Ventilator Induced Lung Injury (VILI) is an acute lung injury that occurs because of volutrauma and excessive use of oxygen. While it not a new concept, the injury occurs when the lung is damaged by the action of mechanical ventilation. Notably, mechanical ventilation has largely been used to support patients who are acutely ill for many decades. However, clinicians and other medical practitioners have become aware of the complications and drawbacks of mechanical ventilation regardless of its life-saving potential. Since its introduction to the medical field and practice, mechanical ventilation for treatment of patients with acute respiratory failure has attracted huge concerns. According to the findings of various researches, the use of mechanical ventilation may severely affect a patient’s lungs. One of the major possible adverse effects of mechanical ventilation of the lungs is Ventilator Induced Lung Injury.
Etiology of VILI:
The main factor that causes Ventilator Induced Lung Injury is the over stretching of the alveoli and the airways. This over stretching is mainly caused by mechanical ventilation since the flow of gas into the lung is likely to take the path of least resistance during the process. During mechanical ventilation, collapsed areas of the lung or those filled with secretions will be underinflated while the relatively normal ones will be overinflated. As a result, these lung areas are likely to become injured or over distended, which can be minimized through the use of smaller tidal volumes.
While several early clinical and experimental studies have suggested that mechanical ventilation could have adverse impacts on the lung, other studies have been conducted in attempts to refute the fact (Dreyfuss & Saumon, 1998). Despite of the lack of clear demonstration of a medical equivalent of the experimental observations, the probability that mechanical ventilation can actually worsen acute lung disease is now widely accepted. The demonstration of super-imposed Ventilator Induced Lung Injury during human acute respiratory distress syndrome may be deceptive. Since the concept is derived from animal studies, it has contributed to the total re-evaluation of the use of mechanical ventilation for patients with acute lung diseases and is the basis of present trends in the medical practice of mechanical ventilation.
In the early years, many patients with acute lung dysfunction could tolerate mechanical ventilation for prolonged periods without any adverse consequences. In the past two decades, it’s generally accepted that mechanical ventilation can either initiate or exacerbate lung injury and lead to patient mortality and morbidity. The process contributes to Ventilator Induced Lung Injury by affecting the lung surfactant and compliance function as well as resulting in air leaks (Tremblay & Slutsky, 2006).
There are several studies that have been conducted to determine whether mechanical ventilation can produce lung injury apart from air leaks. The studies have also focused on determining the specific ventilator settings in which the lung injuries occur. These analyses have demonstrated that ventilation of normal lungs with low pressures does not cause severe injury. Secondly, they have also revealed that ventilation with high pressures tend to produce perivascular edema. Furthermore, the studies have demonstrated that ventilation at high airway pressures without positive end expiratory pressure results in severe lung injury and even death. This is because positive end expiratory pressure bestows protection from alveolar edema because of the high inspiratory pressure ventilation.
Significance of Lung Distention:
The overall degree of lung distention or lung volume at the end of inspiration is usually the major determinant of the severity of Ventilator Induced Lung Injury. This is mainly because this injury and oedema usually occur when a particular degree of lung over-inflation is reached (Ricard, Dreyfuss & Saumon, 2003). Lung over-inflation basically occurs when the ventilation is increased at a specific end-inspiratory pressure. On the contrary, when the positive end expiratory pressure is added to obtain similar end-inspiratory pressure, it tends to slow the development of oedema and lessens the severity of tissue injury. However, the use of positive end expiratory pressure does not prevent the occurrence of microvascular permeability changes. However, greater oedema occurs when the positive end expiratory pressure contributes to extra over-inflation.
Currently, it’s evident that ventilation-induced pulmonary oedema is basically the outcome of significant changes in the permeability of the alveolar-capillary barrier. Oedema severity is likely to be enhanced when small increases in microvascular transmural pressure may add their impacts to those of changed permeability. In specific response to relatively high airway pressures, oedema develops more slowly in larger animals to an extent that they make the situation more complex.
High mechanical ventilation without positive end expiratory pressure may lessen the aerated volume and slowly contribute to mechanical non-uniformity. The resultant lung inhomogeneity will in turn facilitate the over-inflation of the more distensible and relatively healthier zones, which results in more positive feedback aggravation.
