2. POTASSIUM. . .
Maintenance of k balance –
essential for a variety of cellular
functions & neuromuscular transmission
Total body stores : 3000 – 4000mEq
98% - located in the cells
Intracellular K+
concentration : 140 meq/l
Extracellular concentration : 4-5 meq/l
3. POTASSIUM. . .
Difference is maintained by the
Na+
-K+
-ATPase
Ratio of K+
concentration inside cell &
outside - major determinant of resting
membrane potential
10. Hypokalemia
Plasma K < 3.5 mEq/L
Occurs in > 20% of hospitalized
patients
May be asymptomatic
Usually does not require emergency
supplementation over minutes to
hours
Can be dangerous - arrhythmias,
rhabdomyolysis, paralysis.
14. HYPOKALEMIA – DRUG INDUCED
TRANSCELLULAR
K SHIFT
⇑ RENAL K
LOSS
⇑ K LOSS IN
STOOL
Epinephrine
Pseudoephedrine
Salbutomol
Theophylline
Ritodrine
Verapamil
Chloroquine
Insulin overdose
Acetazolamide
Thiazides
Loop diuretics
Fludrocortisone
Pencillin
Aminoglycoside
Amphotericin B
Cisplatin
Phenolphthalein
Na polystrene
sulfonate
18. PSEUDOHYPOKALEMIA
Abnormal WBCs – in large numbers(AML)
– can take up extracellular K when stored
at room temp
Apparent hypokalemia – artefact of
storage procedure
Rapid separation of plasma/storing at 4°C
confirms diagnosis,
avoids this artefact & inappropriate Rx
19. HYPOKALEMIA – ECG CHANGES
•Mild to moderate :
3-3.5mEq/L ----
FLATTENING OR T WAVE INVERSION
•Severe :
2.5-3mEq/L -----QT interval prolongation,
visible U wave ,
mild ST depression(0.5mm) ,
Ventricular extrasystoles.
•Very severe :
<2mEq/L ---- Torsades de pointes ,
Ventricular Fibrillation
20. HYPOKALEMIA - ECG
ST depressions with prominent U waves &
prolonged repolarization
21. HYPOKALEMIA - ECG
Prominent U wave in V3 & V4 giving the conjoined T- U
wave the appearance of "camel's hump“
22. Approach to Hypokalemia
Step 1: Redistribution or depletion?
Redistribution causes
Insulin therapy - DKA
Beta 2 agonists - Salbutomol
Metabolic alkalosis
Beta 2 adrenergic stimulation – AMI
⇑ cell proliferation – Rx of megaloblastic anemia
Barium poisoining
Replacement of potassium in these settings may
lead to overshoot & hyperkalemia
23. Approach to Hypokalemia
Step 1: Redistribution or depletion?
Depletion causes (common)
GI tract losses (diarrhea, vomiting)
Loop/thiazide diuretic therapy
Other medications (e.g. amphotericin B)
Osmotic diuresis (DKA)
Refeeding syndrome (NEVER underestimate!)
Endocrinopathies (mineralocorticoid excess)
Salt wasting nephropathies/RTA’s
Magnesium deficiency (NEVER overlook!)
24. Step 2: Estimate the deficit
Total K+ body stores – 3000-4000mEq
For every 100 mEq below normal,
serum K+
usually drops by 0.27 mEq/L
Roughly 1 mEq /L fall in S.K+ = 200 -400
mEq total body K+ deficit
Highly variable from patient to patient,
however!!
25. S.K
(mEq/L)
>3.5 3 2 <2
TOTAL
K deficit
(mEq/L,70 kg)
0 300 450-600 >600
HYPOKALEMIA & TOTAL K DEFICIT
26. Approach to Hypokalemia
Step 3: Choose route to replace K+
In nearly all situations, ORAL
replacement is PREFERRED over IV
replacement
Oral has less side effects (IV burns!)
Oral is less dangerous
Easy compliance
Choose IV therapy ONLY in patients
who are NPO (for whatever reason) or
who have severe depletion
27. Approach to Hypokalemia
Step 4: Choose K+
preparation
Oral therapy
Potassium Chloride is PREFERRED AGENT
Especially useful in Cl-
responsive metabolic
alkalosis
⇑ in ECF K quicker with KCl compared to other
salts
Potassium Phosphate useful when coexistant
phosphorus deficiency
Often useful in DKA patients
Potassium bicarbonate, acetate, gluconate, or
citrate useful in metabolic acidosis
28. Approach to Hypokalemia
Step 4 (contd…):
Oral therapy :
In mild to moderate hypokalemia
(3.0 to 3.5 mEq/L) :
Avg dose of KCl is 60-80 mEq /d , along with
treatment of underlying disorder
In severe Hypokalemia more rapid replacement
is needed it can be increased upto 40 mEq 6th
hrly.
ORAL SYP. 15 ml POTCHLOR= 2O mEq
Tab. 1 Tab KCl = 8mEq
29. Approach to Hypokalemia
Side effects of oral therapy
GI irritation (therefore patient is advised to
take KCl soln, in a glass of water after food)
oesophageal ,small bowel erosions and
strictures are uncommon
30. Approach to Hypokalemia
IV therapy:
IV thrapy carries high risk of hyperkaelmia
So IV K+ supplementation should be reserved
for severe symptomatic Hypokalemia or for
patients who cannot ingest oral K+
IV 15%POTTASIUM CHLORIDE 1ml = 2
mEq/L
10 ml = 20 mEq/L
31. GUIDELINES
ALWAYS MONITER IV K+ therapy closely with
ECG monitering and frequent Serum K+
estimation.
