Acid Base Balance

Dr. Lokesh arora

Arterial pH
Normal arterial pH 7.36-7.44 (slightly alkaline) o pH less than 7.36 acidemia o pH greater than 7.44 - alkalemia During the course of daily metabolism of protein & carbohydrates ,approximatly 70 meq (1meq/kg) of hydrogen ion is generated. In addition a large amount of Carbon di oxide is formed tht combines with water to from carbonic acid. Arterial pH is product of volatile (CO2), non-volatile acids (fixed).

ECF and ICF Buffers

Major ECF buffers are bicarbonate (HCO3-) and phosphate (HPO4-) Major ICF buffer is hemoglobin
o Oxyhemoglobin releases O2 and takes up CO2 and combines with H2O to form H2CO3 o Organic phosphates (ATP, AMP, ADP) and proteins

 99.9% of filtered HCO3- is reabsorbed

REABSORPTION of Filtered HCO3

o Reabsorbed in proximal convoluted tubule 1. Na/H+ exchanger 2. secreted H+ combines with HCO3- and forms H2CO3. 3. Carbonic anhydrase breaks this down to CO2 and H2O and they diffuse across membrane 4. Inside cell, CO2 and H2O goes thru reverse rxn 5. HCO3- is transported by Na+ cotransport or Clexchange.

H+ is SECRETED into tubule lumen to produce titratable acids

Proximal Convoluted Tubule

H+ secreted and excreted

Secondary active transport

At same time, generate HCO3to reabsorb (secondary active co-transport)

Primary active Transport (90% of H+ secreted into PCT) (Aldosterone control)

Collecting Duct -Intercalated Cell H+ secretion

Secondary active Counter-transport Primary active Transport (aldosterone control)

Acid Base Disorders

(uncompensated responses)
Metabolic
o Acidosis and alkalosis Primary disturbance is HCO3- concentration Acidosis = decreased HCO3- (loss results in increased H+) Alkalosis = increased HCO3- (loss of H+ and gain of HCO3-)

Respiratory

Metabolic disturbances do not include changes in arterial CO2 (PaCO2)

o Acidosis and alkalosis Primary disturbance is Pa CO2 Acidosis = hypoventilation (increased CO2 retention and decreased ph) Alkalosis = hyperventilation (decreased CO2 retention and increased ph)

Compensation for acidosis or alkalosis

Metabolic compensation (rapid minutes) Compensation is respiratory

Respiratory compensation (slow) Compensation is renal

o Acidosis stimulate chemoreceptors hyperventilation decreased PaCO2 o Alkalosis inhibits chemoreceptors hypoventilation increased PaCO2

o Acidosis increase H+ secretion increased HCO3reabsorption (days) o Alkalosis decreased H+ secretion incomplete HCO3- reabsorption decreased plasma HCO3(hours)

Metabolic acidosis
Increased acid production- ketoacidosis, lactic acidosis , salicylate or ethylene glycol ingestion
o Increased anion gap

Excessive bicarbonate loss- severe diarrhea, diuretic treatment, ureterosigmoidostomies

o Normal anion gap

..
Treatment is identifing the underlying cause and crrect it. The long term management is providing sodium bicarbonate tablets or by dietary manipulation.

Metabolic alkalosis
Most common acid base balance in surgical patients Cheyne stroke breathing , tetany Pathogenesiso Loss of gastric secretions o Volume depletion o Potassium depletion

Paradoxical acidurea Treatmento Saline solution,with adequate volume repletion o KCl

Respiratory acidosis Upper abdominal surgeries

Respiratory insufficiency Acute-respiratory arrest No change in bicarbonate level Treatment
o Restoration of adequate ventillation o Tracheal intubation and assisted ventillation

Chronic-chronic respiratory failure Good renal compansation Treatment

o Pulmonary toilet , maintain the ventilltion o Rapid correction is dangerous

High altitude , hyperpyrexia, encephalitis , hyperventillation ,bacterial sepsis Acute Parasthesia, carpopedal spasm , positive chvostek sign Treatment of underlying cause Controlled ventillation

Respiratory akkalosis
Chronic-pulmonary and liver diseases Does not reqire the treatment Treatment of underlying cause