Positive End-Expiratory Pressure

Function

Extrinsic PEEP can be used to increase oxygenation. By Henry’s law, the solubility of a gas in a liquid is directly proportional to the pressure of that gas above the surface of the solution. This applies to mechanical or noninvasive ventilation in that increasing PEEP will increase the pressure in the system. This, in turn, increases the solubility of oxygen and its ability to cross the alveolocapillary membrane and increase the oxygen content in the blood.

Extrinsic PEEP also can be used to improve ventilation-perfusion (VQ) mismatches. The application of positive pressure inside the airways can open or “splint” airways that may otherwise be collapsed, decreasing atelectasis, improving alveolar ventilation, and, in turn, decreasing VQ mismatch.[2]

The application of extrinsic PEEP will, therefore, have a direct impact on oxygenation and an indirect impact on ventilation. By opening up airways, the alveolar surface increases, creating more areas for gas exchange and somewhat improving ventilation. Nevertheless, extrinsic PEEP should never be used for the sole purpose of increasing ventilation. If a patient needs to clear CO2 by improving ventilation, he should receive some level of pressure support for his ventilation, either via BPAP or invasive ventilation.

Extrinsic PEEP also significantly decreases the work of breathing.[3][4] This is especially important for stiff lungs with low compliance. In intubated patients with low compliance, work of breathing can represent an important part of their total energy expenditure (up to 30%). This increases CO2 and lactate production, both of which may be problems of their own. By decreasing work of breathing, CO2 and lactate production decreases, decreasing the need for high minute ventilation (to correct the hypercapnia and acidosis) and thereby decreasing respiratory drive and further decreasing the work of breathing needed by the patient in a positive-effect loop.

Issues of Concern

The use of Extrinsic PEEP also can cause some complications. Normal respiratory physiology works as a negative pressure system. When the diaphragm pushes down during inspiration, negative pressure in the pleural cavity is generated, creating negative pressure in the airways that suck air into the lungs. This same negative intrathoracic pressure decreases the right atrial (RA) pressure and generates a sucking effect on the IVC increasing venous return. The application of extrinsic PEEP changes this physiology. The positive pressure generated by the ventilator or BPAP transmits to the upper airways and finally to the alveoli which are transmitted to the alveolar space and thoracic cavity, creating positive pressure (or at least less negative pressure). This increases RA pressure and decreases venous return, generating a decrease in preload. This has a double effect in decreasing cardiac output: less blood in RV means less blood reaching LV and less blood that can be pumped out decreasing cardiac output, at the same time, the decreased preload means that the heart works at a less efficient point in the frank-startling curve, generating less effective work and further decreasing cardiac output and resulting in a drop in mean arterial pressure (MAP) if there is not a compensatory response by increasing systemic vascular resistance (SVR). This is a very important point to have in mind, especially with patients who may not be able to increase their SVR, such as those with distributive shock (e.g., septic, neurogenic, or anaphylactic).

This effect on RA pressure and venous return (VR) may be beneficial when used in patients with cardiogenic pulmonary edema. In patients with volume overload, decreasing VR will have a dual beneficial effect: the LV may be over distended, also be working at a less-than-optimal point of the frank starling curve. Decreasing VR will again decrease preload, but in this particular case, it has been proposed that the decrease in preload will place the LV at a more efficient workload, possibly increasing cardiac output and improving pulmonary edema, although it has never been shown that higher PEEP directly improves LV function.[5] At the same time, decreased VR means less blood pumped by RV and less pulmonary edema being generated.

Another special circumstance in which extrinsic PEEP’s effect on CO and MAP is important to consider is in patients in whom a cerebral perfusion pressure (CCP) has to be maintained after a stroke or subarachnoid hemorrhage. In this case, although PEEP does not directly affect CCP, and cerebral autoregulation will normally compensate for changes in MAP, special attention has to be given in cases of disturbed cerebrovascular autoregulation, as the decrease in MAP can directly affect CCP causing adverse effects.[6]

Other adverse effects of extrinsic PEEP include its capacity for generating barotrauma, especially in non-compliant lungs by increasing plateau pressures, and its interference with hemodynamic measurements in patients with right-heart catheters.

