Mechanical ventilation

Mechanical ventilation is used to assist or replace spontaneous breathing to reduce the work of breathing and/or reverse life-threatening respiratory derangement in critically ill patients or to maintain respiratory function in those undergoing general anesthesia. It involves the application of positive pressure, which can be invasive (i.e., in intubated patients) or noninvasive (e.g., CPAP or BiPAP). Indications include hypoxemic and hypercapnic respiratory failure, hemodynamic compromise, and the need for close ventilatory control (e.g., therapeutic hyperventilation). Settings such as ventilation modes (e.g., assist-control, pressure-support) and parameters (e.g., tidal volume, respiratory rate, FiO₂, PEEP) should be adjusted to patient needs in order to minimize complications and restore homeostasis. A variety of ventilation strategies have been described for treating different types of respiratory failure. These should be implemented in a critical care setting with close monitoring in collaboration with specialists, nurses, and respiratory therapists. Complications of mechanical ventilation include ventilator-induced lung injury and ventilator-associated pneumonia, as well as extrapulmonary complications such as GI ulcers and venous thromboembolism. A systematic approach to common problems in mechanical ventilation (e.g., sudden deterioration, problems with oxygenation and ventilation, hemodynamic compromise, patient-ventilator dyssynchrony, dynamic hyperinflation) is recommended to prevent morbidity and mortality. Once patients show sufficient spontaneous breathing, they are weaned off ventilation support. See also airway management.

• Mechanical ventilation: use of a ventilator to assist or completely replace spontaneous breathing

Positive-pressure ventilation (PPV) is the underlying mechanism of modern mechanical ventilators [1]

• Definition: Oxygenated air is pushed into the lungs by a mechanical ventilation device that generates a positive pressure gradient.
  • Exhalation occurs through passive elastic recoil.
  • May be administered invasively (e.g., via endotracheal or tracheostomy tube) or noninvasively (e.g., via a secured mask, as in BiPAP or CPAP)
• Effects of positive-pressure ventilation
  • Increased airway pressures
    • Promotes gas exchange and recruitment/stenting of alveoli
    • ↑ Risk of ventilator-induced lung injury (e.g., barotrauma)
    • ↑ Pulmonary artery pressure
    • ↑ Pulmonary vascular resistance
  • Increased intrathoracic pressure → ↑ pulmonary vascular resistance and ↓ venous return → ↓ venous drainage of extrathoracic organs and ↓ cardiac output [2]
    • Right heart: ↓ right atrium filling, ↓ right ventricle (RV) preload, ↓ RV stroke volume, ↑ RV work, ↑ RV afterload
    • Left heart: ↓ left ventricle (LV) preload, ↓ LV stroke volume, ↓ LV afterload, ↓ LV work
    • Abdominal: ↑ gastric distension, ↑ risk of vomiting/aspiration, ↑ abdominal compartment pressure, ↓ organ perfusion

Types of noninvasive positive-pressure ventilation (NIPPV) [3]

Continuous positive airway pressure (CPAP)

• The ventilator delivers one constant airway pressure throughout the respiratory cycle (e.g., 5 cm H₂O).
• Equivalent to providing PEEP without any other support
• Used in hypoxemic respiratory failure; (e.g., cardiogenic pulmonary edema, OSA)

Bilevel positive airway pressure (BIPAP)

• The ventilator delivers two pressure levels and cycles between them.
  • Expiratory positive airway pressure (EPAP): baseline pressure provided
    • Safe range: < 10–15 cm H₂O
  • Inspiratory positive airway pressure (IPAP): EPAP plus added inspiratory pressure support (PS)
    • Safe range: < 20–25 cm H₂O
  • If there is no added inspiratory pressure support (i.e., when IPAP = EPAP), then the EPAP setting is equivalent to CPAP.
  • If there is added inspiratory pressure support (i.e., IPAP > EPAP), then EPAP is equivalent to PEEP (see invasive mechanical ventilation).
• Used in hypercapnic respiratory failure and hypoxemic respiratory failure

CPAP only delivers one airway pressure, equivalent to PEEP. BIPAP cycles between two airway pressures and offers inspiratory pressure support.

Indications for NIPPV [4][5]

• Treatment of respiratory distress in patients with:
  • Acute COPD exacerbation with respiratory acidosis (e.g., pH ≤ 7.35, PaCO₂> 45 mm Hg, RR > 20–24)
  • Cardiogenic pulmonary edema (without shock or ACS)
  • Asthma exacerbations: This is a controversial indication.
• Treatment of acute respiratory failure in patients with:
  • Immunocompromise (e.g., solid organ and bone marrow transplant)
  • Chest trauma
  • Postoperative deterioration
• Bridging to intubation in patients with challenging preoxygenation (e.g., ARDS) [6]
• Bridging back to unassisted breathing
  • Weaning from invasive mechanical ventilation in patients with acute hypercapnic respiratory failure
  • Prophylactic use after planned extubation in patients at high risk for recurrent respiratory failure
• Patients with a level of care precluding invasive mechanical ventilation
  • Patient with a do-not-intubate order [3]
    • Trial of therapy while the underlying disease is treated
    • Temporizing measure to provide life support until the arrival of family/friends
  • Palliative therapy for terminal cancer patients with dyspnea

Contraindications for NIPPV [7][8]

• Impaired/absent spontaneous breathing and/or patient not cooperative with NIPPV
  • Cardiac or respiratory arrest
  • Severe encephalopathy (GCS < 10)
  • Uncontrolled agitation
• Impaired airway protection
  • Upper airway obstruction
  • Inability to clear respiratory secretions
  • Severe upper GI bleeding
  • High risk of aspiration [9]
• Impaired mask seal
  • Facial trauma
  • Surgery
  • Deformity
• High risk of adverse effects from positive pressure
  • Recent upper airway or upper gastrointestinal surgery
  • Hemodynamic instability or cardiac arrhythmia

Uncontrolled agitation is a contraindication for NIPPV.

