Matt Van Zetten
ICU SRMO
 Metabolic Acidosis
 Hyperkalaemia
 Toxicology
 Cardiac arrest
 RTA
 CRRT
 Others?
 NaHCO3
 Available in 8.4% solution, 10/50/100 ml
 1mmol per ml
 Sodibic capsule
 840mg = 10mmol
 Alkalinising agent / buffer
 Na+ and HCO3- dissociate
 HCO3- + H+ -> H2CO3 -> H20 + CO2
 Adverse effects:
 Cardiovascular
 Myocardial dysfunction / decreased cardiac output
 Arrhythmias
 Decreased TPR / hypotension
 Decreased sensitivity to catecholamines
 Pulmonary vasoconstriction
 Neurological
 Decreased LoC
 Metabolic
 Insulin resistance
 Inhibition of glycolysis
 Treatment
 Correction of underlying disorder
 i.e. hypoxia / sepsis / hypoperfusion / DKA
 Mixed opinion in literature regarding buffer therapy
 No evidence that routine buffer use improves outcome
 Studies have shown no improvement in myocardial
contractility with NaHCO3 administration
 Alternative buffers researched, but not in clinical practice
 Buffer therapy generally reserved for severe MA
 Threshold of “severe” MA varies
 Based on Base Excess (to correct 50% of deficit)
 <5kg
 BE x weight/4
 Child
 BE x weight/6
 Adult
 BE x weight/10
 Toxicology / Arrest
 1-2 mmol/kg/dose
 Increased CO2 load
 Worsening of intracellular acidosis
 Hypokalaemia
 Hypernatraemia
 Hypervolaemia
 Hypocalcaemia (decreased ionised Ca)
 Metabolic alkalosis
 Worsening of lactic acidosis
 Decreased O2 delivery to tissues
 Decreased acidosis inhibition of anaerobic metabolism
 Only advised if life threatening and associated with
metabolic acidosis
 Facilitates intracellular shift of K in exchange for
extracellular movement of H
 Temporising measure similar to salbutamol / Insulin
 I.E. K >7 with ECG changes + acidosis
 Toxic effects via:
 Blockade of fast cardiac Na channels
 Noradrenaline reuptake inhibition
 alpha blockade
 Anticholinergic action
 Clinically
 Tachycardia, QRS / QT / PR prolongation, hypotension
 Confusion, drowsiness/coma, fever
 Acidosis (mixed)
 Hypokalaemia
 NaHCO3 MOA:
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Alkalinisation increases TCA protein binding
?Correction of acidosis -> improved myocardial function
?via increasing extracellular sodium
Volume loading
 Therapeutic goal
 Resolution of hypotension, QRS prolongation
 1-2mmol/kg boluses
 Target pH 7.5-7.55
 NB: Hyperventilation and HTS have also been shown to be
effective in reducing QRS prolongation
 Propanolol overdose
 Chloroquine Overdose
 Class 1a / 1c antiarrhythmics overdose
 Venlafaxin overdose
 Bupropion overdose
 Therapeutic goals
 1-2mmol/kg every 2-3 minutes
 Until hypotension and QRS complexes resolve
 Toxic effects via:
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Direct stimulation of respiratory centre
Increased endogenous acid production
Acidity of salicylate itself
Uncoupling oxidative phosphorylation
Inhibiting Krebs cycle enzymes
Inhibiting amino acid synthesis.
 Clinically:
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Raised anion gap acidosis
Hyperventilation
Hyperthermia
Hypotension
Neurological – Tinnitus / Deafness / N+V / Confusion / Seizures
 NaHCO3 MOA:
 Enhances urinary drug elimination
 Increases elimination from tissue and serum
 Prevents redistribution to CNS
 Treatment Goal
 Serum pH <7.5
 Urinary pH >7.5
 Toxic effects via
 Toxic metabolites (first enzyme is ADH)
 (glycoaldehyde, glycolic acid, glyoxylate, oxalic acid)
 Deposition of calcium oxalate in tissues (e.g. kidneys)
 Clinically
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Apparent drunkenness
N+V
Seizures
Coma
Raised anion/osmolar gap metabolic acidosis
Hyperosmolality
ATN / Renal Failure
 NaHCO3 MOA:
 Correct acidosis
 Increase elimination of glycolic acid by kidneys
 Inhibit precipitation of calcium oxalate crystals
 Therapeutic Goal:
 Metabolic acidosis with an arterial pH < 7.3 should be
treated with a sodium bicarbonate infusion to keep the
pH between 7.35 and 7.45
 Aim for urinary pH >7.0
 Toxic effects via:
 Metabolism in liver via ADH to formaldehyde -> formic acid
 Clinically:
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Drunkenness
Headache / nausea / vomiting
Blindness (optic nerve damage)
Drowsiness / coma
Seizures
Raised anion/osmolar gap acidosis
 NaHCO3 MOA:
 Correcting metabolic acidosis
 Decreasing formic acid level
 Therapeutic Goal
 Metabolic acidosis with an arterial pH < 7.3 should be
treated with a sodium bicarbonate infusion to keep the
pH between 7.35 and 7.45
 Routine use of sodium bicarbonate is not
recommended for cardiac arrest by the ARC
 Studies have shown no improvement in outcome
 ?Related to worsened intracellular acidosis
 Consider administration in:
 TCA overdose
 Hyperkalaemia
 Pre-existing metabolic acidosis
 Prolonged cardiac arrest
 ARC guidelines recommend NaHCO3 as 2nd line
therapy for several conditions
 PEA
 As acidosis /hypovolaemia may predispose to PEA
 Asystole / Severe Bradycardia
 Refractory VF/VT
 Distal RTA
 Reduced H+ secretion in DCT
 Na / K wasting
 Hyperchloraemic MA
 Typically require 1-4 mmol/kg/day of Sodibic
 Proximal RTA
 Impaired HCO3 reabsorption in PCT
 K wasting
 May require up to 10mmol/kg/day
 NaHCO3 used as buffer in dialysate fluid
 CRRT rather than NaHCO3 can be used to treat severe
metabolic acidosis
 Also useful to dialyse toxins
 Preventing contrast induced nephropathy
 Mixed outcomes from research in recent years
 Some trials show decreased AKI with NaHCO3 pre-
hydration
 Meta-analysis (Eur J Radiology 2009)
 Many included trials not of high quality
 OR for CIN 0.33 with NaHCO3 vs. NaCl
 No difference in death / CCF / RRT requirement
 Not routinely recommended
 Further research ongoing