Bicarbonate use in cardiac arrest and shock

1. The use of bicarb in cardiac
arrest and shock – is there
any evidence out there?
David Moore CME August 2014

2. What is sodium bicarbonate?
 Bicarbonate is an anion and cannot be given alone. Its
therapeutic use is as a solution of sodium bicarbonate
 It’s a buffer
 An alkalising solution which combines with hydrogen ions to
form a weak carbonic acid.
 This breaks down to produce CO2 and H20.

3. Buffering system

4. When do we use NaHCO3 in the
emergency department?

5. When do we use NaHCO3 in the
emergency department?
 Tricyclic overdose
 Propanolol overdose
 Emergency management of severe hyperkalaemia
 In metabolic acidosis - To counteract the extracellular
acidaemia with the aim of reversing or avoiding the adverse
clinical effects of the acidosis (esp the adverse
cardiovascular effects)

6. What’s the dose?
 Depends on the clinical situation
 In cardiac arrest: 1 mmol/kg is initially given IV over 2-3
minutes, then as guided by arterial blood gases
 An 8.4% solution is a molar solution (ie it contains 1mmol of
HCO3 per ml) and is the concentration clinically available in
Australia.

7. Does NaHCO3 have adverse
effects?

8. Does NaHCO3 have adverse
effects?
 Fluid and sodium load – can cause hypervolaemia,
hyperosmolarity, and hypernatraemia
 Given as a rapid IV bolus can cause a transient fall in MAP and
a transient rise in ICP – probably due to its hypertonicity
 Impaired oxygen unloading at tissue level due to left shift of the
oxyhaemoglobin dissociation curve
 Intracellular acidosis may develop or worsen when the CO2
liberated from NaHCO3 freely enters the cells
 Sodium bicarbonate and adrenaline or calcium when mixed
together may inactivate each other, precipitate and block the IV
line.
….In general, the severity of these effects are related to the
amount of bicarbonate used

9. The use of NaHCO3 in Cardiac
Arrest
 Overall, there is not much good evidence out there- probably
due to the difficulty in obtaining meaningful data – it’s difficult
to standardise the quality of CPR. Also, there are obvious
ethical considerations.
 Current guidelines are based on a few flawed studies in
humans and animals.
 The current guidelines are 4 years old.
 A pubmed and online search found little new evidence
published in the last 4 years to contradict these guidelines

10. Australian Resuscitation Council
guidelines
 They note that: “the vast majority of studies assessing the
effects of drugs on survival have not been able to control for
the quality of cardiopulmonary resuscitation”
 “Furthermore, most drug evaluations to date have been
conducted before recent advances in post-cardiac arrest care
including therapeutic hypothermia”
 “In most cardiac arrests early efficient CPR and adequate
ventilation negate the need for any NaHCO3”

11. Australian Resuscitation Council
guidelines…..evidence?
 They describe 2 studies evaluating buffer agents during CPR.
Both studies had limitations but showed no improvement in
outcome1
 Two retrospective cohort studies also showed no benefit in the
use of buffering agents during CPR
 Two studies demonstrated increased return of spontaneous
circulation, hospital admission and survival at hospital discharge
with bicarbonate use.
 Four cohort studies reported that bicarbonate use was
associated with poor short- and long-term outcome.
1. Deakin CD, Morrison LJ, Morley PT, Callaway CW, Kerber RE, Kronick SL, et al. Part 8: Advanced life support:
2010 International Consensus on Cardiopulmonary resuscitation and Emergency Cardiovascular care science with
treatment recommendations. Resuscitation 2010;81 93-205

12. Australian Resuscitation Council
recommendations:
 Routine administration of NaHCO3 for treatment of in-hospital
and out-of-hospital cardiac arrest is NOT recommended.
{Class A; Expert consensus opinion}
 Consider administration for:
Hyperkalaemia
Treatment of documented metabolic acidosis
Overdose with Tricyclic antidepressants
Protracted arrest (greater than 15 minutes)
{Class A; Expert consensus opinion}

