Ventilator-associated lung injury

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Ventilator-associated lung injury
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Ventilator-associated lung injury (VALI) is an acute lung injury that develops during mechanical ventilation and is termed ventilator-induced lung injury (VILI) if it can be proven that the mechanical ventilation caused the acute lung injury. In contrast, ventilator-associated lung injury (VALI) exists if the cause cannot be proven. VALI is the appropriate term in most situations because it is virtually impossible to prove what actually caused the lung injury in the hospital. [1]

Contents

Cause

It is generally regarded, based on animal models and human studies, that volutrauma is the most harmful aspect of mechanical ventilation. [2] [3] [4] This may be regarded as the over-stretching of the airways and alveoli.[ citation needed ]

During mechanical ventilation, the flow of gas into the lung will take the path of least resistance. Areas of the lung that are collapsed (atelectasis) or filled with secretions will be underinflated, while those areas that are relatively normal will be overinflated. These areas will become overdistended and injured. This may be reduced by using smaller tidal volumes. [5] [6]

During positive pressure ventilation, atelectatic regions will inflate, however, the alveoli will be unstable and will collapse during the expiratory phase of the breath (atelectotrauma). This repeated alveolar collapse and expansion (RACE) is thought to cause VALI. By opening the lung and keeping the lung open RACE (and VALI) is reduced. [7]

Another possible ventilator-associated lung injury is known as biotrauma. Biotrauma involves the lung suffering injury from any mediators of the inflammatory response or from bacteremia.

Finally oxygen toxicity contributes to ventilator-associated lung injury through several mechanisms including oxidative stress.

Possible reasons for predisposition to VALI include:

Pathogenesis

Overdistension of alveoli and cyclic atelectasis (atelectotrauma) are the primary causes for alveolar injury during positive pressure mechanical ventilation. Severe injury to alveoli causes swelling of the tissues (edema) in the lungs, bleeding of the alveoli, loss of surfactant (decrease in lung compliance) and complete alveoli collapse (biotrauma). [1] [8] High flow rates are associated with rheotrauma, high volumes with volutrauma and pressures with barotrauma. Collectively these may be converted into a single unit of mechanical power.[ citation needed ]

Diagnosis

VALI does not need to be distinguished from progressive ALI/ARDS because management is the same in both. Additionally, definitive diagnosis of VALI may not be possible because of lack of sign or symptoms.[ citation needed ]

Prevention

Preventing alveolar overdistension

Alveolar overdistension is mitigated by using small tidal volumes, maintaining a low plateau pressure, and most effectively by using volume-limited ventilation. A 2018 systematic review by The Cochrane Collaboration provided evidence that low tidal volume ventilation reduced post operative pneumonia and reduced the requirement for both invasive and non invasive ventilation after surgery [9]

Preventing cyclic atelectasis (atelectotrauma)

Applied positive end-expiratory pressure (PEEP) is the principal method used to keep the alveoli open and lessen cyclic atelectasis.

Open lung ventilation

Open lung ventilation is a ventilatory strategy that combines small tidal volumes (to lessen alveolar overdistension) and an applied PEEP above the low inflection point on the pressure-volume curve (to lessen cyclic atelectasis).

High frequency ventilation is thought to reduce ventilator-associated lung injury, especially in the context of ARDS and acute lung injury. [7]

Permissive hypercapnia and hypoxaemia allow the patient to be ventilated at less aggressive settings and can, therefore, mitigate all forms of ventilator-associated lung injury

Epidemiology

VALI is most common in people receiving mechanical ventilation for acute lung injury or acute respiratory distress syndrome (ALI/ARDS). [1]

24 percent of people mechanically ventilated will develop VALI for reasons other than ALI or ARDS. [1] The incidence is probably higher among people who already have ALI/ARDS, but estimates vary widely. [1] The variable estimates reflect the difficulty in distinguishing VALI from progressive ALI/ARDS. [1]

