Pathogenesis of Cheyne-Stokes Respiration in Patients With Congestive Heart Failure: Relationship to Arterial Pco2

doi:10.1378/chest.104.4.1079

Chest

Volume 104, Issue 4, October 1993, Pages 1079-1084

https://doi.org/10.1378/chest.104.4.1079 Get rights and content

In order to determine which patients with congestive heart failure (CHF) develop Cheyne-Stokes respiration (CSR) during sleep, we compared the cardiorespiratory profiles of CHF patients with CSR to those of CHF patients without CSR. Overnight polysomnography and continuous transcutaneous Pco₂ (tc Pco₂) monitoring, estimation of left ventricular ejection fraction (LVEF), pulmonary function tests, and chest radiograph were performed on 16 consecutive patients with chronic, stable CHF. The tc Pco₂ monitor (Kontron 7640) was calibrated so that measurements reflected arterial Pco₂ values. A mean value was calculated for wakefulness (W) and total sleep time (TST). Circulation time (CT) from the lung to the carotid body was estimated from the end of an apnea or voluntary breathold to the nadir of oxygen desaturation recorded on an ear oximeter. The duration of CSR was expressed as a percent of TST. Nine patients developed CSR during sleep (52.5 ±31.6 percent TST) (group 1) and 7 did not (group 2). All patients were male and both groups were a similar age (64±8 vs 63±4 years) and weight (body mass index, 28.1±3.5 vs 25.4±3.4 kg/m²). There were no significant intergroup differences between LVEF (22±5.2 vs 24.1 ±5.2 percent), CT (19.1 ±3.6 vs 15.9±6.7 s), SaO₂ (W) (94±1.2 vs 92.4±2.1 percent), and SaO₂ (TST) (90.8 ±2.7 vs 92.4±2.1 percent). The tc Pco₂ (W) was lower in group 1 (34.4 ±3.5 vs 38.1 ± 1.9 mm Hg), increased during sleep by a similar amount in both groups (1.6± 1.5 vs 2.1±2.2 mm Hg), and was significantly lower during sleep in group 1 (36.1 ±3.4 vs 40.2±2.2 mm Hg). We conclude that CHF patients with CSR hyperventilate during sleep and wakefulness and that CHF patients with awake hypocapnia are more likely to develop CSR during sleep. These findings indicate that arterial Pco₂ is important in determining which CHF patients develop CSR.

Section snippets

Patient Population

We studied 16 consecutive patients with severe, stable CHF (New York Heart Association [NYHA] class 3 to 4) whose resting left ventricular ejection fraction (LVEF) was <35 percent. A history of abnormal breathing during sleep was not required for entry into the study. Patients were excluded if they had the following: (1) significant pulmonary, renal, or neurologic disease; (2) medication prescribed that alters respiratory drive; and (3) carbon dioxide retention, defined as awake PaCO₂ <45 mm

Results

The 16 patients we studied had severe, stable CHF due to ischemic heart disease. Each patient had class 3 or 4 (NYHA) CHF and LVEF was <35 percent. Mean LVEF was 22.9±5.5 percent. All patients were male. The mean age was 63.8 ±7.1 years and mean body mass index (BMI) was 26.9±3.8 kg/m². Patients were divided into two groups based on whether they had CSR on the overnight sleep study. Nine patients had CSR that ranged from 15 to 100 percent of the TST (mean±SD, 52.5±31.6 percent TST) and 7

Discussion

We compared the cardiorespiratory profiles of two groups of patients with CHF, one with CSR and one without CSR during sleep. Both groups had similar degrees of LV dysfunction, circulatory delay, and nocturnal hypoxemia. However, PaCO₂ was significantly lower during wakefulness and sleep in CHF patients with CSR compared to those without CSR. The difference in PaCO₂ could not be attributed to the radiologic extent of pulmonary edema, which was similar in both groups. These findings indicate

Acknowledgments

The authors thank Mark Alderson for his technical assistance and Elvie Garcia for typing this manuscript.

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Chest

Clinical Investigations: CardiologyPathogenesis of Cheyne-Stokes Respiration in Patients With Congestive Heart Failure: Relationship to Arterial Pco2

Section snippets

Patient Population

Results

Discussion

Acknowledgments

Am J Med

Clin Chest Med

Lancet

Congestive heart failure: Cheyne-Stokes respiration as the cause of paroxysmal dyspnea at the onset of sleep

Arch Intern Med

A case of apoplexy in which the fleshy part of the heart was converted into fat

Dublin Hospital Rep

Respiration and abnormal sleep in patients with congestive heart failure

Chest

The effect of oxygen on respiration and sleep in patients with congestive heart failure

Ann Intern Med

Cheyne-Stokes breathing during sleep in patients with left ventricular heart failure

South Med J

Mechanisms of hypoxia-induced periodic breathing during sleep in humans

J Appl Physiol

Cheyne-Stokes breathing: an instability in physiologic control

N Engl J Med

Cheyne-Stokes respiration: a review of clinical manifestations and critique of physiological mechanisms

Arch Med

Basic oscillating mechanism of Cheyne-Stokes breathing

Am J Physiol

Sleep apnea and its causes

J Clin Invest

Clinical Investigations: Cardiology
Pathogenesis of Cheyne-Stokes Respiration in Patients With Congestive Heart Failure: Relationship to Arterial Pco₂