

Centre for Sleep Medicine and Circadian Biology

Submit your comments to the author(s).

History

A 27-year-old obese man was referred to the sleep clinic regarding a possible diagnosis of obstructive sleep apnea (OSA). He had developed loud snoring, witnessed apneas and daytime sleepiness in association with an 18 kg weight gain over the last few years. He had no history of hypertension, respiratory, cardiovascular or neurological disease.

Physical Exam

His blood pressure was normal, his height was 183 cm and his weight was 109 kg with a BMI of 32.5 kg/m². His oropharynx was normal (Mallampati class I) without tonsillar enlargement. The neck circumference was 45 cm. The respiratory and cardiovascular examinations were normal.

Lab

None

Figures

Answer: A.

One commonly used definition for hypopneas is ≥ 30% reduction in airflow, but above zero, for ≥ 10 sec accompanied by a ≥ 4% desaturation (1). However, hypopneas are not ordinarily classified as central or obstructive in most sleep laboratories, even though they often make up the majority of respiratory events. Distinguishing central from obstructive hypopneas can be difficult, because in both cases, respiratory efforts continue. However, in many instances, hypopneas are readily classifiable. In this case, the paradoxical or out-of-phase motion of the chest and abdomen during hypopneas indicate upper airway obstruction, and therefore they are classified as obstructive hypopneas.

As a non-U.S.-based sleep laboratory, we have chosen not to use Medicare criteria to define OSA. Indeed, we use the sum channel of respiratory inductance plethysmography (RIP) as our index of airflow. This is a well validated technique for the purpose (2,3), and is an accepted means of identifying apneas and hypopneas according to the The Report of an American Academy of Sleep Medicine Task Force (4). The advantage of RIP over all other techniques is that if the sum of the rib cage and abdominal motion is displayed, it provides an index of airflow and tidal volume that is completely independent of the route of breathing (unlike nasal pressure cannulae or thermistors), and that at the same time the independent movements of the rib cage and abdomen can indicate whether or not upper airway obstruction is present as demonstrated herein.

Cessation of airflow with no motion of the chest and abdomen indicate that these are central apneas. Cheyne-Stokes respiration (CSR) is a form of periodic breathing in which the ventilatory periods are characterized by prolonged waxing and waning of tidal volume alternating with central apneas or hypopneas (5). The length of the hyperpnea and the periodic breathing cycle are inversely proportional to cardiac output (6). In patients with heart failure (HF) and central sleep apnea (CSA), the mean ± SD of the periodic cycle duration is about 60±15 sec, compared with only 37±9 sec in patients with idiopathic CSA without HF (6). Thus, the prolonged periodic cycle and hyperpnea is a sign of low cardiac output. The term "Cheyne-Stokes respiration" should, therefore, probably be restricted to periodic breathing in which the hyperpnea and periodic cycle duration are prolonged. In the present case, the periodic cycle duration of only 25 sec is not in the range associated with CSR, in keeping with the absence of a history of HF. Therefore, these are central apneas without CSR.

The key factor triggering most central apneas is a fall in Pco₂ below the apnea threshold (7). Compared with the diagnostic study (Figure 1), central apneas emerged on CPAP of 4 cm H₂O in association with a decrease in TPCO₂ from 44 to 38 mmHg, probably due to sudden CPAP-induced reduction in airflow resistance and increase in ventilation (Figure 2). Subsequently, on CPAP of 7 cm H₂O (Figure 3), central apneas were alleviated in association with an increase in TPco₂ to 42 mmHg. This observation is compatible with previous demonstrations that raising TPco₂ through inhalation of CO₂ abolishes CSA (8), and that CPAP attenuates CSA in association with a reduction in ventilation and an increase in TPco₂ (9). However, the mechanism through which CPAP raises TPco₂ in such patients has not been identified. In any case, the observation that CPAP emergent CSA was related to a fall in Paco₂ could not have been made without recording of TPco₂. Recording of TPco₂is not a standard measurement in most laboratories, despite its being a well validated means of tracking Paco₂ (10). However, as illustrated by this case, it can provide useful insights into the pathogenesis of various types of CSA, and also for diagnosing and treating hypoventilation syndromes.

References

Iber C, Ancoli-Israel S, Chesson Jr. A, Quan S. The AASM Manual for the Scoring of Sleep and Associated Events. Westchester, IL: American Academy of Sleep Medicine; 2007.
Staats BA, Bonekat HW, Harris CD, Offord KP. Chest wall motion in sleep apnea. Am Rev Respir Dis 1984; 130:59-63.
Gould GA, Whyte KF, Rhind GB, Airlie MA, Catterall JR, Shapiro CM, Douglas NJ. The sleep hypopnea syndrome. Am Rev Respir Dis 1988; 137:895-8.
Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep 1999; 22:667-89.
Cheyne J. A case of apoplexy, in which the fleshy part of the heart was converted into fat. Dublin Hospital Reports and Communications 1818; 2:216-223.
Hall MJ, Xie A, Rutherford R, Ando S, Floras JS, Bradley TD. Cycle length of periodic breathing in patients with and without heart failure. Am J Respir Crit Care Med 1996; 154:376-81.
Yumino D, Bradley TD. Central sleep apnea and Cheyne-Stokes respiration. Proc Am Thorac Soc 2008; 5:226-36.
Xie A, Rankin F, Rutherford R, Bradley TD. Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea. J Appl Physiol 1997; 82:918-26.
Naughton MT, Benard DC, Rutherford R, Bradley TD. Effect of continuous positive airway pressure on central sleep apnea and nocturnal PCO2 in heart failure. Am J Respir Crit Care Med 1994; 150:1598-604.
Naughton M, Benard D, Tam A, Rutherford R, Bradley TD. Role of hyperventilation in the pathogenesis of central sleep apneas in patients with congestive heart failure. Am Rev Respir Dis 1993; 148:330-8.
Morgenthaler TI, Kagramanov V, Hanak V, Decker PA. Complex sleep apnea syndrome: is it a unique clinical syndrome? Sleep 2006; 29:1203-9.
Gay P, Weaver T, Loube D, Iber C. Evaluation of positive airway pressure treatment for sleep related breathing disorders in adults. Sleep 2006; 29:381-401.
Dernaika T, Tawk M, Nazir S, Younis W, Kinasewitz GT. The significance and outcome of continuous positive airway pressure-related central sleep apnea during split night sleep studies. Chest 2007; 132:81-87.

	A.	Obstructive hypopneas Correct!
	B.	Central apneas Incorrect!
	C.	Central hypopneas Incorrect!
	D.	Obstructive apneas Incorrect!

	A.	Obstructive apneas Correct!
	B.	Mixed apneas Incorrect!
	C.	Central apneas without Cheyne-Stokes respiration Incorrect!
	D.	Central apneas with Cheyne-Stokes respiration Incorrect!

	A.	Increase in Sao2 → Decrease in Sao2 Incorrect!
	B.	Decrease in Sao2 →Increase in Sao2 Incorrect!
	C.	Increase in TPco2 → Decrease in TPco2 Incorrect!
	D.	Decrease in TPco2 → Increase in TPco2 Correct!

	A.	CPAP of 4 cm H2O Incorrect!
	B.	CPAP of 7 cm H2O Correct!
	C.	Auto-CPAP Incorrect!
	D.	Adaptive servo ventilation (Auto bilevel-PAP) Incorrect!

A Case of Complex Sleep Apnea?

Submitted by

History

Physical Exam

Lab

Figures

Question 1

Question 2

Question 3

Question 4

References