VentilatorAirway management is one of the defining skills of an emergency physician, but our role in the care of intubated patients may continue long after endotracheal tube placement is confirmed. In mechanically ventilated patients, acute elevations in airways pressures can be triggered by both benign and life-threatening causes. When the ventilator alarms, do you know how to tell the difference? What is your approach in troubleshooting the potential problems?

Work of Breathing

When a patient is on a ventilator, the amount of work needed to deliver a breath can be thought of in terms of pressure. The total amount of work (or pressure) can be divided into two components:

  1. Work to overcome resistance in the airways (resistive work)
  2. Work to distend the lungs and chest wall (elastic work). Elastic work increases as the lung compliance decreases.

As a simplified equation, it can be thought of as:

Ptotal = Presist + Pelastic
Ptotal = Presist + 1/Compliance

Peak inspiratory and plateau pressures

Elevations in airway pressure can thus be thought of being caused by increases in airway resistance and/or decreases in lung compliance. The total amount of airway pressure delivered by the ventilator to overcome resistive and elastic work is defined as the peak inspiratory pressure (Ppeak). The total airway pressure can be separated into component parts by measuring an inspiratory pause. This measures airway pressure at the end of inspiration when flow through the airway has finished. When flow has stopped, the amount of resistive work is zero. Therefore, pressure measured at the end of inspiration represents elastic work; this is defined as plateau pressure (Pplat). A schematic of the ventilator waveform during an inspiratory pause is shown below. The difference between Ppeak and Pplat represents the amount of work needed to overcome airway resistance.


Adapted from 1

Systematic approach to troubleshoot high peak pressures

In the ED, acute elevations in airways pressures can represent potential life-threatening disease and can be systematically evaluated in several steps. Appropriate treatment of elevated airway pressures will be dictated by the underlying cause. The following is a quick checklist of questions to ask yourself:

Is the patient hypotensive?

If so, immediately remove the patient from the ventilator and bag manually. Elevations in intrathoracic pressure limit cardiac output. The constellation of high airway pressures and hypotension suggest critical auto-PEEP or tension pneumothorax. If hypotension improves when the ventilator is removed, auto-PEEP may be the likely cause. If it does not improve, tension pneumothorax and needle decompression should be considered.

Determine a plateau pressure (Pplat)

If the patient is stable, determine a plateau pressure by getting an inspiratory pause on the ventilator.

Determine the difference between Ppeak (Ptotal) and Pplat (Pelastic)

If the difference is high

If the difference between peak and plateau pressures is greater than about 5 cm/H20, increased airway pressure can likely be attributed to increased resistive work. Acute causes of elevated airway resistance are bronchospasm, anaphylaxis, endotracheal tube obstruction or ventilator circuit obstruction (e.g. the ventilator tubing is kinked). During an inspiratory pause, the ventilator waveform would show a tall spike (see below).


Increased resistive work

If the difference is low

If the difference between peak and plateau pressures is low, increased airway pressure is likely secondary to acute decrease of lung compliance and resultant increased elastic work. Acute causes of elevated elastic work are pneumothorax, tension pneumothorax, evolving pneumonia, pulmonary edema, ARDS, and auto-PEEP caused by “breath stacking”. Plateau pressures greater than 30 cm/H20 have been implicated in ventilator-induced lung injury (VILI). In this case, the inspiratory pause waveform would show a small spike (see below).


Increased elastic work

Jain M, Sznajder J. Bench-to-bedside review: distal airways in acute respiratory distress syndrome. Crit Care. 2007;11(1):206. [PubMed]

Expert Peer Review

Nothing grates on the EM physician’s nerves more than the vent alarming incessantly. While the overriding urge is to hit the silence alarm button q2 minutes, this does no good for the patient or the physician who subsequently develops Nintendo thumb. Todd does a nice job here discussing a topic that typically translates poorly in writing.

Two of the keys are knowing what type of physiology the patient has and what parameter is causing the alarm. In relation to peak pressure alarms, alarms typically happen in our patients with obstructive pulmonary diseases (COPD, asthma). In these disorders, high peak pressures are often required to deliver the tidal volume needed and allow for complete exhalation. The peak pressure (Ppeak) often sets our alarms off but this value does not represent the pressure experienced in the alveoli. That pressure is better represented by plateau pressure (Pplat) and thus this parameter is a better measure of vent-induced barotrauma. As Todd points out, the goal is to keep Pplat < 30 mm Hg. If you are over that, breath stacking and dynamic hyperinflation are likely at play. One route to overcome this is to maximize your time of exhalation. This may cause increased Ppeak but will improve Pplat. In a crashing asthmatic where auto-PEEP and breathstacking have led to decreased venous return, disconnecting the vent and forcefully exhaling the patient (sometimes for up to 20-30 seconds) may lead to improved hemodynamic stability.

In past years, a good ED doc needed only to be able to put in the ETT and call the ICU for pickup. With ICU bed crunches and increasingly sick patients, understanding what vent alarms mean and how to address them is a mandatory skill for the Emergency Physician.

Anand Swaminathan, MD MPH
Assistant Residency Director and Assistant Professor of Emergency Medicine, Bellevue/NYU ; Faculty Editor of EM Lyceum
Todd A. Seigel, MD

Todd A. Seigel, MD

ALiEM Featured Contributor
Clinical Fellow in Critical Care Medicine
University of California, San Francisco (UCSF)
Todd A. Seigel, MD

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