METABOLIC ACIDOSIS

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ynm DDUH NEW DELHI 64 1 ACID - BASE BALANCE By Dr Y.N MAURYA M.B.B.S, D.C.H Medical Officer Deen Dayal Upadhyay Hospital Govt. of NCT New Delhi- 64

SOME NORMAL VALUES : 

ynm DDUH NEW DELHI 64 2 SOME NORMAL VALUES pH --- 7.35-7.45 HCO3¯ --- 22-26 mmol/L PaCO2 --- 35-45 mmHg PaO2 --- 60-100 mmHg ALBUMIN-- 4—5.5 g/dl Na+ --- 135-145 mmol/L K+ --- 3.5-5.5 mmol/L Ca+2 --- 1.12-1.23 mmol/L Cl¯ --- 98-106 mmol/L [H+] at pH 7.4 --- 40 nmol/L

Why pH 7.35—7.45 is : 

ynm DDUH NEW DELHI 64 3 Why pH 7.35—7.45 is necessary ?

FOR OPTIMAL FUNCTIONING OF CELLULAR ENZYMES & METABOLIC PROCESSES : 

ynm DDUH NEW DELHI 64 4 FOR OPTIMAL FUNCTIONING OF CELLULAR ENZYMES & METABOLIC PROCESSES

WHICH pH SHOULD BE MAINTAINED ? : 

ynm DDUH NEW DELHI 64 5 WHICH pH SHOULD BE MAINTAINED ? INTRACELLULAR OR EXTRACELLULAR

INTRACELLULAR pH SHOULD BE MAINTAINED : 

ynm DDUH NEW DELHI 64 6 INTRACELLULAR pH SHOULD BE MAINTAINED

IS IT INTRACELLULAR pH WHICH MEASURED NORMALY ? : 

ynm DDUH NEW DELHI 64 7 IS IT INTRACELLULAR pH WHICH MEASURED NORMALY ? NORMALY MEASURED pH IS EXTRACELLULAR pH BECAUSE INTRACELLULAR pH PARALLELS EXTRACELLULAR pH & LATER IS EASY,SO IT IS EXTRACELLULAR pH WHICH IS NORMALY MEASURED

NORMAL PHYSIOLOGY OF ACID- BASE BALANCE : 

ynm DDUH NEW DELHI 64 8 NORMAL PHYSIOLOGY OF ACID- BASE BALANCE

MAINTAINENCE OF EXTRACELLULAR pH & BUFFER : 

ynm DDUH NEW DELHI 64 9 MAINTAINENCE OF EXTRACELLULAR pH & BUFFER WHAT IS BUFFER ? . SUBSTANCES THAT ATTENUATE CHANGE IN pH. THESE ARE WEAK ACIDS OR WEAK BASES. ARE 50% DISSOCIATED AT IT'S pK (diss. Constant) BEST BUFFERS HAVE pK CLOSE TO 7.4

IMPORTANT BUFFERS : 

ynm DDUH NEW DELHI 64 10 IMPORTANT BUFFERS ? BICARBONATE BUFFER H++ HCO3¯ == H2O+ CO2 ( pK 6.1 ) ? NON-BICARBONATE BUFFERS 1. ALBUMIN ( PK 6.5) 2. Hb 3. phosphate H2PO4¯ == H+ + HPO4¯¯ ( pK6.8) 4. Bone

HOW pH IS MAINTAINED B/W 7.35-7.45 : 

ynm DDUH NEW DELHI 64 11 HOW pH IS MAINTAINED B/W 7.35-7.45 WHEN H+ IS ADDED (ACIDOSIS) H++ HCO3¯ H2CO3 H2O + CO2 reaction shifts towards Rt Buffers try to maintain pH, pH decreases ,HCO3- conc. decreases & balancing mechanism start WHEN CO2 IS ADDED (ACIDOSIS) H2O +CO2 H2CO3 H++ HCO3¯ pH decreases, HCO3¯ increases

RESPONSE OF LUNG to acidosis : 

ynm DDUH NEW DELHI 64 12 RESPONSE OF LUNG to acidosis Acidosis is sensed by medulla, aortic & carotid body Signal is send to resp. center Hyperventilation starts & CO2 is washed off,it completes within 12-24 hrs

LIVER ALSO RESPONDS to acidosis : 

ynm DDUH NEW DELHI 64 13 LIVER ALSO RESPONDS to acidosis When organic acids are added eg. Lactic acetic, keto acids etc. HCO3¯ is produced by these acids and acidosis is tried to be balanced

RENAL COMPENSATION to acidosis : 

ynm DDUH NEW DELHI 64 14 RENAL COMPENSATION to acidosis Renal compensation begins 12-24 hr after, hyperventilation starts It takes 3-4 days to complete appropriate metabolic compensation.

