INTRODUCTION:

ARDS is an acute, diffuse, inflammatory form of lung injury and life-threatening condition in
seriously ill patients, characterized by poor oxygenation, pulmonary infiltrates, and acute
onset. On a microscopic level, the
disorder is associated with capillary
endothelial injury and diffuse alveolar
damage.
ARDS is an acute disorder that starts
within seven days of the inciting event
and is characterized by bilateral lung
infiltrates and severe progressive
hypoxemia in the absence of any
evidence of cardiogenic pulmonary edema.
Acute respiratory distress syndrome was first described in 1678 by Ashbaugh and colleagues.

DEFINITION:
Acute respiratory distress syndrome (ARDS) is a sudden and
progressive form of acute respiratory failure in which the alveolar
capillary membrane becomes damaged and more permeable to
intravascular fluid. The alveoli fill with fluid, resulting in severe
dyspnea, hypoxemia refractory to supplemental O2, reduced lung
compliance, and diffuse pulmonary infiltrates.
According to the Berlin definition, ARDS is defined by acute onset,
bilateral lung infiltrates on chest radiography or CT scan of a non-
cardiac origin, and a PaO2/FiO2 ratio of less than 300 mm Hg.

ETIOLOGY:
Direct Lung injury
Common Causes-

 Aspiration of gastric contents or other substances

 Viral/bacterial pneumonia
Less Common Causes-

 Chest trauma
 Embolism: fat, air, amniotic fluid, thrombus
 Inhalation of toxic substances
 Near-drowning
 O2 toxicity
 Radiation pneumonia
Indirect Lung Injury
Common Causes-
  Sepsis (especially gram-negative infection)
 Severe massive trauma
Less Common Causes-
 Acute pancreatitis
 Anaphylaxis
 Cardiopulmonary bypass
 Disseminated intravascular coagulation
 Multiple blood transfusions
 Opioid drug overdose (e.g., heroin)
 Non pulmonary systemic diseases
 Severe head injury
 Shock states

RISK FACTORS:
Some risk factors for ARDS include:
 Advanced age
 Female gender
 Smoking
 Alcohol use
 Aortic vascular surgery
 Cardiovascular surgery
 Traumatic brain injury
 Pancreatitis
 Pulmonary contusion
 Infectious pneumonia
 Drugs (radiation, chemotherapeutic agents, amiodarone)

ANATOMY &
PHYSIOLOGY:
Anatomy:
Physiology:
The four significant aspects of respiratory mechanics are as follows: lung compliance, chest
wall compliance, respiratory rate, and airway resistance. These work in conjunction to create
a negative pressure within the lungs and pleural space, allowing air to be drawn into the
lungs. Conversely, drops in lung volume increase pressure in the lungs, which forces air out.
The function of the pulmonary system is to extract oxygen from the environment and provide
it for aerobic respiration at the cellular level. Oxygen is ultimately used to produce ATP, and
carbon dioxide is breathed out with other metabolic byproducts.
Respiratory tract organs facilitate the process of gas exchange, including the nose, oral cavity,
throat, trachea, bronchi, and lungs. The lungs divide into five major lobes: three lobes on the
right and two lobes on the left. Each lobe is made up of many small alveoli, which are the
primary site of gas exchange. At the alveoli, diffusion of gases into the arterioles occurs
ACUTE RESPIRATORY DISTRESS SYNDROME: PATHOGENESIS
AND CLINICAL FINDINGS:

CLINICAL MANIFESTATION:
At the time of initial injury, & for several hours to 1 to 2 days afterward, the patient may not
experience respiratory symptoms, or the patient may exhibit only the following-

