fluid

HYPOKALEMIA

3.5-5.2 mmol/L) )Potassium
Only 2% is found outside the cells and of this only 0.4% of your K+ is found in the plasma.
Thus as you can see serum K+ measurements have limitations in
reflecting TOTAL body K+ stores.
A 1 mEq/L drop in K+ reflects between 200-400 mEq total body K+ deficit

3.5-5.2 mmol/L) )Pottasium

*Major intracellular cation
*ICF conc. = 150- 160 mEq/ L
*Resting membrane potential
*Regulates fluid, ion balance inside cell
*Contribute to pH balance
Pathophysiology of Hypokalemia
Decrease in K+ causes decreased excitability of cells, therefore cells are less responsive to normal stimuli

Hypokalemia can only occur for four reasons:

Decreased intake
Shift into cells
Extra-renal losses..GIT
Renal losses


*Spurious - i.e. K+ is falsely low..cases of Hyperleukocytosis

Decreased intake normal intake 40-120 daily.

Shift into cells:
1. Alkalosis
2.Insulin
3. Beta adrenergic drugs or epinephrine

*Ketoacidosis – mechanism of Hypokalemia : because of hypoinsulinemia there will be shift of K+ to ECC, H+ replaces K+, which is lost in urine(polyuria)

Examples of

increased potassium entry into cells
Hypokalemic periodic paralysis:
typically oriental men with thyrotoxicosis; ? abnormal Ca++ channel; ? Increased Na/K atp ase activity.
Increased RBC uptake:
e.g. after treatment with B12, folate.

Gastrointestinal losses of potassium

Gastric juice contains 5 – 10 mEq K+/L.
Intestinal fluids contain 20 – 50 mEq/L


Hypokalemia from loss of gastric fluid.
*Loss of hydrogen ion increases plasma bicarbonate(Alkalosis).
*Coexisting volume depletion increases aldosterone secretion.
* In the setting of increased aldosterone levels, sodium is retained and potassium excreted.
Potassium loss is most prominent early.
Actual losses in gastric juice are relatively small.

Diarrheal losses are usually accompanied by metabolic acidosis

1.Villous adenoma
.Laxative abuse2

The kidney and potassium

Renal K+ LossUrine K+ >20 mEq/24 hours
or spot urine K+ of > 30
*Nearly all potassium filtered at the glomerulus is reabsorbed in the proximal nephron.
*Urinary potassium is the result of distal potassium secretion.
* To excrete potassium, the kidney requires an adequate number of nephrons, aldosterone, and a circulation adequate to provide adequate distal delivery of sodium for sodium/potassium exchange.(Na-K-ATPase)

Causes of Renal loss of potassium

Primary hyperaldosteronism ( Conns syndrome),
Cushing syndrome and increased steroids.
Diuretic therapy :Thiazides, loop diuretics and *Diuretics- activate the renin-angiotensin-aldosterone cascade.
Cabonic anhydrase inhibitor



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Clinical manifestations of Hypokalemia

Neuromuscular disorders
Muscle Weakness, flaccid paralysis, respiratory arrest,
GIT :nuasia , constipation paralytic ileus
Acquired Nephrogenic DI( Polyuria,polydypsia)
Heart : Arrhythmias, Postural hypotension
ECG Changes: Flat T-wave appearance of U wave
Cardiac arrest

Management

*treat underlying cause
*correction of alkalosis
*Oral…KCL Tabs
*Parenteral…….beware……infusion of KCL should be slowly….DO NOT exceed 10mmol per hour