Clinical Significance

Using extrinsic PEEP clinically requires an understanding of all the principles discussed and will depend on many factors including the type of ventilation the patient is receiving (nasal intermittent positive pressure ventilation versus invasive mechanical ventilation) and the mode of ventilation (assist control, synchronized intermittent mandatory ventilation, airway pressure release ventilation). All of these different setups have a way to set extrinsic PEEP or an equivalent measure of positive pressure, and their specific set up in each case escapes the scope of this review. Nonetheless, there are some basic principles that apply to all modes of ventilation for PEEP:

• Start low and increase as tolerated and dial to patient comfort and desired oxygenation.
• Constantly check your plateau pressures to prevent barotrauma. As a general rule of thumb, you should aim the keep a plateau pressure below 30 cm H2O.
• Follow the MAP as you are dialing up or down the PEEP.
• When extubating a patient with cardiogenic pulmonary edema who are receiving extrinsic PEEP, consider its effects on VR as removing PEEP may precipitate new pulmonary edema and re-intubation.
• When managing patients with acute respiratory distress syndrome, the ARDSnet protocol provides clear guidance on how to titrate extrinsic PEEP and FiO2%.[7]

Other Issues

Auto-PEEP or intrinsic PEEP

Intrinsic or auto-PEEP is a complication of mechanically ventilated patients.[8] Usually, passive exhalation will permit complete emptying of the air in the lungs until lung pressure equalized with atmospheric pressure, but in some cases the lungs may not completely deflate, leaving air trapped inside the lung at the end of exhalation which generates a positive pressure that remains in the lungs. This pressure is called auto or intrinsic PEEP. When this process repeatedly happens with each respiratory cycle, the amount of air trapping increases with each breath and consequently the intrathoracic pressure increases pathologically, compressing the RA and decreasing VR causing hypotension, as well as increasing plateau pressure (intra-alveolar pressure) and causing barotrauma. The increased air trapping also will make it harder for the patient to bring new air in, increasing the work of breathing, which increases oxygen consumption and CO2 production, thereby increasing the need for ventilation, increasing respiratory rate, and worsening auto-PEEP in a vicious cycle.

Factors leading to auto-PEEP 

• Airway inflammation and mucus plugs generate dynamic airflow obstruction as a forced expiratory effort will increase the pressure around the airway leading to closure around the plugs or inflamed area and trapping air in the alveoli that are dependent on that airway.
• High lung compliance as in chronic obstructive pulmonary disease (COPD) works similarly, as the airways lack scaffolding to stay open during forced exhalation, leading to dynamic airway collapse and air trapping.
• High tidal volume ventilation, where the tidal volume may be too high to be exhaled in a set amount of time, so air is retained by the time the next breath is delivered.
• The high respiratory rate is generating a short exhalation time.
• Slow inspiratory flow generating a higher inspiratory to expiratory time ratio (too much time taken during inhalation does not leave enough time for a full exhalation).

Two types of auto-PEEP

1. Dynamic hyperinflation with intrinsic expiratory flow obstruction is the most common cause of auto-PEEP in COPD patients in whom alveolar collapse during expiration leads to air trapping. It has been stipulated that low-level extrinsic PEEP can help decrease auto-PEEP in these patients by splinting airways open, leading to the easier release of air from the alveoli. Airway inflammation and mucus plugs also cause dynamic hyperinflation in a similar fashion, although the use of extrinsic PEEP in these patients has not been shown to be beneficial as in COPD.
2. Dynamic hyperinflation without airflow obstruction occurs when not enough time is given for the patient to exhale, for example in high respiratory rate, low inspiratory flow, or high tidal volume in which there may not be enough time for the air to leave the lungs before the next respiratory cycle leading to air trapping. In cases like this application of extrinsic PEEP would be detrimental as it would generate backpressure preventing air to flow freely out of the lungs.

