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Too Much, Too Little or Not Sure?



Definition: K+> 5.5 mEq/l

Clinical Presentation:

1. skeletal muscle weakness (even severe flaccid quadriplegia)
2. peaked, tapered, tall T waves...beginning at levels of 6.0 mEq/liter. They are most prominent in leads V2-V4. Decreased and, eventually, absent P waves. Prolonged PR segment. Then, the QRS duration becomes progressively prolonged. Finally, the T wave and the QRS complex fuse to give a sinus wave pattern. The worse complications are ventricular tachycardia and asystole, which may occur in succession after evolution of the above EKG changes or out of the sudden.
3. Metabolic acidosis, because hypokalemia depresses ammoniagenesis in the kidney


1.Transcellular shift 30 mEq/liter. Although this guide is useful, you are not going to wait to see this lab result before starting therapy for life-threatining hyperkalemia.


a) myonecrosis
b) lack of insulin
c) acidosis

During acidosis, H+ in the serum is exchanged for K+ at the cell membrane. This causes an increase in the potassium concentration. The mineral acidoses are more likely to have this effect than lactic acidosis and ketoacidosis. The increase in the potassium levels is of about 1 mEq/liter.

d) digitalis toxicity

The Na/K ATPase normally keeps potassium inside the cell and sodium outside of it. When the pump is excessively inhibited, potassium stays outside and levels rise.

e) beta-blockers- see pseudohyperkalemia

f) hyperosmolar states

g) hemolysis- see pseudohyperkalemia

h) heavily catabolic states, eg. severe sepsis

2. Decreased renal excretion (leading causes)

In these cases, the UK+ is less than 30 mEq/liter.


a) renal insufficiency

Only when the GFR is less than 10 ml/min and urine output falls below 1 liter per day is renal insufficiency the only cause of hyperkalemia. These figures need not be present for hyperkalemia to occur if the cause of the renal insufficiency is interstitial nephritis or hyporeninemic hypoaldosteronism (seen with RTA in elderly diabetics), lupus, sickle cell disease, obstructive uropathy and after renal transplantation.

b) adrenal insufficiency

In this condition, the lack of glucocorticoids leads to hypovolemia with hypotension, hyponatremia, hyperkalemia and acidosis, because the tubule of the kidney can not control these ions and volume in the absence of the hormones.

c) drug effects

- ACE inhibitors
- potassium supplements, K-rich foods, salt substitutes
- heparin (even at small doses to prevent DVT; mechanism: inhibition of aldosterone synthesis)
- potassium-sparing diuretics
- total parenteral nutrition
- high-dose potassium-penicillin


This is a medical emergency. A K+ >6 must prompt:
a) EKG (flat P waves, peaked T waves, prolonged QRS)
b) parenteral calcium preparations (gluconate 10%, gluceptate or chloride)
- administer 2 amps (4.8- 9.6 mEq) of calcium ( or 10 cc of the 10% gluconate solution) over 3 minutes
- side effects: precipitation of Ca-P salts in hyperphosphatemic pts.
- effects start within seconds but last only 30-60 minutes; dose may need to be repeated in 5 minutes after the first dose
- effects of therapy must be guided by EKG
- if the patient is on digitalis, the calcium preparation should be diluted and given over 20-30 minutes.
c) alternatively..insulin and glucose
- administer 50 cc of D50W and 10 units of regular insulin
- effects start within 2-3 minutes
- side effects: hypoglycemia (have more glucose handy or start an infusion)
d) alternatively, bicarbonate
- administer 1-2 amps (44-88 mEq) over 5-10 minutes
- side effects: volume expansion, intracellular acidosis
- should not be given if calcium has been given because precipitation will occur

All of these measures have an immediate effect on the potassium levels. Their effects are short-lived and other measures to keep potassium levels normal must be instituted at the same time:

a) potassium binding resins (Kayexalate)
This is given orally or as an enema. Each reduction of 1 mEq of potassium will be associated with a 2-3 mEq in Na+ levels and volume expansion. Given with sorbitol, a cathartic, to prevent a solid mass of Kayexalate from forming inside the gut.

Dose: a) oral- 30g Kayexalate + 50cc 20% sorbitol. The oral route is preferred.
b) rectal- 50g Kayexalate + 200cc 20% sorbitol. Retain solution for 30-45 minutes if possible.

b) diuretics
1. Furosemide or ethacrynic acid
Effect within 20-30 minutes. These will promote renal excretion of potassium , unless there is oliguric renal failure or no ESRD with anuria. Up to a total of 200 mg may be given until other slower, longer lasting drugs asre given for the control of hyperkalemia.

c) hemodialysis
Needed when urine output is reduced, hyperkalemia is severe and therapy is urgent. Also, when volume overload already exists and the GI tract is not functional or oral/reactal preparations would be dangerous.
d) peritoneal dialysis

e) Digibind- digitalis-binding antibodies for digitalis toxicity cases. Should be given with 2g of parenteral MgSO4. Calcium should be avoided because it may worsen digitalis toxicity. Insulin usually ineffective.

A transvenous pacemaker is necessary when there is an AV block and no response to calcium therapy. Usually insulin and glucose are given at the same time.



a) hemolyzed sample (clotted vein, tight tourniquet)
b) leukocytosis > 50,000
c) thrombocytosis > 1,000,000
To tell if the hyperkalemia is true or not, send clotted and unclotted samples for analysis and compare.

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