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- 1. GANGGUAN PADA KESEIMBANGAN ELEKTROLIT dr. Andi Sulistyo Haribo o! Sp.PD. SPESIALIS PENYAKIT DALAM Pro$ram Studi P&ndidikan Dokt&r UNI(ERSITAS ISLAM MALANG ) * + )
- 2. F L U I D S a n d E L E C T R O LY T E S ELECTROLYTES Functions of Electrolytes Contribute most of the osmotically active particles in body fluids Provide buffer systems for pH re ulation Provide the proper ionic environment for normal neuromuscular irritability ! tissue function
- 4. CA TIONS AND ANIONS IN BODY FLUIDS Figure 27.2
- 5. DISTRIBUTION OF MA OR ELECTROLYTES • Na+ and CL- predominate in extracellular fluids (interstitial fluid and plasma) but are ver low in the intracellular fluid (c toplasm) K+ and $%&4 predominate in intracellular fluid 2- (c toplasm) but are in ver low concentration in the extracellular fluids (interstitial fluid and plasma) • t bod fluid p$ proteins *%- act as anions, total protein concentration *%- is relativel high the second most important anion in the c toplasm *%- is intermediate in blood plasma but *%- is ver low in the interstitial fluid
- 6. DISTRIBUTION OF MINOR ELECTROLYTES • - $C&/ is in intermediate concentrations in all fluids a bit lower in the intracellular fluid (c toplasm), it is an important p$ buffer in the extracellular comparments Ca++ is in low concentration in all fluid compartments but it must be tightl regulated as small shifts in Ca++ concentration in an compartment have serious effects • • 0g++ is in low concentration in all fluid compartments but 0g++ is a bit higher in the intracellular fluid (c toplasm) where it is a component of man cellular en1 mes
- 7. REGULATION OF ELECTROLYTES 0a or Cations in bod fluids □ 3odium (Na+) □ %otassium (K+) □ Calcium (Ca++) □ 0agnesium (0g++)
- 8. PRINCIPLES OF ELECTROLYTE DISTURBANCES 4mplies an underl ing disease process 5reat t the electrol te change but s see6t the cause Clinical maniifestatiions usuall nott specific to a particular electrol te change e.g. sei1ures arrh thmias
- 9. PRINCIPLES OF ELECTROLYTE DISTURBANCES Clinical manifestations determine urgency of treatment, not laboratory values Speed and magniitude of correccttion dependent on clinical circumstances Frequent reassessment of electrolytes required
- 10. ELECTROLYTES / THEIR IMBALANCES SODIUM 0NA1 2 Sodium balan3& □ Sodium 4 ma5or 3ation in &6tra3&llular 7luid 0ECF2 □ Sodium 4 most 3ommon probl&m it8 &l&3trolyt& balan3& □ K&y to balan3&9 in$&stion :ia G;I tra3t 4 &63r&tion :ia kidn&y Aldost&ron& 3ontrols sodium l&:&ls :ia t8& kidn&y □ R&m&mb&r aldost&ron&<s anta$onist 4 ANP □ Sodium 3ontribut&s to r&stin$ m&mbran& pot&ntial Sodium rus8in$ into 3&ll :ia op&n 38ann&ls 3aus&s d&polari=ation o7 n&r:&s and mus3l&s
- 13. DISORDERS OF SODIUM BALANCE ❖ Na+ is the most abundant electrol te in the CF . ❖ Na+ and accompan ing anion Cl- are responsible for normal osmotic activit of the CF ❖ ll gain8loss of Na+ is accompanied b gain8loss of water.