RENAL COMPENSATION to acidosis : 

ynm DDUH NEW DELHI 64 15 RENAL COMPENSATION to acidosis Kidney excrete H+ & conserve HCO3¯. Fixed acids(hydrochloric,sulphuric,phosphoric ) are only excreted by kidney

HOW PH IS MAINTAINED B/W 7.35-7.45 : 

ynm DDUH NEW DELHI 64 16 HOW PH IS MAINTAINED B/W 7.35-7.45 ? WHEN ALKALI IS ADDEED (ALKALOSIS) pH increases , HCO3¯ increases ? WHEN CO2 IS LOST (ALKALOSIS) pH increases, HCO3¯ decreases

RESP. COMPENSATION to alkalosis : 

ynm DDUH NEW DELHI 64 17 RESP. COMPENSATION to alkalosis HYPOVENTILATION STARTS & SMALL INCREASE IN PaCO2 OCCURS

RENAL COMPENSATION to alkalosis : 

ynm DDUH NEW DELHI 64 18 RENAL COMPENSATION to alkalosis IN ALKLOSIS URINARY EXCRETION OF HCO3¯ INCREASES H+ EXCRETION DECREASES

ANION GAP : 

ynm DDUH NEW DELHI 64 19 ANION GAP It represents those negative ions not normally measured in clinical practice i.e PO4¯¯¯,SO4¯¯ lactate, ketoacids & albumin It is diff. b/w conc. of cation except Na+ and conc. of anion except Cl¯& HCO3¯

ANION GAP : 

ynm DDUH NEW DELHI 64 20 ANION GAP [Cl¯+ HCO3¯]+unmeasured anion=[Na+] +unmeasured cation unmeasured anion – unmeasured cation = [Na+]-[Cl¯+ HCO3¯] ANION GAP ===[Na+]-[Cl¯+ HCO3¯] NORMAL ANION GAP IS 8 -12 mmol/L A G is increased if- 1. conc. Of K+,Ca+2 ,Mg+2 dec. 2. conc. Of/charge on protein increases 3. when organic anions are increased ? A G is decreased if cations are increased or albumin decreased

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ynm DDUH NEW DELHI 64 21

ACID – BASE DISORDER : 

ynm DDUH NEW DELHI 64 22 ACID – BASE DISORDER ACIDOSIS METABOLIC RESPIRATORY ALKALOSIS METABOLIC RESPIRATORY

METABOLIC ACIDOSIS : 

ynm DDUH NEW DELHI 64 23 METABOLIC ACIDOSIS WHICH TERM,METABOLIC ACIDOSIS/ACIDEMIA SHOULD BE USED?

METABOLIC ACIDOSIS : 

ynm DDUH NEW DELHI 64 24 METABOLIC ACIDOSIS ACIDEMIA SIMPLY BLOOD pH BELOW 7.35 ACIDOSIS PATHOLOGICAL PROCESS CAUSING ACIDEMIA ALONG WITH SIGNS & SYMPTOMS

METABOLIC ACIDOSIS --PATHOPHYSIOLOSY : 

ynm DDUH NEW DELHI 64 25 METABOLIC ACIDOSIS --PATHOPHYSIOLOSY INCREASED ACID PRODUCTION OTHER THAN H2CO3. DECREASED ACID EXCRETION OTHER THAN H2CO3 @ RATE EOUAL TO THEIR PRODUCTION. LOSS OF ALKALI IN URINE/G.I.T. INGESTIION OF ACIDS.

