Dry drowning
Dry drowning is when a person's lungs become unable to extract oxygen from the air, due primarily to:
- Muscular paralysis
- Puncture wound to the torso (affecting ability of diaphragm to create respiratory movement)
- Changes to the oxygen-absorbing tissues
- Persistence of laryngospasm when immersed in fluid
- Breathing for too long any gas other than oxygen that does not kill the patient on its own. (e.g. Helium)
The person may effectively drown without any sort of fluid. In cases of dry drowning in which the victim was immersed, very little fluid is aspirated into the lungs. The laryngospasm reflex essentially causes asphyxiation and neurogenic pulmonary edema (oedema).
Dry drowning can occur clinically, or due to illness or accident, or be deliberately (and repeatedly) induced in torture (waterboarding).
Pathophysiology
The pathophysiology of this form of pulmonary edema is multifactorial.
In normal breathing, the diaphragm contracts, causing it to drop and increase the air volume of the lungs (lungs are above the diaphragm). This increase causes a partial vacuum in the lungs.
When water or other foreign bodies are inhaled, laryngospasm occurs and the person's larynx spasms shut. As a result, the partial vacuum created by contracting the diaphragm cannot be filled by the inrush of air into the lungs, and the vacuum persists. In an attempt to force air in through the spasmed larynx, the person may breathe deeper and more labored, but this only increases the partial vacuum inside the chest.
The heart continues to beat normally during this time, and blood continues to circulate, though pulmonary oxygen and carbon dioxide gas exchange is markedly reduced. The volume of blood in the pulmonary circulation increases, by pulling in more blood from the abdomen, head, arms and legs - abnormally large volumes of this blood enter the pulmonary circulation via the superior and inferior vena cavae (great veins) in response to the persistent partial vacuum. From the vena cavae, the increased blood volume flows through the right atrium and into the right ventricle. The blood volume is great enough to stretch out the ventricle, similar to water entering a balloon.
The ventricle typically responds to this increased volume of blood by contracting and pumping with increased strength - a phenomenon known as the Frank-Starling mechanism. On being ejected from the right ventricle, the blood is forced into the pulmonary artery and thence to the pulmonary circulation.
In the lungs, the nature of the vasculature changes. The vessels which carry deoxygenated blood (the pulmonary arteries) to the lungs become extremely narrow - narrow enough that red blood cells have to pass through in single file. The walls of the vasculature also become extremely thin to allow oxygen to enter the red blood cells and carbon dioxide to leave. In the case of dry drowning, however, there is no oxygen available in the lungs; there is only a partial vacuum. This partial vacuum draws some of the fluid from the vasculature and into the airspaces of the lungs, creating pulmonary edema, and the patient is now drowning in their own fluids.
At the same time, the sympathetic nervous system responds to the emergency of the closed larynx. Among other things, it constricts much of the body's vasculature. This vasoconstriction increases the blood pressure against which the left ventricle must pump, and may cause enough backpressure to ripple back through the left ventricle, into the left atrium, and into the pulmonary vasculature. This additional pressure on the blood in the lungs' blood vessels exacerbates the edema described above.
Additionally, the actions of the sympathetic nervous system can damage the lungs' vasculature, allowing even more fluid to escape into the lungs' airspaces.
See also
- Splitting of S2 (heart sounds) in which the normal changing intrathoracic (inside the chest) pressures of breathing influence the timing of events in the heart.
- Circulatory system