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SodiumBicarbonateRevisited
Sodium Bicarbonate Revisited
Acidosis is thought to have adverse physiological effects and
generally is associated with increased mortality. Consequently,
therapy to correct acidosis, usually with sodium bicarbonate is
been widely used.
In recent years, however, this approach is changing.
Disease process
Add acid
Loose alkali
acidosisImpaired acid excretion
More than 100 years of Soda Bi Carbonate
Adverse Effects Of
Acidosis ……………….
 Depressed myocardial contractility
 Decreased catecholamine efficacy
 Arrhythmias
 Pulmonary vasoconstriction
 Glycolytic enzyme
phosphofructokinase
is pH dependent resulting in the
impaired utilization of glucose
Below 7.o
Sodium Bicarbonate
 Hypertonicity and hyperosmolality
 Hypercapnia and intracellular acidosis
 Ionized hypocalcaemia
 Decreased oxygen delivery
 Hypokalemia
 Increased organic acid production
 Rebound alkalosis
 Decreased VF threshold , arrhythmias
 Repeated doses : transient hypotension
 Intracellular acidosis / CSF acidosis
 Catecholamine inactivation
 Precipitation ( cal. carbonate )
 Local infiltration necrosis
Hypertonicity and hyperosmolality
7.5 % sodium bicarbonate
Sodium 0.9 mEq / ml
Osmolality : 1700 mOsm /lit.
Normal serum osmolality is around 290
1700 / 6 = 284 , that’s why ideal
dilution of S.B. should be 6 times and
with 5 % dextrose
NaHCO3 Na + HCO3
H HCO3
H2O + CO2
Intracellular
acidosis
60 mmHg
90 %
7.4
7.8
7.0
Impaired tissue oxygenation with
correction of acidemia .
Hb.
Sat.%
RT.
LT.
Oxygendelivery
24 to 48 hrs
Low 2-3 DPG levels
Secondary to reduced glycolysis
Direct effect of
pH
on hemoglobin
reducing
affinity of oxygen
acute acidemia facilitates oxygen delivery, whereas
more chronic acidemia hampers oxygen delivery.
Correcting acute acidemia could be more dangerous
Sodium Bicarbonate
Hypertonicity and hyperosmolality
Hypercapnia and intracellular acidosis
Ionized hypocalcaemia
Decreased oxygen delivery
Hypokalemia
Rebound alkalosis
Decreased VF threshold , arrhythmias
Increased lactate production
Repeated doses : transient hypotension
Intracellular acidosis / CSF acidosis
Catecholamine inactivation
Precipitation ( cal carbonate )
Local infiltration necrosis
Case 1…………………
8 months old child with diarrhea and LRI is in shock
His ABG is
pH 7.01
Pco2 36
HCO3 5.5
ACIDOSIS
LOW BICARB
BUT CO2 IS HIGH ?
WOULD BICARB BE INDICATED ?
NO
Case 2.
Preterm weighing 1.8 kg was on oral feeds and
developed Diarrhea , junior resident noted that the
baby was moderately Dehydrated and had
respiratory rate of 58 / min.
Bolus of normal saline was given followed by a dose
of bicarb , thinking that the baby may be acidotic.
After about 4 hours baby had seizures .
Sugar normal and so was calcium , seizure were
controlled but recurred Again ……………….
Though the serum calcium was “normal ”
These were hypocalcaemic seizures .
Ionic calcium low
CASE 3………….
DKA WITH RT LOWER LOBE CONSOLIDATION AND HYPOXIA
Ph 7.016
CO2 6
BICARB 6
PO2 58
Severe metabolic acidosis with mild hypoxia
Sugar 689 , ketones ++++ , COMA
Received bicarb with other standard protocol for
DKA……………sugar 326 mg %
Ph 7.36
CO2 34
BICARB 18
PO2 63
ABG LOOKS BETTER ,
MILD HYPOTENSION , ON SUPPORT
SUGAR IS OK
Patient deteriorates soon for no obvious
reason , his sugar is OK , ABG = Acidosis
Anion gap still wide , ketones not very high
Ph 7.16
CO2 14
BICARB 9
PO2 57
8 HOURS AFTER
LACTIC ACIDOSIS
Rapid correction of acidosis shifts curve
to left……..tissue hypoxia
Mild hypotension
Diabetics have low 2.3. DPG
Soda bicarb. promotes lactic acidosis
In severe DKA, bicarb therapy is not
supported by the literature. In fact, at
least 2 human studies have shown possible
deleterious effects of bicarbonate
administration even in patients with serum
pH less than 7.0 . Thus the administration
of sodium bicarbonate to patients with
diabetic ketoacidosis cannot be
recommended at any pH ( class 1 )
• Giving bicarbonate to a patient with a true
bicarbonate deficit is not controversial
• Controversy arises when the decrease in
bicarbonate concentration is the result of its
conversion to another base which, given time,
can be converted back to bicarbonate
What are the deleterious effects of acidemia ?