METABOLIC ACIDOSIS –AFFECTED ORGAN SYSTEMS : 

ynm DDUH NEW DELHI 64 26 METABOLIC ACIDOSIS –AFFECTED ORGAN SYSTEMS EVERY CELL IS AFFECTED

METABOLIC ACIDOSIS - BRAIN : 

ynm DDUH NEW DELHI 64 27 METABOLIC ACIDOSIS - BRAIN

METABOLIC ACIDOSIS- HEART : 

ynm DDUH NEW DELHI 64 28 METABOLIC ACIDOSIS- HEART Most common sign is tachycardia Arrythmia may occur pH<7.2 Causes Peripheral vasodilation Hypotention & shock Decr. Resp. to catecholamine

METABOLIC ACIDOSIS- LUNG : 

ynm DDUH NEW DELHI 64 29 METABOLIC ACIDOSIS- LUNG

METABOLIC ACIDOSIS- KIDNEY : 

ynm DDUH NEW DELHI 64 30 METABOLIC ACIDOSIS- KIDNEY Conserve HCO3¯ Excrete H+ and NH3 Renal compensation starts 12-24 hrs after hyperventilation begins.

METABOLIC ACIDOSIS- OTHER EFFECTS : 

ynm DDUH NEW DELHI 64 31 METABOLIC ACIDOSIS- OTHER EFFECTS Hyperkalemia Insulin resistance Incr. protein degradation Decr. ATP production O2 disso. curve shift to Rt—Decr. Oxygenation of Hb in lung

METABOLIC ACIDOSIS- HISTORY TAKING : 

ynm DDUH NEW DELHI 64 32 METABOLIC ACIDOSIS- HISTORY TAKING Anorexia, nausea vomiting Met acidosis with seizure, decr. sensorium in neonate-----Inborn error of metabolism Depressed mental status, lethargy poor feeding—Aortic coarctation , hypoplastic Lt heart syndrome Failure to thrive with Met. Acidosis—RTA Polyuria, polydipsia, wt. loss---DM 1,DKA H/o intoxication---ethanol, methanol, ethylglycol salicylate Chr Med/surg issue—renal failure, DM, ureterosigmoidostomy H/o trauma, fever, sepsis cardiac failure , anaphylaxis

INCREASED ANION GAP ACIDOSIS : 

ynm DDUH NEW DELHI 64 33 INCREASED ANION GAP ACIDOSIS Mneumonic MUDPILES Methanol Uremia DKA Paraldehyde Iron, INH Lactic acid Ethanol ,ethyl glycol salicylate

NORMAL ANION GAP ACIDOSIS : 

ynm DDUH NEW DELHI 64 34 NORMAL ANION GAP ACIDOSIS Mneumonic USEDCARP Ureterostomy Small bowel fistulla Extra chloride Carbonic anhydrase inhibitor Adrenal insufficiency RTA Pancreatic fistula

METABOLIC ACIDOSIS-PATHOPHYSIOLOGY IN DIARRHOEA : 

ynm DDUH NEW DELHI 64 35 METABOLIC ACIDOSIS-PATHOPHYSIOLOGY IN DIARRHOEA HCO3¯LOSS DIARRHOEA VOLUME LOSS SHOCK DEC.IN GFR RENALFAILURE DEC.H+ LOSS ACIDOSIS

METABOLIC ACIDOSIS-PATHOPHYSIOLOGY IN RTA-1 : 

ynm DDUH NEW DELHI 64 36 METABOLIC ACIDOSIS-PATHOPHYSIOLOGY IN RTA-1 RTA-1 INADEQUATE TRANSPOPRT OF H+ IN DISTAL TUBULE OR BACK DIFFUSION OF H+ IN BLOOD CHRONIC ACIDOSIS HYPOKALEMIA AD (mild & most common) mutation in basolateral Cl¯& HCO3¯ EXCHANGER AR (H+ ATPase mutation,also have DEAFNESS) Dec. Ca+2 absorption Renal hypercalciuria 20 hyperparathyroidism Nephrocalcinosis nephrolithiasis Urinary pH>5.5 Growth retardation

METABOLIC ACIDOSIS-PATHOPHYSIOLOGY IN RTA-2 : 

ynm DDUH NEW DELHI 64 37 METABOLIC ACIDOSIS-PATHOPHYSIOLOGY IN RTA-2 RTA-2 Mutation in Na+ HCO3¯cotransporter Defect in HCO3¯absorption Usually along with Fanconi syndrome Urinary pH<5.5 Glycosuria but normal serum glu. hypophosphatemia hypourecemia hypokalemia aminoaciduria LMW protein loss rickets

