potassium homeostasis & its disorders by dr. mohammad el-tahlawi
TRANSCRIPT
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
Causes of hypokalamiaCauses of hypokalamia
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
Causes of hypokalamiaCauses of hypokalamia
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+
Effects of Effects of hypokalamiahypokalamia
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
Effects of Effects of hypokalamiahypokalamia
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)
Potassium replacementPotassium replacement
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
Potassium replacementPotassium replacement
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
Hyperkalemia: Disorders of Hyperkalemia: Disorders of External BalanceExternal Balance
Hyperkalemia: Disorders of Hyperkalemia: Disorders of External BalanceExternal Balance
Excessive Potassium IntakeExcessive Potassium Intake
Oral or Parenteral IntakeOral or Parenteral IntakeK pencillin in high dosesK pencillin in high dosesStored bloodStored blood
Hyperkalemia: Disorders of Hyperkalemia: Disorders of External BalanceExternal Balance
Hyperkalemia: Disorders of Hyperkalemia: Disorders of External BalanceExternal Balance
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