ARDS.pptx

Acute Respiratory Distress SYndrome

1. ACUTE RESPIRATORY DISTRESS SYNDROME Dr. Dipali Dumbre Ph. D Nursing Medical Surgical Nursing SCON

2. Definition “Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of acute respiratory failure in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid”. The alveoli fill with fluid, resulting in severe dyspnea, hypoxemia refractory to supplemental O 2 , reduced lung compliance, and diffuse pulmonary infiltrates

3. E tiology Direct lung injury may cause ARDS. ARDS may develop as a consequence of the systemic inflammatory response syndrome (SIRS ). SIRS may have an infectious or a noninfectious etiology and is characterized by widespread inflammation or clinical responses to inflammation following a variety of physiologic insults, including severe trauma, lung injury, and sepsis. ARDS may also develop as a consequence of multiple organ dysfunction syndrome (MODS). MODS results from organ system dysfunction that progressively increases in severity and ultimately results in multisystem organ failure.

4. An exact cause for the damage to the alveolar-capillary membrane is not known. However , the pathophysiologic changes of ARDS are thought to be due to stimulation of the inflammatory and immune systems, which causes an attraction of neutrophils to the pulmonary interstitium .( a collection of support tissues within the lung that includes the alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues The neutrophils cause a release of biochemical, humoral, and cellular mediators that produce changes in the lung, including increased pulmonary capillary membrane permeability, destruction of elastin(alveolar wall) and collagen, formation of pulmonary micro emboli, and pulmonary artery vasoconstriction .

5. Predisposing Conditions to Acute Respiratory Distress Syndrome DIRECT LUNG INJURY INDIRECT LUNG INJURY Common Causes Aspiration of gastric contents or other substances Viral/bacterial pneumonia Less Common Causes Chest trauma Embolism: fat, air, amniotic fluid, Thrombus Inhalation of toxic substances Near-drowning O 2 toxicity Radiation pneumonitis Common Causes Sepsis (especially gram-negative infection) Severe massive trauma Less Common Causes Acute pancreatitis Anaphylaxis Cardiopulmonary bypass Disseminated intravascular coagulation Multiple blood transfusions Opioid drug overdose (e.g., heroin) Nonpulmonary systemic diseases Severe head injury Shock states

6. PATHOPHYSIOLOGY The pathophysiologic changes in ARDS are divided into three phases: ( 1) Injury or exudative phase, ( 2) Reparative or proliferative phase (3) Fibrotic phase.

7. Injury or Exudative Phase The injury or exudative phase occurs approximately 1 to 7 days (usually 24 to 48 hours) after the initial direct lung injury . Neutrophils adhere to the pulmonary microcirculation, causing damage to the vascular endothelium and increased capillary permeability. In the earliest phase of injury, there is engorgement of the peribronchial and perivascular interstitial space, which produces interstitial edema . Next, fluid from the interstitial space crosses the alveolar epithelium and enters the alveolar space. Intrapulmonary shunt develops because the alveoli fill with fluid, and blood passing through them cannot be oxygenated

8. Alveolar type I and type II cells (which produce surfactant) are damaged by the changes caused by ARDS . This damage, in addition to further fluid and protein accumulation, results in surfactant dysfunction . The function of surfactant is to maintain alveolar stability by decreasing alveolar surface tension and preventing alveolar collapse . Decreased synthesis of surfactant and inactivation of existing surfactant cause the alveoli to become unstable and collapse (atelectasis). Widespread atelectasis further decreases lung compliance, compromises gas exchange, and contributes to hypoxemia

9. Type I alveolar cells  are squamous (giving more surface area to each  cell ) and cover approximately 90–95% of the  alveolar  surface.  Type I cells  are involved in the process of gas exchange between the  alveoli  and blood.

10. Type II cells in the alveolar wall contain secretory granular organelles known as lamellar bodies that fuse with the cell membranes and secrete pulmonary surfactant. This surfactant is a film of fatty substances, a group of phospholipids that reduce alveolar surface tension.

11. Also during this stage, hyaline membranes begin to line the alveoli. The hyaline membrane is composed of necrotic cells, protein, and fibrin and lies adjacent to the alveoli wall. These hyaline membranes are thought to result from the exudation of high-molecular-weight substances (particularly fibrinogen) in the edema fluid. Hyaline membranes contribute to the development of fibrosis and atelectasis, leading to a decrease in gas exchange capability and lung compliance. The primary pathophysiologic changes that characterize the injury or exudative phase of ARDS are interstitial and alveolar edema and atelectasis. Severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia unresponsive to increasing concentrations of O 2 (termed refractory hypoxemia ).

12. Diffusion limitation(occurs when gas exchange across the alveolar-capillary membrane is compromised by a process that thickens or destroys the membrane ), caused by hyaline membrane formation, further contributes to the severity of the hypoxemia. As the lungs become less compliant because of decreased surfactant, pulmonary edema, and atelectasis, the patient must generate higher airway pressures to inflate “stiff” lungs . Reduced lung compliance greatly increases the patient's work of breathing.

