Potassium Homeostasis & Its disorders

Potassium HomeostasisPotassium Homeostasis&&

Its disordersIts disorders

ByBy

Dr. Mohammad El-TahlawiDr. Mohammad El-Tahlawi

ObjectivesObjectives

Potassium homeostasisPotassium homeostasis

HypokalamiaHypokalamia

DefinitionDefinition

CausesCauses

EffectsEffects

DiagnosisDiagnosis

TreatmentTreatment

POTASSIUMPOTASSIUM

Potassium play an important role in:Potassium play an important role in:

1-Electerophysiology of cell membrane 1-Electerophysiology of cell membrane

for all cells in which polarization-for all cells in which polarization-

depolaization cycles are functionally depolaization cycles are functionally

relevant(cardiac and neuromuscular relevant(cardiac and neuromuscular cells).cells).

2-Carbohydrates and protien synthesis2-Carbohydrates and protien synthesis

POTASIUM DISTRIBUTION

In 70 kg

Intracellular 98%3430 meq

K content = 50 meq/kg

Total body K = 3500 meq

Extracellular 2%70 meq

Plasma20%

15 meq

Na-K ATPaseNa-K ATPase

Intracellular

K=140 meq/L

Extra cellular

K=4 meq/L(3.5-4.5meq)

K level in meq / L

intracellular K deficit BY

100 - 200 meq

Decrease in plasma K from 4 - 3 meq/L

intracellular K deficit BY

200 - 400 meq

Decrease in plasma K from 3 - 2 meq/L

Plasma K concentration CorrelatesPlasma K concentration Correlates

poorly with the total body k poorly with the total body k deficitdeficit

Plasma potassium concentrationPlasma potassium concentration

PotassiumIntake

Intercompartmentaldistribution

PotassiumExcretion

Dietary K intakeDietary K intake = = 8080 meq/day meq/day

ExcretionExcretion = = 7070 meq/day meq/day (urine).(urine).

= = 1010 meq/day meq/day (GIT).(GIT).

Regulation of K excretionRegulation of K excretion

The major determinant of urinary K excretion

Extra cellular K Extra cellular K Aldesterone levelAldesterone level

Tubular flow rateTubular flow rate

Intercompartmental shift of Intercompartmental shift of PotassiumPotassium

1- Extracellular pH.1- Extracellular pH.

2- Circulating insulin level.2- Circulating insulin level.

3- Circulating catecholamine 3- Circulating catecholamine activity.activity.

4- Plasma osmolality.4- Plasma osmolality.

5- Hypothermia.5- Hypothermia.

6- Exercise.6- Exercise.

pHK 0.6 meq/L every.01

Change in pH

Acidosis

Alkalosis

InsulinNa-K ATPase

Sympathetic activity (Na-K ATPase)

B2-agonist

B2-blokade

CELL

Plasma osmolality increase K 0.6meq/L per increase10mosm/L

Hypothermia Rewarming

HYPOKALEMIAHYPOKALEMIA

HYPOKALAEMIAHYPOKALAEMIA

(K ion less than 3.5 meq/L)(K ion less than 3.5 meq/L)

CausesCauses::

1-Intercompartmental shift of K.1-Intercompartmental shift of K.

2-Increase k loss.2-Increase k loss.

3-Inadequate k intake.3-Inadequate k intake.

Causes of hypokalamiaCauses of hypokalamia

Intercompartmental shift of K:Intercompartmental shift of K: AlkalosisAlkalosis

Insulin administrationInsulin administration

B2 adrenergic agonistB2 adrenergic agonist

HypothermiaHypothermia

Treatment of megaloplastic anaemiaTreatment of megaloplastic anaemia

Periodic paralasisPeriodic paralasis

Transfusion of frozen bloodTransfusion of frozen blood


Increase K losses Increase K losses (Renal or (Renal or extrarenal)extrarenal)

RenalRenal::DiureticsDiureticsIncrease mineralocorticiod activityIncrease mineralocorticiod activityRenal tubular acidosisRenal tubular acidosisKetoacidosisKetoacidosisHypomagesaemiaHypomagesaemiaUrinary diversion with long ileal loopUrinary diversion with long ileal loopCarbinecillin and Amphotericin BCarbinecillin and Amphotericin B


ExtrarenalExtrarenal:: GITGIT : Diarrhea,Vomiting,Fistula, : Diarrhea,Vomiting,Fistula,

Laxative abuse,Urinary Laxative abuse,Urinary diversion.diversion.

SweetSweet

DialysisDialysis

Decrease K intakeDecrease K intake

Effects of hypokalemiaEffects of hypokalemia

Most of the patients are asymptomatic Most of the patients are asymptomatic until until

K level below 3 meq/L.K level below 3 meq/L.

