Mechanical Ventilation

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Continuing Education Activity

Although mechanical ventilation can be a complex and seemingly elusive topic, expectations are that healthcare professionals who deal with critically ill patients have a basic familiarity with the management of a patient on a ventilator. Additionally, providers must also recognize how applying mechanical ventilation affects patient physiology and response to disease states. The focus of this activity will be on the management of the intubated patient in the first few hours of care on mechanical ventilation and will review the basics of mechanical ventilation, and highlight ventilator strategies when managing a patient by an interprofessional team.

Objectives:

  • Explain the basics of mechanical ventilator management.
  • Describe the different ventilator strategies utilized for different disease processes.
  • Outline major complications of mechanical ventilation.
  • Summarize the advantages of a patient receiving mechanical ventilation.

Introduction

Mechanical ventilation is necessary to sustain life in acute settings hence its management is an essential topic for physicians and healthcare providers to understand and apply safely. This knowledge must be built on a strong foundation of understanding the basic principles of human physiology and airway mechanics. The focus of this article will be on the management of the intubated patient in the first few hours of care on mechanical ventilation. It will review the basics of invasive mechanical ventilation, the common modes of ventilation, initial settings, and supportive care for intubated patients will be discussed in this review. Noninvasive ventilation (NIV) will be discussed separately. [1]

The primary indications for invasive mechanical ventilation can be divided into the following categories:[2]

  1. Airway disease of compromise.
    • Airway protection in a patient who is obtunded or has a dynamic airway, e.g., from trauma or oropharyngeal infection.
    • Airways obstruction is either proximal ( eg angioedema) or distal (asthmatic bronchospasm or acute exacerbation of chronic obstructive pulmonary disease).
  2. Hypoventilation due to impaired drive, pump failure, or inability to exchange gases resulting in hypercapnic respiratory failure. The etiology can be divided into the following subcategories:
    • Impaired central drive (eg drug overdose)[3]
    • Respiratory muscle weakness (eg muscular dystrophy and myositis) [4]
    • Peripheral nervous system defects (eg Guillain-Barré syndrome or myasthenic crisis)[5]
    • Restrictive ventilatory defects (eg chest wall trauma or disease or massive pneumothorax or effusion)
  3. Hypoxemic respiratory failure can be due to the inability to exchange oxygen or delivery to the peripheral tissues due to one of the following reasons: 
    • Alveolar filling defects (eg pneumonia, acute respiratory distress syndrome (ARDS), or pulmonary edema)
    • Pulmonary vascular defects leading to ventilation-perfusion (VQ) mismatch (massive pulmonary embolism or air emboli)
    • Diffusion defects (advanced pulmonary fibrosis)
  4. Increased ventilatory demand due to severe sepsis, shock, or severe metabolic acidosis [6]

Function

Mechanical ventilation (MV) works by applying a positive pressure breath and is dependent on the compliance and resistance of the airway system. During spontaneous inspiration, the lung expands as transpulmonary pressure (P) is produced mainly by a negative pleural pressure generated by the inspiratory muscles. In contrast, during controlled mechanical ventilation, a positive airway pressure drives gas into the lungs, resulting in a positive P. [7] The tidal volume (VT) is the amount of air that moves in or out of the lungs with each respiratory cycle.[8] Physiologically VT is dependent on the height and gender of the person and ranges between 8-10 mL/kg ideal body weight.[2] 

MV can be delivered in different modes including mandatory mode or assisted mode. In the assisted mode the inspiratory effort generated by the patient triggers the MV to deliver the breath while the P is the product of negative pleural pressure and positive alveolar pressure combination.  The most common modes of MV include:

  • Volume-limited assist control ventilation (VAC)
  • Pressure-limited assist control ventilation (PAC)
  • Synchronized intermittent mandatory ventilation with pressure support ventilation (SIMV-PSV)

