METABOLIC ACIDOSIS



Metabolic Acidosis Severe = pH <7.1Effects of metabolic acidosisRS: incr RR, shift of Oxy-Hb curve to R (Hb gives up O2)CV: myocardial depression (when pH <7.1), catecholamine release, pul vasoCMet: hyperK (O.5 K : 0.1 pH); hypoCaNeonates and pregnant women esp susceptible due to decr buffering capacityAGMAIncr anions –Decr cations +Incr AG = incr concentration of unmeasured anions (endogenous / exogenous; due to administration of acid or incr production of acid, or decr acid excretion; eg. Phos, SO4, Ca, Mg) Decr concentration of unmeasured cationsCATMUDPILERSCO, cyanide Lactic acidAlcohol (ETOH alone will never cause severe met acidosis), alcoholic ketoacidosis AcetoacetateToulene HippurateMethanol, metformin Formic / lactic acidUraemia (ie. Renal failure, aminoglycosides) Uric acid, phosphate, sulphate, CrDKA Beta-OH-butyrate, gluParaldehyde, paracetamol, polyethylene glycolIsoniazid / iron / idiopathic / inborn errors of metabolismLactic acidosis = lactate >2.5; most common cause in ED; pure lactic acidosis in only 10% Lactic acidType A Tissue hypoxia / hypoperfusion decr oxidative phosphorylationType B1 Systemic disorders (eg., leukaemia, lymphoma, thiamine def, pancreatitis, short bowel syndrome) Incr production: exercise, seizures, trauma Decr metabolism: hepatic failure, renal failure, hypothermia, DM, sepsis Type B2 Drugs / toxins (eg. ETOH, meth, ethylene glycol, Fe, salicylates, isoniazid, cyanide, CO, metformin uncoupling of oxidative phosphorylation) Type B3 Hereditary metabolic disease (eg. G6PD def) Lactate 2.5-5 = mild = 35% mortality; >2.5 = aerobic capacity exceeded Lactate 5-10 = mod = 75% mortality (severe if >4; NAGMA in 50%) Lactate >10 = severe = 100% mortalityEthylene glycol Glycolic acid, oxylateRhabdoSalicylates, starvation SalicylateIncr AG without acidosis: penicillin, carbenicillinNAGMADue to renal and GI bicarbonate loss, or loss of ability to excrete HCl retained while HCO3 lost incr Cl to maintain electroneutralityUSEDCARPUretersotomy Decr KSmall bowel fistula Decr KExtra Cl (ED resus, HCl ingestion, TPN) Incr KDiarrhoea (accounts for >95%) Decr K Resolving DKA Diuretics (K sparing) Incr K Diuretics (eg. Acetazolamide) Decr KCarbonic anhydrase inhibitors Adrenal insufficiency / Addisons Incr KRenal tubular acidosis (2nd most common cause; decr ability to excrete H in DCT and absorb HCO3 in PCT); other causes = toluene, chronic renal diseases, heavy metal toxicity RTA type 1 (amphotericin, severe hypoK, Sjogrens, SLE, urinary tract obstruction) Decr K RTA type 2 (Fanconi, myeloma, other genetic) Decr K RTA type 4 (hyperK, adrenal insufficiency, rickets, osteomalacia) Incr KPancreatic fistula Decr KEarly ARF usually NAGMA due to HCO3 lossLAGMA <5Incr cations +Decr anions -Increase in unmeasured cations: Lithium, HyperCa / Mg / K, IgG (Multiple Myeloma)Decreased unmeasured anions: HypoAlb / Phos (may mask a AGMA)Chloride over-estimation (anion): Bromide toxicity, Iodide toxicity, Hypercholesterolemia, calculation errorOther: nitritesMngIndications for HCO3: Acidosis (HCO3 <3, pH <7.2) and incr K / Cl ++ 0.5mmol/kg for each desired incr in HCO3; endpoint HCO3 >8 / clinical improvement / pH 7.2; 10-25mmol/hr infusion More likely to be required in NAGMA as 1Y problem is loss of HCO3, as opposed to AGMA where 1Y problem is gain of H Cardiotoxicity due to fast Na channel blockade: TCA OD (severe), type 1a/c antiarrhythmics, cloroquine, propanolol 2mmol/kg IV boluses rpt until stable, then administer as per blood gas results Urinary alkalinisation in OD: salicylate (mod severity not requiring haemodialysis), phenobarb (if continued toxicity despite MDAC), methotrexate 1-2mmol/kg IV bolus 25mmol/hr infusion; aim urinary pH >7.5 Incr urinary solubility: methotrexate, rhabdo Prevention of drug redistribution to CNS (incr unionised amount of drug): salicylate Severe hyperK 50-100mmol (1mmol/kg) slow IV Methanol / ethylene glycol / cyanide / isoniazid >15min cardiac arrest / cardiac arrest in young children or pregnancy HFl acid toxicity RTAComplications of HCO3: extravasation, gastric distension hyperNa, hyperosmolality, alkalosis (pH >7.6 bad for CV function), L shift of O2-Hb diss curve (impaired O2 unloading), hypoK, hypoCa (usually not clinically significant, but if low Ca, then correct Ca before correcting metabolic acidosis to avoid hypoCa); incr lactate production; resp acidosis (ventilation must account for incr CO2 production); paradoxical CSF acidosis; CSF acidosis may be protective and reversal dangerous vol overload, pul oedema In DKA: decr clearance of ketones may precipitate hepatic encephalopathy in susceptible peopleCI to HCO3: hypoK, hypoCa, alkalosis, acute pul oedema, renal failure, severe hyperNaNotes from: METABOLIC ACIDOSIS(PC02 < 35, HC03 , B.E > -2)29375107493000 211455083820ANION GAP(Na + K) – (Cl + HC03) ~ 1200ANION GAP(Na + K) – (Cl + HC03) ~ 122937510150495002937510342900017487903429000403479078740NORMAN ANION GAPDue to loss of HC03, generally with Cl hence normal anion gap00NORMAN ANION GAPDue to loss of HC03, generally with Cl hence normal anion gap560070100965 ANIONGAPDue to H which consumes HCO300 ANIONGAPDue to H which consumes HCO35040630768350056007039560500120015074295001200150-291465002023110118745 ACID LOADKetoacidsDKAStarvationAlcoholicLacticExogenous.00 ACID LOADKetoacidsDKAStarvationAlcoholicLacticExogenous.-8001067945 ACID EXCRETIONARFCRF00 ACID EXCRETIONARFCRF4491990135890Check K levels00Check K levels5040630527050092583052705004491990155575 KLower GIT lossesRenalCA inhibitorsRTAUrinary ‘diversion’Vesico-colicUtero-enterostomy00 KLower GIT lossesRenalCA inhibitorsRTAUrinary ‘diversion’Vesico-colicUtero-enterostomy28575086360 K+ or NormalMineralot corticoid deficiency.eg: Addision’s.Addition of Cl as the anion of an acid, eg, NH4Cl00 K+ or NormalMineralot corticoid deficiency.eg: Addision’s.Addition of Cl as the anion of an acid, eg, NH4Cl ................
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