Gauteng College of Nursing

Postgraduate Diploma In Adult Critical Care Nursing

Regulation 635

ACUTE RESPIRATORY DISTRESS SYNDROME

(ARDS)

31 JULY 2024

MJ SESHOKA
 LEARNING OUTCOMES

The student should be able to:

• Perform a comprehensive health assessment.
• Collect diagnostic data for analysis and interpretation of the
assessment and diagnostic findings.
• Integrate the clinical manifestations to the pathophysiology in the
ARDS patient.

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CONTINUATION

• Formulate a diagnosis based on the findings.

• Develop a comprehensive nursing care plan for ARDS
patients.
• Monitor emergency and complications of critically ill patients
using high-fidelity monitoring equipment.

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CONTINUATION

• Collaborate with the inter and intra professional team on the

management of the patient with ARDS.
• Critically analyse prescribed medications and recommend the
required quantities in line with the patient’s condition and
protocols

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Description

• ARDS is a systemic process that is considered to be

pulmonary manifestation of multi organ dysfunction syndrome.
• It is characterized by non-cardiac pulmonary oedema and
disruption of alveolar capillary membrane as the results of
injury to either the pulmonary vasculature or the airways

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Etiology / Risk factors

• There are several clinical conditions associated with ARDS

• They are categorized as direct or indirect depending on the
primary site of injury
• Direct injury are injuries in which the lung epithelium sustains
a direct insult

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CONTINUATION

Conditions that can cause direct injury

• Corona virus
• Aspiration & near-drowning
• Pulmonary contusion & pneumonia
• Toxic inhalation
• Oxygen toxicity
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CONTINUATION

• Indirect Injury
• When insult occurs elsewhere in the body and mediators are
transmitted via the blood stream to the lungs
• Sepsis, embolism, severe pancreatitis, DIC and trauma were
found to be the causes of indirect injury

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Pathophysiology

ARDS occurs in three phases

• Exudative phase
• Fibro proliferative phase
• Resolution phase

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Exudative phase

• It occurs within 72 hours of initial insult

• Mediators are released causing injury to the pulmonary
capillaries resulting in increased capillary membrane
permeability
• Leading to leakage of fluid filled with protein, blood cells, fibrin
& activated mediators into pulmonary interstitium

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 CONTINUATION

• Damage to pulmonary capillaries also causes development

micro thrombi and elevation of pulmonary arterial pressures
• As fluid enters the pulmonary Interstitium in large amounts
lymphatics are not able to drain all the accumulating fluid ,
resulting in the development of interstitial edema

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CONTINUATION

• Fluid is then forced from the interstitial space into the alveoli,
resulting in alveolar oedema
• Alveolar oedema causes swelling of alveolar epithelial cells
• Eventually alveolar epithelial cells are damaged leading to
impaired surfactant production

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CONTINUATION

• Injury to alveolar epithelial cells and loss of surfactant lead to

further alveolar collapse
• Compression, collapse and flooding of the alveoli and small
airways lead to intrapulmonary shunting & VQ mismatching
resulting in hypoxemia

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CONTINUATION

• Hypoxemia occurs due to Intrapulmonary shunting, VQ

mismatching secondary to compression, collapse and flooding
of the alveoli and small airways
• Increased work of breathing occurs as the results of increased
airway resistance

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CONTINUATION

• Increased work of breathing occurs due to ↑airway resistance

& ↓lung compliance secondary to atelectasis and compression
of the small airway
• Hypoxemia and increased work of breathing lead to patient
fatigue and alveolar hypoventilation

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CONTINUATION

• Pulmonary hypertension occurs as the results of damage to

the pulmonary capillaries, micro thrombi and hypoxic
vasoconstriction leading to increased right ventricular afterload
• Increased right ventricular afterload lead to right ventricular
dysfunction and a decreased Cardiac Output (CO)

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 Fibro proliferative phase

• This phase involves the disordered healing process of the lung.