Related Research Articles

<span class="mw-page-title-main">Mechanical ventilation</span> Method to mechanically assist or replace spontaneous breathing

Mechanical ventilation or assisted ventilation is the medical term for using a machine called a ventilator to fully or partially provide artificial ventilation. Mechanical ventilation helps move air into and out of the lungs, with the main goal of helping the delivery of oxygen and removal of carbon dioxide. Mechanical ventilation is used for many reasons, including to protect the airway due to mechanical or neurologic cause, to ensure adequate oxygenation, or to remove excess carbon dioxide from the lungs. Various healthcare providers are involved with the use of mechanical ventilation and people who require ventilators are typically monitored in an intensive care unit.

<span class="mw-page-title-main">Tidal volume</span> Volume of air displaced between normal inhalation and exhalation

Tidal volume is the volume of air moved into or out of the lungs in one breath. In a healthy, young human adult, tidal volume is approximately 500 ml per inspiration at rest or 7 ml/kg of body mass.

<span class="mw-page-title-main">Pulmonary edema</span> Fluid accumulation in the tissue and air spaces of the lungs

Pulmonary edema, also known as pulmonary congestion, is excessive liquid accumulation in the tissue and air spaces of the lungs. It leads to impaired gas exchange and may cause hypoxemia and respiratory failure. It is due to either failure of the left ventricle of the heart to remove oxygenated blood adequately from the pulmonary circulation, or an injury to the lung tissue directly or blood vessels of the lung.

<span class="mw-page-title-main">Acute respiratory distress syndrome</span> Human disease

Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). For those who survive, a decreased quality of life is common.

Positive end-expiratory pressure (PEEP) is the pressure in the lungs above atmospheric pressure that exists at the end of expiration. The two types of PEEP are extrinsic PEEP and intrinsic PEEP. Pressure that is applied or increased during an inspiration is termed pressure support.PEEP is a therapeutic parameter set in the ventilator, or a complication of mechanical ventilation with air trapping (auto-PEEP).

High-frequency ventilation is a type of mechanical ventilation which utilizes a respiratory rate greater than four times the normal value and very small tidal volumes. High frequency ventilation is thought to reduce ventilator-associated lung injury (VALI), especially in the context of ARDS and acute lung injury. This is commonly referred to as lung protective ventilation. There are different types of high-frequency ventilation. Each type has its own unique advantages and disadvantages. The types of HFV are characterized by the delivery system and the type of exhalation phase.

Pulmonary hygiene, formerly referred to as pulmonary toilet, is a set of methods used to clear mucus and secretions from the airways. The word pulmonary refers to the lungs. The word toilet, related to the French toilette, refers to body care and hygiene; this root is used in words such as toiletry that also relate to cleansing.

<span class="mw-page-title-main">Diffuse alveolar damage</span> Medical condition

Diffuse alveolar damage (DAD) is a histologic term used to describe specific changes that occur to the structure of the lungs during injury or disease. Most often DAD is described in association with the early stages of acute respiratory distress syndrome (ARDS). It is important to note that DAD can be seen in situations other than ARDS (such as acute interstitial pneumonia) and that ARDS can occur without DAD.

<span class="mw-page-title-main">Airway pressure release ventilation</span> Pressure control mode of mechanical ventilation

Airway pressure release ventilation (APRV) is a pressure control mode of mechanical ventilation that utilizes an inverse ratio ventilation strategy. APRV is an applied continuous positive airway pressure (CPAP) that at a set timed interval releases the applied pressure. Depending on the ventilator manufacturer, it may be referred to as BiVent. This is just as appropriate to use, since the only difference is that the term APRV is copyrighted.

Modes of mechanical ventilation are one of the most important aspects of the usage of mechanical ventilation. The mode refers to the method of inspiratory support. In general, mode selection is based on clinician familiarity and institutional preferences, since there is a paucity of evidence indicating that the mode affects clinical outcome. The most frequently used forms of volume-limited mechanical ventilation are intermittent mandatory ventilation (IMV) and continuous mandatory ventilation (CMV). There have been substantial changes in the nomenclature of mechanical ventilation over the years, but more recently it has become standardized by many respirology and pulmonology groups. Writing a mode is most proper in all capital letters with a dash between the control variable and the strategy.

