The tremendous impact of hypoxia on any critical organ, namely the brain and the heart, are well known, at least because of their obvious result. The question asked by many: “For how long can the patient tolerate apnoea?” cannot be answered with certainty for any given patient. The long list of possible problems that may arise during the transport of O2 from the anesthetic circuit to the very last cell of the human organism precludes any possibility of precise calculation. Hypoxia of critical tissues (the brain and the heart) has deleterious pathophysiologic effects on them. The abrupt and intense rise in systemic and pulmonary blood pressure combined with tachycardia, adds an excessive work load (and so an extra ATP deficit) to the myocardium. Thus it can increase morbidity from myocardial ischemia, rupture of aneurysms in the systemic and cerebral circulation, acute heart failure, pulmonary hypertension and failure of the right heart. The severity of these consequences may be augmented by the cellular effects of hypoxia like disruption of cell structure and sensitization to arrhythmias. The Central Nervous System accepts an excessive work load too. It has to fulfill auto regulation requirements: regulation of the perfusion pressure to the brain while systemic blood pressure presents with at least biphasic fluctuation during hypoxia and apnoea, manage the responses of reflex mechanisms, conservation of electrical activity in order to continue its central role as command center and sympathetic and parasympathetic outflow to the heart and other organs in gravely hypoxic conditions, over viewing hormonal and catecholamine discharge etc. All these responsibilities should have to be concluded in a milieu of strenuous efforts to conserve or replace ATP and get rid of the products of anaerobic metabolism. This is obviously a titanic work.
It could be more devastating, if all these procedures should be completed in subjects who may already suffer from serious derangements of their physiology like systemic hypertension, coronary artery disease, carotid artery disease, chronic pulmonary disease, diabetes mellitus, intracranial hypertension and cerebral oedema. And it becomes worse, when hypoxia and apnoea ensues in patients, who are trying to conserve homeostasis while suffering from multiple trauma, sepsis or acute respiratory insufficiency. Finally, possibly under the systemic effects of anesthetic agents, cells of critical organs respond to protracted hypoxia with programmed cell death after stressful combat to retain structural and operational integrity.
Some anesthetic agents are considered to have protective effects to the brain and the heart against ischemic – reperfusion injury. Unfortunately, we are lacking almost any data on their possible positive or negative effect on hypoxemic hypoxia during apnoea.
A few agents have been discovered that could offer in time protection against hypoxia. Even less would be applicable in every day clinical practice, as the cases of difficult airway come up unexpectantly. So what should be done?
Apparently we should be able to understand and learn any critical information that has been discovered about the systemic effects of hypoxia and apnoea. And most important, we should make any effort to continuously apply structured and well organized procedures of administering anesthesia in order to minimize the rate of hypoxic accidents and their effect on human tissues that are obviously completely dependant on oxygen.