Ventilator-Induced Lung Injury (VILI): An Overview (2025)

A ventilator-induced lung injury (VILI) is a critical concern in the management of patients requiring mechanical ventilation. While mechanical ventilation is a lifesaving intervention, improper settings or prolonged use can lead to VILI, causing significant damage to the lungs.

This injury results from factors such as excessive pressure, volume, or oxygen, which can compromise lung tissue integrity and exacerbate underlying conditions.

Understanding the mechanisms, risk factors, and preventive strategies for VILI is essential for optimizing patient outcomes and minimizing harm.

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What is a Ventilator-Induced Lung Injury (VILI)?

Ventilator-induced lung injury (VILI) refers to the lung damage that occurs as a result of mechanical ventilation, particularly when ventilator settings are not properly adjusted. This type of injury can be caused by excessive pressure, large tidal volumes, high oxygen concentrations, and repetitive opening and closing of alveoli.

VILI can exacerbate pre-existing lung conditions or create new lung pathologies, leading to complications such as acute respiratory distress syndrome (ARDS).

Understanding the mechanisms and implementing lung-protective ventilation strategies are essential to prevent or minimize the occurrence of VILI in patients requiring mechanical ventilation.

Causes

Ventilator-induced lung injuries (VILI) result from the mechanical forces exerted on the lungs during mechanical ventilation, particularly when the lungs are stretched beyond their natural capacity for expansion.

This type of injury primarily occurs due to elevated transpulmonary pressure—the difference between the pressure inside the alveoli and the pleural space—during positive-pressure ventilation. High levels of positive end-expiratory pressure (PEEP) can also contribute to lung damage by maintaining excessive pressure within the lungs.

Several factors increase the risk of VILI, including the use of high oxygen concentrations, elevated airway pressures, prolonged mechanical ventilation, and pre-existing lung conditions in the patient.

Note: Careful management of ventilator settings and consideration of the patient’s underlying lung health are crucial in minimizing the risk of VILI.

Types

Various types of ventilator-induced lung injuries can occur, depending on the specific mechanism of injury:

• Barotrauma: Occurs when excessive pressure is applied to the lungs during mechanical ventilation. High inspiratory pressures can cause overdistension of the alveoli, leading to ruptures in the lung tissue, air leaks, and the development of conditions like pneumothorax or subcutaneous emphysema.
• Volutrauma: Caused by the delivery of excessively large tidal volumes during ventilation. Overdistension of alveoli due to high tidal volumes leads to mechanical stress on lung tissues, resulting in inflammation, cell damage, and potential long-term injury to the lung parenchyma.
• Atelectrauma: Occurs due to the repetitive opening and closing of collapsed alveoli during the ventilatory cycle. This repetitive stress can cause shear forces on the alveolar walls, leading to inflammation, increased permeability, and subsequent injury to the lung tissue.
• Oxygen Toxicity: Prolonged exposure to high concentrations of oxygen can lead to oxygen toxicity, which damages the delicate epithelial cells lining the alveoli. This oxidative stress can result in inflammation, cell death, and exacerbation of lung injury.
• Biotrauma: Refers to the inflammatory response triggered by mechanical ventilation. The physical forces exerted on lung tissues during ventilation can activate the release of pro-inflammatory cytokines and other mediators, leading to a systemic inflammatory response that can worsen lung injury and contribute to the development of ARDS.
• Shear Stress: Occurs when there is a significant difference in the pressure or volume between adjacent lung units during mechanical ventilation. This can cause mechanical disruption at the interface of these units, leading to lung tissue damage.

Note: Preventing these types of VILI requires careful adjustment of ventilator settings, adherence to lung-protective ventilation strategies, and close monitoring of the patient’s respiratory status.

Risk Factors

The risk factors for a ventilator-induced lung injury (VILI) include:

