Usually, when blood oxygen levels fall because of inflammation in the lungs, the waste gas of carbon dioxide rises. It is this rise in the level of uncleared carbon dioxide that produces the distressing symptom of ‘air hunger’. Even when levels of oxygen in the blood of the COVID patients (as measured by an oxygen saturation monitor) dropped from the usual SaO2 of 95-99% to a level of around 80% (which would normally be considered life-threatening), some people with the virus seemed comfortable, and were not gasping for air. The phenomena became known as ‘happy hypoxia’.
The physiology of this happy hypoxia can be explained by noting the following: although the COVID patients’ lungs were so inflamed that oxygen could not be extracted into the blood, and even though they were clearly hypoxic, there was still good clearance and elimination of the waste gas, carbon dioxide.
Happy hypoxia has also been associated with deaths resulting from lung infections and pneumonia. When William Osler, one of the founders of the Johns Hopkins Hospital, described in 1892, a death from pneumonia as ‘the old person’s friend’, it was happy hypoxia that he was referring to (See the COVID-19 Chapter in this book). The goal, therefore, is to ensure the hypoxic death will be a happy one. Happy hypoxia depends on cerebral oxygen levels dropping to lethal levels, while avoiding any increase in carbon dioxide (with the associated distressing symptoms).
The Cardiac Switch
The ischemic hypoxia that is brought about by interfering with the heart is rarely peaceful. A heart attack (AMI), for example, leads to the heart being suddenly unable to pump blood and is often accompanied by severe chest pain. Some cardiotoxic drugs can also stop the heart and cause ischaemic hypoxia.