The secret behind shallow water blackouts and drownings revealed
Over the past several years, an epidemic of drownings has occurred nationwide. The drownings include a surprising population of individuals. It involves trained athletes and swimmers who have engaged in an extremely dangerous practice of underwater swimming with breath-holding as an endurance training technique. This involves athletes and students who are high achievers and competitors, and all of them have died while breath-holding under water in an attempt to achieve a competitive edge and improve their endurance.
The medical literature is replete with a collation of drowning cases and near drownings in individuals who have purposely hyperventilated before attempting lengthy underwater swimming exercises. What made this alarming was that these individuals were all excellent swimmers and almost always those tragedies occurred in pools that had lifeguards.
Most swimmers who died from this practice hyperventilated thinking that in doing so this would increase their oxygen stores, so that they could stay underwater longer.
Hyperventilation actually decreases the body's natural stores of carbon dioxide while adding very little to its oxygen reserves. The common misconception is that the drive to breathe is triggered by a lack of oxygen. However, the level of carbon dioxide in the blood is a much stronger stimulus that prompts the breathing reflex.
By hyperventilating and blowing off excess carbon dioxide, the swimmer loses that respiratory drive and because of depleted oxygen reserves, shallow water blackout occurs. A loss of consciousness under water can trigger a series of events including inhalation of water, cardiac arrest, brain damage and death.
In 1976, 58 cases of shallow water blackout drownings were reported and commented on in the Journal of Medicine and Sciences in Sports. In most fatalities, the persons were known to have learned the value of and had previously employed hyperventilation to increase their breath-holding time. The coroners concluded that in almost all instances the death, which occurred underwater, constituted "death by drowning" without any pathologic evidence to support this conclusion.
It is conceivable that the hypoxia (low oxygen state) led to loss of consciousness, which in turn would cause total relaxation of the muscles suspending respiration. If the lung volume at that time was greater than the expiratory reserve volume of the lungs under those conditions, air would be expelled passively. The effect of severe hypoxia would then prevent the effort to inhale, which would be expected after expiration, and in the next few seconds death would occur.
Most autopsies observed that the heart was dilated, the liver became passively congested and acute pulmonary hypertension ensued. Acute hypoxia has this classic effect on the pulmonary circulation.
What can confuse coroners at the time of autopsies is that once the muscles of respiration relax and spontaneous breathing movements ensue, the individual as a terminal event aspirates water, which leads then to their conclusions of "death by drowning."
The increase of oxygen consumption must shorten the time course from the beginning of the apnea (cessation of breathing) to unconsciousness with relaxation of the muscles and subsequent inhalation of water then death within 2.5 minutes or less. This is in contradistinction to what we know about drowning in the non-breath-holding situation when it takes approximately eight minutes from the cessation of respiration until death.
One characteristic aspect of hypoxia is that loss of consciousness occurs with little specific warning. It is much different from a faint caused by hypotension or drop in blood pressure. In the latter instance, the subject usually has several seconds warning. But, hypoxic subjects can sometimes continue their previous activity in the moment between loss of consciousness and final collapse.
In addition, there remains a subset of young athletes who possess the congenital long-QT syndrome (LQTS) and other cardiac channel defects or abnormalities that may suffer a swimming-triggered cardiac event precipitated by this form of hypoxic training.
It is true that most aquatic staffs, lifeguards, pool managers and coaches understand and are familiar with shallow water blackout and how it results from underwater breath-holding exercises, training techniques and games. It is alarming and worrisome, however, that some primary organizations that train and certify pool lifeguards provide only vague references to this dangerous training practice in their manuals.
It is imperative that these institutions update their teaching manuals and make paramount in their lifeguard certification procedures that underwater breath-holding training exercises should be strictly forbidden. It is important that swim coaches not employ hypoxic training as part of their training exercises. The medical profession must become more aware of this dangerous practice in order to add their considerable weight to seeing that the practice of hypoxic underwater breath-holding is abolished.
Jeffrey A. Ratner, MD, is a board-certified physician specializing in pulmonary and internal medicine. He is in private practice in State College and is a credentialed physician on the medical staff at Mount Nittany Medical Center.