• High Tidal Volumes: Using large tidal volumes during mechanical ventilation can overstretch the alveoli, leading to volutrauma, which is a major contributor to VILI. Overdistension of the lung tissue increases the risk of alveolar rupture and subsequent lung injury.
• Elevated Airway Pressures: High peak and plateau pressures can cause barotrauma, resulting in physical damage to the lung structures. This is especially risky in patients with already compromised lung compliance, where the lungs are less able to tolerate excessive pressure.
• High Positive End-Expiratory Pressure (PEEP): While PEEP is used to keep the alveoli open and improve oxygenation, excessively high PEEP levels can lead to overinflation of the lungs, increasing the risk of VILI. It can also elevate transpulmonary pressures, further stressing the lung tissue.
• Prolonged Duration of Mechanical Ventilation: The longer a patient remains on mechanical ventilation, the greater the cumulative exposure to the mechanical forces that can cause VILI. Extended ventilation periods increase the likelihood of lung injury, particularly if ventilator settings are not carefully managed.
• High Oxygen Concentrations (FiO2): Prolonged exposure to high fractions of inspired oxygen (FiO2) can lead to oxygen toxicity, causing oxidative stress and inflammation in the lungs. This increases the susceptibility to VILI by damaging the lung tissue.
• Pre-existing Lung Conditions: Patients with underlying lung diseases, such as chronic obstructive pulmonary disease (COPD), acute respiratory distress syndrome (ARDS), or pulmonary fibrosis, are at higher risk of developing VILI. These conditions often involve reduced lung compliance and increased vulnerability to the mechanical forces of ventilation.
• Inappropriate Ventilator Settings: Poorly adjusted ventilator settings, such as excessive respiratory rates or inadequate PEEP, can contribute to the development of VILI. Tailoring ventilator parameters to the individual patient’s lung mechanics is essential to minimize the risk.
• Repetitive Alveolar Opening and Closing: The repeated collapse and reopening of alveoli during ventilation, often due to insufficient PEEP, can cause atelectrauma. This shear stress on the alveoli contributes significantly to VILI.
• Systemic Inflammatory Response: Mechanical ventilation can trigger a systemic inflammatory response, particularly in the context of biotrauma. This inflammatory process not only exacerbates lung injury but can also lead to multi-organ dysfunction.

Note: Understanding these risk factors is key to implementing protective ventilation strategies that reduce the incidence of VILI and improve patient outcomes.

Signs and Symptoms

The signs and symptoms of a ventilator-induced lung injury (VILI) can vary depending on the severity of the injury and the underlying cause.

Some examples include:

• Worsening Oxygenation: A decline in the patient’s oxygenation status, despite adjustments in ventilator settings, can be an early sign of VILI. This may manifest as a decrease in arterial oxygen levels (PaO2) or an increase in the need for supplemental oxygen.
• Increased Peak Airway Pressures: A rise in peak airway pressures during mechanical ventilation, without a corresponding change in tidal volume or respiratory rate, may indicate increased resistance in the airways or decreased lung compliance, both of which can be associated with VILI.
• Decreased Lung Compliance: Reduced lung compliance, where the lungs become stiffer and less able to expand, is a hallmark of VILI. This can be observed as an increase in plateau pressures and a decrease in the amount of air the lungs can hold for a given pressure.
• Radiographic Changes: Chest X-rays or CT scans may reveal new or worsening infiltrates, consolidation, or signs of pulmonary edema, all of which can be indicative of VILI. These imaging findings suggest that the lung tissue has been damaged or inflamed.
• Dyspnea and Respiratory Distress: Patients may exhibit signs of respiratory distress, such as labored breathing, tachypnea (increased respiratory rate), and use of accessory muscles. Although patients on mechanical ventilation may not be able to communicate these symptoms, monitoring their respiratory patterns can provide clues.
• Pulmonary Edema: VILI can lead to non-cardiogenic pulmonary edema, where fluid accumulates in the alveoli due to increased capillary permeability. This condition can severely impair gas exchange and is often seen in advanced stages of lung injury.
• Hypotension: As VILI progresses, it may lead to a systemic inflammatory response, which can result in hypotension (low blood pressure). This can be a sign of worsening lung injury and the development of complications like acute respiratory distress syndrome (ARDS) or septic shock.
• Hypocapnia or Hypercapnia: Depending on the type and extent of lung injury, patients may develop abnormalities in carbon dioxide levels. Hypocapnia (low CO2) may occur due to hyperventilation, while hypercapnia (high CO2) may result from impaired gas exchange due to lung damage.
• Respiratory Acidosis: As VILI impairs the lungs’ ability to remove carbon dioxide, respiratory acidosis can develop. This condition is characterized by an increase in blood acidity and may be detected through arterial blood gas (ABG) analysis.
• Air Leaks: Barotrauma from VILI can cause air leaks, leading to conditions like pneumothorax (collapsed lung), pneumomediastinum, or subcutaneous emphysema. These are serious complications that require prompt intervention.

Note: Recognizing these signs and symptoms is essential for early identification and management of VILI, allowing for timely adjustments to ventilator settings and other therapeutic interventions.

Treatment

The treatment of ventilator-induced lung injury (VILI) focuses on implementing lung-protective strategies that minimize further damage to the lungs.

