Membrane ventilators with interventional lung assist have been used as a bridge to lung transplant on over 1,200 patients in Europe with marked ventilation-refractory respiratory acidosis, severe hypercapnia, or significant hypoxia.1 The device acts as an artificial lung that promotes gas exchange outside the body with the main objective of removing carbon dioxide.2 It facilitates advanced protection of the lung from disease processes that cause acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and vital organ failure (such as renal failure or hepatic failure.)2
How it works
Unlike conventional mechanical ventilation, the membrane ventilator uses simple diffusion across a membrane to oxygenate the blood. Catheters are threaded into the femoral artery on either leg of the patient and connected to the membrane ventilator to form a loop through which blood flows.3 The device itself is a plastic gas exchange model with polymethylpentene material woven into hollow fibers and then interlaced into bundles to form membranes that permit diffusion. The PMP membrane surfaces are heparinized to prevent clotting as a result of direct contact with the blood. Oxygen flows through the hollow fibers and blood flows over their exterior surfaces which oxygenates the blood.2 Carbon dioxide is removed by varying sweep rates, which are regulated by an oxygen control meter with a maximum flow of 10 L/min.1 That capacity makes this device well-suited for patients with chronic obstructive pulmonary disease who are experiencing an acute hypercapnic exacerbation.3
Full oxygenation support can be achieved through a veno-venous route which requires a mechanical pump. A mean arterial pressure of 60 mmHg is required for proper use because the device is attached to systemic circulation instead of pulmonary circulation. With this set-up, the patient's natural breathing can assist the device in optimizing oxygenation.2 It should be noted that increasing mixed-venous oxygen saturation may result in an initial decrease in PaO2, which may produce a decrease in hypoxic pulmonary vasoconstriction and an increase in the pulmonary right-to-left shunt.1
Conventional mechanical ventilation comes with the risk of barotrauma or volutrauma and lung infection, which can further damage already compromised lung tissue and increase mortality rates. The membrane ventilator provides ultra-protective lung ventilation because it attaches to the systemic circulation and has no direct contact with already injured lung tissue. It often is used to prevent postoperative complications such as bronchopleural fistulas and inflammatory responses.3
Guidelines from the Newcastle upon Tyne Hospitals recommend that reduction or discontinuation of sedation may be attempted sooner with this device than conventional mechanical ventilation, which helps speed patient recovery. Sedation promotes shallow breathing and can cause atelectasis; therefore a more rapid reduction in sedation may result in larger spontaneous tidal volumes and reduce the occurrence of atelectasis. Breathing spontaneously also helps prevent diaphragm muscle atrophy, which can impede patient recovery. The membrane ventilator lessens rates of re-intubation, tracheotomy, mortality, and other complications ordinarily associated with conventional mechanical ventilation. In addition, the weaning success rate can be dramatically improved by this membrane ventilator.3
Membrane ventilators are used in an ICU setting and oxygen saturation must be monitored.3 The device must be used in conjunction with anti-coagulation therapy to prevent blood clots, vasopressors to keep mean arterial pressure of 60 mmHg, and a systolic blood pressure of less than 200 mmHg.
Manufacturer's guidelines specify that the device is indicated when the elimination of carbon dioxide or sufficient gas exchange cannot be accomplished by protective ventilation on a conventional mechanical ventilator. It also is indicated as a prophylactic treatment for respiratory acidosis and its effects. While the membrane ventilator with interventional lung assist is more conducive to certain disease processes that effect oxygenation and ventilation such as pneumonia, pneumothorax, primary and secondary acute respiratory distress syndrome (ARDS), and COPD exacerbations, it is not limited to a specific diagnosis. The membrane ventilator should be considered whenever the acceptable limits for conventional mechanical ventilation have been surpassed or are unsuccessful. However, the ventilator cannot be used if the patient has heparin-induced thrombocytopenia or unstable hemodynamics with an insufficient perfusion pressure following shunt opening such as cardiogenic or septic shock. It also is contraindicated if the patient has advanced atherosclerotic occlusive peripheral vascular disease or small femoral arteries because it could result in deterioration of perfusion to the cannulated limbs. The membrane ventilator should not be used on newborns, infants, or children who have a body weight less than twenty kilograms. Finally, dietary fat should not be included in the patient's daily nutritional supplements because fatty deposits could block the PMP membranes.1
Patients must have sufficient cardiac function to perfuse the artificial lung in the same way the heart perfuses the natural lung. Researchers at The Newcastle upon Tyne Hospitals, NHS Foundation Trust note that an oxygen saturation of 75 to 85 percent may be acceptable in the beginning phase of treatment so long as the patient has an adequate blood pressure and urine continues to be produced. The device should be sustained at or below the level of the heart and flow should be stopped momentarily when the patient is moved or repositioned. Insertion sites and arterial pedal pulses should be examined every hour to ensure collateral blood flow to the legs and feet. The device can be used without replacement for a maximum of 29 days after which a percentage of the device's heparin coating is lost.3
Certain device settings are recommended and hemodynamic criteria must be met to maximize the function of the membrane ventilator, including a gas flow of 10-15 L/min, a maximum gas pressure of 30 mmHg, a maximum blood flow rate of 4.5 L/min, a maximum blood side mean pressure (systolic blood pressure) of 200 mmHg, and a mean arterial pressure of 60 mmHg.2 The device also must have a gas and vent port size of one quarter of an inch, a static priming volume of 175 mL, and a blood outlet/inlet connector size of three eighths of an inch to function properly.2
The device is not currently approved for use in the United States, although clinicians have petitioned the Food and Drug Administration to secure compassionate release use of the device on two occasions. Currently, 601 patients are enrolled in a worldwide registry to study the mechanism, clinical effects, and range of indications associated with the ventilator.4
Janay Moore, BS, CRT, Ashley Oliver, BS, CRT, and Taryn Dunn, BS, CRT, (pictured above) are recent graduates of the respiratory therapy program at the University of Alabama at Birmingham.
- Novalung: iLA Membrane Ventilator®. C2011. [cited 2011 June 1] Available from: http://www.novalung.com/en/ila/
- Fischer S, Streuber M. The Novalung® iLA Membrane Ventilator: Technical Aspects. c2006 [updated 2006 Aug 11; cited 2011 June 1] Available from: http://www.ctsnet.org/portals/thoracic/newtechnology/article-9.html
- The Newcastle upon Tyne Hospitals, NHS Foundation Trust. Novalung Guideline. c2010 [updated 2012 Feb; cited 2011 June 2] Available from: http://www.newcastle-hospitals.org.uk/downloads/clinical-guidelines/Perioperative%20and%20Critical%20Care/NovalungProtocolCurrent2010.pdf
- iLA Registry. C2011. [cited 2011 Aug 8] Available from: http://www.novalung.com/en