This document discusses hyperkalemia, defined as a plasma potassium level greater than 5.0 mEq/L. True hyperkalemia results from transcellular shifts of potassium, increased potassium exposure, or decreased renal excretion. Severe hyperkalemia can cause cardiac arrhythmias. Treatment involves reducing extracellular potassium through medications like calcium gluconate, insulin, sodium bicarbonate, and beta-agonists. Long-term management may include dietary modifications, correcting acidosis, promoting potassium excretion with diuretics, and administering mineralocorticoids for hypoaldosteronism.

1. Dr. Bikal Lamichhane
Ist year Resident
Internal Medicine
Hyperkalemia

2. Definitions
 Hyperkalemia is defined as a plasma [K+] >5.0 mEq/L.
 Etiology
 Pseudohyperkalemia represents an artificially elevated plasma [K+] due to K+
movement out of cells immediately before or following venipuncture.
 Contributing factors include repeated fist clenching, hemolysis, and marked
leukocytosis or thrombocytosis.

3.  True hyperkalemia occurs as a result of
 (a) transcellular shift,
 (b) increased exposure to K+, and most commonly,
 (c) decreased renal K+ excretion.
(a)Transcellular shift.
 Insulin deficiency, hyperosmolality, nonselective b-blockers,digitalis, metabolic acidosis
(excluding those from organic acids), and depolarizing muscle relaxants, such as succinylcholine,
release K+ from predominate ICFstores into the ECF compartment.
 Exercise-induced hyperkalemia results from release of K+ from muscles.
 Familial periodic paralysis a rare cause of hyperkalemia.
 Massive cellular destruction, as seen in tumor lysis syndrome, also liberates cellular K+ into ECF.

4. (b)Increased exposure to K+ :-
-rare unless assosciated with renal impairment.
- Foods with a high content of K+ include salt substitutes, dried fruits, nuts,
tomatoes, potatoes, spinach, bananas, and oranges.
- Juices derived from these foods may be especially rich sources.

5. (c)Decreased renal K+excretion.
 intrinsic renal disease,
 decreased delivery of filtrate to the distal nephron,
 adrenal insufficiency, and
 hyporeninemic hypoaldosteronism (type 4 RTA).
 Drugs
 Common culprits include angiotensin-converting enzyme inhibitors and
angiotensin receptor blockers, potassium-sparing diuretics, NSAIDs, and
cyclosporine.
 Heparin and ketoconazole can also contribute to hyperkalemia through the
decreased production of aldosterone.

6. DIAGNOSIS
Clinical Presentation
 The most serious effect of hyperkalemia is cardiac arrhythmogenesis secondary
to potassium's pivotal role in membrane potentials.
 May present with palpitations, syncope, or even sudden cardiac death.
 Severe hyperkalemia causes partial depolarization of the skeletal muscle cell
membrane and may manifest as weakness, potentially progressing to flaccid
paralysis & hypoventilation if the respiratory muscles are involved.

7. Diagnostic Testing
Laboratories
 pseudohyperkalemia should be excluded by rechecking laboratory data.
 Assessment of renal [K+] excretion and the renin-angiotensin-aldosterone
axis can help narrow the differential diagnosis when the etiology is not apparent.
 Renal [K+] excretion can be assessed using the TTKG(Trans-tubular potassium
gradient).
 A TTKG >10 suggests that renal tubular mechanisms for K+ secretion are intact.
 Persistence of hyperkalemia despite an intact renal response suggests poor
filtrate delivery to the distal mechanisms of K+ regulation, due to ↓ed effective
circulating volume.

8. A TTKG <7 implies impaired K+ secretion caused by hypoaldosteronism,
aldosterone resistance, or hyporeninemic hypoaldosteronism.
 Low aldosterone levels suggest either adrenal disease (renin levels elevated;
TTKG improves with fludrocortisone) or
 hyporeninemic hypoaldosteronism (renin levels low; occurs with type 4 RTA as
well as chloride shunting, or Gordon's syndrome).
 High aldosterone levels, typically accompanied by high renin levels, suggest
aldosterone resistance (pseudohypoaldosteronism) but can also be seen in K+-
sparing diuretics.

9. Electrocardiography
 ECG changes include increased T-wave
amplitude, or peaked T waves.
 More severe degrees of hyperkalemia result
in a prolonged PR interval and QRS
duration
 atrioventricular conduction delay, and loss
of P waves.
 Progressive widening of the QRS complex
and its merging with the T wave produce a
sine wave pattern.
 The terminal event is usually ventricular
fibrillation or asystole.

10. Tall teneted symmetrical T-waves (K level-
6.5)

11. Sine wave appearance with severe
hyperkalaemia (K+ 9.9 mEq/L – loss of p- wave ,
wide QRS )

12. TREATMENT
 Severe hyperkalemia with ECG changes is a medical emergency and requires
immediate treatment directed at minimizing membrane depolarization by reducing the ECF [K+].
 Medications
 Administration of calcium gluconate decreases membrane excitability.
 Usual dose is 10 mL of a 10% solution infused over 2 to 3 minutes.
 The dose can be repeated if no improvement in the ECG is seen after 5 to
10 minutes.

13. Insulin causes K+ to shift into cells,
Commonly used combination is 10 to 20 U of regular insulin & 25 to 50 g
glucose administered intravenously. Hyperglycemic patients should be given the
insulin alone.
 NaHCO3 is effective for severe hyperkalemia associated with metabolic acidosis.
In the acute setting, it can be given as an IV isotonic solution (3 ampules of
NaHCO3 in 1 L of 5% dextrose).
 ß2-Adrenergic agonists promote cellular uptake of K1. The onset of action is
30 minutes, lowering the plasma [K+] by 0.5 to 1.5 mEq/L, & the effect lasts
for 2 to 4 hrs.

14.  Longer term means for [K+] removal.
 Increasing distal Na+ delivery in the kidney enhances renal K+ clearance.
 Achieved with the administration of saline in patients who appear volume
depleted. Otherwise, diuretics can be used if renal function is adequate.
 Cation exchange resins, such as sodium polystyrene sulfonate
(Kayexalate),promote the exchange of Na+ for K1 in the GI tract.
 Dose is 25 to 50 g mixed with 100 mL 20% sorbitol to prevent constipation.

15.  Dialysis should be reserved for patients with renal failure and those with severe
life-threatening hyperkalemia who are unresponsive to more conservative
measures.
 Chronic therapy may involve dietary modifications to avoid high K+ foods ,
correction of metabolic acidosis with oral alkali, promoting kaliuresis with
diuretics, and administration of exogenous mineralocorticoid in states of
hypoaldosteronism.