Key approaches include:

• Low Tidal Volume Ventilation: Reducing the tidal volume—the amount of air delivered with each breath—helps prevent lung overdistension, thereby decreasing the risk of volutrauma. This strategy is particularly effective in protecting the alveoli from excessive stretching.
• Low Airway Pressure Ventilation: Lowering the pressures applied to the lungs during mechanical ventilation reduces the risk of barotrauma, which occurs when excessive pressure damages the lung tissue. This approach aims to maintain ventilation while minimizing pressure-induced injury.
• Low Plateau Pressures: Plateau pressure is the pressure in the lungs at the end of inspiration, just before exhalation begins. Keeping plateau pressures low is crucial for preventing overdistension of the lungs and protecting the delicate alveolar structures from damage.
• Low Driving Pressures: Driving pressure, calculated as the difference between plateau pressure and PEEP (positive end-expiratory pressure), represents the force used to deliver air into the lungs. Lowering driving pressure can reduce the risk of barotrauma by limiting the mechanical stress on the lung tissue.
• Optimized FiO2: To avoid oxygen toxicity, it’s essential to use the lowest fraction of inspired oxygen (FiO2) that still maintains adequate oxygenation. This strategy reduces the harmful effects of high oxygen levels while ensuring the patient receives sufficient oxygen.
• Appropriate PEEP Levels: Setting PEEP at the lowest level that still supports adequate oxygenation helps prevent alveolar collapse without overinflating the lungs. This balance is particularly important in patients with ARDS, where lung-protective ventilation is critical.

Note: Effective management of VILI requires a multifaceted approach, with careful monitoring and adjustment of ventilator settings, combined with supportive therapies to minimize lung injury and promote healing.

Lung Protective Strategies

Lung protective strategies are a set of clinical practices and techniques used in mechanical ventilation to minimize the risk of ventilator-induced lung injury (VILI) and to protect the lungs from further damage.

To minimize the risk of lung injury during mechanical ventilation, the following key parameters should be adhered to:

• Tidal Volume: 4–8 mL/kg of predicted body weight
• Plateau Pressure: Less than 28 cmH2O
• Driving Pressure: Less than 15 cmH2O
• FiO2: Adjusted to maintain PaO2 between 55–80 mmHg
• SpO2: Target range of 88–95%

Reducing tidal volume helps prevent alveolar overdistension, thereby lowering the risk of volutrauma. Keeping plateau pressure below 28 cmH2O minimizes the risk of barotrauma and protects the alveoli from excessive mechanical stress.

Maintaining a low driving pressure (the difference between plateau pressure and PEEP) reduces the mechanical load on the lungs, helping to prevent barotrauma. FiO2 should be titrated to ensure adequate oxygenation while minimizing the risk of oxygen toxicity.

Furthermore, maintaining oxygen saturation within the normal range ensures sufficient oxygen delivery to tissues while avoiding excessive oxygen exposure.

Additional Considerations

• Patient-Ventilator Dyssynchrony: Strive to avoid dyssynchrony between the patient’s breathing efforts and the ventilator’s delivered breaths, as this can increase the risk of lung injury.
• Auto-PEEP and Air Trapping: Preventing auto-PEEP (unintended positive end-expiratory pressure) and air trapping is essential, as these can lead to increased intrathoracic pressure and exacerbate lung injury.

Individualized Approach

The most appropriate treatment plan should be tailored to the specific cause and severity of the patient’s ventilator-induced lung injury (VILI), as well as their underlying health condition.

Close monitoring and regular reassessment of the patient’s clinical status are crucial to ensure that the chosen ventilation strategy is both effective and safe. Adjustments should be made as needed to optimize outcomes and minimize the risk of further lung damage.

FAQs About Ventilator-Induced Lung Injuries

What is VILI in Medical Terms?

VILI, or ventilator-induced lung injury, refers to lung damage that occurs as a result of mechanical ventilation.

This injury arises when the mechanical forces applied during ventilation—such as excessive pressure, large tidal volumes, or high oxygen concentrations—compromise lung tissue integrity.

VILI can exacerbate pre-existing lung conditions or create new lung pathologies, leading to complications like acute respiratory distress syndrome (ARDS).

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How to Diagnose a VILI?

Diagnosing VILI involves a combination of clinical assessment, imaging, and monitoring of ventilator parameters.

Clinicians look for signs of worsening oxygenation, increased airway pressures, and reduced lung compliance. Imaging studies like chest x-rays or CT scans may reveal new infiltrates, pulmonary edema, or other signs of lung injury.

