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Disturbances of Fluid and Electrolyte Balance PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Disturbances of fluid and electrolyte balance" by Csaba Hermann MD.

This medical PowerPoint presentation talks about fluid and electrolyte balance which is essential for the proper functioning of the body. Disturbances in fluid and electrolyte balance can occur due to various reasons such as dehydration, overhydration, vomiting, diarrhea, excessive sweating, hormonal imbalances, and kidney disease, among others.

Some of the common disturbances of fluid and electrolyte balance are Dehydration, Overhydration, Hyponatremia, Hypernatremia, Hypokalemia, and Hyperkalemia, etc.

It is important to maintain proper fluid and electrolyte balance in the body, as disturbances can lead to serious health complications. Treatment depends on the underlying cause of the disturbance and may include rehydration, electrolyte replacement, and medication. It is important to consult a healthcare professional if you experience symptoms of fluid and electrolyte imbalance.

Tags : electrolyte balance, dehydration, overhydration, vomiting, diarrhea, excessive sweating, hormonal imbalances, kidney disease, Emergency Medicine, Emergency Medicine PowerPOint presentation

Published on : Apr 12, 2023 | Views : 1983 | Downloads : 4

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Slide 1-

Disturbances of fluid and electrolyte balance Csaba Hermann MD Dept. of Anesthesiology and Intensive Care Semmelweis University
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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
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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
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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
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Intracellular space Extracellular space Interstitial space Intravasal space Capillary wall Oncotic pressure Colloids Electrolytes Water Cell membrane Osmotic pressure
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Body Fluid Volumes
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Daily Water Balance (liters) 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 INPUT OUTPUT
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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 Composition of fluids (mmol/l)
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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
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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.
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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
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Water Deficit INCREASED OSMOLARITY SENSED BY HYPOTHALAMIC RECEPTORS FALL IN ECF VOLUME FALL IN ARTERIAL BLOOD PRESSURE STIMULATION OF HYPOTHALAMIC NEURONS INCREASED THIRST INCREASED WATER INTAKE DECREASED PLASMA OSMOLARITY INCREASED VASOPRESSIN OPEN PORES IN COLLECTING DUCT MORE WATER REABSORBED FALL IN URINE OUTPUT ARTERIOLAR VASOCONSTRICTION DECREASED PLASMA OSMOLARITY RELIEVES RELIEVES
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Blood pressure and renal handling of sodium FALL IN SODIUM LOAD FALL IN ARTERIAL PRESSURE FALL IN GFR FALL IN FILTERED SODIUM INCREASE IN ALDOSTERONE SECRETION INCREASE IN SODIUM ABSORPTION FALL IN EXCRETION OF SODIUM, CHLORIDE, AND FLUID INCREASED CONSERVATION OF SODIUM AND FLUID RELIEVES
Slide 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)
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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
Slide 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
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Dehydration Isotonic Hypertonic Hypotonic Se Na n + - Se osmolarity n + - Hb + + + Htk + + + Blood volume - - - Thirst mod. increase increased no
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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
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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)
Slide 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
Slide 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 + + +
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Isotonic hyperhydration Intracellular fluid volume remains constant Causes: renal failure, heart failure; decreased oncotic pressure, increased isotonic fluid intake Therapy: decrease intake, diuretics
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Hypertonic hyperhydration Infrequent Causes: renal failure, excessive hypertonic fluid input Increased thirst, fever, convulsion, coma Therapy: diuretics, dialysis + slow replacement with hypotonic solutions
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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)
Slide 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)
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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)
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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)
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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
Slide 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
Slide 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
Slide 31-

Hyperkalaemia Therapy Removal K from the body Loop diuretics Sodium polystyrene sulfonate Dialysis
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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
Slide 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
Slide 34-

Acid-base disorders
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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
Slide 36-

Analysis of acid-base balance Respiratory Metabolic Buffer system (HCO3-, BE) Strong ion difference (Na+, K+, Cl-, lactate-) – Stewart method
Slide 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.
Slide 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
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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
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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) BGA
Slide 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
Slide 42-

Iatrogenic Fixed Symptom of an ongoing acute illness Only metabolic acidosis has real clinical importance Practical classification of metabolic acid-base disorders
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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)
Slide 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
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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
Slide 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
Slide 47-

Metabolic alkalosis Symptoms Hypoventilation, repiratory depression Neuromuscular excitability Hypokalaemia Seizures Increased oxy-Hgb affinity Altered coronary blood flow, vasoconstriction Decreased cerebral blood flow
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Metabolic alkalosis Therapy Therapy of underlying disease Chloride responsive alkalosis: NaCl Chloride-unresponsive alkalosis: HCl, KCl Mineralocorticoid excess: Spironolactone
Slide 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
Slide 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