RESPIRATORY Last edited: 3/9/2024

3. ARDS
I. PATHOPHYSIOLOGY OF ARDS COMPLICATIONS OF ARDS IV. DIAGNOSTIC APPROACH TO ARDS
PULMONARY SHUNT A. HYPOXEMIC RESPIRATORY FAILURE WITH MULTI- A. ASSESS FOR TYPE OF RESPIRATORY FAILURE
II. CAUSES OF ARDS ORGAN DYSFUNCTION B. ASSESS FOR THE CAUSE OF TYPE I (HYPOXEMIC) RESPIRATORY FAILURE
A. DIRECT LUNG INJURY B. PULMONARY HYPERTENSION V. TREATMENT OF ARDS
B. INDIRECT LUNG INJURY C. VENTILATOR-ASSOCIATED PNEUMONIA (VAP) A. TREAT THE CAUSE OF ARDS
III. CLASSIC FINDINGS OF ARDS D. VENTILATOR INDUCED LUNG INJURY (VILI) B. SUPPORTIVE CARE OF ARDS
HYPOXEMIC RESPIRATORY FAILURE

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I. Pathophysiology of ARDS
Pulmonary Shunt
o Lung Injury → Diffuse alveolar damage → o Lung Injury → Diffuse alveolar damage →
Type I alveolar injury → ↑Alveolar permeability → Type II alveolar injury → ↓Surfactant production →
Severe Alveolar filling → No ventilation and poor gas Severe alveolar collapse → No ventilation and poor gas
exchange to alveoli → Severe hypoxemia exchange to alveoli → Severe hypoxemia

+ V

Diffuse Alveolar
Damage O2

Exudative Q
Phase
+ Diffuse Alveolar
Alveolar Filling RR WOB
Damage

O2

Q
Surfactant Alveolar
Collapse
RR WOB

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II. Causes of ARDS
A. Direct Lung Injury
a) Pneumonia
o Severe bacteria or COVID-19 pneumonia → PNA
Diffuse lung inflammation → Diffuse alveolar damage
 Assess for fever, productive cough, leukocytosis, and fevers
Aspiration
Inhaled Toxins
b) Aspiration
o Gastric content aspiration → Diffuse pneumonitis →
diffuse alveolar damage
 Assess for impaired level of consciousness that may be
associated with aspiration

B. Indirect Lung Injury

a) Sepsis
o Systemic infection → Widespread systemic inflammation →
Diffuse pulmonary capillary and alveolar cell injury
 Assess for fever, leukocytosis, tachypnea, and hypotension
(e.g. shock)
• The most common cause of ARDS

b) Pancreatitis
o Widespread systemic inflammation →
Diffuse pulmonary capillary and alveolar cell injury
 Assess for epigastric pain and ↑↑Lipase (3 x ULN)

c) Transfusion-Associated Lung Injury (TRALI)

o Transfusion → Donor antibodies react against neutrophils →
Widespread systemic inflammation →
Diffuse pulmonary capillary and alveolar cell injury
 Monitor within 6 hours post-transfusion Systemic
Inflammation

III. Classic Findings of ARDS

Hypoxemic Respiratory Failure
o Dyspnea, Tachypnea, ↑Work of breathing (WOB) Berlin Criteria
 ↓O2 → Stimulates chemoreceptors →
↑Respiratory drive to breathe
• Hypoxia (SpO2 < 90%) on pulse oximetry

Acute Hypoxemia (< 1 wk)

Ratio (P/F < 300)
Diffuse B/L Infiltrates
Swan (PCWP < 18)
Cardiogenic
Pulmonary
Edema
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 IV. Complications of ARDS
A. Hypoxemic Respiratory Failure with Multi-Organ Dysfunction
Pathophysiology:
o Severe hypoxia → ↑Oxygen delivery to tissues → Multi-Organ Dysfunction
Organ ischemia → Organ dysfunction
Presentation:
o Hypoxia not responsive to oxygen supplementation (e.g. shunt
physiology) PH
o Encephalopathy:
 Confusion → Stupor → Coma Lactate
o Arrhythmias: +

