ICU SRMO Sodium Bicarbonate use in critical care Metabolic Acidosis Hyperkalaemia Toxicology Cardiac arrest RTA CRRT Others Potential Sodium Bicarbonate Uses NaHCO3 Available in 84 solution 1050100 ml ID: 224828
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Matt Van ZettenICU SRMO
Sodium Bicarbonate
- use in critical careSlide2
Metabolic AcidosisHyperkalaemiaToxicologyCardiac arrestRTACRRTOthers?
Potential Sodium Bicarbonate Uses:Slide3
NaHCO3Available in 8.4% solution, 10/50/100 ml1mmol per mlSodibic capsule840mg = 10mmolAlkalinising agent / buffer
Na+ and HCO3- dissociate
HCO3- + H+ -> H2CO3 -> H20 + CO2
Sodium BicarbonateSlide4
Adverse effects:CardiovascularMyocardial dysfunction / decreased cardiac outputArrhythmiasDecreased TPR / hypotensionDecreased sensitivity to catecholamines
Pulmonary vasoconstriction
Neurological
Decreased LoC
Metabolic
Insulin resistanceInhibition of glycolysis
AcidaemiaSlide5
TreatmentCorrection of underlying disorderi.e. hypoxia / sepsis / hypoperfusion / DKAMixed opinion in literature regarding buffer therapyNo 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
Metabolic acidosisSlide6
Based on Base Excess (to correct 50% of deficit)<5kgBE x weight/4ChildBE x weight/6Adult
BE x weight/10
Toxicology / Arrest
1-2 mmol/kg/dose
NaHCO3 DosingSlide7
Increased CO2 loadWorsening of intracellular acidosisHypokalaemiaHypernatraemiaHypervolaemiaHypocalcaemia (decreased ionised Ca)
Metabolic alkalosis
Worsening of lactic acidosis
Decreased O2 delivery to tissues
Decreased acidosis inhibition of anaerobic metabolism
Complications of NaH2CO3 TherapySlide8
Only advised if life threatening and associated with metabolic acidosisFacilitates intracellular shift of K in exchange for extracellular movement of HTemporising measure similar to salbutamol / Insulin
I.E. K >7 with ECG changes + acidosis
HyperkalaemiaSlide9
Toxic effects via: Blockade of fast cardiac Na channelsNoradrenaline reuptake inhibitionalpha blockadeAnticholinergic actionClinically
Tachycardia, QRS / QT / PR prolongation, hypotension
Confusion, drowsiness/coma, fever
Acidosis (mixed)
Hypokalaemia
TCA OverdoseSlide10
NaHCO3 MOA:
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
TCA OverdoseSlide11
Propanolol overdoseChloroquine OverdoseClass 1a / 1c antiarrhythmics overdoseVenlafaxin overdoseBupropion overdose
Therapeutic goals
1-2mmol/kg every 2-3 minutes
Until hypotension and QRS complexes resolve
Cardiotoxicity
from Fast Na channel blockadeSlide12
Toxic effects via:
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:
Raised anion gap acidosis
Hyperventilation
Hyperthermia
Hypotension
Neurological – Tinnitus / Deafness / N+V / Confusion / Seizures
Salicylate
OverdoseSlide13
NaHCO3 MOA:Enhances urinary drug eliminationIncreases elimination from tissue and serumPrevents redistribution to CNSTreatment Goal
Serum pH <7.5
Urinary pH >7.5
Salicylate OverdoseSlide14
Toxic effects viaToxic metabolites (first enzyme is ADH)(glycoaldehyde, glycolic acid, glyoxylate, oxalic acid)
Deposition of calcium oxalate in tissues (e.g. kidneys)
Clinically
Apparent drunkenness
N+V
Seizures
Coma
Raised anion/osmolar gap metabolic acidosis
Hyperosmolality
ATN / Renal Failure
Ethylene Glycol OverdoseSlide15
NaHCO3 MOA:Correct acidosisIncrease elimination of glycolic acid by kidneysInhibit precipitation of calcium oxalate crystalsTherapeutic 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
Ethylene Glycol OverdoseSlide16
Toxic effects via:Metabolism in liver via ADH to formaldehyde -> formic acid
Clinically:
Drunkenness
Headache / nausea / vomiting
Blindness (optic nerve damage)
Drowsiness / coma
Seizures
Raised anion/osmolar gap acidosis
Methanol OverdoseSlide17
NaHCO3 MOA:Correcting metabolic acidosisDecreasing formic acid levelTherapeutic GoalMetabolic 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
Methanol OverdoseSlide18
Routine use of sodium bicarbonate is not recommended for cardiac arrest by the ARCStudies have shown no improvement in outcome?Related to worsened intracellular acidosisConsider administration in:
TCA overdose
Hyperkalaemia
Pre-existing metabolic acidosis
Prolonged cardiac arrest
Cardiac ArrestSlide19
ARC guidelines recommend NaHCO3 as 2nd line therapy for several conditionsPEAAs acidosis /hypovolaemia may predispose to PEA
Asystole / Severe Bradycardia
Refractory VF/VT
Cardiac Arrest - APLSSlide20
Distal RTAReduced H+ secretion in DCTNa / K wastingHyperchloraemic MATypically require 1-4 mmol/kg/day of SodibicProximal RTA
Impaired HCO3 reabsorption in PCT
K wasting
May require up to 10mmol/kg/day
RTASlide21
CRRTSlide22
NaHCO3 used as buffer in dialysate fluidCRRT rather than NaHCO3 can be used to treat severe metabolic acidosisAlso useful to dialyse toxins
CRRTSlide23
Preventing contrast induced nephropathyMixed outcomes from research in recent yearsSome trials show decreased AKI with NaHCO3 pre-hydrationMeta-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
Other uses?