Acute Respiratory Distress Syndrome

(ARDS)
ARDS
• Life threatening disorder.
• Presents across a continuum. New Berlin Definition
(2012) developed by ARDS Definition Task Force.
• A wide spectrum of clinical severity.
• A condition of non-cardiac pulmonary edema.*
• Results from direct and indirect pulmonary insults.

*PAOP < 18 mmHg.

Refer to reference chart at end of PPT for normal values.
 Terms, Definitions Change, Much Still Unknown

• Short story
– ALI eliminated, ARDS has 3 categories, progressive

• Concise, pros/cons to change

https://lifeinthefastlane.com/ccc/acute-respiratory-distress-syndrome-ards-definitions/

• Elaborated
– Acute respiratory distress syndrome: new definition, current and future
therapeutic options.
 Compare the
CXR’s
included in
this PPT to
get a sense
of the
spectrum of
clinical
severity.
The formula to calculate P/F Ratio will be discussed in the next slide.
P/F Ratio
Calculate the PaO2 / FiO2 Ratio
• Divide the PaO2 by the FiO2 to get the P/F ratio.
Example
• If patient’s PaO2 is 80 mm Hg on 100 % oxygen then:
• P/F = 80 / 100% (1.0)
• P/F = 80
• P/F Ratio is < 100 mm Hg. Patient has Severe ARDS.

• Try this one: PaO2 100 mm Hg, FiO2 21%. (0.21)

• What’s a normal value?

Go to https://lifeinthefastlane.com/ccc/pao2fio2-ratio/ for the answer.
 Multi-Transfusion / TRALI

Transfusion Associated Lung Injury Note bilateral opacities, often

(TRALI). If risk factor/temporal referred to as “white out”.
relationship exist to support ARDS dx,
may be dx’ed as transfused ARDS, if
not, may be dx’ed as TRALI.
 ARDS
Direct Insults Indirect Insults
• Aspiration • Sepsis (most common cause
of ARDS)
• Pneumonia
• Shock
• Pulmonary trauma • Multi-trauma (non-thoracic)
• O2 toxicity • DIC
• Inhalation injury • Burns
• Radiation • Multiple transfusions
• PE / Fat emboli
• Pancreatitis
Inflammatory Response • Drug Overdose
Release of inflammatory mediators
Alveolar / Capillary Barrier

• Composed of 2 layers
– microvascular epithelium
– alveolar epithelium
• Alveolar endothelium
– Type I pneumocytes
– Type II pneumocytes

• http://www.ardsnet.org/ Explore. What treatment was identified?

Capillary Leak
When does this develop?
.

Fu Z, JAP 1992; 73:123

Alveolar Collapse
When is surfactant inactivated?
When does alveolar collapse develop?
.

CT Scan: Heterogeneous
Non-dependent alveoli

Dependent alveoli
Compare CXR: ARDS
to CT Scan: ARDS

Do different
diagnostic
tools provide
different
perspectives?
 CT Scan of Chest
Consider idea that dependent areas of lung most affected.
 Phases of ARDS
Define:

• Exudative

• Fibroproliferative

• Resolution

Apply knowledge of effects of cardiac remodeling. What might you anticipate about lung function?
 Diagnosis & Treatment
• Clinical presentation Definitive therapy ?
• ABG
• CXR ARDS
• CT Scan
Prevention

Support
 5 P’s of Therapy
• Perfusion
• Positioning
• Protective lung ventilation (permissive hypercapnia)
• Protocol weaning
• Preventing complications

How does it all relate?

Positioning & Rotational Therapy
Continuous Lateral Rotation

Goals
Improve ventilation of collapsed alveoli
Mobilize secretions and lung H2O
Redistribution of perfusion to ventilated lung units
Proning
• Can you imagine turning a critically ill person onto their belly?

• Read the article Prone positioning for patients with ARDS to

learn about your role. (Article posted on Sakai.)

• Visit the link to browse an interesting dialogue between nurses

about proning. Note how it mentions nurses’ “tolerance” for first
15 minutes of instability.
http://allnurses.com/ccu-nursing-forum/ards-prone-position-336889.html

• What do you think about this?

