In Sekhon, Ainslie and Griesdale’s model they discuss primary and secondary brain injury following a cardiac arrest. Looking more closely at the primary brain injury they state that with a reduction in cerebral oxygen ATP production decreases and there is a switch to anaerobic respiration. This in turn leads to a reduction in ATP dependent ion channel action. There are three main effects
- Accumulation of Na+ ions
- Accumulation of lactate with acidosis
- An influx of Calcium ions into the cells
Hypoxic Ischaemic Brain Injury
Sekhon, Ainslie and Griesdale have written an open access article on hypoxic ischaemic brain injury titled “Clinical Pathophysiology of Hypoxic Ischemic Brain Injury after Cardiac Arrest:A “two-hit” Model“. This paper can be used as a starting point for discussion of the events that lead to brain injury following hypoxia. This in turn is relevant to the question of energy usage in the Brain Hypometabolism Hypothesis.
Sekhon, Ainslie and Griesdale posit a simple two stage model of brain injury following cardiac arrest in which injury results from
- Primary cerebral hypoxia
- Secondary mechanisms after return of cerebral perfusion
What is the Brain Hypometabolism Hypothesis?
The Brain Hypometabolism Hypothesis broadly states that
‘Hypometabolism in the brain leads to neuropathology‘
What is Metabolism?
Metabolism can be defined as the chemical processes that occur in living organisms. There are three types of metabolic processes
(a) Generation of energy
(b) Generation of basic chemicals including fatty acids, amino acids and sugars
(c) Elimination of Nitrogen waste products
Restating the Brain Hypometabolism Hypothesis
The Brain Hypometabolism Hypothesis focuses on energy metabolism. More specifically the hypothesis states that
‘Energy hypometabolism in the brain leads to neuropathology‘
Glycolysis is one of the key pathways for energy metabolism in the human body. In this metabolic pathway the molecule Glucose is converted into Pyruvate. This pathway generates energy in the form of ATP. This pathway however does not use oxygen although the products generated are metabolised using oxygen. This is relevant to the bigger picture of energy metabolism in the brain.
Sekhon MS, Ainslie PN, Griesdale DE. Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest: a “two-hit” model. Crit Care. 2017 Apr 13;21(1):90. doi: 10.1186/s13054-017-1670-9.
Thorens B, Mueckler M. Glucose transporters in the 21st Century. American Journal of Physiology – Endocrinology and Metabolism. 2010;298(2):E141-E145. doi:10.1152/ajpendo.00712.2009.
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