THE ACUTE RESPIRATORY

DISTRESS SYNDROME

Daniel Brockman, DO

Objectives

Describe the history and evolution of the diagnosis

of ARDS

Review the diagnostic criteria for ARDS

Discuss the primary interventions in ARDS

Address salvage therapies for severe hypoxia in

ARDS.

Case Presentations

A

23 year old male college student…

18 year old female…

60 year old male SNF resident…

40 year old female with an SBO

Case presentations

...is found down after ODing on Heroin.

…comes to the ICU after DCS for abdominal trauma

from an MVC.

…is sent to the ED with a fever and cough.

…vomits on the wards and collapses.

Next they

develop severe hypoxia.

And a CXR reveals

Or this

Or this

Or maybe it was a CT to r/o PE

Epidemiology

Approximately 190,000-200,000 cases annually

reported.

Incidence estimated to be 86 case per 100,000

Increased incidence in the elderly

306 case per 100,000

Estimated mortality between 30-40%.

Historical Perspective

During the Vietnam War a clinical syndrome of

severe hypoxia was identified soldiers who suffered

serious injuries.

The Adult Respiratory Distress

Syndrome

In 1967 a case series reported 12 cases of sudden

onset severe hypoxia associated with diffuse patchy

infiltrates on chest X-ray.

The condition was termed the Adult Respiratory

Distress Syndrome.

The X-ray appeared very similar to the Infant

Respiratory Distress Syndrome.

Pediatricians are for babies

As the condition was diagnosed more it became

apparent that ARDS occurred in all ages.

Pediatricians REALLY don’t like writing the word

adult and were quite vocal about it.

Therefore the name was changed to ACUTE

Respiratory Distress Syndrome

Shortly there after

Tom Petty, MD had a new ABG machine

Discovered in a patient with what was later identified

as ARDS after trauma that retarding expiratory flow

resulted in an increase in PaO2(40->130).

This maneuver was repeated in 12 additional patients

with similar clinical picture with consistent improvements

in oxygenation.

So what is ARDS?

Diffuse pulmonary edema due to fluid leaking in to

alveolar spaces and damage to lung tissues from

inflammation and loss of oncotic forces.

So all of these:

Neurogenic Pulmonary Edema

Fat Embolism

Shock Lung

TRALI

Pump Lung

Capillary Leak Syndrome

Are just ARDS

Clinical Diagnosis

AECC Definition:

Due to the disparate causes and unclear definition a

diagnostic criteria was composed in 1994 to

standardize the definition of ARDS

Main diagnostic points were

Acute Onset

Hypoxia

Bilateral Infiltrates

Absence of Heart Failure

Refining the Diagnosis

The Berlin Criteria was devised by a panel of

experts in 2011 and released in 2012.

Provided more concrete criteria for some of the

diagnostic requirements.

Added a severity scale to diagnosis.

Not very different from AECC in actuality.

AECC vs. Berlin

Acute Onset.

Diffuse patchy infiltrates on CXR.

Absence of LV dysfunction on Echo or PAWP<18.

PaO2/FiO2 <200.

Onset within 7 days.

Diffuse patchy infiltrates on CXR or CT scan.

No clinical suspicion of heart failure or absence of LV dysfunction on Echo.

PaO2/FiO2<300 on at least 5 of PEEP or EPAP.

Berlin Criteria Severity Scale

Based on PaO2/FiO2 ratio.

Mild 201-300

Moderate 101-200

Severe <101

Correlates with mortality

Mild: 27%

Moderate: 32%

Severe: 45%

So if you want to be technical

Patient’s with cardiomyopathies can’t have ARDS.

Patient’s with a pneumonectomy can’t have ARDS

Pathophysiology

Inciting event causes release of inflammatory

markers causing damage to capillaries and alveoli

resulting in fluid exiting the vascular space into the

lung parenchyma resulting in filling of or collapse

of alveoli.

Pathophysiology

Results in patches of alveoli that receive no

ventilation causing shunting of deoxygenated

venous blood through portions of the lung without

oxygenation.

Phases of ARDS

Acute(or exudative) Phase

Edema and diffuse alveolar damage.

Generally Days 1-6

Phases of ARDS

Healthy Lung

Acute ARDS

Phases of ARDS

Proliferative Phase

Edema begins to improve,

overgrowth of Type 2

Aveolar Cells, myofibroblasts

invade into interstitium and

collagen deposition occurs.

Thank you Pediatricians

Chronic Acute Respiratory Distress Syndrome

Also called Fibrotic Phase of ARDS

Fibrosis of lung parenchyma,

formation of cysts in

damaged parts of the

Lung.

Inciting Events

Pulmonary

Pneumonia

Aspiration

Pulmonary Contusion

Near Drowning

Smoke Inhalation

Extrapulmonary

Sepsis

Severe Trauma

Burns

Pancreatitis

Blood Transfusions

Drug Overdose/Reaction

Head Injury

Cardiac Bypass

Bone Marrow Transplant

Complications

Pneumothorax

Pneumomediastinum

Decreased venous return-hypotension

Worsening of pulmonary edema and worsening oxygenation

Organ dysfunctiomn

Many are actually are complications of mechanical ventilation in ARDS

Barotrauma

Injury to lung due to High Ventilatory pressures.