• Cellular granulation & collagen deposition occur within the alveolar
capillary membrane
• The alveoli become enlarged & irregularly shaped
• The pulmonary capillaries become scarred & obliterated
• The lungs become stiff, pulmonary hypertension worsens &
hypoxemia continued
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Resolution phase

• Recovery occurs over several weeks

• Structural and vascular remodeling takes place to re-establish
the alveolar-capillary membrane
• The hyaline membranes are cleared & the intra alveolar fluid is
transported out of the alveolus into the interstitium
• The alveolar epithelial cells multiply & the alveolar
macrophages remove cellular debris to facilitate the restoration
of the alveolus
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DIAGNOSTIC STUDIES

• Auscultation – fine crackles

• Chest x-ray – infiltrates – progressing to consolidation which
appears as a “whiteout”
• CT chest
• Pulmonary function tests - decreased lung compliance &
decreased functional residual capacity

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 CONTINUATION

ABG analysis
• Refractory hypoxemia with persistent low saturation due to
intrapulmonary shunting
• Respiratory alkalosis in the early phases due to hyperventilation
• Respiratory acidosis in the later phases as gas exchange &
ventilation become increasingly impaired
• Increased A-a gradient & reduced PF ratio
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CLINICAL MANIFESTATIONS

Stage 1 (first 12hours)

• Dyspnea, tachypnea, restlessness
• Moderate to extensive use of accessory muscle
• Normal CXR, Respiratory alkalosis
• Hemodynamics - Elevated pulmonary artery pressure (PAP)
• Blood results may vary depending on the cause of ARDS e.g.
elevated WCC
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CONTINUATION

Stage 2 - Exudative phase (24hours)

• Severe dyspnea, tachypnea, cyanosis, tachycardia
• Increased agitation & restlessness
• Decreased air entry to dependent lung fields
• Coarse bilateral crackles
• Low saturation despite supplemental oxygen
• CXR – patchy bilateral infiltrates
• Hemodynamics – increasingly elevated PAP

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CONTINUATION
Stage 3 - Fibro proliferative phase (2-10 days)
• Decreased air entry bilaterally
• Decreased gut motility
• Generalized edema & poor skin integrity & breakdown
• Worsening hypoxemia
• CXR – air Broncho grams ,decreased lung volumes
• Blood results - ↓platelets & Hb, ↑WCC & abnormal clotting
factors
• Hemodynamics – becoming increasingly worse

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CONTINUATION
Stage 4 - Resolution phase (more than 10 days)
• Symptoms of MODS (decreased urine output, impaired
coagulation)
• Worsening hypoxemia & hypercapnia
• Sepsis, pneumonia
• CXR – air Broncho grams & pneumothoraxes
• Hemodynamics – becoming increasingly worse

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MEDICAL MANAGEMENT

• Management includes
• Treating the underlying course
• Promoting gas exchange
• Supporting tissue oxygenation
• Preventing complications

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 1. VENTILATION

• Patient must be intubated & mechanically ventilated to facilitate

adequate gas exchange
• Use of assist control ventilation or SIMV
• Set rate of 20 to 30 breath/minute and maximum tidal volume

(TV) as possible for elimination of CO2

• TV to be at least at 6ml/kg to prevent barotrauma & Volutrauma

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Permissive Hypercapnia

• Use Low TV Ventilation in conjunction with normal respiratory

rates in an attempt to limit the effect of Atelectrauma & bio
trauma

• Increasing rate can worsen alveolar damage, therefore CO2

level is allowed to increase for patient to be hypercapnic

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CONTINUATION

• PaCO2 must not exceed 80-100mmHg because of the negative

cardiopulmonary effects of severe acidosis

• The arterial pH is maintained at 7.20 or more by giving IV
Sodium Bicarbonate or increase the T/V or Respiratory rate
• Permissive hypercapnia is contradicted in patients with raised
ICP, pulmonary hypertension, seizures and heart failure
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PRESSURE CONTROL VENTILATION (PCV)

• In PCV Mode each breath is delivered or augmented by the

preset amount of inspiratory pressure as opposed by T/V
which is used in volume ventilation.
• Thus the actual TV patient receives, vary with every breath.
• PCV is used to limit and control amount of pressure in the
lungs & decrease the incidence of Volutrauma

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CONTINUATION

• The goal is to keep patient plateau pressure (End Inspiratory

static pressure) of < 30cmH2O
• As the lungs become stiffer, it become harder to maintain an
adequate TV and hypercapnia can occur.

