Detailed mechanisms for Step 1.
| Cause | Mechanism / Pathophysiology |
|---|---|
| Metabolic Acidosis (High Anion Gap) | |
| Lactic acidosis | Why: Poor tissue perfusion (shock, sepsis) forces cells into anaerobic metabolism. The byproduct is lactate (an organic acid). The accumulation of unmeasured anions (lactate) consumes bicarbonate and raises the Anion Gap. |
| Diabetic ketoacidosis (DKA) | Why: Severe insulin deficiency leads to uninhibited lipolysis. The liver converts fatty acids into ketone bodies (ketoacids like beta-hydroxybutyrate). These act as unmeasured anions, consuming bicarbonate. |
| Kidney failure (Uremia) | Why: The kidneys fail to excrete the daily load of fixed acids (sulfates, phosphates) generated by protein metabolism. These retained acids accumulate in the blood. |
| Methanol / Ethylene Glycol | Why: These alcohols are metabolized by alcohol dehydrogenase into toxic organic acids (Formic acid for Methanol; Oxalic/Glycolic acid for Ethylene Glycol). These acids accumulate and consume bicarbonate. |
| Metabolic Acidosis (Normal Anion Gap) | |
| Severe diarrhea | Why: The GI tract below the stomach is rich in bicarbonate. Diarrhea causes direct physical loss of HCO3- in the stool. The kidney retains Chloride (Cl-) to maintain electroneutrality, resulting in a hyperchloremic (Normal AG) acidosis. |
| Renal tubular acidosis (RTA) | Why: A defect in the renal tubules preventing either the excretion of H+ (Distal/Type 1) or the reabsorption of HCO3- (Proximal/Type 2). Bicarbonate is lost in urine or not regenerated. |
| Excess normal saline infusion | Why: "Dilutional acidosis." Large volumes of NaCl load the body with Chloride. The high serum Cl- forces HCO3- to decrease to maintain electrical balance in the extracellular fluid. |
| Metabolic Alkalosis | |
| Vomiting / NG Suction | Why: Gastric secretions are very acidic (HCl). Vomiting leads to direct loss of H+ from the body. Additionally, volume depletion creates "contraction alkalosis" (RAAS activation increases HCO3- reabsorption). |
| Diuretic overuse | Why: Loop and thiazide diuretics cause volume depletion. This activates the RAAS system (Aldosterone). Aldosterone saves Na+ but excretes H+ and K+ in the urine, generating metabolic alkalosis. |
| Primary hyperaldosteronism | Why: A tumor or hyperplasia pumps out excess Aldosterone. Aldosterone works at the collecting duct to reabsorb Na+ and excrete H+, leading to direct alkalosis (and hypokalemia). |
| Respiratory Acidosis (Hypoventilation) | |
| Opioid overdose | Why: Opioids bind to mu-receptors in the brainstem respiratory center, blunting the drive to breathe. Decreased respiratory rate leads to CO2 retention (Hypercapnia). |
| Neuromuscular weakness | Why: The diaphragm and intercostal muscles act as the "pump" for ventilation. In conditions like Guillain-Barré or Myasthenia Gravis, the muscles are too weak to expand the chest wall effectively. This "pump failure" causes alveolar hypoventilation and CO2 retention. |
| COPD | Why: Airway obstruction and air trapping increase dead space and reduce effective gas exchange. This chronic inability to exhale fully leads to CO2 accumulation. |
| Respiratory Alkalosis (Hyperventilation) | |
| PE / Pneumonia | Why: These conditions cause hypoxemia (low O2) or irritate lung receptors. The body compensates by increasing respiratory drive (hyperventilation) to get more oxygen, inadvertently blowing off too much CO2. |
| High Altitude | Why: Low atmospheric oxygen pressure causes hypoxemia. This stimulates the peripheral chemoreceptors to increase ventilation (hypoxic drive), blowing off CO2. |
| Pregnancy | Why: High levels of Progesterone directly stimulate the respiratory center in the medulla to increase ventilation/tidal volume. This is a normal physiologic adaptation to clear fetal CO2. |