METABOLIC ACIDOSIS-PATHOPHYSIOLOGY IN RTA-4 : 

ynm DDUH NEW DELHI 64 38 METABOLIC ACIDOSIS-PATHOPHYSIOLOGY IN RTA-4 RTA-4 Abnormal H+,K+ secretion at distal tubule Absence of ALDST. (CAH i.e 21 alfa hydroxylase defficiency) ALDST. Resistance ( transplanted kidney) hyperkalemia hyponatremia Volume loss hyperkalemia Drugs NSAID ACE Inhibitor. Trimethoprim Heparin

METABOLIC ACIDOSIS - LAB INVESTIGATIONS : 

ynm DDUH NEW DELHI 64 39 METABOLIC ACIDOSIS - LAB INVESTIGATIONS Electrolyte, BUN, S.Gravity……….. If BUN : creatinine > 20—---prerenal azotemia / hypovolumia Hypoglycemia with acidosis—--adrenal insufficiency, liver disorder Normoglycemia, glycosuria, met. Acidosis—---RTA2 O.G >20 with met acidosis—---methanol, ethanol OSMOLE GAP=2Na+(glucose/18)+(BUN/2.8) Hypoalbunemia is most common cause of low anion gap Decrease in 1 gm/dl albumin=Decrease in AG of 2.5 mosmol/L

METABOLIC ACIDOSIS -TREATMENT : 

ynm DDUH NEW DELHI 64 40 METABOLIC ACIDOSIS -TREATMENT Treatment of underlying disorder is must. If HCO3¯ > 10-12 --- no need of bicarbonate replacement unless renal dysfunction.

MET. ACIDOSIS – HCO3¯ THERAPY : 

ynm DDUH NEW DELHI 64 41 MET. ACIDOSIS – HCO3¯ THERAPY For CRF, RTA bicarbonate therapy is necessory---d/t ongoing loss. Salicylate poisoning—short term bicarbonate therapy—incr. excretion. If bicarbonate <8 –myocardial & CNS dysfunction---HCO3¯ therapy is must.

METABOLIC ACIDOSIS- BICARBONATE THERAPY : 

ynm DDUH NEW DELHI 64 42 METABOLIC ACIDOSIS- BICARBONATE THERAPY HCO3¯ deficit= (desired-measured HCO3¯ ) x wt(kg) x 0.6 Half of total HCO3¯ is given within few hrs, rest is given in rest of 24 hrs. Do’t overcorrect/rapid infusion—can cause—tetany, seizure, hypokalemia , hypocalcemia Dose>1meq/kg/dose---alkaline overshoot C.I—alkalosis,hypernatremia,hypocalcemia,pulm edema ,preg. ICH ©,avoid extravasation

METABOLIC ACIDOSIS -hemodialysis : 

ynm DDUH NEW DELHI 64 43 METABOLIC ACIDOSIS -hemodialysis Not responding to medical treatment Renal failure Methanol Ethyl glycol Salicylate

METABOLIC ACIDOSIS - THIAMINE : 

ynm DDUH NEW DELHI 64 44 METABOLIC ACIDOSIS - THIAMINE Thiamine acts as co-enzyme for various decarboxylation reaction. Deficiency occurs in those babies who are on exclusive breast milk & mother having thiamine deficiency. present as lactic acidosis with shock which is resistant to inotropic agents and volume resuscitation Thiamine deficiency should be suspected in Pt. on TPN without multivitamin >2 wks. DOSE –10—25 mg IM/IV.

METABOLIC ACIDOSIS- T H A M : 

ynm DDUH NEW DELHI 64 45 METABOLIC ACIDOSIS- T H A M THAM (tris-hydroxylmethylaminomethane) is a buffer, used to treat acidosis when CO2 accumulates d/t administration of bicarbonate. THAM + H2CO3 = THAM--H + HCO3¯ DOSE –0.5—1mg/kg/dose C.I -- hypersensitivity, renal failure, uremia. Use with © in resp. depression, hypoglycemia

METABOLIC ACIDOSIS-VENTILATION : 

ynm DDUH NEW DELHI 64 46 METABOLIC ACIDOSIS-VENTILATION Resistant met. Acidosis Shock, sepsis Hypoxia Increased ICT Respiratory failure

Slide 47: 

ynm DDUH NEW DELHI 64 47 THANK YOU