RESPIRATORY FAILURE

• Respiratory failure is not really a disease; it is a general term to describe any circumstance that interferes with the ability to maintain adequate gas exchange.
• Respiratory failure is defined as a life threatening condition of an alteration in an individual's oxygenation (PaO₂) to fall below 60 mm Hg (hypoxemia) and/or the partial pressure of arterial carbon dioxide (PaCo₂) to rise above 50 mm Hg (hypercapnia), on room air as determined by arterial blood gas (ABG) analysis.
• It is considered to exist when the respiratory system is no longer able to meet metabolic demand.

Classification

Respiratory failure classified as acute or chronic.

Acute Respiratory Failure

1. Characterized by hypoxemia (Pao₂ less than 50 mm Hg) and/or hypercapnia (Paco₂ greater than 50 mm Hg) and acidemia (pH less than 7.35).
2. Occurs rapidly, usually in minutes to hours or days.

Chronic Respiratory Failure

1. Characterized by hypoxemia (decreased Pao₂) and/or hypercapnia (increased Paco₂) with a normal pH (7.35 to 7.45).
2. Occurs over a period of months to years-allows for activation of compensatory mechanisms.

Etiology / Types

There are two different types of respiratory failure.

Type I - hypoxemic respiratory failure - is also known as Oxygenation Failure; in this type, oxygenation is compromised but carbon dioxide levels may be either normal or low. (Hypoventilation with V/Q mismatch)

• Decreased alveolar oxygenation

  Influenced by many factors, including conditions modifying environmental oxygen tension

  • Affected by altitude - FiO₂ reduces to less than 21%
  • Fire - consume the environmental oxygen
  • Oxygen supplementation
• Ventilation/perfusion (V/Q) mismatch

  Affected by factors such as bronchoconstriction, the presence of secretions in the airway and the surface area of the alveoli.

  • Atelectasis (alveolar collapse) decreases surface area,
  • Emphysema and fluid within the alveoli
  • Pulmonary artery vasospasm and
  • Pulmonary embolism
  • Hypoxia, hypoxic pulmonary vasoconstriction
  • Cardiogenic pulmonary edema (left ventricular failure; mitral stenosis).
  • Acute respiratory distress syndrome (ARDS)
• Decreased oxyhaemoglobin saturation

  Apart from the factors impeding gas exchange, other influences can affect the amount of oxygen binding to haemoglobin.

  • Carbon monoxide poisoning

Type II - Hypercapnia respiratory failure - is also known as ventilatory failure; in this type, both oxygenation and carbon dioxide elimination are compromised. (Hypoventilation with or without V/Q mismatch)

Ventilatory Failure with Normal Lungs

• Decreased central ventilatory drive

  Conditions that alter the respiratory drive include -

  • Brain stem compression from haemorrhage or tumour,
  • Metabolic encephalopathy and
  • Overdose of depressant drugs, such as anaesthetic agents, narcotics or benzodiazepines.
• Decreased neuromuscular transmission

  Conditions affecting the neuromuscular units supplying respiratory muscles include

  • Spinal cord injury,
  • Multiple sclerosis,
  • Myasthenia gravis and
  • Gullain-barré syndrome.
  • Drugs with neuromuscular junction antagonistic affects can also cause ventilatory failure.
• Chest wall or muscle pathology

  Conditions that affect respiratory muscles include

  • Fatigue,
  • Disuse atrophy,
  • Polymyositis and
  • Muscular dystrophy.
  • Flail chest,
  • Kyphoscoliosis,
  • Morbid obesity
  • Pneumothorax

Ventilatory Failure with Intrinsic Lung Disease

• Intrinsic Lung Disease
  • Chronic obstructive pulmonary disease (COPD) (chronic bronchitis, emphysema).
  • Severe asthma.
  • Cystic fibrosis.

