Metabolic alkalosis


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Metabolic alkalosis

  2. 2.  A metabolic condition in which the arterial pH is elevated beyond the normal range ( 7.35-7.45 )  Result of decreased hydrogen ion concentration, leading to increased bicarbonate and increased PaCo2  As a result of compensatory alveolar hypoventilation
  3. 3.  Often associated with hypochloremia and hypokalemia.  Often occurs in association with other disorders like respiratory acidosis or alkalosis or metabolic acidosis.  Arterial pH makes the diagnosis as it is increased in metabolic alkalosis and may b normal or decreased in respiratory acidosis.
  4. 4. CAUSES I. Exogenous HCO3 overload • Acute alkali administration • Milk alkali syndrome
  5. 5. II. Effective ECF contraction  Gastrointestinal origin • Vomiting • Gastric aspiration • congenital Chloride diarrhoea • villous adenoma
  6. 6.  Renal origin • Diuretcs • Posthypercapnic stage • Hypercalcemia/hypoparathyroidism • Recovery from lactic acidosis or ketoacidosis • Delivery of nonreabsorbable anions including Penicillin, Carbenicilline • Hypomagnesemia • Bartter’s syndrome • Gitelman’s syndrome
  7. 7. III. ECF expansion, hypertension, mineralocorticoid excess  High renin • Renal artery stenosis • Accelerated hypertension • Renin secreting tumor • Oestrogen therapy
  8. 8. Low renin • Primary aldosteronism (adenoma, hyperplasia, carcinoma) • Adrenal enzyme defects (11 B hydroxylase deficiency, 17 a-hydroxylase deficiency) • Cushing’s syndrome or disease
  9. 9. IV. OTHERS  Liddle’s syndrome  Cystic fibrosis  Ingestion of licorice, carbenolone, chewer’s tobacco
  10. 10. Causes associated with contracted ECF volume
  11. 11. Vomiting or nasogastric suction  Results in the loss of hydrochloric acid with the stomach contents.  Loss of fluid and Nacl in vomitus results in contraction of ECF and increased secretion of renin and aldosterone.  Severe vomiting also causes loss of potassium (hypokalaemia) and sodium (hyponatremia).  The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions by the action of aldosterone, leading to metabolic alkalosis
  12. 12. Congenital chloridorrhea  Rare autosomal recessive disorder which causes severe diarrhea, fecal acid loss and HCO3 retention  The main mechanism is loss of ileal HCO3/Cl anion exchange mechanism which results in decreased Cl reabsorption.  Na/H exchange mechanism remains normal so normal H+ is secreted in stool which causes Na and HCO3 to be retained  This results in metabolic alkalosis
  13. 13. Villous adenoma  High adenoma derived K secretory rate  Colonic secretion is alkaline  K and volume depletion most probably causes alkalosis
  14. 14. Diuretics  Loop diuretics and thiazide reduce the ECF without affecting the total body bicarbonate content.  Diuretics blocks Na+ and Cl- channels  More Na is delivered to DCT
  15. 15.  Na exchange with K+ under the effect of aldosterone  Kaliuresis and hypokalemia occurs  Depleted ECF causes contraction alkalosis  Hypokalemia augments renal ammoniagenesis
  16. 16. Posthypercapnia  During respiratory acidosis prolonged co2 retention occurs (chronic hypoventilation and hypercapnia) resulting in increased plasma HCO3 concentration  Due to increased reasbsorption and generation of HCO3  When hypercapnia resolves increased HCO3 content and associated ECF contraction will cause metabolic alkalosis  Alkalosis persists until chloride supplementation is given
  17. 17. Nonreabsorbable anions  Administration of large amount of non reabsorbable anions like penicillin or carbenicillin can enhance distal acidification and K+ excretion  H+ secretion occurs without Cl- dependant HCO3 secretion.  Mg deficiency also results in hypokalemic alkalosis by enhancing distal acidification by stimulation of renin and hence aldosterone secretion.
  18. 18. Bartter’s syndrome  Autosomal recessive disorder involving impaired Thick Ascending Limb salt reabsorption  Results in salt wasting, volume depletion, and activation of renin-angiotensin system  It is associated with metabolic alkalosis, hypokalemia and normal to low blood pressure
  19. 19. Gitelman syndrome  autosomal recessive disorder  characterised by metabolic alkalosis, hypokalemia, hypocalciuria and hypomagnesemia  It is caused by loss of function of the thiazidesensitive sodium-chloride symporter located in the distal convoluted tubule.