This Confusion is Confusing. What’s the story?

Think about it this way…

LUNGS ARE STIFF?
Damaged lung(s) less compliant

LUNGS ARE SMALL?

Heterogeneous areas of lung damage
lead to reduced amount of functioning lung

The next several slides will help you to think more about this. It begins
with some background information and continues with therapies that you can encounter.
 ARDS

• Alveolar changes result in 66% reduction of TLC

• Only 33% can be ventilated (baby lung)
https://ccforum.biomedcentral.com/articles/10.1186/s13054-017-1905-9

• Vt based on “normal” TLC is too large

Total Lung Capacity (TLC)

Definition 1. the inspiratory capacity plus the functional residual capacity; the volume of air contained
in the lungs at the end of a maximal inspiration; also equals vital capacity plus residual volume.

Visit https://www.cliffsnotes.com/study-guides/anatomy-and-physiology/the-respiratory-system/lung-
volumes-and-capacities to review values.
 Compare Normal Vt with ARDS Vt
Tidal Volume (Vt) for 70 kg person

Normal lungs
ARDS
Vt = 10 - 12 ml x kg Account for reduced TLC (66%)

Calculate using 10 ml. Vt = 700 ml - 462 ml (66%)

Vt = 10 ml x 70 kg Vt = 238 ml
Vt = 700 - 840 ml
 Is Hypoxemia Responsive or Refractory to O2 therapy?

This graphic
depicts severity of
injury and
relationship
between P/F Ratio
and therapy.

Which side of the

graphic represents
a patient with
ARDS that is
refractory to
therapy?
Multidisciplinary Plan of Care
Mechanical Ventilation: Modes, Adjunct, and Concepts
• PEEP
• Permissive Hypercapnia
• Inverse Ratio Ventilation
• Pressure Control Ventilation
• Pressure Regulated Volume Control (PRVC)
• High Frequency Ventilation (HFV)
• (Alveoli) Recruitment Maneuvers
Complications of Mechanical Ventilation

Ventilator Induced Lung Injury (VILI)

“Volutrauma”
Volutrauma caused by over-expansion or over
distention of alveoli from ventilation with volumes
in excess of relative lung capacity.

• Correlates to trans-alveolar pressures of 30-35 cm H2O

• Static “plateau” pressures of > 35-50 cm H2O
Complications of Mechanical Ventilation
Over-Expansion/Over-Distention
Alveoli Lungs
• Epithelial damage
• Alveolar wall stress fractures
• Capillary compression
Complications of Mechanical Ventilation
• Repeated end-tidal alveolar collapse / shearing force
• “Milking” of surfactant from alveoli with repeat closure

Inspiratory phase
Expiratory phase
Lung Protective Ventilation
Used to prevent/minimize complications of mechanical ventilation
Goals
• Maintain safe trans-alveolar pressures (< 30 cm H20 )
– Pressure Targeted Ventilation

• Prevent end-tidal alveolar collapse

– PEEP
Lung Protective Ventilation
Low Tidal Volume Ventilation (LTVV)
Use Tidal Volume
• 5-8 ml / kg (Normally 10-12 ml/kg)

Use volume control modes

• AC
• SIMV

Is LTVV considered a way to deliver lung protective ventilation?

What happens to CO2 with LTVV?
 Permissive Hypercapnea
Expected, allowable rise in PaCO2 levels that
results from hypoventilation of the lungs
Vt PaCO2

• Maintain normoxic conditions to minimize

metabolic effects (arterial pH)

Can oxyhemoglobin dissociation curve be applied here?

 Permissive Hypercapnea

What’s effect of elevated CO2?

Are patient’s with cardiovascular dysfunction or

cerebral injury/compromise candidates for permissive
hypercapnea?
PEEP
Goal
Alveolar recruitment
• Maintains alveolar opening threshold
– Pressure stays above zero line.
• Reduces shear force injury to alveoli
– Less force to open alveoli.
• Displacement of lung H2O

Can PEEP also cause harm?

