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Bicarbonate i.v. for PEM

Discussion in 'General ME/CFS Discussion' started by JollyRoger, Jun 16, 2017.

  1. JollyRoger

    JollyRoger Senior Member

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    I noticed that all my PEM problems are in relation with lactate- nausea, vomiting, muscle weakness and extrem pain.

    A usual lactat acidosis is usually treated with bicarbonate I.v.
    Could this treatment prevent my PEM?
     
  2. Mary

    Mary Senior Member

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    I don't know if IV bicarbonate could prevent PEM though it might help. Many people here supplement orally with baking soda to try to avoid or lessen PEM or to help with recovery. I've been doing it myself lately and it has been helpful with muscle aches.

    Also, thiamine deficiency has been linked to lactic acidosis: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3388689/
    https://med.virginia.edu/ginutrition/wp-content/uploads/sites/199/2014/06/Parrish-March-17.pdf
     
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  3. Mary

    Mary Senior Member

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    JollyRoger likes this.
  4. JollyRoger

    JollyRoger Senior Member

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    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
     
  5. Mary

    Mary Senior Member

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    @JollyRoger - I'm afraid I can't comment on this, too complex for me right now! :confused: However, you might find these threads interesting and hopefully find people who may be able to better answer your questions:

    http://forums.phoenixrising.me/index.php?threads/relation-between-lactic-acid-and-fatigue-pem.49241/
    http://forums.phoenixrising.me/index.php?threads/research-on-lactic-acid.48556/#post-798696
    http://forums.phoenixrising.me/inde...-study-to-measure-blood-lactate-levels.40152/
    If you want to ask a particular member a question, tag them in your post by putting the "@" sign before their name (e.g., @Mary, or as I did with your name above)
     
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