 Dyspnea
 Tachypnea
 Cough & restlessness
 Chest auscultation may be normal or reveal fine, scattered crackles.
 ABG usually indicates mild hypoxemia & respiratory alkalosis caused by
hyperventilation.
  The chest x-ray may be normal or exhibit evidence of minimal scattered interstitial
infiltrates.
 Ederna may not show on the x-ray until there is a 30% increase in fluid content in the
lung.
As ARDS progresses, symptoms worsen because of
 increased fluid accumulation and decreased lung compliance
 respiratory discomfort becomes evident as the work of breathing increases,
 tachypnea and intercostal and suprasternal retractions may be present
 pulmonary function tests in ARDS reveal decreased compliance and decreased long
volumes, particularly a decreased functional residual capacity (FRC).
 tachycardia, diaphoresis. changes in sensorium with decreased mentation, cyanosis,
and pallor may be present.
 chest auscultation usually reveals scattered to diffuse crackles and rhonchi.
 the chest x-ray demonstrates diffuse and extensive bilateral interstitial and alveolar
infiltrates.
 a pulmonary artery catheter may be inserted. Pulmonary artery wedge pressure does
not increase in ARDS because the cause is non-cardiogenic (not related to
cardiac function)
 associated with profound respiratory distress requiring endotracheal intubation and
PPV.
 the chest x-ray is often termed whiteout or white lung, because consolidation and
coalescing infiltrates are widespread throughout the lungs leaving few recognizable
air spaces
 pleural effusions may also be present.
 severe hypoxemia, hypercapnia, and metabolic acidosis

COMPLICATIONS:
Complications may develop as a result of ARDS itself or its treatment. The major cause of
death in ARDS is MODS, often accompanied by sepsis.
Hospital-Acquired Pneumonia- A frequent complication of ARDS is hospital acquired
pneumonia, occurring in as many as 68% of patients with ARDS.
Barotrauma- Barotrauma may result from rupture of over distended alveoli during mechanical
ventilation.
Volu-Pressure Trauma- Volu-Pressure Trauma can occur in patients with ARDS when large
tidal volumes (e.g., 10 to 15 ml kg) are used to ventilate noncompliant langs. Volu-pressure
trauma results in alveolar fractures and movement of fluids and protein into the alveolar spaces.
Physiologic Stress Ulcers- Critically ill patients with acute respiratory failure are at high risk
for stress ulcers. Bleeding from stress ulcers occurs in 30% of patients with ARDS who require
PPV, a higher incidence than other causes of acute respiratory failure.
Renal Failure- Renal failure can occur from decreased renal tissue oxygenation as a result of
hypotension, hypoxemia, or hypercapnia. Renal failure may also be caused by administration
of nephrotoxic drugs (e.g., aminoglycosides), which are used to treat infections associated with
ARDS.
Other complications include-
 Catheter related infection
 Pulmonary emboli
 Pulmonary fibrosis
 VAP
 Paralytic ileus
 Dysrhythmias
 Decreased cardiac output
 Anemia
 DIC
 Thrombocytopenia
 Delirium
 Sleep deprivation
 PTSD

Diagnostic Studies:
ABG
Bronchoscopy
Echocardiogram
Sputum culture & analysis
Refractory Hypoxemia
PaO2 < 50 mmHg on FIO2 > 40% PEEP > 5 cm H2 O
PaO2/ FIO2 ratio < 200

Chest X-Ray & chest CT-scan

New bilateral interstitial & alveolar infiltrates

chest x-ray
Pulmonary Artery Wedge Pressure
< 18 mm Hg and no evidence of heart failure
Predisposing Condition
Identification of a predisposing condition for ARDS within 48 hours of clinical
manifestations.
MEDICAL MANAGEMENT:
For treatment of acute respiratory distress syndrome (ARDS), think ARDS
A- Antibiotics
R- Respiratory support
D- Diuretics
S- Situate patient in prone position

5 P”s of ARDS therapy-

Managing patients with ARDS requires maintaining the airway, providing adequate
oxygenation, and supporting hemodynamic function.
The five P’s of supportive therapy include perfusion, positioning, protective lung ventilation,
protocol weaning, and preventing complications.
Drug Therapy-
Different classes of drugs & fluids prescribed for management of ARDS:
Classes Drugs Doses
Corticosteroids 1. Methyl prednisolone 40 mg(IV)
2. Hydrocortisone 500 mg (IV)
3. Dexamethasone 4 mg (IV)
Neuromuscular 1. Pancuronium
blocking agents 2. Vecuronium
Diuretics Frusemide 20 mg (IV)
Anti microbials 1. Piperacillin tazobactam 2.25 gm
2. Doxycycline 100 mg
3. Meropenem 500 mg
4. Linezolid 600 mg
5. Macrolides 500 mg
6. Levofloxacin 500 mg
7. Vancomycin 500 mg
8. Tigecycline 50 mg
IV Fluids 1. DNS
2. NS 500 ml
3. RL
4. 5% Dextrose

