GeriQBank · Paper II · Q45
Respiratory failure, including acute type 2 respiratory failure
- Topic
- Respiratory Medicine
- Chapter
- Part II — Respiratory Medicine and Sleep
- Years asked
- Not recorded in the source
- Frequency
- No university frequency data for this paper yet
Detailed answer
Pro · free in betaAttempt it firstOutline your answer before revealing it — definition, causes, evaluation, management and the geriatric angle.Reveal answer
7-Mark Answer | 6 textbook points + 1 latest update | Asked ×2
Textbook Core – 6 Points
Definition and classification. Respiratory failure is failure of the lungs to maintain adequate gas exchange, defined on arterial blood gas as PaO < 60 mmHg (8 kPa) breathing room air, with or without PaCO > 50 mmHg (6.7 2 2 kPa). Type 1 (hypoxaemic) Type 2 (hypercapnic / ventilatory)
Gases PaO2 ↓, PaCO2 normal or ↓ PaO2 ↓, PaCO2 ↑
Mechanism V/Q mismatch, shunt, Alveolar hypoventilation (pump failure)
diffusion defect A–a Widened Normal in pure hypoventilation; widened if lung disease coexists gradient Examples Pneumonia, pulmonary oedema, COPD exacerbation, opioid/sedative overdose, neuromuscular disease, kyphoscoliosis, PE, ARDS, ILD obesity hypoventilation, severe asthma (late)
Acute versus chronic — read the bicarbonate. In acute type 2 failure the pH is low with a normal bicarbonate; in chronic failure the bicarbonate is raised with a near-normal pH (renal compensation); in acute-on-chronic failure the bicarbonate is raised AND the pH is low. This single distinction determines urgency and is a guaranteed examination mark. Also calculate the alveolar–arterial oxygen gradient, which rises normally with age (approximately age/4 + 4 mmHg).
Why older people are predisposed. Ageing produces loss of elastic recoil with small airway closure and V/Q mismatch, reduced chest wall compliance from kyphosis and rib cage stiffening, reduced respiratory muscle mass and strength, and a lower PaO . Most importantly there is a marked decline in efferent neural output and 2 a blunted ventilatory response to hypoxia and hypercapnia, giving a lower threshold for ventilatory decompensation. Add sarcopenia, malnutrition, sedatives and opioids, aspiration and immobility, and small insults precipitate failure.
Clinical features. Hypoxaemia — dyspnoea, tachypnoea, restlessness, confusion, cyanosis (a late and unreliable sign), tachycardia, arrhythmia; chronically, polycythaemia, pulmonary hypertension and cor pulmonale. Hypercapnia — headache (especially morning), warm peripheries with a bounding pulse, flushing, drowsiness progressing to coma, flapping tremor (asterixis) and papilloedema. In older adults the earliest and often the only sign is unexplained delirium or drowsiness — always check an arterial blood gas. Pulse oximetry cannot detect hypercapnia and is misleading on supplemental oxygen.
Investigations. Arterial blood gas is the diagnostic test (record the FiO ). Add chest radiograph, ECG, full 2 blood count, urea and electrolytes, glucose, and where relevant CT chest or CTPA, echocardiography, sputum culture, toxicology, thyroid function, creatine kinase and nerve conduction studies for neuromuscular causes. In chronic disease do spirometry, overnight oximetry and transcutaneous CO monitoring. Look actively for 2 reversible precipitants — infection, pneumothorax, pulmonary embolism, heart failure, sedative drugs, electrolyte disturbance and pain-related hypoventilation.
Management of acute type 2 respiratory failure. (i) Treat the precipitating cause — bronchodilators, corticosteroids, antibiotics, drainage of pneumothorax, reversal of opioids with naloxone. (ii) Controlled oxygen therapy targeting SpO 88–92% using a 24–28% Venturi mask — excessive oxygen worsens hypercapnia 2 through loss of hypoxic drive, the Haldane effect and increased V/Q mismatch, and increases coronary and cerebral vascular resistance. (iii) Non-invasive ventilation (BiPAP) when pH < 7.35 with PaCO > 6 kPa 2 despite maximal medical therapy — it reduces mortality, intubation rate and hospital stay. (iv) Repeat the ABG at 1 hour; failure to improve, pH < 7.25, reduced consciousness or intolerance of the mask indicates intubation and invasive ventilation — or, in a frail patient, that NIV is the agreed ceiling of care. (v) Respiratory stimulants (doxapram) are now rarely used. (vi) Document a ceiling-of-treatment and resuscitation decision early, and provide palliation of breathlessness with opioids and benzodiazepines where treatment is not succeeding.
Latest Update – 1 Point (2023–Present)
High-flow nasal oxygen (HFNO) has become an established third option between conventional oxygen and NIV. Delivering heated, humidified gas at 30–60 L/min with a precise FiO , it generates modest PEEP 2 and washes out anatomical dead space. ERS/ATS guidance and the GOLD reports support HFNO in acute hypoxaemic respiratory failure (where it reduces intubation compared with conventional oxygen), and it is safe and effective in exacerbated COPD with both normocapnic and hypercapnic failure. It is especially valuable in older patients as a comfort-preserving option where intubation is not appropriate (do-not-intubate orders) or to provide intermediate care outside the intensive care unit — although NIV remains first-line for acidotic hypercapnic failure.
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References
- PAPERS-2-3-4_COMBINED.pdf — page 247
- GeriQBank source PDF — p. 247
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