Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome : 

Acute Respiratory Distress Syndrome By Chest Department Ain Shams University

Objectives : 

Objectives Define ALI and ARDS. Describe the pathophysiology of ARDS. Detail types of Ventilator Associated Lung Injury. Describe strategies to avoid VALI. Describe ARDS network study and consequent protocols. Define lung recruitment maneuvers.

History : 

(Ashbugh et al, Lancet, 1967) History In 1967, when Ashbaugh and colleagues described 12 patients with acute respiratory distress, cyanosis refractory to oxygen therapy, decreased lung compliance, and diffuse infiltrates evident on the chest radiograph.

History : 

(Murray et al, Am Rev Respir Dis 1989;139:1065) History In 1988, an expanded definition was proposed that quantified the physiologic respiratory impairment through the use of a four-point lung-injury scoring system that was based on: level of positive end-expiratory pressure ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen static lung compliance degree of infiltration evident on chest radiographs.

Definitions : 

Am J Respir Crit Care Med Vol 149. pp 818-824,1994 Definitions (1) Oxygenation abnormality, a PaO2/FIO2 200 ARDS, 300 ALI. (2) Chest radiograph criterion, bilateral infiltrates. (3) Pulmonary artery wedge pressure 18 mm Hg, or no clinical evidence of left atrial hypertension.

Risk Factors : 

Risk Factors

The Acute Phase : 

The Acute Phase

The Acute phase : 

(Lorraine and Mathay, N Eng J Med, 2000) The Acute phase Characteristic hyaline membrane With associated intraalveolar red cells and neutrophils.

Fibrosing Alveolitis : 

(Lorraine and Mathay, N Eng J Med, 2000) Fibrosing Alveolitis

Outcome : 

Outcome Complete resolution. Pneumothorax. Fibrosing alveolitis. Mortality rate has declined from 66-80% to 34% (Abel et al, Thorax, 1998)

Mechanism : 

Mechanism Neutrophil activation and accumulation in alveoli. Other proinflammatory cytokines. VILI. Inflammation-Coagulation interaction. Deposition of collagen and fibronectin.

Mechanism : 

Mechanism Resolution is done by active sodium and chloride transport from distal alveoli and then water follows. Removal of insoluble proteins is achieved by: Endocytosis. Transcytosis. Phagocytosis. Removal of cells depends mainly on apoptosis.

All of the following can lead to ARDS except : 

All of the following can lead to ARDS except Burns. CHF. Sickle cell disease. Acute pancreatitis. Drowning. Fat embolism.

All of the following can lead to ARDS except : 

All of the following can lead to ARDS except Burns. CHF. Sickle cell disease. Acute pancreatitis. Drowning. Fat embolism.

Slide 17: 

(NEJM, 2005)

Treatment : 

Treatment Search, prevent and treat infection. GI prophylaxis. Anticoagulation. Nutrition. Supportive Care.

History of Ventilation Strategies : 

History of Ventilation Strategies

Slide 20: 

Alveoli filled with inflammatory cells Stiff lungs Low V/Q relationship Shunts Surfactant dysfunction alveolar collapse Hypoxemia

ARDS : 

ARDS Increased pulmonary shunt. Increased dead space ventilation. Reduced pulmonary compliance. Increased work of breathing. Hypoxemia. Respiratory failure requiring mechanical ventilation.

The role of mechanical ventilation in ARDS is: : 

The role of mechanical ventilation in ARDS is: 1. Treat the syndrome. 2. Prevention of further lung injury. 3. Support gas exchange functions of the lungs allowing it time to heal. 4. Giving more oxygen to the body so it can fight MODS.

The role of mechanical ventilation in ARDS is: : 

The role of mechanical ventilation in ARDS is: 1. Treat the syndrome. 2. Prevention of further lung injury. 3. Support gas exchange functions of the lungs allowing it time to heal. 4. Giving more oxygen to the body so it can fight MODS.

Mechanical ventilation of ARDS the old way : 

Biggatello L, Cairo 2003 Mechanical ventilation of ARDS the old way Vt: 10-15 ml/Kg. PEEP 10 cm H2O. High PEEP 30-40 cm H2O. Normal ABG.

Ventilator Associated Lung Injury : 

Ventilator Associated Lung Injury Barotrauma Volutrauma Atelectrauma Biotrauma

Barotrauma : 

Barotrauma Excess PP >50 mmHg can lead to air leaks pneumothorax, pneumomediastinum, SC emphysema, pneuopericardium.

Volutrauma : 

(Dreyfuss et al., 1988). Volutrauma High end inspiratory volume can lead to a more subtle alveolar stress injury leading to increased lung water and is reversed by PEEP.

Atelectrauma : 

Atelectrauma Low lung volume surfactant is squeezed out leading to alveolar collapse, repeated collapse and reopening leads to a shear stress particularly early in the course of lung injury.

Biotrauma : 

Biotrauma Inflammatory products are released secondary to mechanical factors lead to MODS.

Slide 30: 

Slutsky, A. S. Chest 1999;116:9S-a-15S-a

VALI is more liable to occur in: : 

VALI is more liable to occur in: Healthy lung regions. Diseased lung regions.

