Acute respiratory distress syndrome (ARDS) is a condition which sees widespread inflammation and increased permeability of the lungs of critically ill or wounded patients. It cannot be explained by - but may coexist with - left atrial or pulmonary capillary hypertension.1
Risk factors include sepsis, accidents that caused damage to the brain, smoking, and pneumonia. Patients often experience severe shortness of breath though also low blood pressure, confusion and exhaustion, fast breathing and dizziness might be symptoms.
Acute respiratory distress syndrome has proven to be a difficult problem to solve in respiratory medicine. Underdiagnosis has resulted in high morbidity and mortality2,3,4 and improvement in its management is crucial to reducing this burden.
Acute respiratory distress syndrome is a clinically defined condition with acute respiratory failure triggered by a wide variety of pathologies including trauma, pulmonary infection, severe burns, near-drowning and as a reaction to drugs. Although most ARDS predisposing conditions are well known3,6,7, there is a notable lack of awareness about environmental and individual risk factors.
Sex, age, weight, height
Alcohol abuse, cigarette smoke exposure
Underlying illness/indicators of organ health
Pneumonia, sepsis, simplified acute physiology score (SAPS), creatinine, albumin, alanine aminotransferase (ALT).
Due to the damage to the alveolar epithelium, the alveolar-capillary membrane and the endothelium, the lung compliance decreases progressively, and hypoxemia becomes refractory.8 Therefore, mechanical ventilation should be applied.8
However, while respiratory support is needed in ARDS, in some cases mechanical ventilation as a treatment can actually serve to worsen lung injury.9 To improve survival in ARDS mechanical ventilation, it’s important to achieve adequate gas exchange while limiting additional injury by incorporating low tidal volume (6 mL/kg based on ideal body weight) ventilation and low airway plateau pressure (Pplat) with permissive hypercapnia, if required.10 To monitor ventilation it's recommended to use capnography. To explain how to correctly apply and interpret the capnograhpy waveform results in a meaningful manner, G. Farquharson and G. K. Spratt recently published 'Algorithms for Interpreting Capnography'.
In addition, the use of positive end-expiratory pressure (PEEP) and/or recruitment manoeuvres may be helpful in reducing injury related to the repeated expansion and collapse of alveoli.11,12,13
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1. Bernard GR et al. The American European consensus conference on ARDS: definitions mechanisms, relevant outcomes and clinical trial coordination. Am J Respir Crit Care Med 1994;149:818–824
2. Brun-Buisson C, Minelli C, Bertolini G, et al. Epidemiology and outcome of acute lung injury in European intensive care units. Results from the ALIVE study. Intensive Care Med 2004; 30: 51–61.
3. Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury. N Engl J Med 2005; 353: 1685–1693.
4. Villar J, Blanco J, Añón JM, et al. The ALIEN study: incidence and outcome of acute respiratory distress syndrome in the era of lung protective ventilation. Intensive Care Med 2011; 37: 1932–1941.
5. Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, Fan E, Camporota L, Slutsky AS. JAMA. Acute respiratory distress syndrome: the Berlin Definition. ARDS Definition Task Force 2012; Jun 20; 307(23):2526-33.
6. Matthay MA, Ware LB, Zimmerman GA. The acute respiratory distress syndrome. J Clin Invest 2012; 122: 2731–2740.
7. Moss M, Bucher B, Moore FA, et al. The role of chronic alcohol abuse in the development of acute respiratory distress syndrome in adults. JAMA 1996; 275: 50–54.
8. Grigorakos, L. Evaluating mechanical ventilation in patients with ARDS. Arch Pulmonol Respir Care 2018; 4(1): 001-005
9. Xiaoming J, Malhotra A, Saeed M, et al. Risk Factors for Acute Respiratory Distress Syndrome in Patients Mechanically Ventilated for Greater Than 48 Hours. Chest. 2008; 133(4): 853–861.
10. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N. Engl. J. Med.: 2000, 342(18);1301-8.
11. Gattinoni L et al. Physical and biological triggers of ventilator-induced lung injury and its prevention. Eur Respir J 2003; 22: Suppl. 47, 15s–25s.
12. Malo J et al. How does positive end-expiratory pressure reduce intrapulmonary shunt in canine pulmonary edema? J Appl Physiol Respir Environ Exerc Physiol 1984;57(4):1002-10.
13. Halter et al. Positive end-expiratory pressure after a recruitment maneuver prevents both alveolar collapse and recruitment/derecruitment. Am J Respir Crit Care Med. 2003;167(12):1620-6.