Pressure support ventilation (PS) is usually not used alone instead it is commonly used during weaning from MV. Other types of modes of MV include controlled mechanical ventilation (CMV; volume-limited or pressure-limited), intermittent mandatory ventilation (IMV), and airway pressure release ventilation (APRV) or Bilevel MV are less commonly used as initial settings. [9]

In general, breath delivery can be divided into either volume-limited or pressure-limited types. Depending on the respiratory compliance and airway resistance and the type or mode of MV, the breath's VT and airway pressure will change. For example, in cases of using volume assist control VAC mode, VT is set to a fixed amount hence the static airway pressure (or plateau pressure at end inspiration) will be dependent on lung compliance. On the other hand, when pressure assist control PAC mode is used the driving pressure is set and fixed hence VT is variable from breath to breath and dependent on lung compliance (ie when the lung compliance is high, VT is high and when lung compliance is low, VT is low). 

There are four stages of mechanical ventilation. There is the trigger phase, the inspiratory phase, the cycling phase, and the expiratory phase. The trigger phase is the initiation of an inhalation which is triggered by an effort from the patient or by set parameters by the mechanical ventilator. The inhalation of air into the patient defines the inspiratory phase. The cycling phase is the brief moment when inhalation has ceased but before exhalation has begun. The expiratory phase is the passive exhalation of air from the patient.

Setting MV

Mode selection: It is recommended to use commonly used MV modes listed above for initiation of MV. The selection of MV mode should be individualized to achieve safety via optimization of ventilation-perfusion matching and pressure-volume relationship of the lungs. [10] In addition,patient-ventilator synchrony and comfort are important factors for the mode selection. 

VAC mode: When VAC  mode is chosen the following parameters have to be set on the ventilator:

  • Tidal volume: VT is usually selected based on ideal or predicted body weight (PBW) not actual weight. In conditions such as ARDS that require a protective lung strategy, the VT is set at a low range of 4 to 8 mL/kg PBW. [11]
  • Respiratory rate (RR): RR is typically set at 12 to 16 breaths/minute, and higher RR ( up to 35 breaths/minute) is selected to achieve adequate minute ventilation such as during protective lung strategy in ARDS to avoid severe hypercapnia or to offset severe acidosis. [12]
  • Inspiratory flow rate (IFR): IFR is usually set at 40 to 60 L/minute to target an inspiratory: expiratory ratio of 1:2 or 1:3. Higher IFR is usually recommended (up to 90 L/min) in cases of severe distal airway obstruction such as acute COPD exacerbation or severe asthma exacerbation which will allow longer expiratory time to empty the lung and hence target I:E ratio of more than 1:3. [10]
  • Fraction of inspired oxygen (FI02): FI02 should be set to the lowest level to achieve pulse oximetry (SP02) of 90% to 96%, as hyperoxemia has been shown to increase mortality in critically ill patients.[13] [14]
  • Positive end-expiratory pressure (PEEP): PEEP is used to increase the functional residual capacity and stent open collapsable alveoli, thus reducing atelectatic trauma.[2] The level of PEEP is usually set at 5 cmH2O and titrated based on the underlying condition and oxygenation needs. For example, in ARDS there is a specific level of PEEP titrated according to respiratory system mechanics or to ARDSNetwork table. [15]
  • Trigger sensitivity: The triggers are two types flow-trigger and pressure-trigger. For pressure-trigger it is usually set at -2 cmH2O but should be avoided in cases where auto-PEEP is suspected and instead, flow-trigger should be used and set at a 2 L/min threshold. 

PAC mode: When PAC mode is selected the following parameters have to be set on the ventilator:

  • Inspiratory Pressure (Pi): Pi level is usually selected (10-20 cmH2) to achieve adequate tidal volume based on the patient's underlying condition as discussed above.
  • Inspiratory time (Ti): Ti is typically set to  1 second and adjusted to achieve an I:E ratio of 1:2 to 1:3. 
  • PEEP and FiO2 are selected similarly to VAC mode. However, the Pi adds additional pressure to the peak airway pressure and may further increase the risk of barotrauma. 