Procedure [3][5][8]

The following steps are pertinent to adults newly requiring NIPPV. Stable patients continuing home therapy (e.g., CPAP for longstanding OSA) should be started on their preferred interface and baseline settings.

• Preparation
  • Obtain baseline ABG if feasible.
  • Make sure the patient is comfortable, alert, and in sitting position.
  • Monitor pulse oximetry, blood pressure, ECG, ABG, exhaled tidal volume, and respiratory mechanics.
  • Explain the procedure to the patient.
  • Prepare for intubation in case respiratory and clinical status deteriorates.
• Choice of interface [8]
  • Oronasal mask
  • Total-face masks
  • Nasal mask or nasal pillows
  • Helmet
• NIPPV settings [5]
  • BIPAP mode [3]
    • Low-high approach: Start with low pressures and adjust upward as needed and tolerated.
      • Start EPAP at 3–5 cm H₂O.
      • Start IPAP at 10 cm H₂O.
    • High-low approach: Start with high pressures and adjust downward as needed and tolerated.
      • Start EPAP at 5–8 cm H₂O.
      • Start IPAP at 20–25 cm H₂O.
  • CPAP mode: Set PEEP to 5–12 cm H₂O.
  • Titrate FiO₂ (between 30% and 50%) to the desired oxygenation target (e.g., SpO₂ 88–92% for COPD).
• Monitoring and adjustments
  • Initially administer NIPPV for 30–60 minutes.
  • Titrate initial pressures (PEEP/EPAP and IPAP) to:
    • ↓ Work of breathing and dyspnea
      • ↓ Respiratory rate
      • ↑ Tidal volume
    • ↓ Patient-ventilator dyssynchrony
  • Check ABG after 20–30 minutes.
    • If SpO₂ is low, increase FiO₂ and PEEP/EPAP.
    • If PaCO₂ is high, increase IPAP.
  • If patient's condition worsens , prepare to switch to invasive mechanical ventilation (see endotracheal intubation).

Do not delay invasive mechanical ventilation (e.g., intubation) if a patient's condition is worsening with NIPPV.

Complications [8]

• Air leaks
• Aspiration and potential aspiration pneumonia
• Ventilator-associated lung injury: barotrauma or pneumothorax
• Severe gastric distention that necessitates NG tube insertion
• Skin irritation, abrasions, and nasal bridge ulceration
• Mucus plugging
• Mucosal dryness

General principles [3][10]

• Description: positive pressure ventilation administered through an invasive airway device, e.g., endotracheal (ET) or tracheostomy tube (see “Airway management” for details)
• Goals
  • Reduce work of breathing (WOB). [11]
    • Prevent respiratory arrest.
    • Alleviate myocardial oxygen demand.
    • Prevent multiorgan dysfunction.
  • Treat life-threatening hypoxemia and hypercarbia.
  • Ensure aggressive bronchopulmonary hygiene.
  • Support breathing in patients requiring intubation for airway protection.
• Risks: The ET tube and ventilator tubing/circuit increase instrumental dead space, which leads to higher airway resistance and pressure, thereby raising the risk of ventilator-induced lung injury.

Indications for invasive mechanical ventilation [12][13]

• Hypercapnic respiratory failure
• Hypoxemic respiratory failure
• Hemodynamic compromise
  • Early mechanical ventilation offloads the heart by reducing the MVO₂ required to maintain the work of breathing. [12]
  • Useful in conditions with ↑ systemic oxygen demand and/or ↓ cardiac output (e.g., polytrauma, burns, septic shock, severe MI, cardiogenic shock)
  • The benefits must be weighed against the hemodynamic risks of positive-pressure ventilation (see PPV).
• Hyperventilation therapy: short-term measure to treat patients with increased ICP [14]
• GCS ≤ 8 [15]

Contraindications

• No absolute contraindications
• Relatively contraindicated in patients with advanced directives against mechanical ventilation

Initiating mechanical ventilation in patients with severe obstructive lung disease, acidosis, and shock is associated with significant morbidity and mortality. These conditions require special care and preparation (see high-risk indications for mechanical ventilation).

Adjunctive care of ventilated patients

Sedation, analgesia, and muscle relaxants [16][17][18]

• Goals
  • Decrease patient discomfort.
  • Suppress respiratory drive.
  • Decrease muscular resistance to mechanical ventilation.
  • Decrease patient-ventilator dyssynchrony.
• Sedation
  • Start immediately after intubation for patient comfort: Do not mistake paralysis for sedation, especially if a long-acting muscle relaxant (e.g., rocuronium) was used during the induction.
  • Titrate to patient comfort (e.g., RASS range 0 to -5).
  • Consider lighter sedation in patients requiring serial neurological examination.
  • Agents
    • Propofol
    • Midazolam
    • Dexmedetomidine
    • Ketamine [19]
• Analgesia
  • Spontaneously breathing patients should be monitored for respiratory depression.
  • Agents
    • Fentanyl (off-label)
    • Morphine (off-label)
• Muscle relaxants [20][21]
  • Allow a higher level of ventilatory control when desired (e.g., in refractory ARDS)
  • Should only be used in sedated patients.
  • Agents
    • Rocuronium
    • Pancuronium
    • Cisatracurium -

Sedation should be started immediately after intubation and should not be mistaken or confused for the paralysis caused by some induction agents. Paralysis without sedation should be avoided at all costs!

