Continuing Education Activity
Shallow water blackout is a loss of consciousness caused by cerebral hypoxia towards the end of a breath-hold dive in shallow water. It is typically caused by hyperventilating just before a dive, which lowers the carbon dioxide (CO2) level and delays the diver's urge to breathe. This activity reviews the role of the healthcare team in the prevention and treatment of this condition.
- Identify the etiology and epidemiology of shallow water blackout risk factors and emergencies.
- Outline the appropriate history, physical, and evaluation of shallow water blackout patients.
- Review the treatment and management options available for shallow water blackout.
- Describe interprofessional team strategies for improving care coordination and communication to prevent and treat shallow water blackout emergencies.
The term shallow water backout has been commonly used as a term for drowning, particularly when preceded by hyperventilation. Other terms used to describe this syndrome include: “underwater blackout,” “underwater blackout syndrome,” “sudden underwater blackout syndrome (SUBS),” “breath-holding blackout,” and “free-diver blackout.” Shallow water blackout means unconsciousness in water typically less than 15 feet (5 m) either due to equipment failure or prolonged breath-holding. This language can be misleading as drowning can occur at depths greater than 5m as well. The American Red Cross, YMCA, and U.S.A. swimming have since redefined the term as a hypoxic blackout. Hypoxic blackout is defined as “the loss of consciousness in the underwater swimmer or diver, during an apnea submersion preceded by hyperventilation, where alternative causes of unconsciousness have been excluded.” Shallow water blackout has the potential to affect anyone in the water, even fit and experienced swimmers. This condition can occur in any body of water, no matter the depth. Some people survive such an event as a result of prompt and effective rescue efforts. Others are not as fortunate. Preventive measures through an increased understanding of hypoxic blackouts are crucial to prevent tragic and unnecessary deaths.
The underlying cause of hypoxic blackouts is usually multifactorial. It generally stems from poor situational awareness, inadequate safety measures, and poor technique. The average person can hold their breath for between 30 to 90 seconds. It is very rare for people to be able to hold their breath for much longer without specialized training or preparation. Most hypoxic events occur when people attempt prolonged breath-holding and push past their safety threshold. This situation becomes particularly dangerous when there is little rest in between prolonged breath-holding attempts. While trained breath holders can survive submerged for more than 6 minutes, they are still at risk for drowning. Drowning that happens with previously fit and asymptomatic swimmers usually occur during breath-holding training, competition races, and endurance underwater swimming and diving. Those most at risk for hypoxic blackouts are novice divers going to moderate depths.
Additionally, hypoxic blackout directly links to hyperventilating or taking a series of short breaths before going underwater. This behavior is the leading cause of drowning for experienced swimmers. In public settings, if lifeguards are not aware of behaviors such as intentional hyperventilation, the risks of adverse events are significantly increased.
In the United States, there are about 4000 drowning deaths annually. However, over the last four decades, the U.S. has decreased the death rate from drowning by over 300%. 1970 there were 3.87 drowning deaths per 100000 population, which in 2000 had decreased to 1.24 per 100000. This downward trend is attributed to improved knowledge of the pathophysiology and treatment of drowning. However, many remaining deaths are avoidable with relatively minimal effort. Drowning still ranks as the fifth leading cause of unintentional injury leading to death in the United States.
Interestingly, however, the rates of fatalities following prolonged breath-holding, preceded by a period of hyperventilation, have not fallen. Shallow water blackout most commonly involves males under the age of 40 years old and has a high fatality rate. Of note, in a CDC case series, 13 of the 16 dangerous breath-holding cases identified in New York were males. Of the 16 cases, four resulted in a fatality, and three of those four fatalities were associated with the military. From 2008 to 2015, there have been a total of 24 Marine Corps drowning fatalities, 3 of which occurred while on duty. During the same time frame, there were 46 total Navy drowning fatalities, 14 of which happened while on duty.