Piperacillin–tazobactam was most frequently prescribed antimicrobial combination,

followed by doxycycline and then macrolides.

The underlying cause for ARDS should be determined so appropriate treatment can be
initiated.
 Low VT by mechanical ventilation (6 ml/kg of predicted body weight) reduces
mortality compared to high volume ventilation. Monitor for respiratory acidosis.
Protective ventilation (i.e., maximum inspiratory pressure [MIP] of < 35 cm) should
be instituted. PEEP should be used to improve PaO2. PEEP keeps the alveoli open,
thereby improving gas exchange. Therefore, a lower oxygen con- centration (FiO2)
may be used to maintain satisfactory oxygenation.
 Fluid management must be maintained. The patient may be hypovolemic due to the
movement of fluid into the interstitium of the lung. Pulmonary artery catheter
monitoring and inotropic medication can be helpful.
 Medications are aimed at treating the underlying cause. Corticosteroids are used
infrequently due to the controversy regarding benefits of usage.
 Nutritional therapy: require 35 to 45 kcal/kg/day to meet caloric requirements.
Enteral feeding is the first consideration; however, parenteral nutrition also may be
required.
 Inhaled nitric oxide (an endogenous vasodilator) may help to reduce V/Q mismatch
and improve oxygenation
 ECMO: It is an extracorporeal technique of providing prolonged cardiac and
respiratory support to persons whose heart and lungs are unable to provide an
adequate amount of gas exchange or perfusion to sustain life.
 Nebulizer therapy: with budesonide, salbutamol, duolin.
 Chest physiotherapy: to loosen the secretions
 VAP prevention/bundle:
 Oral care with chlorhexidine
 Peptic ulcer prophylaxis
 Deep vein thrombosis prophylaxis
 Head end elevation
 Daily sedation assessment & spontaneous breathing trials
 DVT prophylaxis: medical treatment to prevent the development of DVT in a patient
at risk of this condition. In patients with DVT, a blood clot forms in the deep veins of
the arm or leg, occluding blood flow and potentially leading to complications. The
most serious complication is a pulmonary embolism (PE). e.g. enoxaparin, heparin.
NURSING MANGEMENT:
Nursing diagnosis:
1. Impaired gaseous exchange related to damage to the alveolar capillary membrane,
change in lung compliance as evidenced by abnormal arterial pH, cyanosis,
bradypnea, hypoxemia, hypoxia.
2. Impaired spontaneous ventilation related to respiratory muscle fatigue, disease
process, damage to the alveolar capillary membrane as evidenced by decreased
arterial oxygen saturation, decreased tidal volume, increased heart rate,
restlessness.
3. Ineffective airway clearance related to excessive mucus, airway spasm, lung
injury as evidenced by altered respiratory rate & rhythm, tachypnea, tachycardia,
cyanosis, shortness of breath.
4. Ineffective breathing pattern related to alveolar impairment, poor lung expansion,
lung fibrosis, fluid in the lungs as evidenced by tachypnea, dyspnea, anxiety,
restlessness, respiratory muscle fatigue.
5. Risk for infection related to sepsis, invasive lines, prolonged immobility.
 Application of Roy’s Adaptation Model on ARDS
Input Stimulus Interaction Capsulate Output
Environmental changes – Focal stimuli – 1. Impaired gaseous exchange related
When lung tissues are injured, to damage to the alveolar capillary
Temp- 98.60F the alveoli become permeable membrane, change in lung Pulse- 90 bpm
Pulse- 106 bpm to large molecules, allowing compliance as evidenced by Respiration- 28 bpm
Respiration- 36 bpm more proteins, debris, and abnormal arterial pH, cyanosis, ABG- PaO2/ FIO2 ratio < 250
Bp- 140/ 90 mm Hg fluids to enter lungs. bradypnea, hypoxemia, hypoxia. SPO2-98%
Type-2 DM from 6 years Inflammation also breaks  Assessed
HTN from 4-5 years. down surfactant making the Pulse- 106 bpm
Infection on lungs lungs less compliant & causes Respiration- 36 bpm
Chain smoker for 15- 20 ARDS  Assessed chest x-ray.
years,  Assessed ABG- PaO2/ FIO2 ratio <
ABG- PaO2/ FIO2 ratio < Contextual stimuli – 200
200, SPO2- 86% Bp- 140/ 90 mm Hg  Prone position is given to the patient.
Chest x-ray shows bilateral ABG- PaO2/ FIO2 ratio < 200  Administered inj.
lung infiltrates, SOB, restlessness Methylprednisolone 40 mg IV.
SOB, restlessness  Oxygen support is provided.