  20. 20. Causes associated with normal or increased ECF volume
  21. 21. High renin  States with high renin may be accompanied by hyperaldosteronism and alkalosis  Renin levels may be increased due to increased renin secretion or decreased circulating blood volume  Examples of high renin HTN are Accelerated hypertension and renovascular hypertension  Estrogen increase renin substrate and hence angiotensin II formation  Primary tumor overproduction of renin can also cause Metabolic alkalosis
  22. 22. Low renin I. Hyperaldosternism  Adenoma, carcinoma and hyperplasia of adrenal gland results in aldosterone overproduction  Adrenal enzyme defects (11 B hydroxylase deficiency, 17 a- hydroxylase deficiency)  Aldosterone causes hypokalemia which results in an increased indirect reabsorption of HCO3 via the rise in proximal tubular intracellular H+  Hypokalemia reduces GFR and thereby maintains the elevated blood HCO3
  23. 23. II. Cushing’s syndrome or disease  Abnormally high glucocorticoid hormone production caused by adrenal gland adenoma or carcinoma or ectopic corticotrophin production can cause metabolic alkalosis
  24. 24. Liddle’s syndrome  Autosomal dominant disorder  Characterized by early, and frequently severe, hypertension associated with low plasma renin activity, metabolic alkalosis, hypokalemia, and normal to low levels of aldosterone  Liddle syndrome involves abnormal kidney function, with excess reabsorption of sodium and loss of potassium from the renal tubule
  25. 25. CYSTIC FIBROSIS Cystic fibrosis Mutation in CF gene on CHR-7 (del 3 bp in CFTR protein ) Na+ & Clˉ loss Volume depletionHrponatremia (rare) alkalosis hypokalemia
  26. 26. Milk-Alkali syndrome  Ingestion of large amount of milk and absorbable antacids: CaCO3  Patient excrete large amount of Ca and HCO3 in the urine  Ca deposits more in alkaline urine  Deposition of Ca leads to renal function impairment  Thus HCO3 increased in plasma
  27. 27. ORGAN SYSTEM CONSEQUENCES Cardiovascular Arteriolar vasoconstriction Decreased coronary blood flow, decreased myocardial contractility Increased risk of arrhythmia Respiratory Hypoventilation Metabolic Decreased K+ , Ca+ , Mg + , PO4 Neurological Seizures
  28. 28. COMPENSATION  Respiratory compensation for metabolic alkalosis is less predictable than that for metabolic acidosis  PCO2 can be estimated by adding 15 to the HCO3 when HCO3 range is from 25 to 40 meq/l  Further elevation in PCO2 is limited by hypoxemia and to some extent hypokalemia, which normally accompanies metabolic alkalosis
  29. 29.  Compensation for metabolic alkalosis occurs mainly in the lungs, which retain carbon dioxide (CO2) through hypoventilation.  CO2 is then consumed toward the formation of the carbonic acid, thus decreasing pH.  The decrease in H+ suppresses the peripheral chemoreceptors, which are sensitive to pH.  But, because respiration slows, there's an increase in PCO2 which offsets the depression because of the action of the central chemoreceptors which are sensitive to the partial pressure of CO2 in the cerebral spinal fluid.  So, because of the central chemoreceptors, respiration rate would be increased.
  30. 30.  Renal compensation for metabolic alkalosis consists of increased excretion of HCO3 -  Filtered load of HCO3 - exceeds the ability of the renal tubule to reabsorb it.  The development of metabolic alkalosis hence means the failure of kidneys to eliminate HCO3 at normal capacity
  31. 31. CLINICAL PRESENTATION  Symptom of metabolic alkalosis are not specific.  Include changes in central and peripheral nervous system function  Hypoventilation develops because of inhibition of the respiratory center in the medulla.  Mental confusion, obtundation, predisposition to seizure is common
  32. 32.  Aggravation of arrhythmia and hypoxemia in COPD may also be seen  Symptoms of hypokalemia like muscle cramps, myalgia and muscle weakness may also be seen  Symptoms of hypocalcemia (eg, jitteriness, perioral tingling, muscle spasms) may be present.