Bronchopulmonary hygiene [22]

• Oral and airway hygiene
• Tracheal suctioning
• Mucolytics
• Bronchoscopy
• Chest physiotherapy and kinetic therapy

Supportive care

• Orogastric or nasogastric tube insertion
• Pressure ulcer prophylaxis
• VTE prophylaxis
• Consider stress ulcer prophylaxis (routine use is controversial)

Basic ventilation parameters [1][3][10][23][24][25]

1. Tidal volume (V_t): the volume of air delivered to or taken by the patient per breath
   • Set by the clinician in volume-controlled modes (e.g., 8–12 mL/kg ideal body weight)
   • Measured by the ventilator in pressure-controlled or pressure-supported modes (e.g., PRVC and PSV)
2. Respiratory rate (RR): breaths taken or delivered per minute
   • Set by the clinician in the absence of patient-initiated breaths (e.g., ∼ 10–15/min)
   • Set by the patient in spontaneous breathing modes
   • Commonly a combination of patient-triggered assisted breaths and a clinician-set backup RR
3. Fraction of inspired oxygen (FiO₂): the fraction of oxygen (by volume) in the inspired air
   • FiO₂ of room air = 21%
   • FiO₂ up to 100% can be delivered in perfectly sealed ventilator circuits.
4. Positive end-expiratory pressure (PEEP):
   • Definition
     • Positive pressure in the lung maintained over the entire inhalation and expiration phases
     • Measured in centimeters of water (cm H₂O)
     • Also known as extrinsic PEEP (as it is applied to the patient by the device)
   • Mechanism of action: keeps airway pressure above the atmospheric level at the end of exhalation → increases alveolar pressure and volume → reopens collapsed or unstable alveoli → improves ventilation/perfusion relation
   • Indications: PEEP is typically justified when a PaO₂ of 60 mm Hg cannot be achieved with an FiO₂ of 60%.
     • Almost all patients need a minimum amount of PEEP (3–5 cm H₂O).
     • Higher PEEP is indicated in conditions involving a right-to-left pulmonary shunt pathology.
   • Advantages
     • Prevent atelectasis
     • ↑ Oxygenation without increasing the risk of oxygen toxicity
     • ↑ Gas exchange area
     • ↑ Functional residual capacity
     • ↑ Pulmonary compliance
   • Adverse effects
     • Ventilator-induced lung injury
     • Patient-ventilator dyssynchrony
     • See “adverse effects” of positive pressure ventilation.
     • See hemodynamic compromise in mechanically ventilated patients.

Ventilator modes [1][3][10][23][24][25]

Mandatory ventilation modes

Mandatory modes are useful when respiratory musculature is weak/paralyzed and respiratory drive is impaired.

• Examples
  • Assist-control (AC) ventilation: can consist of volume-control ventilation (VCV) or pressure-control ventilation (PCV)
  • Pressure-regulated volume control (PRVC)
• Description
  • Breath frequency and waveforms are mostly controlled by the clinician.
  • A minimum number of breaths per minute are delivered by the ventilator.
  • Patients can trigger additional breaths above the minimum set rate.
  • The breath volume and/or pressure are fixed and are independent of patient effort.

Spontaneous ventilation modes

Spontaneous modes are useful for when respiratory musculature is intact/weak and respiratory drive is intact.

• Example: pressure-support ventilation (PSV)
• Description:
  • Breath frequency and waveforms are mostly controlled by the patient.
  • The ventilator only provides inspiratory pressure to support breathing.
  • Almost all breaths are patient-triggered.
  • Breath volume and duration depend on patient effort and the degree of inspiratory pressure provided.

Comparison of commonly used ventilator modes

Advanced settings

1. Pressure support (PS): positive pressure added on top of PEEP during inspiration in pressure-supported ventilation modes (e.g., PSV)
   • Ranges from 5 cm H₂O (minimal support) to 30 cm H₂O (maximal support)
   • Work of breathing is mostly accomplished by the ventilator if PS > 20 cm H₂O.
   • PS is typically increased to compensate for respiratory muscle fatigue, then gradually decreased during weaning from mechanical ventilation to allow patients to strengthen their respiratory musculature, with the goal of them breathing unassisted.
2. Peak inspiratory pressure (P_IP) limit/target: preset parameter in pressure-controlled and pressure-regulated ventilation modes
   • In other ventilator modes, P_IP is a variable (see “monitoring” below).
   • Typically set at ∼ 20–25 cm H₂O to prevent barotrauma
3. Inspiratory flow rate (VI): the rate of airflow sent into lungs during the inspiratory phase
   • Adjustable; flow rate typically set at at 60 L/min
4. Inspiratory:expiratory ratio (I:E ratio): the ratio of inspiratory time to expiratory time in a given breathing cycle
   • Usually expressed in whole numbers (e.g., 1:2, 1:3)
   • Can be adjusted directly or indirectly depending on the device
   • Target I:E ratios are desirable in certain conditions (e.g., 1:4–1:5 for obstructive lung disease).
     • Lower I:E ratios improve CO₂ clearance, minimize air trapping (auto-PEEP), and minimize the effect of positive-pressure on hemodynamics.
     • Higher I:E ratios increase mean airway pressure and may enhance oxygenation and recruitment.
   • Depends on other parameters
     • ↑ RR→ ↓ time available for passive expiration → ↑ I:E ratio
     • ↑ V_t → ↑ time required for inspiration → ↑ I:E ratio
     • ↑ VI → ↓ time required for inspiration → ↓ I:E ratio
     • Inspiratory time = Vt/VI
     • Expiratory time = [breath cycle time (1/RR) - inspiratory time]
     • I:E ratio = inspiratory time/expiratory time
5. Trigger sensitivity (mechanical ventilation): the threshold of inspiratory pressure or flow-gradient at which the ventilator identifies the patient's attempt to initiate a breath
   • Typically standard to the device (1–3 cm H₂O)
   • Not commonly adjusted by clinicians
     • Low sensitivity helps to decrease work of breathing
     • High sensitivity helps to decrease oversensing of breaths

