Disturbances of fluid and electrolyte balance

1. Disturbances of fluid and electrolyte balance Csaba Hermann MD Dept. of Anesthesiology and Intensive Care Semmelweis University

2. Homeostasis • The maintenance of normal volume and normal composition of the extracellular fluid is vital to life. • Homeostasis: the various physiologic arrangements which serve to restore the normal state, once it has been disturbed • Fluid balance • Electrolyte balance • Osmotic balance • Acid-base balance

3. General principles • Diffusion: movement of the particles in a solution from the area of high concentration to the area of lower concentration • Electrolyte: inorganic substance that dissociates into ions • Osmosis: diffusion of solvent molecules (water) into region in which there is a higher concentration of a solute (electrolyte) to which the membrane is impermeable • Osmotic pressure: the pressure necessary to prevent solvent migration • Osmol: concentration of osmotic active particles

4. General principles • Osmolarity : number of osmoles per liter of solution • Osmolality: number of osmoles per kilogram of solvent • Measurement: depression of freezing point • Calculation (plasma): 2x(Na+K)+glucose+BUN (mmol/l) • Tonicity: effective osmolality of a solution relative to plasma • Colloids: high molecular weight particles (> 20000 D) • Oncotic pressure (colloid osmotic pressure): the pressure necessery to prevent diffusion of solvent molecules (water) into region in which there is a higher concentration of a colloid to which the membrane is impermeable

5. Extracellular space Intracellular space Intravasal space Interstitial space Water Electrolytes Colloids Cell membrane Osmotic pressure Capillary wall Oncotic pressure

6. Body Fluid Volumes

7. FLUID INTAKE 1.5 IN FOOD 0,8 METABOLIC 0.3 Total 2,6 INSENSIBLE 0.8 SWEAT 0,1 FECES 0.2 URINE 1.5 Total 2.6 Daily Water Balance (liters) OUTPUT INPUT

8. Composition of fluids (mmol/l) Fluid Na+ K + HCO3- Cl - ICF 12 140 12 4 Plasma 140 4-5 26 112 ISF 145 4,4 27 117 Liquor 147 3 23 113 Verejték 20-40 5 - 15-40 Nyál 10 26 15 10 Gastric juice 20-80 5-20 - 100-150 H+: 40-60 Intestinal juice 120-140 5-15 20-40 10

9. Fluid replacement • 0-10 kg: 100 ml/kg/d • 11-20 kg: 50 ml/kg/d • > 20 kg: 20 ml/kg/d • 4-2-1 (ml/kg/h) Patient (70 kgs) (4-2-1) • 1-10 kg 4 ml/kg/h 40 ml/h • 11-20 kg 2 ml/kg/h 20 ml/h • >20 kg 1 ml/kg/h 50 ml/h Together: 110 ml/h 2640ml/d

10. Fluid Balance • The main way to regulate body water gain is by adjusting the volume of water intake, mainly by drinking more or less fluid. The thirst center in the hypothalamus governs the urge to drink. • Although increased amounts of water and solutes are lost through sweating and exhalation during exercise, loss of excess water or excess solutes depends mainly on regulating excretion in the urine. • The extent of urinary Na (and Cl) loss is the main determinant of body fluid volume, whereas the extent of urinary water loss is the main determinant of body fluid osmolarity.

11. Fluid Balance • Angiotensin II and aldosterone reduce urinary loss of Na+ and Cl- and thereby increase the volume of body fluids (baroreceptors: sinus caroticus, kidney) • Stimulation of ANP production: elevation of atrial wall tension (Angiotensin) • ANPpromotes natriuresis, elevated excretion of Na+ (and Cl- ), which decreases blood volume. • The major hormone that regulates water loss and thus body fluid osmolarity is ADH (Hypothalamus) • The regulation of the volume of body fluids superior to the regulation of osmolarity

12. INCREASED OSMOLARITY SENSED BY HYPOTHALAMICRECEPTORS FALL IN ECF VOLUME FALL IN ARTERIAL BLOOD PRESSURE Water Deficit RELIEVES RELIEVES STIMULATION OF HYPOTHALAMIC NEURONS INCREASED VASOPRESSIN OPEN PORES IN COLLECTING DUCT ARTERIOLAR VASOCONSTRICTION INCREASED THIRST MORE WATER REABSORBED INCREASED WATER INTAKE FALL IN URINE OUTPUT DECREASED PLASMA OSMOLARITY DECREASED PLASMA OSMOLARITY

