Acid-Base Balance

A cause of metabolic alkalosis is hyperaldosteronism; increased aldosterone levels cause increased H+ secretion by the distal tubule and increased reabsorption of “new” HCO3–. Diarrhea causes loss of HCO3–from the gastrointestinal (GI) tract and acetazolamide causes loss of HCO3–in the urine, both resulting in hyperchloremic metabolic acidosis with normal anion gap. Ingestion of ethylene glycol and salicylate poisoning leads to metabolic acidosis with increased anion gap.

ABC of Biochemistry 6th - P: 376

Maintenance stage of metabolic alkalosis
1.Hypovolemia
2.Hypocloremia
3.Hypokalemia
4.Primary hyperaldosteronism

Total daily production of fixed H+ from catabolism of proteins and phospholipids (plus any additional fixed H+ that is ingested) must be matched by the sum of excretion of H+ as titratable acid plus NH4+ to maintain acid–base balance.

HCO₃ deficit= ( Normal HCO₃- Measured HCO³)* HCO₃ space

HCO₃ space=30-50 % of TBW

ABC biochem 7th -401

Explanations:
Normal pH value is 7.4 and lethal values only about 0.5 on either side of normal.

The history in this case suggests the patient's chest pain is due to muscular injury rather than anything more sinister. The patient's anxiety about cardiovascular morbidity has ultimately resulted in hyperventilation causing an acute respiratory alkalosis . Acid base abnormalities can be solved by either considering the Henderson-Hasselbach equation (CO2 + H2O → H2CO3 → H+ + HCO3-), whereby change in the product(s) on one side of the equation is balanced by a shift in equilibrium. For example, in this case the patient's hyperventilation causes a reduction in CO2, in order to increase the CO₂ the equilibrium shifts towards CO₂ + H₂O which causes a reduction in H+ (alkalosis) and HCO3-. This process occurs in respiratory alkalosis with metabolic compensation (C). If the patient had a true cardiac arrest it would cause a surge in lactic acidosis hence H+ concentration increases causing a metabolic acidosis (B). In order to balance this change, the equilibrium shifts away from H+ and causes increased CO2 production which can manifest as an increased respiratory rate, otherwise called 'metabolic acidosis with respiratory compensation' (D). In a respiratory acidosis with metabolic compensation (A) scenario, a patient may have a respiratory abnormality such as chronic hypoventilation. The accumulation of CO2 which leads to increased H+ is compensated for by bicarbonate which is subsequently reduced. In more chronic conditions, the bicarbonate becomes elevated.

Clinical safe range of pH is 7.3-7.5

ABC of Biochemistry 6th - P:342

Features of proximal acidification:
1. It is a high capcity system used for huge bicarbonate reabsorption mainly in PCT and partly in ALH (if HCO3- escape reabsorption in PCT).
2. Here secreted Ht from tubular cell is titrated in tubular fluid by filtered HCO3- for its reabsorption with no net loss of H+ from body and no net gain of HCO3- to blood. Merely proportional replacement of filtered HCO3- in blood occur by this mechanism.
3. Simply it helps to maintain the present bicarbonate status (alkali reserve) of body without urinary HCO3- loss. It does nothing to change the acid base status of body.
4. It does not create high luminal H+ concentration.
5. It creates a very low pH gradient by decreasing filtrate pH from 7.4 to 6.8.
6. It is important because it saves huge amount of HCO3- per day (about 4500 mmol) by preventing their urinary loss. Kidney cannot be in a position to excrete non volatile acid load without prior reabsorption of all filtered HCO3- because one HCO3- loss from the body is equivalent to one H+ gain to the body.

 ABC of Biochemistry 6th - P: 359

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