To understand the pathophysiology of a hypoxic blackout, we will first examine the physiology of diving. The underwater environment has increasingly higher pressures, the deeper it is. These pressures are dramatically higher than the land’s atmospheric pressure. For every additional 10 meters of depth, the ambient pressure rises by 1 bar (about 750 mm Hg). As a result of this high-pressure environment, the lungs become compressed (Boyle’s law: P1xV1 = P2xV2), which results in increased pressure within both the thoracic cavity and peripherally. This situation ultimately promotes the central shunting of peripheral blood flow. These systemic shunting mechanisms work to conserve oxygen and delay the effects of hypoxia and hypercapnia. This increase in intrathoracic blood volume increases cardiac output and central venous pressure. The volume of blood displaced into the thoracic cavity is proportional to the depth of the dive. The thoracic vessels become engorged and compress the surrounding airspace, further decreasing lung volume via alveolar compression, increasing the blood volume available to participate in alveolar gas exchange, which improves the body’s adaptability to the underwater environment. Interestingly, with training, tolerance of hypoxia and hypercapnia can be prolonged as the body adapts.
With this understanding, we can better understand the physiology of drowning. After prolonged breath-holding, the oxygen reserve becomes depleted. This lack of oxygenation, along with the inability to successfully carry out respiratory drive, can lead to unconsciousness and possibly death. When a drowning person can no longer keep his/her airway clear, the water is either spat out or swallowed, either of which can induce laryngospasm and lead to further aspiration followed by worsening hypoxemia and eventually unconsciousness. Hypoxic cardiac arrest ensues after a period of bradycardia and pulseless electrical activity. This entire process occurs within seconds to a few minutes.
Hyperventilation before breath-holding lowers the arterial partial pressure of CO2 and delays the re-emergence of the stimulus to breathe. Hyperventilation also modestly increases the alveolar O2 concentration, thus increasing arterial pO2. This increase, however, does not safely compensate for the O2 deficiency that occurs toward the end of breath-holding limits. Urges to breathe normally happen when the pCO2 is 45 to 60 mm Hg. Receptors sense CO2 in the medulla, which fire synapses to the frontal cortex to cause the irresistible impulse to inspire. Hyperventilation before a breath-hold decreases pre-dive CO2 levels significantly. Thus, the subsequent CO2 rise during submersion may not be sufficient to trigger the impulse to breathe before the loss of consciousness secondary to hypoxemia. Additionally, arterial oxygen rapidly drops at the tail end of the oxygen curve; this is a dangerous combination that can lead to rapid unconsciousness before the breath holder has time to come to the surface for air.
A similar phenomenon called ascent blackout can occur in deep-water diving when the loss of consciousness occurs merely meters below the surface. In breath-hold diving, the risk of hypoxic blackouts is increased during the ascent as arterial oxygen saturation drops to less than the threshold for consciousness. This threshold is 25 to 30 mm Hg. Unconsciousness during ascent results from reduced arterial pO2 resulting from metabolic consumption of O2, combining with decreasing ambient pressure during ascent. The reduced pressure enables ‘stealing’ of blood back to the periphery. As the decreased partial pressure in the alveoli allows for them to expand from their compressed underwater state, the blood available for gas exchange becomes vastly reduced. This combination of a rapid drop in gas exchange, peripheral redistribution of blood, and a depleted pO2 at the end of a breath-hold leads to an increased risk of unconsciousness (ascent blackout). Ascent blackout falls within the category of hypoxic and/or shallow water blackout.
History and Physical
The assessment of a patient who is found unconscious in the water requires rapid intervention. Remove the person from the water and get them safely on shore or in the boat. The most critical step is mouth-to-mouth ventilation, which should begin as soon as the patient’s airway can open, and the rescuer is safe. Prompt initiation of rescue breathing is associated with an increased likelihood of survival. Once resuscitation efforts are underway, activate emergency medical services (EMS) immediately. The patient will require transport to the closest medical facility if/when stabilized. Have someone else locate any medical equipment that may be nearby. History and physical will be brief in this situation. If possible, get a prompt situational history from bystanders (first-person observers, lifeguards, swimming instructors, or relatives/companions). This information gathering should occur as one physically assesses the patient. This information may help form diagnostic and treatment decisions. Further history is obtainable when/if the patient stabilizes.
The physical exam will also be brief. Once the patient is out of the water, rapidly assess the patient’s level of consciousness as you initiate evaluation with the BLS/ACLS protocol using CAB: circulation, airway, and breathing. The resuscitation efforts should start even as one examines the patient.