General principles

All mechanically ventilated patients require close clinical, biomechanical, and laboratory monitoring in a critical care unit. This should include:

• One-to-one nursing care
• Continuous cardiac and hemodynamic monitoring
• Respiratory monitoring: Sensors can be externally applied or built into modern ventilators.
• Temperature monitoring
• Blood gas analysis monitoring

External monitoring [27]

• Pulse oximetry
  • Advantages
    • Widely available and portable
    • Easy to interpret in real-time
    • High accuracy if SpO₂ > 70%
  • Disadvantages: not as accurate as PaO₂
    • ↓ Accuracy in the case of: hypovolemia, hypothermia, vasopressor use, dyshemoglobinemia (e.g., carboxyhemoglobin, methemoglobin)
    • Poor sensitivity for hyperoxia
• Capnometry (portable): numerical measurement of end-tidal CO₂ (EtCO₂) [28]
  • Description
    • Externally-applied devices are being used with increasing frequency.
    • Expired air is sampled through a tube.
    • A transducer detects CO₂ and the amount is displayed on the monitor.
  • Primary uses
    • Determining the adequacy of ventilation
    • Confirming ET tube placement
    • RR monitoring
  • Secondary uses
    • Short term guidance of hyperventilation therapy (e.g., treating ↑ ICP)
    • Diagnosing pulmonary embolism
    • Preventing hypercapnia, e.g., in brain-injured and post-cardiac arrest patients
    • Assessing CPR quality
  • Disadvantages: underestimates PaCO₂ compared to ABG
• Advanced monitoring to consider: especially for conditions exacerbated by positive pressure ventilation.
  • Hemodynamically unstable patients: CVP monitoring; IVC diameter and collapsibility
  • Patients at risk of abdominal compartment syndrome: abdominal compartment pressures

Ventilator-based monitoring [3][10][27]

The following are standard measurements built into most newer generation ventilators.

Capnography

• Description
  • Waveform version of capnometry displaying CO₂ measurements in exhaled air over time
  • The EtCO₂ is measured at the end of the expiratory phase of the breathing cycle.
  • Sensors are typically integrated into the ventilator but can be portable in rare cases.
• Interpretation
  • Normal waveform: rapid increase of the CO₂ concentration → plateau → rapid decrease in the CO₂ concentration during inspiration.
  • Loss of waveform
    • Cardiac arrest
    • Accidental extubation
    • Complete tube obstruction
  • Significant decrease in waveform amplitude
    • Partial tube obstruction
    • Airway leak
    • Hypotension

Pressure monitoring [13][29]

• Peak inspiratory pressure (P_IP):
  • Definition: the maximum pressure measured at any point throughout the inspiratory phase
  • Description: primarily reflects airway resistance; lung compliance reflected to a lesser degree
    • VCV
      • Measured P_IP is greatly influenced by airway resistance.
      • Less reflective of alveolar pressure and risk of VILI
    • PCV/PRVC
      • P_IP = inspiratory pressure target + PEEP
      • Accurately reflects alveolar pressure and correlates well with VILI risk
  • Interpretation: P_IP > 35–40 cm H₂O is generally considered elevated.
• Plateau pressure (P_Plat)
  • Definition: the maximum air pressure measured during a pause at the end of inspiration
  • Description: reflects lung compliance
    • VCV: more accurately reflects alveolar pressure and risk of VILI than P_IP
  • Interpretation: P_plat > 30 cm H₂O is considered elevated.
• Auto-PEEP (intrinsic PEEP) [30]
  • Definition: PEEP remaining in the circuit at the end of expiration that is not delivered by the ventilator, i.e., generated by the patient
  • Description
    • Tends to occur in conditions in which the expiratory outflow is impaired (e.g., asthma)
    • Expiration is incomplete at the end of a breath cycle → air trapping → dynamic hyperinflation
    • Estimated using expiratory hold maneuver
      • The circuit is paused for 3–5 seconds at the end of expiration.
      • The change in pressure waveform back to baseline is measured as it reaches equilibrium in the circuit, which is the total PEEP.
      • Auto-PEEP = total PEEP - extrinsic PEEP
  • Interpretation:
    • Ideally, no auto-PEEP should be present.
    • The presence and degree of auto-PEEP correlates with a higher risk of complications (e.g., dynamic hyperinflation, adverse effects of positive pressure ventilation).