SIMV/PSV mode: When SIMV/PSV  mode is selected the initial settings include:

  • Pressure support (PS): The PS typically starts with 5 to 15 cm H2O for spontaneous breaths taken by the patient above the set rate. The PS can be adjusted as needed to maintain certain Minute ventilation. 
  • Tidal volume: VT is set similarly to VAC mode at levels to achieve targeted minute ventilation without causing ventilator-associated lung injury (4-8 mL/kg PBW) for the non-spontaneous breaths. 

Airway Pressure Release Ventilation Mode

APRV is a form of continuous positive airway pressure (CPAP) characterized by a timed pressure release while allowing for spontaneous breathing.[16] (See Figure 1) APRV functions by providing continuous pressure to keep the lungs open with a timed release to lower set pressure.[17][18] The continuous pressure phase of APRV transmits pressure to the chest wall, which allows for the recruitment of both proximal and distal alveoli.  The prolonged continuous pressure phase with the short release phase avoids the continuous cycles of recruitment-derecruitment in pressure/volume control vent settings.[19] This helps to avoid atelectrauma, barotrauma, and resulting ventilator-induced lung injury.[19] (See Figure 2) The timed release allows for a passive exhalation and improved clearance of CO2. Since APRV relies upon spontaneous ventilation, it requires less sedation than conventional modalities, thus mitigating adverse events due to sedation. Spontaneous breathing has the benefit of increasing end-expiratory lung volume, decreasing atelectasis, and improving ventilation to dependent lung regions. [19] Spontaneous breathing further improves the hemodynamic profile by decreasing intrathoracic pressure, thus improving preload and cardiac output. 

Setting up APRV requires adjusting four main variables, P-high, P-low, T-high, and T-low. [17][18] P-high is the continuous pressure set, while P-low is the pressure release part of the cycle.  T-high is how long the continuous pressure is set to last, while T-low is the release phase duration.  The patient should initially be set on AC/VC immediately post-intubation until the paralysis wears off.  Then, an inspiratory hold should be performed to determine the plateau pressure.  This plateau pressure becomes the P-high and should generally be around 27-29cm H2O, though obese patients may require higher pressure. The P-low is generally set to 0. However, there is generally intrinsic PEEP as full exhalation does not occur.  The T-high is generally set to 4-6 seconds, while the T-low to .2-.8 seconds in restrictive lung disease and .8-1.5 seconds in obstructive lung disease.  To properly set the T-low, you should examine the Flow-Time Waveform on the ventilator.  The T-low should be set to approximately 75% of the Peak Expiratory Flow Rate (PEFR).[19][17] (See Figure 3)  The T-low needs to be continuously readjusted to 75% of the PEFR as lung recruits over time.  FI02 should be titrated downwards once the patient is on APRV and comfortable. 

Spontaneous breathing is paramount in APRV; thus, a small amount of pressure support or automatic tube compensation should be added to account for the endotracheal tube’s intrinsic resistance. [17]  Hypoxemia can be corrected by increasing the P-high and T-high.[17] Hypoxemia can also be corrected by shortening the T-low.  Permissive hypercapnia is allowed in APRV. However, hypercapnia can be corrected if needed by decreasing sedation and/or increasing P-high and T-high.  It can further be corrected by increasing the T-low. However, increasing the T-low can be problematic as APRV relies upon intrinsic PEEP (iPEEP) to keep the lungs open during P-low.  If the T-low increases, the iPEEP will decrease, thus risking the derecruitment of alveoli.

