In the United States, patients with acute respiratory distress syndrome (ARDS) occupy 1 in 10 critical care beds. Each year, ARDS kills 150,000 Americans. Most of the deaths are triggered by an event, such as sepsis or pneumonia. What is ARDS?
What distinguishes ALI from ARDS is the P/F ratio, the comparison of arterial partial pressure of oxygen (PaO2) with inspired fractional concentration of oxygen (FiO2). Simply put, the P/F ratio is a comparison of the amount of oxygen given to a patient with the amount of oxygen actually entering the patient’s bloodstream. The higher the P/F ratio, the better the gas exchange. The normal measurement is around 500 mm Hg. A P/F ratio below 300 mm Hg regardless of the positive end-expiratory pressure (PEEP) measurement indicates ALI. A P/F ratio below 200 mm Hg regardless of the PEEP measurement indicates ARDS. If a patient’s oxygen requirements continue increasing while oxygen saturation levels (based on finger-probe readings and arterial blood gas [ABG] measurements) remain low, ALI is progressing to ARDS. This condition is called refractory hypoxemia. A patient with ARDS has decreased functional residual lung capacity, which may lead to organ failure and death. Typically, ARDS requires admission to an intensive care unit (ICU) and mechanical ventilation. What’s the damage? Normally, surfactant decreases surface tension and allows the alveoli to open easily. In ARDS, the edema and reduced surfactant level compromise gas exchange, causing decreased oxygen and increased carbon dioxide in the blood. The result is hypoxemia, pulmonary hypertension, and decreased pulmonary compliance. In later stages of ARDS, progressive alveolitis and fibrosis—stiff lungs—further decrease pulmonary function. Signs and symptoms A chest X-ray shows diffuse infiltrates, and ABG results indicate respiratory alkalosis with very low PaO2 levels. In the later stages, hypercapnia may develop. Further metabolic imbalances can lead to mixed acidosis, signaling a low ventilation-to-perfusion (V./Q.) ratio and a deteriorating P/F ratio. To rule out a cardiogenic cause of pulmonary edema, a physician may order PAWP measurements. 5 P’s of ARDS therapy The five P’s of supportive therapy include perfusion, positioning, protective lung ventilation, protocol weaning, and preventing complications. Perfusion Evaluate the patient’s volume status by measuring blood pressure, respiratory variations of pulmonary and systemic arterial pulse pressure, central venous pressure, and urine output. Confirm intravascular status with pulmonary artery catheter data, cardiac output, cardiac index, pulmonary vascular resistance, and venous oxygen saturation (SvO2). Certain drugs can also help increase perfusion. Inotropics such as dobutamine (Dobutrex) can increase cardiac output to boost oxygenation. Milrinone lactate (Primacor), another inotropic, improves perfusion by causing vasodilation in the pulmonary bed Vasopressors, such as norepinephrine and dopamine, promote systemic vasoconstriction, thus increasing blood pressure and perfusion. When administering these drugs, monitor vital signs, skin color and temperature, and the patient’s tolerance to therapy. Positioning The same thing happens with PEEP, which primarily aerates the anterior, nondependent areas of the lungs instead of the dependent areas that would benefit most. Immobility, a major cause of pulmonary complications, greatly influences perfusion distribution. Three positioning therapies can decrease these complications and improve perfusion in ARDS patients:
These therapies improve oxygenation by mobilizing secretions, resolving atelectasis, improving V./Q. ratio, recruiting functional but collapsed or consolidated alveolar units, and decreasing interstitial fluid accumulation. Rotational therapy reduces nosocomial pneumonia, skin breakdown, ICU length of stay, and the number of ventilator days. There’s a correlation between the degree of rotation and the therapeutic benefit. With rotational therapy, the patient must be turned consistently to 40 degrees; otherwise, the therapy doesn’t significantly affect the clearance of secretions, risk of pneumonia, or the length of ICU stay. Kinetic Therapy is effective in immobilized patients at angles up to 62 degrees. Using the prone position Prone positioning can be achieved with or without a device, such as the Stryker frame, Triadyne Proning Accessory Kit, Vollman Proner, and RotoProne. If you’re not using a device, turn the patient from the supine position toward the ventilator, using the chest and pelvic area to allow for better diaphragm motion and lung mechanics. Depending on the size of the patient, the turn may take four to eight nurses. Place the patient in the prone position with pillows or cushions supporting the chest and pelvis to allow the abdomen to hang free. When the patient is in