13. Blood pressure and renal handling of sodium FALL IN SODIUM LOAD RELIEVES FALL IN ARTERIAL PRESSURE INCREASE IN ALDOSTERONE SECRETION FALL IN GFR FALL IN EXCRETION OF SODIUM, CHLORIDE, AND FLUID FALL IN FILTERED SODIUM INCREASE IN SODIUM ABSORPTION INCREASED CONSERVATION OF SODIUM AND FLUID

14. Disturbances of fluid homeostasis • Disturbance of fluid balance (intake≠output) • Dehydraton, Overhydration (hyperhydration) • Disturbance of osmolarity (electrolyte intake≠water intake) • Isonatremic (isotonic) • Hyponatremic (hypotonic) • Hypernatremic (hypertonic)

15. Disturbances of fluid homeostasis Diagnosis: • Physical signs: skin turgor, oedema, mucous membranes, neck veins, puls, liver, level of consciousness, capillary refill, fontanel (children) • Vital sings: blood pressure; heart rate; (respiratory rate); body temperature; CVP; urine output; serum and urine Na, osmolarity; Htk; serum total protein

16. Dehydration • Signs: increased thirst (except: advanced age, hypotonic dehydration), weakness, decreased skin turgor, dry mucous membranes, empty neck veins, decreased urine output, elevated Htk, fever, tachycardia, hypotension, decreased CVP,lethargy, stupor, coma • Mild (loss: 4% of body weight): decresed skin turgor, sunken eyes, dry mucous membranes • Moderate (loss: 5-8 % of body weight): + oliguria, orthostatic hypotension, tachycardia • Severe (loss: 8-10 % of body weight): + hypotension, decreased level of consciusness, stupor

17. Dehydration Isotonic Hypertonic Hypotonic Se Na n + - Se osmolarity n + - Hb + + + Htk + + + Blood volume - - - Thirst mod. increase increased no

18. Isotonic dehydration • Intracellular fluid volume remains constant • External loss: vomiting, diarrhoea, haemorrhage, burning • Internal loss: ileus, ascites, pleural effusion • Therapy: volume replacement wiht isotonic solution

19. Hypertonic dehydration • Extracellular + intracellular fluid loss; elevated osmolarity • Causes: inadequate replacement of hypotonic fluid loss, osmotic diuresis (diabetes), decreased ADH secretion, high fever, heat stroke, massive diarrhoea • Therapy: slow water replacement, hypotonic solutions are contraindicated in the first phase of replacement • Water deficit (l): 0,6*kg*((Nameasured/Nanormal)-1)

20. Hypotonic dehydration • Decreased extracellular fluid volumen, elevated intracellular fluid volume • Causes: inadequate fluid replacement with hypotonic solution, elevated ADH secretion + extracellular fluid loss, Addison’s disease, diuretics, vomiting • Usually no thirst • Therapy: Isotonic fluid replacement, Na replacement in case of severe hyponatraemia

21. Hyperhydration • Signs: oedema, increased skin turgor, elevated CVP, distended neck veins, pulmonary oedema Isotonic Hypertonic Hypotonic SeNa n + - Se osmolarity n + - Hb - - - Htk - -- (-) Blood volume + + +

22. Isotonic hyperhydration • Intracellular fluid volume remains constant • Causes: renal failure, heart failure; decreased oncotic pressure, increased isotonic fluid intake • Therapy: decrease intake, diuretics

23. Hypertonic hyperhydration • Infrequent • Causes: renal failure, excessive hypertonic fluid input • Increased thirst, fever, convulsion, coma • Therapy: diuretics, dialysis + slow replacement with hypotonic solutions

24. Hypotonic hyperhydration • Intracellular fluid volume is also increased • Water poisoning • Causes: heart failure, near drowning (fresh-water), increased input of hypotonic solutions (TUR syndrome) • Symptomes: weakness, nausea, vomiting,altered mental status • Therapy: diuretics + fluid replacement with isotonic solution (+ Natrium)

25. Hyponatraemia • Serum Na < 135 mmol/l • Causes: • Water problem (excess of water relative to sodium) • Water excretion by the kidney is impaired • Pseudohyponatraemia (hyperlipidaemia, hyperproteinaemia) • Symptoms: • Cerebral oedema • Nausea, vomiting, lethargy, confusion, seizures, coma • Therapy: • Hypertonic saline (Se Na < 125 mmol/l) • Isotonic saline (se na > 125 mmol/l) • Increase rate of se Na level should be less than 2 mmol/h (cave: Central pontin myelinolysis)