13. UK Resuscitation Council 2010 –
use of bicarbonate
 “Best treatment of acidaemia in cardiac arrest is chest compression;
some additional benefit is gained by ventilation. During cardiac arrest,
arterial gas values may be misleading and bear little relationship to the
true acid-base state, analysis of central venous blood may provide a
better estimation of tissue pH”
 “Bicarbonate causes generation of carbon dioxide, which diffuses
rapidly into cells and has the following effects:
 It exacerbates intracellular acidosis;
 It produces a negative inotropic effect on ischaemic myocardium;
 It presents a large, osmotically active, sodium load to an already
compromised circulation and brain;
 It produces a shift to the left in the O2 dissociation curve, further
inhibiting release of oxygen to the tissues.

14. UK resuscitation council 2010
Recommendations:
 “Giving Sodium Bicarbonate routinely during cardiac arrest
and CPR , or after ROSC, is NOT recommended.
 Give sodium bicarbonate (50mmol) if cardiac arrest is
associated with hyperkalaemia or tricyclic antidepressant
overdose.
 Repeat the dose according to the clinical condition of the
patient and the result of repeated blood gas analysis.

15. Use of NaHCO3 in shock
 Again, there is not a lot of recent evidence…..the most cited
papers date from 2000 and before!
 The preferred management of metabolic acidosis secondary to
shock is to correct the primary cause
 Bicarbonate is probably NOT useful in most cases of high anion
gap acidosis – Lactic acidosis can get worse if bicarbonate is
given (removal of acidotic inhibition of glycolysis). NaHCO3 also
impairs tissue oxygen unloading (left shift of ODC due to
increased pH)
 Clinical studies have shown NO benefit from bicarbonate in DKA
 In these cases, the only indication for bicarbonate use is
probably for the management of severe hyperkalaemia.

16. What about a normal anion gap
acidosis?
 Consensus opinion is that bicarbonate therapy may be useful
for correction of acidaemia due to non-organic acidosis (ie
normal anion gap acidosis)
 This is because there is no organic anion which can be
metabolised to regenerate bicarb.
 Once the primary cause is corrected, resolution of the
acidaemia occurs more rapidly if bicarbonate therapy is used
 The aim is to increase arterial pH to above 7.2 to minimise
adverse effects of the acidaemia and to avoid the adverse
effects of bicarbonate therapy

17. Chest American college of chest physicians 2000;117;260-267
 “Sodium bicarb clearly raises the arterial pH in critically ill patients with lactic
acidosis.
 The impact on intracellular pH is unknown in such patients, but extrapolation
from several animal studies suggest it is negative.
 Despite the correction of arterial acidaemia, sodium bicarb has no
favourable cardiovascular effects, even for patients with severe acidaemia.
 Even theoretical arguments in favour of sodium bicarb administration rely on
a naïve representation of acid-base physiology, ignoring the complex
compartmentalization of pH, the impact of carbon dioxide generation, and
the second-level effects of bicarb infusion
 The oft-cited rationale for bicarb use, that it might ameliorate the
haemodynamic depression of metabolic acidaemia has been disproved
convincingly.
 Given the current lack of evidence supporting its use, it should not be used
for patients with lactic acidosis.”

18. Conclusion
 There have been few meaningful studies in recent years on the use of
bicarbonate in Cardiac arrest or shock.
 Current consensus guidelines state that NaHCO3 should NOT be
routinely used during or immediately after cardiac arrest and CPR
 ….Unless cardiac arrest is associated with tricyclic/propanolol overdose
or severe hyperkalaemia.
 Current consensus also appears NOT to recommend the use of
NaHCO3 in patients in shock with raised anion gap acidaemia
 Bicarbonate can be useful in patients with normal anion gap acidosis
but only once the primary cause is corrected
 If bicarb is used, ventilation must be adequate to eliminate the CO2
produced from bicarbonate
 Emergency physicians should be aware that bicarbonate may cause
clinical deterioration if tissue hypoxia is present and should not be
“thrown into the mix” without careful consideration.

19. Questions?