Stop Giving Amps of Bicarb!

Chapter 1: What dafuq is in an amp of bicarb?

Take a look!

  • 50mL

  • 8.4% NaHCO3 -> 50mEq

  • The osmolarity of this solution is 2,000mOsm/L - twice that of 3% saline. < (click for emcrit)

Screen Shot 2020-11-05 at 7.56.02 PM.png

Chapter 2: Sodium bicarbonate doesn't just magically raise pH...

Remember this thing?

CO2 + H20 <=> H2CO3 <=> HCO3 + H

It's complicated. Bicarb binds to acid. Then it turns to CO2 and water, so you can breathe it out.

Basically if you're giving bicarb, you can only raise your pH as long as you can breathe off your CO2, increasing your RATE or VOLUME.

**This is particularly a problem in patients who are not in control of their breathing (vented), aren't breathing (arrest), or who have maximized the efficiency of their breathing (Kussmal breathing in DKA).**

That's right - you need to increase your minute ventilation to have a change in pH.

Here's Weingart's take.

Chapter 3: Sodium bicarb amps can cause harm!

FIRST:

One amp of bicarb is like giving 100cc of 3% hypertonic saline!! But as Josh Farkas points out, we typically have no hesitation giving "a couple of amps of bicarb."
This is a huge osmotic load which can lead to huge fluid shifts - prepare for that amp to increase intravascular fluid by 1/4 liter with every push. (Is this what you want to give to your renal failure pt? Your heart failure pt?)

SECOND:

You are worsening acidosis.
What? Huh? But I thought...
No. Stop. Shush. You're worsening acidosis.

Remember, you're increasing CO2 - whether you can breathe it off or not, this CO2 rises in but blood BUT ALSO rises in the tissues and may worsen acidosis in these tissues. < (click for litfl.com article)

THIRD:

Be ready to cause hypernatremia - expect a rise of 1mEq Na per amp of bicarb.

FOURTH:

Extravasation can cause tissue necrosis.

FIFTH:

CSF acidosis, hypocalcemia. Increased lactate. (Some may argue that's not a bad thing.)

If you do manage to fix the acidosis, you can overshoot and create an alkalosis and even screw up the oxygen dissociation curve (in a bad way).

Chapter 4: It just doesn't f&$%ing work
Cardiac arrest: it doesn't do anything. No increased survival. and AHA says it should not be given routinely.

Lactic acidosis: There's a whole section on UpToDate - there's minimal research for pH < 7.1 so you can consider it at that point... but otherwise, nah.

DKA: Take it from a nephrologist: In ketoacidosis, it is almost never necessary to give bicarbonate even though the patient is bicarbonate deficient unless renal function is permanently impaired. Therapy with fluids and electrolytes restores extracellular volume and renal blood flow, thus enhancing the renal excretion of acid and regenerating bicarbonate.

Hyperkalemia: Amps of bicarb, even in hyperK emergencies, have not been shown to lower potassium. Click that UpToDate link or listen to Scott Weingart talk about it on EMRAP.
Patients with hyperK should be started on isotonic bicarbonate drips for 4-6hours, a treatment that works better in acidotic patients.

CHAPTER 5: Soooo who gets bicarb?
AMPS:

  • Bicarb ampules in sodium channel blockade (like TCAs) are, as Dr. Bogoch said yesterday, the cornerstone of therapy

  • Bicarb ampules may be appropriate to alkalinize urine in certain toxicities

  • Seizing hyponatremic patients

DRIPS:

  • Appropriate in hyperK patients who can handle fluid

  • Appropriate in patients with AKI and pH < 7.2 (BICAR-ICU Trial)

  • May be appropriate for pH < 7.0 or 7.1, depending on who you talk to...

**If the pH is < 7.1 and you wanna give an amp of bicarb, there isn't enough data to say you're wrong. If it's a last-ditch effort, you might as well.

https://www.uptodate.com/contents/bicarbonate-therapy-in-lactic-acidosis?search=sodium%20bicarbonate&source=search_result&selectedTitle=3~148&usage_type=default&display_rank=2

Other references embedded in text.


