Acid-Base Balance PDF

Acid-Base Balance Acid-Base Homeostasis  The pH of body fluids is maintained within a narrow range despite the ability of the kidneys to generate large amounts of HCO3 - and the normal large acid load produced by metabolism.  This endogenous acid load is efficiently neutralized by buf...

Acid-Base Balance Acid-Base Homeostasis  The pH of body fluids is maintained within a narrow range despite the ability of the kidneys to generate large amounts of HCO3 - and the normal large acid load produced by metabolism.  This endogenous acid load is efficiently neutralized by buffer systems and ultimately excreted by the lungs and kidneys.  Important buffers include intracellular proteins and phosphates and the extracellular bicarbonate–carbonic acid system.  Compensation for acid-base derangements can be by respiratory mechanisms (for metabolic derangements) or metabolic mechanisms for respiratory derangements).  Changes in ventilation in response to metabolic abnormalities are mediated by hydrogen sensitive chemoreceptors found in the carotid body and brain stem.  Acidosis stimulates the chemoreceptors to increase ventilation, whereas alkalosis decreases the activity of the chemoreceptors and thus decreases ventilation.  The kidneys provide compensation for respiratory abnormalities by either increasing or decreasing bicarbonate reabsorption in response to respiratory acidosis or alkalosis, respectively.  Unlike the prompt change in ventilation that occurs with metabolic abnormalities, the compensatory response in the kidneys to respiratory abnormalities is delayed.  Significant compensation may not begin for 6 hours and then may continue for several days.  The predicted compensatory changes in response to metabolic or respiratory derangements are listed in Table below. Predicted changes in acid-base disorders DISORDER PREDICTED CHANGE DISORDER PREDICTED CHANGE Metabolic Metabolic acidosis Metabolic alkalosis Pco2 = 1.5 × HCO3- + 8 Pco2 = 0.7 × HCO3- + 21 Respiratory Acute respiratory acidosis Δ pH = (Pco2 – 40) × 0.008 Chronic respiratory acidosis Acute Δ pH = (Pco2 – 40) × 0.003 Δ pH = (40 – respiratory alkalosis Chronic respiratory Pco2) × 0.008 Δ pH = (40 – Pco2) × 0.017 alkalosis 1 Metabolic Derangements Metabolic Acidosis. Etiology of metabolic acidosis Increased Anion Gap Metabolic Acidosis 1. Exogenous acid ingestion a. Ethylene glycol b. Salicylate c. Methanol 2. Endogenous acid production a. Ketoacidosis b. Lactic acidosis c. Renal insufficiency Normal Anion Gap 1. Acid administration (HCL) 2. Loss of bicarbonate 3. GI losses (diarrhea, fistulas) 4. Ureterosigmoidostomy 5. Renal tubular acidosis. 6. Carbonic anhydrase inhibiton.  The body responds by several mechanisms, including producing buffers (extracellular bicarbonate and intracellular buffers from bone(phosphate) and muscle(protein) ) by 1. increasing ventilation (Kussmaul's respirations). 2. increasing renal reabsorption and generation of bicarbonate.  The kidney also will increase secretion of hydrogen and thus increase urinary excretion of NH4+ (H+ + NH3+ = NH4+).  Evaluation of a patient with a low serum bicarbonate level and metabolic acidosis includes determination of the anion gap (AG), an index of unmeasured anions. Anion Gap(AG) = (Na) – (Cl + HCO3)  The normal AG is 20 mEq/L) i. Mineralocorticoid excess ii. Profound potassium depletion. b. Chloride sparing (urinary chloride