3Potassium play an important role in: 1-Electerophysiology of cell membranefor all cells in which polarization-depolaization cycles are functionallyrelevant(cardiac and neuromuscular cells).2-Carbohydrates and protien synthesis
4POTASIUM DISTRIBUTION Extracellular 2%70 meqIntracellular 98%3430 meqPlasma20%15 meqNa-K ATPaseK content = 50 meq/kgIn 70 kgTotal body K = 3500 meq
5K level in meq / L K=140 meq/L Extra cellular K=4 meq/L (3.5-4.5meq) IntracellularK=140 meq/LExtra cellularK=4 meq/L( meq)
6intracellular K deficit Decrease in plasma K from meq/Lintracellular K deficitBYmeq
7intracellular K deficit Decrease in plasma K from meq/Lintracellular K deficitBYmeq
8Plasma K concentration Correlates poorly with the total body k deficit
15HYPOKALAEMIA Causes: (K ion less than 3.5 meq/L) 1-Intercompartmental shift of K.2-Increase k loss.3-Inadequate k intake.
16Intercompartmental shift of K: Causes of hypokalamiaIntercompartmental shift of K:AlkalosisInsulin administrationB2 adrenergic agonistHypothermiaTreatment of megaloplastic anaemiaPeriodic paralasisTransfusion of frozen blood
17Increase K losses (Renal or extrarenal) Renal: Causes of hypokalamiaIncrease K losses (Renal or extrarenal)Renal:DiureticsIncrease mineralocorticiod activityRenal tubular acidosisKetoacidosisHypomagesaemiaUrinary diversion with long ileal loopCarbinecillin and Amphotericin BPrim and Sec hyper alderostenism
18Extrarenal: Decrease K intake GIT : Diarrhea,Vomiting,Fistula, Causes of hypokalamiaExtrarenal:GIT : Diarrhea,Vomiting,Fistula,Laxative abuse,Urinary diversion.SweetDialysisDecrease K intake
19Effects of hypokalemia Most of the patients are asymptomatic untilK level below 3 meq/L.Cariovascular effects are most prominent
20Effects of hypokalamia CardiovascularECG changesDysrhythmiaMyocardial dysfunctionMyocardial fibrosisOrthostatic hypotensionIncrease digitalis toxicity
21Effects of hypokalamia Prominent U-waveFlat TDepressed STsegmentNormalDecreasing Serum K+CardiovascularECG changesT wave flatteningProminent U waveST segment depresionIncrease P wave amplitudeProlongation of PR interval
22Effects of hypokalamia NeuromuscularSkletal ms. Weakness up to respiratory failure.TetanyRhabdomyolysisIleus , Urine retentionRenalPolyuriaIncrease amonium productionIncrease HCO3 reabsorptionIncrease Na retensionIncreased renin secretion→ increase AngII→ thirst
23Effects of hypokalamia MetabolicDecrease insulin secretionDecrease growth hormone secretionDecrease aldesterone secretionHormonalNegative nitrogen balanceEncephalopathy in liver disease
25Hypokalemia Urine K Urine Chloride Less than 30 meq/L More than 30meq/LUrine ChlorideDiarrheaLess than 15meq/LMore than 15meq/LNG DrainageDiureticsAlkalosisMg depletion
26Treatment of hypokalemia The goal of therapy:Is to remove the patient from immediatedanger and not necessarily to correct theentire K deficit.Firstly concern :Any condition that promotes transcellularK shift.
27Potassium replacement Oral replacement with KcL solution is generally safe(60-80 meq/d)IV replacement :(Remember )Serious cardiac manifestation.Peripheral line not exceed 8 meq/h.More than 8meq/h, centeral line is indicated.Dextrose containing solution should be avoided.ECG monitoring is mandatory in high rate infusion.