Issues of Concern

Ventilator-associated lung injury (VALI): Lung injury related to ventilator use is common when the setting is not selected based on PBW, particularly in cases of stiff lungs such as ARDS that require lung protective strategy using low tidal volume and targeted airway pressures to prevent lung injuries. [20]

Ventilator-associated events (VAE): VAE is defined as "deterioration in respiratory status after a period of stability or improvement on the ventilator, with evidence of infection or inflammation, and laboratory evidence of respiratory infection". [21] Risk factors for VAE include sedation (such as with benzodiazepines or propofol), fluid overload, high tidal-volume ventilation, and high inspiratory driving pressures.[22] Potential strategies to prevent VAEs include ventilator bundles by minimizing sedation, using daily spontaneous awakening and breathing trials, encouraging early mobilization, using conservative fluid and transfusion strategies, and lung protective strategy. Recent studies have tested some of these interventions on patients' outcomes such as the utilization of ventilator bundles.[23][24][23]

Hemodynamic changes: When placing a patient on mechanical ventilation, there is a change in their natural negative pressure ventilation to one of positive pressure ventilation; this will affect the heart-lung physiology and can alter the patient's hemodynamic status. The addition of positive pressure ventilation increases intrathoracic pressure.  The increase in intrathoracic pressure will lead to a decrease in right ventricular preload and left ventricular preload and afterload.  It will also increase the right ventricular afterload.[25] While these effects could have a minimal change on a healthy person's hemodynamics, they can cause profound alterations in the hemodynamics of a critically ill patient. For example, a patient with acute pulmonary edema will benefit from the reduced preload while someone in septic shock would not.

Clinical Significance

Three clinical strategies may be chosen to assist in ventilator management.

Lung Protective Strategy

This strategy should be used for any patient with the potential to develop acute lung injury (ALI) or whose disease state risks progression to acute respiratory distress syndrome (ARDS).  This low tidal volume strategy was developed after the landmark ARDSnet trials, specifically, the ARMA study, which showed low tidal volume ventilation in patients with ARDS improved mortality. [26] This method is used to avoid barotrauma, volume trauma, and atelectatic trauma. Pneumonia, severe aspiration, pancreatitis, and sepsis are examples of patients with the acute potential to develop ALI and should be managed with the lung protective strategy. 

Tidal volume should be initially set at 6 ml/kg based on ideal body weight.[27][26][28][29] As patients develop ALI and progress into ARDS, their lungs become progressively recruited and develop shunts, which leads to decreased functional lung volume.[30] A low tidal volume strategy offsets the decreased functional lung volume. Tidal volume should not be adjusted based on minute ventilation goals. The respiratory rate is adjusted based on minute ventilation goals and the acid-base status of the patient. An initial rate of 16 breaths/minute is appropriate for most patients to achieve normocapnia.[31] A blood gas should be sent approximately 30 minutes after initiation of mechanical ventilation and RR adjusted based on the acid-base status and PaCO2 of the patient. If the PaCO2 is significantly greater than 40 mmHg, then the RR should be increased. If the PaCO2 is significantly lower than 40, then the RR should be decreased. It is important to remember that the ETCO2 is not a reliable indicator of PaCO2 as the ETCO2 can be affected by the physiological shunt, dead space, and decreased cardiac output. The inspiratory flow rate should be set at 60L/minute. If the patient appears to be trying to inhale more during the initiation of inspiration, it can increase.[30]

Immediately after intubation, an attempt should be made to reduce the FI02 to 40% to avoid hyperoxemia.[13] From there, adjustments of the FI02 and PEEP are simultaneously controlled in the lung-protective strategy. Difficulty in oxygenation in ALI is due to de-recruited alveoli and physiological shunt. To counteract this, you should increase the FIO2 and PEEP together. The oxygenation goal of 88%-95% should follow the ARDSnet protocol.[28] 

Table 1. ARDSnet PEEP/FIO2 Protocol[28]