There will not be sufficient time for more detailed evaluation or studies in the setting of a water emergency. Proceed with resuscitation efforts.
Treatment / Management
Respond promptly to restore oxygenation, ventilation, and perfusion as quickly as possible. Basic and advanced life support protocols: Assess responsiveness as above. Rescue breaths should be initiated first and foremost as above. Then check for a pulse. If the patient has a pulse, reassess the airway and breathing portion of the algorithm, which involves the jaw thrust or tilt-chin (if head injury) maneuver. Provide ten breaths per minute if the patient is not spontaneously breathing and recheck pulses every two minutes.
If no pulse is present, initiate CPR for five cycles (about 2 min) starting with chest compressions, 30 compressions then two rescue breaths in the cycle. Initiate advanced life support early, which includes advanced airway and use of an automated AED as equipment availability permits. Regurgitation of stomach contents is the most common complication during drowning resuscitation. Active efforts to expel water from the airway with abdominal thrusts or head down positioning should be avoided as they delay ventilation and increase the risk of vomiting and mortality. All water rescue patients who lost consciousness, even if brief, should undergo hospital evaluation. Most patients who require resuscitation efforts will require ICU hospital admission and possibly mechanical ventilation.
The unexpected demise of a swimmer can have multiple causes. When evaluating a patient who has lost consciousness in the water, it is crucial to consider all possible causes to intervene effectively. Hypoxic blackout (unconsciousness due to hypoxia) is one of the most common underlying causes of morbidity and mortality in the water. Other differentials to consider are preexistent organic cardiac disease (coronary artery disease or cardiomyopathy), preexistent cardiac arrhythmias, and epilepsy. All of these conditions undergo exacerbation in the oxygen-starved apneic environment of being underwater. Some data has shown that a prolonged QT can also contribute to an increased risk of underwater unconsciousness. Prolonged QT is inducable by medications, metabolic disturbances (hypokalemia), or even alcohol. In general, with cardiac-related drowning, the swimmer is usually observed to have stopped swimming on the surface and may demonstrate unusual non-sustained behavior. On the other hand, in a hypoxic blackout, the swimmer may be seen hyperventilating before going underwater, which is followed by failure to surface. Considering these differentials will increase the efficacy of rescue efforts.
The outcome of a hypoxic blackout is multifactorial. The most significant factor is the duration of hypoxia. The longer the patient is hypoxic, the poorer the outcome. A mediating factor is the baseline fitness and health status of the patient before the incident. The other factor that influences outcomes is the timeliness and quality of rescue efforts. This depends on the training and skill of those providing resuscitation, the availability of medical supplies, and the proximity of a medical facility to continue stabilization and workup following initial resuscitation. All of these variables make it challenging to concretely predict how an individual will fare after a hypoxic blackout event. If conditions are optimized, and there is only a minimal duration of hypoxia, coupled with rapid and effective resuscitation followed by prompt medical evaluation and workup, patients will fare well. Patients who have spontaneous circulation and breathing at the time of hospital arrival usually have a successful recovery. However, if any of these parameters are missing, the event will likely be fatal, or the patient will suffer long-term functional neurological deficits. Patients were able to return home without adverse sequelae in 95% of drowning cases in which CPR was successful in restoring conscious.
If a patient is successfully resuscitated after a hypoxic blackout, there are four main complications with which to be concerned.
Respiratory complications are the most common following a drowning event. Patients are usually managed on a ventilator for about 48 hours. This period allows for surfactant regeneration as surfactant is often destroyed and washed out by the presence of water in the alveoli. Weaning from ventilation earlier than 48 hours may increase the risk of pulmonary edema requiring reintubation. Respiratory management is similar to that of patients with acute respiratory distress syndrome (ARDS).
Pneumonia is not commonly a result of aspirated water during a drowning event. Pulmonary edema secondary to aspirated water from the drowning incident is commonly misdiagnosed as pneumonia in the short-term. Pools, rivers, and beaches generally do not have sufficient bacteria to promote pneumonia in the short-term post-drowning period of 48 to 72 hours. Aspirated water is usually a small volume, and it rapidly absorbs into the central circulation. Prophylactic antibiotics are not recommended immediately following drowning and are not associated with a reduction in the prevalence of pneumonia or decreased mortality.
