Gopichand hypokalemia final

hypokalemia

1. APPROACH
TO
HYPOKALEMIA
By ;
Dr. A.GOPI CHAND ,
UNIT VII.

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

4. POTASSIUM METABOLISM

7. K HOMEOSTASIS – KEY HORMONES

8. Na & K transport in Principal cell
in Cortical Collecting Duct

9. ALDOSTERONE ACTION IN PRINCIPAL CELLS

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.

11. Hypokalemia classification
Mild to moderate : 3-3.5mEq/L
Severe : 2.5-3mEq/L
Very severe : <2mEq/L

12. HYPOKALEMIA
Clinical manifestations determine
urgency & magnititude of treatment,
not laboratory values
Frequent reassessment of K required
ABG - useful

13. HYPOKALEMIA - CAUSES
DRUGS
GI LOSS : Vomiting,NG suction,diarrohea
SKIN :Profuse sweating,extensive burns
HORMONES : Aldosterone,Steroids,Renin
secreting tumors , CAH
MAGNESIUM DEFICIENCY
INTRINSIC RENAL TRANSPORT DEFECTS :
Bartter´s,Gitelman´s,Liddle´s
syndromes

14. HYPOKALEMIA – DRUG INDUCED
TRANSCELLULAR
K SHIFT
Ý RENAL K
LOSS
Ý 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

15. HYPOKALEMIA – CLINICAL
MANIFESTATIONS
CVS : ECG changes,atrial/ventricular
arrhythmias,
SKELETAL MUSCLE :
Weakness,cramps,tetany,paralysis,
rhabdomyolysis
SMOOTH MUSCLE :
Constipation,Ileus,urinary retention
ENDOCRINE : Carbohydrate intolerance

16. HYPOKALEMIA – RENAL EFFECTS
Impaired concentrating ability – polyuria
& polydipsia – Nephrogenic DI
This appears to occur because hypokalemia
causes defective activation of renal
adenylate cyclase, preventing antidiuretic
hormone-stimulated urinary concentration.
Impaired ammonia production – hepatic
failure
hypokalemia increases proximal tubule
ammoniagenesis.

17. HYPOKALEMIA – RENAL EFFECTS
Impaired urinary acidification
Hypokalemia
inhibits aldosterone secretion
Interstitial nephritis

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
Ý 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
Ý 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 6
th

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 FluidIso MIso PIso GIso ERL
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

42. RELATION BETWEEN
HYPOKALEMIA AND HYPOMAGNESEMIA
Basolateral surface

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

44. Median effective intracellular Mg2+concentration for ROMK
inhibition: 1.0 mM

45. HYPOMAGNESEMIA WITHOUT HYPOKALEMIA
Seen in
 Familial
Hypomagnesemia Hypercalcuria
And Nephrocalcinosis
Hypomagnesemia with secondary hypocalcemia
Where serum K+ and U.K+ excretion are normal.

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)

48. HYPOKALEMIA & ABG

51. HYPOKALEMIA,HTN,METABOLIC
ALKALOSIS - DIFFERENTIALS

53. HYPOKALEMIC METABOLIC
ALKALOSIS WITHOUT HTN

54. HYPOKALEMIA & PARALYSIS

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.