Risk Factors:
Generally, Ventilator Induced Lung Injury is common to patients receiving mechanical ventilation for acute respiratory distress syndrome or acute lung injury. While Ventilator Induced Lung Injury is mainly attributed to mechanical ventilation, there are other risk factors that are likely to contribute to the injury. These risk factors can be considered as factors that predispose a patient or an individual to the injury. According to the findings of several bench studies, several risk factors have been identified such as underlying lung disease, heterogeneous lung ventilation, aspiration, extremes of age, systemic inflammation, pulmonary edema, and surfactant dysfunction. These risk factors enhance the vulnerability of lungs to injury originating from mechanical ventilation. In most cases, a synergistic link was identified between mechanical ventilation and an underlying lung dysfunction or abnormality.
There are various reasons for the fact that pre-existing lung dysfunctions and abnormalities enhance vulnerability to mechanical Ventilator Induced Lung Injury. First, underlying abnormalities contribute to the need for excessive magnitude of force beyond the resilience of the existing parenchyma, which causes structural disruption. Secondly, the factors that predispose to injury originate as force is applied to the regions of the lung or weaken lung tissue. Similar to the genetic predisposition, the abnormalities also contributes to factors that promote inflammatory response or restrain tissue healing that enhance the lung’s susceptibility to Ventilator Induced Lung Injury.
Minimizing Ventilator Induced Lung Injury:
Even though mechanical ventilation is one of the positive outcomes of global technology developments with positive life-saving potential, it has contributed to Ventilator Induced Lung Injury. However, the prevalence of the injury is difficult to determine since pathology and occurrence of the injury is usually inseparable from that of acute respiratory distress syndrome and acute lung injury (Galvin & Granton, 2011). While various clinical initiatives should be taken to lessen the disease, the respiratory therapy field should be at the forefront since it’s associated with acute lung injury. Actually, the need for a respiratory therapist to take necessary measures in lessening the injury is linked to the fact that almost every patient with ALI/ARDS are increasingly vulnerable and at risk for Ventilator Induced Lung Injury.
A respiratory therapist needs to be aware that the necessity for mechanical ventilation in the operating room puts patients at risk for the injury. These medical practitioners also need to know that tidal hyperinflation in this population may be similarly harmful. Since no treatment for acute lung injury is definite, respiratory therapists need to adopt impeccable intensive care since it’s the cornerstone of management. The impeccable intensive care involves early anticipatory management and treatment of the primary cause. Initial anticipatory management helps in avoiding late complications and poor outcomes while treating the primary cause lessens the risk of Ventilator Induced Lung Injury (Feng et. al., 2011).
Notably, there are various approaches that can be used by respiratory therapists and other clinical practitioners to lessen Ventilator Induced Lung Injury. First, the therapists can adopt a lung protective strategy that incorporates the avoidance of lung over-inflation using a tidal volume restrictive strategy. The lung protective strategy can also include the use of an optimal level of positive end expiratory pressure in order to ensure that alveolar patency with successive permissive hypercapnia is a standard of care in the management of ALI/ARDS patients. Some of the major objectives of the strategy include lessening regional alveolar distension, atelectasis, oxygen mediated injury, diaphragm injury, and inflammation. The other approaches that can be used to lessen the injury include using high frequency oscillatory ventilation, positioning, neuromascular blocking agents, fluid therapy, and immunomodulation.
Conclusion:
Ventilator Induced Lung Injury is one of the common illnesses that occur among patients with acute lung injury. This disease is mainly attributed to the use of mechanical ventilator to save these patients though there are other risk factors that contribute to the injury.
References:
Dreyfuss, D. & Saumon, G. (1998, January 1). Ventilator-induced Lung Injury — Lessons from Experimental Studies. American Journal of Respiratory and Critical Care Medicine, 157(1), 294-323. Retrieved from http://ajrccm.atsjournals.org/content/157/1/294.long
Feng et. al. (2011, July 19). Pediatric Acute Respiratory Distress Syndrome Treatment and Management. Retrieved September 26, 2012, from http://emedicine.medscape.com/article/803573-treatment
Galvin, S. & Granton, J. (2011, March 3). Reducing Ventilator Lung Injury. Retrieved September
26, 2012, from http://respiratory-care-sleep-medicine.advanceweb.com/Features/Articles/Reducing-Ventilator-Induced-Lung-Injury.aspx
Ricard, J.D., Dreyfuss, D. & Saumon, G. (2003). Ventilator-induced Lung Injury. European Respiratory Journal, 22(42). Retrieved from http://erj.ersjournals.com/content/22/42_suppl/2s.full.pdf
Tremblay, L.N. & Slutsky, a.S. (2006). Ventilator-induced Lung Injury: From the Bench to the Bedside. Intensive Care Med, 32, 24-33. Retrieved from http://www.ccmpitt.com/ebm/ards/ventilator-induced%20lung%20injury_from%20the%20bench%20to%20the%20bedside.pdf
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