VALI is more liable to occur in: : 

VALI is more liable to occur in: Healthy lung regions. Diseased lung regions.

Mechanical Ventilation Strategies : 

Mechanical Ventilation Strategies Low Vt, low PP with permissive hypercapnia. PEEP Recruitment maneuvers. APRV. BIPAP. HFOV.

ARDS Network Study : 

ARDS Network Study 861 ARDS and ALI pts 429 12 ml/Kg PP < 50 cm H2O 432 6 ml/Kg PP < 30 cm H2O

Contraindications to permissive hypercapnia include the following except: : 

Contraindications to permissive hypercapnia include the following except: Acute head injury. Acute myocardial infarction. Acute metabolic acidemia. TCA overdose. Severe Pneumonia. Sickle cell disease.

Contraindications to permissive hypercapnia include the following except: : 

Contraindications to permissive hypercapnia include the following except: Acute head injury. Acute myocardial infarction. Acute metabolic acidemia. TCA overdose. Severe Pneumonia. Sickle cell disease.

PEEP : 

PEEP Improves oxygenation. Increases lung volume by increasing FRC. At optimum levels PEEP increases respiratory system compliance. In patients with airflow limitation PEEP antagonizes auto PEEP.

PEEP : 

PEEP PEEP can prevent atelectrauma (prevent derecruitment) not only improves oxygenation. Incremental steps. Decremental steps. P-V curve.

Pressure-Volume Curve : 

Pressure-Volume Curve

ARDS Curve : 

ARDS Curve

The Problem : 

The Problem Posterior need high PEEP Anterior need low PEEP Collapse Overdistension

Recruitment Maneuvers : 

Recruitment Maneuvers

Recruitment Maneuvers : 

Recruitment Maneuvers High level continuous positive airway pressure: sustained inflations 40-50 cmH2O for 30-60 seconds (Amato et al., NEJM 1998). Intermittent sighs. Three consecutive sighs per minute 40-50 cmH2O each (Pelosi, AJRCCM 1999). Intermittent and stepwise high positive end-expiratory pressure levels with a fixed pressure control maneuver (Foti et al., 2001).

Prone : 

Prone Prone positioning increases PaO2 in 70% of ARDS patients. This effect fades off in the supine position (Catte et al., AJRCCM 1997). No effect on mortality (Gattinoni et al., NEJM 2001).

Pressure Controlled Ventilation : 

Pressure Controlled Ventilation Control airway and alveolar pressure. Improved efficiency of gas exchange. Ease and safety of prolonged inspiratory times. Improved patient comfort.

Negative effects of PPV include the following except: : 

Negative effects of PPV include the following except: 1) Increased intrathoracic pressure. 2) Reduced venous return. 3) Reduced cardiac output. 4) Improved renal perfusion. 5) Reduced blood pressure.

Negative effects of PPV include the following except: : 

Negative effects of PPV include the following except: 1) Increased intrathoracic pressure. 2) Reduced venous return. 3) Reduced cardiac output. 4) Improved renal perfusion. 5) Reduced blood pressure.

Spontaneous Breathing : 

(Kuhlen R, Rossaint R,2002). Spontaneous Breathing Spontaneous breathing Prevents all negative effects of positive pressure ventilation. Compared with controlled mechanical ventilation, spontaneous breathing results in reduced atelectasis and improved ventilation-perfusion relationship. Less use of sedation and muscle relaxation.

BIPAP & APRV : 

BIPAP & APRV

HFOV : 

(Derdak et al., AJRCCM 2002) HFOV High frequency Oscillatory Ventilation Jet. Percussive. Provides: very small Vt with minimal distending alveolar pressures. high mean airway pressure maintaining a high end expiratory lung volume.

Nitric Oxide : 

(Hurford and Bigattello, Anesthesiology 2002) Nitric Oxide 5-10 ppm NO leads to decreased PAP and increases PaO2 in 60% of ARDS pts. No persistent effect. Can be used as rescue therapy.

Liquid Ventilation : 

(Hirschl et al., AJRCCM 2002) Liquid Ventilation Perfluorocarbon ventilation may enhance gas exchange. Randomized trial: No effect on mortality.

Others : 

Others Steroids Surfactant ECMO

Steroides can be given in ARDS: : 

Steroides can be given in ARDS: Early in its course. When infection is not suspected. In the stage of fibrosing alveolitis. Routinely. Never. As rescue therapy.

Steroides can be given in ARDS: : 

Steroides can be given in ARDS: Early in its course. When infection is not suspected. In the stage of fibrosing alveolitis. Routinely. Never. As rescue therapy.

Mortality from ARDS : 

Mortality from ARDS 40-60 % 20-30% 30-40% 60-80%

Mortality from ARDS : 

Mortality from ARDS 40-60 % 20-30% 30-40% 60-80%

All in All : 

All in All Mechanical ventilation is a means of improving gas exchange while the lung is healing in ARDS. VALI should be avoided by using lung protective strategies. Pressure controlled mechanical ventilation allow better control and comfort for the patient.

All in All : 

All in All Vt 5-7 ml/Kg PP < 30 mmHg PEEP that produces best PaO2 with FIO2 < 0.6. Prone positioning should be tried in resistant cases.

Thank you : 

Thank you