ELECTROLYTE IMBALANCE Hypokalemia in ICU

Presented By: Mentored ByDr.Shahzad A.Mumtaz Dr.M.Asim RanaCritical 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

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.

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.

Clinical Case32 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.

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

May 18 May 17 May 16 May 15 May 14 May 13 May 12

4.0 3.4 1.9 2.9 3.5 3.0 2.5 K +

0.89 0.78 0.95

0.92 0.90 0.68 0.75 Mg +

20meq KCL I/V

30meq KCL I/V

40meq KCL I/V

Replacement

40meq KCL I/V

100ml NaHCO3

4gm Mgso4

Answer & Rationale

End of slide show

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.

•

Hypokalemia = S.K+ level less than 3.5mMol/LB/C K+ is mainly IC ion,hypokalemia may occur in

low, normal or high total body K+.

1 2 2.5 3 S.K +

If PH nor 400+Meq 400Meq 300Meq 200Meq Total Deficit

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.

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

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

Clinical EffectsCardiovascular: Arrhythmias then conduction

defects/Myocardial DysfunctionVascular: Postural hypotension

Neuro Muscular:Skeletal muscle weakness:fatigue,myalgia.

Smooth muscles—paralytic ileusRespiratory muscle weakness—hypoventilationTetany,Rhabdomyolysis,Hyporeflexia– impaired mentation

Renal Effects: Reduced GF to renal damage GIT : Nausea,Vomiting,Paralytic ileusMetabolic : Glucose intolerance,Metabolic Alkalosis

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

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.

Go back to the Case

• Calculate K+ deficit.• Answer• Rationale of Question

Clinical Case32 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.

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 .

May 18 May 17 May 16 May 15 May 14 May 13 May 12

4.0 3.4 1.9 2.9 3.5 3.0 2.5 K +

0.89 0.78 0.95

0.92 0.90 0.68 0.75 Mg +

20meq KCL I/V

30meq KCL I/V

40meq KCL I/V

Replacement

40meq KCL I/V

100ml NaHCO3

4gm Mgso4

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

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.

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.

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.

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

Central Line Peripheral Line

80Meq/L 40Meq/L LVI Maximum Conc

80Meq/L 40Meq/L TPN Maximum Conc

S.K+ = 2.5mMol/L……………Pls Help