Pneumothorax

Pneumomediatinum

Volutrauma

Increase in inflammatory markers caused by

distension of alveola.

Leads to further lung injury from inflammation and

extrapulmonary organ injury.

Atelectrauma

Increase in both inflammatory cytokines and

alveolar injury due to shearing caused by the

repeated opening and closing of alveolar units.

Optimizing Treatment in ARDS

Low Tidal Volume Ventilation

Controlling Plateau Pressures

Permissive Hypercapnia

Providing adequate Oxygentaion

Early Neuromuscular Blockade

The ARMA Trial

Randomized control trial

861 patients meeting AECC definition of Acute Lung

Injury (PaO2/FiO2<300)

Randomized to:

6 ml/kg(PBW) and Plateau pressure <30

12 ml/kg(PBW) and Plateau pressure <50

Stopped early due to significantly higher mortality in

12 ml/kg group

Demographics

Results

12 ml/kg 6 ml/kg P-value

Mortality 39.8% 31.0% 0.007

Ventilator free days 10 12 0.007

Days without other organ failure 11 15 0.006

Barotrauma Events 11 10 0.43

PEEP strategies

Best PEEP using flow volume loops

Super PEEP

Optimum PEEP for compliance

Minimum PEEP for oxygenation

No good evidence to support one strategy over

another for determining PEEP.

Some points about PEEP

It takes time to recruit alveoli with PEEP, don’t

expect rapid changes in oxygenation.

A lung opening procedure or recruitment maneuver

can be used to more rapidly open the lung and

improve oxygenation.

Increase PEEP to 30-40 for 20-30 seconds.

Early Neuromuscular Blockade

Randomized Double Blind Placebo Controllede Trial

340 patients with AECC definition of ARDS and

PaO2/FiO2<150 on at least 5 of PEEP

Randomized to

Deep Sedation for 24 hours

Deep Sedation plus Neuromuscular Blockade with

cisatricurium for 48 hours.

Demographics

Results

Results

Adjust 90 day Hazard Ratio for Death: 0.68 (p-value: 0.04)

Neuromuscular Blockade

Subgroup analysis based on severity of ARDS

defined by PaO2/FiO2 ratio demonstrated that

mortality benefit occurred in patients with

PaO2/FiO2 ratio <120.

Fluid Management(The FACCT Trial)

Randomized Controlled Trial

Two major questions:

Do PAC’s help management of ARDS

Keep this short: NO

Liberal(give fluid) vs restrictive(diurese) management

The FACCT Trial

1000 patient meeting AECC definition of Acute

Lung Injury (PaO2/FiO2<300)

Randomized to:

Demographics

Results

Salvage/Rescue Therapies

Proning

Inhaled Vasodilators

APRV

HFOV

ECMO

Proning

Proning

Reverses dependant areas of lung leading to

decreased V/Q mismatch.

Creates increase in extrathoracic pressure.

Recent NEJM study showed improved mortality in

patients with severe ARDS (PaO2/FiO2<100 after

36 hours of treatment) kept prone for 14 hrs a day.

Inhaled Nitric Oxide

Vasodilator

Enters opened areas of lung and dilates capillaries increasing blood flow to open areas of lung.

Improves V/Q matching.

Expensive.

Improves oxygenation but no proven mortality benefit.

Increased incidence of renal failure.

Epoprostenol

Same mechanism of action as INO.

Administered as continuous NEB @ 50 ng/kg/min

Again improves oxygenation but no proven mortality

benefit

Significantly cheaper than INO.

No evidence of increased renal failure.

Iloprost

Another inhaled vasodilator

Administered Ever 2 to 4 hours

Has the least evidence supporting its effectiveness.

Cheapest option of Inhaled Vasodilators

APRV

APRV

Alternate mode of ventilation high steady airway

pressure that drops to a lower pressure for a brief

period of time.

Allows higher airway pressures.

Some small studies show decreased rates of

developing ARDS, but no other evidence of

outcomes differences in patients with ARDS.

HFOV

HFOV

Continuous high airway pressures, a piston rapidly

pushes tiny amounts of air into and out of the lungs.

Allows higher mean airway pressures without large

tidal volumes or shearing improving recruitment and

oxygenation.

In 2 large studies no benefit or worsened outcomes

if used in early ARDS.

ECMO

ECMO

By running Venous blood through a membrane

oxygenator the patient can have effective CO2

removal and oxygenation without relying on the

lungs.

Allows for minimal vent settings to rest the lungs.

Evidence is limited but shows some potential benefit

in severe ARDS.

Key Points

ARDS is a clinical diagnosis with specific criteria.

Acute Onset <7 days

PaO2/FiO2 <300

Bilateral patchy infiltrates

Not cardiac related

Key Points

Low tidal volume ventilation improves mortality.

6 mL/kg PBW(based on Height)

Diuresis decreases ventilator days and organ failure in

hemodynamically stable patients.

Early Neuromuscular Blockade of benefit in moderately

severe cases

Variety of salvage therapies

Proning, Inhaled Vasodilators, APRV, HFOV, ECMO

Only proning has shown any mortality benefit.

Key Points

Variety of salvage therapies

Proning, Inhaled Vasodilators, APRV, HFOV, ECMO

Only proning has shown any mortality benefit.