Is acidemia severe enough to warrant therapy ?
How much bicarbonate ?
what are deleterious effects of Bicarbonates ?
In considering acute
bicarbonate replacement four
questions should be thought of
 SEVERE METABOLIC ACIDOSIS WITH
ADEQUATE VENTILATORY SUPPORT
 HYPERKALEMIA
 HYPERMAGNESEMIA
 TRICYCLIC ANTI DEPRESSANT POISONING
 SODIUM CHANNEL BLOCKER POISONING
Indications as per A.H.A.
Sodium bicarbonate is further indicated in the
treatment of certain drug intoxications, including
barbiturates (where dissociation of the
barbiturate-protein complex is desired), in
poisoning by salicylates or methyl alcohol and in
hemolytic reactions requiring alkalinization of the
urine to diminish nephrotoxicity of hemoglobin and
its breakdown products.
How do I give soda bicarb
×
 Indication : if pH is less than 7.15
in DKA ( less than 7.1 and not improving )
 HCO3 required = half of BW × ( 15 – HCO3 )
 Dilute 4 to 6 times give over 2 hours
 Diluent : water for injection/5%dextrose
Ensure adequate ventilation
carbicarb, an
equimolar mixture of
sodium bicarbonate and
sodium carbonate.
Carbonate preferentially
combines with hydrogen
ions resulting in production
of bicarbonate rather than
CO2. Carbonate can also
combine with carbonic acid,
a reaction which also
produces bicarbonate. Thus
the acidosis is titrated
without the production of
CO2 or the lowering of
intracellular pH.
ALTERNATIVE
 Post resuscitation ..role of Soda Bicarbonate ?
 I don’t have ABG facility and the patient is in shock
Should I give Soda Bicarbonate
 Child with diarrhea and shock I would like to add S.B..
 to normal saline bolus , comment
 If the child admitted with me has received large dose of
 S.B. what should I monitor ?
 How do I dilute S.B., Rate of infusion
 Role of S.B. in wide anion gap acidosis
 Intratracheal administration for treatment of metabolic A
 Can S.B. be used for treatment of hyponatremia ?
( equivalent to 6 % saline,7.5 % contains 0.9 mEq./ml)
FAQ,S ………………………….
OVERDOSAGE:
Should alkalosis result, the
bicarbonate should be stopped
and the patient managed
according to the degree of
alkalosis NORMAL SALINE may
be given, potassium chloride is
indicated if there is
hypokalemia. Severe alkalosis
may be accompanied by
hyperirritability or tetany and
these symptoms may be
controlled by calcium gluconate.
THANKS

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Sodium Bicarbonate Revisited

  • 2. Acidosis is thought to have adverse physiological effects and generally is associated with increased mortality. Consequently, therapy to correct acidosis, usually with sodium bicarbonate is been widely used. In recent years, however, this approach is changing. Disease process Add acid Loose alkali acidosisImpaired acid excretion More than 100 years of Soda Bi Carbonate
  • 3. Adverse Effects Of Acidosis ……………….  Depressed myocardial contractility  Decreased catecholamine efficacy  Arrhythmias  Pulmonary vasoconstriction  Glycolytic enzyme phosphofructokinase is pH dependent resulting in the impaired utilization of glucose Below 7.o
  • 4. Sodium Bicarbonate  Hypertonicity and hyperosmolality  Hypercapnia and intracellular acidosis  Ionized hypocalcaemia  Decreased oxygen delivery  Hypokalemia  Increased organic acid production  Rebound alkalosis  Decreased VF threshold , arrhythmias  Repeated doses : transient hypotension  Intracellular acidosis / CSF acidosis  Catecholamine inactivation  Precipitation ( cal. carbonate )  Local infiltration necrosis
  • 5. Hypertonicity and hyperosmolality 7.5 % sodium bicarbonate Sodium 0.9 mEq / ml Osmolality : 1700 mOsm /lit. Normal serum osmolality is around 290 1700 / 6 = 284 , that’s why ideal dilution of S.B. should be 6 times and with 5 % dextrose
  • 6. NaHCO3 Na + HCO3 H HCO3 H2O + CO2 Intracellular acidosis
  • 7. 60 mmHg 90 % 7.4 7.8 7.0 Impaired tissue oxygenation with correction of acidemia . Hb. Sat.% RT. LT.