Cariovascular effects are most Cariovascular effects are most prominentprominent

Effects of hypokalamiaEffects of hypokalamia

CardiovascularCardiovascular ECG changesECG changes

DysrhythmiaDysrhythmia

Myocardial dysfunctionMyocardial dysfunction

Myocardial fibrosisMyocardial fibrosis

Orthostatic hypotensionOrthostatic hypotension

Increase digitalis toxicityIncrease digitalis toxicity

Effects of Effects of hypokalamiahypokalamia

CardiovascularCardiovascular

ECG changesECG changesT wave flatteningT wave flattening

Prominent U waveProminent U wave

ST segment depresionST segment depresion

Increase P wave amplitudeIncrease P wave amplitude

Prolongation of PR intervalProlongation of PR interval

Prominent U-wave

Flat T-wave

Depressed ST-segment

Normal

Dec

rea

sing

Ser

um

K+


NeuromuscularNeuromuscular Skletal ms. Weakness up to Skletal ms. Weakness up to respiratory failure.respiratory failure. TetanyTetany RhabdomyolysisRhabdomyolysis Ileus , Urine retentionIleus , Urine retentionRenalRenal PolyuriaPolyuria Increase amonium productionIncrease amonium production Increase HCO3 reabsorptionIncrease HCO3 reabsorption Increase Na retensionIncrease Na retension Increased renin secretionIncreased renin secretion→ → increase AngII→ thirstincrease AngII→ thirst


MetabolicMetabolic

Decrease insulin secretionDecrease insulin secretion

Decrease growth hormone Decrease growth hormone secretionsecretion

Decrease aldesterone secretionDecrease aldesterone secretion

HormonalHormonal

Negative nitrogen balanceNegative nitrogen balance

Encephalopathy in liver diseaseEncephalopathy in liver disease

Approach to diagnosisApproach to diagnosis

Hypokalemia

Urine K

Less than 30 meq/L More than 30meq/L

Diarrhea

Urine Chloride

Less than 15meq/L More than 15meq/L

NG Drainage

AlkalosisDiuretics

Mg depletion

Treatment of Treatment of hypokalemiahypokalemia

The goal of therapy:The goal of therapy:

Is to remove the patient from Is to remove the patient from immediate immediate

danger and not necessarily to danger and not necessarily to correct the correct the

entire K deficit.entire K deficit.

Firstly concernFirstly concern : :

Any condition that promotes Any condition that promotes transcellular transcellular

K shift.K shift.

Potassium replacementPotassium replacement

Oral replacementOral replacement with KcL solution is with KcL solution is generally safe(60-80 meq/d)generally safe(60-80 meq/d)

IV replacement IV replacement :(Remember ):(Remember )

Serious cardiac manifestation.Serious cardiac manifestation.

Peripheral line not exceed 8 meq/h.Peripheral line not exceed 8 meq/h.

More than 8meq/h, centeral line is More than 8meq/h, centeral line is indicated.indicated.

Dextrose containing solution should be Dextrose containing solution should be avoided.avoided.

ECG monitoring is mandatory in high rate ECG monitoring is mandatory in high rate infusion.infusion.

Potassium Potassium replacementreplacement

SolutionsSolutionsPotassium chloride and potassium Potassium chloride and potassium

phosphatephosphate

Kcl:Kcl: is available in 2meq/mL (5ml) is available in 2meq/mL (5ml)

is of choice with metabolic alkalosis is of choice with metabolic alkalosis as it corrects chloride shifts.as it corrects chloride shifts.

Osmolality = 4000 mosm/kgH2OOsmolality = 4000 mosm/kgH2O

K phosphate:K phosphate: is of choice with coexisting is of choice with coexisting hypophatemia (e.g DKA)hypophatemia (e.g DKA)


DeficitDeficit =(3.5 - acutal serum K ) x 0.4 =(3.5 - acutal serum K ) x 0.4 BWBW

MaintenenceMaintenence = 1 meq / kg BW / day = 1 meq / kg BW / day


Infusion rate (pripheral line)Infusion rate (pripheral line) Not exceed 8 meq / hNot exceed 8 meq / h

Infusion rate (centeral line)Infusion rate (centeral line) Standard method = 20 meq KcL in 100 ml Standard method = 20 meq KcL in 100 ml

saline/hsaline/h

Maximum rate (serum k less than 1.5 meq/L)Maximum rate (serum k less than 1.5 meq/L) We need peripheral lineWe need peripheral line

= 40 meq kcL / h = 40 meq kcL / h = ( ½ BW meq/h)= ( ½ BW meq/h)

Practical approachPractical approach

1.1. If K level <2 mEq/L, deficit= 0.4 x If K level <2 mEq/L, deficit= 0.4 x wt(normal – measured K) we can wt(normal – measured K) we can give up to 0.5 mEq/kg/hr.give up to 0.5 mEq/kg/hr.