- 14. HYPONATREMIA $ povolemic h ponatremia • • • • 9omiting :iarrhea :iuretics drenal insufficienc Normovolemic h ponatremia • • • 3 ndrome of inappropriate secretion of antidiuretic hormone ;enal failure <ater intoxication $ pervolemic h ponatremia • • • C$F Liver failure Nephrotic s ndrome
- 16. CLINICAL MANIFESTATIONS OF HYPONATREMIA Neurologic • • • 3ei1ure Coma gitation =astrointestinal • norexia • Nausea8vomiting 0uscular • Cramps • wea6ness • $eadache Cerebral edema Confusion • •
- 17. TREATMENT OF HYPONATREMIA ❖ Fluid restriction ❖ dministration of h pertonic saline and an osmotic or loop diuretic ❖ >>>Correction of serum sodium levels too rapidl can result in neurologic damage and central pontine m elinol sis>>>
- 18. HYPONATREMIA cute s mptomatic h ponatremia □ Correct no faster than 1 m @8L per hour for the first A-B m @8L □ No more than 1-12 m @8L in first 24 hours □ DE saline is almost never needed □ Calculate the Na deficit Na m @ (*Na desired - *Na measured ) G 5H< 5H< .D or .A G weight in K=
- 19. CAUSES OF HYPERNATREMIA ❖ 0ost common cause is water deficienc d8tI • • xcessive loss 4nade@uate inta6e ❖ lso ma be caused b I • • • • xogenous Na+ load %rimar h peraldosteronism :iabetes insipidus ;enal d sfunction
- 21. CLINICAL MANIFESTATIONS OF HYPERNATREMIA ❖ 5remulousness ❖ 4rritabilit ❖ taxia ❖ 0ental confusion ❖ Coma d8t cerebral water loss
- 22. TREATMENT OF HYPERNATREMIA ❖ ;enal tubular diuretics ❖ $emodial sis ❖ 5reat central diabetes insipidus with vasopressin ❖ >>>Correction of serum sodium level too rapidl can result in neurologic damage secondar to cerebral edema>>>
- 24. HYPERNATREMIA 5reatment □ Severe ECFV depletion is the priority and should be corrected with NS first. 3ubse@uent fluid replacement can be h potonic □ 0a or complication of overl rapid correction is cerebral edema □ 3afe rate is no more than .D- 1 m @8L per hour □ 3hould ta6e /A-72 to hours to completel correct
- 25. HYPERNATREMIA 5reatment □ Calculate the water deficit □ $2& deficit 5H< G (*Na meas - *Na des )8*Na des □ 4mportant to ta6e into account ongoing losses insensible losses .D - 1 liter824 hours with fever these losses increase b A -B ml824 hrs for each degree Farenheit
- 26. POTASSIUM REGULATION 0a or electrol te and principle cation in the extracellular fluid □ ;egulates metabolic activities □ ;e@uired for gl cogen deposits in the liver and s6eletal muscle □ ;e@uired for transmission of nerve impulses normal cardiac conduction and normal smooth and s6eletal muscle contraction □ ;egulated b dietar inta6e and renal excretion
- 27. ELECTROLYTES / THEIR IMBALANCES POTASSIUM 0K1 2 Potassium balan3& □ Ma5or intra3&llular 3ation □ Balan3&9 in$&stion 4 &63r&tion 0:ia kidn&ys2 Aldost&ron& primarily 3ontrols potassium •It &638an$&s potassium 7or sodium Insulin also r&$ulat&s potassium • It dri:&s it into 3&lls 0 it8 su$ar2 / t8us produ3&s 8ypokal&mia pH also a77&3ts potassium s&3r&tion • A3idosis9 mor& H1 in blood 8i38 7inds its ay into 3&ll / pus8&s K1 into blood Also $&t kidn&y to &638an$& H1 7or K1 A3idosis ;$i:&s; 8yp&rkal&mia • Alkalosis9 l&ss H1 in blood Kidn&ys &638an$& K1 7or H1> t8us $&t 8ypokal&mia
