hyperkalemia

Hyperkalemia .pre -dialysis

definition

Plasma K conc. > 5.0 mmol/l Hyperkalemia is a potentially life-threatening metabolic problem caused by inability of the kidneys to excrete potassium, impairment of the mechanisms that move potassium from the circulation into the cells, or a combination of these factors.

Etiology:
inc. K intake Rare Potassium adaptation Ensures rapid K excretion in response to K intake Iatrogenic Overzealous parental K replacement

 Pseudohyperkalemia
Due to movement of K out of cells following venipuncture Contributed by: torniquet hemolysis leucocytosis & thrombocytosis K release following clot formation

 K release from cells due to tissue breakdown

Intravascular hemolysis Tumor lysis syndrome rhabdomyolysis

 Metabolic acidosis
Redistribution of K from ICF to ECF Or due to intracellular buffering of H

 Insulin deficiency & hyperglycemia Promote K shift from ICF to ECF Exercise induced hyperkalemia Related to degree of exertion Due to release of K from muscle cells Reversible Beta blockers Contribute to elevation of K in other conditions

 Hyperkalemic periodic paralysis

Rare, autosomal dominant disorder Episodic weakness or paralysis , precipitated by exercise

Severe digitalis toxicity

Inhibition of Na-K-ATPase pump

 Renal failure
Usually in acute oliguric renal failure Due to inc. release of K from cells ( acidosis, catabolism) and dec. excretion Chronic --- initial compensation but eventually fails to maintain K level

Drug-induced interstitial nephritis Lupus nephritis Sickle disease Diabetic nephropathy

Dec. effective circulating arterial volume: Volume depletion CHF Dec. K secretion Aimpaired Na reabsorption B--enhanced Cl reabsorption

Aimpaired Na reabsorption
Primary hypoaldosteronism
Adrenal insufficiency (Addisons disease) Adrenal enzyme deficiency

Secondary hypoaldosteronism
Hyporeninemia Drugs ( ACE-i ,NSAIDS, heparin )

 ACE-inhibitors and ARBs

cause impaired aldosterone release Inc. risk in
DM Renal insufficiency

Heparin
Inhibits production of aldoterone by cells of zona glomerulosa severe disease in
Renal disease ,dm, using K-sparing diuretics, ACE-I,NSAIDS

 Hyporeninemic Hypoaldosteronism
Syndrome Euvolemia or ECF volume expansion & supressed renin and aldosterone levels Common in
Mild renal insufficiency Diabetic nephropathy Ch. Tubulo-interstitial disease

Pts. Have impaired kaliuretic response to mineralocorticoids

 Degree of hyperkalemia in hypoaldostreronism is mild in absence of inc. K intake or renal dysfunction NSAIDS
Inhibit renin sec. and vasodilator prostaglandins leading to
Dec. GFR and dec. K secretion

 Resistance to aldosterone
Pseudoaldosteronism Tubulointerstitial disease
SLE, Renal transplant Obstruction, infection

Drugs ( K sparing diuretics, trimethoprim, pentamidine )

 Pseudohypoaldosteronism
Rare familial disorder Hyperkalemia Metabolic acidosis Renal Na wasting Hypotension High renin and aldosterone levels End-organ resistance to aldosterone

 Electrolyte abnormalities can be reversed by high doses of exogenous mineralocorticoids { fludrocortisone } Spironolactone
Mineralocorticoid antagonist

Amiloride and triamterene

Block apical channel of Na in principal cells

Trimethoprim & pentamidine

Block distal nephron Na reabsorption

 Benhanced Cl reabsorption [ chloride shunt ]

Gordons synd
Hyperkalemia Metabolic acidosis Normal GFR Volume expanded, dec. renin and aldosterone levels, refractory to exogenous mineralocorticoids

Cyclosporine toxicity

 Type 4 renal tubular acidosis

Due to :
Hypoaldosteronism or Cl shunt ( aldosterone- resistant )

Clinical features
Prolonged depolarization of cell membranes
Weakness Flaccid paralysis Hypoventilation

Inhibits renal ammonia-genesis leading to dec. acid excretion

metabolic acidosis

Cardiac toxicity

ECG changes

 Effects on P wave
Diminishes progressively in amplitude & disappears completely

Effects on the P-R interval

lengthening of the P-R interval.

Effects on the QRS complex

widened, and this affects mainly the terminal deflexion. The appearance suggests a bundle branch block, but this is not necessarily the mechanism. It seems likely that the conduction may be within the Purkinje network itself or even at the cellular level. Resembles right bundle branch block with either left anterior or left posterior hemiblock.

 Effects on the T wave

The T wave, at first, becomes tall and peaked , then somewhat widened. It develops a characteristic appearance. The proximal limb has a rapid, almost vertical ascent. The distal limb, while still steep, has a somewhat more gradual descent and slope.

Effects on the S-T segment

S-T segment virtually disappears, becoming, incorporated into the proximal limb of the T wave.

Effects on the Q-T interval

Either normal or actually decreased, however if the hyperkalamia is associated with hypocalcaemia, the Q-T interval may be prolonged, a situation which occurs with the chronic renal faliure and uraemia.

diagnosis
assess K secretion
TTKG < 5
Response to fludrocortisone

TTKG > 10 Inc. distal flow

DEC. EFFECTIVE CIRCULATING VOLUME

TTKG < 10
HYPERTENSION LOW RENIN & ALDOSTERONE
GORDONS SYND CYCLOSPORINE,DISTAL TYPE4 RTA

HYPOTENSION HIGH RENIN & ALDOSTERONE

PSEUDOHYPOALDOSTERONISM K-SPARING DIURETICS,TRIMITHOPRIM

TTKG>10
PRIMARY/SEC HYPOALDOSTERONISM
MEASURE RENIN & ALDOSTERONE LEVELS

Medications Used in Acute Treatment of Hyperkalemia

Medication * Dosage
Calcium gluconate

Onset

Length of effect

Mechanism of action Cautions

Protects myocardium from toxic effects of calcium; no effect on serum potassium level Can worsen digoxin toxicity

10 to 20 Immed 30 mL of 10 iate minutes percent solution IV over two to three minutes

Insulin

Regular insulin 10-20 units IV with 25-50 mL of 50 percent glucose

15 to 30 minu tes

Two to six hours

Shifts potassium out of the vascular space and into the cells; no effect on total body potassium

Consider 5 percent dextrose solution infusion at 100 mL per hour to prevent hypoglycemia with repeated doses. Glucose unnecessary if blood sugar elevated above 250 mg per dL (13.9 mmol per L)

Albuterol 10 to 20 15 to 30 (Ventolin) mg by minutes nebulizer over 10 minutes (use concentrat ed form, 5 mg per mL)

Two to three hours

Shifts potassium into the cells, additive to the effect of insulin; no effect on total body potassium

May cause a brief initial rise in serum potassium

Furosemide (Lasix)

20 to 40 mg IV, give with saline if volume depletio n is a concern

15 minutes to one hour

Four Increases hours renal excretion of potassium

Only effective if adequate renal response to loop diuretic

Sodium polystyrene sulfonate (Kayexalat e)

Oral: 50 g in 30 mL of sorbitol solution Rectal: 50 g in a retention enema

One to two hours (rectal route is faster)

Four to six hours

Removes potassium from the gut in exchange for sodium

Sorbitol may be associated with bowel necrosis. May lead to sodium retention

 i/v NaHCO3
Shifts K into cells 3 ampules / litre (134 mmol/l NaHCO3 ) Reserved for severe hyperkalemia assoc. with Acidosis or ACE-I and ARBs + renal failureS