26. Hypernatraemia • Se Na > 145 mmol/l • Causes: inadequate water intake and increased free water loss; intake of hypertonic sodium solution • Symptoms: • Increased thirst • Central nervous system abnormalities (confusion, weakness, lethargy, seizures, coma) • Therapy: water repletion, correction rate of Na level should be no greater than 2 mmol/h (cave: cerebral oedema)

27. ADH • SIADH (syndrome of inappropriate ADH secretion) • Ectopic production • Brain diseases • Lung diseases • Therapy: decrease of water intake • Diabetes insipidus • Decreased ADH secretion (central), decreased ADH effect in the kidneys (renal) • Therapy: ADH (central), hydrochlorothiazide, indomethacine (renal)

28. Potassium • Most abundant cation of ICF, helps maintain ICF volume • Key role in the resting membrane potential and action potential of neurons and muscle fibers • K+ level is controlled by aldosterone • Hydrogen-potassium exchange in cell membrane • Minimal potassium intake: 1 mmol/kg

29. Hyperkalaemia • Se K > 5 mmmol/l • Causes • Impaired excretion • Renal failure, mineralocorticoid deficiency, pseudohypoaldosteronism, drugs (potassium sparing diuretics, ACE-inhibitors NSAID, cyclosporin) • Shifts of K out of cells • Tissue breakdown, acidosis, insulin deficiency

30. Hyperkalaemia • Symptoms: • Cardiac (peaked T waves, loss of P waves, heart blocks, ventricular arrhytmias, widening of QRS complexes, asystole) • Paresthesias, weakness, paralysis • Acidosis • Therapy • Direct antagonism of hyperkalemic effect on cell membrane polarization • Calcium gluconate • Movement of extracellular K into intracellular compartment • Insulin (+glucose) • Sodium bicarbonate • β2-adrenergic agonists

31. Hyperkalaemia • Therapy • Removal K from the body • Loop diuretics • Sodium polystyrene sulfonate • Dialysis

32. Hypokalaemia • Se K < 3,5 mmmol/l • Causes: • Increased excretion: diarrhoea, renal losses, mineralocorticoid excess, magnesium depletion • Shifts of K into cells: drugs (insulin, β2-adrenergic agonists, theophylline, caffeine), alkalosis, hyperthyreoidism • Symptoms: • Cardiac: flat t waves, ST depression, U wave, QT interval prolongation, arrhytmias • Muscle paralysis, rhabdomyolysis • Coma • Metabolic alkalosis

33. Hypokalaemia • Therapy • Supplementation of K • (Knormal-Kmeasured) * ttkg * 0.2 + daily need • Infusion rate: no more, than 20 (30) mmol/h • Oral supplementation • 1 gr potassium-chloride containes 13,4 potassium, 1 gr potassium-citrate containes 9,2 mmol/l potassium

34. Acid-base disorders

35. Acid-base balance • H2O  H+ + OH- (steady state: pH 7 (6,8)) • A Henderson-Hasselbach Equation pH = - log [H+]= pK+log [anion/undissociated acid] • Extracellular space: 7.38pH  7.42 • Intracellular space: pH ~6.8 • Source of H+: intake, metabolism (50 mmol/d), CO2: 12500 ,mmol/d) • Elimination of H+: kidney, lung (CO2), gastrointestinal tract, liver

36. Analysis of acid-base balance • Respiratory • Metabolic • Buffer system (HCO3-, BE) • Strong ion difference (Na+, K+, Cl-, lactate-) – Stewart method

37. Buffers • A buffer is a substance, that has the ability to bind or release H+ in solution, thus keeping the pH of the solution relatevily constant despite of considerable quantities of acid or base • The important buffer systems in blood include proteins, carbonic acid-bicarbonate buffers and phosphates.