Others: High Frequency Ventilation (HFV)

Types of HFV
• High Frequency Jet Ventilation (HFJV)
Up to 600 bpm
• High Frequency Oscillatory Ventilation (HFOV)
300 to 3000 bpm
• High Frequency Percussive Ventilation (HFPV)

If you want to read more about this, visit

http://www.rtmagazine.com/2012/02/high-frequency-
ventilation-what-is-the-best-choice/
High Frequency Oscillator
 Due to the large pressure changes under
Alveolar conventional ventilation, the alveolus will
Changes expand (perhaps dynamically hyperinflate*) and
then deflate during expiration. The dynamic
During HFV hyperinflation can lead to barotrauma, while the
deflation can collapse the alveolus, not allowing
HFOV it to contribute in gas exchange. To counteract
the deflation, PEEP is added, which increases
the pressure..
Inspiration
~ During HFV the pressure is nearly constant,
Expiration leading to a nearly constant volume during
inhalation and exhalation.

Since the alveolus does not collapse, it can

contribute in gas exchange, and can do it at
lower pressures. These lower pressures
prevent dynamic hyperinflation and its adverse
effects.
Note: dy·nam·ic hy·per·in·fla·tion
The increase in lung volume that occurs during mechanical ventilation when insufficient exhalation time prevents the
respiratory system from returning to its resting end-expiratory equilibrium volume between breath cycles.
Others: Non-Ventilatory Gas Exchange
• Extracorporeal Lung Support/Assist (ECLS)
• Low-frequency positive pressure ventilation with
extracorporeal CO2 removal (ECCO2R)
• Intravenous oxygenation (IVOX)
If you want to know more about this, visit
http://www.signavitae.com/2016/10/lung-replacement-therapies-for-acute-
respiratory-failure/
Therapeutic Goals

Optimize Oxygen Delivery (DO2)

• Avoid fluid overload

– Keep PAOP < 12 mm Hg)
• Augment cardiac output
– Inotropic agents
• Optimize hemoglobin (10 g/dL)
Therapeutic Goals

Reduce Oxygen Consumption (VO2)

• Reduce or space patient care activities

• Treat fever
– avoid shivering
– 200% increase in VO2
• Treat pain, anxiety, agitation
• Limit excessive carbohydrate load
Pharmacologic Adjuncts
• Analgesics
• Anxiolytics
– Maximize use of sedation before using NMBs

• Neuromuscular Blockade (NMB)

– Provide appropriate levels of concomitant analgesia and anxiolytics
when using NMB’s
– Titrate NMB’s by peripheral nerve stimulation (TOF)
• Train of 4
• https://www.gosh.nhs.uk/conditions-and-treatments/clinical-
guidelines/train-four-monitoring-how-carry-out-procedure
Remember…
Nutrition
• Feed Early And Feed Enterally
• “Immunonutrition”
– Manipulate nutrition to impact immune system
Psycho-Social Support
• Patient
• Family
Outcome
• Mortality 40-60%
– Range will vary by source
• Associated with
– Severity of lung injury
– Associated disorders
– Additional organ dysfunction
• Early deaths related to lung injury
• Late deaths related to sepsis
• Hepatic function a major factor in survival
 Next Slide
• The next slide is a textbook chapter squeezed
onto a single page.
• Take a look at it.
• What do you already know?
• What do you need to know?
• How does PAOP relate to ARDS?
 Relationship of Hemodynamic Parameters

Cardiac Output/Index (CO/CI)

Heart Rate (HR) X Stroke Volume (SV)
60-100 ml/beat

Contractility
Preload Afterload
Stroke work
RVSWI- 8.5-12 g/m
LVSWI- 35-85 g/m
Left Ventricle Right Ventricle
Right Ventricle Left Ventricle
(PAOP) Pulmonary Vascular
(CVP) Resistance (PVR) Systemic Vascular
5-15 mmHg
Resistance (SVR)
1-8 mm Hg 20-120 d/s/cm
800-1400 d/s/cm
I’m sick as a dog. Dude! I know the 5 P’s!