Download Metabolic acidosis fact sheet

Metabolic Acidosis
Severe = pH <7.1
Effects of
metabolic
acidosis
RS: incr RR, shift of Oxy-Hb curve to R (Hb gives up O2)
CV: myocardial depression (when pH <7.1), catecholamine release, pul vasoC
Met: hyperK (O.5 K : 0.1 pH); hypoCa
Neonates and pregnant women esp susceptible due to decr buffering capacity
AGMA
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 cations
Incr anions –
Decr cations +
CATMUDPILERS
CO, cyanide
Lactic acid
Alcohol (ETOH alone will never cause severe met acidosis), alcoholic ketoacidosis
Acetoacetate
Toulene
Hippurate
Methanol, metformin
Formic / lactic acid
Uraemia (ie. Renal failure, aminoglycosides)
Uric acid, phosphate, sulphate, Cr
DKA
Beta-OH-butyrate, glu
Paraldehyde, paracetamol, polyethylene glycol
Isoniazid / iron / idiopathic / inborn errors of metabolism
Lactic acidosis = lactate >2.5; most common cause in ED; pure lactic acidosis in only 10%
Lactic acid
Type A
Tissue hypoxia / hypoperfusion  decr oxidative phosphorylation
Type 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% mortality
Ethylene glycol
Glycolic acid, oxylate
Rhabdo
Salicylates, starvation
Salicylate
NAGMA
Incr AG without acidosis: penicillin, carbenicillin
Due to renal and GI bicarbonate loss, or loss of ability to excrete H
Cl retained while HCO3 lost  incr Cl to maintain electroneutrality
USEDCARP
Uretersotomy
Decr K
Small bowel fistula
Decr K
Extra Cl (ED resus, HCl ingestion, TPN)
Incr K
Diarrhoea (accounts for >95%)
Decr K
Resolving DKA
Diuretics (K sparing)
Incr K
Diuretics (eg. Acetazolamide)
Decr K
Carbonic anhydrase inhibitors
Adrenal insufficiency / Addisons
Incr K
nd
Renal tubular acidosis (2 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)
Pancreatic fistula
Decr K
Incr K
Early ARF usually NAGMA due to HCO3 loss
LAGMA <5
Incr cations +
Decr anions Mng
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 error
Other: nitrites
Indications 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
RTA
Complications 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 people
CI to HCO3: hypoK, hypoCa, alkalosis, acute pul oedema, renal failure, severe hyperNa
Notes from:
METABOLIC ACIDOSIS
(PC02 < 35, HC03 , B.E > -2)
ANION GAP
(Na + K) – (Cl + HC03) ~ 12
 ANIONGAP
Due to H which
consumes HCO3
NORMAN ANION GAP
Due to loss of HC03, generally with
 Cl hence normal anion gap
 ACID
EXCRETION
ARF
CRF
 ACID LOAD
1. Ketoacids
 DKA
 Starvation
 Alcoholic
2. Lactic
3. Exogenous.
Check K levels
 K+ or Normal
1. Mineralot corticoid deficiency.
eg: Addision’s.
2. Addition of Cl as the anion of an acid,
eg, NH4Cl
K
1. Lower GIT losses
2. Renal
 CA inhibitors
 RTA
3. Urinary ‘diversion’
 Vesico-colic
 Utero-enterostomy