ards old problem current strategies november 4, 2013
DESCRIPTION
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 - PowerPoint PPT PresentationTRANSCRIPT
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ARDS OLD PROBLEM
CURRENT STRATEGIES
NOVEMBER 4, 2013
David W. Chang, EdD, RRT University of South Alabama
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Outline1. Definition2. History3. Pathophysiology4. Mechanical Stress5. Clinical presentations6. Management Strategies7. Complications
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Outline1. Definition2. History3. Pathophysiology4. Mechanical Stress5. Clinical presentations6. Management Strategies7. Complications
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Definition of ALI and ARDS (1994 AECC)
Acute onset Hypoxemia (PaO2/FIO2 = 200 or 300 mm
Hg) Bilateral infiltrates PCWP <18 mm Hg
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Outline1. Definitions of ALI and ARDS
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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
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Outline1. Definition2. History3. Pathophysiology4. Mechanical Stress5. Clinical presentations6. Management Strategies7. Complications
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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)
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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)
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Outline1. Definition2. History3. Pathophysiology4. Mechanical Stress5. Clinical presentations6. Management Strategies7. Complications
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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)
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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
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Pathophysiology
Direct injury may lead to (E) pathological abnormality in the intra-
alveolar space(F) alveolar filling by edema, fibrin,
collagen, neutrophilic aggregates or blood
(G) V/Q mismatch and intrapulmonary shunting
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Pathophysiology
Indirect injury may 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
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Pathophysiology
Indirect injury may 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 Transudate is caused by disturbance of
hydrostatic pressure and colloid osmotic pressure
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Pathophysiology
Indirect injury may 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
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Outline1. Definition2. History3. Pathophysiology4. Mechanical Stress5. Clinical presentations6. Management Strategies7. Complications
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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 overdistended at high pressures (video)
Barotrauma or volutrauma is more likely to occur in normal lung units
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Outline1. Definition2. History3. Pathophysiology4. Mechanical Stress5. Clinical presentations6. Management Strategies7. Complications
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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 ventilatory failure Acute ventilatory failure
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Clinical presentations (radiographic)
Bilateral infiltrates No signs of large pleural effusion (normal
costophrenic angles) 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)
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Outline1. Definition2. History3. Pathophysiology4. Mechanical Stress5. Clinical presentations6. Management Strategies7. Complications
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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
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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
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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
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Management Strategies
Mechanical ventilation (volume-controlled or pressure-controlled) to reduce work of breathing
Keep airway pressures below thresholdsPIP < 50 cm H2OPlateau pressure < 35 cm H2O (ARDSNet recommends < 30 cm H2O)Mean airway pressure < 30 cm H2OPEEP < 10 cm H2O
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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 mPaw may be used to monitor hemodynamic
effects plateau pressure may be used to monitor
overdistentionRecommended FIO2/PEEP combinations (Table)Recruitment maneuver to determine optimal PEEP (Video)
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Management Strategies
Low VT and Permissive Hypercapnia to 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
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Management Strategies
Airway Pressure Release Ventilation (APRV) (Figure)↓decreased airway pressure requirement↓ minute ventilation↓ dead-space ventilationpromote spontaneous breathing
↓ use of sedation & neuromuscular blockade optimized ABG results↑ FRC↑ cardiac output
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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)
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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
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Management Strategies
Prone positioning Lung zones Lung volume distribution
* Improvement in oxygenation is temporary
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Outline1. Definition2. History3. Pathophysiology4. Mechanical Stress5. Clinical presentations6. Management Strategies7. Complications
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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)
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Summary Early intervention Team approach Tailor management strategies to patient’s need Prevent complications
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