- 28. 5he relation between potassium and h drogen ions in the plasma 3aladinJs natom K %h siolog fourth edition 0c=raw $ill
- 29. %otassium balance in the bod Costan1o %h siolog second edition 3aunders
- 30. POTASSIUM ION REGULATION IN ECF 27-/
- 31. HYPOKALEMIA ❖ Causes • • • • • • =astrointestinal losses 3 stemic al6alosis :iabetic 6etoacidosis :iuretic therap 3 mpathetic nervous s stem stimulation dministration of beta-adrenergic receptor agonists
- 32. HYPOKALEMIA 3purious h po6alemia □ 0ar6ed leu6oc tosis □ dose of insulin right before the blood draw ;edistribution h po6alemia □ l6alosis (K decreases ./ for ever .1 increase in p$) □ 4ncreased Heta2 adrenergic activit □ 5heoph lline toxicit □ Familial
- 33. HYPOKALEMIA xtrarenal depletion □ diarrhea □ laxative abuse □ sweat losses □ fasting or inade@uate inta6e
- 34. HYPOKALEMIA ;enal potassium depletion □ urine potassium 2 m @824 hrs □ spot urine with 2 m @K8gram creatinine □ classified whether the occur with a metabolic al6alosis vomiting8N= suction diuretic tx 0ineralocorticoid excess s ndromes
- 35. HYPOKALEMIA ;enal losses □ metabolic acidosis ; 5 5 pe 4and 4 :K Carbonic anh drase inhibitor therap Mreterosigmoidostom □ No acid-base disorder 0g deficienc :rugs
- 36. CLINICAL MANIFESTATIONS OF HYPOKALEMIA utonomic neuropath 36eletal muscle wea6ness 4ncreased sensitivit to :igoxin Cardiac • • :ecreased m ocardial contractilit lectrical conduction abnormalities • rrh thmias 5ach cardia 9entricular fibrillation • •
- 37. POTASSIUM Copyright 2008 by Pearson Education, Inc.
- 38. HYPOKALEMIA AND THE EKG • %rolonged %; interval • %rolonged 5 interval • <idening of ;3 • Flattened 5 wave
- 39. TREATMENT OF HYPOKALEMIA ❖ 3low 49 potassium supplements ❖ nesthesia related concernsI • • • • 4ncreased ris6 of m ocardial irritabilit K+ O2.A void h perventilation of the lungs void glucose containing 49 solutions void rapid infusion of 49 K+ supplements
- 40. HYPERKALEMIA 3evere h per6alemia is a medical emergenc Neuromuscular signs (wea6ness ascending paral sis respirator failure) %rogressive C= changes (pea6ed 5 waves flattened % waves prolonged %; interval idioventricular rh thm and widened ;3 complex sine wave pattern 9 fib)
- 41. HYPERKALEMIA ❖ Causes • 4ncreased total bod potassium • ;enal failure %otassium-sparing diuretics xcessive 49 K+ supplements xcessive use of salt substitutes • • • • ltered distribution of potassium • 0etabolic or respirator acidosis :igitalis intoxication 4nsulin deficienc $emol sis 5issue and muscle damage after burns dministration on succin lcholine • • • • •
- 42. CLINICAL MANIFESTATIONS OF HYPERKALEMIA ❖ reflexia ❖ <ea6ness ❖ %aral sis ❖ %aresthesia ❖ Cardiac conduction abnormalities
- 43. HYPERKALEMIA AND THE EKG • Narrowing and pea6ing of 5 waves • 1st degree 9 bloc6 • ;3 widening • 35 segment depression • %rogression to merging of ;3 an 5 waves to a sine wave • 5ach cardia • 9entricular fibrillation
