Normal Acid-Base Homeostasis

Normal Acid-Base Homeostasis

• Systemic arterial pH is maintained between 7.35 and 7.45.
• This is achieved via extracellular and intracellular chemical buffering.
• Respiratory and renal regulatory mechanisms are also important.
• Arterial CO2 tension (PaCO2) is controlled by the central nervous system and respiratory systems.
• Plasma bicarbonate is controlled by the kidneys.
• Kidneys stabilize arterial pH by excretion or retention of acid or alkali.
• The Henderson-Hasselbalch equation describes the metabolic and respiratory components that regulate systemic pH: PH= 6.1 + log HCO3/PaCO2 X 0.0301

Regulation of Acid-Base Balance

• Acid and base originate within the body.
• Volatile acids: H2CO3 (15 mol/day)
• Fixed acids (90 mmol/L): sulfuric acid, phosphoric acid, uric acid, and mesostate.
• Bases include salts of organic acids and NH3.

Role of Buffers

• Bicarbonate/carbonic acid (HCO-3/H2CO3) buffer system accounts for 53% of buffering.
• Hemoglobin (Hb-/HHb) : 35%
• Proteins (Pr-/HPr): 7%
• Phosphate: 5%
• pH can be calculated using the Henderson-Hasselbalch equation: pH = pKa + log [HCO-3]/[H2CO3]; an example calculation yields pH = 7.4
• The buffer for fixed acids is HCO-3/H2CO3.
• The buffer for volatile acids is Hb-/HHb.

Respiratory Regulation

• Ventilation alters the amount of breathe out of CO2.
• Central receptors increase PaCO2.
• Peripheral receptors increase [H+].
• PaO2 increases receptors
• PaCO2 > 80mmHg inhibits the respiratory center.

Cellular Action

• Involves exchanges of H+ and K+.

Parameters of Acid-Base

• pH is an important, inexact parameter with a normal range of 7.35-7.45.
• PaCO2 is the partial pressure of CO2 dissolved in arterial plasma, and is a respiratory parameter.
• Normal PaCO2 range: 4.4-6.25 kPa (33-46 mmHg)
• Primary change in respiratory acidosis: PaCO2 increases.
• Primary change in respiratory alkalosis: PaCO2 decreases.
• Secondary change in metabolic acidosis: PaCO2 decreases.
• Secondary change in metabolic alkalosis: PaCO2 increases.

Anion Gap

• Represents the unmeasured anions in plasma such as albumin, sulfate, and phosphate.
• Normal range: 12 ± 2 mmol/L.

Metabolic Acidosis

• Primary disturbance: decrease of [HCO-3] in the arterial plasma.

Causes and Pathogenesis of Metabolic Acidosis

• Lactic acidosis: hypoxia, diabetes, and liver disease.
• Ketoacidosis: diabetes, and starvation.
• Severe renal failure: accumulation of fixed acids.
• Salicylic acid poisoning.
• Acid intake can be caused by certain foods.
• Can also occur due to increased endogenous acid production (lactate and ketoacids).
• Loss of bicarbonate as in diarrhea.
• Accumulation of endogenous acids as in renal failure.
• Effects respiratory, cardiac and nervous systems.
• A fall in blood pH leads to increased ventilation, especially the tidal volume (Kussmaul respiration).
• Intrinsic cardiac contractility may be depressed.
• Peripheral arterial vasodilation and central venoconstriction may occur.
• Predisposition to pulmonary edema with minimal volume overload.
• CNS function may be depressed, leading to headache, lethargy, stupor, or coma.
• High Anion Gap (AG) metabolic acidosis can be caused by DKA, lactic acidosis, alcoholic ketoacidosis, and toxins.
• Normal Anion Gap or Hyperchloremic Acidosis includes GIT HCO3 loss from diarrhea and renal acidosis.
• Metabolic acidosis with normal AG is associated with diarrhea, intestinal suction, intestinal fistula, and biliary fistula.
• Early renal failure results in decreased NH3 and H+ secretion.
• Renal tubular acidosis results in decreased H+ secretion and is impacted by depressants of carbonic anhydrase (C.A.) such as acetazolamide, intake of Cl- (NaCl, NH4Cl), and hyperkalemia.

Metabolic Alkalosis

• Manifested by an elevated arterial pH, an increase in serum HCO3, and an increase in PaCO2 as a result of compensatory alveolar hypoventilation.
• Often accompanied by hypochloremia and hypokalemia.
• Often associated with other ACID BASE disorders.

Respiratory Acidosis

• Can be due to severe pulmonary disease, respiratory muscle fatigue, or abnormalities in ventilatory control.

Respiratory Alkalosis

• Characterized by an increase in PaCO2 and decrease in pH.
• Alveolar hyperventilation decreases PaCO2 and increases the HCO3/PaCO2 ratio, increasing the pH.

Causes and Pathogenesis of Respiratory Alkalosis

• Hypotonic hypoxia.
• Pneumonia.
• Hyperventilation due to hysteria, fever, or [NH3].
• Hyperthyroidism.
• Misoperation of a ventilator.

Mixed Acid-Base Disturbances

• Dual acid-base disturbances involve combinations of different acid-base disorders.
• Metabolic acidosis plus respiratory acidosis involves decreased [HCO-3], increased PaCO2, and decreased pH. Respiration stops to characterize disorder.
• Metabolic alkalosis plus respiratory alkalosis: increased NH3, PaCO2, [HCO-3] and pH. Character is diuretic or hepatic
• Respiratory acidosis plus metabolic alkalosis: Pulmonary heart disease or duiretic. The pH is approximately equal

Summary of Acid-Base Disorders

• Metabolic Acidosis: pH is low, HCO3 is low, PaCO2 is low.
• Metabolic Alkalosis: pH is high, HCO3 is high, PaCO2 is high.
• Respiratory Acidosis: pH is low, HCO3 is high, PaCO2 is high.
• Respiratory Alkalosis: pH is high, HCO3 is low, PaCo2 is low.