Upon connecting a patient to mechanical ventilation, it is essential to frequently reassess its effects on the patient, especially the alveoli. This assessment is done by examining the plateau pressure and driving pressure. The plateau pressure is the pressure applied to small airways and alveoli. The plateau pressure should be under 30 to prevent volume trauma, which is an injury to the lung secondary to overdistension of the alveoli.  To obtain the plateau pressure, one must perform an inspiratory pause. Most ventilators have a button to calculate it. The driving pressure is the ratio of the tidal volume to the lung's compliance, providing an approximation of the "functional" amount of lung that hasn't been de-recruited or shunted.[32] The driving pressure can be calculated simply by subtracting the amount of PEEP from the plateau pressure.[32] The driving pressure should remain below 14.  If plateau and driving pressures start to exceed these limits, then decrease TV to 4ml/kg. The respiratory rate can be increased to compensate for the decrease in minute ventilation, though permissive hypercapnia might be necessary.  Permissive hypercapnia is a "ventilation strategy to allow for an unphysiologically high partial pressure of carbon dioxide (PCO2) to permit lung-protective ventilation with low tidal volumes."[33] Recruitment maneuvers have been found to increase mortality in moderate to severe ARDS and should not be routinely used.[34]  

Obstructive Strategy

Generally, patients with obstructive lung disease (OLD), such as asthma and COPD, are often treated with non-invasive ventilation. However, they sometimes require intubation and placement on mechanical ventilation.  Obstructive lung disease is characterized by narrowed airways and the collapse of the small airways on expiration. [2] This condition leads to increased airflow resistance and decreases the expiratory flow, resulting in more time required to exhale the tidal volume fully.  If inhalation begins before the full tidal volume has been exhaled, then some residual air is left inside the chest.  The intrathoracic pressure increases as more and more air are trapped inside the alveoli. This pressure is termed auto-PEEP, and this pressure must be overcome during inhalation. As the amount of air trapped inside the chest increases, you have to flatten off the diaphragm and expand the lungs, decreasing compliance, called dynamic hyperinflation. As auto-PEEP and dynamic hyperinflation progress, there is an increased work of breathing, decreased efficiency of inhalation, and potential for hemodynamic instability due to the high intrathoracic pressure. Given these unique circumstances in OLD, the ventilator strategy employed must offset these pathologically increased intrathoracic pressures. Furthermore, ventilatory management must be combined with maximal medical therapy such as in-line nebulizers to reverse the obstructive process. 

The most important thing to accomplish when managing the ventilator for an obstructive patient is to increase the expiratory phase, allowing for more time to exhale, which will reduce auto-PEEP and dynamic hyperinflation.[2][30][31] It is important to recall that most patients will require deep sedation in order not to over-breathe the ventilator and inspire too often. The tidal volume should be set at 8ml/kg, while the respiratory rate should start at ten breaths per minute.[30] These settings will allow for ample time for a full expiration and hence decreased auto-PEEP, which tends to employ the above-described permissive hypercapnia strategy by focussing on lowered tidal volumes and oxygenation over elevated PaCO2. The inspiratory flow rate should be set at 60 L/minute. FI02 should be set at 40% after the initiation of ventilation.  As obstructive lung disease is typically a problem with ventilation and not oxygenation, the FIO2 should not need to be increased.  Minimal PEEP should be employed, with some studies advocating for a PEEP of zero while some advocate for a small amount of PEEP to help overcome auto-PEEP. 

The ventilator waveform requires careful assessment. If the waveform does not reach zero by the beginning of the new breath, then the RR must be decreased, or else hyperinflation and auto-PEEP will rise.  If an obstructive patient suddenly desaturates or drops their blood pressure, they should be disconnected from the vent to allow for a full exhalation with a clinician pushing on their chest to facilitate exhalation. After this, a full workup specifically ruling out pneumothorax due to volume trauma should be undertaken.[31] If plateau pressures are chronically high, then pneumothorax must also be ruled out.  