- 44. HYPERKALEMIA tiolog Prenal failure transcellular shifts cell death drugs pseudoh per6alemia 0anifestations P cardiac neuromuscular
- 45. TREATMENT OF HYPERKALEMIA %rimar goal void adverse cardiac effects 4nsulin and glucose to shift K+ into cells 49 calcium to antagoni1e cardiac effects of h per6alemia nesthesia related concernsI serum K+ of D.Dm @8L is upper limit for elective procedures
- 46. HYPERKALEMIA 5reatment □ 3top potassium> =et and C= □ Hyperkalemia with ECG changes is a medical emergency
- 47. HYPERKALEMIA 5reatment □ First phase is emergenc treatment to counteract the effects of h per6alemia 49 Calcium □ 5empori1ing treatment to drive the potassium into the cells glucose plus insulin Heta2 agonist Na$C&/
- 48. HYPERKALEMIA 5reatment □ 5herap directed at actual removal of potassium from the bod sodium pol st rene sulfonate (Ka exalate) dial sis □ :etermine and correct the underl ing cause
- 49. ELECTROLYTES / THEIR IMBALANCES CALCIUM 0CA1 1 2 Cal3ium balan3& □ Cal3ium is most abundant min&ral in body □ Cal3ium is important as an &6tra3&llular 3ation □ Cal3ium / p8osp8orus 8a:& a r&3ipro3al r&lations8ip □ Cal3ium balan3& is d&p&nd&nt on9 Parat8yroid 8ormon& 0PTH2 Cal3itriol 0a3ti:& :itamin D2 Cal3itonin 07rom t8yroid2 □ 9@ o7 3al3ium r&absorb&d at t8& kidn&ys Cal3ium 7un3tions □ Stru3tural str&n$t8 7or bon&s / t&&t8 □ Maintains stability o7 n&r:& m&mbran& □ R& uir&d 7or mus3l& 3&ll 3ontra3tion □ N&3&ssary 7or blood 3lottin$
- 50. REGULATION OF CALCIUM IONS ;egulated within narrow range □ levated extracellular levels prevent membrane depolari1ation □ :ecreased levels lead to spontaneous action potential generation 5erms □ $ pocalcemia □ $ percalcemia %5$ increases Ca2+ extracellular levels and decreases extracellular phosphate levels 9itamin : stimulates Ca2+ upta6e in intestines Calcitonin decreases extracellular Ca2+ levels 27-D
- 51. REGULATION OF CALCIUM IONS 27-D1
- 52. HYPOCALCEMIA ❖ CausesI • • • • • • :ecreased serum albumin concentration Chelation of calcium b citrate ;habdom ol sis $ poparath roidism %ancreatitis ;enal failure
- 53. CLINICAL MANIFESTATIONS OF HYPOCALCEMIA ❖ Neuromuscular irritabilit • • • 5etan Lar ngospasm $ peractive deep tendon reflexes ❖ <ea6ness ❖ 9asodilation ❖ 0 ocardial d sfunction ❖ Hrad cardia ❖ $eart bloc6
- 54. TREATMENT OF HYPOCALCEMIA ❖ Calcium replacement ❖ 4ntraoperative P h perventilation and respirator al6alosis
- 55. HYPERCALCEMIA ❖ CausesI • Calcium mobili1ation from bone due to immobilit • 5umors • $ perparath roidism
- 56. CLINICAL MANIFESTATIONS OF HYPERCALCEMIA ❖ norexia ❖ Nausea ❖ Constipation ❖ Cognitive depression ❖ K= changes • • • %rolonged %; interval 3hortened 5 interval %9CJs
- 57. TREATMENT OF HYPERCALCEMIA ❖ 5reatment of underl ing cause ❖ 9olume expansion ❖ 4ntraoperative h percalcemia should be managed with administration of ade@uate fluids and maintenance of urine output.
- 58. Copyright 2008 by Pearson Education, Inc.
