Cyclical breathing in heart failure patients
April 1, 2000 3 minutes read
Cyclical breathing in heart failure patients
Synopsis: Cyclical breathing in CHF patients is associated with autonomic dysfunction and a poor prognosis, and modulation of peripheral chemosensitivity may have beneficial effects.
Source: Ponikowski P, et al. Circulation 1999; 100:2,418-2,424.
Ventilatory rate acceleration and deceleration with apnea or Cheyne-Stokes respiration (CSR) are common during sleep in CHF patients, and ventilatory oscillation without apnea or periodic breathing (PB) can be seen in awake patients. However, the clinical significance of cyclical breathing (CSR or PB) in CHF patients is not fully understood. Thus, Ponikowski and colleagues studied 74 stable CHF patients in sinus rhythm by observing breathing patterns, analyzing heart rate variability and baroreflex sensitivity, and assessing the response to peripheral chemoreceptor suppression. Cyclical respiration was exhibited by 66% of the patients with approximately equal numbers displaying CSR and PB. Cyclical breathing was associated with more advanced CHF symptoms, impaired autonomic balance, and increased peripheral chemosensitivity. Also, cyclical breathing was associated with nonsustained ventricular tachycardia on ambulatory ECG monitoring (more than 50% of cyclical patients vs. 10% of normal breathing patients; P < 0.01). In addition, mortality was higher over an average 524 days follow-up on cyclical compared to normal breathers (37% vs. 12%) and cyclical breathing was independent of peak oxygen (O2) consumption and NYHA class. Finally, hyperoxia abolished cyclical breathing in seven of eight patients tested and dyhydrocodeine reduced peripheral chemosensitivity, abolishing PB in four patients and converting CSR to PB in two. Ponikowski, et al conclude that cyclical breathing in CHF patients is associated with autonomic dysfunction and a poor prognosis, and that modulation of peripheral chemosensitivity may have beneficial effects in CHF patients.
Comment by Michael H. Crawford, MD, Robert S. Flinn Professor, Chief of Cardiology, Univer-sity of New Mexico, Albuquerque
CSR is well-described in CHF patients and has been related to the severity of hemodynamic abnormalities in other studies. In fact, an inverse relationship between cardiac output and the total cycle length of a CSR cycle has been proposed. Also, the poor prognosis of CSR and its relationship to ventricular tachyarrhythmias has been reported. CSR is usually observed during sleep. This study shows that the more common awake breathing abnormality is PB without apnea. Also, this study shows that CSR and PB are a continuum and have the same implications and should be considered one entity — cyclical breathing. Although there are no hemodynamic measurements in this study, cyclical breathing was related to NYHA class, ventricular tachycardia, and reduced survival, supporting their hypothesis that CSR and PB are different manifestations of the same phenomenon.
That concepts suggest that cyclical breathing is a consequence of CHF and poor cardiac output, which would delay transmission of signals related to O2 and CO2 levels to the brain because of reduced circulation time. However, Ponikowski, et al hypothesize that enhanced peripheral sensitivity to O2 and CO2 may be the dominant mechanism and demonstrate that two therapies (oxygen and dihydroxodeine) that reduce hemosensitivity improve cyclic breathing. If cyclical breathing is the real culprit leading to periods of hypoxia, increased sympathetic drive, ventricular arrhythmias, and sudden death (as in sleep apnea), then therapies to reduce it could decrease mortality in CHF. This is a novel concept that their study supports, but it also raises further questions. What is the best therapy for cyclical breathing? Is specific therapy better than just intensifying standard CHF care? Is reduced cyclical breathing associated with reduced arrhythmias and death? Further experimentation along these lines seems justified and is in concert with the current approach to treating CHF — blocking every adverse neurohormonal effect with a designer drug. Until gene therapy for CHF emerges, improving the modulation of peripheral chemosensitivity may be a worthy goal for the pharmaceutical industry.
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