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Disorders of electrolyte balance
- 2. SODIUM METABOLISM INTAKE BODY DISTRIBUTION LOSES100 -300 mmoles/DAY Bones and tissues 25% Exchangeable 75% ECF ICF Interstitial fluid Renal = IntakeRenal = Intake Faeces 5mmoles/day Sweat 5mmoles/day Normal level of Na+ in plasma is 136-145 mEq/L and in cells 12 mEq/L. Sodium is the major cation of extracellular fluid Dr. N. Sivaranjani 2
- 3. • Functions of sodium • Maintenance of resting membrane potential • Nerve impulse transmission • Muscle contraction • Maintenance of EC osmotic pressure and Water balance • Regulation of A-B balance • Glucose , galactose, amino acid absorption • Functioning of NaK ATPase and Na-H exchanger. Dr. N. Sivaranjani 3
- 4. Regulation of sodium balance • Kidney plays a predominant role. • Renin/angiotensin – Aldosterone mechanism effective circulating volume is the major stimulus • Atrial Natriuretic peptide increase in ECF, increase BP - stimulus Dr. N. Sivaranjani 4
- 5. Disorders of sodium balance • Hyponatremia • Abnormally low serum sodium <136 mEq/L • Decrease in plasma osmolality Clinical features : Hyponatremia –due to excess H2O & Na :- Edema , ascites , increased JVP Hponatremia - due to loss of Na & H2O :- Decreased skin turgor , dry mucus membrane, hypotension and tachycardia.Dr. N. Sivaranjani 5
- 6. HYPONATREMIA Hypervolemia Excess of H2O & Na retention Presents with Edema PSEUDOHYPONATREMIA RENAL loss SALT LOSING NEPHROPATHY ADDISONS DISEASE Diarrhea Vomiting Burns SIADH CCF NEPHROTIC SYNDROME CIRRHOSIS HYPERLIPIDEMIA HYPERPROTEINEMIA Hyponatremia N or raised P.Osmolality plasma water fraction falls TRUE HYPONATREMIA ATN Euvolemia Excess of H2O NO Edema Increased intake of water – PSYCHOGENIC POLYDIPSIA IATROGENIC FLUID OVERLOAD Hypovolemia H2O & Na loss Dehydration NON RENAL loss Dr. N. Sivaranjani 6
- 7. Diagnostic approach • Plasma Na – decreased • Plasma osmolality – decreased • If pt Dehydrated – due to loss of Na and H2O • Not dehydrated – due to excess Na and H2O • Urine Na – • Renal loss more than 20 mEq/L • Non renal loss less than 10 mEq/L Dr. N. Sivaranjani 7
- 8. 8 Treatment of Hyponatremia • Treat the underlying cause • Administered sodium should be closely monitored • Fluid restriction and diuretics – edematous state Dr. N. Sivaranjani
- 9. 9 Hypernatremia – Plasma Na+ > 145 mEq / L – Total body Na Content is high with respect to water – Common cause – excessive water loss - Cells dehydrate C/F :- If Hypernatraemia is due to water loss- symptoms of Dehydration Intense thirst, mental confusion, fever & decreased urine output Due to excess salt gain- Hypertension ,Edema Dr. N. Sivaranjani
- 10. CAUSES OF HYPERNATREMIA Water depletionRetention of sodium GIT loss S.Vomiting S.Diarrhea Excessive sweating Ch.Fever S.ExerciseDI Hypothalamic Nephrogenic Ingestion Infusion of Na HCO3 for treatment of acidosis 1̊ Hyperaldosteronism Conn’s syndrome Cushing’s syndrome Na & H2O depletion Decreased intake Increased loss Unconscious patient Diuretic therapy , nephropathy , polyuric phase of ATN , DM Dr. N. Sivaranjani 10
- 11. • Diagnostic approach • Serum sodium and osmolality – elevated HYPERNATREMIA Urine osmolality >300 mOsmo/Kg Diarrhea – 700 mOsmol/Kg Excessive sweating DM – Osmotic diuresis < 300 mOsmo/Kg Diabetes insipidusADH stimulation No response Nephrogenic DI Response Central DI Dr. N. Sivaranjani 11