Laboratory monitoring [31]

Arterial blood gas monitoring

• General considerations
  • More accurate than pulse oximetry for assessing oxygenation
  • Essential for calculation of P/F ratio
  • Consider an arterial line for patients requiring frequent arterial sampling.
  • Normal physiological/compensated ranges are typically desirable (exceptions include permissive hypercapnia).
• Sampling frequency
  • Within 30 minutes of intubation
  • Within 1 hour of changes in ventilator settings or patient status
  • Every 8–24 hours otherwise
• Interpretation: See also arterial blood gas analysis.
  • Ventilation: pH, PaCO₂, HCO₃
    • Respiratory acidosis pattern: insufficient minute ventilation
    • Respiratory alkalosis patterns: iatrogenic hyperventilation
    • Metabolic acidosis/alkalosis patterns: Consider adjusting minute ventilation for compensation.
    • See improving ventilation in mechanically ventilated patients.
  • Oxygenation: PaO₂
    • For interventions, see improving oxygenation in mechanically ventilated patients.

Venous blood gas [10]

• Generally correlates well with ABG for pH
• Venous PCO₂ is not as reliable as capnography.
• Venous PO₂ is not as reliable as pulse oximetry.

Ventilator-induced lung injury (VILI) [3][27]

VILI refers to both pulmonary and extrapulmonary injuries resulting from any combination of the following.

• Pulmonary barotrauma [34]
  • Mechanism: excess pressure in circuit → ↑ extra-alveolar air dissecting into other fascial planes and compartments
  • Aggravating factors
    • ↑ PEEP
    • ↓ Lung compliance
    • ↑ Airway resistance
    • ↑ Inspiratory flow rate
  • Consequences
    • Pneumothorax and/or tension pneumothorax
    • Pneumomediastinum
    • Pneumoperitoneum
    • Subcutaneous emphysema
• Volutrauma
  • Mechanism: excess volume delivered → alveolar overdistention → disruption of alveolar-capillary membrane → release of inflammatory mediators
  • Aggravating factors: ↑ V_t and ↓ lung compliance
• Atelectrauma
  • Mechanism: repeated opening and closing of alveoli (i.e., atelectasis) → shear stress → release of inflammatory mediators
  • Aggravating factors: ↓ PEEP , ↓ V_t, ↓ pulmonary surfactant
• Biotrauma
  • Mechanism: release of inflammatory mediators from lung → systemic organ dysfunction
  • Aggravating factors: volutrauma, atelectrauma
• Oxygen toxicity [32][33]
  • Mechanism: excess oxygen concentration → free radical formation, causing direct tissue injury (e.g., diffuse alveolar damage, tracheobronchitis) [13]
  • Aggravating factor: ↑ FiO₂
  • Consequences: Hyperoxia is associated with higher mortality in critically ill patients than normoxemia.

Other complications

Intrapulmonary

• VAP: See “Prevention of ventilator-associated infections” and “Empiric antibiotic therapy for ventilator-associated pneumonia.”
• Inspiratory muscle weakness and deconditioning [35]
• Ventilator-associated pulmonary fibrosis: occurs in the subacute phase of ARDS [36][37]

Extrapulmonary [27]

• Gastric mucosal injury (e.g., PUD, GI bleed)
• Venous thromboembolism [27]
• Systemic deconditioning
• Pressure ulcers
• Contractures

We list the most important complications. The selection is not exhaustive.

See "Mechanical ventilation in children" for pediatric ventilation strategies.

Normal lung mechanics [10][13][42]

• Common uses
  • Healthy patient undergoing elective surgery
  • Intubation for airway protection (e.g., TBI, poisoning)
• Typical settings
  • Mode: initially any mandatory or mixed mode (AC/VCV, PCV, PRVC), then switch to PSV or SIMV
  • V_t: 8–10 mL/kg ideal body weight
  • RR: 10–15 breaths/min
  • FiO₂: Start at 100%, then rapidly titrate to < 40%
  • PEEP: Start at 3–5 cm H₂O.
• Additional parameters
  • I:E ratio: 1:2
  • If switching to pressure support: See ventilator weaning.
  • Positioning: supine

Permissive hypercapnia [43][44][45][46][47]

• Definition: the acceptance of hypercapnia (PaCO₂> 45 mm Hg) as a byproduct of a given ventilation strategy
• Rationale
  • In some conditions (e.g., ARDS, asthma, AECOPD), targeting normocapnia increases the risk of VILI.
  • Generally considered safe [48][49][50]
• Relative contraindication: acute intracranial disorders [49][51]
• Procedure
  • Ventilatory parameters are adjusted according to patient needs: See lung-protective ventilation strategy and obstructive lung disease ventilation strategy.
  • Arterial blood gas targets
    • PaCO₂: no clear upper limit; Experts suggest maintaining < 50 mm Hg as much as possible. [49]
    • pH ≥ 7.25 generally acceptable [52]
• Complications
  • Acute cor pulmonale
  • Organ dysfunction: cardiovascular and renal

Ventilation strategy for obstructive lung disease [10][13][42]

These are conditions with a high-risk of periintubation mortality.

• Challenges
  • Oxygenation
    • Rapid desaturation, impaired lung dynamics, high oxygen demand and consumption
    • Poor patient cooperation during preoxygenation due to hypoxia and distress
  • Ventilation
    • Severe bronchospasm/airway inflammation leads to increased resistance in the circuit and increased risk of barotrauma.
    • Breath stacking leads to dynamic hyperinflation (DHI) and auto-PEEP.
• Prevention
  • Maximize noninvasive therapy prior to mechanical ventilation if time allows.
  • Optimize periintubation medical treatment
  • See high-risk indications for mechanical ventilation for the prevention of hypoxia, respiratory acidosis, and DHI.

Patients with obstructive lung disease are at high risk of periintubation mortality.

