ARDS & Mecanical ventilation

1. {
ARDS &Mecanical Ventilator
Done by : khadeeja nofal(200273)
Supervisor : Dr. Mazen Almasri
Dr.Ameen harb
Palestine Polytechnic University

2. Acute respiratory distress syndrome
 General characteristic
 Causes
 Clinical features
 Diagnosis
 Treatment
 Complications
:
Outline

3. Acute respiratory distress syndrome
ARDS

4.  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.
 ARDS is not a primary disease, but rather a disorder that arises due to other
conditions that cause a widespread inflammatory process.
 2012 Berlin definition:
a. Acute onset (<1 week of known clinical insult).
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
General Characteristics

5.  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.
Pathophysiology

6.  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.
 Decreased pulmonary compliance—leads to increased work of breathing.
 Increased dead space—secondary to obstruction and destruction of pulmonary–
capillary bed.
 Low vital capacity, low FRC.

7. 1. Sepsis is the 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.
Causes

8. 1. Dyspnea, tachypnea, and tachycardia due to increased work of breathing.
2. Progressive hypoxemia—not responsive to supplemental oxygen.
3. Patients are difficult to ventilate because of high peak airway pressures due to stiff,
noncompliant lungs.
Clinical Features

9. 1. CXR—shows diffuse bilateral pulmonary infiltrates
 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.
 CXR improvement follows clinical improvement after 1 to 2
weeks or more.
Diagnosis

10. 2. ABG
 Hypoxemia (PaO2 <60)
 Initially, respiratory alkalosis (PaCO2 <40) is present, which gives way to respiratory acidosis as
the work of breathing increases and PaCO2 increases.
 If the patient is septic, metabolic acidosis may be present, with or without respiratory
compensation.
3. Pulmonary artery catheter—enables a determination of PCWP. PCWP reflects left heart filling
pressures and is an indirect marker of intravascular volume status.
 PCWP is the most useful parameter in differentiating ARDS from cardiogenic pulmonary
edema.
 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.
 However, routine placement of pulmonary artery catheters has not been shown to be
beneficial in ARDS or sepsis.
4. Bronchoscopy with bronchoalveolar lavage
 This may be considered if patient is acutely ill and infection is suspected.
 Fluid collected can be cultured and analyzed for cell differential, cytology, Gram stain, and
silver stain.

11. 1. Oxygenation—try to keep O2 saturation >90%.
2. Mechanical ventilation is based on the ARDSNet studies. The most important
principles include using a high PEEP with low tidal volumes. Sedation and short term
paralysis may be needed to improve compliance with mechanical ventilation.
3. Fluid management
 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.
 On the other hand, patients with sepsis have high fluid requirements, so determining the
appropriate fluid management may be difficult.
4. Treat the underlying cause, for example, infection.
5. Do not forget to address the patient’s nutritional needs. Tube feedings are preferred
over parenteral nutrition .
Treatment

12. 1. Permanent lung injury—resulting in lung scarring or honeycomb lung.
2. Complications associated with mechanical ventilation:
 Barotrauma secondary to high-pressure mechanical ventilation, possibly causing
a pneumothorax or pneumomediastinum
 Nosocomial pneumonia
3. Line-associated infections: central lines and pulmonary artery catheters (line
infection sepsis), urinary catheters (UTI), and nasal tubes (sinus infection).
4. Renal failure—may be due to nephrotoxic medication, sepsis with hypotension, or
underlying disease.
5. Ileus, stress ulcers
6. Multiorgan failure
7. Critical illness myopathy and polyneuropathy
Complications

33. Thank you
Reference: Step Up to Medicine
U WORLD