13. Progressive increase in pressures required to deliver a controlled ventilation may occur as a result of worsening lung compliance . Hypoxemia and the stimulation of juxtacapillary receptors( J-receptors ( juxtacapillary ) are nerves innervating into the body of the lung. J-receptors  (respond to events such as pulmonary edema , pulmonary emboli pneumonia, and barotrauma, which cause a decrease in oxygenation and thus lead to an increase in ventilation/respiration .) in the stiff lung parenchyma (J reflex) initially cause an increase in respiratory rate and a decrease in tidal volume . This breathing pattern increases CO 2 removal, producing respiratory alkalosis. Cardiac output increases in response to hypoxemia, a compensatory effort to increase pulmonary blood flow. However , as atelectasis, pulmonary edema, and pulmonary shunt increase, compensation fails, and hypoventilation, decreased cardiac output, and decreased tissue O 2 perfusion eventually occur.

14. Reparative or Proliferative Phase The reparative or proliferative phase of ARDS begins 1 to 2 weeks after the initial lung injury. During this phase, there is an influx of neutrophils, monocytes, and lymphocytes and fibroblast proliferation as part of the inflammatory response. The injured lung has an immense regenerative capacity after acute lung injury. The proliferative phase is complete when the diseased lung becomes characterized by dense, fibrous tissue. Increased pulmonary vascular resistance and pulmonary hypertension may occur in this stage because fibroblasts and inflammatory cells destroy the pulmonary vasculature.

15. Lung compliance continues to decrease as a result of interstitial fibrosis. Hypoxemia worsens because of the thickened alveolar membrane, causing diffusion limitation and shunting. If the reparative phase persists, widespread fibrosis results. If the reparative phase is arrested, the lesions resolve.

16. Fibrotic Phase The fibrotic phase of ARDS occurs approximately 2 to 3 weeks after the initial lung injury. This phase is also called the chronic or late phase of ARDS. By this time, the lung is completely remodeled by sparsely collagenous and fibrous tissues. There is diffuse scarring and fibrosis, resulting in decreased lung compliance. In addition, the surface area for gas exchange is significantly reduced because the interstitium is fibrotic, and therefore hypoxemia continues. Pulmonary hypertension results from pulmonary vascular destruction and fibrosis.

17. Clinical Manifestations The initial presentation of ARDS is often insidious. At the time of the initial injury, and for several hours to 1 to 2 days afterward, the patient may not experience respiratory symptoms, or the patient may exhibit only dyspnea, tachypnea, cough, and restlessness. Chest auscultation may be normal or reveal fine, scattered crackles. ABGs usually indicate mild hypoxemia and respiratory alkalosis caused by hyperventilation . Respiratory alkalosis results from hypoxemia and the stimulation of juxtacapillary receptors.

18. The chest x-ray may be normal or exhibit evidence of minimal scattered interstitial infiltrates. Edema may not show on the x-ray until there is a 30% increase in fluid content in the lung . As ARDS progresses, symptoms worsen because of increased fluid accumulation and decreased lung compliance. Respiratory discomfort becomes evident as the work of breathing increases. Tachypnea and intercostal and suprasternal retractions may be present.

19. Pulmonary function tests in ARDS reveal decreased compliance and decreased lung volumes, particularly a decreased functional residual capacity (is the volume of air present in the lungs at the end of passive expiration ). Tachycardia , diaphoresis, changes in sensorium with decreased mentation, cyanosis, and pallor may be present. Chest auscultation usually reveals scattered to diffuse crackles and rhonchi . The chest x-ray demonstrates diffuse and extensive bilateral interstitial and alveolar infiltrates. A pulmonary artery catheter may be inserted. Hypoxemia and a PaO 2 /FIO 2 ratio below 200 (e.g., 80/0.8 = 100) despite increased FIO 2 by mask, cannula, or endotracheal tube are hallmarks of ARDS.

20. ABGs may initially demonstrate a normal or decreased PaCO 2 despite severe dyspnea and hypoxemia. Hypercapnia signifies that hypoventilation is occurring, and the patient is no longer able to maintain the level of ventilation needed to provide optimum gas exchange. As ARDS progresses, it is associated with profound respiratory distress requiring endotracheal intubation and PPV. The chest x-ray is often termed whiteout or white lung, because consolidation and coalescing infiltrates are widespread throughout the lungs, leaving few recognizable air spaces. Pleural effusions may also be present. Severe hypoxemia, hypercapnia, and metabolic acidosis, with symptoms of target organ or tissue hypoxia, may ensue if prompt therapy is not given.

21. Complications Hospital-Acquired Pneumonia. A frequent complication of ARDS is hospital-acquired pneumonia, occurring in as many as 68% of patients with ARDS . Risk factors include impaired host defenses, contaminated medical equipment, invasive monitoring devices, aspiration of GI contents (especially in patients receiving tube feedings), and prolonged mechanical ventilation, as well as colonization of the respiratory tract. Strategies to prevent hospital-acquired pneumonia include infection control measures (e.g., strict hand washing and sterile technique during endotracheal suctioning) and elevating the head of the bed 30 to 45 degrees to prevent aspiration.