- 12. 12 Treatment of Hypernatremia • Treat the underlying cause • Correct the free water deficit at a rate of 1mEq/L/hr • Check serum Na every 4hr • Use isotonic salt -free IV fluid • acute hypernatremia - correction can be quicker. • chronic cases should be treated slowly to prevent cerebral edema Dr. N. Sivaranjani
- 13. POTASSIUM METABOLISM INTAKE BODY DISTRIBUTION LOSES30 -100 mmoles/DAY ECF 55 MMOLES/L ICF 3600 MMOL/L Renal 20-100 MMOL/L Faeces 5mmoles/day LOSS Normal level of K+ in plasma is 3.5-5 mEq/L and in cells 150 mEq/L. Dr. N. Sivaranjani 13
- 14. Functions of potassium • Nerve impulse transmission • Maintenance of IC osmotic pressure • Function of H-K ATPase and HCL secretion • Activation of intracellular enzyme- PK, GS • Cardiac muscle activities • Neuromuscular excitability Dr. N. Sivaranjani 14
- 15. Uptake of K into cells - Na K ATPase / pump Renal regulation K balance – 67% reabsorbed by PCT H+-K ATPase Aldosterone – increase excretion of K+ from DCT High K diet, H+ – increases the excretion of K. Regulation of plasma Potassium Increase uptake of K into cell Decrease uptake of K Insulin DM Alkalosis Acidosis – H+ Beta adrenergic stimulation Alpha Adrenergic stimulation Inhibition of Na K ATPase Dr. N. Sivaranjani 15
- 16. K K H+ H+ Dr. N. Sivaranjani 16
- 17. 17 Hypokalemia • Serum K+ < 3.5 mEq /L • Beware if diabetic – Insulin pushes K+ into cells – D.Ketoacidosis – H+ replaces K+, which is lost in urine Dr. N. Sivaranjani
- 18. HYPOKALEMIA Intake Altered cellular uptake GI loss Renal loss Alkalosis Insulin Renal Tubular acidosis Hyper Aldosteronism – Cushing’s disease Dietary deficiency Diuretics Vomiting Diarrhea GI fistula Hypokalemic periodic paralysis (abnormal calcium channels) Dr. N. Sivaranjani 18
- 19. 19 Clinical manifestations of Hypokalemia Non specific symptoms - Anorexia, Nausea, Vomiting ,Muscle cramps, confusion. • Neuromuscular disorders – Weakness, decreased reflexes. – ECG - appearance of U wave , Flat or inverted T wave, ST segment depression. Arrhythmias and cardiac arrest Rx- supplement K+ slowly, preferably by foods Be cautious in administering drugs that are not potassium-sparing Monitor acid-base balance, pulse, BP and ECG Dr. N. Sivaranjani
- 20. Diagnostic approach Hypokalemia True hypokalemiaRedistribution Insulin therapy Urine K excretion - More than 25 mEq/day Renal Loss less than 25 mEq/day Non Renal Loss Diarrhea Plasma bicarbonate Decreased – seen in metabolic acidosis Proximal RTA Increased – Met Alkalosis Cushing’s syndrome Dr. N. Sivaranjani 20
- 21. 21 Hyperkalemia • Serum K+ > 5.5 mEq /L • Beware of diabetic – Insulin deficiency pushes K+ outside cells. Dr. N. Sivaranjani
- 22. HYPERKALEMIA Intake Pseudo hyperkalemia Altered Cellular Uptake Renal Excretion Acidosis Insulin deficiency Renal failure Hypo Aldosteronism – Addison’s disease HemolysisK rich food – banana ,orange Leukocytosis Thrombocytosis Factitious (K+ leaches out when blood is kept for a long time before separation Dr. N. Sivaranjani 22
- 23. 23 Clinical manifestations of hyperkalemia • Early – hyperactive muscles , paresthesia • Late - muscle weakness, flaccid paralysis ECG – wide QRS complex, Peaked T-waves, Prologed PR interval. • Dysrhythmias – Bradycardia, heart block, cardiac arrest Dr. N. Sivaranjani
- 24. ECG Changes Dr. N. Sivaranjani 24