POTD: TPA in PE

POTD: TPA in PE

  • Massive PE can lead to hemodynamic instability and death

  • Smaller but clinically significant PEs can lead to pulmonary hypertension, RV dysfunction and subsequently poor quality of life (decreased exercise tolerance and even dyspnea at rest)

  • TPA in PE is surrounded by controversy with various opinions on the matter

AHA:

  • Massive: hemodynamic instability defined as SBP<90 (or 40 point drop from baseline) for >15 minutes=

  • Thrombolysis indicated unless there are contraindications

  • Sub-massive: hemodynamically stable but with signs of RV strain (elevated troponin/BNP, echo findings of RV dysfunction) = Thrombolysis may be considered (level IIb/C)

ACEP:

  • Hemodynamically unstable patients: Thrombolysis indicated if benefits outweigh risks of bleeding

  • Level B recommendation

  • Hemodynamically stable patients: insufficient evidence to do thrombolysis

MOPETT (Moderate Pulmonary Embolism Treated with Thrombolysis):

If

  • Symptomatic moderate defined as ≥2 signs/symptoms (7 total in inclusion criteria) in addition to CTPA involvement of >70% involvement of thrombus in ≥2 lobar, or left or right main pulmonary arteries

  • Ventilation/perfusion scan showing mismatch in ≥2 lobes

  • SBP<95 excluded

Then

  • enoxaparin/heparin only vs enoxaparin/heparin + half dose tPA (10mg bolus then 40mg over 2 hours)

  • primary end point: pulmonary HTN at 28 months

  • rates in treatment group=16%, control group=57%

  • combined end point: pulmonary HTN at 28 months + recurrent PE

  • treatment group=16%, control group=63%

  • no patients in either group bled

Conclusion:

  • Studies suggest that half-dose thrombolysis is safe/effective in the treatment of moderate PE, with a significant immediate reduction in pulmonary artery pressure that was maintained at 28 months

  • ”Thrombolytics have demonstrated faster improvements in RV function and pulmonary perfusion, but these benefits have not translated to improvements in mortality.”

  • So the measured outcome is of questionable significance as opposed to actual measurements of quality-of-life

  • Perhaps consider in your young patient in whom potential improvement in exercise tolerance in remaining lifetime may be more relevant than in older, immobile patients

Stay well,

TR Adam

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POTD: Myxedema Coma

POTD: Myxedema Coma

Clinical Features (Remember LOW and SLOW: low HR, BP, Temp, sugar, RR, Na, Mentation, reflexes):

  • Decreased mental status

  • Hypothermia (<95.9F)

  • Hypotension  

  • Hyponatremia

  • Hypoglycemia  

  • Bradycardia

  • Bradypnea


Work-Up:

  • CMP- looking for hyponatremia, elevated CPK, elevated creatinine, transaminasas

  • CBC- looking for anemia, leukopenia

  • TSH, FT4, FT3- In primary hypothyroidism, TSH will be elevated and T4 and T3 will be low. In secondary hypothyroidism (Pituitary dysfunction) the TSH can be low or normal and T4 and T3 will be low

  • Blood cultures- looking for a secondary sepsis source

  • Cortisol level

  • Lipid panel-  Hyperlipidemia

  • VBG-  looking for hypoglycemia, respiratory acidosis

  • CXR- looking for pleural effusions

  • ECG- looking for bradycardia and rhythm

  • Cardiac POCUS- looking for pericardial effusion


Treatment:

  • Levothyroxine(T4)  100 to 500 mcg IV (Potentially safer in patients with CAD) or

  • Liothyronine (T3) 20mcg IV (Start with 10mcg if elderly or has CAD)

  • Hydrocortisone 100mg IV q8hr

  • Passive rewarming (Do not actively rewarm as rapid peripheral vasodilation may induce worsening hypotension)

  • Mechanical ventilation early may prevent respiratory collapse and severe respiratory acidosis

  • IVFs- dextrose containing fluids for hypoglycemia. If patient is hyponatremic, be cautious of too rapid fluid correction

  • Broad spectrum Antibiotics


Prognosis:

  • Mortality reaches as high as 60%  


Dispo:

  • ICU admission 

Stay well,

TR Adam

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