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Disturbances of fluid and electrolyte balance

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

8 Composition of fluids (mmol/l)
Fluid Na+ K + HCO3- Cl - ICF Plasma ISF , Liquor Verejték Nyál Gastric juice H+: 40-60 Intestinal juice

9 Fluid replacement 0-10 kg: 100 ml/kg/d 11-20 kg: 50 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 ml/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) ANP promotes 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 Water Deficit RELIEVES RELIEVES STIMULATION OF HYPOTHALAMIC NEURONS
INCREASED OSMOLARITY SENSED BY HYPOTHALAMIC RECEPTORS FALL IN ECF VOLUME FALL IN ARTERIAL BLOOD PRESSURE 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 * 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: ,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. Buffer pK Concentration Buffer capacity Bicarbonate 6,1 24 mmol/l 75 % Hgb 8,25 24 mmol/l 25 % oxyHgb 6,95 Proteins - Phosphates 6,8

38 Buffers Carbonic acid – bicarbonate system:
H2CO3  H+ + HCO3-  H2O + CO2 A Henderson-Hasselbach Equation pH = - log [H+]= pK+log [anion/undissociated acid] pH= 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) (4,9-6,6) actual/standard 21-26/ /21-26 bicarbonate (mmol/l) BE (mmol/l) -2,5 - +2,5 -2,5 - +2,5 Anion gap (mmol/l) (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 pH<7.35, HCO3<20 mmol/l, BE<-3 mmol/l
Metabolic acidosis pH<7.35, HCO3<20 mmol/l, BE<-3 mmol/l Anion gap (Na++K+) - (Cl-+HCO3-) normal range: 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 pH>7.45, HCO3>26 mmol/l, BE>3 mmol/l
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


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