Acute Respiratory Distress Syndrome

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.

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Acute Respiratory Distress Syndrome - The Berlin Definition5
TIMING Within one week of a known clinical insult or new/worsening respiratory symptoms
Chest imaginga Bilateral opacities – not fully explained by effusions, lobar/lung collapse or nodules
Origin of edema Respiratory failure not fully explained by cardiac or fluid overload. Need objective assessment (e.g. echocardiography) to exclude hydrostatic edema if no risk factor is present
Mild 200 mmHg < PaO2/FIO2 ≤300 mmHg with PEEP or CPAP ≥5 cmH2Oc  
Moderate 100 mmHg < PaO2/FIO2 ≤200 mmHg with PEEP ≥5 cmH2O
Severe PaO2/FIO2 ≤100 mmHg with PEEP ≥5 cmH2O 


CPAP: Continuous Positive Airway Pressure;

FIO2: Fraction of Inspired Oxygen;

PaO2: Partial Pressure of Arterial Oxygen;

PEEP: Positive End-Expiratory Pressure; 


a Chest radiograph or computed tomography scan;

b If altitude is higher than 1,000 m, the correction factor should be calculated as follows: [PaO2/FIO2_(barometric pressure/760)]; c This may be delivered noninvasively in the mild acute respiratory distress syndrome group.

Acute Respiratory Distress Syndrome - The Berlin Definition5

Risk factors of ARDS

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.

Risk factors of Acute Respiratory Distress Syndrome3,6,7

Demographic information

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).

Risk factors of Acute Respiratory Distress Syndrome3,6,7

Demographic information

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

Discover below which  respiratory and monitoring products from Medtronic can help in the  treatment of patients who have been diagnosed with acute respiratory  distress syndrome. 


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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.