  • 8. Oxygendelivery 24 to 48 hrs Low 2-3 DPG levels Secondary to reduced glycolysis Direct effect of pH on hemoglobin reducing affinity of oxygen acute acidemia facilitates oxygen delivery, whereas more chronic acidemia hampers oxygen delivery. Correcting acute acidemia could be more dangerous
  • 9. Sodium Bicarbonate Hypertonicity and hyperosmolality Hypercapnia and intracellular acidosis Ionized hypocalcaemia Decreased oxygen delivery Hypokalemia Rebound alkalosis Decreased VF threshold , arrhythmias Increased lactate production Repeated doses : transient hypotension Intracellular acidosis / CSF acidosis Catecholamine inactivation Precipitation ( cal carbonate ) Local infiltration necrosis
  • 10. Case 1………………… 8 months old child with diarrhea and LRI is in shock His ABG is pH 7.01 Pco2 36 HCO3 5.5 ACIDOSIS LOW BICARB BUT CO2 IS HIGH ? WOULD BICARB BE INDICATED ? NO
  • 11. Case 2. Preterm weighing 1.8 kg was on oral feeds and developed Diarrhea , junior resident noted that the baby was moderately Dehydrated and had respiratory rate of 58 / min. Bolus of normal saline was given followed by a dose of bicarb , thinking that the baby may be acidotic. After about 4 hours baby had seizures . Sugar normal and so was calcium , seizure were controlled but recurred Again ………………. Though the serum calcium was “normal ” These were hypocalcaemic seizures . Ionic calcium low
  • 12. CASE 3…………. DKA WITH RT LOWER LOBE CONSOLIDATION AND HYPOXIA Ph 7.016 CO2 6 BICARB 6 PO2 58 Severe metabolic acidosis with mild hypoxia Sugar 689 , ketones ++++ , COMA Received bicarb with other standard protocol for DKA……………sugar 326 mg % Ph 7.36 CO2 34 BICARB 18 PO2 63 ABG LOOKS BETTER , MILD HYPOTENSION , ON SUPPORT SUGAR IS OK Patient deteriorates soon for no obvious reason , his sugar is OK , ABG = Acidosis Anion gap still wide , ketones not very high Ph 7.16 CO2 14 BICARB 9 PO2 57 8 HOURS AFTER LACTIC ACIDOSIS
  • 13. Rapid correction of acidosis shifts curve to left……..tissue hypoxia Mild hypotension Diabetics have low 2.3. DPG Soda bicarb. promotes lactic acidosis In severe DKA, bicarb therapy is not supported by the literature. In fact, at least 2 human studies have shown possible deleterious effects of bicarbonate administration even in patients with serum pH less than 7.0 . Thus the administration of sodium bicarbonate to patients with diabetic ketoacidosis cannot be recommended at any pH ( class 1 )
  • 14. • Giving bicarbonate to a patient with a true bicarbonate deficit is not controversial • Controversy arises when the decrease in bicarbonate concentration is the result of its conversion to another base which, given time, can be converted back to bicarbonate
  • 15. What are the deleterious effects of acidemia ? Is acidemia severe enough to warrant therapy ? How much bicarbonate ? what are deleterious effects of Bicarbonates ? In considering acute bicarbonate replacement four questions should be thought of
  • 16.  SEVERE METABOLIC ACIDOSIS WITH ADEQUATE VENTILATORY SUPPORT  HYPERKALEMIA  HYPERMAGNESEMIA  TRICYCLIC ANTI DEPRESSANT POISONING  SODIUM CHANNEL BLOCKER POISONING Indications as per A.H.A. Sodium bicarbonate is further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturate-protein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of hemoglobin and its breakdown products.
  • 17. How do I give soda bicarb ×  Indication : if pH is less than 7.15 in DKA ( less than 7.1 and not improving )  HCO3 required = half of BW × ( 15 – HCO3 )  Dilute 4 to 6 times give over 2 hours  Diluent : water for injection/5%dextrose Ensure adequate ventilation
  • 18. carbicarb, an equimolar mixture of sodium bicarbonate and sodium carbonate. Carbonate preferentially combines with hydrogen ions resulting in production of bicarbonate rather than CO2. Carbonate can also combine with carbonic acid, a reaction which also produces bicarbonate. Thus the acidosis is titrated without the production of CO2 or the lowering of intracellular pH. ALTERNATIVE
  • 19.  Post resuscitation ..role of Soda Bicarbonate ?  I don’t have ABG facility and the patient is in shock Should I give Soda Bicarbonate  Child with diarrhea and shock I would like to add S.B..  to normal saline bolus , comment  If the child admitted with me has received large dose of  S.B. what should I monitor ?  How do I dilute S.B., Rate of infusion  Role of S.B. in wide anion gap acidosis  Intratracheal administration for treatment of metabolic A  Can S.B. be used for treatment of hyponatremia ? ( equivalent to 6 % saline,7.5 % contains 0.9 mEq./ml) FAQ,S ………………………….
  • 20. OVERDOSAGE: Should alkalosis result, the bicarbonate should be stopped and the patient managed according to the degree of alkalosis NORMAL SALINE may be given, potassium chloride is indicated if there is hypokalemia. Severe alkalosis may be accompanied by hyperirritability or tetany and these symptoms may be controlled by calcium gluconate.
  • 21.