Ch 28 Management of patient with fluid & electrolyte disturbances

1. Ch 28 Management of patient with fluid & electrolyte disturbances R1 최 정 현

2. Fluid compartment

3. Intracellular fluid • (ATP)-dependent pump • Na+ : K+ = 3:2 • K+  concentrated intracellularly • Na+  extracelluarly • 이러한 unequal exchange는 Nondiffusible protein으로 인한 intracellular hyperosmolality를 방지 • Ischemia, hypoxia시 pump기능 감소  swelling of cells

4. Extracellular fluid • Provide • a medium for • cell nutrients and electrolyte • Cellular waste products • 1.interstitial fluid • 대부분 free fluid보다는 proteoglycan과 chemical association을 통해 gel형태로 존재 • Negative pr.를 가짐(-5mmHg) • Vol.이 증가하여 free fluid증가하여 positive pr.되면 edema가 됨. • 2.intravascular fluid • Commonly referred to as plasma • Plasma protein(주로 albumin)은 ISF로 나갈 수 없기 때문에 유일한 osmotically active solute이 됨.

5. edema • ECF가 계속 증가하게 되면 blood volume은 증가하지 않고 결국 ISF만 증가하게 되어 tissue edema가 생기게 됨.

7. Exchange between fluid compartments • Diffusion:random movement of molecule due to their kinetic energy • Rate of diffusion • Membrane permeability • Substance concentration difference • Pressure difference • Electrical potential에 의해 결정됨.

8. 1. Diffusion through cell membrane • ISF와 ICF사이의 diffusion • Lipid bylayer를 직접 통과 • Oxygen, CO2, water, lipid soluble molecule • Protein channel을 통해 • Na+, K+, Ca+과 같은 cation • Carrier protein을 통해(facilitated diffusion) • Glucose, amino acid • Fluid exchange는 nondiffusible solute concentration의 차이에 의한 osmotic force에 의하게 됨.

9. 2. Diffusion through capillary endothelium • Oxygen, CO2, water, lipid soluble substance memb.직접 통과 • Low-molecular-weight water-soluble substances(Na+, Cl-, K+, glc.)  intercellular cleft를 잘 통과. • High molecular-weight substances cleft잘 통과 못함.(liver, lung제외) • Fluid exchage는 osmotic force와 hydrostatic force에 의함.

10. Venous end에서 재흡수 되지 않은 fluid는 lymphatic flow를 통해 돌아감.

11. Disorders of water balance • Normal adult daily water intake • 2500mL (energy substrate의 대사산물 300mL포함) • Daily water loss • 1500mL : urine • 400mL : respi. Tract evaporation • 400mL : skin evaporation • 100mL : sweat • 100mL : feces • Water content및 cell volume의 변화는 특히 뇌와 같은 곳의 심각한 기능 이상을 초래할 수 있다.

12. Plasma sodium conc.과 ECF,ICF osmolality와의 relationship • Plasma osmolality(mOsm/kg) = [Na+]*2 + BUN/2.8 + glc./18 • Effective Plasma osmolality(mOsm/kg) = [Na+]*2 + glc./18 • Normally varies 280 ~ 290 mOsm/L • Osmolal gap : 측정치와 계산치의 차이 • Ethanol, mannitol, methanol, ethylen glycol, isopryl alchohol • CRF, ketoacidosis, 다량의 glycine • Marked hyperlipidemia, hyper proteinemia

13. Control of plasma osmolality 1. Secretion of ADH hypothalamus의 supraoptic and paraventricular nuclei에서 감지. ECF osm. ￪  cell shrink  ADH분비(from post. Pituitary)  renal collecting tubule에서 재흡수 증가 ECF osm. ￬  반대 2. Nonosmotic release ADH carotid baroreceptor, atrial stretch receptor  blood vol.이 5~10%감소시 stimulate ADH pain, emotional stress, hypoxia시도 자극가능. 3. Thirst hypothalamus의 lat. Preoptic area에서 ECF osm.증가시 thirst 생기게 함.

14. Hyperosmolality & Hypernatremia • Hyperosmolaity가 항상 hypernatremia([Na+]>145 mEq/L)와 연관이 있는 것은 아님. • Ex.) Marked hyperglycemia • Glc. 100 mg/dL 증가시 plasma Na+ 1.6 mEq감소 • Hypernatremia(loss of water)는 보통 thirst에 의한 수분섭취로 예방이 되기 때문에 주로 unable to drink, very aged, very young, altered consciousness pt.에서 나타나게 됨.

