ards old problem current strategies november 4 2013
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ARDS Old Problem Current strategies november 4, 2013. David W. Chang, EdD , RRT University of South Alabama. Outline. 1. Definition 2. History 3. Pathophysiology 4. Mechanical Stress 5. Clinical presentations 6. Management Strategies 7. Complications. Outline. 1. Definition

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ards old problem current strategies november 4 2013

ARDSOld ProblemCurrent strategiesnovember 4, 2013

David W. Chang, EdD, RRT

University of South Alabama

outline
Outline

1. Definition

2. History

3. Pathophysiology

4. Mechanical Stress

5. Clinical presentations

6. Management Strategies

7. Complications

outline1
Outline

1. Definition

2. History

3. Pathophysiology

4. Mechanical Stress

5. Clinical presentations

6. Management Strategies

7. Complications

slide4

Definition of ALI and ARDS (1994 AECC)

  • Acute onset
  • Hypoxemia (PaO2/FIO2 = 200 or 300 mm Hg)
  • Bilateral infiltrates
  • PCWP <18 mm Hg
outline2
Outline

1. Definitions of ALI and ARDS

slide6

Definition of ARDS (2011 Berlin)

  • P/F index
    • mild ARDS: 201 - 300 mmHg (≤ 39.9 kPa)
    • moderate ARDS: 101 - 200 mmHg (≤ 26.6 kPa)
    • severe ARDS: ≤ 100 mmHg (≤ 13.3 kPa)
  • Radiographic severity
  • Respiratory compliance ≤ 40 mL/cm H2O
  • PEEP ≥ 10 cm H2O
  • Corrected minute ventilation ≥ 10 L/min
outline3
Outline

1. Definition

2. History

3. Pathophysiology

4. Mechanical Stress

5. Clinical presentations

6. Management Strategies

7. Complications

slide8

History

  • 1950’s – Pulmonary edema (respirator lung, DaNang lung, shock lung, post-traumatic lung, wet lung)
  • 1959 – Neonatal RDS (Avery and Mead)
  • 1967 – ARDS (Ashbaugh et al)
slide9

History

  • Late 1960s – intensive care units became common in the U.S.
  • 1930s to 1950s – Drinker respirator (negative pressure ventilation, iron lung, chest cuirass)
  • 1950s to present – manual ventilation, positive pressure breathing, mechanical ventilator, microprocessor controlled ventilator

Mortality ranges from 90% (untreated)

to 25% (treated aggressively)

outline4
Outline

1. Definition

2. History

3. Pathophysiology

4. Mechanical Stress

5. Clinical presentations

6. Management Strategies

7. Complications

slide15

Pathophysiology

  • Direct injury

(e.g., pneumonia, aspiration, inhalation of toxins, near drowning, pulmonary contusion, fat embolism)

  • Indirect injury

(e.g., sepsis, severe trauma, acute pancreatitis, cardiopulmonary bypass, transfusion of blood products, drug overdose)

slide16

Pathophysiology

Direct injury may lead to

(A) activation of alveolar macrophages

(B) development of inflammatory response within the lungs

(C) alveolar epithelial damage

(D) alveolar walls are thickened due to acute distention of capillaries and interstitial edema

slide17

Pathophysiology

Direct injury may lead to

(E) pathological abnormality in the intra-alveolar space

(F) alveolar filling by edema, fibrin, collagen, neutrophilicaggregates or blood

(G) V/Q mismatch and intrapulmonary shunting

slide18

Pathophysiology

Indirect injurymay lead to

(A) Inflammatory mediators released from the extrapulmonary foci into the systemic circulation

(B) target of damage is the pulmonary vascular endothelial cell

(C) Endothelial dysfunction causes fluid extravasation from the capillaries and impaired drainage of fluid from the lungs

slide19

Pathophysiology

Indirect injurymay lead to

(D) Dysfunction of type II pulmonary epithelial cells leads to reduction of surfactant

(E) Increase of vascular permeability (transudate – a pale esinophilic finely granular, replaces the air)

*Exudate is caused by inflammation

Transudateis caused by disturbance of hydrostatic pressure and colloid osmotic pressure

slide20

Pathophysiology

Indirect injurymay lead to

(F) Recruitment of monocytes, polymorphonuclear leukocytes, platelets, and other abnormal cells

(G) Primary pathological alteration is microvascular congestion and interstitial edema

(H) V/Q mismatch and intrapulmonary shunting

outline5
Outline

1. Definition

2. History

3. Pathophysiology

4. Mechanical Stress

5. Clinical presentations

6. Management Strategies

7. Complications

slide24

Mechanical Stress

  • In ARDS, lung structure and function are not homogenous (i.e., healthy and sick lung units are mingled)
  • Collapsed lung units require higher positive pressure
  • Normal lung units become overdistendedat high pressures (video)
  • Barotrauma or volutraumais more likely to occur in normal lung units
outline6
Outline

