Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome
A. General characteristics

1. ARDS is a diffuse inflammatory process (not necessarily infectious) involving
   both lungs—neutrophil activation (due to a variety of causes) in the systemic or
   pulmonary circulations is the primary mechanism (see Clinical Pearl 2-10).
2. ARDS is not a primary disease, but rather a disorder that arises due to other conditions that cause a widespread inflammatory process.
3. New 2012 Berlin definition:
   a. Acute onset (<1 week).
   b. Bilateral infiltrates on chest imaging.
   c. Pulmonary edema not explained by fluid overload or CHF (e.g., no clinical evidence of CHF or pulmonary capillary wedge pressure (PCWP) <18 mm Hg).
   d. Abnormal PaO2/FiO2 ratio.
   • 200 to 300: mild ARDS
   • 100 to 200: moderate ARDS
   • 100: severe ARDS
4. Pathophysiology
   a. Massive intrapulmonary shunting of blood is a key pathophysiologic event in
   ARDS—severe hypoxemia with no significant improvement on 100% oxygen
   (requires high PEEP to prop open airways). Shunting is secondary to widespread atelectasis, collapse of alveoli, and surfactant dysfunction.
   • Interstitial edema and alveolar collapse are due to an increase in lung fluid,
   which leads to stiff lungs, an increase in alveolar–arterial oxygen difference
   (A–a gradient), and ineffective gas exchange.
   • Note that the effects of the increase in pulmonary fluid are identical to those
   seen in cardiogenic pulmonary edema, but the cause is different: An increase
   in alveolar capillary permeability causes ARDS, whereas congestive hydrostatic forces cause cardiogenic pulmonary edema.

b. Decreased pulmonary compliance—leads to increased work of breathing.
c. Increased dead space—secondary to obstruction and destruction of pulmonary
capillary bed.
d. Low vital capacity, low FRC.
B. Causes

1. Sepsis is most common risk factor—can be secondary to a variety of infections
   (e.g., pneumonia, urosepsis, wound infections)
2. Aspiration of gastric contents
3. Severe trauma, fractures (e.g., femur, pelvis), acute pancreatitis, multiple or massive transfusions, near-drowning
4. Drug overdose, toxic inhalations
5. Intracranial HTN
6. Cardiopulmonary bypass
   C. Clinical features
7. Dyspnea, tachypnea, and tachycardia due to increased work of breathing.
8. Progressive hypoxemia—not responsive to supplemental oxygen.
9. Patients are difficult to ventilate because of high peak airway pressures due to stiff,
   noncompliant lungs.
   D. Diagnosis
10. CXR—shows diffuse bilateral pulmonary infiltrates (see Figure 2-13)
    a. There is a variable correlation between findings on CXR and severity of hypoxemia or clinical response. Diuresis improves and volume overload worsens the
    infiltrates—regardless of CXR findings, the underlying ARDS may or may not
    be improved.
    b. CXR improvement follows clinical improvement after 1 to 2 weeks or more.
11. ABG
    a. Hypoxemia (PaO2 <60)
    b. Initially, respiratory alkalosis (PaCO2 <40) is present, which gives way to respiratory acidosis as the work of breathing increases and PaCO2 increases.
    c. If the patient is septic, metabolic acidosis may be present, with or without
    respiratory compensation.
12. Pulmonary artery catheter—enables a determination of PCWP. PCWP reflects left
    heart filling pressures and is an indirect marker of intravascular volume status.
    a. PCWP is the most useful parameter in differentiating ARDS from cardiogenic
    pulmonary edema.
    b. If PCWP is low (<18 mm Hg), ARDS is more likely, whereas if PCWP is high (>18 mm Hg), cardiogenic pulmonary edema is more likely.
    c. However, routine placement of pulmonary artery catheters has not been
    shown to be beneficial in ARDS or sepsis.
13. Bronchoscopy with bronchoalveolar lavage
    a. This may be considered if patient is acutely ill and infection is suspected.
    b. Fluid collected can be cultured and analyzed for cell differential, cytology,
    Gram stain, and silver stain.
    E. Treatment
14. Oxygenation—try to keep O2 saturation >90%.
15. Mechanical ventilation is based on the ARDSNet studies. The most important
    principles include using a high PEEP with low tidal volumes.
16. Fluid management
    a. Volume overload should be avoided. A low-normal intravascular volume is preferred; the goal should be a CVP 4 to 6 cm H2O. Vasopressors may be needed
    to maintain BP.
    b. On the other hand, patients with sepsis have high fluid requirements, so determining the appropriate fluid management may be difficult.
17. Treat the underlying cause, for example, infection.

A: Chest radiograph showing typical findings in ARDS. B: Another example of ARDS. Also
note presence of an ET and Swan–Ganz central venous catheter.
(A from Miller WT, Miller WT Jr. Field Guide to the Chest X-Ray. Philadelphia, PA: Lippincott Williams & Wilkins, 1999:4,
Figure 1.2B.) (B from Daffner RH. Clinical Radiology: The Essentials. 2nd ed. Philadelphia, PA: Lippincott Williams &
Wilkins, 1999:175, Figure 4.117A.)
A
B

