GMED3009- Respiratory failure (ARDS) Flashcards

1
Q

Definition of acute respiratory distress syndrome (ARDS)

A

acute, diffuse, inflammatory form of lung injury that is associated with a variety of etiologies. characterised by noncardiogenic pulmonary oedema and severe refractory hypoxaemia

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2
Q

What conditions are associated with direct and indirect lung injury?

A

direct= penumonia, aspiration of gastric contents, pulmonary contusion, fat emboli, inhalation injury, near drowning, reperfusion pulmonary edema

Indirect- sepsis, multiple trauma, multiple blood transfusions, cardiopulmonary bypass, burns, acute pancreatitis,drug overdose

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3
Q

Pathophysiology of ARDS

A
  • It is unregulated systemic inflammatory response to acute injury or inflammation
  • Inflammatory cellular responses and biochemical mediators damage the alveolar-capillary membrane
  • In response to direct lung injury or a systemic insult such as endotoxin, an increase in pulmonary or circulatory pro- inflammatory cytokines occurs.
  • Activated neutrophils secrete cytokines, such as tumour necrosis factor-alpha and interleukins, which increase the inflammatory response
  • Neutrophils also produce oxygen radicals and proteases that can injure the capillary endothelium and alveolar epithelium
  • Epithelial and endothelial damage, in turn, leads to increased permeability and the subsequent influx of protein-rich fluid into the alveolar space. In addition to these structural changes, there is evidence of impaired fibrinolysis in ARDS that leads to capillary thrombosis and microinfarction.
  • Some patients achieve complete resolution of lung injury before progressing into the fibroproliferative stage, whereas others progress directly to develop fibrosis.
  • The extent of fibrosis may be determined by the severity of the initial injury, toxic oxygen effects, and ventilator-associated lung injury
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4
Q

Definition of respiratory failure

A

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic or hypercapnic

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5
Q

Types of respiratory failure

A

1) Hypoxemic respiratory failure (type I)= is characterized by Pa O2 <60 mm Hg with a normal or low Pa CO2. This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary oedema, pneumonia, and pulmonary hemorrhage.

2) Hypercapnic respiratory failure (type II) is characterized by a PaCO2 > 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common aetiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and COPD).

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6
Q

Common causes of type I (hypoxemic) respiratory failure

A

● COPD
● Pneumonia
● Pulmonary edema
● Pulmonary fibrosis
● Asthma
● Pneumothorax
● Pulmonary embolism
● Pulmonary arterial hypertension
● Pneumoconiosis
● Granulomatous lung diseases
● Cyanotic congenital heart disease
● Bronchiectasis
● Acute respiratory distress syndrome (ARDS)
● Fat embolism syndrome

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7
Q

Common causes of type 2 (hypercapnic) respiratory failure

A

● COPD
● Severe asthma
● Drug overdose
● Poisonings
● Myasthenia gravis
● Primary muscle disorders
● Cervical cordotomy
● Head and cervical cord injury
● Pulmonary edema
● ARDS
● Myxedema
● Tetanus

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8
Q

Describe the typical signs and symptoms of Respiratory Failure

A

Type 1 RF: Dyspnoea, Tachypnoea, Use of accessory muscle, decreased SaO2
Type 2 RF: Dypnoea, ^RR with shallow respirations, decreased tidal volume and decreased minute ventilation

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8
Q

Describe the typical signs and symptoms of Respiratory Failure

A

Type 1 RF: Dyspnoea, Tachypnoea, Use of accessory muscle, decreased SaO2
Type 2 RF: Dypnoea, ^RR with shallow respirations, decreased tidal volume and decreased minute ventilation

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9
Q

Discuss the clinical and physical assessment of a patient with Respiratory Failure

A

RESP: Tachypnea slowly progressing to bradypnoea. Shallow breathing, use of accessory muscles, Dyspnoea
CNS: General agitation due to hypoxia, restlessness, fluctuating GCS depending on PaCO2 levels. Confusion, delirium, tremors, siezures
CVS: Tachycardia progressing to bradycardia. Arrhythmias (from the acidosis), bounding pulse, hypertension progressing to hypotension, JVP distended. Cyanosis, a bluish color of skin and mucous membranes, indicates hypoxemia.

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10
Q

What diagnostic studies would be performed on a patient with Respiratory failure?

A

CXR

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11
Q

Discuss the specific routine nursing care of a patient with respiratory failure

A

● Main goals of care for RF include ensuring adequate oxygenation and ventilation. Ensure that oxygen delivery device is appropriate administering for administering supplemental oxygen.
● Oxygen therapy may require humidification to aid in loosening secretions. Thick secretions are hard to expel
● Adequate fluid intake- to maintain hydration status, also helps in keeping the secretions thin and easier to remove
● Chest physio- assists with secretion removal and positioning to help improve oxygenation. Postural draining may also assist secretion removal
● Airway suctioning- if the patient is unable to expel own secretions.
● Encourage adequate nutritional support- The hypermetabolic state in critical illness increases the energy requirements therefore increase in nutritional support is required to maintain body weight and muscle mass
● Encourage deep breathing and coughing to prevent obstruction caused by secretions
● Position patient in upright position at 45 degrees to help maximize chest expansion

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12
Q

Discuss common complications of Respiratory failure

A

Common cardiovascular complications in patients with acute respiratory failure include hypotension, reduced cardiac output, arrhythmia, pericarditis, and acute myocardial infarction. These complications may be related to the underlying disease process, mechanical ventilation, or the use of pulmonary artery catheters.