Pathophysiology

Clinical Manifestations

• Hypoxemia-restlessness, agitation, dyspnoea, disorientation, confusion, delirium, loss of consciousness.
• Hypercapnia-headache, somnolence, dizziness, confusion.
• Tachypnea initially; then when no longer able to compensate, bradypnea
• Accessory muscle use
• Asynchronous respirations

Diagnostic Evaluation

• ABG analysis-show changes in PaO2, PaCO2, and pH from patient's normal; or PaO2 less than 50 mm Hg, PaCO2 greater than 50 mm Hg, pH less than 7.35.
• Pulse oximetry-decreasing SaO2.
• End tidal CO2 monitoring-elevated.
• Complete blood count, serum electrolytes,
• chest X-ray,
• Urinalysis,
• Electrocardiogram (ECG),
• Blood and sputum cultures-to determine underlying cause and patient's condition.

Management

• Oxygen therapy to correct the hypoxemia.
• Chest physical therapy and hydration to mobilize secretions.
• Bronchodilators and possibly corticosteroids to reduce bronchospasm and inflammation.
• Diuretics for pulmonary congestion.
• Mechanical ventilation as indicated. Non-invasive positive-pressure ventilation using a facemask may be a successful option for short-term support of ventilation.

Note- Avoid administration of oxygen at Fio₂ of 100% for COPD patients because you may depress the respiratory center drive. For COPD patients, the drive to breathe may be hypoxemia.

Complications

1. Oxygen toxicity if prolonged high Fio₂ required.
2. Barotrauma from mechanical ventilation intervention

Nursing Management

Nursing Assessment

• Assess changes suggesting –
  • increased work of breathing - tachypnea, diaphoresis, intercostal muscle retraction, fatigue
  • Pulmonary edema - fine, coarse crackles or rales, frothy pink sputum.
• Assess breath sounds.
• Assess level of consciousness (LOC) and ability to tolerate increased work of breathing.
• Assess for signs of hypoxemia and hypercapnia.
• Determine vital capacity (VC), respiratory rate, and negative inspiratory force (NIF) and compare with values indicating need for mechanical ventilation:
• Analyse ABG and compare with previous values.
• Determine hemodynamic status (blood pressure, pulmonary wedge pressure, cardiac output, SvO2) and compare with previous values. If patient is on mechanical ventilation and positive end-expiratory pressure (PEEP), venous return may be limited, resulting in decreased cardiac output.

Nursing Diagnoses

1. Impaired Gas Exchange related to inadequate respiratory center activity or chest wall movement, airway obstruction, and/or fluid in lungs

• Goal: Improving Gas Exchange
• Administer antibiotics, cardiac medications, and diuretics as ordered.
• Administer oxygen to maintain PaO₂ of 60 mm Hg or SaO₂ > 90%.
• Monitor fluid balance by intake and output measurement.
• Provide measures to prevent atelectasis and promote chest expansion and secretion clearance.
• Monitor adequacy of alveolar ventilation by frequent measurement of respiratory rate, VC, inspiratory force, and ABG levels.
• Prepare to assist with non-invasive ventilation or intubation and initiation of mechanical ventilation, if indicated.

1. Ineffective Airway Clearance related to increased or tenacious secretions.

• Goal: Maintaining Airway Clearance
• Administer medications to increase alveolar ventilation-bronchodilators.
• Perform chest physiotherapy to remove mucus.
• Administer I.V. fluids and mucolytics to reduce sputum viscosity.
• Suction patient as needed to assist with removal of secretions.
• If the patient becomes increasingly lethargic, cannot cough or expectorate secretions, cannot cooperate with therapy, or if pH falls below 7.30, despite use of the above therapy, report and prepare to assist with intubation and initiation of mechanical ventilation.

Health Education

• Instruct patient with pre-existing pulmonary disease to seek early intervention for infections to prevent acute respiratory failure.
• Teach patient about medication regimen.
  • Proper technique for inhaler use
  • Dosage and timing of medications
  • Monitoring for adverse effects of corticosteroids: weight gain due to fluid retention, polyuria and polydipsia due to hyperglycemia, mood changes; report to health care provider