  33. 33. DIAGNOSIS Clˉ Responsive (urinary Clˉ<10 meq/L) Clˉ Resistant (urinary Clˉ>20 meq/L) HIGH BP NORMAL BP 1) Gastric losses 2) Loop diuretics (frusemide) 3) Clˉ loosing diarrhoea 4) Clˉ Deficient formula 5) Cystic fibrosis 6) Post hypercapnoea 1) Adrenal adenoma/hyperplasia 2) Hyperaldosteronism(remedial) 3) Renovascular disease 4) Renin secreting tumor 5) 17 alfa hydro.deficiency 6) 11 beta hydro.deficiency 7) Cushing syndrome 8) 11 beta hydroxysteriod dehydrogenase deficiency 9) Licorice ingestion 10) Liddle syndrome Gitelman syndrome Bartter syndrome Excess base intake METABOLIC ALKALOSIS
  34. 34. Chloride-Sensitive (Responsive) Metabolic Alkalosis:  The initial problem is a sustained loss of chloride out of proportion to the loss of sodium (either by renal or GI )  This chloride depletion results in renal sodium conservation leading to a corresponding reabsorption of [HCO3 -] by the kidney.  In this category of metabolic alkalosis, the urinary [Cl-] is <10 mEq/L,  and the disorders respond to treatment with intravenous NaCl.
  35. 35. Chloride-Insensitive (Resistant) Metabolic Alkalosis:  The pathogenesis in this category is direct stimulation of the kidneys to retain bicarbonate irrespective of electrolyte intake and losses.  The urinary [Cl-] >15-20 mEq/L, and these disorders do not respond to NaCl administration.
  36. 36. ynm dduh new delhi 64 HISTORY  vomiting,  medication diuretics in CHF  Salty sweats CYSTIC FIBROSIS  Intake of sodabicarbonate  Massive blood transfusion, (citrate bicarbonate)  Total parenteral nutrition (TPN) ( acetate bicarbonate)  POLYHYDRAMNIOS IN MOTHER antenatal Bartter syndrome  Deafness , Recurrent dehydration Bartter syndrome  Hypertension hypermineralocorticoid state
  37. 37. ABG in Metabolic Alkalosis  Arterial pH increased (> 7.45)  Serum bicarbonate increased (> 26meq/l)  PaCO2 increased  PaCO2 rises 7 mmHg per 10 meq/L bicarbonate rise  PaCO2 = 0.75 x HCO3
  38. 38.  The anion gap is frequently elevated to a modest degree in metabolic alkalosis because of the increase in the negative charge of albumin and the enhanced production of lactate.  Serum bicarbonate concentration can be calculated from a blood gas sample using the Henderson- Hasselbalch equation, as follows: pH = 6.10 + log (HCO3 - ÷ 0.03 × PaCO2) Alternatively, HCO3 - = 24 × PaCO2 ÷ [H+]
  39. 39.  Normally, arterial PaCO2 increases by 0.5-0.7 mm Hg for every 1 mEq/L increase in plasma bicarbonate concentration  If the change in PaCO2 is not within this range, then a mixed acid-base disturbance occurs.  if the increase in PaCO2 is more than 0.7 times the increase in bicarbonate, then metabolic alkalosis coexists with primary respiratory acidosis.  If the increase in PaCO2 is less than the expected change, then a primary respiratory alkalosis is also present.
  40. 40. INVESTIGATIONS  Urinary chloride  Renin & aldosterone renovascular HTN,renin secret. tumor  Renin & aldosterone adrenal adenoma, glucocort. Remedial hyperaldostero.  Renin & aldosterone cushing & Liddle synd. Licorice, 17 alfa hydro.deficiency 11 beta hydro.deficiency 11 beta hydroxysteriod dehydrogenase deficiency  Elevated 24 hr urine cortisol Cushing syndrome  Elevated 11 de-oxycortisol 17 alfa hydro.deficiency, 11 beta hydro.deficiency
  41. 41. MANAGEMENT chloride- Responsive metabolic alkalosis  Re-expand volume with Normal Saline ( Primary Therapy)  Supplement with Potassium to treat hypokalemia (alkalosis associated with severe hypokalemia will be resistant to volume resuscitation until K is repleted)  H+ blockers or PPIs if vomiting/NG suction to prevent further losses in H+ ions
  42. 42.  Discontinue diuretics  Acetazolamide if NS contraindicated due to CHF. (Monitor for hypokalemia)  HCl or NH4Cl in emergency. (HCl can cause hemolysis, NH4Cl should not be used in liver disease)  Hemodialysis in patients with marked renal failure
  43. 43. Chloride– Unresponsive metabolic alkalosis  Surgical removal of mineralocorticoid producing tumor  Aldosterone inhibitor  ACE inhibitor.  Discontinue steroids  Potassium repletion (only intervention needed to treat the alkalosis)
  44. 44. REFERENCE  Brenner and Rector’s THE KIDNEY 9th edition  Harrison’s principles of internal medicine, 17th edition   Webmd
  45. 45. THANK YOU!!!!!