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Sodium homeostasis
- 1. ANGAN KARMAKAR (JUNIOR RESIDENT) CHAIRPERSON:PROF. A.K. SAHA
- 3. Functions of sodium Sodium and its attendant anions (Cl- and HCO3-) account for 90% to 95% of osmotic pressure in ECF Determine membrane potential and neuromuscular excitability Influences acid-base balance Influences the activity of enzymes
- 4. Balance of sodium The content of sodium is 40~50 mmol /Kg of BW Sodium can be divided into two parts: 1)Exchangeable pool 60% of sodium is exchangeable in ECF (50%) and in ICF(10%) 2)Non-exchangeable pool 40% of Na+ is bound to polyanionic proteoglycans in bone ,cartilage,skin
- 6. NORMAL SODIUM METABOLISM Sodiumabsorption Via two mechanisms 1.freely permeable across the interstitial cell 2. symport with glucose and aminoacids
- 7. Sodium excretion Majordeterminant of balance Kidneys : extremely efficient eliminates more if the intake of sodium is more and vice- versa does not eliminate sodium if there is no intake Gastrointestinal tract : second way ≤10% of the sodium intake is lost in feces
- 8. Sodium handling bykidney Absorbed at 3 main regions in the nephron 1.PCT– 2/3 of Na+ reabsorbed 2.TALH– 25-30% is reabsorbed via apical Na+ K+ 2Cl- transporter 3.DCT– 5% by thiazide sensitive Na+ Cl- cotransporter Finally Na+ reabsorption also occurs in cortical and medullary collecting ducts via ENaC
- 9. Regulation of waterand sodium metabolism Thirst neural regulation Antidiuretic hormone hormonal Aldosterone regulation Atrial natriuretic peptide
- 10. no thirst increase ofECF osmolality (1~2%) hypovolemia elevated angiotensin II dryness of mouth osmoreceptor (anterior hypothalamus) volume receptor in venae cavae and atrium thirst center (anterior hypothalamus) sense of thirst and drink of water decrease of ECF osmolality increase of ECF volume decrease of angiotensin concentration II dryness disappears Is it enough? THIRST
- 11. Thirst onlyis not enough to regulate the balance of water and sodium The defects of (neuro-regulation) thirst are: 1)no obvious thirst in hypovolemia if osmolality is not increased 2)in coma- no sense of thirst 3) too young baby, too old man
- 12. Antidiuretic hormone synthesis-hypothalamus storage & release- Posterior pituitary major regulator for water output and reabsorption in kidney
- 13. increase of ECFosmolality (1~2%) via osmoreceptor hypovolemia via volume receptor reduction of BP via baroreceptors synthesis and release of ADH drugs (stimulate), alcohol (inhibit) Stress,Pain Nausea elevated angiotensin II + + + + +
- 15. ALDOSTERONE Major regulatorof sodium excretion and reabsorption. steroid hormone produced by the adrenal cortex Factors stimulating aldosterone secretion: 1) Angiotensin II - major stimulator 2) decrease of sodium level in ECF 3) increase of potassium level in ECF
