A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.

1. ELECTROLYTE IMBALANCE
Hypokalemia in ICU
Presented By: Mentored By
Dr.Shahzad A.Mumtaz Dr.M.Asim Rana
Critical Care Fellow CCD Consultant
References:
1)Oh intensive care manual
2)KSMC CCD Protocols (Review)
3)www.uptodate.com
4)The washington manual of critical
care

2. Objectives
•Review causes & clinical manifestations of
electrolyte disturbances.
•Outline emergent management of electrolytes
disturbances.
•Learning when to refer & when to admit.
•Recognize & treat the cause.

3. Principles of Electrolyte Disturbances
• Implies an underlying disease process.
• Treat the electrolyte change but seek the
cause.
• Determine urgency of treatment according to
clinical manifestations, not by laboratory
values.
• Speed & magnitude of correction dependent
on clinical circumstances.
• Frequent re-assessment of electrolytes
required.

4. Clinical Case
32 years old female 70 kg with Type 1 DM presented in
E/R as unresponsive,history of vomiting,abdominal
pain. Vital signs were BP 114/70,HR 120/min,RR
24/min,& afebrile.ABGs revealed 7.11/10/180/5 on
O2 5l/min.Initial lab results showed Na 139 mMol/L,
K+ 2.5mMol/L,Cl 105 and Glucose 368.ECG is
normal, Mild renal impairment. Anion Gap
calculated as 28.Normal albumin,amylase,lipase.
DKA protocol was applied. Electrolyte replacement
protocol was also followed.

5. May 12 May 13 May 14 May 15 May 16 May 17 May 18
K+ 2.5 3.0 3.5 2.9 1.9 3.4 4.0
Mg+ 0.75 0.68 0.90 0.92 0.95 0.78 0.89
20meq
KCL I/V
30meq
KCL I/V
40meq
KCL I/V
Replacement
40meq
KCL I/V
100ml
NaHCO3
4gm
Mgso4
Pt condition deteriorated,ABGs revealed as 7.1/26/89/3 got wide complex
tachycardia,arrested,ABGs showing K+ 1.9.Immediate replaced,Pt reverted back, followed
closely. Next 2 days, AG closed,electrolytes normailzed.She was extubated,out of DKA,Stable
and ready for discharged from ICU today.
Q: What was the most likely event happened that pt arrested?
1)Silent Myocardial Ischemia in Diabetic pt
2) Administration of 100 ml 8.4% Bicarbonate.
3)Administration of 40 Meq Kcl was not adequate.
4)Potassium replacement/DKA protocol was not followed
5)Administration of Mgso4

6. Answer & Rationale
End of slide show

7. Hypokalemia(k+ major IC cation)
• S.K+ range is 3.5-5.0 mMol/L
• 98% of total body K+ is intracellular
• A decrement of 1mMol/L of SK+ concentration
means a loss of about 200-300mMol/L in body
K+ stores.
•
S.K+ 3 2.5 2 1
Total Deficit 200Meq 300Meq 400Meq 400+Meq If PH nor
Hypokalemia = S.K+ level less than 3.5mMol/L
B/C K+ is mainly IC ion,hypokalemia may occur in
low, normal or high total body K+.

10. Functions
• Main function is the stability of action potential
of the cell membrane.
• Main effect of hypokalemia is hyperpolarization
of resting membrane potential affecting mainly:
The heart producing arrhythmias
Brain affecting nerve conduction
• K+ also plays a role as co factor in enzymatic
reactions.
• Maintain the normal cell volume
• Also affects IC H+ conc & participate in
regulation of Intracellular PH.

11. Causes of Hypokalemia
1)Decreased Intake: Starvation,IVF without K+
Clay Ingestion-(Geophagia)
2)Redistribution e.g,Shift of K+ from ECF to ICF
a)Metabolic Alkalosis
b)Hormonal : Insulin,Beta 2 adrnergic agonist
c)Anabolism: TPN,Vit B12 or Folic Acid,GMCSF
d)Others: Pseudohypokalemia,Hypothermia,
Barium Toxicity,HPP
3)Increased Loss
Renal & Non Renal

12. Causes
a)Renal Losses of K+
Diuretics-leads to increased renal tubular flow
Aldosterone secretion causing k+ wasting in
presence of Na ions.
Renal Tubular Damage-from nephrotoxic drugs
osmotic diuresis & increased excretion of
non-absorbable ketoacid anions.
RTA 1,2 BS,LS,GS
Exogenous Mineralocorticoid
b) Non-Renal loss of K+ e.g. GIT loss

13. Clinical Effects
Cardiovascular: Arrhythmias then conduction
defects/Myocardial Dysfunction
Vascular: Postural hypotension
Neuro Muscular:
Skeletal muscle weakness:fatigue,myalgia.
Smooth muscles—paralytic ileus
Respiratory muscle weakness—hypoventilation
Tetany,Rhabdomyolysis,Hyporeflexia– impaired mentation
Renal Effects: Reduced GF to renal damage
GIT : Nausea,Vomiting,Paralytic ileus
Metabolic : Glucose intolerance,Metabolic Alkalosis