Hospital acquired infections, such as pneumonia, urinary tract infections, and catheter-related sepsis, are frequent complications of acute respiratory failure. These usually occur with the use of mechanical devices. The incidence of nosocomial pneumonia is high and associated with significant mortality.

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13
Q

Pharmological treatment

A

Salbuatmol
Ipratropium

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14
Q

Aetiology of ARDS

A

acute condition characterised by bilateral pulmonary infiltrates. Cardiogenic pulmonary edema must be excluded, severe hypoxemia in the absence of evidence for cardiogenic pulmonary edema.

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15
Q

Risk factors of ARDS

A

no identified risk factor. ARDS risk factors include direct lung injury (most commonly, aspiration of gastric contents), systemic illnesses, and injuries. Most common cause of ARDS is Sepsis followed by
● Trauma, with or without pulmonary contusion
● Fractures, particularly multiple fractures and long bone fractures
● Burns
● Massive transfusion
● Pneumonia
● Aspiration
● Drug overdose
● Near drowning
● Post perfusion injury after cardiopulmonary bypass
● Pancreatitis
● Fat embolism

16
Q

Stages of ARDS

A
  • diffuse alveolar damage and lung capillary endothelial injury. The early phase is described as being exudative, whereas the later phase is fibro-proliferative in character.

● Injury/Exudative phase: Occurs between 1-7 days after the initial direct lung insult. Is characterised by an increase in the permeability of the alveolar-capillary barrier, leading to an influx of fluid into the alveoli. Intrapulmonary shunts develop and as the alveoli have filled with fluid, blood passing through cannot be oxygenated. Alveoli collapse and atelectasis develops further reducing lung compliance.
● Proliferative phase. Begins 1-2 weeks after initial lung injury. Influx of neutrophils monocytes, fibroblasts and lymphocytes to lung injury site and destroy the pulmonary vasculature. Connective tissue and other structural elements in the lungs proliferate in response to the initial injury, including development of fibroblasts (cells giving rise to connective tissue).Under a microscope, lung tissue appears densely cellular. Terms “stiff lung” have been known to characterize this phase. Two to four weeks after the onset of lung injury, abnormally enlarged air spaces and fibrotic tissue (scarring) are increasingly apparent. If the proliferative stage is stopped the lesions will resolve.
● Fibrosis/Repair Phase (healing stage). 2- 3 weeks after the initial lung injury. The lung reorganizes and recovers during this phase. Resolution of inflammation, excess cellularity, and fibrosis settles. Oxygenation improves to the point of removing mechanical ventilation. This phase may take up to 12 months to resolve depending on the severity of the ARDS.

17
Q

Criteria of diagnosis of ARDS

A

● Clinical presentation - Tachypnea and dyspnea; crackles upon auscultation
● Clinical setting - Direct insult (aspiration) or systemic process causing lung injury (sepsis)
● Radiologic appearance - 3-quadrant or 4-quadrant alveolar flooding/fluid
● Lung mechanics - Diminished compliance (< 40 mL/cm H 2 O)
● Gas exchange - Severe hypoxia refractory to oxygen therapy

18
Q

Criteria of diagnosis of ARDS

A

● Clinical presentation - Tachypnea and dyspnea; crackles upon auscultation
● Clinical setting - Direct insult (aspiration) or systemic process causing lung injury (sepsis)
● Radiologic appearance - 3-quadrant or 4-quadrant alveolar flooding/fluid
● Lung mechanics - Diminished compliance (< 40 mL/cm H 2 O)
● Gas exchange - Severe hypoxia refractory to oxygen therapy

19
Q

Treatment management of ARDS

A

treatment of the underlying condition is essential, along with:
1) supportive care
2) noninvasive ventilation or mechanical ventilation using low tidal volumes
3) conservative fluid management

Other supportive therapies include: Nutritional support, Extracorporeal Membrane Oxygenation (ECMO)
Pharmacological therapies include: Inhaling Nitric oxide and corticosteroids

19
Q

Treatment management of ARDS

A

treatment of the underlying condition is essential, along with:
1) supportive care
2) noninvasive ventilation or mechanical ventilation using low tidal volumes
3) conservative fluid management

Other supportive therapies include: Nutritional support, Extracorporeal Membrane Oxygenation (ECMO)
Pharmacological therapies include: Inhaling Nitric oxide and corticosteroids

20
Q

How is oxygen delivered to ARDS patients?

A

CPAP or BiPAP

21
Q

If prompt therapy is not initiated for the patient with ARDS, what ABG results would you suspect?

A

hypercapnia and metabolic acidosis