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Special Report: Do All Drowning Victims Drown?

Morgan, Paddy, J., MD; Tipton, Michael, J., PhD

doi: 10.1097/01.EEM.0000535017.40449.29
Special Report

Dr. Morgan is a postgraduate student in the Extreme Environments Laboratory in the Department of Sport and Exercise Science at the University of Portsmouth in the United Kingdom and an anesthetist at Southmead Hospital, North Bristol NHS Trust, Bristol, UK. Follow him on Twitter @drpaddymorgan. Dr. Tipton is a professor of human and applied physiology, also in the Extreme Environments Laboratory. Follow him on Twitter @ProfMikeTipton.





It may be that many immersion deaths attributed to drowning are actually caused by cardiac problems, casting a different light on how to diagnose and treat these conditions. Deaths from immersion represent the third leading cause of unintentional injury death worldwide, according to the World Health Organization (, and drowning is a common but not the only cause of these deaths.

Instead, cardiac problems are the likely cause of some immersion deaths, but these are underestimated because the incapacitation caused by cardiac conditions often results in agonal gasping and the aspiration of water, which leads to a drowning diagnosis. That is complicated further because the fatal cardiac arrhythmias experienced in immersion are not detectable post-mortem.

The incidence of cardiac arrhythmias in the initial minute of immersion is one to three percent, but that number rises to 81 percent if the face is immersed and maximum breath-holding is involved. (J Appl Physiol 2006;100[6]:2057.) An accidental immersion is, in fact, likely to involve face immersion and breath-holding, but these also occur even in some non-accidental scenarios, like the somewhat chaotic mass start of a triathlon. A case series of U.S. Triathlon participant deaths found that 67 percent occurred in the swim phase, and these were thought to be cardiac-related. (USA Triathlon Fatality Incidents Study. 2012.

Complex interplay between the two arms of the autonomic nervous system occurs in these situations, with multiple combinations of variables (relative magnitudes of sympathetic and parasympathetic stimuli, constant or pulsatile in nature) being applied to myocardial tissue that has a variable response according to an individual's genetics, medications that induce changes to repolarization, and metabolic status at a cellular level (acidosis, hypoxia, hypercapnia). The result may be a fatal arrhythmia or a simple ectopic beat. This has been termed autonomic conflict (AC), defined as the strong and coincidental activation of the two limbs of the autonomic nervous system via the cold shock response or the exercise (sympathetic stimuli) and the diving response (parasympathetic stimuli). (J Physiol 2012;590[14]:3219.)

The cold shock response occurs when cold thermoreceptors are rapidly stimulated during immersion, and that triggers profound sympathetic activation. (Clin Sci [Lond] 1989;77[6]:581.) It is characterized by a rapid and large respiratory gasp, uncontrollable hyperventilation, peripheral vasoconstriction, hypertension, and tachycardia. The parasympathetic component is activated by stimulation of receptors in the distribution of the ophthalmic and maxillary divisions of the trigeminal nerve during submersion (head under) or wave splash resulting in the dive reflex.

This features a profound sinus bradycardia, breath-hold, and peripheral vasoconstriction. (J Physiol 2012;590[14]:3219.) During the breath-hold, stretch receptors of the lungs will contribute an additional neural component to the bradycardia. (Acta Physiol Scand 1968;73[1]:139.) The bradycardia will also have mechanical contributions from the cephalic redistribution of blood volume due to the hydrostatic pressure of water on the body and intrathoracic pressure changes at the break of breath-hold. (Pflugers Arch 1978;374[2]:115.)

The anxiety and stress associated with an unexpected immersion or the mass start or congested turns of a triathlon are, along with anger, profound sympathetic stimulants. Equally, the enforced, potentially prolonged breath-hold associated with unexpected immersions or the submersion of the head and water entering the nasopharynx during the congested periods of a triathlon swim will produce profound parasympathetic stimulation. These conditions do not occur in training, making the problems more profound in competition because the swimmers have never experienced them before. (Br J Sports Med 2014;48[15]:1134.)

Strong associations exist between fatal cardiac arrhythmias and the stress of a “drowning” event. The inherited long QT syndrome (LQTS) type 1 has been described as a trigger for torsades de pointes associated with swimming, and sudden death has been described in LQTS type 2 when a sudden surge of sympathetic activity occurs on a background of high parasympathetic tone. (Mayo Clin Proc 1999;74[11]:1088; Circulation 2001;103[1]:89.) Recent work demonstrates that AC is a pro-arrhythmic stimulus in LQTS. (J Mol Cell Cardiol 2018;116:145.) Combined adrenergic and parasympathetic stimulation has a complex relationship with arrhythmogenicity, with differences in the effects of steady-state adrenergic activation vs. sudden adrenergic stress. Specifically, sudden adrenergic stress appears to be the more arrhythmogenic.

Understanding AC is important for prevention, diagnosis, and treatment. Knowledge of AC enables those at risk to be screened for long QT syndrome; open water swims can have intelligent courses and rescue provision at high-risk points. (J Mol Cell Cardiol 2018;116:145.) AC also explains some deaths associated with immersion that are not explained by drowning-induced hypoxic cardiac arrest. It is possible that an immersion victim may be in cardiac arrest as a result of arrhythmia and that the arrhythmia may be torsade de pointes.

Appropriate treatment and the prognosis may be better based on cardiac arrest of cardiogenic origin, with near-immediate cessation of cerebral blood flow, rather than the progressive hypoxia leading to hypoxic cardiac arrest seen in drowning, where the hypoxemia occurring before cessation of cerebral blood flow exacerbates the neuronal injury post-return of spontaneous circulation. (Resuscitation 1997;35[1]:41.) Theory and increasing evidence suggest that AC is not confined to immersion, and may act as an arrhythmogenic factor in other situations. (High Alt Med Biol 2014;15[3]:356.)

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