1. Definition

2. History

3. Pathophysiology

4. Mechanical Stress

5. Clinical presentations

6. Management Strategies

7. Complications

slide27

Clinical presentations (ventilation & oxygenation)

  • Tachypnea
  • Rapid shallow breathing (↑f/VT)

↑VD/VT

↓VA (VA = VT– VD)

↑V/Q mismatch

  • ↑Intrapulmonary Shunting
  • ↓PaO2/FIO2 (P/F) index
  • ↑PaCO2 due to fatigue of respiratory muscles
  • Impending ventilatoryfailure
  • Acute ventilatoryfailure
slide28

Clinical presentations (radiographic)

  • Bilateral infiltrates
  • No signs of large pleural effusion (normal costophrenicangles)
  • No signs of atrial enlargement
  • No signs of heart failure (e.g., PCWP >18 mm Hg) or volume overload (high systemic blood pressure, peripheral edema)
outline7
Outline

1. Definition

2. History

3. Pathophysiology

4. Mechanical Stress

5. Clinical presentations

6. Management Strategies

7. Complications

slide30

Management Strategies

(ineffective, controversial, transient positive effects or not validated in large studies)

  • Drugs
    • Inhaled synthetic surfactant, IV antibody to endotoxin, ketoconazole (anti-fungal), ibuprofen (NSAID), simvastatin (cholesterol reduction), and inhaled nitric oxide (pulmonary vasodilator)
  • Nutritional support and supplement
  • Devices
    • ECMO, HFOV
slide31

Management Strategies

(reasonable and potentially useful)

  • Fluid management
  • Infection control (early intervention)
  • Prevention of VAP
  • Noninvasive ventilation (early intervention)
  • Nutritional support (enteral feeding tube)
  • Frequent position changes and range of motion
slide32

Management Strategies

(current practice)

  • Mechanical ventilation with PEEP
  • Decramental recruitment maneuver for optimal PEEP
  • Low VT and permissive hypercapnia
  • Airway pressure release ventilaiton
  • Inverse ratio ventilation
  • Prone positioning
slide33

Management Strategies

  • Mechanical ventilation(volume-controlled or pressure-controlled) to reduce work of breathing
  • Keep airway pressures below thresholds

PIP < 50 cm H2O

Plateau pressure < 35 cm H2O

(ARDSNet recommends < 30 cm H2O)

Mean airway pressure < 30 cm H2O

PEEP < 10 cm H2O

slide34

Management Strategies

Oxygen and PEEP to provide oxygenation

  • Note effects of PEEP and other factors on airway pressures (Figure)
    • mPaw= (f x I time / 60) x (PIP – PEEP) + PEEP
    • mPawmay be used to monitor hemodynamic effects
    • plateau pressure may be used to monitor overdistention

Recommended FIO2/PEEP combinations (Table)

Recruitment maneuver to determine optimal PEEP (Video)

slide40

Management Strategies

Low VT and Permissive Hypercapniato minimize lung injury (Table)

  • 6 mL/Kg
    • as low as 4 mL/Kg to keep PPLAT < 30 cm H2O
    • permit PaCO2 to rise
    • acidosis is managed by bicarbonate or tromethamine
slide42

Management Strategies

Airway Pressure Release Ventilation (APRV) (Figure)

↓decreased airway pressure requirement

↓ minute ventilation

↓ dead-space ventilation

promote spontaneous breathing

↓ use of sedation & neuromuscular blockade optimized ABG results

↑ FRC

↑ cardiac output

slide44

Management Strategies

Inverse ratio ventilation (IRV)

Pressure-Controlled + IRV

(pressure titrated to low VT 4 to 7 mL/kg)

Long inspiratory time

(inspiratory flow titrated to desired inverse ratio)

slide45

Management Strategies

Inverse ratio ventilation (IRV)

  • Facilitate gas exchange (esp. O2)
  • Reduce FIO2 and PEEP requirement
  • Require sedation and neuromuscular blockade
  • Monitor for improvement & hemodynamic effects
slide47

Management Strategies

Prone positioning

  • Lung zones
  • Lung volume distribution

* Improvement in oxygenation is temporary

outline8
Outline

1. Definition

2. History

3. Pathophysiology

4. Mechanical Stress

5. Clinical presentations

6. Management Strategies

7. Complications

slide55

Complications

  • Ventilator-associated pneumonia
    • Prevention and intervention
  • Hypoxic-ischemic encephalopathy
    • Brain (2% body weight, 15% energy consumption, cannot hold or store energy in the form of glycogen, cannot utilize fatty acids, depends on a constant supply of oxygen and glucose)
    • CPP = MAP – ICP (normal 70 to 80 mm Hg)
summary
Summary
  • Early intervention
  • Team approach
  • Tailor management strategies to patient’s need
  • Prevent complications
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