Has Anyone Seen My Executive Function Recently?

To the Editor:

We enjoyed George Rodway's Wilderness Essay, ¹ which was intriguingly entitled “Decision making at extreme altitude: has anyone seen my executive function recently?” Obvious and potentially illuminating parallels can be drawn with cerebral function in patients undergoing locoregional carotid endarterectomy (CEA). During CEA, a crucial step during the operation is the cross-clamping of the common carotid artery. At that point, there is no flow in the ipsilateral internal carotid artery, and patients may exhibit signs of hemispheric hypoperfusion. During the operation, we try to converse with our patients to assess the adequacy of their cerebral oxygen delivery (COD). Patients often begin to deteriorate in a fairly subtle and graded fashion. Initially, they will often lose their sense of humor, and then they begin to struggle to initiate new lines of conversation. Their answers become shorter and less expansive; after that, the thought processes appear to be blunted, until finally affected patients become monosyllabic. At this point, it could be argued that they have lost their executive function, and certainly it would appear they would not to be capable of complex strategic decision making. Some patients may then go on to have mild focal neurological deficits before finally becoming profoundly obtunded. The subtle and incremental neurological degradation can usually be picked up at an early stage. Pharmacological augmentation of the blood pressure or increasing the fraction of inspired oxygen (F_Io₂) may be beneficial. If the deterioration in cerebral function is slow, that implies that there is only a modest imbalance between the regional cerebral oxygen delivery (rCOD) and regional cerebral oxygen consumption (rCOC), and any strategy that improves rCOD or decreases rCOC may reverse the deficit. ² Carotid shunt insertion is the final option.

Adequate oxygen delivery to the brain is also crucial for normal function at altitude. Oxygen carriage within the blood at altitude has conventionally been maintained a number of physiological processes (including erythropoiesis, hyperventilation, tachycardia, and increased cardiac output) and is often termed “acclimatization.” Specific to the cerebral circulation is an increase in middle cerebral artery flow. ³ It has recently been shown that exposure to both acute and extreme hypoxia is also associated with an increase in middle cerebral artery diameter. ⁴ In acclimatized subjects ascending to extreme altitude, the changes in vessel caliber appeared to be of greater importance to increasing flow (and so COD) than changes in the velocity of the blood within it. Oxygen supplementation at 7950 m rapidly reversed the observed middle cerebral artery dilation. Such vessel dilation and its rapid reversal through administration of supplemental oxygen has not previously been described, and challenges currently accepted concepts relating to adaptive mechanisms.

The reported mortality rate on Everest between 1921 and 2006 was 1.3%. ⁵ During the spring climbing seasons from 1982 to 2006, 94 mountaineers died after climbing above 8000 m. Profound fatigue (n = 34), cognitive changes (n = 21), and ataxia (n = 12) were the most common symptoms reported for nonsurvivors. At 8400 m, blood gas analysis (n = 4) demonstrated mean Pao₂ was 3.28 kPa and PaCo₂ was 1.77 kPa, ⁶ and it has been postulated that acute hypoxic cerebral dysfunction at such extreme altitude might involve pathophysiological mechanisms apart from high altitude cerebral edema, ⁷ possibly a result of an imbalance between rCOD and rCOC.

It is not unreasonable to suggest that some climbers have acute hypoxic cerebral dysfunction or “loss of executive function” as a result of reaching the adaptive limits of the convective mechanisms for maintaining adequate Cao₂ and cerebral oxygen delivery. We suggest this loss of executive function may account for some deaths at extreme altitude.