ARDS

Diana May B. Laraya, MD

Acute

Respiratory

Distress

Syndrome

Definition:

Severe dyspnea of rapid onset

Hypoxemia

Diffuse pulmonary infiltrates

RESPIRATORY FAILURE

ARDS• Caused by diffuse lung injury

• Medical or surgical disorders

• Direct or Indirect

18th ed HPIM

• ALI: PaO2/FiO2 ≤ 300mmHg• ARDS: PaO2/FiO2 ≤ 200mmHg

etiology

• >80% caused by sepsis and Pneumonia• 40-50% : trauma, transfusion-related,

aspiration of gastric contents• Trauma ~ pulmonary contusion, multiple rib

fracture, chest wall trauma/flail chest• Rare causes: head trauma, near-drowning,

toxic inhalation, burns

ARDS• Clinical course

1. Exudative

2. Proliferative

3. Fibrotic

ARDS: pathophysiol

ogy

ARDS: exudative

ARDS: exudative

• Early alveolar edema• Neutrophil-rich leukocyte infiltration• Hyaline membrane from diffuse alveolar

damage• ~First 7 days

ARDS: exudative

• Prominent interstitial inflammation• Early fibrotic changes• ~Day 7-day21

Neutrophillymphocyte ↑type II pneumocytedifferentiate into type I

pneumocyte Synthesis of new pulmonary surfactant

ARDS: proliferative

• Alveolar type III procollagen peptide ~↑ mortality from ARDS

• Extensive alveolar duct and interstitial fibrosis• Emphysema-like changes with bullae• Intimal fibroproliferation in the pulmonary

microcirculation vascular occlusionpulmonary HPN

ARDS: fibrotic

• Long-term support on MV and supplemental O2

• INCREASED RISK pneumothorax• REDUCTION in lung compliance• Increased pulmonary dead space

↑↑↑ Morbidity and Mortality

ARDS: fibrotic

Time course for the development of ARDS

ARDS: MANAGEMENT

• GENERAL PRINCIPLESRecognition and treatment of the underlying medical and

surgical disorderMinimizing procedures and their complicationsProphylaxis against VTE, GI bleeding, aspiration, excessive

sedation and central venous catheter infectionPrompt recognition of nosocomial infectionsProvision of adequate nutrition

• Mechanical ventilation management

• VENTILATOR-induced lung injury:• Repeated alveolar lung overdistention• Recurrent alveolar collapse

ARDS: MANAGEMENT

• National Institute of Health:ARDS Network– RCT comparing low VT (6mL/kg BW) ventilation

vs conventional VT (12mL/kg BW)

- Significantly low mortality rate in the low VT pxs (31%) compare to conventional VT (40%)

ARDS: MANAGEMENT

VT=6mL/kg BW

• Mechanical ventilation management

• VENTILATOR-induced lung injury:Repeated alveolar lung overdistention• Recurrent alveolar collapse

ARDS: MANAGEMENT

• Prevention of alveolar collapse• ALVEOLAR COLLAPSE due to– Presence of alveolar and interstitial fluid– Loss of surfactant– Decrease in lung compliance

ARDS: MANAGEMENT

• Positive end-expiratory pressure (PEEP)– Minimize FiO2

– Maximize PaO2

• “Optimal PEEP” in ARDS: 12-15mmHg

ARDS: MANAGEMENT

• Inverse-ratio ventilation– Increase mean airway pressure– Longer inspiration time than expiration time

I:E >1:1• ↓ time to exhale => dynamic hyperinflation =>

increased end-expiratory pressure => oxygenation improved

No benefit in ARDS mortality

ARDS: MANAGEMENT

• PRONE position– Improve arterial oxygenation– Uncertain effect on survival and outcomesHazards:

Accidental endotracheal extubationLoss of central venous cathetersOrthopedic injury

ARDS: MANAGEMENT

• Other mechanical ventilation strategies:1. High-frequency ventilation (HFV) • High respiratory rates (5-20 cycles per second) and• Low VTS (1-2mLkg)

2. Partial liquid ventilation (PLV) • Perfluorocarbon

No survival benefit from ARDS

ARDS: MANAGEMENT

• Lung-replacement therapy with extracorporeal membrane oxygenation (ECMO)– Neonates– With survival benefit

ARDS: MANAGEMENT

adjunctive ventilator therapy (PEEP, HFV, PLV, ECMO, etc)

incomplete efficacy datarescue therapy

ARDS: MANAGEMENT

ARDS: Fluid Management

• Fluid restriction• Diuretics

reduce left atrial filling pressure↓

Minimizes pulmonary edema prevents further decrements in arterial oxygenation and lung compliance

NEUROMUSCULAR blockade

• EARLY Neuromuscular blockade for 48H– Cisatracurium besylate

lung-protective ventilation px-ventilator synchrony

ARDS: Glucocorticoids

• Reduce pulmonary inflammation• Benefit in some studies

• Current evidence does not support the use of glucocorticoids

OTHER THERAPIES

1. SURFACTANT replacement2. Inhaled nitric oxide3. Inhaled epoprostenol

improve oxygenation-transient***do not improve survival or decrease

time on Mech Vent

ARDS: Prognosis

• Mortality ~ 26%-44%

Nonpulmonary causes >80% Sepsis Nonpulmonary organ failure

ARDS: Mortality Risk Factors

• Nonpulmonary cause – major• Advanced age (>75yo)• Preexisting organ failure• Direct lung injury (2x)• Severe hypoxemia (PF ratio <100)

Functional Recovery in ARDS survivors

• Maximal lung fxn – 6months• 1yr after extubation ~ 1/3 have N spirometry• Most have mild abnormalities in pulmo fxn• 5yr assessment ~ exercise limitation and

decreased physical quality of life

ARDS

Thank

you…?