When breathing too much can “kill” you
By J. Howard Jaster, MD
Respiratory therapy for sleep apnea
If your doctor has just told you that you have sleep apnea, you may be about to walk into a dark and dangerous alley. Some might reasonably advise you to update your last will and testament. It seems that the disease itself can be more capriciously lethal than most patients imagine. And the treatments may add a significant risk for sudden unexpected death – which many doctors do not understand or acknowledge.
Clinical Trials
At the dawn of the new millennium there had been a decades-long tradition of treating sleep apnea with nocturnal respiratory therapy, but only small and imperfect clinical studies were available to guide doctors regarding which type of respiratory therapy to use, and how much – and whether or not it was really even helpful. Shortly thereafter doctors embarked on two major international clinical trials, which together were like a Manhattan Project involving several major universities, to produce data that would determine once and for all whether respiratory therapy was beneficial to patients with sleep apnea.
And the results, published in 20151 and 20162 in the New England Journal of Medicine (NEJM), stunned doctors around the world. The study groups of patients who received nocturnal respiratory therapy for sleep apnea had more deaths than the control groups that had no treatment. Yet it seems that after obtaining these expensive trial results, doctors then proceeded to minimize them and ignore them. The actual trial methodology and results are simple and can be read by many patients who have no healthcare schooling3.
Why can nocturnal respiratory therapy kill sleep apnea patients?
Blood flow to the brain is controlled somewhat separately from the rest of the body. Carbon dioxide (CO2) is a potent dilator of blood vessels in the brain, and thereby increases blood flow in the brain. CO2 does not have this effect elsewhere in the body. When respiratory therapy is used to treat sleep apnea, CO2 is reduced everywhere in the body, and blood flow in the brain is reduced. Why does that make any difference?
The heart is an electric pump. The brain is a computerized electronic guidance system. The vagus nerve is an electric cable cord attached to the heart, used to plug the heart into the brain, just as you would plug an electric pump cord into a wall socket – but of course the attachment is permanent. The cable holds two wires, each insulated from the other: an up-stream wire from the heart to the brain, and a down-stream wire from the brain to the heart. At the end of the cable cord are two metal prongs that fit into an electric socket in the brain. Each metal prong attaches to one of the two wires in the vagus nerve. The two metal prongs that are ‘plugged into’ the brain are thereby imbedded in the brain and receive their blood supply from the brain vessels, which are dramatically influenced by CO2 levels.
When someone initially begins to develop sleep apnea, their heart begins to suffer from lack of oxygen. The heart then sends signals to the brain through the vagus nerve up-stream wire to make adjustments in the heart rate and contractility. The brain then makes those adjustments through the down-stream wire. As sleep apnea becomes progressively more severe, the two metal prongs are unable to handle the high volume of signaling, and they begin to overheat, and require increased blood flow. But just as they need greater blood flow, respiratory therapy is initiated, thereby decreasing CO2 and decreasing their blood flow. An electrical short circuit occurs, sending abnormal electrical discharges from the prongs though the down-stream wire to the heart – sometimes causing cardiac arrest.
Passing out
Did you ever see a tall slender young man have a panic attack as he began to speak publicly for the first time? First his heart started racing, and then his breathing began racing to keep up. A minute later he was lying on the floor beside the podium. What happened? He lost consciousness because the blood flow to his brain dropped precipitously. Why did that happen? By hyperventilating he severely reduced the CO2 in his blood stream.
Mouth-to-mouth is out
Meanwhile, have you ever heard of “Hands-only CPR (cardio-pulmonary resuscitation)”? It has been recommended for over a decade because field data shows that cardiac arrest patients do as well or better when given only chest compressions – and not mouth-to-mouth breathing. Can that be possible? By not breathing for the patient the CO2 levels in brain remain very high – maximally dilating blood vessels and increasing blood flow – while the blood is being circulated by chest compressions. Cardiac arrest outside of the hospital is just one more special occasion when breathing too much can kill you.
View the HCA disclaimer here>>
About the author: Dr Jaster is affiliated with the Department of Medicine, London Corporation in Kuala Lumpur. Read more of his work in the Journal of Thoracic Disease; Reperfusion injury to ischemic medullary brain nuclei after stopping continuous positive airway pressure-induced CO2-reduced vasoconstriction in sleep apnea.
1. Cowie MR, Woehrle H, Wegscheider K, et al. Adaptive Servo-Ventilation for Central Sleep Apnea in Systolic Heart Failure. N Engl J Med. 2015 Sep 17;373(12):1095-105. doi: 10.1056/NEJMoa1506459. Epub 2015 Sep 1. PMID: 26323938
2. McEvoy RD et al. SAVE Investigators and Coordinators. CPAP for Prevention of Cardiovascular Events in Obstructive Sleep Apnea. N Engl J Med. 2016 Sep 8;375(10):919-31. doi: 10.1056/NEJMoa1606599. Epub 2016 Aug 28.
3. Read related reports on-line at https://www.nejm.org/doi/pdf/10.1056/NEJMoa1606599
