Heart Failure

Cheyne-Stokes breathing in heart failure

Cheyne-Stokes’s breath got its name in honor of those who described it in the middle of XIX century in patients with severe heart failure and stroke of Scottish military doctor John Caine and Irish doctor, Professor William Stokes.

Cheyne-Stokes’ breath looks like this. Rare surface breaths and exhalations gradually become more frequent and deeper. Once the respiratory intensity reaches its maximum, the respiratory movements begin to weaken again, sometimes up to their complete cessation and stopping of breathing, an episode of central apnea. The abnormal respiratory cycle repeats itself again.

The physiology of this process is this. At decrease in pulmonary ventilation and the subsequent apnea there is an increase in concentration of carbon dioxide in blood, the respiratory center is excited, as a result of which there is a renewal of breathing and the period of compensatory hyperventilation, leading to another extreme – a significant decrease in the level of carbon dioxide in blood. This again leads to respiratory depression and apnea.

For a long time, it has been thought that Cheyne-Stokes’ breathing in heart failure not only reflects the patient’s serious condition, but is also an independent factor in increasing the risk of death. Therefore, it should be treated. The most effective and technological method of treatment of Chain-Stokes breathing was adaptive servoventilation.

This is a variant of masked auxiliary ventilation in which the device adapts to the peculiarities of the patient’s breathing to the maximum extent possible: it helps to fully compensate for the lack of breathing in case of hypopnea and apnea, but turns off for the time when the person normally breathes.

However, in large studies an unexpected and paradoxical result was obtained – adaptive servoventilation in patients with chronic heart failure as a result of a significant decrease in the function of the left ventricle causes an increase in mortality. As a result, the controversy about the role of Chain-Stokes’ breathing and approaches to its treatment flared up with a new layer.

“Chain-Stokes’ breath: friend or foe?” – A publication with this title by M. Noton was the beginning of a heated discussion that is still ongoing. The scientist put forward the idea that the periodic breathing of Chain-Stokes in patients with chronic heart failure can be considered a compensatory mechanism. But soon, Sh.

Javakheri presented counterarguments proving that this is a serious pathology that threatens patients with impaired heart muscle function.


лю. Noton believes that the phenomenon of Chain-Stokes manifests itself in heart failure and indirectly indicates the weakening of the heart muscle and its inability to pump enough blood.

The scientist proves that the unique mechanism of this respiratory disorder can reduce the consequences of heart failure as a blood pump. The following contributes to the preservation of cardiac function.

Apnea hyperventilation, which occurs after the episode, increases the volume of the lungs, and positive pressure increases the release of blood from the heart. At the same time, excessive sympathetic activity of the nervous system is suppressed.

In addition, the acid-alkaline state of the blood is returning to normal. Lack of breathing effort during central apnea provides periodic rest for the respiratory muscles.


The opponents have their own “trumps”. They refer to research that points to the connection between Cheyne-Stokes’ breathing and various pathological consequences, including hypertension, which is extremely dangerous in a heart patient.

And this condition is reversible in the effective treatment of central sleep apnoea. By suppressing Chain-Stokes’ breath, we eventually eliminate the excessive excitement of the sympathetic system. The same thing happens when treating obstructive sleep apnoea with SiPAP therapy.

Hyperventilation, which occurs after each episode of apnea, further increases the load on breathing. At the same time, there is an increase in intrabreast pressure fluctuations, which creates an even greater obstacle to blood access to the heart.

By eliminating intermittent respiration, we eliminate abnormal hyperventilation and increase the efficiency of diaphragm muscles. All of this proves that Cheyne-Stokes’ breathing is a dangerous enemy for patients with reduced blood flow from the left ventricle.

Both scientists, proving their position, give many arguments, describe in detail the mechanisms of intermittent breathing and analyze the potential links of this disorder with heart failure.

But none of the works can claim the final truth yet, it is just a discussion of experts. Each of the concepts requires more detailed study and additional research.