Pulmonary edema should improve within 3 to 4 days following a drowning incident. If there are new or persistent pulmonary infiltrates in the setting of fever and sustained or worsening leukocytosis, this is a sign of developing pneumonia, and antibiotic treatment should be initiated. A diagnosis of pneumonia following drowning is most often secondary to aspiration of stomach contents vomited during resuscitation efforts. Ventilator-associated pneumonia risk is also increased (34% to 52%) on day 3 to 4 of hospitalization
With this in mind, a low threshold for initiating empiric antimicrobials is reasonable in patients who have evidence of systemic toxicity or hemodynamic instability without a clear source. This threshold may be slightly lower if the drowning occurred in a contaminated (chemical or microbial) body of water; however, specific treatment guidelines based on water type remain unestablished.
Cardiac complications can also arise after drowning incidents. Decreased cardiac output is common immediately after a severe drowning event. This reduction in blood pressure has the potential to lead to hypotension. Initial management involves rapid crystalloid infusion, maintaining euthermia, and improved oxygenation. If hypotension is refractive to these interventions, initiate pressors. When crystalloid resuscitation has failed, further assessment of cardiac function and cardiac output with an echocardiogram is the recommendation to guide management further. Although there is no guidance on the use of Swan-Ganz catheter in drowning patients, consider this as an option as one would with any other hypotensive ICU patient requiring pressors.
Prolonged hypoxia can lead to cerebral hypoxia and long-term cerebral tissue damage. Most late-term morbidity and mortality are of neurological etiology. The key to prevent this is aggressive oxygenation during and after resuscitation. Patients who remain unresponsive after successful CPR should undergo frequent neurological function reevaluation.
Lastly, metabolic acidosis occurs in 70% of hospital patients following drowning. It is attributed to lactic acidosis resulting from widespread tissue hypoxia. The degree of acidosis can serve as a marker of the severity of the hypoxemia incurred. Downstream consequences include acute renal impairment and multisystem organ failure. Manage with appropriate ventilator support and consider bicarbonate repletion when pH is less than 7.2.
Deterrence and Patient Education
The most effective way to reduce drowning incidence is to prevent it. 80% to 90% of all drownings are preventable. It has been noted that qualified special dive operators have previously recommended for trainees to attempt hyperventilation to improve breath-holding abilities, which is false. The diving and medical communities must play a role to dispel these false claims and inform the public that doing so actually decreases breath-holding capability and safety. The American Red Cross, U.S.A. Swimming, and the YMCA have released a joint press release to increase awareness of the risks of hyperventilation before submersion breath-holding; this is a crucial step in increasing awareness.
Additionally, at public pools or other locations with lifeguards, prevention requires prompt lifeguard recognition of and response to dangerous and/or emergent situations such as hyperventilation. If lifeguards are vigilant, they can significantly reduce the incidence of death from drowning. However, the mere presence of a lifeguard without vigilance can give pool patrons a false sense of security and contribute to catastrophes. Another factor that can play a role is the maintenance of swimming facilities. Water should ideally be clear for visualization to the bottom of the water, the pH requires close monitoring, and hazards minimized. In public settings, it is advisable to have quick access to rescue equipment, continuous lifeguard surveillance, and phone access within the proximity of the pool. The key is the prevention of the need for rescue. If rescue efforts become necessary, prompt retrieval of drowning swimmers provides the only chance of success with resuscitation.
Enhancing Healthcare Team Outcomes
The key to preventing hypoxic blackout is prevention through education and correction of risky behaviors; this begins with the general public, especially those who swim or are supervising swimmers. Such individuals include parents, teachers, public community health nurses, swim coaches, SCUBA diving instructors, and military trainers. Secondly, during a resuscitation effort, it requires a rapid response that ideally has one resuscitation leader to delegate tasks to others, which will optimize efficiency and efficacy. If resuscitation is successful, patient care relies on an interprofessional team comprised of emergency medical services (EMS) personnel, emergency medical personnel, and intensive care staff to treat the aftermath of a drowning incident. Prehospital and flight nurses are often involved in care. If neurological deficits remain, the patient will require neurological rehabilitation. Specialty care nurses in neuroscience and rehabilitation care for these patients and coordinate care by allied health personnel. [Level 5]