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
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).
Occurs rapidly, usually in minutes to hours or days.
Chronic Respiratory Failure
Characterized by hypoxemia (decreased Pao2) and/or hypercapnia (increased Paco2) with a normal pH (7.35 to 7.45).
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
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.
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
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
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
Oxygen toxicity if prolonged high Fio2 required.
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
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.
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