15. Hypernatremia • & low total body sodium content • Water and Na+ loss • Osmotic diuresis, diarrhea, sweat • Sign of hypovolemia • & normal total body sodium content • Pure water loss • M/c cause : dibetes insipidus • Central : ADH 분비 감소 • Nephrogenic : ADH 반응성 감소 • & increased total body sodium content • Hypertonic saline solution주입시 • Hyperaldosterinism, cushing synd.에서 나타날 수도 있음.

16. Clinical manifestation of hypernatremia • Neurological (cellular dehydration으로) • Restlesness, lethargy, hyperreflexia • Seizure, coma, death로 발전 가능 • Brain volume의 급격한 감소시 cerebral vein rupture로 ICH, SAH도 발생 가능.

17. Tx. Of hypernatremia • Rapid correction주의 : Sz.,brain edema, permanent neurological damage, death가능 • 시간당 0.5 mEq이상속도로 교정 되지 않게 주의

18. Anesthetic consideration • Hypernatremia • 동물실험에서 MAC 증가 • 주로 fluid deficit과 관련 • Elective surgery에서 150 mEq이상시 원인교정이 될때까지 수술 연기되어야 함.

19. Hypoosmlality & hyponatremia • Hypoosmolality와 hyponatremia([Na+]<135 mEq/L)는 거의 항상 연관되어 있다. • 예외 : pseudohyponatremia

20. Primary polydipsia SIADH Glucocorticoid deficiency Hypothyrodism Drug-induced Hypoosmolal hyponatremia 분류 및 치료 CHF Cirrhosis Nphrotic syndrome Vomiting Diarrhea Sweat, burn Third spacing Diuretics Mineralocorticoid deficiency Salt-losing nephropathy Osmotic diuresis Renal tubular acidosis • 예외 : Vomiting시 Una가 20 mEq이상일 수 있다.:metabolic alkalosis 교정을 위해 HCO3배출될때 Na+함께 배출되기 때문. • 단, Urine Cl-가 10 mEq이하

21. Clinical manifestation of hyponatremia • Sx.(주로 neurological, intracellular water증가 때문) • 125 mEq/L이상의 mild to moderate에서는 종종 asymptomatic • Early Sx. • Anorexia, nausea, weakness • Progressive cerebral edema lethargy, confusion, seizure, coma, death • Serious manifestation은 보통 120 mEq/L이하에서 나타남. • Risk : premenopausal women

22. Hyponatremia 교정 • 보통 125 mEq/L 이상으로 교정시 Sx.이 완화됨. • Na+ defic = TBW*(desired[Na+]-present[Na+]) • 교정속도 • Mild Sx.시 : 0.5 mEq/L/h or less • Moderate : 1 mEq/L/h or less • Sevre : 1.5 mEq/L/h or less • 급속교정시 central pontine myelinolysis로 permanent neurological sequelae생길 수

23. Anesthetic consideration • General anesthesia시 130 mEq/L이상이면 safe • Elective op.시 Sx.없더라도 130 mEq/L이상으로 교정해 주어야 함. • MAC감소 • Postop. Agitation, confusion, somnolence • TUR-P 를 받는 환자는 irrigation fluid로 부터 다량의 water흡수하여 acute water intoxication의 high risk가 됨.

24. Disorders of sodium balance • ECF volume 은 totoal body sodium content와 직접적으로 비례관계 • Positive sodium balance  ECF vol. ￪ • Negative sodium balance  ECF vol. ￬ • ECF volume과 total body sodium content는 renal Na+ excretion의 조정에 의해 조절됨.

25. Control mechanism(sodium balance) • Sensors of volume • Baroreceptor • At carotid sinus : SNS activity, nonosmotic ADH • Afferent renal arteriols : RAA system • Stretch receptor in both atria : atrial natriuretic h., ADH를 modulation

26. Control mechanism(sodium balance) • Effectors of volume change • Renin-angitensin-aldosterone • Renin  angiotensin II ￪  aldosterone ￪  enhancing Na+ reabsorption(prox. Renal tubule) • Angiotensin II : direct vasoconstrictor, norepi. Potentiate • ANP • Atrial distention시 분비 • 2 major action • Arterial vasodilation • Increased urinalry sodium and water excretion

27. Control mechanism(sodium balance) • Effectors of volume change • Brain natriuretic peptide • Ventricle overdistention시 ventricle에서 분비 • 보통 ANP의 20% level이지만 acute CHF시 ANP level exceed • Pressure natriuresis • BP가 조금만 증가해도 urinary Na+ excretion 상대적으로 크게 증가 • SNS activity • 활성화시 • Na+ reabsorption증가(prox. Renal tubule) • Renal vasoconstruction  renal blood flow 감소