- 16. ATRIAL NATRIURETIC PEPTIDE •released from atrium in response to increased atrial stretch via mechanoreceptors • Effects: 1.dilates renal blood vessels increase GFR 2.inhibits reabsorption of Na+ from collecting ducts 3.inhibit release of renin, aldosterone and ADH 4.endogenous antagonist to angiotensin II • increases excretion of both water and sodium
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- 18. ECF NORMAL PERIPHERAL PERFUSION NORMAL PERFUSION PRESSURES Normal Albumen Normal plasmaoncotic pressure NORMAL CARDIAC OUTPUT Normal Sodium Normal tonicity Holds the fluid volume in circulation Holds the fluid volume in ECF NORMAL PATIENT APPROACH TO SODIUM IMBALANCE
- 19. ECF NORMAL PERIPHERAL PERFUSION NORMAL PERFUSION PRESSURES NORMAL CARDIAC OUTPUT True hyponatremia represents anincrease in free water relative to sodium in the extracellular fluids HYPONATREMIA
- 20. ECF NORMAL PERIPHERAL PERFUSION NORMAL PERFUSION PRESSURES NORMAL CARDIAC OUTPUT True hyponatremia represents anincrease in free water relative to sodium in the extracellular fluids HYPONATREMIA
- 21. ECF NORMAL PERIPHERAL PERFUSION NORMAL PERFUSION PRESSURES NORMAL CARDIAC OUTPUT RESULTS FROM LOSSOF WATER AND SODIUM AND REPLACEMENT WITH PURE WATER HYPONATREMIA
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- 23. ECF PERIPHERAL PERFUSION PERFUSION PRESSURES CARDIAC OUTPUT Hyponatremia CLINICAL PICTURE Hypovolemic CEREBRAL EDEMA • INCREASEDICP • SEIZURES • ARDS • RESPIRATORY ARREST
- 24. ECF PERIPHERAL PERFUSION PERFUSION PRESSURES CARDIAC OUTPUT Hyponatremia CLINICAL PICTURE Hypovolemic CEREBRAL EDEMA • INCREASEDICP • SEIZURES • ARDS • RESPIRATORY ARREST MANAGEMENT • MANAGE THE VOLUME STATUS • REPLACE THE SODIUM DEFICIT
- 25. ECF Hyponatremia CLINICAL PICTURE Hypovolemic CEREBRAL EDEMA • INCREASEDICP • SEIZURES • ARDS • RESPIRATORY ARREST SODIUM DEFICIT CALCULATION NORMAL TBW X (130 – CURRENT Na) MANAGEMENT • MANAGE THE VOLUME STATUS • REPLACE THE SODIUM DEFICIT
- 26. ECF Hyponatremia CLINICAL PICTURE Hypovolemic CEREBRAL EDEMA • INCREASEDICP • SEIZURES • ARDS • RESPIRATORY ARREST SODIUM DEFICIT CALCULATION NORMAL TBW X (130 – CURRENT Na) CAN BE REPLACED WITH • 3% SODIUM CHLORIDE (513 mmol/litre) • ISOTONIC SALINE (308 mmol/litre) MANAGEMENT • MANAGE THE VOLUME STATUS • REPLACE THE SODIUM DEFICIT
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- 28. Hyponatremia- Diagnostic Approach Theconcentration of sodium in a random (spot) urine sample and its osmolality shows the sodium loss is renal or extra-renal in origin.
- 29. MANAGEMENT Hyponatremia- Diagnostic Approach HYPOVOLEMICHYPONATREMIA • Hypertonic saline (3% NaCl) in symptomatic patients • Isotonic saline in asymptomatic patients Important : Never increase the Na levels by > 0.5 mmol/L per hour The concentration of sodium in a random (spot) urine sample and its osmolality shows the sodium loss is renal or extra-renal in origin.
