AAhhh.....thiamin is important for the pdh enzyme.... known from the latest research.
I read somewhere that lactic acidosis can happen through mitochondrial dysfunction by shock (low blood volume)
Frequent urination and low blood volume are well known in the cfs world.
I wonder if it could maybe the reason for it......
I copy and paste it.
Aspects which contribute to the formation of acidosis
In shock;
1. Increase acid production (Type A lactic acidosis)
- Insufficient O2 delivered to tissues Flux = Q x O2 content
- ↑anaerobic metabolism through glycolysis with the formation of lactic acid
from pyruvate. This is an energy-inefficient process (yields 2ATP for each
mol of glucose) resulting in the formation of large amounts of lactic acid.
- Hepatic hypoperfusion means that lactic acid is unable to enter the Cori
cycle to convert the lactic acid back to glucose.
Effect on the body:
- Respiratory:
o ↓pH detected by peripheral & central chemoreceptors. Activate
respiratory centre of the medulla and ↑MV through hyperventilation
rapidly ↓PaCO2. ↓pH by 1 → ↑MV by 3L/min
May lead to eventual exhaustion
Hyperventilation ↑metabolic demand of mm of respiration
further compounding acidosis
- Cardiovascular:
Compounding ‘shocked’ state
o ↓pH is negatively inotropic
o Vascular resistance:
acidosis → direct ↓SVR (metabolic autoregulation), ↑PVR
Hypovolaemia → ↑SVR 2° ADH (V1 receptor), ATII (AT1R)
activation
o Impaired SNS response, as ↓response to catecholamines <7.2
o Depressed myocardial function and ↑arrythmogenicity through
↑K+ (through cellular H+
/K+ exchange) and ↑Ca2+ (through
dissociation from albumin)
- Right-shift of O2Hb-dissociation curve, ↑O2 delivery to tissues
- CNS effects:
o Impaired consciousness
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