Hyperkalemia: Physiology ↓ Renal Excretion
↑ Intake
↓ Intracellular Shift
Acute and chronic kidney disease; CHF
Principal Cell Dysfunction (TTKG < 7) ACEi/ARB; AI; heparin Hypovolemia (TTKG > 7)
↓ EABV
↓ distal flow of Na+ and H2O
Urine [Na+] < 20 mmol/L Cell lysis ↑ osmolarity H2O efflux Solvent drag β2 inhibition α1 stimulation Digoxin ↓ A NAGMA ↓ insulin ↓ NHE1 activity Diabetic nephropathy; NSAIDs ↓ A: ↓ R K+ sparing diuretics; voltage- dependent RTA ↓ Na+/K+ ATPase activity ↓ GFR ↓ A: ↑ R ↑ A: ↑ R ↓ CCD K+ secretion ↑ K+ availability ↑ K+ release ↓ intracellular K+ influx Chronic: Desensitize voltage- gated Na+ channels and ↓ membrane excitability ECG: Peaked T-waves, ↑ PR interval, flat/absent P-wave, ↑ QRS, QRST “sine wave” Hyperkalemia Serum [K+] > 5.1 mmol/L
Acute: ↑ extracellular [K+] makes the RMP less (-)
Abbreviations:
A: Aldosterone
AI: Adrenal Insufficiency
CCD: Cortical Collecting Duct
CHF: Congestive Heart Failure
EABV: Effective Arterial Blood Volume H+: Hydrogen ion
K+: Potassium ion
Na+: Sodium ion
NAGMA: Normal Anion Gap Metabolic Acidosis
NSAIDs: Non-steroidal anti-inflammatory drugs Note:
Muscle weakness or paralysis, ↓ urinary acid excretion
R: Renin
RTA: Renal Tubular Acidosis
RMP: Resting Membrane Potential TTKG: Transtubular Potassium Gradient
• Pseudohyperkalemia should always be excluded; can be caused by thrombocytosis, leukocytosis or improper blood withdrawal technique.
Authors: Mannat Dhillon Joshua Low Reviewers: Andrea Kuczynski Kevin McLaughlin* * MD at time of publication
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published March 6, 2019 on www.thecalgaryguide.com