Intermediate Strategy

The PReVENT trial showed no difference in an intermediate tidal volume strategy (10ml/kg) versus a low tidal volume strategy (6ml/kg) in patients without ARDS.[35] If the patient is being placed on mechanical ventilation and has no obstructive physiology or risk of developing acute lung injury, an intermediate tidal volume strategy using 8-10ml/kg could be employed.  Generally, as this patient would not have oxygenation or ventilation difficulties, minimal ventilator settings could be employed. Starting with a tidal volume of 8ml/kg, RR of 16, IFR of 60 L/minute, FIO2 of 40%, and PEEP of 5, with titration as needed, is a reasonable starting point.     

Other Issues

Ventilator bundles play a vital role in preventing ventilator-associated events. Some of these measures include minimizing sedation, using daily spontaneous breathing trials, early mobilization, using conservative fluid and transfusion strategies, and lung protective strategies.

Sedation: Before initiating mechanical ventilation, one should also consider what medications to provide for post-intubation pain control and sedation.  An "analgesia first" sedation strategy is recommended, with the most commonly used agent being fentanyl due to its forgiving, i.e., minimally hypotension-inducing hemodynamic properties.[36][37] If the patient is still agitated while getting an analgesia sedation regimen, additional agents, such as propofol, can be added depending on the patient's hemodynamics and clinical needs. A chest x-ray and blood gas should be obtained to determine proper endotracheal placement and to assess minute ventilation. Many centers are now utilizing ultrasound to confirm endotracheal tube (ETT) placement; however, its use has not become the standard of care. Plateau pressures should be checked frequently to assess alveolar integrity.

Head of the bed elevation: All patients on mechanical ventilation should have the head of the bed elevated to at least 30 degrees. According to a 2016 Cochrane review on ventilator-associated pneumonia (VAP), "a semi-recumbent (30º to 60º) position reduced clinically suspected VAP by 25.7% when compared to a 0° to 10° supine position", however, they acknowledge that the data is severely limited.[38]

Airway maintenance: If the patient suddenly desaturates, then the DOPES mnemonic should be followed to determine the causes of the problem. DOPES stands for displacement, obstruction of the ETT or airways, pneumothorax/pulmonary embolism/pulmonary edema, equipment failure, and stacked breaths. The patient should immediately be disconnected from the ventilator and switched to a bag valve mask. The person bagging should ventilate calmly and allow for a full exhalation. Following this, a systematic approach should be followed.  Does the patient still have a good waveform on their ETCO2? If not, then the ET tube may have become dislodged.  Does the patient bag easily or with difficulty? If bagging is difficult, this will inform you of some obstructive problems such as an obstructed ET tube, pneumothorax, or bronchospasm. If the patient bags easily and SpO2 rises rapidly, then it points to equipment failure. While this is under evaluation, another provider should be assessing the patient with an ultrasound of the lungs and heart, and a chest X-ray should be obtained ASAP. Pulmonary embolism should be a consideration if no other cause of the desaturation is found.

Venous thromboembolism prophylaxis: Invasive mechanical ventilation is an independent risk factor for increased odds of venous thromboembolism in the intensive care unit.[39] Hence adding prophylactic measures are important to prevent additional morbidities. 

Gastrointestinal prophylaxis: Gastrointestinal bleeding occurs in approximately 5 % of critically ill patients not receiving prophylaxis.[40] In a multicenter study, invasive mechanical ventilation was one of two independent risk factors for GI bleeding (odds ratio for bleeding, 15.6; 95% CI, 3.0 to 80.1).[41] Therefore the use of an acid suppression strategy for patients on mechanical ventilation has been recommended.[42] proton pump inhibitors (PPIs) are the most effective agents in preventing clinically important gastrointestinal bleeding, but they may increase the risk of pneumonia. It is however unnecessary to continue acid suppression after discharge from the ICU. [43]

