Back to #Basics: When to Use Sodium Bicarb in the ICU

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Basic ABG Review review: http://pulmcast.com/abg

The body needs to keep blood pH in a very tight range, 7.35 - 7.45.

  • Outside of this range you have abnormalities in electrolyte concentrations (esp K and Ca), membrane potentials, protein folding and cellular function

  • May seem narrow - its because small changes in pH mean larger changes in H+ concentration (logarithmic scale)

We are constantly exposed to substances/metabolic changes that would result in large changes in pH. Our body works against this by:

  • Bicarbonate buffer equation: LeChatlier’s principle

  • The lungs: hypo or hyperventilation

  • The kidneys: secrete or retain acid, secrete or retain bicarb, produce de novo bicarb

  • Honorable mention: Hgb acts as potent buffer by binding CO2 to form carbaminohemoglobin

Problems with severe acidemia

  • Reduction in cardiac output (mediated by both depression of myocardial contractility AND increased afterload in the pulmonary and systemic circulation)

  • Inappropriate tachycardia

  • Decreased arrhythmia threshold

  • K+ shift out of cells ---> hyperkalemia (further depressing myocardial contractility and increasing risk of arrhythmia)

What happens when we give one ‘amp’ of bicarb? (50mL of 8.4% sodium bicarbonate)

  1. SODIUM

    1. One amp of 8.4% sodium bicarbonate is profoundly concentrated - 2000mOsm/L (in context, this is more than double the osmolality of hypertonic saline)

    2. This sodium load enters the extracellular space

    3. Serum sodium increases by approx 2mEq

    4. The intracellular compartment is dehydrated - 125mL exits cells and enters the extracellular compartment

  2. BICARBONATE

    1. Almost all bicarbonate is used up as buffer (converted into CO2 and H2O)

    2. Remainder is diluted by the 125mL water removed from the intracellular compartment

    3. If there is no significant acidemia and renal function is normal, nearly all the remaining bicarb will by excreted by the kidney.

Importance of ventilation

https://www.ncbi.nlm.nih.gov/pubmed/10923730

J Pediatr. 1972 Apr;80(4):681-2.

J Pediatr 1977;91(2):287

In a patient with metabolic acidosis, administration of sodium bicarbonate in a closed system where you CANNOT increase minute ventilation will NOT increase the serum pH. In other words, if you cannot blow off all of the CO2 generated by using bicarb as a buffer, your pH will essentially remain the same. All you are doing in this scenario is exchanging one acid for another (H+ for CO2).

Situations we agree to give bicarbonate

  • Non anion gap metabolic acidosis

    • Hyperchloremic acidosis

    • Diarrhea

    • Adrenal insufficiency

    • Renal tubular acidoses 

    • THE CAUSE IS - DIRECT BICARB LOSS - fix is quite simple. Replace the bicarb that the patient lost

  • Hyperkalemia

    • Reducing serum proton concentration 

    • Cause a shift of potassium INTO cells in exchange for intracellular H+ ions

    • Temporize the situation while you address the underlying cause

  • Treatment of sodium channel blocker overdose with ECG changes

    • Local anesthetics

    • TCAs

    • Carbamazepine

    • Antiarrhythmics like flecanide

  • Urinary alkalinzation in salicylate toxicity

  • And that’s pretty much it - that’s all we can truly agree on w/ regard to bicarbonate

Disagreements

Diabeteic Ketoacidosis

Bicarb is not effective at raising the serum pH in DKA. There’s minimal clinical benefit and even some element of harm including:

        • Cerebral edema, coma

          • (rapid fluid shifts from osmolality changes)

        • Prolonged hospitalization

        • Paradoxical worsening of ketosis

          • Acidosis inhibits enzymes responsible for beta oxidation

          • Reversing this = more ketone production

        • Worsening tissue hypoxia

          • Acidosis decreases hemoglobin’s affinity for oxygen

          • Reversing this = less O2 delivery to tissues

        • Hypokalemia - from shifts

Don’t give.

Lactic Acidosis

Because of these potential harms, most experts agree that we should NOT be administering bicarbonate to patients with lactic acidosis and a serum pH greater than 7.15

    • This is supported by the surviving sepsis campaign recs

      • Recommend AGAINST bicarbonate therapy for the purpose of improving hemodynamics or reducing vasopressor requirements in patients with hypoperfusion induced lactic acidosis and a pH >7.15 (Grade 2B)

      • They conveniently don’t comment on what to do when the pH is less than 7.15

  • There are a few physiologic studies - both small human clinical trials and canine studies - to support the idea in patients with severe acidemia (pH < 7.1) that bicarbonate

    • Improves hemodynamics

    • Improves tissue perfusion

    • Reduces risk of arrhythmia

  • Severe lactic acidosis has a high mortality, sometimes approaching up to 80%

    • Physiologic data to support bicarb administration

    • No mortality data to support

    • Probably not a panacea to fix everything when the situation is THAT dire

    • At the end of the day - case by case basis, sometimes bridge to CRRT

Cases where you should consider bicarbonate in lactic acidosis:

  1. Lactic acidosis + NAGMA (delta ratio or corrected bicarbonate - see ABG episode)

  2. Lactic acidosis + AKI (applies to uremic acidosis without lactic acidosis as well) - check out BICAR-ICU trial https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)31080-8/fulltext (similar principles for uremic acidosis with AKI and no lactic acidosis)

Cardiac arrest

  • AHA recommends AGAINST routine bicarb administration in patients with cardiac arrest.

    • We know some clinicians choose to give bicarb intra-arrest especially if pH is <7.1, but we need to recognize that this is a data-free zone

Potential harms in cardiac arrest:

    • Fluid shifts and hypernatremia

    • Hypocalcemia

    • Changes in oxygen affinity (right shift in acidosis)

    • Unreliable ventilation esp if no advanced airway

    • Metabolic alkalosis as soon as perfusion is restored (harmful)


SUMMARY: 

  • When to definitely give

    • HyperK

      NAGMA

    • Drug OD (sodium channel blockers, salicylate)

  • When to consider giving

    • Lactic acidosis and pH < 7.1

    • Lactic acidosis with AKI and uremia

    • Lactic acidosis with concurrent NAGMA

    • Uremic acidosis

    • ?Cardiac arrest - empiric vs severe acidemia

      • Definitely give if hyperK or sodium channel blocker suspected etiology

  • When not to give

    • DKA, especially in peds

    • Lactic acidosis and pH > 7.15

  • What kind of to give

    • Isotonic over hypertonic

    • SBE equations/weight based (for bolus dosing)

    • Vs continuous infusion with trending labs

Further reading:


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