28. Control mechanism(sodium balance) • Effectors of volume change • GFR and plasma sodium concentration • Filtered Na+양과 비례 • Tubuloglomerular balance • Rate of renal tubular flow • Changes in peritubular capillary hydrostatic and oncotic pressure • Antidiuretic hormone

29. Volume regulation VS Osmoregulation

30. Anesthetic consideration • Hypovolemic patient • Sensitive to vasodilating, negative inotropic effect • Volatile anesthetics, barbiturate, histamine release agent(morphine, meperidine, curare, atracurium) •  dosage 줄여야 함. • 또한 spinal or dpidural anesthesia시 sympathetic blockade에도 sensitive • 만약 마취전 hypovolemia를 교정할수 없다면 •  ketamine이 induction agent of choice • Etomidate가 suitable alternative

31. Anesthetic consideration • Hypervolemia • 술전 diuretics로 교정 • 가능하다면 Cardiac, renal, hepatic function의 이상을 교정해줌. • Major hazard • Pulmonary interstitial edema • Alveolar edema • Large collection of pleural or ascitic fluid

32. Disorders of potassium balance • Potassium • Cell membrane의 electrophysiology • Carbohydrate, protein synthesis에 주요역할 • Intracellular concentration : 140 mEq/L • Extracellular conc. : 4 mEq/L

33. Normal potassium balance • Dietary potassium intake : • 평균 80 mEq/d (40~140) • Excreted • Urine : 70 mEq (distal tubule) • GI tract : 10 mEq

34. Intercompartment shift of potassium • Occur following • Changes in extracellular pH • Circulating insulin level • Circulating catecholamine activity • Plasma osmolality • hypothermia

35. Intercompartment shift of potassium • Insulin & catecholamine : Na+-K+ ATPase 에 직접작용하여  plasma [K+] 낮춤. • Exercise시 muscle에서 K+ release  plasma [K+] 증가(synd. of periodic paralysis) • Acidosis시 H+ 이 cell안으로 들어가며 K+ 나옴 plasma [K+] 증가 • Alkalosis  plasma [K+] 감소 • B2-adrenergic agonist투여시 m.과 liver의 uptake로  plasma [K+] 감소 • Acute increase in plasma osmolality시 solvent drag현상으로  plasma [K+] 증가 • Hypothermia시 cellular uptake로  plasma [K+] 감소 • Rewarming시 reverse되므로 hypothermia상태에서 K+투여는 rewarming시 transient hyperkalemia야기할 수 있다.

36. Hypokalemia Gastmintestinal losses • Vomiting • dirrhea, particularly secretory diarrhea ECF  ICF shift • Acute a|ka|osis • Hypoka|emic periodic para|ysis • Barium ingestion • |nsulin therapy • Vitamin B12 therapy • Thyrotoxicosis (rare|y) lnadequate intake Cf.) frozen red cell수혈시 발생가능.  이 cell들은 potassium loss상태로 수혈 수 K+을 흡수하게 됨. • [K+] < 3.5 mEq/L • 원인 Excess renal loss • MineraloCorticoid excess • Primary hypera|dosteronism (Conn’s syndrome) • G|ucoconicoid--remediable hyperaldosteronism • Renin excess • Renovascular hypertension • Bartterl’s syndrome • Lidd|e’s syndrome • Diuresis • Chronic metabo|ic a|kalosis • Antibiotics • Carbenicil|in • Gentamicin • Amphotericin B • Rena| tubu|ar acidosis • Dista|, gradient-limited • Proxima| • Ureterosigmoidostomy

37. Hypokalemia • Clinical manifestation • 보통 3mEq/L 이하로 떨어지기 전까지는 asymtomatic <Effects of hypokalemia> • Cardiovascular • Electrocardiographic changes/arrhythmia5 • Myocardia| dysfunction • Neuromuscular • Skeletal murk weakness • Tetany • Rhabdomyo|ysis • Ileus • Renal • Polyuria (nephrogenic diabetes insipidus) • Increased ammonia production • Increased bicarbonate reabsorption • Hormonal • Decreased insulin secretion • Decreased aldosterone secretion • Metabolic • Negative nitrogen balance • Encephalopathy in patients with liver disease

38. Due to Delayed ventricular repolarization • T wave flattening and inversion • Prominent U wave • ST segment depression • Increased P wave amplitude • Prolongation of the PR interval