22. Barotrauma. Barotrauma may result from rupture of overdistended alveoli during mechanical ventilation. The high peak airway pressures that may be required in patients with ARDS predispose to this complication. Barotrauma results in the presence of alveolar air in locations where it is not usually found. This can lead to pulmonary interstitial emphysema, pneumothorax, subcutaneous emphysema, pneumoperitoneum , pneumomediastinum , pneumopericardium , and tension pneumothorax. To avoid barotrauma and minimize risk associated with elevated plateau and peak inspiratory pressures, the patient with ARDS may be ventilated with smaller tidal volumes (e.g., 6 ml/kg) and varying amounts of positive end-expiratory pressure (PEEP) in order to minimize oxygen requirements and intrathoracic pressures.

23. Volu-Pressure Trauma Volu-pressure trauma can occur in patients with ARDS when large tidal volumes (e.g., 10 to 15 ml/kg) are used to ventilate noncompliant lungs. Volu-pressure trauma results in alveolar fractures and movement of fluids and proteins into the alveolar spaces. To limit this complication, it is recommended that smaller tidal volumes or pressure ventilation be used in patients with ARDS .

24. Physiologic Stress Ulcers. Critically ill patients with acute respiratory failure are at high risk for stress ulcers . Bleeding from stress ulcers occurs in 30% of patients with ARDS who require PPV, a higher incidence than other causes of acute respiratory failure. Management strategies include correction of predisposing conditions such as hypotension, shock, and acidosis . Prophylactic management includes antiulcer agents such as H 2 -histamine receptor antagonists (e.g., ranitidine [Zantac]), as well as proton pump inhibitors (e.g., pantoprazole [ Protonix ]) and mucosal-protecting agents (e.g., sucralfate [Carafate ]). Early initiation of enteral nutrition also helps prevent mucosal damage

25. Renal Failure Renal failure can occur from decreased renal tissue oxygenation as a result of hypotension, hypoxemia, or hypercapnia . Renal failure may also be caused by administration of nephrotoxic drugs (e.g., aminoglycosides), which are used to treat infections associated with ARDS.

26. Diagnostic Findings Refractory Hypoxemia PaO 2 <50 mm Hg on FIO 2 >40% with PEEP >5 cm H 2 O PaO 2 /FIO 2 ratio <200 Chest X-Ray New bilateral interstitial and alveolar infiltrates Pulmonary Artery Wedge Pressure ≤18 mm Hg and no evidence of heart failure Predisposing Condition Identification of a predisposing condition for ARDS within 48 hr of clinical manifestations

27. COLLABORATIVE THERAPY Respiratory Therapy Oxygen Administration Mechanical Ventilation: Endotracheal intubation and mechanical ventilation provide additional respiratory support . During mechanical ventilation, it is common to apply PEEP at 5 cm H 2 O to compensate for loss of glottic function caused by the presence of the endotracheal tube . In patients with ARDS, higher levels of PEEP (e.g., 10 to 20 cm H 2 O) may be used. The mechanism of action of PEEP is related to its ability to increase FRC and recruit (open up) collapsed alveoli. PEEP is typically applied in 3 to 5 cm H 2 O increments until oxygenation is adequate with FIO 2 of 60% or less . PEEP may improve V/Q in respiratory units that collapse at low airway pressures, thus allowing the FIO 2 to be lowered.

28. Positioning Strategies Some patients with ARDS demonstrate a marked improvement in PaO 2 when turned from the supine to the prone position (e.g., PaO 2 70 mm Hg supine, PaO 2 90 mm Hg the prone) with no change in inspired O 2 concentration

29. In the early phases of ARDS, fluid moves freely throughout the lung. Because of gravity, this fluid pools in dependent regions of the lung . As a consequence, some alveoli are fluid filled (dependent areas), whereas others are air filled (nondependent areas). In addition, when the patient is supine the heart and mediastinal contents place more pressure on the lungs than in the prone position, which changes pleural pressure and predisposes to atelectasis. If the patient is turned from supine to prone, air-filled, nonatelectatic alveoli in the ventral (anterior) portion of the lung become dependent.

30. Perfusion may be better matched to ventilation, causing less V/Q mismatch. Not all patients respond to prone positioning with an increase in PaO 2 , and there is no reliable way of predicting who will respond. Prone positioning is typically reserved for patients with refractory hypoxemia who do not respond to other strategies to increase PaO 2 . When this positioning strategy is used, there must be a plan in place for immediate repositioning for cardiopulmonary resuscitation in the event of a cardiac arrest.

31. Other positioning strategies that can be considered for patients with ARDS include continuous lateral rotation therapy (CLRT) and kinetic therapy. The purpose of CLRT is to provide continuous, slow, side-to-side turning of the patient by rotating the actual bed frame less than 40 degrees. The lateral movement of the bed is maintained for 18 of every 24 hours to simulate postural drainage and to help mobilize pulmonary secretions.