38. Buffers • Carbonic acid – bicarbonate system: • H2CO3 H+ + HCO3-  H2O + CO2 • A Henderson-Hasselbach Equation pH = - log [H+]= pK+log [anion/undissociated acid] • pH= 6.1 + log[HCO3/0.03xPaCO2 (amount of carbonic acid)] • Plasma proteins • Dissociation of their carboxyl or free amino groups • Hemoglobin • Dissociation of imidazole groups • Phosphates : low plasma concentration

39. Acid-base disorders • Acidosis: pH<7.35 • Alkalosis: pH>7.45 • Metabolic disturbance: addition of acid or alkali (stronger, than the buffers) or removal of acid or alkali • Respiratory disturbance: rise or decline in arterial pCO2 • Compensation: • Kidneys • Lung

40. BGA arterial mixed venous pH 7.37-7.45 7.35-7,43 pCO2 Hgmm(kPa) 35-46(4,6-6,1) 37-50 (4,9-6,6) actual/standard 21-26/21-26 21-26/21-26 bicarbonate (mmol/l) BE (mmol/l) -2,5 - +2,5 -2,5 - +2,5 Anion gap (mmol/l) 10-14 10-14 (Siggaard-Andersen Curve Nomogram)

41. Metabolic acid-base disorders • Dysfunction of the primary regulating organs • Renal failure • Exogenous administration of drugs or fluids that alter the body’s ability to maintain normal acid-base balance • Methanol, ethylene glycol, salicylates • Abnormal metabolism that overwhelms the normal defense mechanisms • Ketoacidosis (diabetic, alcoholic, starvation, metabolic error) • Lactic acidosis

42. Practical classification of metabolic acid-base disorders • Iatrogenic • Fixed • Symptom of an ongoing acute illness • Only metabolic acidosis has real clinical importance

43. Metabolic acidosis pH<7.35, HCO3<20 mmol/l, BE<-3 mmol/l Anion gap (Na++K+) - (Cl-+HCO3-) normal range: 10-15 mmol/l • Elevated anion gap: lactic acidosis, ketoacidosis, renal failure, exogenous administration of acids • Non-anion gap acidosis: renal tubular acidosis, gastrointestinal acidosis, Iatrogenic acidosis (administration of Cl, dilutional acidosis)

44. Metabolic acidosis • Symptoms: • Increased sympathetic activity • Decreased inotropy, arterial vasodilatation – critical pH (7,2) • Decreased oxy-Hgb binding • Hyperkalaemia • Insulin resistance • Free radical formation • Bone demineralization • Emesis • Decreased sensorium • Hyperventilation

45. Metabolic acidosis • Therapy • Therapy of underlying disease • Maximizing respiratory compensation • NaHCO3 mmol = -BE* 0,3 * kg • Maximal rate of infusion: 1.5 mmol/kg/h • Adverse effects: hypernatraemia, increased CO2 production, intracellular acidosis • Tromethamin (Tris-buffer, Tham) • Penetrates cells • Maximal daily dose: 5 mmol/kg • Adverse effect: hypoglycaemia, respiratory depression, fatal hepatic necrosis

46. Metabolic alkalosis pH>7.45, HCO3>26 mmol/l, BE>3 mmol/l Causes: • Chloride responsive • Vomiting, gastric drainage • Chloride wasting diarrhea (villous adenoma) • Diuretics • Post-hyperpnoe • Chloride-unresponsive • Mineralocorticoid excess • Cushing’s syndrome • Bartter’s syndrome • Hypokalaemia • Sodium salt administration (acetate, citrate) • Massive blood transfusion • Sodium-lactate (Ringer’s solution) • Parenteral nutrition

47. Metabolic alkalosis • Symptoms • Hypoventilation, repiratory depression • Neuromuscular excitability • Hypokalaemia • Seizures • Increased oxy-Hgb affinity • Altered coronary blood flow, vasoconstriction • Decreased cerebral blood flow

48. Metabolic alkalosis Therapy • Therapy of underlying disease • Chloride responsive alkalosis: NaCl • Chloride-unresponsive alkalosis: HCl, KCl • Mineralocorticoid excess: Spironolactone

49. Respiratory alkalosis pH>7.45, pCO2<35 Hgmm • Causes: • Hypoxic respiratory failure • Salicylate intoxication • Early sepsis • Hepatic failure • Arteficial hyperventilation • Symptomes • Decreased cerebral or coronary blood flow • Neuromuscular excitability • Therapy: • Therapy of underlying disease • Increasing the dead space

50. Respiratory acidosis pH<7.35, pCO2>45 Hgmm • Cause: • Respiratory failure • Symptoms: • Symptoms of metabolic acidosis + coma • Therapy: • Therapy of underlying disease • Mechanical ventilation