Continuous mandatory ventilation (CMV) is a mode of mechanical ventilation in which breaths are delivered based on set variables. Still used in the operating room, in previous nomenclature, CMV referred to "controlled mechanical ventilation", a mode of ventilation characterized by a ventilator that makes no effort to sense patient breathing effort. In continuous mandatory ventilation, the ventilator can be triggered either by the patient or mechanically by the ventilator. The ventilator is set to deliver a breath according to parameters selected by the operator. "Controlled mechanical ventilation" is an outdated expansion for "CMV"; "continuous mandatory ventilation" is now accepted standard nomenclature for mechanical ventilation. CMV today can assist or control itself dynamically, depending on the transient presence or absence of spontaneous breathing effort. Thus, today's CMV would have been called ACV in older nomenclature, and the original form of CMV is a thing of the past. But despite continual technological improvement over the past half century, CMV may still be uncomfortable for the patient.

Within the medical field of respiratory therapy, Open lung ventilation is a strategy that is utilized by several modes of mechanical ventilation to combine low tidal volume and applied PEEP to maximize recruitment of alveoli. The low tidal volume aims to minimize alveolar overdistention and the PEEP minimizes cyclic atelectasis. Working in tandem the effects from both decrease the risk of ventilator-associated lung injury.

Fraction of inspired oxygen (FIO2), correctly denoted with a capital I, is the molar or volumetric fraction of oxygen in the inhaled gas. Medical patients experiencing difficulty breathing are provided with oxygen-enriched air, which means a higher-than-atmospheric FIO2. Natural air includes 21% oxygen, which is equivalent to FIO2 of 0.21. Oxygen-enriched air has a higher FIO2 than 0.21; up to 1.00 which means 100% oxygen. FIO2 is typically maintained below 0.5 even with mechanical ventilation, to avoid oxygen toxicity, but there are applications when up to 100% is routinely used.

Dynamic hyperinflation is a phenomenon that occurs when a new breath begins before the lung has reached the static equilibrium volume. In simpler terms, this means that a new breath starts before the usual amount of air has been breathed out, leading to a build-up of air in the lungs, and causing breathing in and out to take place when the lung is nearly full.

Acute inhalation injury may result from frequent and widespread use of household cleaning agents and industrial gases. The airways and lungs receive continuous first-pass exposure to non-toxic and irritant or toxic gases via inhalation. Irritant gases are those that, on inhalation, dissolve in the water of the respiratory tract mucosa and provoke an inflammatory response, usually from the release of acidic or alkaline radicals. Smoke, chlorine, phosgene, sulfur dioxide, hydrogen chloride, hydrogen sulfide, nitrogen dioxide, ozone, and ammonia are common irritants.

Prone ventilation, sometimes called prone positioning or proning, refers to mechanical ventilation with the patient lying face-down (prone). It improves oxygenation in most patients with acute respiratory distress syndrome (ARDS) and reduces mortality. The earliest trial investigating the benefits of prone ventilation occurred in 1976. Since that time, many meta-analyses and one randomized control trial, the PROSEVA trial, have shown an increase in patients' survival with the more severe versions of ARDS. There are many proposed mechanisms, but they are not fully delineated. The proposed utility of prone ventilation is that this position will improve lung mechanics, improve oxygenation, and increase survival. Although improved oxygenation has been shown in multiple studies, this position change's survival benefit is not as clear. Similar to the slow adoption of low tidal volume ventilation utilized in ARDS, many believe that the investigation into the benefits of prone ventilation will likely be ongoing in the future.

<span class="mw-page-title-main">Mechanical power (medicine)</span>

In medicine, mechanical power is a measure of the amount of energy imparted to a patient by a mechanical ventilator.