 Atrial fibrillation O2
 Ventricular tachycardia
o Myocardial Ischemia:
 Angina, ST changes, and a ↑Troponin + + Arrhythmias
o Lactic Acidosis:
 ↑Lactate level Encephalopathy Myocardial
 ABG with ↓pH and ↓HCO3-
+ Ischemia

B. Pulmonary Hypertension 12:24 C. Ventilator-Associated Pneumonia (VAP) 15:21

Pathophysiology: Pathophysiology:
o Extremely severe acute hypoxemia → ↑Hypoxic pulmonary o Severe ARDS that requires intubation →
vasoconstriction → ↑PVR → ↑Pulmonary BP Prolonged intubation (> 48 hrs) → Risk of bacterial infection
Presentation: (e.g. MRSA or Pseudomonas) in the presence of ETT and
o Dyspnea on exertion microaspiration around ETT
o ↑Risk of Right Heart Failure (e.g. Cor Pulmonale) Presentation:
 JVD o Fevers and Leukocytosis
 Ascites o ↑Purulent sputum Production
 Hepatomegaly o Worsening infiltrates on CXR
 Lower extremity edema o ↑Oxygen/ventilator requirements
o Sputum culture (+) for MDR pathogen (e.g. Pseudomonas or
MRSA)
Pulmonary Hypertension
Ventilator Associated PNA
(VAP)
+
Vasoconstriction

>2 days

O2

CVP PVR V/Q Mismatch

Pulm HTN

Pseudomonas
RHF S. aureus (MRSA)
JVD Pedal Edema

Hepatomegaly Ascites

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 D. Ventilator Induced Lung Injury (VILI) 17:15

1. Barotrauma 3. Atelectrauma
Pathophysiology: Pathophysiology:
o ARDS with ↓Lung compliance → Ventilator delivers excessive o ARDS with ↓lung compliance →
airway pressure via (↑Plateau pressures and ↑PEEP) → Ventilator delivers very little PEEP →
↑Alveolar rupture alveoli minimally expand and quickly collapse →
Presentation: ↑Inflammation (which worsens lung injury)
o ↑Plateau pressures (> 30) Presentation:
o ↑Risk of Pneumothorax and pneumomediastinum o CXR with worsening atelectasis
o ↑FiO2 requirements on ventilator
Barotrauma
Atelectrauma

PEEP w/
Lung Compliance
PEEP w/
Lung Compliance

Pneumomediastinum +
PTX
Inflammation
WOB

Alveolar
Derecruitment

2. Volutrauma 4. Hyperoxia
Pathophysiology: Pathophysiology:
o ARDS with ↓lung compliance → Ventilator delivers larger tidal o ARDS with ↓lung compliance → Ventilator delivers too
volumes→ Alveolar overdistention → ↑Alveolar rupture and much FiO2 → Worsens V/Q mismatch and
inflammation (↑Lung injury severity) ↑Inflammation (↑Lung injury severity)
Presentation: Presentation:
o ↑Tidal volumes (> 6cc/kg of IBW) o ABG with ↑PaO2 while on ↑FiO2
o ↑Risk of Pneumothorax and pneumomediastinum
Hyperoxia
Volutrauma

TV w/
Lung Compliance
FiO2

V/Q Mismatch
Inflammation

Inflammation

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V. Diagnostic Approach to ARDS