- 59. REGULATION OF CHLORIDE / MAGNESIUM IONS Chloride ions %redominant anions in CF 0agnesium ions Capacit of 6idne to reabsorb is limited xcess lost in urine :ecreased extracellular magnesium results in greater degree of reabsorption 27-DQ
- 60. MAGNESIUM REGULATION ssential for en1 me activities Neurochemical activities Cardiac and s6eletal muscle excitabilit ;egulation □ :ietar □ ;enal mechanisms □ %arath roid hormone action D PAE of magnesium contained in bones □ 1E in CF □ 0inimal amount in cell
- 62. HYPOMAGNESEMIA ❖ 3erum magnesium less than 1.Dm @8L ❖ CausesI • • • • • • • • 4nade@uate inta6e of magnesium 5%N =astrointestinal losses %ancreatitis %arath roid hormone disorders $ peraldosteronism Ketoacidosis Chronic alcoholism
- 63. CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA ❖ CN3 irritabilit • 3ei1ures • $ perreflexia • 36eletal muscle spasm
- 64. TREATMENT OF HYPOMAGNESEMIA ❖ 49 administration of magnesium sulfate
- 65. HYPERMAGNESEMIA ❖ 3erum magnesium level greater than 2.D m @8L ❖ CausesI • 4atrogenic administration • %reeclampsia ntacids8laxatives • • ;enal failure
- 66. CLINICAL MANIFESTATIONS OF HYPERMAGNESEMIA ❖ CN3 depression stupor coma ❖ 36eletal muscle wea6ness respirator failure ❖ :ecreased peripheral vascular tone ❖ :ecreased m ocardial contractilit ❖ 5ocol sis
- 67. HYPERMAGNESEMIA AND THE EKG ❖ %rolonged % interval ❖ <idened ;3
- 68. TREATMENT OF HYPERMAGNESEMIA ❖ 3upportive care ❖ Fluid loading ❖ :iuresis ❖ cute h permagnesemia P49calcium to counter the elevated magnesium levels
- 69. IONS CONT<D. A • N %hosphate (%& 4 ---) ▫ Huffer ion found in 4CF ssists in acid-base regulation $elps to develop and maintain bones and teeth ▫ Calcium and phosphate are inversel proportional %romotes normal neuromuscular action and participates in carboh drate metabolism ▫ bsorbed through =4 tract ; egulated b diet renal excretion intestinal absorption and %5$ • Mnder normal conditions reabsorption of phosphate occurs at maximum rate in the nephron • nincrease in plasma phosphate increases amount of phosphate in nephron be ond that which can be reabsorbed, excess is lost in urine
- 71. OTHER ELECTROLYTE DEFICITS CA! POC! MG 0a produce serious but nonspecific cardiac neuromuscular respirator and other effects ll are primaril intracellular ions so deficits difficult to estimate 5itrate replacement agai inst t clinical findings
- 72. PHOSPHATE 4nvolved in acidPbase buffering s stem 5% production and cellular upta6e of glucose 0aintenance re@uires ade@uate renal functioning ssential to muscle ;HCs and nervous s stem function
- 73. HYPERPHOSPHATEMIA $igh serum %&4 caused b / □ cute or chronic renal failure □ Chemotherap □ xcessive ingestion of phosphate or vitamin : 0anifestations □ Calcified depositionI oints arteries s6in 6idne s and corneas □ Neuromuscular irritabilit and tetan
- 74. HYPERPHOSPHATEMIA 0anagement □ 4dentif and treat underl ing cause □ ;estrict foods and fluids containing %&4/ □ de@uate h dration and correction of h pocalcemic conditions
- 75. HYPOPHOSPHATEMIA 4 Low serum %& /− caused b □ 0alnourishment8malabsorption □ lcohol withdrawal □ Mse of phosphate-binding antacids □ :uring parenteral nutrition with inade@uate replacement
- 76. HYPOPHOSPHATEMIA 0anifestations □ CN3 depression □ Confusion □ 0uscle wea6ness and pain □ : srh thmias □ Cardiom opath
- 77. HYPOPHOSPHATEMIA 0anagement □ &ral supplementation − □ 4ngestion of foods high in %&4 / □ 49 administration of sodium or potassium phosphate
- 78. +99
- 79. Saya akan perlakukan teman sejawat saya seperti saudara kandung Saya akan memperlakukan teman sejawat saya sebagaimana saya ingin diperlakukan. ) * +*