9.7 Potassium Disorders & Systematic Acid-Base Analysis
Key Takeaways
- Hypokalemia, hyperkalemia, and metabolic and respiratory acidosis and alkalosis with mixed disturbances are all enumerated under water and electrolyte balance.
- Intravenous calcium is given first in hyperkalemia with ECG changes to stabilize the myocardium, but it does not lower the serum potassium.
- Insulin with glucose and inhaled beta-agonists shift potassium intracellularly, while only dialysis, diuretics and binders remove it from the body.
- Assess compensation with the appropriate formula, since inadequate or excessive compensation indicates a second acid-base disorder.
- A delta-delta ratio outside the expected range reveals a coexisting non-gap acidosis or metabolic alkalosis hidden behind an anion gap acidosis.
Last updated: August 2026
1. Hyperkalemia: ECG Manifestations & Emergency Management
Hyperkalemia (Serum Potassium > 5.0–5.5 mEq/L) reduces cardiac myocyte resting membrane potential, impairing myocardial conduction velocity and triggering fatal ventricular dysrhythmias.
Order of Electrocardiographic (ECG) Progression
- Peaked T Waves: Narrow-based, symmetrical, pointed "tented" T waves (earliest finding, typically K+ > 5.5–6.0 mEq/L).
- PR Interval Prolongation & Loss of P Waves: Flattening and eventual disappearance of P waves, bradycardia, or nodal rhythms (K+ > 6.5–7.0 mEq/L).
- QRS Complex Widening: Conduction delay across His-Purkinje system (K+ > 7.0–7.5 mEq/L).
- Sine Wave Pattern: Merging of wide QRS complexes with tall T waves, forming a continuous biphasic sine wave (K+ > 8.0 mEq/L).
- Ventricular Fibrillation, PEA, or Asystole.
The 3-Step Emergency Treatment Protocol
| Step | Intervention & Dosage | Mechanism of Action | Onset & Duration | Clinical Pearls |
|---|---|---|---|---|
| Step 1: Membrane Stabilization (Immediate) | • IV Calcium Gluconate (10%): 10–20 mL (1–2 g) IV over 2–3 min<br/>• IV Calcium Chloride (10%): 10 mL (1 g) via central line | Antagonizes potassium-induced membrane depolarization by raising cardiac threshold potential | Onset: 1–3 min<br/>Duration: 30–60 min | Does NOT lower serum K+; repeat dose if ECG changes persist after 5–10 min. Calcium chloride has 3x more elemental calcium but causes tissue necrosis if extravasated from peripheral IV. |
| Step 2: Intracellular K+ Shifting (Temporary) | • IV Regular Insulin 10 Units + 50 mL 50% Dextrose (D50W, 25 g)<br/>• Nebulized Albuterol: 10–20 mg in 4 mL saline over 15 min<br/>• IV Sodium Bicarbonate: 50–100 mEq IV | Stimulates Na+/K+-ATPase to drive extracellular K+ into intracellular compartment | Onset: 15–30 min<br/>Duration: 2–4 hours | Insulin is most reliable (lowers K+ by 0.5–1.2 mEq/L; omit D50 only if glucose >250 mg/dL). Albuterol dose is 4x standard asthma dose. IV Bicarbonate is only effective if concurrent severe metabolic acidosis is present. |
| Step 3: Total Body K+ Elimination (Definitive) | • Loop Diuretics: IV Furosemide 40–80 mg<br/>• Sodium Zirconium Cyclosilicate (SZC / Lokelma): 10 g PO TID<br/>• Patiromer (Veltassa): 8.4 g PO daily<br/>• Emergent Hemodialysis | Physically removes potassium from the body via renal excretion, fecal binding, or extracorporeal clearance | Onset:<br/>• Furosemide: 30 min<br/>• SZC: 1–2 hours<br/>• Patiromer: 4–7 hours<br/>• Dialysis: Immediate | Hemodialysis is the most definitive and rapid clearance method. Sodium Polystyrene Sulfonate (Kayexalate) is discouraged due to FDA black-box warning for intestinal necrosis and bowel perforation (especially with sorbitol). |
2. Systematic Acid-Base Analysis: GOLDMARK, Osmolar Gap & Delta-Delta
Interpretation of arterial blood gases (ABGs) and serum chemistries requires a disciplined 6-step approach:
Stepwise Analysis
- pH: Acidemia (<7.35) vs. Alkalemia (>7.45).
- Primary Disturbance: Check PaCO2 (respiratory) and HCO3- (metabolic).
- Assess Secondary Compensation:
- Metabolic Acidosis: Winter's Formula: $\text{Expected PaCO2} = 1.5 \times [\text{HCO3}^-] + 8 \pm 2$
- If Actual PaCO2 > Expected PaCO2: Concurrent Respiratory Acidosis (e.g., respiratory depression, severe COPD).
- If Actual PaCO2 < Expected PaCO2: Concurrent Respiratory Alkalosis (e.g., hyperventilation, sepsis, salicylates).