the prone position, arrange the arms in the swimmer’s pose—one at the side of the body and the other extended above the head. Using positioning devices Both the Triadyne Proning Accessory Kit and the Vollman Proner make positioning the patient easier and more effective. The Triadyne Proning Accessory Kit consists of a sheet to aid in positioning the patient and position packs to support the patient in the prone position. The RotoProne bed is an automated system that combines Kinetic Therapy with prone positioning for up to 62 degrees. This device allows one nurse to make position changes and to provide several intervals of prone positioning throughout the day. In a 24-hour period, an ARDS patient should be in the prone position for at least 18 hours. Disadvantages of prone positioning Typically, patients with refractory hypoxemia are placed in the prone position when ventilator settings are already maximized, with FiO2 at 100% and high levels of PEEP. We are learning that outcomes are better when positioning starts early in the course of ARDS. Protective Lung Ventilation During the early stages of ARDS, use mechanical ventilation to open collapsed alveoli. The primary goal of ventilation is to support organ function by providing adequate ventilation and oxygenation while decreasing the patient’s work of breathing. But mechanical ventilation itself can damage the alveoli, making protective lung ventilation necessary. In the past, ventilatory management of ARDS meant using high tidal volumes (VT) of 10 to 15 ml/kg to prevent atelectasis and normalize partial pressure of carbon dioxide with increased levels of PEEP to reduce FiO2. But high VTs overstretch the alveoli, causing shearing forces on them and thus increasing the inflammatory response. The less affected lung regions must then accommodate most of the VT, which can lead to ventilator-induced lung injury (VILI)—a condition that exacerbates the physiologic responses to ARDS. VILI is a complex process caused by repetitive application of excessive stress or strain to the lung’s fibroskeleton, microvasculature, terminal airways, and delicate alveolar tissue. PEEP opens collapsed alveoli and prevents end-tidal alveolar collapse. This pressure also keeps the alveoli clear of fluid. For ARDS patients, ARDSNet guidelines recommend titration of PEEP up to a high level of 22 to 24 cm. Because PEEP can increase intrathoracic pressure that lowers cardiac output, you should use hemodynamic monitoring to determine the best PEEP setting for each ARDS patient. Research also shows that using continuous positive airway pressure at 35 to 40 cm H2O for 30 to 40 seconds can also open collapsed alveoli without severe hemodynamic compromise or barotrauma. Current recommendations for protective lung ventilation include:
Be sure to monitor the patient for changes in respiratory status—such as increased respiratory rate, adventitious breath sounds, decreased oxygenation saturation, and dyspnea—at least every 4 hours and after every change in PEEP or VT. Protocol weaning
Preventing complications Deep vein thrombosis Treatment for DVT includes these interventions:
Pressure ulcers Poor nutrition VAP Putting the 5 P’s into practice Selected references Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, 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(3):818-824. Available at: http://ajrccm.atsjournals.org/cgi/content/abstract/149/3/818. Accessed January 17, 2007. Ely EW. Mechanical ventilator weaning protocols driven by nonphysician health-care professionals. Chest. 2001;120:454S-463S. Grap MJ, Munro CL. Preventing ventilator-associated pneumonia: evidence-based care. Crit Care Nurs Clin North Am. 2006;16(3):349-358. Kollef M. Ventilator-associated pneumonia and ventilator-induced lung injury: two peas in a pod. Crit Care Med. 2002;30(10):2391-2392. Markowicz P, Wolff M, Djedaini K, Cohen Y, Chastre J, Delclaux C, et al. Multicenter prospective study of ventilator-associated pneumonia during acute respiratory distress syndrome: incidence, prognosis, and risk factors. ARDS Study Group. Am J Respir Crit Care Med. 2000;161(6):1942-1948. Marini JJ, Gattinoni L. Ventilatory management of acute respiratory distress syndrome: a consensus of two. Crit Care Med. 2004;32(1):250-255. Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1334-1349.www.ihi.org/IHI/Programs/Campaign/Campaign.htm?TabId=2#PreventVentilator-AssociatedPneumonia For a complete list of selected references, see March 2007 references. Janice Powers, MSN, RN, CCRN, CCNS, CNRN, CWCN, is a Clinical Nurse Specialist at Critical Care and Neuroscience Methodist Hospital, Clarian Health Partners, in Indianapolis, Indiana. Ms. Powers has disclosed that she has received a speaker honorarium from KCI and Eli Lilly and Company within the previous 12 months.
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