Asthma and anaphylaxis [53][54]

See “Intubation and mechanical ventilation in asthma” and “Airway management and ventilation in anaphylaxis” for details on indications and initial management.

• Typical settings
  • Mode
    • Use caution with continuing AC/VCV.
    • Consider switching to PCV or PRVC.
  • V_t: 4–8 mL/kg, then adjust according to ABG
  • RR: Adjust according to permissive hypercapnia.
    • Increase if pH < 7.25.
    • Acceptable ranges: 8–10 breaths/min
  • FiO₂
    • Initially 100%; rapid titration to < 30–50%
    • Target minimum required to maintain SpO₂ 88–92%
  • PEEP: Keep < 80% of auto-PEEP value (0–5 cm H₂O).
• Additional parameters
  • Maximize expiratory time (e.g., consider I:E ratio 1:4 rather than 1:2).
  • VI: 60–80 L/min
  • Auto-PEEP: Keep to a minimum.

AECOPD [13][42]

• Indication: See indications for intubation in patients with AECOPD.
• Typical settings
  • Mode:
    • Use caution with continuing AC/VCV.
    • Consider switching to PCV or PRVC.
  • V_t: 6–8 mL/kg
  • RR: Adjust according to permissive hypercapnia.
    • Increase if pH < 7.25.
    • Acceptable ranges; 10–12 breaths/min
  • FiO₂
    • Initially 100%; rapid titration to < 30–50%
    • Target minimum required to maintain SpO₂ 88–92%.
  • PEEP: Keep < 80% of auto-PEEP value.
• Additional parameters
  • Maximize expiratory time (e.g., consider I:E ratio 1:4 rather than 1:2).
  • VI: 60–80 L/min
  • Auto-PEEP: Keep to a minimum.

Use the I:E ratio to maximize expiratory time and prevent auto-PEEP in obstructive lung disease.

Ventilation strategy for severe acidosis [10][13]

These are conditions with a high-risk of peri-intubation mortality.

• Challenges
  • The maximal respiratory compensation achievable by a ventilator is inferior to the patient's endogenous capacity.
  • Apneic periods during intubation can dangerously lower pH due to CO₂ buildup.
• Preparation: See high-risk indications for mechanical ventilation.
• Common uses: respiratory muscle fatigue in cases of salicylate toxicity, DKA, toxic alcohol poisoning, renal failure, COPD
• Typical settings
  • Mode: AC/VCV
  • V_t/RR: needs to be optimized to match respiratory compensation [55]
    • Use the Winter formula to identify desired PaCO₂.
    • In adults, can estimate initial target minute ventilation (V_t × RR) based on desired PaCO₂
      • 40 mm Hg: 6–8 L
      • 30 mm Hg: 12–14 L
      • 20 mm Hg: 18–20 L
    • Adjust subsequent targets using the following formula:
      • Target minute ventilation = (measured PaCO₂ × current minute ventilation) ÷ desired PaCO₂ [56]
  • FiO₂: Start at 100%, then rapidly titrate to < 40%.
  • PEEP: Start at 3–5 cm H₂O.

Optimizing the tidal volume and respiratory rate to match the patient's respiratory compensation is critical in patients with severe acidosis to avoid cardiac arrest.

Lung-protective ventilation strategy [10][13][20][31][42][57][58][59][60]

This is used in very high-risk and challenging clinical situations. Expert consultation is crucial during initiation and adjustment.

• Rationale: LPV improves gas exchange while reducing the risk of VILI.
  • Permissive hypercapnia is applied.
  • Low tidal volumes to prevent volutrauma
  • Low pressures (P_Plat ≤ 30 cm H₂O) to prevent barotrauma
  • Collapsed alveoli are recruited through various methods, e.g., PEEP titration and treatment of the underlying disease
  • Deep sedation to reduce patient-ventilator dyssynchrony and oxygen demand (see adjunctive care of ventilated patients).
• Common uses
  • ARDS
  • Acute lung injury (e.g., inhalational injury, TRALI)
  • Severe VILI
• Typical settings
  • Mode: AC/VCV or AC/PCV [61]
  • V_t: 6–8 mL/kg; Decrease to 4–6 mL/kg if P_Plat > 30 cm H₂O.
  • RR
    • Increase if pH < 7.25.
    • Acceptable ranges: 20–35 breaths/min
  • FiO₂ and PEEP: should be adjusted in tandem to the lowest PEEP/FiO₂ combination defined in the ARDSnet protocol (see ARDS)
    • FiO₂: Start at 100% and wean down as soon as possible.
    • PEEP: Start at 5 cm H₂O and adjust upwards as needed.
    • Further titration of these parameters should follow the ARDSnet protocol increments.

Ventilation strategy for elevated ICP [14][62]

Elevated ICP is a high-risk condition primarily due to the adverse effects of induction medications and laryngoscopy. See intubation of patients with high ICP for airway management.

• Common use
  • High ICP refractory to other lowering measures
  • Should only be used as a temporizing measure
  • Avoid in the first 24 hours after head injury. [10][63]
• Typical settings
  • Mode: AC/VCV
  • FiO₂: 100%
  • PEEP: ≤ 5 cm H₂O
  • Vt/RR
    • First 30 minutes
      • Set initial V_t ≥ 8 mL/kg.
      • Adjust RR to target PaCO₂ 30–35 mm Hg.
    • Subsequently can reduce V_t to 6–8 mL/kg and adjust RR to target normocapnia (i.e., 35–40 mm Hg).
• Additional parameters: Raise the head of the bed.

