Skyler Lentz Profile picture
Jul 10, 2019 11 tweets 4 min read Read on X
You intubated the asthmatic! What to look for on the vent and what to do about it.

It gets complicated, but the basics are in the thread below

#foamcc #foamed #tweetorial mini
1/
The problem is bronchospasm and secretions narrow the airways and lead to obstruction, limitations in exhalation and high airway resistance.

On the vent, this is seen as a high peak pressure (high resistance) and a prolonged expiratory flow or incomplete exhalation.
2/
The high peak pressure isn’t really a problem unless the plateau (obtained by an end insp hold) is also high. The delicate alveoli only feel the plateau pressure. Best to keep the plateau pressure < 30 cm H20 by minimizing auto-PEEP as the auto-PEEP contributes to plat press
3/
Auto-peep/dynamic hyperinflation/breath stacking (similar terms) develops because the patient does not have enough time to exhale. Each breath leads to a larger and larger lung volume. Not good!

Figure from: ncbi.nlm.nih.gov/pubmed/26033128
4/
How do you fix the air trapping?

By maximizing the expiratory time.

5/
Basic Math. If RR is 30/min = 2 seconds per resp cycle with I time of 1 sec, then E time is 1 sec or I:E of 1:1. Drop the RR to 12 with same I time and get 1:4.

Dropping the rate is the best way to maximize the exhalation time!

6/
Goal is to give a low enough rate that allows for near full exhalation on the flow waveform. A high normal tidal volume ~ 8ml/kg IBW can help maintain minute ventilation.

These patients will have a respiratory acidosis from deadspace and the low RR but that is usually ok!
7/
What is more dangerous than a low pH from a resp acidosis? High intrathoracic pressure or a pneumothorax leading to a PEA arrest.

Many patients require deep sedation or paralysis to avoid a spontaneously high RR that would lead to worsening of air trapping

8/
Maximize the bronchodilators and be patient. It may take hours to days for the lungs to improve. Keep them safe on the vent in the meantime.

If all else fails, there’s ECMO

9/
Tips:
Look for air trapping on flow waveform
Decrease RR to maximize expiratory time, as low as 10-15/min
Keep plateau pressure < 30
Tolerate a respiratory acidosis and deeply sedate +/- paralyze if needed
Maximize bronchodilators
V-V ECMO if unmanageable on the vent

10/
Please share and add your tips below!

11/

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More from @SkylerLentz

Dec 22, 2023
A patient presents in shock:

BP is 100/35

A wide pulse pressure (low diastolic) is suggestive of a distributive shock

With an important exception

👇

1/

#FOAMcc #foamed #MedTwitter
A narrow pulse pressure ~ BP 80/60 makes me think low cardiac output and high SVR

Simplistically, the stroke volume is low so a high systolic pressure is not generated

Compensation = increase SVR and a higher diastolic pressure

Causes cardiogenic shock, hypovolemia, etc.

2/
When I see a BP of 100/35 I think of a low SVR (vasodilated) state and imagine the simplified equation

Mean arterial pressure ⬇️= cardiac output ↔️x systemic vascular resistance ⬇️

Common causes: sepsis, anaphylaxis, iatrogenic (vasodilators), etc

3/
Read 6 tweets
Sep 11, 2023
Can epinephrine cause hypotension?

A patient is transferred the ICU with hypotension on 4 mcg/min (.05 mcg/kg/min) epinephrine. Thought to be a GI bleed, resuscitated but was still hypotensive with a HR in the 60s, BP100/40 (60)

Takes carvedilol

Epi stopped MAP 60->90 🤯

How
It is related to the dose dependent effects of epinephrine

At lower doses (<.1 mcg/kg/min) it has more beta 1 and beta 2 activity than alpha 1 (vasoconstriction)

Beta 1 increases inotropy (⬆️ stroke volume) and chronotropy (⬆️ HR)

Beta 2 reduces vascular tone (vasodilates)
Epi is thought of as a inoconstrictor
(Increased inotropy and vasoconstriction)

But, I have had few cases (like this one) where at low doses it acts more like an inodilator (inotropy and vasodilation)

I like this visual journals.sagepub.com/doi/10.1177/10…
Image
Read 5 tweets
Mar 20, 2023
🧪Can you have a metabolic acidosis with a normal plasma bicarbonate?

Lessons learned from a case

👇

#FOAMed #foamcc

1/
A patient presents ill after being found down and altered

Sepsis from a pneumonia is suspected

Labs:
Na 130 K 5.0 Cl 75 Bicarb 25
Cr 3.8 BUN 120 (Acute renal failure)
Glucose 520 (h/o type 2 DM)
Lactate 3
Ca 13.0
pH 7.41 pCO2 45

2/
Is there an acidosis?

The pH is normal, bicarb is normal 🧐

What’s the anion gap?

130 – [75+25] = anion gap of 30

There is an elevated anion gap = there IS a high anion gap metabolic acidosis (HAGMA)

3/
Read 11 tweets
Apr 1, 2022
Important lessons 📜 from ICU case:

🚨Not everything is septic shock
🚨A limited echo has limitations

Older patient in shock on 3 vasopressors, who initially presented with dyspnea and a CXR like 👇

What the diagnosis?

#FOAMed #FOAMcc

Image credit: ahajournals.org/doi/10.1161/CI…
Presented to the ED with acute onset dyspnea, new O2 requirement 6 L NC, minimal PMH

BP 95/70, HR ~ 100, afebrile

Hypoxemia worsened during ED stay requiring intubation

Now hypotensive

CT obtained with unilateral right sided pulm infiltrates, small pleural effusions, no PE
Labs 🧪

WBC 20k

Troponin mild elevation

Lactic acid 5.0

Cr mild elevation

U/A with > 50 WBC

Antibiotics, 2 L IVF given and admitted to ICU
Read 8 tweets
Jun 18, 2021
New heart failure presentation and a BP like this 114/33?

👇

😯🚨

#FOAMed #FOAMcc Image
We often see a large pulse pressure in distributive shock (sepsis) from a low SVR (vasodilation)

Not everything is sepsis, don't be fooled! 🧐

When seen with an acute heart failure presentation 🫀🫁 it may be acute aortic valve regurgitation

Endocarditis is a common cause
Diastolic back flow into the LV through an incompetent aortic valve = low diastolic BP & elevated pulse pressure

Regurgitation can lead to pulmonary edema (LVEDP ⬆️, Left atrial pressure ⬆️ = pulmonary edema)

And poor forward cardiac output may cause hypoperfusion (Shock)
Read 5 tweets
Apr 18, 2020
Can you be in shock and HYPERtensive?

I think so. Our patients teach us many lessons

#FOAMed
#FOAMcc
@UVMEmergencyMed

👇
A patient presents with 7 days of dyspnea, LE edema and fatigue. They have run out of all meds 2 weeks ago #COVID. They had an MI with ishcemic cardiomyopathy EF ~30%, also has a-fib.
Exam:
Afebrile, BP consistently >160/110, HR 110 afib, RR 30, POx 86%-> 94% 4LNC

Mild confusion
JVD+
Mild resp distress, crackles BL
No murmur
Hands, legs COLD and mottled to knees, toes and fingers purple, cap refill delayed
Pitting LE edema
Read 8 tweets

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