aka Pulmonary Puzzler 014 Having overcome his worrying episode of post-intubation hypotension in the emergency department, the man who was intubated for severe asthma in Pulmonary Puzzle 013 is now in the intensive care department. He remains mechanically ventilated. You are asked to review him because the high airway pressure alarm is going off. QuestionsQ1. Why is the airway pressure alarm important? Answer and interpretation
For at least three reasons:
Q2. What are the potential adverse effects of excessive airway pressure? Answer and interpretation
High airway pressures do not correlate with lung barotrauma. Airway pressure itself is not particularly deleterious unless it reflects excessive alveolar pressure. Excessive alveolar pressure can have a number of adverse effects:
Inadequate ventilation can occur because many ventilators are set to terminate the inspiratory flow if the upper pressure limit setting is reached. When this occurs inspiratory volumes are markedly reduced, resulting in low tidal volumes and minute ventilation. Other ventilators do not do this but will simply hold the airway pressure at the pressure limit, resulting in a smaller reduction in tidal volume. Q3. How is airway pressure related to alveolar pressure? Answer and interpretation
airway pressure = flow x resistance + alveolar pressure Thus if flow or resistance is markedly altered, a change in airway pressure will not be indicative of a change in the alveolar pressure. Airway pressure is more conveniently measured than alveolar pressure. Peak inspiratory pressure (PIP) is displayed on most ventilators. A maximum acceptable PIP of <35 cmH20 is widely used. Q4. How can alveolar pressure be estimated? Answer and interpretation
Alveolar pressure is estimated by determining the inspiratory pause pressure, which corresponds to the plateau pressure. The inspiratory pause pressure is determined by observing the plateau pressure in an apneic ventilated patient when when the ‘inspiratory pause hold‘ control is activated. Because flow is reduced to zero, airway pressure and alveolar pressures will equalise and the airway pressure will correspond to the alveolar pressure at full inspiration. airway pressure = 0 x resistance + alveolar pressure = alveolar pressure
Figure: PIP vs Pplat: Normal curve – demonstrates normal PIP , Pplat , PTA (transairway pressure), and Ti (inspiratory time). High Raw curve – A significant increase in the PTA is associated with increased airway resistance. High Flow curve – the inspiratory time is shorter than normal, indicating a higher inspiratory gas flow rate. Decreased Lung Compliance curve – An increase in the plateau pressure and a corresponding increase in the PIP is consistent with decreased lung compliance. Q5. What is an excessive alveolar pressure? Answer and interpretation
To prevent lung injury, alveolar pressure (aka the plateau pressure) should be kept <30 cmH2O. High alveolar pressures can be due to excessive tidal volume, gas trapping, PEEP or low compliance as shown by this relationship: alveolar pressure = (volume/ compliance) + PEEP Q6. What are the two main categories of causes of high airway pressure? Answer and interpretation
When it comes to ventilated patients you need to think: Man versus Machine
Q7. What is the most useful first step in isolating the cause of high airway pressures? Answer and interpretation
Disconnect the patient from the ventilator and manually bag the patient using high-flow oxygen. If the patient is difficult to ventilate the problem is not with the ventilator or the circuit, but the patient or endotracheal tube. That’s right — deja vu …again! Q8. What are the possible causes of high airway pressures in the intubated and ventilated patient? Answer and interpretation
First, let’s consider the machine:
And now the man:
Q9. How will you go about identifying the cause of the high airway pressure? Answer and interpretation
The key steps are:
Upon assessing the patient you decide that the high airway pressure alarms are due to patient-ventilator dyssynchrony, in addition to ongoing bronchoconstriction…
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives. After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education. He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference. His one great achievement is being the father of three amazing children. On Twitter, he is @precordialthump. | INTENSIVE | RAGE | Resuscitology | SMACC |