Superficially, tissue hypoxia might look similar to Ischemia but differs in one important aspect. Though the hypoxic myocardium is short of oxygen, the respiratory excreta from cells ie Co2, lactic acid, and free radicles are promptly cleared and flushed as blood flow is normal. Hence, generally acute Ischemia of tissues is more cell threatening than regional hypoxia at any organ level.
How do you classify hypoxia? we need to go to physiology classes again.
There are 4 types. Ischemic -Hypoxia, systemic hypoxia, Anemic hypoxia, Histo-toxic hypoxia.A good reference to read (Ošt’ádal B., Kolář F. (1999) Myocardial Hypoxia and Ischemia. In: Cardiac Ischemia: From Injury to Protection. Basic Science for the Cardiologist, vol 4. Springer, Boston, MA.)
The question we want to address here is the effect of systemic hypoxia on LV function.
We encounter this in different settings.
Chronic hypoxia :In COPD, there can be slow adaptation, still there will be some definite impairment of myocardial function.(Which may not be important in normal times but will tell at times of other stress ) Many studies have documented COPD to compromise LV function. In fact, DCM has a link with some severe forms of COPD (Personal observation, will try to get the evidence )
In acute hypoxia(Non-Ischemic) it causes organ dysfunction.(Acute pulmonary embolism, and sepsis.) We see this often in IMCU with ventilated patients with multisytem defects a poorly contractile ventricles. Some of us used to report this entity with a empirical term global hypokinesia due to hypoxia. The effect of systemic hypoxia on cardiac metabolism is complex as the heart has a unique ability to survive with ketones in anaerobic metabolism at least for a few hours to days.
It is truly fascinating to note, how the human donor heart makes a stunning statement (to the coronary blood flow obsessed cardiologists) when it is shipped in ice bags with exclusive support of metabolic juices without a single drop of blood and come alive in the recipients without any damage. Is it not a wholesome proof? , for temporary survival, the heart just require ATPs and high energy bonds, not blood in the real sense.
Here is a 1962 paper that analyzed how the heart is able to survive hypoxia. Walter F. BallingerII and Heinz Vollenweider Anaerobic Metabolism of Heart Circulation Research. 1962;11:681–685
How to study the effect of chronic hypoxia on LV function?
We may lack animal models but Ironically we have perfect human hearts to study the effect of hypoxia on the myocardium. They are cyanotic congenital heart disease. Here is one of the rare reports based on only two patients that address this issue. The authors (Neeraj Awasthy et al) to be appreciated for this pertinent observation.I think we need to look further. Even in TGA, the urgency to perform an arterial switch within a month or so is not only hemodynamic regression in LV mass facing pulmonary circuit but also early hypoxic injury to LV myocardium.
Reference