2.2. If K level reaches 2.5 mEq/L, slowly If K level reaches 2.5 mEq/L, slowly corrects K by giving 10 mEq/hr.corrects K by giving 10 mEq/hr.

3.3. Add the daily intake (1 mEq/kg)Add the daily intake (1 mEq/kg)

It is advisable to give K salts into large It is advisable to give K salts into large but not central vein.but not central vein.

Potassium products:Potassium products:1.1. IV preparationsIV preparations2.2. Oral: 15ml= 40 mEq (if conc. Of KCl in Oral: 15ml= 40 mEq (if conc. Of KCl in

sol. is 10%)sol. is 10%)3.3. Natural sources:Natural sources: -Orange: one orange=300mg K-Orange: one orange=300mg K one litre juice=2.8gm Kone litre juice=2.8gm K -Bananas: one piece= 750mg K-Bananas: one piece= 750mg K K therapy in pediatrics: 1-3mEq/kg/every K therapy in pediatrics: 1-3mEq/kg/every

1mEq decrease in K level with max. 1mEq decrease in K level with max. 3mEq/kg/day 3mEq/kg/day

Response to the Response to the treatmenttreatment

At firstAt first The serum K may be slow to The serum K may be slow to rise particularly if K losses are ongoingrise particularly if K losses are ongoing

Full replacementFull replacement usually takes few usually takes few days.days.

If there is If there is refractory hypokalemiarefractory hypokalemia check check magnessium levelmagnessium level

CONCLUSIONCONCLUSION

Potassium has important role to vital body function .Potassium has important role to vital body function .

Plasma K concentration is a function of relationship Plasma K concentration is a function of relationship between entry, the inbetween entry, the intercompartemental distribution and tercompartemental distribution and excretion of K.excretion of K.

HypokalemiaHypokalemia : serum K less thd 3.5meq/L : serum K less thd 3.5meq/L

Cause Cause : Decrease intake, Losses and : Decrease intake, Losses and Intercompartemental Intercompartemental shift.shift. Effects Effects : : Cardiovascular,Neuromuscular,renal,Hormonal Cardiovascular,Neuromuscular,renal,Hormonal and metabolic.and metabolic. DiagnosisDiagnosis . .

TreatmentTreatment :Goals, replacement and response :Goals, replacement and response

HyperkalemiaHyperkalemia

HyperkalemiaPlasma [K+] > 5.0

Hyperkalemia may be the result of disturbances in external balance (total body K+ excess) or in internal balance (shift of K+ from intracellular to extracellular compartments)

HyperkalemiaPlasma [K+] > 5.0

Hyperkalemia may be the result of disturbances in external balance (total body K+ excess) or in internal balance (shift of K+ from intracellular to extracellular compartments)

Hyperkalemia: Disorders of Hyperkalemia: Disorders of External BalanceExternal Balance

ExcessiveK+ intake

Distal tubularflow

Mineralocorticoiddeficiency

Acute & chronicrenal failure

Distal tubulardysfunction

Pseudohyperkalemia

PseudohyperkalemiaPseudohyperkalemia

Movement of K+ out of cells during Movement of K+ out of cells during or after blood drawingor after blood drawing

HemolysisHemolysis

Fist clenching (local exercise Fist clenching (local exercise

effect)effect)

Marked leukocytosisMarked leukocytosis



Excessive Potassium IntakeExcessive Potassium Intake

Oral or Parenteral IntakeOral or Parenteral IntakeK pencillin in high dosesK pencillin in high dosesStored bloodStored blood



Decreased Renal ExcretionDecreased Renal Excretion

Acute and Chronic Renal FailureAcute and Chronic Renal Failure

Decreased Distal Tubular FlowDecreased Distal Tubular Flow Volume depletionVolume depletion Decreased effective arterial blood volume (CHF, cirrhosis)Decreased effective arterial blood volume (CHF, cirrhosis) Drugs altering glomerular hemodynamics with a decrease in Drugs altering glomerular hemodynamics with a decrease in

GFR (NSAIDs, ACE inhibitors, ARBs)GFR (NSAIDs, ACE inhibitors, ARBs)

Mineralocorticoid DeficiencyMineralocorticoid Deficiency Combined glucocorticoid and mineralocorticoid (adrenal Combined glucocorticoid and mineralocorticoid (adrenal

insufficiency)insufficiency) Hyporeninemic hypoaldosteronism (diabetes mellitus)Hyporeninemic hypoaldosteronism (diabetes mellitus) Drug-induced (ACE inhibitors, ARBs)Drug-induced (ACE inhibitors, ARBs)

Distal Tubular DysfunctionDistal Tubular Dysfunction Disorders causing impaired renal tubular function with Disorders causing impaired renal tubular function with

hyporesponsiveness to aldosterone (interstitial nephritis)hyporesponsiveness to aldosterone (interstitial nephritis) Potassium-sparing diuretics (amiloride, triamterene, Potassium-sparing diuretics (amiloride, triamterene,

spironolactone)spironolactone)

