potassium

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.
 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. 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.

11. 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.

12.  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.

13.  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.