- Metabolic Alkalosis: $\text{Expected PaCO2} = 0.7 \times [\text{HCO3}^-] + 21 \pm 2$
- Metabolic Acidosis: Winter's Formula: $\text{Expected PaCO2} = 1.5 \times [\text{HCO3}^-] + 8 \pm 2$
- Calculate Serum Anion Gap (AG):
- Normal AG = 8 to 12 mEq/L.
- Hypoalbuminemia Correction: For every 1.0 g/dL decrease in serum albumin below 4.0 g/dL, add 2.5 mEq/L to the calculated Anion Gap (uncorrected AG will falsely miss high anion gap acidosis in malnourished/nephrotic patients).
High Anion Gap Metabolic Acidosis (HAGMA > 12): The GOLDMARK Mnemonic
| Letter | Etiology | Key Diagnostic Tests & Clinical Pearls |
|---|---|---|
| G | Glycols (Ethylene glycol, Propylene glycol) | Ethylene Glycol: Windshield washer/antifreeze; metabolized by alcohol dehydrogenase to glycolate and oxalate; causes severe HAGMA, high osmolar gap, envelope-shaped calcium oxalate crystals, acute tubular necrosis, and cranial nerve palsies. Treatment: IV Fomepizole (ADH inhibitor) and emergent hemodialysis.<br/>Propylene Glycol: Solvent in continuous IV lorazepam/diazepam infusions. |
| O | Oxoproline (5-Oxoproline / Pyroglutamic Acid) | Develops in malnourished women on chronic high-dose Acetaminophen (depletes hepatic glutathione). |
| L | L-Lactate | Type A (tissue hypoperfusion, septic shock, cardiogenic shock, mesenteric ischemia) vs. Type B (toxins, linezolid, metformin toxicity, hepatic failure, malignancy). |
| D | D-Lactate | Occurs in patients with Short Bowel Syndrome / jejunoileal bypass due to bacterial fermentation of unabsorbed carbohydrates; presents with episodic encephalopathy, ataxia, slurred speech, and high AG acidosis; standard lab lactate assay measures only L-lactate and will be normal. |
| M | Methanol | Found in windshield de-icer, moonshine; metabolized to formaldehyde and formic acid; produces severe optic disc hyperemia, "snowstorm" visual loss/blindness, putaminal necrosis, and high osmolar gap. Treatment: Fomepizole + hemodialysis. |
| A | Aspirin / Salicylates | Direct stimulation of medullary respiratory center causes early respiratory alkalosis; uncoupling of oxidative phosphorylation causes HAGMA -> classic Mixed Respiratory Alkalosis & High Anion Gap Metabolic Acidosis. Presents with tinnitus, hyperventilation, fever, confusion. Treatment: IV Sodium Bicarbonate (urinary alkalinization to pH 7.5–8.0) and hemodialysis. |
| R | Renal Failure / Uremia | Impaired excretion of organic sulfates, phosphates, and urates in advanced AKI/CKD (typically when GFR <15–20 mL/min). |
| K | Ketoacidosis | DKA (hyperglycemia, elevated beta-hydroxybutyrate); Alcoholic Ketoacidosis (AKA) (binge drinker with starvation and nausea; high beta-hydroxybutyrate, normal or low glucose; treated with D5W + normal saline, NOT insulin); Starvation Ketoacidosis. |
Toxic Alcohols & The Serum Osmolar Gap
- Calculated Serum Osmolality:
- Serum Osmolar Gap = Measured Osmolality - Calculated Osmolality.
- Normal Osmolar Gap is < 10 mOsm/kg.
- An osmolar gap > 10–15 mOsm/kg strongly confirms the presence of unmeasured exogenous osmoles (Ethylene glycol, Methanol, Isopropanol [causes high osmolar gap and ketonemia without metabolic acidosis], Propylene glycol).
The Delta-Delta Ratio ($\Delta - \Delta$)
Used in HAGMA to detect hidden underlying non-anion gap acidosis or metabolic alkalosis:
- Ratio < 0.8: Mixed High Anion Gap & Normal Anion Gap Metabolic Acidosis (e.g., patient with DKA who also has severe diarrhea or early renal failure).
- Ratio 0.8 to 2.0: Pure High Anion Gap Metabolic Acidosis.
- Ratio > 2.0: Mixed High Anion Gap Metabolic Acidosis & Metabolic Alkalosis (e.g., patient with lactic acidosis or DKA who has concurrent severe vomiting or nasogastric suction).
Test Your Knowledge
A 68-year-old man with end-stage kidney disease on maintenance hemodialysis misses two consecutive dialysis sessions and is brought to the emergency department with profound generalized muscular weakness. On physical examination, his heart rate is 38 bpm and blood pressure is 88/50 mmHg. The 12-lead ECG demonstrates profound loss of P waves, marked QRS complex widening (180 ms), and merging of the QRS with peaked T waves into a continuous biphasic sine-wave pattern. Stat serum potassium is 7.8 mEq/L. What is the single most urgent initial step in management?
A
B
C
D