A. Assess for type of Respiratory Failure

1. Obtain an ABG 2. Administer 100% FiO2 Challenge
Purpose: Purpose:
o Differentiate between Type I and Type II respiratory failure o Differentiate between V/Q mismatch and Shunt in Type I
o Assess the severity of ARDS via the P/F ratio respiratory failure
Abnormal Findings: Abnormal Findings:
o Type I (Hypoxemic) Respiratory Failure: o V/Q Mismatch:
 PaO2 < 60mmHg  Hypoxemia improves with oxygen supplementation
 Normal or Low PaCO2 o Shunt:
o Type II (Hypercapnic) Respiratory Failure:  Hypoxemia DOES NOT improve with oxygen
 PaO2 < 60mmHg supplementation
 ↑PaCO2 (> 45mmHg)
o ARDS Severity via P/F Ratio:
 P/F ~ 200-300 → Mild ARDS
 P/F ~100-200 → Moderate ARDS
 P/F < 100 → Severe ARDS

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 B. Assess for the cause of type I (Hypoxemic) Respiratory Failure
1. Obtain CXR or Chest CT 2. Obtain an Echocardiogram
Purpose: Purpose:
o To assess for the presence of pneumonia, pulmonary edema, o Assess for intracardiac shunt (e.g. ASD, PFO, VSD)
atelectasis, alveolar hemorrhage, ARDS o Assess for evidence of cardiogenic pulmonary edema
o To assess for the presence of PE (use CTPA study) Findings in ARDS:
Abnormal Findings in ARDS: o Normal LVEF or Normal Diastolic function helps support
o Diffuse infiltrates → ARDS diffuse infiltrates are not from cardiogenic pulmonary edema
and suggests ARDS

FIGURE 1. CXR SHOWING BILATERAL PULMONARY INFILTRATES FIGURE 3. APICAL 4 CHAMBER VIEW SHOWING NORMAL LVEF & DIASTOLIC FUNCTION

FIGURE 2. CT SHOWING BILATERAL PULMONARY INFILTRATES FIGURE 4. PARASTERNAL SHORT AXIS SHOWING NORMAL LVEF & DIASTOLIC FUNCTION

3. Obtain Right Heart Catheterization (RHC)

Purpose:
o Definitively assess for evidence of cardiogenic pulmonary
edema
Findings in ARDS
o PCWP < 18 mmHg helps support diffuse infiltrates that are not
from cardiogenic pulmonary edema and suggests ARDS

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VI. Treatment of ARDS

A. Treat the cause of ARDS

1. Pneumonia, Aspiration, and Sepsis
Treatment:
o Antibiotics for bacterial infections
 Vancomycin and Piperacillin-tazobactam empirically.
Narrowly based on sputum/blood cultures

B. Supportive Care of ARDS

1. Invasive Oxygen Supplementation 2. Heavy Sedation and Analgesia
Types of Supplementation: Types of Supplementation:
o Intubation and mechanical ventilation o Sedation:
Indications:  Propofol infusion
o Hypoxemia refractory to non-invasive ventilation (e.g. HFNC)  Midazolam infusion
Modes of Ventilation: o Analgesia:
o Controlled mechanical ventilation (CMV)  Fentanyl infusion
 Used in patients who require diaphragmatic rest, allowing  Dilaudid infusion
the ventilator to do the work Indications:
Purpose: o Worsening Hypoxemia while on LTVV causing ventilator
o Improve oxygenation
dyssynchrony
 Use of FiO2
Purpose:
• ↑FiO2 in hypoxia
o Hypoxemia while on LTVV causing ventilator dyssynchrony and
 Use of PEEP
worsening P/F ratio
• ↑PEEP in hypoxia to reduce
o These agents inhibit the respiratory center, facilitating
atelectrauma (VILI)
mechanical ventilation by preventing the patient from resisting
o Reduce risk of mortality via Low tidal
the ventilator's settings, particularly when they instinctively
volume ventilation (LTVV)
attempt to take deeper breaths than the machine permits
 Use of Tidal volume and RR
Monitoring:
• ↓TV in ARDS to reduce volutrauma (VILI)
o Monitor the ventilator for any dyssynchrony and titrate the
• ↑RR to allow clearance of CO2 but can allow permissive
hypercapnia infusions to the goal of vent synchrony
Monitoring:  Ventilator alarms signal high breathing frequency or high
o Monitor Tidal Volumes (TV): tidal volumes along with hypoxia indicates dyssynchrony
 ↑TV (> 6cc/kg of IBW) → ↑Risk of volutrauma in ARDS o Monitor the P/F ratio on ABG for the progression of ARDS
o Monitor Plateau pressures (Pplat):
 ↑Pplat (> 30) in ARDS → Assess for increased risk of
barotrauma in ARDS
o Monitor the P/F ratio on ABG for the progression of ARDS