<span class="mw-page-title-main">Atelectotrauma</span> Damage caused to the lung by mechanical ventilation

Atelectotrauma, atelectrauma, cyclic atelectasis or repeated alveolar collapse and expansion (RACE) are medical terms for the damage caused to the lung by mechanical ventilation under certain conditions. When parts of the lung collapse at the end of expiration, due to a combination of a diseased lung state and a low functional residual capacity, then reopen again on inspiration, this repeated collapsing and reopening causes shear stress which has a damaging effect on the alveolus. Clinicians attempt to reduce atelectotrauma by ensuring adequate positive end-expiratory pressure (PEEP) to maintain the alveoli open in expiration. This is known as open lung ventilation. High frequency oscillatory ventilation (HFOV) with its use of 'super CPAP' is especially effective in preventing atelectotrauma since it maintains a very high mean airway pressure (MAP), equivalent to a very high PEEP. Atelectotrauma is one of several means by which mechanical ventilation may damage the lungs leading to ventilator-associated lung injury. The other means are volutrauma, barotrauma, rheotrauma and biotrauma. Attempts have been made to combine these factors in an all encompassing term: mechanical power.

<span class="mw-page-title-main">Pathophysiology of acute respiratory distress syndrome</span>

The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure. It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. Additional common findings in ARDS include partial collapse of the lungs (atelectasis) and low levels of oxygen in the blood (hypoxemia). The clinical syndrome is associated with pathological findings including pneumonia, eosinophilic pneumonia, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, and diffuse alveolar damage (DAD). Of these, the pathology most commonly associated with ARDS is DAD, which is characterized by a diffuse inflammation of lung tissue. The triggering insult to the tissue usually results in an initial release of chemical signals and other inflammatory mediators secreted by local epithelial and endothelial cells.

<span class="mw-page-title-main">Pendelluft</span>

Pendelluft refers to the movement of gas between two regions of the lung, usually between regions of differing compliance or airway resistance. Pendelluft is an important physiological concept to take into account during mechanical ventilation, particularly in patients with an open thorax, severe bronchospasm, or with heterogeneous lung compliance. It was first published as a physiological concept in 1956.

References

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  4. Donn, S M (13 October 2005). "Minimising ventilator induced lung injury in preterm infants". Archives of Disease in Childhood: Fetal and Neonatal Edition. 91 (3): F226–F230. doi:10.1136/adc.2005.082271. PMC   2672704 . PMID   16632652.
  5. Ng Calvin SH, Arifi Ahmed A, Wan Song, Ho Anthony MH, Wan Innes YP, Wong Eric MC, Yim Anthony PC (2008). "Ventilation during Cardiopulmonary Bypass: Impact on Cytokine Response and Cardiopulmonary Function". Ann Thorac Surg. 85 (1): 154–62. doi: 10.1016/j.athoracsur.2007.07.068 . PMID   18154801.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. Ng Calvin SH, Wan Song, Ho Anthony MH, Underwood Malcolm J (2009). "Gene Expression Changes with "Non-injurious" Ventilation Strategy". Crit Care. 13 (2): 403. doi: 10.1186/cc7719 . PMC   2689456 . PMID   19291277.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. 1 2 Krishnan JA, Brower RG (2000). "High-frequency ventilation for acute lung injury and ARDS". Chest. 118 (3): 795–807. doi: 10.1378/chest.118.3.795 . PMID   10988205. Free Full Text.
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  9. Guay, Joanne; Ochroch, Edward A; Kopp, Sandra (2018-07-09). "Intraoperative use of low volume ventilation to decrease postoperative mortality, mechanical ventilation, lengths of stay and lung injury in adults without acute lung injury". Cochrane Database of Systematic Reviews. 7 (10): CD011151. doi:10.1002/14651858.cd011151.pub3. ISSN   1465-1858. PMC   6513630 . PMID   29985541.