- 30. Hyponatremia- Diagnostic Approach NORMOVOLEMICHYPONATREMIA • FLUID RESTRICTION • Furosemide diuresis, combined with • Hypertonic saline (3% NaCl) in symptomatic patients • VAPTANS MANAGEMENT The concentration of sodium in a random (spot) urine sample and its osmolality shows the sodium loss is renal or extra-renal in origin. Important : Never increase the Na levels by > 0.5 mmol/L per hour
- 31. SIADH…a diagnosis ofexclusion Bartter et al. American Journal of Medicine 1957
- 32. Hyponatremia- Diagnostic Approach HYPERVOLEMICHYPONATREMIA • FLUID RESTRICTION • Furosemide diuresis, in asymptomatic patients • Furosemide diuresis, with judicious use of hypertonic saline in symptomatic patients MANAGEMENT The concentration of sodium in a random (spot) urine sample and its osmolality shows the sodium loss is renal or extra-renal in origin. Important : Never increase the Na levels by > 0.5 mmol/L per hour
- 34. ECF Loss of HypotonicfluidNORMAL PERIPHERAL PERFUSION NORMAL PERFUSION PRESSURES NORMAL CARDIAC OUTPUT CLINICAL SCENARIO
- 35. ECF Loss of HypotonicfluidNORMAL PERIPHERAL PERFUSION NORMAL PERFUSION PRESSURES NORMAL CARDIAC OUTPUT CLINICAL SCENARIO •Vomiting •Diarrhoea •Profuse diuresis
- 36. ECF Loss of Hypotonicfluid PERIPHERAL PERFUSION PERFUSION PRESSURES CARDIAC OUTPUT CLINICAL SCENARIO •Vomiting •Diarrhoea •Profuse diuresis
- 37. ECF Loss of Hypotonicfluid PERIPHERAL PERFUSION PERFUSION PRESSURES CARDIAC OUTPUT CLINICAL SCENARIO •Vomiting •Diarrhoea •Profuse diuresis Eg: Serum sodium > 165 mmol/L Hypovolemic Hypernatremia
- 38. ECF Loss of Hypotonicfluid PERIPHERAL PERFUSION PERFUSION PRESSURES CARDIAC OUTPUT CLINICAL SCENARIO •Vomiting •Diarrhoea •Profuse diuresis Brain cell shrinkage Eg: Serum sodium > 155 mmol/L ENCEPHALOPATHY • depressed consciousness • frank coma • generalized seizures • focal neurological deficits up to 50% mortality Hypovolemic Hypernatremia
- 39. ECF Loss of Hypotonicfluid PERIPHERAL PERFUSION PERFUSION PRESSURES CARDIAC OUTPUT CLINICAL SCENARIO •Vomiting •Diarrhoea •Profuse diuresis Brain cell shrinkage Eg: Serum sodium > 155 mmol/L ENCEPHALOPATHY • depressed consciousness • frank coma • generalized seizures • focal neurological deficits Brain cells behave like osmometers ! Hypovolemic Hypernatremia
- 40. ECF Loss of Hypotonicfluid PERIPHERAL PERFUSION PERFUSION PRESSURES CARDIAC OUTPUT CLINICAL SCENARIO •Vomiting •Diarrhoea •Profuse diuresis Brain cell shrinkage Eg: Serum sodium > 155 mmol/L Idio-osmoles Partially restored Partially restored Partially restored Hypovolemic Hypernatremia
- 41. ECF Loss of Hypotonicfluid PERIPHERAL PERFUSION PERFUSION PRESSURES CARDIAC OUTPUT CLINICAL SCENARIO •Vomiting •Diarrhoea •Profuse diuresis Brain cell size restored Eg: Serum sodium > 155 mmol/L Idio-osmoles Partially restored Partially restored Partially restored Hypovolemic Hypernatremia
- 42. ECF Loss of Hypotonicfluid PERIPHERAL PERFUSION PERFUSION PRESSURES CARDIAC OUTPUT CLINICAL SCENARIO •Vomiting •Diarrhoea •Profuse diuresis Brain cell size restored Eg: Serum sodium > 155 mmol/L Idio-osmoles Partially restored Partially restored Partially restored Management …to restore the perfusion status and sodium deficit quickly… …and to replace the free water deficit slowly (to prevent intracellular overhydration). Hypovolemic Hypernatremia
- 43. ECF Management … to replacethe free water deficit slowly (to prevent intracellular overhydration). FREE WATER DEFICIT= {(PLASMA Na-140)/140}*TBW Estimating the water deficit
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- 46. why only inbrain cells?
- 47. Consequences of rapidchange of plasma sodium concentration
- 48. TAKE HOME MESSAGES… Do not just be carried away by Na levels Asses the patient clinically Asses volume status Correct intravascular volume first Correct deficit or excess slowly unless symptomatic Recheck response clinically & by lab tests
- 49. THANK YOU FORLISTENING