2. Ineffective airway clearance related

Nursing Diagnosis- Residual stimuli – to excessive mucus, airway spasm,
1. Impaired gaseous HTN for 4-5 years lung injury as evidenced by altered
exchange related to Chain smoker for 15- 20 respiratory rate & rhythm,
damage to the years tachypnea, tachycardia, cyanosis, Patient is maintaining a patent
alveolar capillary No knowledge on heath shortness of breath. airway & an effective breathing
membrane, change in matter. pattern.
 Assessed breathing sounds.
lung compliance as
 Monitored SPO2- 86%
evidenced by
abnormal arterial pH,  Provided oral & nasopharyngeal
suctioning.
cyanosis, bradypnea,
hypoxemia, hypoxia.  Administered nebulization Duolin (1
respule) + budecort(1 respule)
 2. Ineffective airway 3. Ineffective breathing pattern related
clearance related to to alveolar impairment, poor lung Patient is maintaining an
excessive mucus, expansion, lung fibrosis, fluid in the effective breathing pattern.
airway spasm, lung lungs as evidenced by tachypnea, Respiration- 28 bpm
injury as evidenced dyspnea, anxiety, restlessness, ABG- PaO2/ FIO2 ratio < 250
by altered respiratory respiratory muscle fatigue. SPO2-98%
rate & rhythm,  Oxygen support is provided.
tachypnea,  Assessed ABG- PaO2/ FIO2 ratio <
tachycardia, cyanosis, 200
shortness of breath.  Administered inj. Pipzo 2.25 gm then
inj. Doxycycline 100 mg & then inj.
3. Ineffective breathing Macrolides 500 mg.
pattern related to  Administered inj. Lasix 40 mg.
alveolar impairment,  Administered inj.
poor lung expansion, Methylprednisolone 40 mg IV.
lung fibrosis, fluid in the  Chest physiotherapy is provided.
lungs as evidenced by
tachypnea, dyspnea,
anxiety, restlessness,
respiratory muscle
fatigue.
CONCLUSION:
 ARDS is a multisystem syndrome - not a "disease"
 Characterized by accumulation of excessive fluid in the lungs with resulting
hypoxemia and ultimately some degree of fibrotic changes.
 The most frequent causes of ARDS include sepsis, aspiration, pneumonia and severe
trauma
 Treatment is primarily supportive and can non-traditional types of ventilation and
oxygenation strategies.
 Many theoretical therapies
 The best proven strategy to improve survival is low tidal volume ventilation.
BIBLIOGRAPHY:

 Lewis’s et.al. Medical Surgical Nursing Assessment & Management of Clinical

Problems. 4th edition. South Asia: Elsevier
 Brunner & Suddarth’s. Textbook of Medical Surgical Nursing. 13th edition. South Asian
Edition: Wolters Kluwer (India) Pvt. Ltd.
 Black JM. Black’s Medical Surgical Nursing: Clinical Management for positive
Outcomes. 1st edition. South Asia: Elsevier India.