Drowning is labeled by the World Health Organization as one of the leading causes of death, with 375,000 reported annual cases, although the actual figures might be four to five times greater.
Drowning can occur due to immersion (when we enter the water up to our necks or when we swim) or submersion (when our airways are in the water, as when diving). Let’s look at each of these and their individual factors in more detail.
The cause of drowning in this case has to do with temperature, either too high or too low. Most cases occur below the thermoneutral point of ~35C but some occur above it, in hot water immersion like in hot baths or swimming in hot water.
We usually thermoregulate by sweating because sweat evaporates and this phase change removes heat from the skin thereby cooling us down.
In hot water immersion though, the ambient air is too humid so our sweat does not evaporate efficiently enough and what sweat we
produce under water does not evaporate at all and thus does not help is cooling us down.
Our body detects the higher skin temperature and sends signals which cause, among other things, vasodilation, which raises the heart rate.
This in turn might trigger arrhythmias, which, coupled with the dehydration and increased blood viscosity can prove fatal.
Hyperthermia can also prove fatal in competitive swimming (see the Fran Crippen case) or diving in warm water.
Being immersed in cold water can shunt your breathing reflex. This response, cold shock, is evoked by skin cooling and starts in water of ~25C,
peaking at ~15 - 10C. Below 5C, we sense intense cold pain. Cold receptors respond to the sudden decrease in skin temperature resulting from
immersion in cold water with a dynamic response that evokes gasping, hyperventilation, increased cardiac output, peripheral vasoconstriction,
and hypertension. This in turn increases the metabolic rate which decreases breath hold time, something that is crucial because it can lead to
aspiration (breathing in water) and drowning. The incidence of arrhythmias can also increase from 2% to 82% when we immerse our face in the
water and hold our breaths. Superficial tissue cooling can lead to fatigue and a muscular dysfunction akin to peripheral paralysis, which can
occur before our core temperature falls below 35C.
Hypothermia, as you can imagine, is even more dangerous. The progressive signs and symptoms are shivering (36°C), confusion, disorientation,
introversion (35°C), amnesia (34°C), cardiac arrhythmias (33°C), clouding of consciousness (33-30°C), Loss Of Consciousness (30°C), Ventricular
Fibrillation (28°C), and death (25°C). There is however great individual variability in these symptoms, so for instance someone who is shivering
might have a normal core temperature and someone who isn’t might have a dangerously low one.
Panic or fear of drowning can lead to actual drowning because the swimmer (80% of triathlete deaths occur during the swim phase) or diver may
be confronted with new and unexpected conditions like colder water, currents, low visibility, entanglement etc which can lead to a mental and
physical incapacitation. We might also fear the onset of a previous condition, such as a cardiac problem, which can lead to sensory deprivation,
illusions, irrational logic and cognition etc., thereby limiting our problem solving abilities.
It is possible that a high activation of the sympathetic nervous system in this case can lead to loss of muscle strength and hyper-arousal.
It has been reported that the diving response, an autonomic response many diving animals have, may have a role in protecting us from drowning by its selective peripheral vasoconstriction, bradycardia etc. Nevertheless, its role is probably not that important as a protective measure. Rapid cooling of the brain brought on by colder blood and cooling of the heart by aspiration of cold water are potentially more important protective factors. Breath holding in cold water can cause an “autonomic conflict”, wherein the sympathetic and parasympathetic nervous systems are simultaneously stimulated, sending conflicting signals to the heart, which can lead to an arrhythmia. These don’t commonly lead to drowning though and would have to be combined with other pre-existing conditions to prove fatal.
This is an effect where the laryngeal muscles may reflexively close to protect the laryngeal tree from foreign objects. This may prevent the entrance of water into the lungs in a case of drowning but there isn’t substantial research to back this claim.
When we breathe in water, this reaches and damages the alveoli. The increase of surface tension can lead to a lower perfusion of gases, which can then lead to blood bypassing the lungs, worsening the patient’s condition. Seawater aspiration seems to be worse as it draws liquid from the plasma into the alveoli and causes further damage. In both fresh and sea water aspiration though, plasma enters the alveoli, incapacitating normal gas exchange. This can also generate foam with further decreases pulmonary efficiency.
Swallowing water during the drowning process may increase the risk of vomiting, spontaneously or during resuscitation, eventually leading to aspiration of gastric content. Swallowing water may also contribute to life-threatening electrolyte disorders. But overall, there doesn’t seem to be a strong correlation between swallowing water and drowning and it is also very difficult to study if drowning victims had ingested a significant - or any - amount of water.
Emesis, or throwing up, is another factor that doesn’t bear a conclusive connection to drowning per se. What is interesting is that besides “normal” factors, one of which could be ingestion of sea water, emesis can also be triggered by a chemoreceptor zone detecting stimulants like hypoxia and ketoacidosis. The actual problem is that if we throw up in the water while panicking, gastric contents can be aspirated, leading to infection and eventual drowning.
Ingestion or aspiration of water can also potentially lead to electrolyte disorders in the body, which can lead to a ventricular fibrillation or hypoxemia and metabolic acidosis via pulmonary oedema. Research suggests though that this only occurs in exceptional cases.
The brain’s response to drowning is most likely an interaction between hypoxemia, submersion in cold water, cold shock and aspiration of water. Loss of consciousness is a critical event in drowning and is often attributed to asphyxia following submersion, loss of pulmonary oxygen uptake, brain energy failure, and deterioration of brain function. Hypoxemia in normothermic healthy humans causes an initial cerebral vasodilatory response to preserve oxygen delivery. As immersion causes hyperventilation which can cause problems, it seems important to train to suppress it in emergency situations. In the end though, a sustained decrease in oxygen delivery will eventually cause cell and neuron death. Many survived drowning victims sustain permanent brain damage.
Now that we understand the physiology of drowning a little bit better, we can find ways to prevent it or give ourselves a fighting chance if we are ever in such an emergency scenario. Further research is definitely needed to understand the various mechanisms in more depth and to potentially prevent or treat drowning.
You can read the full paper here.