14. Question
• Which one of the following EKG changes is
least likely to occur with Hypokalemia
A) ST-T segment Depression
B) T-wave inversion
C) AV Blocks(2nd & 3rd degree)
D) Pre mature ventricular contractions
E) U waves
F) QT Prolongation

15. Management approach
Careful history e.g. Vomiting,Laxative abuse,Diuretics
Eliminate decreased intake .
Exclude Pseudohypokalemia
• Calculate K+ Deficit and replace.
• Calculate Transtubular K+ gradient
• Do Urinary K+,CL & S.HCO3,Renin,Follow
algorithm.
Kdeficit (mmol) = (Knormal lower limit - Kmeasured) x kg body weight x 0.4
Daily potassium requirement is around 1 mmol/Kg body weight.
Add normal daily requirement + losses along with deficit.

16. Go back to the Case
• Calculate K+ deficit.
• Answer
• Rationale of Question

17. Clinical Case
32 years old female 70 kg with Type 1 DM presented in
E/R as unresponsive,history of vomiting,abdominal
pain. Vital signs were BP 114/70,HR 120/min,RR
24/min,& afebrile.ABGs revealed 7.11/10/180/5 on
O2 5l/min.Initial lab results showed Na 139 mMol/L,
K+ 2.5mMol/L,Cl 105 and Glucose 368.ECG is
normal, Mild renal impairment. Anion Gap
calculated as 28.Normal albumin,amylase,lipase.
DKA protocol was applied. Electrolyte replacement
protocol was also followed.

18. May May 12 May 13 May 14 May 15 May 16 May 17 18
K+ 2.5 3.0 3.5 2.9 1.9 3.4 4.0
Mg+ 0.75 0.68 0.90 0.92 0.95 0.78 0.89
20meq
KCL I/V
30meq
KCL I/V
40meq
KCL I/V
Replacement
40meq
KCL I/V
100ml
NaHCO3
4gm
Mgso4
Pt condition deteriorated,ABGs revealed as 7.1/26/89/3 got wide complex
tachycardia,arrested,ABGs showing K+ 1.9.Immediate replaced,Pt reverted back, followed
closely. Next 2 days, AG closed,electrolytes normailzed.She was extubated,out of DKA,Stable
and ready for discharged from ICU today.
Q: What was the most likely event happened that pt arrested?
1)Silent Myocardial Ischemia in Diabetic pt
2) Administration of 100 ml 8.4% Bicarbonate.
3)Administration of 40 Meq Kcl was not adequate.
4)Potassium replacement/DKA protocol was not followed
5)Administration of Mgso4.

19. Transtubular K+ concntration Gradient
• TTKG can distinguish renal from non-renal loss of K+.
• Ratio of k+ conc in lumen of cortical collecting duct to that of potassium in plasma
• TTKG is simple & rapid calculation of net K+ secretion calculated as follows:
TTKG = (U. potassium /S. potassium) ÷ (U. osmolality / S. osmolality)
Hypokalemia + TTKG < 2
Hypokalemia + TTKG > 4 + Metabolic Acidosis
Hypokalemia + TTKG > 4 + Metabolic Alkalosis + Hypertensive or Normotensive

21. Treatment
 Diagnosis & treatment of underlying cause.
 Therapeutic goals are to correct potassium
deficit & minimize ongoing losses.
 Treat aggressively in severe metabolic acidosis
 Correction of Hypomagnesaemia.
 Discontinue offending drugs.
 It is safer to correct hypokalemia via Oral route.
 K+ should be diluted in nonglucose solutions.
 Avoid over infusions or Hyperkalemia.

22. Treatment contd:
Replace either Oral or intravenous.
Intravenous------Central or Peripheral line.
Oral------Tablet or Syrup
Orally Tablets are available 600mg or 750mg.
Intravenous allowed max dose/hour is controversial
However
IV KCL replacement 20mEq/hr via Infusion pumps
via central line or 10mEq/hr via infusion pumps via
peripheral line.

23. Treatment Contd:
Never give potassium I.M or rapid I.V push.
Never give more than 26.8meq/2gm KCl over 1
hour without any continuous ECG monitor.
Do not just add the KCl solution to the hanging I.V
fluid bag. Fully invert it around 10 times to ensure
proper mixing.
1 tab(600mg) of( Slow K) gives around 8 mmol
potassium.
Peripheral veins are damaged by a potassium
concentration greater than 30 mmol/L. For higher
concentrations, central lines are preferred.

24. Treatment Recommendations
Small Volume Infusions •
10Meq/100ml –Preferred peripheral line •
10Meq/50ml– Preferred central line •
20Meq/100ml—C.monitoring+peripheral or central •
20Meq/50ml--- C.monitoring+central •
Large Volume Infusions •
Peripheral Line Central Line
LVI Maximum Conc 40Meq/L 80Meq/L
TPN Maximum Conc 40Meq/L 80Meq/L

25. S.K+ = 2.5mMol/L……………Pls Help