Acid-Base, Blood Gases, And Electrolytes

Blood gases and the Henderson-Hasselbalch equation

Arterial blood gas (ABG) interpretation is high-yield. The governing equation is Henderson-Hasselbalch: pH = 6.1 + log([HCO3-] / (0.03 x pCO2)). The numerator (bicarbonate) is the metabolic/renal component; the denominator (pCO2) is the respiratory/lung component. Memorize the normals: arterial pH 7.35-7.45, pCO2 35-45 mmHg, HCO3- 22-26 mEq/L, pO2 80-100 mmHg.

Classify a disorder in three steps: (1) Is the pH acidotic (<7.35) or alkalotic (>7.45)? (2) Which system explains it -- does pCO2 move the pH the same direction (respiratory) or does HCO3- (metabolic)? (3) Is the opposite system compensating?

Worked example: pH 7.28, pCO2 60 mmHg, HCO3- 27. Low pH + high pCO2 = respiratory acidosis with early renal compensation (HCO3- slightly up). Remember CO2 acts as acid: hypoventilation (COPD, sedation) retains CO2.

The anion gap

Anion gap (AG) = Na+ - (Cl- + HCO3-), normal 8-12 mEq/L (or 12-16 if K+ is included). A high anion gap metabolic acidosis comes from added unmeasured anions -- mnemonic MUDPILES: Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates. A normal-gap (hyperchloremic) acidosis comes from bicarbonate loss (diarrhea, renal tubular acidosis). Worked example: Na 140, Cl 100, HCO3 12 -> AG = 140 - 112 = 28 mEq/L (high gap; think DKA or lactic acidosis).

Electrolytes

• Sodium (135-145 mEq/L): main extracellular cation; hyponatremia <120 is a critical value risking seizures.
• Potassium (3.5-5.0 mEq/L): intracellular cation; <2.5 or >6.0 is critical and causes arrhythmias. Pseudohyperkalemia is a classic trap -- hemolysis, fist clenching, thrombocytosis, or delayed serum separation falsely elevate K+ as cells leak potassium.
• Chloride (98-107 mEq/L): follows sodium; shifts inversely with bicarbonate.
• Bicarbonate / total CO2 (22-28 mEq/L): the metabolic buffer.
• Calcium: 45% ionized (active), 40% albumin-bound. Correct total calcium up by 0.8 mg/dL for every 1.0 g/dL the albumin is below 4.0. Ionized calcium is the physiologically active fraction.

Proper specimen handling matters: ABGs are drawn anaerobically in heparin and run promptly on ice; air bubbles falsely raise pO2 and lower pCO2. Allowing whole blood to sit shifts potassium up and glucose down through glycolysis (~5-7%/hour).

Compensation and mixed disorders

The exam distinguishes acute from chronic and compensated from uncompensated. In full compensation the pH returns into the 7.35-7.45 range while pCO2 and HCO3- remain abnormal in the same direction. If the pH is still outside the range, compensation is partial. Remember that the body never overcompensates -- it will not push the pH past 7.40 in the opposite direction.

A mixed disorder is suspected when the expected compensation does not occur; for example, a salicylate overdose produces a simultaneous respiratory alkalosis (low pCO2) and metabolic acidosis (low HCO3-), so the pH may sit near normal while both systems are abnormal.

Winter's formula predicts respiratory compensation in metabolic acidosis: expected pCO2 = (1.5 x HCO3-) + 8 (+/- 2). If the measured pCO2 is higher than predicted, a concurrent respiratory acidosis exists.

Electrolyte correlation and osmolality

Calculated serum osmolality = 2(Na) + glucose/18 + BUN/2.8; normal is 275-295 mOsm/kg. An osmolal gap (measured minus calculated > 10) signals an unmeasured osmotically active substance such as methanol, ethylene glycol, or ethanol. Hyponatremia must be interpreted with osmolality: pseudohyponatremia from severe hyperlipidemia or hyperproteinemia is an artifact of older indirect ion-selective electrodes.

Severe hyperglycemia drags water into plasma and lowers measured sodium by about 1.6 mEq/L for every 100 mg/dL of glucose above normal -- a translational correction the exam expects you to apply rather than reporting a falsely alarming sodium.

Buffer systems and measurement methods

The bicarbonate-carbonic acid buffer is the body's most important and the one the equation describes, but hemoglobin, phosphate, and plasma proteins also buffer. Electrolytes are measured by ion-selective electrodes (ISE), which come in direct (whole blood, unaffected by lipids/protein) and indirect (diluted, susceptible to pseudohyponatremia) configurations -- knowing which one explains a discrepant sodium is a tested distinction. pCO2 is measured by a Severinghaus electrode and pO2 by a Clark electrode. Bicarbonate on a chemistry analyzer is usually reported as total CO2, which is mostly bicarbonate plus dissolved CO2.

Because potassium is critical, recognize that even small preanalytical errors -- a tourniquet left on too long, fist pumping, or a hemolyzed draw -- can push a normal potassium into the critical range and trigger an unnecessary clinical response. The exam consistently asks you to identify the preanalytical cause before accepting an alarming electrolyte value, rather than reporting it blindly.

Clinical correlations of common imbalances

Map each electrolyte to its classic clinical context. Hyperkalemia accompanies renal failure, acidosis (potassium shifts out of cells), and tissue breakdown, and it produces peaked T waves and cardiac arrest. Hypokalemia accompanies vomiting, diuretics, and alkalosis. Hypernatremia reflects free-water deficit (dehydration, diabetes insipidus), while hyponatremia reflects water excess or SIADH. Hypercalcemia points to hyperparathyroidism or malignancy (the two most common causes), while hypocalcemia accompanies renal failure, hypoparathyroidism, and vitamin D deficiency.

Magnesium often moves with potassium and calcium, and unexplained refractory hypokalemia frequently will not correct until magnesium is replaced. When an electrolyte result and the clinical scenario conflict, the exam wants you to first rule out a preanalytical or analytical artifact, then interpret the value within the acid-base and osmolality context rather than in isolation -- the same integrated reasoning that governs the entire chemistry domain.