28Potassium replacement SolutionsPotassium chloride and potassium phosphateKcl: is available in 2meq/mL (5ml)is of choice with metabolic alkalosis as it corrects chloride shifts.Osmolality = 4000 mosm/kgH2OK phosphate: is of choice with coexisting hypophatemia (e.g DKA)
29Potassium replacement Deficit =(3.5 - acutal serum K ) x 0.4 BWMaintenence = 1 meq / kg BW / day
30Potassium replacement Infusion rate (pripheral line)Not exceed 8 meq / hInfusion rate (centeral line)Standard method = 20 meq KcL in 100 ml saline/hMaximum rate (serum k less than 1.5 meq/L)We need peripheral line= 40 meq kcL / h= ( ½ BW meq/h)
31Practical approachIf K level <2 mEq/L, deficit= 0.4 x wt(normal – measured K) we can give up to 0.5 mEq/kg/hr.If K level reaches 2.5 mEq/L, slowly corrects K by giving 10 mEq/hr.Add the daily intake (1 mEq/kg)
32It is advisable to give K salts into large but not central vein. Potassium products:IV preparationsOral: 15ml= 40 mEq (if conc. Of KCl in sol. is 10%)Natural sources:-Orange: one orange=300mg Kone litre juice=2.8gm K-Bananas: one piece= 750mg KK therapy in pediatrics: 1-3mEq/kg/every 1mEq decrease in K level with max. 3mEq/kg/day
33Response to the treatment At first The serum K may be slow to rise particularly if K losses are ongoingFull replacement usually takes few days.If there is refractory hypokalemia check magnessium level
35CONCLUSION Potassium has important role to vital body function . Plasma K concentration is a function of relationship between entry, the intercompartemental distribution and excretion of K.Hypokalemia : serum K less thd 3.5meq/LCause : Decrease intake, Losses and Intercompartementalshift.Effects : Cardiovascular,Neuromuscular,renal,Hormonaland metabolic.Diagnosis .Treatment :Goals, replacement and response
37Hyperkalemia Plasma [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)
39Fist clenching (local exercise effect) PseudohyperkalemiaMovement of K+ out of cells during or after blood drawingHemolysisFist clenching (local exercise effect)Marked leukocytosis
40Hyperkalemia: Disorders of External Balance Excessive Potassium IntakeOral or Parenteral IntakeK pencillin in high dosesStored blood
41Hyperkalemia: Disorders of External Balance Decreased Renal ExcretionAcute and Chronic Renal FailureDecreased Distal Tubular FlowVolume depletionDecreased effective arterial blood volume (CHF, cirrhosis)Drugs altering glomerular hemodynamics with a decrease in GFR (NSAIDs, ACE inhibitors, ARBs)Mineralocorticoid DeficiencyCombined glucocorticoid and mineralocorticoid (adrenal insufficiency)Hyporeninemic hypoaldosteronism (diabetes mellitus)Drug-induced (ACE inhibitors, ARBs)Distal Tubular DysfunctionDisorders causing impaired renal tubular function with hyporesponsiveness to aldosterone (interstitial nephritis)Potassium-sparing diuretics (amiloride, triamterene, spironolactone)
42Hyperkalemia: Disorders of Internal Balance Insulin deficiency2-Adrenergic blockadeHypertonicityAcidemiaCell lysis
43Clinical Manifestations of Hyperkalemia Clinical manifestations result primarily from the depolarization of resting cell membrane potential in myocytes and neuronsProlonged depolarization decreases membrane Na+ permeability through the inactivation of voltage-sensitive Na+ channels producing a reduction in membrane excitabilityCardiac toxicityEKG changesCardiac conduction defectsArrhythmiasNeuromuscular changesAscending weakness, ileus
47Emergency measures:-Dextrose 10%:ml over 30min.ml over the next few hours.-Dextrose/insulin infusionInsulin: 0.1U/kg then 1U/kg/hr (add minimum 2-3 glucose/U insulin). Onset of effect is 1-5 min.-NaHCO3: 150mEq over several minutes?increased pH causes K shift into cells.
48Definitive measures:Key oxalate (Na polysterene)-Oral: 15-30g 2-4 times/day + sorbitol 20-25% (50ml/15gm resin)The resin induces diarrhea and leads to K loss.-Retention enema: 50gm in 200ml sorbitol 25%.Every gm resin combines with 1mEq K in GIT.Dialysis : in cases of RF.