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Metabolic acidosis & Metabolic alkalosis
Dr.R.Anitha Prof.S.Shivakumar unit
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Metabolic acidosis
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Primary Change Secondary change Net effect Hco3 Pco2 pH ( H+)
Pco2 should by 1.2 mmHg for each mEq plasma Hco3
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Causes of metabolic acidosis
Inability to excrete dietary acid load Renal failure Renal tubular acidosis type 1 &4 Increased H+ load Lactic acidosis Ketoacidosis Toxin ingestions Increased HCO3 loss diarrhoea
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Normal anion gap or hyper chloremic acidosis
AG = Na+– (Hco3 + Cl ) Normal = 12 ± 4 ( 8 16 ) Measure of unmeasured anion (protiens) Normal anion gap or hyper chloremic acidosis High anion gap
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Metabolic acidosis Lactic acidosis Ketoacidosis Diarrhoea
High anion gap Normal anion gap Lactic acidosis Ketoacidosis Renal failure Toxin ingestions Salicylate Methanol Ethylene glycol Diarrhoea Renal tubular acidosis
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Clinical features Kussmals respiration (increased depth than rate)
Neurologic symptoms: lethargy to coma In severe acidosis (pH< 7.1): Cardiac arrhythmia Reduced cardiac contractility Decreased inotropic response to catecholamines. Chronic acidosis Impaired growth in children Osteomalacia/osteopenia
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Treatment Treat the underlying cause NaHCO3 therapy:
Severe metabolic acidosis (pH<7.1) Chronic acidosis (sodium or potassium citrate) To alkalanise urine in salicylate poisoning
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NaHCO3 therapy in severe acidosis: pH <7.1
Always treat the pH and not the HCO3 Only one half of bicarbonate deficit to be corrected in initial 12 hrs NaHCO3 dose= desired HCO3 – observed HCO3 * 50%of body wt desired HCO3 =12 meq/L in HAG acidosis and meq/L in NAG
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Example A 24 yr old type 1 diabetic male, weighing aroud 50 Kg presenting with fever, tachypnoea and abd pain to the EMU pH HCO pCo Urine ketones + BP 100/70 PR 128/min Start IV saline 0.9%, insulin bolus &continuous infusion drip, start NaHCO3 therapy to bring the pH to 7.2
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Calculation of desired HCO3
H = 24 x Pco2 (Modified Henderson equation) Hco3 pH = HC03 = PCo2 =20.8 When pH is 7.0, H+ = 100 neq To make the pH 7.2, H+ = 63, the desired HCO3(y) 63 = 24 x 20.8/ y y = 24 x 20.8/ 63 = 7.9 = desired HCO3 NaHCO3 dose= desired HCO3 – observed HCO3 * 50%of body wt = 7.9 – 5 * 25 = 73 meq
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Complications of NaHCO3 therapy
Sodium and volume overload – dangerous in states of shock – slow continuous UF/ CVVH/intermittent dialysis(HD/PD) Hypernatremia Hypokalemia Overshoot alkalosis On correction of the cause metabolism of organic anions(lactate, ketoacids) will produce HCO3 – potential HCO3
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CHRONIC ACIDOSIS Imeq/kg/day of alkali either as Shohl’s solution or NaHCO3 tablets Shohl’s solution = 140g citric acid + 98g hydrated crystalline salt of sodium citrate in dist water to make 1000ml ( 1ml=1meq)
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Potassium in metabolic acidosis
Usually hyperkalemia occurs Potassium depletion common – GI loss/renal loss/treatment of DKA Initial plasma K relatively normal or high – metabolic acidemia cause K to move out of cells in to ECF. Careful freq monitoring of potassium during treatment and correct hypokalemia (<3.5) at once.
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Summary AG Normal Anion Gap High Anion Gap cause
H/O diarrhoea,DM, Toxin ingestion, C/F of shock Sr Ketone, lactate, urine pH/osm gap/AG, pl osm gap Treat The cause The pH only in severe acidosis pH<7.1
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Metabolic alkalosis
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Pco2 should by 0.6 mmHg for each mEq plasma Hco3
Primary Change Secondary change Net effect Hco3 Pco2 pH ( H+) Pco2 should by 0.6 mmHg for each mEq plasma Hco3
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Metabolic alkalosis Generation Maintenance
H+ loss in GIT (vomiting or NG suction) or in urine (diuretics) Maintenance Perpetuation of metabolic alkalosis – requires impairment in renal HCO3 excretion
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Maintenance Decreased effective arterial volume Decreased GFR
Secondary hyperaldosteronism Na retention/H+ excretion
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Chloride depletion Chloride loss reabsorption Bicarbonate Increase
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Potassium depletion Intracellular acidosis Paradoxical aciduria
k k k H k H H H H k k k k H H k k k H H H k H k H Paradoxical aciduria Extracellular alkalosis
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Cause of metabolic alkalosis
Gastrointestinal loss vomiting or NG suction Renal loss Loop or thiazide diuretic Mineralocorticoid excess Postchronic hypercapnea H+ movement into cells Hypokalemia
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For a clinically relevant etiologic classification
Urine Cl- conc <10meq/L Chloride Depletion Alkalosis Decreased effective arterial volume CDA >20meq/L Potassium Depletion Alkalosis Mineralocorticoid excess KDA
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CDA KDA Gastric acid loss Chloruretic diuretics Posthypercapnic state
With hypertension Primary aldosteronism Secondary aldosteronism With normotension Bartter syndrome Gitelman syndrome
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Clinical features Signs of volume depletion in CDA (hypotension, tachycardia..) Singn of volume expansion in KDA (hypertension) Signs of hypokalemia In severe metabolic alkalosis (pH > 7.55) hepatic encephalopathy, cardiac arrhythmia, digitalis cardiotoxicty or altered mental status
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General management principles
Correction of fluid defecit Correction of hypokalemia and hypochloremia Correction of pH if it is severe alkalosis (pH > 7.55)
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Chloride Depletion Alkalosis
ECF volume contraction Volume correction by NaCl Further repletion KCl ECF volume overload NaCl contraindicated T.Acetazolamide 250mg bd/tds
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Potassium depletion alkalosis
Potassium replacement Removal of source of mineralocorticoid excess Blockade – Amiloride 5-10mg Triamtrene 100 mg bd Spiranalactone mg Hypomagnesemia to be corrected
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Severe hypokalemia (<2meq/l)
Make the metabolic alkalosis and hypovolemia resistant to saline therapy Because severe hypokalemia cause impairment in Cl- reabsorption in distal tubule Replacement of only one half of potassium defecit will normalise Cl- reabsorption
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In very severe alkalosis (pH > 7.55)
c/f of hepatic encephalopathy, cardiac arrhythmia, digitalis cardiotoxicty or altered mental status HCl (0.1N)administration in central venous catheter 25meq/hr Amount of HCl= 0.5* body wt*(plasma HCO3-24)
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Summary Urine cl Chloride depletion alkalosis (CDA)
Potassium depletion alkalosis (KDA) CDA ECF vol contraction – NaCl, KCl ECF vol overload – acetazolamide, K supp KDA K replacement Remove or block the source
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Summary cont… pH >7.55 Hcl therapy
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Take home message Identify the cause with history, C/F, ABG, lab analysis. Single HCO3 value cannot replace ABG Treat the cause Treat the pH only when there is severe acidosis or alkalosis Always correct the pH not the HCO3
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Thank you
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