Enhancing Healthcare Team Outcomes

The management of a patient on mechanical ventilation requires an interprofessional team involving physicians, nurses, and respiratory therapists. Good communication among the team is paramount.  Respiratory therapists provide a crucial role in managing ventilated patients, and their expertise should be utilized extensively.[44] Finally, only one dedicated professional should be in charge of the ventilator, and vent changes should not be made without communication with others in charge of the patient. [Level III]



(Click Image to Enlarge)
Figure 1. APRV Pressure cycles with superimposed Spontaneous Breathing
Airway pressure release ventilation is a form of continuous positive airway pressure (CPAP). The Phigh is equivalent to a CPAP level; Thigh is the duration of Phigh. The CPAP phase (Phigh) is intermittently released to a Plow for a brief duration (Tlow) reestablishing the CPAP level on the subsequent breath. Spontaneous breathing may be superimposed at both pressure levels and is independent of time-cycling.
Figure 1. APRV Pressure cycles with superimposed Spontaneous Breathing Airway pressure release ventilation is a form of continuous positive airway pressure (CPAP). The Phigh is equivalent to a CPAP level; Thigh is the duration of Phigh. The CPAP phase (Phigh) is intermittently released to a Plow for a brief duration (Tlow) reestablishing the CPAP level on the subsequent breath. Spontaneous breathing may be superimposed at both pressure levels and is independent of time-cycling.
Habashi NM. Other approaches to open-lung ventilation: Airway pressure release ventilation. Critical Care Medicine. 2005;33(Supplement).

(Click Image to Enlarge)
Figure 2. Tidal Volume during APRV vs Conventional Ventilation
Ventilation during airway pressure release ventilation is augmented by release volumes and is associated with decreasing airway pressure and lung distension. Conversely, tidal volumes during conventional ventilation are generated by increasing airway pressure and lung distension.
Figure 2. Tidal Volume during APRV vs Conventional Ventilation Ventilation during airway pressure release ventilation is augmented by release volumes and is associated with decreasing airway pressure and lung distension. Conversely, tidal volumes during conventional ventilation are generated by increasing airway pressure and lung distension.
Habashi NM. Other approaches to open-lung ventilation: Airway pressure release ventilation. Critical Care Medicine. 2005;33(Supplement).

(Click Image to Enlarge)
Figure 3: Depiction of a Peak Expiratory Flow Curve
A patient with a lung that initially has low compliance has a steeper expiratory flow curve (30°) and will require a short release phase (TLow) (0.3 s in this example) to terminate the expiratory flow rate at 75% of the peak expiratory flow (PEFR). As the lung recruits and becomes more compliant, the slope decreases to 45°, requiring an extension in the TLow time, in this example to 0.5 s. With alveolar recruitment and increasing compliance, the lung is able to accommodate larger tidal volumes. Thus, airway pressure release ventilation allows for mechanical ventilation that is time controlled and adaptive to the patient's respiratory system mechanics (time-controlled adaptive ventilation).
Figure 3: Depiction of a Peak Expiratory Flow Curve A patient with a lung that initially has low compliance has a steeper expiratory flow curve (30°) and will require a short release phase (TLow) (0.3 s in this example) to terminate the expiratory flow rate at 75% of the peak expiratory flow (PEFR). As the lung recruits and becomes more compliant, the slope decreases to 45°, requiring an extension in the TLow time, in this example to 0.5 s. With alveolar recruitment and increasing compliance, the lung is able to accommodate larger tidal volumes. Thus, airway pressure release ventilation allows for mechanical ventilation that is time controlled and adaptive to the patient's respiratory system mechanics (time-controlled adaptive ventilation).
Habashi NM. Other approaches to open-lung ventilation: Airway pressure release ventilation. Critical Care Medicine. 2005;33(Supplement).
Article Details

Article Author

Sean M. Hickey

Article Editor:

Al O. Giwa

Updated:

11/26/2022 5:26:27 PM

PubMed Link:

Mechanical Ventilation

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