Ventilation strategy for neuromuscular weakness and chest wall injury [10][13]

• Common uses
  • Myelopathy
  • Guillain-Barré syndrome
  • Myasthenia gravis
  • Flail chest
• Typical settings
  • Mode: AC/VCV, PCV, PRVC
  • V_t: 8–10 mL/kg ideal body weight
  • RR: 15–25 breaths/min
  • FiO₂: Start at 100%, then rapidly titrate to < 50%.
  • PEEP: Start at 5–8 cm H₂O.
• Additional parameters
  • VI: 60–80 L/min

Ventilator weaning

• Definition: the process of easing a patient off mechanical ventilatory support
• Typical settings
  • Mode: PSV
  • V_t/RR: set by patient
  • FiO₂: Begin at level from prior ventilatory mode (e.g., AC/VCV) and reduce to < 40%.
  • PEEP: Begin at level from prior ventilatory mode (e.g., AC/VCV) and reduce to 3–5 cm H₂O.
  • Pressure support (PS)
    • Range: 5–20 cm H₂O
    • Initially choose the amount required to match the V_t delivered on the previous ventilation mode.
    • Progressively reduce, as tolerated by the patient's clinical status and ventilatory parameters.
• Spontaneous breathing trial [64]
  • A test that is used to determine whether a mechanically ventilated patient is ready to breathe without a ventilator
  • Criteria for extubation
    • Patient is able to spontaneously initiate an inspiratory effort (i.e., good neuromuscular function).
    • Underlying lung disease is stable/resolving.
    • Adequate PaO₂ and SpO₂ on minimal support (e.g., PS ≤ 5 cm H₂O)
    • pH ≥ 7.25
    • Hemodynamically stable with little or no vasopressor therapy

Extubation with inadequate weaning (i.e., without proper muscle restrengthening) can lead to respiratory failure and require reintubation.

Approach to mechanically-ventilated patient in respiratory distress [3][10][13][27][38]

• If hemodynamically unstable: Disconnect the patient from the ventilator and switch to manual ventilation with 100% FiO₂.
• If hemodynamically stable: Increase FiO₂ to 100% until further assessment is complete.
• Perform focused clinical evaluation.
  • Historical clues
    • Changes in ventilator settings
    • Changes in patient symptoms
    • Recent instrumentation
    • Attempts at repositioning
  • Physical examination
    • Airway: position, patency, and presence of leaks
    • Breathing: chest rise, lung auscultation, skin crepitus
    • Circulation: signs of perfusion and hemodynamic status
• Check monitors and alarms: Review P_IP and P_Plat.
• Inspect ventilator equipment and tubing.
• Perform bedside ultrasound or order portable CXR, as guided by clinical suspicion (e.g., to rule out pneumothorax).

In patients who are hemodynamically unstable, disconnect them from the ventilator and start manual ventilation with 100% FiO₂.

Causes of sudden deterioration post-intubation [65][66]

• Displacement/disconnection
  • See airway management for ET tube troubleshooting.
  • Check for disconnection in the circuit.
• Obstruction: See airway management for causes.
  • Deep suctioning with saline flushes
  • Undo kinks in tubing.
  • Evaluate patients biting ET tubes for causes of pain/discomfort.
    • Adjust sedation and analgesia accordingly
    • Apply a bite block.
• Pneumothorax
  • See “diagnostics” in pneumothorax for bedside ultrasound assessment.
  • All mechanically ventilated patients with pneumothorax require urgent tube thoracostomy.
  • If a tension pneumothorax is suspected, perform an urgent needle decompression.
• Equipment failure
  • If suspected, disconnect the patient from the ventilator and manually ventilate with 100% FiO₂ until it can be replaced.
  • Troubleshoot with a respiratory therapist.

Causes of sudden deterioration after intubation can be recalled using the DOPE mnemonic: Displacement/Disconnection, Obstruction, Pneumothorax, Equipment failure.

Improving oxygenation in mechanically ventilated patients

• Especially challenging in patients with hypoxemic respiratory failure
• Adjust FiO₂ and PEEP.
  1. Increase FiO₂ to rapidly deliver a higher oxygen concentration.
     • Avoid prolonged exposure to high FiO₂ levels (> 60%) to prevent hyperoxia/oxygen toxicity. [32][33]
       • Avoid SpO₂ ≥ 95% for prolonged periods, unless specifically indicated.
       • If SpO₂ is persistently 100%, check PaO₂ on ABG (see “monitoring” above).
  2. Increase PEEP if FiO₂ > 60% is required. [67][68][69][70]
     • Titrate up as needed to allow FiO₂ to be reduced to less risky levels.
     • Avoid prolonged exposure to high PEEP to minimize VILI.
     • Aim for the lowest PEEP tolerated to maintain oxygenation target.
• Treat reversible underlying causes of hypoxemia.
• Consider lung recruitment maneuvers for refractory hypoxemia.

Improving ventilation in mechanically ventilated patients

• Especially challenging in patients with hypercapnic respiratory failure
• Adjust minute ventilation (RR + V_t)
  • If ABG is consistent with alkalosis (hypocapnia): Decrease minute ventilation.
    • Decrease V_t.
    • Decrease RR.
  • If ABG is consistent with acidosis (hypercapnia): Increase minute ventilation.
    • Increase V_t: limited by risk of VILI
    • Increase RR: limited by expiration time (risk of DHI)
    • If in PSV mode, acidosis and/or hypercapnia may indicate low volumes inspired.
      • If due to oversedation: Reduce sedative dose.
      • If due to respiratory muscle fatigue or decrease in lung compliance:
        • Add inspiratory pressure.
        • Switch to mode with greater assistance (e.g., AC, PRVC).
        • Address reversible underlying disorders (e.g., asthma exacerbation, AECOPD, acute heart failure, pneumothorax).
• If patient-ventilator dyssynchrony present: Increase sedation and consider paralysis.