When to suspect auto-PEEP

• Exhalation is still ongoing when the next respiratory cycle starts. This can be easily checked by looking at the volume curve in the ventilator display. If this curve fails to go back to zero, then it is a sign that air is being trapped.[9]
• Increasing plateau pressures on the ventilator.
• Active exhalation by the patient as seen by the use of accessory muscles of respiration during exhalation.
• Drop-in blood pressure.
• Long expiratory times.
• Respiratory distress.

Although there is a big differential for an intubated patient, who develops respiratory distress, the presence of a volume curve that does not go back to zero before the next breath is delivered is very highly suggestive of auto-PEEP.

Treating auto-PEEP

It is important to minimize or prevent the development of auto-PEEP in the ventilated population as its consequences may be dire.

In the most extreme case in which patients are in respiratory distress and shock, disconnecting the patient from the ventilator and allowing enough time for exhalation before manually bagging the patient is a quick life-saving measure.

For less dramatic cases, several measures can be taken to reduce the amount and prevent the development of auto-PEEP.

Assuring enough time for exhalation so that all the air in the lungs can get out is the most important principle governing the prevention of auto-PEEP. This may be achieved by multiple methods:[10]

• Decreasing respiratory rate will increase the time between breaths and decrease the inspiratory to expiratory (I:E) ratio to 1:3 to 1:5.
• Increasing the inspiratory rate to 60 to 100 L/min will assure fast delivery of air during inspiration, lending more time for exhalation.
• Utilize a square waveform for ventilation delivery. This is uncomfortable for the patient but speeds the inspiration process.
• Decrease tidal volume. When there is less air being pushed into the lungs, there is less air needed to be pushed out and less time is required to finish a full exhalation.
• Decrease respiratory demand by decreasing CO2 and lactate production (minimize work of breathing, control fever and pain, ensure adequate sedation, control anxiety, treat sepsis)

If there is also flow obstruction, minimize it by treating bronchoconstriction with bronchodilators and suctioning mucus plugs. Treat airway inflammation with steroids when indicated.

The use of extrinsic PEEP is tricky, and although it may be beneficial, it has to be guided by good clinical sense. In cases of dynamic flow obstruction, especially in COPD where there is alveolar collapse, (Note: This does not include asthma where there is inflammation of the airway but not necessarily airway collapse.) the application of extrinsic PEEP will splint the airways open, permitting this way for air to be flushed from alveolar pouches and decreasing auto-PEEP. Extrinsic PEEP will also decrease the work of breathing in the appropriate setting. Nevertheless, when applied in the wrong setting, like in patients without dynamic airflow obstruction, the application of extrinsic PEEP will generate back pressure that will prevent air from getting out of the lungs, worsening air trapping. It is also important to understand that the extrinsic PEEP initially will add to the auto-PEEP, increasing the intrathoracic pressure. When used, it is recommended to maintain extrinsic PEEP below 75% to 85% of the auto-PEEP. Again, the use of extrinsic PEEP to treat auto-PEEP has to be driven by strong clinical sense as not all patients will benefit from it and others will be harmed. A practical way to assess the effects of extrinsic PEEP in auto-PEEP is to apply small increments of extrinsic PEEP and check the static pressures in the lungs. If the static pressures do not increase, then applying extrinsic PEEP may benefit the patient, but if the pressures increase, then it is time to back down on this strategy.

Enhancing Healthcare Team Outcomes

All healthcare professionals who look after ventilated patients should know the indications and potential adverse effects of PEEP. The ventilator settings should only be changed by one dedicated person- namely the respiratory therapist. Anytime a change is made, it should be charted. Nurses who look after ventilated patients should be aware that high PEEP can lead to barotrauma and a drop in cardiac output- thus protocols should be in place to counter these complications. Daily rounds should be conducted on each ventilated patient to determine the patient's progress and need for changes in the ventilator settings.