Hyperkalemia: Disorders of Hyperkalemia: Disorders of Internal BalanceInternal Balance

Hyperkalemia: Disorders of Hyperkalemia: Disorders of Internal BalanceInternal Balance

– Insulin deficiencyInsulin deficiency

22-Adrenergic -Adrenergic blockadeblockade

– HypertonicityHypertonicity

– AcidemiaAcidemia

– Cell lysisCell lysis

Clinical Manifestations of Clinical Manifestations of HyperkalemiaHyperkalemia

Clinical manifestations result primarily from the depolarization of resting cell Clinical manifestations result primarily from the depolarization of resting cell membrane potential in myocytes and neuronsmembrane potential in myocytes and neurons

Prolonged depolarization decreases membrane NaProlonged depolarization decreases membrane Na++ permeability through permeability through the inactivation of voltage-sensitive Nathe inactivation of voltage-sensitive Na++ channels producing a reduction in channels producing a reduction in membrane excitabilitymembrane excitability

Cardiac toxicityCardiac toxicity

– EKG changesEKG changes– Cardiac conduction defectsCardiac conduction defects– ArrhythmiasArrhythmias

Neuromuscular changesNeuromuscular changes

– Ascending weakness, ileusAscending weakness, ileus

EKG Manifestations of EKG Manifestations of HyperkalemiaHyperkalemia

EKG Manifestations of EKG Manifestations of HyperkalemiaHyperkalemia

Wide QRS ComplexShortened QT IntervalProlonged PR Interval

Further Widening of QRS ComplexAbsent P-Wave

Sine-Wave Morphology(e.g. Ventricular Tachycardia)

Peaked T-wave

Normal

Incr

eas

ing

Se

rum

K+

Medical Treatment of Medical Treatment of HyperkalemiaHyperkalemia

Membrane StabilizationMembrane Stabilization– IV calciumIV calcium

Internal RedistributionInternal Redistribution– IV insulin (+ glucose)IV insulin (+ glucose) -adrenergic agonist (albuterol inhaled)-adrenergic agonist (albuterol inhaled)

Enhanced EliminationEnhanced Elimination– Kayexalate (sodium polystyrene sulfonate) Kayexalate (sodium polystyrene sulfonate)

ion exchange resinion exchange resin– Loop diureticLoop diuretic– HemodialysisHemodialysis

Practical approachPractical approach

Mild cases: K<6.5mEq/LMild cases: K<6.5mEq/L→causal →causal managementmanagement

Moderate cases: K=6.5-8mEq/L:Moderate cases: K=6.5-8mEq/L:

-glucose infusion.-glucose infusion.

-glucose insulin infusion.-glucose insulin infusion.

-NaHCO3-NaHCO3 Severe cases: K>8mEq/L→calcium Severe cases: K>8mEq/L→calcium

injectioninjection

Emergency measures:Emergency measures:-Dextrose 10%:-Dextrose 10%: 200-500ml over 30min.200-500ml over 30min. 500-1000ml over the next few hours.500-1000ml over the next few hours.-Dextrose/insulin infusion-Dextrose/insulin infusionInsulin: 0.1U/kg then 1U/kg/hr (add Insulin: 0.1U/kg then 1U/kg/hr (add

minimum 2-3 glucose/U insulin). Onset of minimum 2-3 glucose/U insulin). Onset of effect is 1-5 min.effect is 1-5 min.

-NaHCO3: 150mEq over several minutes-NaHCO3: 150mEq over several minutes?increased pH causes K shift into cells. ?increased pH causes K shift into cells.

Definitive measures: Definitive measures: Key oxalate (Na polysterene)Key oxalate (Na polysterene)

--OralOral: 15-30g 2-4 times/day + sorbitol 20-25% : 15-30g 2-4 times/day + sorbitol 20-25% (50ml/15gm resin)(50ml/15gm resin)

The resin induces diarrhea and leads to K loss.The resin induces diarrhea and leads to K loss.

--Retention enemaRetention enema: 50gm in 200ml sorbitol : 50gm in 200ml sorbitol 25%.25%.

Every gm resin combines with 1mEq K in GIT.Every gm resin combines with 1mEq K in GIT. Dialysis : in cases of RF.Dialysis : in cases of RF.

Potassium DisordersPotassium DisordersNormal homeostasisNormal homeostasisHypokalemiaHypokalemia

– Etiologic factorsEtiologic factors– Algorithm for diagnosisAlgorithm for diagnosis

HyperkalemiaHyperkalemia

– Etiologic factorsEtiologic factors– Algorithm for diagnosisAlgorithm for diagnosis

Potassium Homeostasis & Its disorders

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