Avoid IV K+ till Urine output is established
Never give injection direct IV It can cause
sudden Hyperkalemia and instant death from
cardiac arrest.
Never add KCl to Isolyte -M
Treatment of Acidosis with IV NaHCO3 may
aggravate or precipitate Hypokalemia due to
intracellular shift of K+.
32. GUIDELINES contd…
In severe hypokalemia KCl should be mixed
with Isotonic Saline .
Don’t use 5% Dextrose as diluent Because
Dextrode stimulates Insulin release which will
shift the potassium intracellularly .
So initially , aggravtes the hypokalemia, here
transient reduction of serum K+ can be 0.2
-1.4 mEq/L if 20 mEq of KCl in 1unit 5% D .
Commonest indications --- DKA ,HONKC / HHS
33. REMEMBER – THAT
HYPOKALEMIA IS SAFER THAN
HYPERKALEMIA
AVOID OVERENTHUSIASM in Rx
DON’T GIVE MORE THAN
10-20mEq/hr
40 mEq/L
240 mEq/day
34. How to give IV ??
100mEq of K+ { 5amps of 15% KCl } is mixed
with 1 lit of 0.9% NS .
Infusion of this Saline at rate of 100ml /hr
which will deliver 10mEq of KCl /hr.
Avg raise in K+ is 0.25mEq/L when 20 mEq of
KCl /hr.
35. IN UP TO DATE
For 1000 ml NS never give more than 3
amp.(60 mEq)
For 100-200 ml NS ,
If it is in central vein max upto 40 mEq,(2
amps KCL)
If it is in peripheral vein upto 10 mEq
36. How long to give IV ??
As soon as cardiac rhythm returns to normal or
muscle strength is restored to normal .
IV K+ is gradually tapered and discontinued
and oral KCl is initiated
37. ADVERSE EFFECTS
Severe Phlebitis if >40mEq/l infused into the
peripheral veins
So , > 40 mEq/L K+ should be infused into
large {femoral> subclavian } .
Sudden severe hyperkalemia
38. K RICH FOOD
Fruit juices
Tender coconut
water
Banana
Juicy fruits
Dry fruits
Chocolate
Coffee
Soups
Salt substitutes
39. IV Fluid Iso M Iso P Iso G Iso E RL
K(mEq/L) 35 20 17 10 4
K CONCENTRATION OF IV FLUIDS
40. Monitoring…..
Severe hypokalemia, DKA patients
Reassess labs Q4-6 hours
Moderate hypokalemia patients
Reassess labs BID to TID as needed
Mild hypokalemia
Reassess labs QDay or less as needed
41. Housekeeping/follow up
BE AGGRESSIVE in DKA patients patients
May want to keep K+
over 4.0 or even 4.5
mEq/L in cardiac patients, especially in
those with arrhythmias
BE GENTLE in patients with acute or chronic
renal failure
May wish to cut doses in half, double
intervals, or not replace at all
May need to monitor very closely
43. Old concept :
Na-K-ATPasechannel dysfunction by
hypoMg2+
New theory:
ROMK as an inward rectifying
K+channel
Intracellular Mg2+ binds and blocks
the pore of the channel from the
inside
LimitK+efflux from the cell
NOT limitK+influx into the cell
45. HYPOMAGNESEMIA WITHOUT HYPOKALEMIA
Seen in
Familial
Hypomagnesemia Hypercalcuria
And Nephrocalcinosis
Hypomagnesemia with secondary hypocalcemia
Where serum K+ and U.K+ excretion are normal.
46.
47. Transtubular Potassium Gradient
TTKG = Uk x Posm
Sk x Uosm
Plasma osmolality :
Urine Osmolality:
Normal TTKG –- 8-9
2 × Na + glucose (mg/dl) + BUN (mg/dl)
18 2.8
2 × Na + glucose (mmol/L) + BUN (mmol/l)
55. HYPOKALEMIC PERIODIC PARALYSIS
HOKPP1CACNA1S (a voltage-gated calcium channel found
in the transverse tubules of skeletal muscle cells)
HOKPP2SCN4A (a voltage-gated sodium channel found at
the neuromuscular junction)
56. Attacks often begin in adolescence and most commonly
occur on awakening or after sleep or rest following
strenuous exercise (attacks during exercise are rare),
high carbohydrate meals, meals with high sodium content,
sudden changes in temperature, and even excitement,
noise, flashing lights and induced by cold temperatures.
Weakness may be mild and limited to certain muscle
groups, or more severe full-body paralysis.
Attacks may last for a few hours or persist for several
days. Recovery is usually sudden when it occurs, due to
release of potassium from swollen muscles as they
recover.
57. PREVENTION
Normal intake should be 60 mEq/d prevent Hypokalemia.
But patient receiving Digitalis and long term diuretics
should receive K+ supplement.
Post operative patients on parenteral fluid therapyshould
receive 40-50 mEq/d to prevent Hypokalemia.
Editor's Notes
Hypokalemia produces distinctive changes in the ST-T complex. The most common pattern seen is ST depressions with prominent U waves and prolonged repolarization. With hypokalemia, the U waves typically become enlarged and may even exceed the height of the T waves.
Particularly important in Digitalis patients!