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Inverse ratio ventilation (IRV)

• IRV can be used either in volume or pressure control.

• IRV prolongs inspiratory (I) time & shortens expiratory (E) thus
reversing the normal I:E ratio
• The Goal is to maintain a Constant Mean Airway Pressure
throughout the ventilator cycle to keep the alveolar open and
for a better gas exchange

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CONTINUATION

• It also increase functional residual capacity (FRC) and

decrease the work of breathing
• As the breath is delivered over a longer time, Peak Inspiratory
Time in the lungs decreases

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High-Frequency Oscillatory Ventilation (HFOV)

• This mode uses constant airway pressure to promote Alveolar

Recruitment while avoiding over distention of the alveoli
• It is used in patients who remain severely hypoxemic despite
other treatments.
• It deliver low TV (1 TO 3ml/breath at a very fast rates or
oscillations (300-900 breaths/min)

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2. OXYGEN THERAPY

• O2 is administered at the lowest level to support tissue

oxygenation
• The goal is to prevent oxygen toxicity

• Up to 50% O2 can be administered to maintain the Saturation

of 90%

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POSITVE END EXPIRATORY PRESSURE

• The purpose of using PEEP in Patients with ARDS is to

improve oxygenation while reducing FiO2 to less toxic level.

• PEEP opens collapsed alveoli, stabilizes flooded alveoli &

increases FRC
• Thus decreasing intrapulmonary shunting and increase
compliance

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CONTINUATION

• Extracorporeal membrane oxygenation (ECMO) can be done

as the last resort in case of severe ARDS when conventional

therapy has failed.
• This method allow the lungs to rest by facilitating removal of

CO2 & providing O2 external to the lungs using an artificial lung

or membrane or fiber oxygenator.

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3. Tissue perfusion

• Adequate Tissue Perfusion depend on the Cardiac output (CO)

and hemoglobin level
• Cardiac output depend on Preload, Afterload, Contractility and
Heart Rate
• To manipulate CO, fluids & medications are used

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CONTINUATION

• Fluid management include maintaining low Intravascular

volume, fluid restriction & diuretics while supporting CO with
vasoactive & inotropes
• The goal is to reduce fluid leakage into the lungs

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Nursing management

The goal is to:

• Optimize oxygenation and ventilation
• Provide comfort and emotional support
• Maintain surveillance for complications

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Optimize oxygenation and ventilation

Interventions to optimize oxygenation and ventilation

include:
• Positioning
• Preventing desaturation
• Promoting secretion clearance

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Positioning

• Nurse in semi fowlers position for lung expansion

• Frequent repositioning at least 2 hourly to optimize
oxygenation

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Preventing desaturation

• Hyper oxygenate before suctioning

• Limit physical activities
• Provide adequate rest & recovery time between activities
• Monitoring of saturation

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Promoting secretion clearance

• Provide adequate systemic hydration

• Administer humidified supplemental oxygen
• Encourage coughing
• Suction patient when necessary
• Post extubation deep breathing exercises & incentive
spirometry must be started
• Auscultation for lung sounds
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• Formulate nursing diagnoses for patient with
ARDS

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REFERENCES

• Hartjes, T.M., (2023). AACN Core curriculum for progressive and critical
care nursing. Elsevier/Saunders. P139-141
• Morton, P.G., Fontaine, D.K., Hudak, C.M. and Gallo, B.M., (2023). 12TH
edition, Critical care nursing: a holistic approach (Vol. 1). Philadelphia:
Lippincott Williams & Wilkins. P519- 534
• Urden, L.D., Stacy, K.M. and Lough, M.E., (2022). 9th edition, Critical
Care: Diagnosis and Management. Elsevier Health Sciences. P470-476

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