Hemodynamic compromise in mechanically ventilated patients [3][11][71]

• Mechanism: PPV can cause or exacerbate shock (see “Effects” in “Positive pressure ventilation”).
• Aggravating factors
  • Induction agents with vasodilatory side effects (e.g., propofol)
  • RV dysfunction
  • Hypovolemia, peripheral vasodilation
  • ↑ PEEP and auto-PEEP
• Consequences
  • Obstructive shock
  • Circulatory collapse
  • Cardiac arrest
• Management
  • Treat DHI if present.
  • Decrease PEEP if tolerated.
  • Optimize fluid resuscitation.
  • Consider vasopressor infusions and push-dose pressors.

Patient-ventilator dyssynchrony [72]

• Description
  • A mismatch between patient and equipment
    • Airflow: The flow delivered by the ventilator is inconsistent with the patient's demand.
    • Phase: The timing and cycle of ventilator-delivered breaths are misaligned with the patient's respiratory drive.
• Recognition
  • Often identified by nursing staff or respiratory therapists
  • Possible clues [72]
    • Biological: unstable vital signs, pressure/flow waveform patterns, changes in ABG parameters, EtCO₂
    • Behavioral: coughing, signs of increased respiratory effort , agitation
• Aggravating factors
  • Patient-related
    • ↑ Respiratory drive: hypoxemia, hypercapnia, metabolic acidosis, hypermetabolic states, anxiety, fever, pain, medications
    • ↓ Respiratory drive: metabolic alkalosis, medications (e.g., sedatives, opioids), hypometabolic states
    • Lung mechanics: weak respiratory musculature, prolonged expiration time (e.g., obstructive lung disease), impaired neuromuscular control
    • Underlying disease: delirium, obstructive lung disease, ARDS, pulmonary edema, pulmonary embolism, pneumothorax
    • Other conditions: poor positioning, chest wall splinting, abdominal distention
  • Ventilator-related
    • Airway: mucus plugs, poor sizing
    • Leaks and disconnections in system
    • Increased instrumental dead space
    • FiO₂ too low
    • Inappropriate PEEP setting
    • Inappropriate triggers sensitivity
• Consequences
  • Discomfort
  • Hypoxia, barotrauma
  • Prolonged mechanical ventilation
  • Patient biting on ET tube, causing obstruction
• Management
  • Check ventilator circuitry for reversible malfunction.
  • Check ventilation monitors, waveforms, and alarms.
  • Examine the patient and order appropriate diagnostic tests (see “aggravating factors” above).
  • Collaborate with nursing staff and respiratory therapists for guidance.
  • Identify and treat the underlying cause.
  • Change ventilation parameters or mode to match patient needs.
  • Ensure adequate patient sedation in line with patient needs and goals of care.

Dynamic hyperinflation (DHI) [30][66]

• Description: progressively increased airway and intrathoracic pressures with each ventilation cycle
• Mechanism: Initiation of new breath before full expiration → breath stacking → progressively increased intrathoracic pressure
• Recognition
  • Respiratory distress
  • High pressure or low volume alarms
  • Hemodynamic instability
• Aggravating factors
  • Patients at high risk of developing auto-PEEP (e.g., patients with obstructive lung disease)
  • Poorly set ventilatory parameters (e.g., Vt/RR that are too high)
• Consequences
  • Increased work of breathing
  • Ineffective ventilation
  • Ventilator dyssynchrony
  • Barotrauma and volutrauma (see VILI)
  • Shock and circulatory collapse (see “hemodynamic comprise” above)
  • Unreliable monitoring
• Management
  • Disconnect the patient from the ventilator.
  • Externally compress the chest to deflate the lung.
  • Adjust ventilator settings before reconnecting (see “prevention” below).
  • Identify and treat any underlying reversible conditions.
    • Treat expiratory airflow obstruction: e.g., bronchodilators, suctioning.
    • Treat central drivers of hyperventilation: e.g., analgesia, sedation.
    • Treat refractory patient-ventilator dyssynchrony; e.g., muscle relaxants.
• Prevention
  • Goal: Allow more expiratory time to minimize auto-PEEP.
  • Choose mode with ↓ risk of DHI: e.g., PCV
  • Parameter adjustments
    • Decrease V_t.
    • Decrease RR.
    • Decrease I:E ratio.
    • Increase VI.

There are currently no accepted consensus guidelines on appropriate alarm settings or responses. Ranges vary by patient, ventilator model, type of critical care unit, and institution. Refer to local alarm thresholds and ranges, or consult an experienced critical care specialist and/or respiratory therapist. [27][54][73][74]

Treat ventilator alarms as a critical issue. Beware of alarm fatigue.

• One-Minute Telegram 145-2026-3/3: Less restraint for ventilated ICU patients does not improve outcomes
• One-Minute Telegram 145-2026-1/3: High-flow vs. standard O2 in the ICU: less intubation, similar mortality
• One-Minute Telegram 108-2024-1/3: Can high-intensity NIPPV prevent intubation in AECOPD?
• One-Minute Telegram 20-2021-1/3: Better outcomes after implementation of critical care management protocols?

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