- 25. Diagnostic approach Hyperkalemia Exclude psuedohyperkalemia and Redistribution Plasma bicarbonate High Anion Gap DKA, LA Normal Anion Gap RTA RF Mineralocorticoid deficiency Increased Respiratory acidosis Decreased Anion Gap Normal Periodic paralysis Dr. N. Sivaranjani 25
- 26. Treatment Acute treatment – • Infusion of Ca. gluconate – antagonize K • Insulin and glucose administration – enhance entry of K into cell from plasma • Administration of HCO3 – correct acidosis Chronic treatment – • Administration of K binding resins orally • Dialysis – hemodialysis and peritoneal dialysis. Dr. N. Sivaranjani 26
- 27. Cl ˉ (Chloride) • Major extracellular anion • Plasma conc. 95 -105 mEq/ L Regulation in kidney through: • Reabsorption with sodium • Reciprocal relationship with bicarbonate Dr. N. Sivaranjani 27
- 28. Functions of chloride • Regulation of A-B balance, Water balance and osmotic pressure • Formation of HCl • Chloride shift • Enzyme salivary amylase is activated by Cl. Dr. N. Sivaranjani 28
- 29. • Most commonly from gastric losses – Excessive vomiting - compensatory increase in plasma bicarbonate. This is called hypochloremic alkalosis – Excessive sweating. • Renal loss - Addisons disease, salt losing nephropathy . • Often presents as a contraction alkalosis with paradoxical aciduria (Na+ retained and H+ wasted in the kidney) Rx: resuscitation with normal saline Hypochloremia Dr. N. Sivaranjani 29
- 30. • Dehydrtaion , • Cushing’s synd, • Severe diarrhea - loss of bicarbonate and compensatory retention of chloride. • Renal tubular acidosis. • often presents as a hyperchloremic acidemia with paradoxical alkaluria (H+ retained and Na+ wasted in the kidney) Rx: stop normal saline and replace with hypotonic crystalloid Hyperchloremia Dr. N. Sivaranjani 30
- 31. IV FLUID REPLACEMENT THERAPY Indications Replacement of abnormal fluid & electrolyte losses [surgery, trauma, burns, GI bleeding] Maintenance of daily fluid & electrolyte needs Correction of fluid disorders Correction of electrolyte disorders Dr. N. Sivaranjani 31
- 32. Assessment of fluid compartment Plasma volume – • BP, JVP, Pulse rate, CVP central venous pressure Interstitial volume – • Edema Intracellular volume – • Difficult to assess clinically • Disorders of cerebral function is important Dr. N. Sivaranjani 32
- 33. What fluids to give : 5% dextrose – replace deficit in total body water 0.9% sodium chloride – expands only ECF volume Hypotonic - Water moves from ECF to ICF by osmosis Usually maintenance fluids 0.45% sodium chloride 0.33% sodium chloride Hypertonic – expands and rise osmolality of ECF 3% NaCl Dr. N. Sivaranjani 33
- 34. Plasma Expanders • Stay in vascular space and increase osmotic pressure • Colloids (protein solutions) – Packed RBCs – Albumin – Plasma Dr. N. Sivaranjani 34
- 35. Essay (15) What are the functions of Na in the body? What is the reference range for levels of serum Na. describe working of RAA system o maintain optimal amounts of sodium in the body. Briefly disorders associated with derangements in Na homeostasis. Short notes (5) Water toxicity Dehydration Give an account of water distribution and its balance in the body Explain the metabolic inter relation b/w Na conc and water volume. Hyponatremia Very short notes (2) Normal Na and K level Name the major intra and extra cellular anion Osmolality Dr. N. Sivaranjani 35