5. Do not forget to address the patient’s nutritional needs. Tube feedings are preferred
   over parenteral nutrition (see Appendix).
   F. Complications
6. Permanent lung injury—resulting in lung scarring or honeycomb lung
7. Complications associated with mechanical ventilation
   a. Barotrauma secondary to high-pressure mechanical ventilation, possibly causing a pneumothorax or pneumomediastinum
   b. Nosocomial pneumonia
8. Line-associated infections: central lines and pulmonary artery catheters (line infection sepsis), urinary catheters (UTI), and nasal tubes (sinus infection)
9. Renal failure—may be due to nephrotoxic medication, sepsis with hypotension, or
   underlying disease
10. Ileus, stress ulcers

6. Multiple organ failure
7. Critical illness myopathy
   Mechanical Ventilation
   A. General characteristics
8. In treating respiratory failure, mechanical ventilation has two major goals: to
   maintain alveolar ventilation and to correct hypoxemia
9. The decision to initiate mechanical ventilation should be a clinical one. Generally,
   patients with the following require mechanical ventilation:
   a. Significant respiratory distress (e.g., high RR) or respiratory arrest
   b. Impaired or reduced level of consciousness with inability to protect the airway
   (look for absent gag or cough reflex)
   c. Metabolic acidosis (if the patient is unable to compensate with adequate hyperventilation)
   d. Respiratory muscle fatigue
   e. Significant hypoxemia (PaO2 <70 mm Hg) or hypercapnia (PaCO2 >50 mm
   Hg); respiratory acidosis (pH <7.2) with hypercapnia
10. ABGs are used to assess response to initiation of mechanical ventilation.
    Acceptable ranges of gas values include a PaO2 of 50 to 60 with PaCO2 of 40 to
    50, and pH between 7.35 and 7.50.
11. General principles
    a. Initial settings should rest the respiratory muscles.
    b. The goal is to reduce the likelihood of barotraumas (high static airway pressures, overinflation) and atelectasis (low static airway pressures, underinflation).
    c. A volume-cycled ventilator is most commonly used.
    B. Ventilator settings
12. Assist control (AC) ventilation
    a. This is the initial mode used in most patients with respiratory failure.
    b. Guarantees a “backup” minute ventilation that has been preset, but the patient
    can still initiate breaths at a faster rate than the backup rate.
    c. AC and other ventilator modes can be volume targeted or pressure targeted. If
    volume targeted is selected, the ventilator will give a preset tidal volume for each
    breath regardless of the pressure required to give that breath (ensures ventilation
    but could lead to high pressures and barotrauma); if pressure targeted is ­selected,
    the ventilator will deliver a fixed inspiratory pressure regardless of the tidal volume (avoids barotraumas but adequate ventilation may not be achieved).
    d. All breaths are supported by the ventilator (in contrast to intermittent mandatory ventilation).
13. Synchronous intermittent mandatory ventilation (SIMV)
    a. Patients can breathe on their own above the mandatory rate without help from
    the ventilator (i.e., the tidal volume of these extra breaths is not determined by
    the ventilator, as it is in the assisted controlled mode).
    b. If no spontaneous breath is initiated by the patient, the predetermined mandatory breath is delivered by the ventilator.
    c. May increase respiratory fatigue and prolonged mechanical ventilation.
14. Continuous positive airway pressure (CPAP)
    a. Positive pressure (0 to 20 cm H2O) is delivered continuously (during expiration
    and inspiration) by the ventilator, but no volume breaths are delivered (patient
    breathes on his or her own).
15. Pressure support ventilation (PSV)
    a. Inspiratory pressure is set to support each patient-triggered breath, with a constant PEEP. This is mostly used during weaning trials (Clinical Pearl 2-11).
16. Noninvasive mechanical ventilation
    a. CPAP: Positive pressure (0 to 20 cm H2O) is delivered continuously (during
    expiration and inspiration) by the ventilator, but no volume breaths are delivered (patient breathes on his or her own).

b. BiPAP: Similar to PSV but done with a face or nasal mask rather than intubation. Delivers a set inspiratory pressure with a constant PEEP.
C. Key parameters

1. Settings that affect PaCO2: Minute ventilation (RR × VT)
   a. This should be adjusted to achieve the patient’s baseline PaCO2.
   b. An initial tidal volume (VT) of 4 to 8 mL/kg is appropriate in most cases (lower
   tidal volumes are recommended in patients with ARDS and COPD).
   c. A rate of 10 to 12 breaths/min is appropriate.
2. Settings that affect PaO2: FiO2 and PEEP
   a. FiO2: The initial FiO2 should be 100%. Quickly titrate down and use the lowest
   possible FiO2 to maintain a PaO2 of 50 to 60 or higher (or saturation >90%) to
   avoid oxygen toxicity (theoretical, FiO2 < 60% is usually safe).
   b. PEEP is positive pressure maintained at the end of a passive exhalation—
   keeps alveoli open—5 cm H2O is an appropriate initial setting. High levels of
   PEEP increase the risk of barotrauma (injury to airway = pneumothorax) and
   decrease cardiac output (decreased venous return from increased intrathoracic
   pressure).
   D. Complications
3. Anxiety, agitation, discomfort
   a. Both sedation and analgesia are important; paralytics should be used during
   intubation and can be used after intubation if the patient continues to be agitated and fight the ventilator.
4. Difficulty with tracheal secretions—suction on a regular basis.
5. Ventilator-associated pneumonia (risk is ∼1% per day).
6. Barotrauma—caused by high airway pressures.
7. Tracheomalacia (softening of the tracheal cartilage)—due to the prolonged presence of an endotracheal tube (ET).
8. Laryngeal damage during intubation.
9. Gastrointestinal effects (stress ulcers and cholestasis)—increased risk in mechanically ventilated patients. All patients should be on a PPI or H2 blocker.