Home » Surgical Notes » Applied Physiology

Acid-base

pH = -log10[H+]

Normal range is 7.36 - 7.44

Base-Deficit: Amount of acid/alkali required to restore 1l of blood to a normal pH (at pCO2 of 5.3kPa at 37'C).

Base-deficit = -[HCO3 - 24.8 + (16.2 x (pH - 7.4))]

 

Normal ranges

  • pH: 7.36 - 7.44
  • pCO2
  • pO2
  • HCO3-: 22 - 28
  • BE -2 +2

 

Sources of H+

  1. Lungs: CO2 + H2O <-> H2CO3 <-> HCO3- + H+
  2. Anaerobic metabolism (generating lactic acid from pyruvate)
  3. Generation of ketone bodies: acetone, acetoacetate, B-hydroxybutyrate

Sources of Buffer / Bases

  1. Bicarbonate system
  2. Phosphate system
  3. Plasma proteins
  4. Hemoglobin

 

Organs involved in regulating acid-base balance

  1. Respiratory
  2. Kidneys: HCO control
  3. Blood: plasma protein buffer
  4. Bone
  5. Liver: produce HCO3 and ammonia

 

  Acidosis
 Alkalosis 
Effects
  1. Respiratory
    • Oxygen: Right shift of curve (reduced O2 affinity, increased tendency to oxygenate tissue)
    • Pulmonary hypertension
  2. Cardiac
    • Decreased myocardial contractility
    • Resistance to catecholamines
    • Cardiac arrythmias
    • Increased sympathetic activity
  3. Proteins
    • Denatured
  
Workup
  1. ABG -
    • pH
    • pCO2
    • HCO3: Loss from gut, depletion through buffering, impaired generation
  2. Chloride (chloride retained at expense of bicarbonate); hypercholraemia results in low bicarbonate and thus generates acidosis
    • May be due to dehydration
    • Can be due to defects in tubular function
  3. Serum lactate: Metabolic acidosis - classified by Cohen + Woods
    1. Common disorders - liver disease, renal failure, DKA, malignancy, short-bowel
    2. Drugs/toxins: paracetamol / salicylate, metformin, epinephrine
    3. Inborn error of metabolism: pyruvate dehydrogenase deficiency
    • Type A: From Tissue hypoxia - anaerobic metabolism of pyruvate to lactate (any cause of shock)
    • Type B: Not due to Hypoxia
  4. Urine dipstick - ketones
  5. Calculate anion gap (Na + K) - (HCO3- + Cl-)
    • Normal Anion Gap: HCO replaced with chloride ions to maintain electrochemical neutrality
    1. Addisons (hypoaldosteronism - hyperkalaemic acidosis)
    2. RTA: - group of conditions that exhibit renal tubular dysfunction in presence of normal GFR
      • Type I (distal) - loss of ability to excrete acid at CCD; leads to acidosis
      • Type II (proximal) - loss of HCO3 resorptive capacity; leads to acidosis
      • Type IV: Hypoaldosteronism - hyperkalaemic acidosis
    3. Ileal conduit
    4. Carbonic anhydrase inhibitor
    • Increased Anion Gap:
    1. MUDPALES - Methanol, Uraemia, DKA, Paraldehyde, Alcohol, Lactic acidosis, Ethyl glycol, Salicylates
  6. Check renal functrion

Causes:

  1. Addition of bicarbonate
    • Iatrogenic
    • Milk-Alkali syndrome
  2. Loss of chloride (with gain of bicarbonate)
    • Vomiting
    • Diuretics
  3. Hypokalaemia - shift of protons into cell 
Treatment  Sodium Bicarbonate
  1. 8.4%
  2. Generates extra CO2, therefore ventilation must be adequate
  3. Worsens intracellular acidosis
 

 


‹ Applied PhysiologyupAction potential ›