Alarms from the ventilator: Troubleshooting high peak pressures

Alarms from the ventilator: Troubleshooting high peak pressures


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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  • Michal Pisár

    Great post! So important in the daily practice.
    Worth mentioning though, that it only applies to the classical volume controled mode, not so much to the pressure controled or some of the “advanced” modes like PRVC.

    • Todd Seigel

      Thank you for bringing this up, this is a great point. The approach to managing elevated airway pressures presented in the post can only be applied to patients are who are on a ventilator mode in which plateau pressures can be obtained. This is done most easily in traditional volume-controlled ventilation. PRVC (pressure-regulated volume control) is a dual mode of ventilation that dynamically changes pressure to deliver a set tidal volume. Plateau pressures can be measured in this mode but obtaining them can be more challenging. Notably, in pressure-controlled ventilation, the maximum airway pressure is set by the provider, and tidal volume is a dependent variable. In this case, acute elevations in resistance or decreases in compliance would result in decreased tidal volume rather than elevated airway pressure (as pressure is set to remain constant).

  • Wes Pierce

    Great post. I am an ICU pharmacist that manages analgo-sedation under a protocol I developed with my pulmonary group. Despite my efforts to provide light sedation using a pain-first, benzo sparing approach, I am commonly asked by my docs to deeply sedate patients that have high peak pressures. Although deeper sedation can improve compliance, I am not always convinced elevated peak pressures are a sedation issue and worry about increased delirium and ICU/vent days from unnecessary deep sedation. How do you approach analgo-sedation in patients with high peak pressures, especially if the Pp – Pplat is low (compliance elasticity issue)?

    • Todd Seigel

      This is a fantastic question. Under-sedation can lead to discomfort and
      dyssynchrony, both of which may lead to an increase in peak pressures. In addition, as you point out, deeper sedation may improve overall compliance. That said, I think you make a important point that sedation may not always improve elevated peak pressures and, for the the reasons you mention, can be deleterious. To your direct question, for patients with low Pp-Pplat (for example, severe ARDS), I would first address any other potential cause of immediate compliance changes, such as pneumothorax. If compliance changes are relatively gradual, I would think about what changes had been made in sedation over that time period (eg has the team been gradually decreasing sedation over the past 24-48 hours), whether the severity of the underlying pathology has changed, or both. If there were no other way to modulate elevated peaks or plateau pressures, I think trying additional sedation to address any component of chest wall compliance is reasonable (in ARDS, for example, many patients with intractably high plateau pressures and refractory hypoxemia will receive paralysis). If the increases in sedation don’t improve lung mechanics, I would rethink whether additional sedation was actually necessary. Overall, I think that use of sedation should be judicious and constantly evaluated. Though additional sedation can improve elevated peak pressures, I think reflexively administering additional sedation for this problem may not be warranted. I hope this answers your question, and please feel free to email me as well.