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!
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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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.
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
The Berlin criteria: Acute onset within one-week, bilateral opacities on CXR not explained by cardiogenic pulmonary edema, pleural effusion etc. and a PaO2/FiO2 ratio of <300 mm Hg with PEEP 5 cm H2O.
More simply in the ED or acute setting I consider anyone with bilateral infiltrates + inflammation (sepsis, pneumonia, trauma etc) + hypoxemia to be at risk for ARDS and if intubated manage them with lung protective ventilation. 3/