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3. Paralysis 5. Inhaled Pulmonary Vasodilators
Types of Supplementation: Types of Supplementation:
o Neuromuscular Blockade (NMB): o Inhaled Nitric Oxide (iNO)
 Cisatracurium infusion Indications:
• Combined with sedation and analgesia o Worsening Hypoxemia while on LTVV refractory to heavy
Indications: sedation, analgesia, and NMB with P/F ratio <150 and presence
o Worsening Hypoxemia while on LTVV → Refractory to heavy of pulmonary HTN or RV dysfunction on echocardiogram
sedation and analgesia with P/F ratio < 150 Purpose:
Purpose: o Worsening Hypoxemia while on LTVV refractory to heavy
o Hypoxemia while on LTVV and heavy sedation/analgesia sedation, analgesia, NMB with P/F ratio < 150, and presence of
causing ventilator dyssynchrony and worsening P/F ratio < 150 pulmonary HTN or RV dysfunction on echocardiogram
 NMBs paralyze the diaphragm and intercostals → Allow the  iNO → Pulmonary vasodilation → Improves perfusion to
ventilator to do the work, preventing the patient from well-ventilated alveoli → Improves V/Q matching with
resisting the ventilator's settings, particularly when they pulmonary vasodilation → Less stress on the right heart
instinctively attempt to take deeper breaths than the Monitoring:
machine permits o Monitor methemoglobin levels to avoid methemoglobinemia
Monitoring: with prolonged infusions
o Monitor the ventilator for any dyssynchrony and titrate the o Monitor the P/F ratio on ABG for the progression of ARDS
infusions to the goal of vent synchrony 6. Veno-Venous Extracorporeal Membrane Oxygenation
 Ventilator alarms signal high breathing frequency or high
(V-V ECMO)
tidal volumes along with hypoxia indicates dyssynchrony
Indications:
o Monitor the P/F ratio on ABG for the progression of ARDS
o Refractory Hypoxemia despite LTVV on heavy sedation,
4. Prone Positioning analgesia, NMB, and iNO with P/F ratio < 150
Indications: Purpose:
o Worsening Hypoxemia while on LTVV → Refractory to heavy o Refractory Hypoxemia despite LTVV on heavy sedation,
sedation, analgesia, and NMB with P/F ratio < 150 analgesia, NMB, and iNO with P/F ratio < 150
Purpose:  V-V ECMO takes over the job of the lungs by oxygenating
o Hypoxemia while on LTVV and heavy sedation, analgesia, and the blood and removing CO2 → This allows time for the lungs
NMB causing ventilator dyssynchrony and worsening P/F ratio to heal from such an extensive injury
< 150 Monitoring:
 Proning → ↓Compression of the posterior bases of lungs → o Monitor for reduction in FiO2, PEEP, and improvement in
↓Dependent atelectasis → Improves V/Q matching oxygen saturation, as well as improving CXR
Monitoring: o Monitor the P/F ratio on ABG for the progression of ARDS
o Monitor for reduction in FiO2, PEEP, and improvement in o Monitor for ECMO complications such as bleeding or circuit
oxygen saturation as well as improving CXR thrombosis
 Usually, 16 hours of lying prone and 8 hours of lying supine
o Monitor the P/F ratio on ABG for the progression of ARDS

Supine Prone

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