Blood gas analysis may show abnormalities in oxygen and carbon dioxide levels. Diagnosis also includes ruling out other causes of lung injury, such as infection or heart failure.

What is the Difference Between VALI and VILI?

Ventilator-associated lung injury (VALI) and ventilator-induced lung injury (VILI) are related but distinct terms. VILI refers specifically to lung injury directly caused by the mechanical forces of ventilation, such as high pressures or volumes.

VALI, on the other hand, is a broader term that encompasses any lung injury associated with the use of mechanical ventilation, including those caused by factors like infection or inflammation, which may not be directly related to the mechanical forces.

What are the Risks of Ventilator-Induced Lung Injury?

The risks of ventilator-induced lung injury include the potential for barotrauma (damage from high airway pressures), volutrauma (damage from large tidal volumes), oxygen toxicity (damage from high oxygen concentrations), and atelectrauma (damage from repetitive opening and closing of alveoli).

Patients with pre-existing lung conditions, those requiring prolonged mechanical ventilation, and those exposed to inappropriate ventilator settings are at higher risk for developing VILI.

These injuries can lead to severe complications, such as acute respiratory distress syndrome (ARDS), prolonged ventilator dependency, and increased mortality.

What Damage Does a Ventilator Do to Your Lungs?

A ventilator can cause several types of lung damage if not properly managed. This includes:

• Barotrauma: Injury from excessive pressure in the airways, which can cause alveolar rupture and air leaks such as pneumothorax.
• Volutrauma: Damage from delivering large tidal volumes, leading to overstretching and tearing of the lung tissue.
• Oxygen Toxicity: Prolonged exposure to high concentrations of oxygen can result in oxidative stress and damage to the lung’s delicate structures.
• Atelectrauma: Injury from the repetitive collapse and reopening of alveoli, causing shear stress on the lung tissue.
• Biotrauma: An inflammatory response triggered by mechanical forces, which can exacerbate lung injury and potentially lead to systemic inflammation.

How Common Is a Ventilator-Induced Lung Injury?

The exact incidence of ventilator-induced lung injury (VILI) varies, but it is a significant concern in critical care settings. Patients with conditions such as acute respiratory distress syndrome (ARDS) or those requiring prolonged mechanical ventilation are at higher risk.

Studies suggest that a considerable percentage of patients on mechanical ventilation, especially those with ARDS, may develop some degree of VILI, making its prevention a critical focus in critical care.

What is Permissive Hypercapnia Used For?

Permissive hypercapnia is a lung-protective strategy used during mechanical ventilation where higher levels of carbon dioxide (CO2) are tolerated in the blood to minimize lung injury.

By allowing for higher CO2 levels, this approach enables the use of lower tidal volumes and reduced airway pressures, which can help prevent volutrauma and barotrauma.

Permissive hypercapnia is particularly useful in managing patients with acute respiratory distress syndrome (ARDS) to reduce the risk of ventilator-induced lung injury.

How to Prevent a Ventilator-Induced Lung Injury?

Preventing ventilator-induced lung injury (VILI) involves using lung-protective ventilation strategies:

• Low Tidal Volume Ventilation: Using smaller tidal volumes (4–8 mL/kg) to prevent overdistension of the alveoli.
• Low Plateau Pressure: Keeping plateau pressures below 28 cmH2O to avoid excessive pressure on the lungs.
• Appropriate PEEP Levels: Using PEEP to keep alveoli open without causing overinflation.
• Minimized Oxygen Concentrations: Reducing FiO2 to the lowest level necessary to maintain adequate oxygenation, avoiding oxygen toxicity.
• Avoiding Patient-Ventilator Dyssynchrony: Ensuring that the ventilator settings are in sync with the patient’s breathing effort to prevent additional lung stress.
• Close Monitoring: Regularly assessing the patient’s respiratory status and adjusting ventilator settings as needed to optimize ventilation while minimizing the risk of lung injury.

Final Thoughts

Ventilator-induced lung injury (VILI) represents a significant challenge in the management of patients requiring mechanical ventilation. Despite its lifesaving potential, mechanical ventilation can lead to severe lung damage if not carefully managed.

Understanding the mechanisms, risk factors, and types of VILI is crucial for implementing effective lung-protective strategies.

By adhering to key parameters such as low tidal volumes, optimized PEEP levels, and careful management of FiO2, healthcare providers can minimize the risk of VILI.

Ultimately, a personalized approach that includes regular reassessment and adjustment of ventilator settings is essential to ensure the safety and well-being of patients undergoing mechanical ventilation.