You have asked some very good questions, particularly the last two. I think we are entering uncharted “waters” medically when dealing with deep and prolonged diver blackouts.
What happens to the heart and brain after a person blacks out from hypoxia? It is the physiology of asphyxia, which is most commonly due to choking, suffocation, entering oxygen-depleted spaces, or loss of aircraft cabin pressure. There is actually very little quality data from humans. You cannot study this problem very well for obvious ethical reasons. You will find partial answers in three places: altitude chamber blackouts, dying patients taken off life support, and freedivers. Free diving is a form of controlled asphyxia. There are some animal experiments conducted to simulate hypoxic cardiac arrests in infants and children. Here is some of what is known.
LIFE SUPPORT TERMINATION
Person chokes on food and collapses after 1 or 2 minutes (rough time frame for loss of consciousness after complete arrest of breathing with normal air volume in lungs). Patient arrives in ER after long period of CPR. We find an obstructed airway and remove a chunk of food or vomit. Vigorous CPR, airway management and oxygen ventilation, a few doses of epinephrine and atropine restore a strong pulse and we get a nice return of blood pressure (usually just before we are about to give up and pronounce). The patient goes from looking dusky and blue to being pink with great circulation, a successful and somewhat unexpected resuscitation. But unfortunately pupils are dilated, there are no reflexes, and the brain is dead from prolonged anoxia. This person is in a vegetative coma from which meaningful recovery is not possible. I’ve had two cases like this in past year alone.
What happens next is insightful as to what might happen to a diver following black out. After discussion with family and various consultations, a decision is made to withdraw life support. Sedation is given and the ventilator is turned off. Heart rate begins to drop after a minute or two 60… 50… 40... 30. Some people drop faster than others. There are occasional extra random beats on the monitor. The sinus node (pacemaker) stops firing (sinus arrest) and slower beats originate from the lower conduction fibres (junctional rhythm) then finally from the ventricles alone (escape beats). This can take 5 minutes or longer. Blood pressure drops as the anoxic heart muscle weakens, and peripheral pulses are lost. The weak ventricles may fibrillate, but this is actually uncommon due to myocyte electrical uncoupling and loss of cellular energy. Defibrillation shocks would be ineffective. Finally there are only very weak electrical impulses every few seconds that have vanishing influence on muscle contraction. This is called pulseless electrical activity (PEA). Finally the heart stops (asystole). The brain is too hypoxic to drive spontaneous breathing. Respiratory drive is essentially lost below arterial PaO2 of about 10 mmHg, whereas consciousness is normally lost below about 25 mmHg. A few small spontaneous gasps (agonal breaths) are seen, triggered by uncoupling of neural oscillators in the brainstem, the last vestiges of a primitive survival response that is ineffective. Death is formally pronounced, although different parts of the body die at different rates.
This is of interest to diving because it is likely the same course of events that can be expected with a seriously hypoxic diver who is not resuscitated, or suffers from excessive delay. Breathing stops, same as having the machine turned off. Brain arrest (black out) followed by respiratory arrest (loss of drive) followed by gradual progression to cardiac arrest (loss of circulation).
How much delay is tolerable after initial BO? How much oxygen debt can your cells get into before things become irreversible (immediate cell death or triggering of delayed apoptosis) despite life support measures? At what point can circulation be restored before the brain is irreversibly damaged and the heart becomes too weak to revive with ventilation or CPR. That is the key question. The exact timing is not known and is really a statistical distribution.
The classic “four-minute rule” goes back to an article published in 1956 based on 132 patients who had cardiac arrest during surgery at a U.S. hospital. Of these, 42 percent survived if revived in less than 4 minutes, and 7 percent if over 4 minutes. A rather arbitrary cut off based on a small sample. This is not very representative study of arrest and resuscitation in the real world. Animal studies demonstrate damage to the most vulnerable areas of cortex and hippocampus (higher centres) as early as 3 minutes after asphyxia, but other lower centres can survive remarkably long periods without oxygen. More recent human data from various large studies show a drop in survival of roughly 5 to 10 percent for each minute delay after cardiac (not respiratory) arrest, but say nothing of neurological outcomes. Generally adults tend to die from cardiac arrest due to arrhythmias like ventricular fibrillation, whereas children die from respiratory arrest causing subsequent anoxic cardiac arrest. Much less data is available on survival after respiratory arrest, which is most relevant to apnea-induced BO.
Case reports of diver blackouts might shed some light on the process, and maybe allow us to prepare better for rescue situations. It is worth asking if we can use specific observations of diver BO to calibrate physiological expectations? We should at least take a look.
STATIC APNEA
Dry surface (not depth) apnea studies show slow increase in heart rate with progressive hypoxia (increased sympathetic drive to maintain cerebral oxygen delivery), followed by drop in HR possibly due to the myocardium itself becoming hypoxic, or maybe from increasing vagal tone that kicks in as a survival response. Just prior to BO there may be an abrupt control instability where HR suddenly drops (sympathetic withdrawal), possibly similar to strong competing reflex instabilities causing vasovagal syncope (common faint). This phenomenon has been reported in various studies. It is also seen as terminal response in lab animal asphyxia. There is complex interplay between autonomic nervous system control and direct myocardial response to hypoxia. Incompletely studied and not well understood.
DIVER BLACKOUT
Bahamas 2009, diver blacks out at 20 metres on ascent from 90 metres. Safety diver covers airway and carries to surface. No response, deeply unconscious. No spontaneous breathing seen. Removed from water to deck with 42 seconds passing from BO time until manual oxygen ventilation begins. Carotid pulse is present, weak but reasonable rate, meaning systolic pressure is likely at least 60 mmHg. CPR is not necessary as diver responds well to oxygen ventilation and begins spontaneous breathing. Awake but dazed after one minute, fully alert and sitting up after two minutes looking well.
Dominican 2002, Audrey Mestre reaches 170 metres then blacks out at 120 metres 3:40 minutes into the dive. Tragic story well known. High negative chest pressure sucks water into the lungs. Laryngospasm if present would not likely prevent this, and would relax with further hypoxia. Dive profile and times documented with precision thanks to data recorder. Witness reports pulse present after surfacing at 8:38 minutes. Seems very remarkable. Agonal breaths reported. This suggests perhaps marginal circulation is present, but consequences of prolonged brain anoxia tragically apparent. Oxygen stores in brain and myocardium are long since depleted.
The heart can shift from fatty acid metabolism using oxygen over to glycogen utilization in the absence of oxygen, ultimately a losing battle if not corrected, but it must drop contractility and pump output dramatically to sustain itself. The brain cannot do this. Some animals and hibernators have a neuroprotective strategy to down-regulate metabolism to pilot light levels. Many species of newborn animals can actively lower their metabolism and oxygen consumption when exposed to hypoxia, probably a birth survival mechanism, but this response is largely lost into adulthood. Adult humans require large continuous brain energy consumption, and so far appear to lack this capacity.
CONCLUSION
Time course of brain and heart physiology is not known after the point of BO. Might be estimated based on case reports and computer simulation. Data from divers is lacking. We should be encouraging reporting and analysis of significant prolonged hypoxic events, and certainly those requiring any level of resuscitation.