In my response to Melody Maxim’s question I failed to explain why anoxic CPS presents additional challenges. Compression-only CPR (with no accompanying positive pressure ventilation) is still effective at generating some ventilation. This may seem impossible because the tidal volumes during compression-only ventilation are very small (~40 ml), in fact much smaller than the anatomical dead space of the large airways (~250 ml). In theory, all that should happen is that gas will move to and fro in the oropharynx and trachea with no ventilation of the alveoli and thus no gas exchange. In practice, modest gas exchange does occur due to pressure waves and stirring of the large airway gas presumably in a way similar to that in which gas exchange occurs in high frequency ventilation where tidal volumes are also very small (and well below the anatomical dead space). Deakin, et al., have measured ventilation in compression-only CPR in hospital patients who have failed resuscitation (Deakin C, O'Neill J, Tabor T. Does compression-only cardiopulmonary resuscitation generate adequate passive ventilation during cardiac arrest? Resuscitation , 75: 53 - 59C; 2003.) and found that median tidal volume per compression was 41.5ml (range 33.0–62.1ml), with a peak end-tidal CO2 of 0.93kPa (range 0.0–4.6kPa)and a minute CO2 of 19.5ml (range 15.9–33.8; normal range 150–180ml). While this not enough to support life it is more than enough to drive oxygen radical mediated reperfusion injury.
If compression-only active compression-decompression CPR (ACD-CPR) is used, minute ventilation rates (at ~100 compressions per minute) will be in the range of 2,500 to 3,000 ml with an alveolar ventilation rate in the range 1,200 to 1,500 ml/min. This is roughly a normal alveolar ventilation rate. In fact, gas exchange is somewhat better than would be predicted by the alveolar ventilation rate because non-tidal mechanisms of gas exchange (again, similar to those seen in high frequency jet and high frequency oscillating ventilation) come into play as a result of the high ventilation rate (100 breaths per minute) and the shock waves generated in the large airways as a result of chest compression. This effect becomes even more pronounced if high impulse CPR is being used in conjunction with ACD-CPR.
An added problem is that when cardiac arrest occurs both the arterial and venous blood will still have a large amount of oxygen present. Typically, life is not sustainable and death occurs when the central venous oxygen saturation (SVO2) reaches ~50%. Arterial blood oxygen saturation may range from just over 50% to as high as 98% depending upon the agonal course. While oxygen in the capillaries and small caliber arterioles and venules is quickly used up during circulatory arrest (ischemia) the oxygen in the large vessels persists for a long time after cardiac arrest. If circulation is restarted after a significant ischemic interval (>5 min) this reservoir of oxygenated blood provides a very damaging source of oxygen free radicals which cause reperfusion injury – even absent any exogenous ventilation.
The take-home message from the foregoing is that anoxic ventilation (ideally) would require more than simple occlusion of the airway; perhaps short-term ventilation with an inert gas (such as nitrogen) to facilitate desaturation of both the pulmonary blood (presumably nearly 100% saturated) and of the venous blood (~50% saturated). Inert gas ventilation may also be necessary to remove CO2. It will also be necessary to ameliorate red cell stickiness and rigidity as well as white blood cell and platelet adhesion and this will require pharmacological intervention; possibly inhaled nitric oxide, or more likely, intravenous administration of one or more nitrite compounds. It may also be necessary to provide some kind of substrate to provide energy to the vascular smooth muscle so that vascular tone and auto-regulation, and thus perfusion pressure, can be maintained during prolonged CPS. This will require formidable technical skill and thorough theoretical understanding. This is impossible given the current lack of biomedical acumen in cryonics.
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