In the early 1900s many animal experiments conducted both in Europe and North America demonstrated that if an animal was immersed and drowned in water containing chemical traces or dyes, these would spread through the tracheo-bronchial tree to the alveolar surfaces. In the case of fresh water, this was also absorbed into the bloodstream.
A consistent fall in arterial oxygen content was observed, followed by a rise in arterial carbon dioxide and sometimes cardiac arrhythmias.
Swann and his colleagues from Texas3,4, in a series of accurate but misleading experiments, flooded animals’ lungs with fresh or salt water and demonstrated the significant differences between the two, attributable to osmotic pressures. In both cases, flooding of the lungs produced a reduction in PaO2 and pH, with a rise in the arterial partial pressure of carbon dioxide (PaCO2).
Because fresh water was osmotically much weaker than blood, it moved into the bloodstream and produced haemodilution – reducing blood concentrations of proteins, sodium, chloride and so forth. The subsequent reduction in the osmotic pressure of the blood caused haemolysis and a liberation of both haemoglobin and potassium, with resultant metabolic and renal complications, aggravated by hypoxia. Deaths were often cardiac and resulted from ventricular fibrillation.
When, however, the animals’ lungs were flooded with sea water – which has a higher osmotic concentration than blood – water was drawn from the bloodstream into the lungs, thereby producing pulmonary oedema and haemoconcentration. This caused an increase in the haematocrit, blood proteins and electrolytes.
For many years physicians attempted to correct these presumed electrolyte, metabolic and cardiac abnormalities in human drownings, but their cases did not replicate the animal model (Figure 21.1).
Earlier workers had shown that in dogs that drowned, there were still large volumes of air in the lungs, as there are in humans.
Colebatch and Halmagyi5, working in Australia in 1961, produced an animal model more relevant to the clinical management of patients, by aspiration of only 1 to 3 ml/kg body weight. By using these smaller volumes, these researchers demonstrated the sudden arterial hypoxia, not directly proportional to the amount of fluid inhaled. Pulmonary hypertension, vagal inhibition and reduced compliance were also observed. These investigators demonstrated that the weight of the lungs increased threefold the weight of the instilled sea water. Sea water aspiration usually caused significant pulmonary oedema, but aspirated fresh water was often absorbed from the lungs within 2 to 3 minutes.
Subsequent animal experiments by Modell6 and others, using intermediate volumes of aspirant, demonstrated that shunting of blood was the predominant cause of persistent arterial hypoxaemia, as a result of perfusion of blood through non-ventilated areas of lung. Destruction of lung surfactant in fresh water installation also resulted in alveolar wall damage and pulmonary oedema.