Predictive Factors of Failure For Non-invasive Positive Pressure Ventilation (NPPV)

Ventilator Management: Risk Management Pitfalls

1. “My patient’s peak inspiratory pressure alarm kept beeping, so I decided to decrease the tidal volume.” Did you check the plateau pressure first? Plateau pressure represents the force required to overcome the lung’s elastic recoil. It will increase with decreased compliance, overdistention of the lungs, or hyperinflation. It is important to note the difference between overdistention (too much tidal volume and subsequent alveolar stretching) and hyperinflation (trapped air in the lungs). If the plateau pressure did not change then the lung’s recoil force did not change, and the ventilator alarmed for another reason.

Peak inspiratory pressure (PIP) also reflects the total force required to flow air through the lungs. Increases in PIP without change in plateau pressure may be due to an obstruction to airflow or an increase in airway resistance. In this case, higher PIP levels would not indicate overdistention. Consider increased secretions (suction the airway), bronchospasm (give bronchodilators), and obstruction (check ETT placement).

2. “My patient’s peak inspiratory alarm kept beeping, and I couldn’t find the silent button.” What if the increase in PIP was the result of decreased compliance? If the plateau pressure increased to the same extent that peak pressure increased without a difference between the two (no change in resistance: R = PIP – Pplat/Flow) then decreased compliance is to blame. Factors that decrease compliance include alveolar collapse/atelectasis (measure auto-PEEP and apply PEEP), lung collapse (decompress the pneumothorax), overdistention of the lung (decrease tidal volume), air trapping (reduce I-time or rate), and right mainstem intubation (confirm with CXR).

Please compare pitfall 1 and 2. Note that the PIP alarm in pitfall 1 resulted from increased airway resistance whereas it represents an increase in plateau pressure due to decreased compliance in this example. While these events may appear similar and the alarms sound the same, understand that their etiologies and management are quite different.

3. “Since my asthmatic had extremely high inspiratory resistance, I chose to use a lower inspiratory flow rate.” While a high inspiratory flow may exaggerate the high resistance in asthma and result in increased peak inspiratory pressures, a short inspiratory time is necessary to allow for a prolonged expiratory time. The expiration phase of breathing must be extended so air trapping is avoided. A careful balance must be obtained between adequate inspiratory flow, PIP, and sufficient expiratory times. Longer E-times are necessary to minimize air trapping and hyperinflation. Setting the ventilator to deliver a high inspiratory flow rate shortens I-time (thus, longer exhalation time).

This will increase inspiratory flow and increase PIP. The severe airway resistance seen in asthmatics actually prevents the complete transference of this pressure to the alveoli (Poiseuille’s law) thus averting alveoli from experiencing the full effect of the PIP. Recall the difference between PIP and plateau pressures. If you raise the PIP, there may not be a corresponding change in the plateau pressure after you shorten the I-time and lengthen the expiration because you’ve reduced the auto-PEEP somewhat. As a result, the plateau pressure will tend to decrease. A high peak airway pressure is not necessarily dangerous unless it corresponds to a dangerously high transalveolar pressure (Pplat).

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Ventilator Management: Case Study

Case Study:

You realize that it’s been just a little too quite tonight when the radio suddenly cackles to life: “Teenage girl asthma can’t breathe diaphoretic giving nebs No IV 2-minute ETA.” Within minutes, two medics rush in with a diaphoretic cyanotic girl perched forward on her hands. Her pleading glance catches yours as you watch her take her last voluntary breath; intubation is obviously required ventilator management is your concern since you realize her life depends on it

As you resuscitate the crashing asthmatic, your 60-year-old male patient on the other side of the curtain, who has been sleeping comfortably, begins to complain that his breathing is getting worse. He is a frequent flyer with a known history of bad emphysema and a worse attitude. He adamantly refuses ‘the mask’ ventilation. You think back about his chest x-ray, which showed extensive bilateral pulmonary infiltrates, and wonder how long your luck can hold up before you need to intervene with him. His voice and attitude sound oddly weak, but you remember that the last time he was intubated he developed a pneumothorax.

Just as you ponder these thoughts, a seasoned pair of medics burst into the ED. The hiss of nebs can be heard under the rushing sound of high pressure CPAP. “Sorry Doc, tried to raise you on the radio but no one answered. This lady is sick and not moving much air. We got her on CPAP at 20, 100%, but we’re not making much progress; heart rate of 170 and can’t get her sats higher than 60%. She’s got CHF. Had no time to intubate.” Just then their short, morbidly obese, pale, diaphoretic patient rips her CPAP mask aside and screams, “I can’t breathe.” Her eyes then roll back, and she begins to have a hypoxic seizure.

Case Study Conclusion:
Case #1: You intubate the young asthmatic and start her on pressure control ventilation. She is adequately sedated and paralyzed as you obtain your initial settings. Because of severe obstruction and prolonged expiratory phase, you have the following settings: FIO2 100% and PCAC to achieve target tidal volume of 400 mL. The inspiratory occlusion maneuver reveals an acceptable plateau pressure of 27 cm H2O. After initial PEEP of 5, the P-flex suggests you set the PEEP at 8 cm H2O. The patient is adequately sedated with ketamine and morphine and therefore tolerates a respiratory rate of 6 breaths per minute and a short inspiratory time with a prolonged expiratory time. With these settings, you get an ABG of pH 7.28, PaO2 85, and PaCO2 of 110. The nurses are uncomfortable and ask to increase the respiratory rate and oxygen. Instead, you recognize the role of permissive hypercapnia and lung protective strategies. The whistling of the continuous nebs comforts you as you arrange an ICU admission.

Case #2: Your frail COPD patient deteriorated soon after you stabilized the asthmatic. You wondered if this man would ever come off the vent as you deftly slid the 8.0 ETT through the cords. After airway stabilization, you set your ventilator as follows: PCAC, FIO2 100%, PIP 22 (corresponds to volumes between 600 cc and 800 cc), PEEP 14 (based on P-flex), sedated with midazolam drips and morphine, short inspiratory time with a prolonged expiratory time, and a respiratory rate of 8. This gives you an ABG of pH 7.40, PaO2 170, and PaCO2 of 30. You ask the respiratory therapist to reduce the FIO2 based on the oxygenation pleth (there is a good wave) and to reduce the PIP. She remarks that the plateau pressures are already below 30, but you explain that the corresponding volumes are a bit too large for a 60 kg man.

Case #3: Stabilizing this patient was a chore that involved management of her myocardial infarction, flash pulmonary edema, and new onset seizure (either hypoxic or a run of ventricular tachycardia). Her short neck, large size, and frothy pink sputum made intubation difficult. She ended up with a 7-0 ETT tube, volume control ventilation, FIO2 100%, set tidal volumes of 400 (corresponding plateau pressure 35), initial PEEP of 5, sedated with morphine and propofol, and a respiratory rate of 14. A P-flex shows an optimal PEEP of 15. You set this and notice, with satisfaction, that her plateau pressures come down as you recruit more lung volume. You adjust her tidal volumes up to 500 as you maintain her plateau pressures < 30. You also reduce your FIO2 to 50% to avoid absorption atelectasis.

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