HYPOKALEMIA

BASIC PHYSIOLOGY
 CAUSES OF HYPOKALEMIA

1. DECREASED INTAKE-
(A) STARVATION
(B) CLAY INGESTION

2. REDISTRIBUTION INTO CELLS

3. INCREASED LOSSES
(A) EXTRA-RENAL LOSSES
(B) RENAL LOSSES
 REDISTRIBUTION INTO CELLS

I) ACID-BASE DISTURBANCES
II) HORMONAL
III) ANABOLIC
IV) OTHER

I) ACID-BASE-
METABOLIC ALKALOSIS PROMOTES NA/K+ PUMP MEDIATED
SHIFT OF K+ INTO CELLS
II) HORMONAL
INSULIN
i) Exogenous- Iatrogenic
Hypokalemia
ii) Endogenous- Malnourished
patients given a carbohydrate
meal, Total Parenteral Nutrition
INCREASD SYMPATHETIC THYROID
ACTIVITY 1. Thyrotoxic Periodic Paralysis
i) Increased B adrenergic activity- 2. Hyperthyroidsim
Alcohol withdrawal, Post MI,
Post severe Head injury,
Hyperthyroidism
ii) Beta adrenergic drugs-
Bronchodilator, Tocolytics
iii) Alpha Antagonists
iv) Other sympathomimetic drugs
v) Downstream stimulation of
Na/K+ pump- Theophylline,
Caffeine
III) ANABOLIC STATES
1. VITAMIN B12 / FA ADMINISTRATION (RBC PRODUCTION)
2. GM-CSF ADMIN (WBC PRODUCTION)
3. TOTAL PARENTERAL NUTRITION

IV) OTHERS
4. PSEUDOHYPOKALEMIA- PROFOUND LEUKOCYTOSIS
5. FAMILIAL HYPOKALEMIC PERIODIC PARALYSIS
6. HYPOTHERMIA
7. BARIUM TOXICITY
 INCREASED LOSSES

• NON RENAL LOSSES

A) GI LOSS
I) DIARRHEA- INFECTIOUS/ NONINFECTIOUS- CELIAC, ILEOSTOMY, VILLOUS
ADENOMA, VIPOMA, CHRONIC LAXATIVE ABUSE, IBD, COLONIC PSEUDO OBSTRUCTION
II) VOMITING/ NG SUCTIONING- DIRECT LOSSES FEW, PREDOMINANTLY RENAL
B) INTEGUMENTARY LOSSES- SWEATING

• RENAL LOSSES

A) INCREASED DISTAL FLOW AND NA+ DELIVERY

I. DIURETICS: THIAZIDES > LOOP DIURETICS
II. OSMOTIC DIURESIS- HIGH DOSES OF PENICILLIN RELATED ANTIBIOTICS
B) HYPOMAGNESEMIA
C) EXCESSIVE SECRETION OF K
1. MINERALOCORTICOID EXCESS-
I) PRIMARY HYPERALSDOSTERONISM- ALDOSTERONE:PRA >50
GENETIC- FH1/FH2/FH3, CONGENITAL ADRENAL HYPERPLASIA
ACQUIRED- ALDOSTERONE PRODUCING ADENOMA, UNILATERAL ADRENAL HYPERPLASIA (PAH),
BILATERAL ADRENAL HYPERPLASIA (IHA) , ADRENAL ADENOMA
II) SECONDARY HYPERALDOSTERONISM
RENAL ARTERY STENOSIS (MC)
RENIN SECTING TUMORS
MALIGNANT HYPERTENSION
III) CUSHINGS SYNDROME- MORE IN ECTOPIC ACTH VS CUSHING’S DISEASE
IV) BARTERS SYNDROME, GITELMAN SYNDROME
2. APPARENT MINERALOCORTICOID EXCESS
I) SAME ( SYNDROME OF APPARENT MINERALOCORTICOID EXCESS) –
DEFICIENCY OF
11B HSD TYPE 2
II) INHIBITION OF 11B HSD TYPE 2 BY- GLYCYRRHIZINIC ACID/ CARBENOXOLONE;
ITRACONAZOLE & POSACONAZOLE
III) LIDDLE’S SYNDROME

3. DISTAL DELIVERY OF NON REABSORBABLE ANIONS- VOMITING/ NG SUCTION

( HCO3), PROXIMAL RTA, DKA
DIAGNOSTIC APPROACH TO HYPOKALEMIA
THE TRANS-TUBULAR POTASSIUM GRADIENT (TTKG) IS AN INDEX REFLECTING
THE CONSERVATION OF POTASSIUM IN THE CORTICAL COLLECTING DUCTS (CCD)
OF THE KIDNEYS.
NOTE THAT THIS FORMULA IS VALID ONLY WHEN UOSM >300 AND UNA >25

THE EXPECTED VALUES OF THE TTKG ARE LARGELY BASED ON HISTORICAL DATA,
AND ARE 7–8 IN THE PRESENCE OF HYPERKALEMI
 ECG CHANGES IN HYPOKALEMIA

• PROMINENT U WAVES- BEST SEEN IN V2- V3 AND WHEN

S. K+<3 MM
• FLAT T WAVE/ T WAVE INVERSIONS
• ST DEPRESSION
• PR INTERVAL PROLONGATION
• INCREASE IN P-WAVE AMPLITUDE (PSEUDO-P PULMONALE_
• QT PROLONGATION
 TREATMENT

• TOTAL POTASSIUM DEFICIT- SERUM K+ DROPS BY ~0.27 MM FOR EVERY 100-MMOL REDUCTION
IN TOTAL-BODY STORES; LOSS OF 400–800 MMOL OF TOTAL-BODY K+ RESULTS IN A REDUCTION
IN SERUM K+ BY ~2.0 MM
• POTASSIUM PREPARATIONS
• POTASSIUM PHOSPHATE- PREFERRED IN COIMBINED HYPOKALEMIA AND HYPOPHOSPHATEMIA
EXAMPLE- TYPE 2 RTA
• POTASSIUM BICARBONATE/ CITRATE- PREFERRED IN PTS WITH CONCOMITANT METABOLIC ACIDOSIS
• POTASSIUM CHLORIDE- PREFERRED BECAUSE PTS WITH HYPOKALEMIA OFTEN CHLORIDE DEPLETED.
RAISES POTASSIUM AT FASTER LEVELS COMPARED TO OTHER PREPARATIONS
 ORAL VS IV

• ORAL POTASSIUM PREFERRED OVER IV.

• THE USE OF INTRAVENOUS ADMINISTRATION SHOULD BE LIMITED TO PATIENTS
UNABLE TO USE THE ENTERAL ROUTE OR IN THE SETTING OF SEVERE
COMPLICATIONS (E.G., PARALYSIS, ARRHYTHMIA) AND CAN BE CONSIDERED IN
SEVERE HYPOKALEMIA ( <2.5-3 MM)
• SHOULD ALWAYS BE ADMINISTERED IN SALINE SOLUTIONS, RATHER THAN
DEXTROSE, BECAUSE THE DEXTROSE-INDUCED INCREASE IN INSULIN CAN
ACUTELY EXACERBATE HYPOKALEMIA
• THE PERIPHERAL INTRAVENOUS DOSE IS USUALLY 20–40 MMOL OF K+-CL– PER
LITER
• IF HYPOKALEMIA IS SEVERE ( <2.5 MM) OR CRITICALLY SYMPTOMATIC, IV KCL
THROUGH A CENTRAL VEIN WITH CARDIAC MONTORING IN INTENSIVE CARE
THANK YOU