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hyperkalemia-pathophysiology-intracellular-shift-and-intake
hyperkalemia-pathophysiology-intracellular-shift-and-intake
![Hyperkalemia (intracellular shift and ↑ intake): Pathophysiology
↑ K+ dietary intake (rarely causative)
β2 receptor inhibition (i.e. beta blockers)
Digoxin
α1 receptor stimulation (i.e. epinephrine, norepinephrine)
Insulin deficiency or resistance (i.e. diabetes mellitus)
↓ Stimulation of NHE1 (moves 1 Na+ into cell, 1 H+ out of cell) throughout body
Normal Anion- Gap Metabolic Acidosis (NAGMA)
Excess serum H+ results in ↓ NHE1 activity (See NAGMA: Pathogenesis and Laboratory Findings slide)
↑ Serum osmolarity (i.e. hyperglycemia)
Osmotic movement of water from cells to serum
Cell lysis (i.e. tumour lysis syndrome, rhabdomyolysis, hemolytic anemia)
↑ K+ release from lysed cells into the serum
Na+/K+ ATPase (moves 3K+ into cell, 2 Na+ out) activity inhibited on cells throughout body
↓ Activity of Na+/K+ ATPase on cells throughout the body
↓ Amount of K+ entering cells
↓ NHE1 activity prevents Na+ from entering the cell
Lack of high intracellular [Na+] needed to drive the Na+/K+ ATPase on cells
Loss of water from cells ↑ intracellular [K+]
K+ moves down concentration gradient from cell into serum
↑ K+ available for absorption
Since K+ is dissolved in water, some K+ is carried by water as water osmotically moves through water channels into the serum (phenomenon known as “solvent drag”)
See Hyperkalemia: Clinical Findings slide
Authors:
Mannat Dhillon, Joshua Low, Emily Wildman Reviewers:
Huneza Nadeem, Marissa (Ran) Zhang, Andrea Kuczynski, Yan Yu*, Kevin McLaughlin*, Adam Bass*
* MD at time of publication
↑ K+ in serum
Hyperkalemia
Serum [K+] > 5.1 mmol/L
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published July 17, 2022 on www.thecalgaryguide.com](https://calgaryguide.ucalgary.ca/wp-content/uploads/2022/07/Hyperkalemia-shift-1.jpg "Hyperkalemia (intracellular shift and ↑ intake): Pathophysiology
↑ K+ dietary intake (rarely causative)
β2 receptor inhibition (i.e. beta blockers)
Digoxin
α1 receptor stimulation (i.e. epinephrine, norepinephrine)
Insulin deficiency or resistance (i.e. diabetes mellitus)
↓ Stimulation of NHE1 (moves 1 Na+ into cell, 1 H+ out of cell) throughout body
Normal Anion- Gap Metabolic Acidosis (NAGMA)
Excess serum H+ results in ↓ NHE1 activity (See NAGMA: Pathogenesis and Laboratory Findings slide)
↑ Serum osmolarity (i.e. hyperglycemia)
Osmotic movement of water from cells to serum
Cell lysis (i.e. tumour lysis syndrome, rhabdomyolysis, hemolytic anemia)
↑ K+ release from lysed cells into the serum
Na+/K+ ATPase (moves 3K+ into cell, 2 Na+ out) activity inhibited on cells throughout body
↓ Activity of Na+/K+ ATPase on cells throughout the body
↓ Amount of K+ entering cells
↓ NHE1 activity prevents Na+ from entering the cell
Lack of high intracellular [Na+] needed to drive the Na+/K+ ATPase on cells
Loss of water from cells ↑ intracellular [K+]
K+ moves down concentration gradient from cell into serum
↑ K+ available for absorption
Since K+ is dissolved in water, some K+ is carried by water as water osmotically moves through water channels into the serum (phenomenon known as “solvent drag”)
See Hyperkalemia: Clinical Findings slide
Authors:
Mannat Dhillon, Joshua Low, Emily Wildman Reviewers:
Huneza Nadeem, Marissa (Ran) Zhang, Andrea Kuczynski, Yan Yu*, Kevin McLaughlin*, Adam Bass*
* MD at time of publication
↑ K+ in serum
Hyperkalemia
Serum [K+] > 5.1 mmol/L
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published July 17, 2022 on www.thecalgaryguide.com")
