Adaptive Pressure Control Ventilation and Severe Sepsis a Grueling Combination

Mentioned in previous postings Adaptive Pressure Control (APC) should be used cautiously in patients with high inspiratory drives. In patients with sepsis APC can become problematic by weaning the driving pressure prematurely due to a vigorous respiratory drive associated with lactic acidosis. The lower driving pressures will not efficiently off load the respiratory muscles leading to increased work of breathing, ventilatory muscle fatigue, and may initiate lung injury. 

Provided are two examples of APC utilized in sepsis patients:

Case 1

5’-1” female patient with the following ventilator settings:

Mode- APC, Set Frequency 14, I-time 1.0 second, Set Tidal Volume 500 ml, FiO2 45%, PEEP +5 cmH2O.

A mean measured peak inspiratory pressure for 36 hours was 15 cmH2O.  (A low PIP is an indication of an excessive inspiratory drive).

Initial ABG: pH 7.24, paCO2 20, PaO2 112, HCO3 8.7, BD -19 (measured minute ventilation of 16.3)

Patient appeared very uncomfortable presenting with diaphoresis, nasal flaring, and accessory muscle use. The Airway Occlusion at 0.1 second was assessed to evaluate the patients work load of inspiration.

The patients P0.1 measured were -5.7 to -5.2 indicating a large inspiratory effort or increased central drive. This large effort may be due to pain or agitation so the patient should be assessed further.

One way to assess if the large inspiratory effort is due to work of breathing is to increase support and reevaluate the patient & P0.1 for changes.

Patient was switched to PC-CMV to provide a fixed driving pressure. The patient’s tidal volume dramatically increased, this is common with the vigorous inspiratory efforts. The tidal volumes should become smaller as the patients work of breathing decreases and the muscles off-load.

Also assess the respiratory rate, the respiratory rate should slow down if the discomfort is due to purely work of breathing (this is a key finding). If the high drive is due to agitation or pain the respiratory rate will remain the same.

The patient’s frequency decreased from a rate of 25-to-20 and tidal volume started to decrease. This indicates that the respiratory muscles are off-loading and work of breathing is decreasing. The patient’s agitation was most likely due to work of breathing.

Once again evaluate P0.1 to compare if the new settings have decreased the inspiratory effort.

The Airway Occlusion at 0.1 second was reevaluated to compare the ventilator modes, settings, and patient’s comfort level.

The P0.1 measurement changed dramatically in a short amount of time (~ 3 minutes). The P0.1 changed to -1.9 cmH2O associated with a low level of muscular inspiratory activity.

This demonstrates that the patient experienced a large amount of inspiratory work when ventilated with APC.

The patient remained ventilated on PC-CMV over night.

AM ABG’s on PC-CMV:

pH 7.39, paCo2 19.1, paO2 210, HCO3 11.6, BD -13

Case 2

Male patient with a diagnosis of sepsis.

Ventilator settings: Mode- APC, RR-14, Vt- 550, PEEP +5, FiO2 90%.

Measured PIP 15 cmH2o

Measured rate-30

Measured P0.1 was -4

ABG: pH 7.33, PaCO2 25.2, PaO2 51, HCO3 13.3, BD -13

Changed mode of ventilation to PC-CMV, with a pressure setting of 20 cmH2O, set frequency 25 (to off load spontaneous efforts).

Measured P0.1 with these changes was -2.2

Switched patient back to initial settings for a comparison, and the measured P0.1 was -6.6 after the change.

Findings were discussed with attending physician, and the patient was placed back on PC-CMV.



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