39. Treatment of hypokalemia • Associated organ dysfunction의 severity에 따라 결정됨. • Significant ECG change시(ST segment change, arrhythmia)  continuous ECG monitoring (특히 IV K+ replacement중) • Weakness가 있는 환자는 주기적인 muscle strength 평가가 필요

40. Treatment of hypokalemia • Oral replacement • potassium chloride solution • Safest • 60 ~ 80 mEq/d • Require several days • IV replacement • Serious cardiac manifestation또는 muscle weakness시 • 8 mEq/h속도를 넘지 않게 , 240mEq/d넘지 않게 • Dextorse-containing solution은 피함  insulin분비로 plasma K+낮춤. • 빠른 주입시(10-20mEq/h)  central line필요(femoral catheter가 좋음. ), close ECG monitoring 필요 • Metabolic alkalosis시  potassium chloride사용. : 부족한 chloride도 같이 교정 가능 • Metabolic acidosis시  potassium bicarbonate or equivalent(K+ acetate, K+ citrate) • Diabetic ketoacidosis시  potassium phosphate사용 : concomitant hypophosphatemia도 교정

41. Anesthetic consideration • Common preoperative finding • Elective surgery시 lower limit를 가짐 • 3~3.5 mEq/L • ECG change가 없는 chronic mild hypokalemia시 anesthetic risk는 증가하지 않음. • But, digoxin 투여 환자에서는 risk증가하므로 4mEq/l이상으로 유지하는 것이 좋음. • Intraop.에서 • Atrial or ventricular arrhythmia시 IV potassium보충해야함. • Hyperventilation을 피하여 K+감소를 방지

42. Hyperkalemia • 5.5 mEq/L 이상 • Kidney의 tremendous excretion capacity로 정상인에서는 거의 생기지 않음. • 하루 500mEq 배출 가능. • SNS & insulin분비가 plasma [K+]의 급격한 증가를 막는데 중요한 역할.

43. Hyperkalemia의 원인 • Due to extracellular movement • Succinylcholine  평균 0.5 mEq/L증가 • Acidosis • Cell lysis following chemotherapy • Hemolysis • Rhabdomyolysis • Massive tissue trauma • Hyperosmolality • Digitalis overdose • Arginine hydrocloride and b2-adrenergic blockade • Hyperkalemic periodic paralysis

44. Hyperkalemia의 원인 • Decreased renal excretion • Renal failure • AIDS • Spironolactone • ACEi • NSAID • Pentamidine • Trimethoprim • Increased potassium intake • Salt substitutes • Stored whole blood transfusion시 : 21일이 지난 후에는 1unit가 30 mEq/L까지 증가시킬 수 있음.  plasma의 양을 최소화 함으로써 예방.

45. clinical manifestation • Most important effect • Skeletal muscle weakness • Cardiac manifestation

46. clinical manifestation • Most important effect • Skeletal muscle weakness • 보통 8 mEq/L 이상이 될때까지는 생기지 않음. • Sustained spontaneous depolarization 과 inactivation of Na+ channel에 의함(succinylchoiline과 비슷)  결국 ascending paralysis초래 • Cardiac manifestation

47. clinical manifestation • Most important effect • Skeletal muscle weakness • Cardiac manifestation • Delayed depolarization에 의함 • 7mEq/L이상에서 생김 • ECG change • Peaked T-wave(종종 shortened QT동반) • Widening of QRS complex • PR prolongation • Loss of P wave • Loss of R wave amplitude • ST depression(occationally elevation) • Sine wave • Ventricular fibrillation and asystole

48. Treatment of hyperkalemia • Hyperkalemia associated with hypoaldostronism  mineralocorticoid replacement • Calcium • partially antagonize cardiac effect • Rapid but short • Digoxin toxicity를 potentiation하므로 주의 • Metabolic acidosis  sodium bicarbonate • B-agonist  massive transfusion으로 인한 hyperkalemia시 유용. • Epinephrine  rapidly decrease • Glucose and insulin : peak effect 도달에 1h 걸림. • Furosemide  renal excretion 증가 • Kayexalate • Dialysis

49. Anesthetic consideration • ECG : carefully monitored • Contraindicated • succinylcholine • H/S : K+ containing • Metabolic or respiratory acidosis피함. • Mild hyperventilation이 desirable • NMBAs effect를 accentuation할 수 있으므로 neuromuscular function을 주의깊게 minitoring.

50. Disorders of calcium balance • Total body calcium의 98%는 bone이지만 normal extracellular calcium conc.의 유지는 homeostasis에 중요 • Biological function • Muscle contraction • Release of neurotransmitter and hormone • Blood coagulation • Bone metabolism