Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Heart failure and chronic lung disease in frailty
Medicine of older adults · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
!
Acute cardiorespiratory failure
Severe breathlessness, exhaustion, cyanosis, altered consciousness, shock, acute pulmonary oedema, silent chest, rising carbon dioxide, chest pain or arrhythmia requires immediate diagnosis and organ support.
Action: Use ABCDE, controlled oxygen with blood gases when hypercapnia risk exists, ECG and urgent chest assessment, treat pulmonary oedema or obstructive exacerbation, and obtain senior and critical-care input for non-invasive ventilation, vasopressor or escalation decisions.
Overview
Distinguish cardiac, pulmonary and mixed decompensation, treat congestion, bronchospasm, infection and respiratory failure without destabilising other organs, and align long-term disease therapy, rehabilitation and escalation with frailty and personal goals.
Establish stable baseline breathlessness, exercise distance, orthopnoea, oedema, sputum, oxygen use, exacerbations, weight and self-care. Ask onset, chest pain, palpitations, fever, pleurisy, haemoptysis, medication and inhaler use, diuretic response, salt and fluid change and recent admission. Collateral and pharmacy supply may reveal missed therapy or a device the person cannot physically operate.
Use ABCDE and diagnose physiology. Record oxygen on the exact delivery device, work of breathing, speech, fatigue, perfusion, blood pressure, jugular venous pressure, oedema and mental state. Wheeze can occur in pulmonary oedema; crackles can be absent in COPD with heart failure. Unilateral signs, murmur, rhythm, calf findings and infection sources broaden the differential.
Obtain ECG, chest radiograph, FBC, renal and electrolytes, liver, glucose and CRP as indicated. Blood gas is urgent for severe disease, drowsiness, oxygen change or hypercapnia risk. Natriuretic peptides support heart-failure assessment but rise with age, renal disease and atrial fibrillation and may be lower in obesity. Troponin needs clinical interpretation because acute illness can cause myocardial injury without plaque rupture.
Practice
Two practice questions
Your practice draft is saved in this browser.
Question 1 of 2
0 correct
Medicine of older adultsOriginal SBA
Treating COPD exacerbation
An 80-year-old admitted with a clinically significant COPD exacerbation has no contraindication to systemic corticosteroids. Which NICE regimen is appropriate?
Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Give oxygen for hypoxaemia, not breathlessness alone. If COPD or another hypercapnia risk exists, use controlled oxygen to a target commonly 88% to 92% until gases define the plan. Repeat gas after oxygen or clinical change. A normal saturation does not exclude respiratory distress, and over-oxygenation can worsen carbon dioxide retention in susceptible patients.
Treat acute congestion with IV loop diuretic, using a higher dose than the pre-admission oral dose when already treated, as NICE advises, and titrate to urine, weight and clinical decongestion. Avoid routine nitrates unless a specific indication such as severe hypertension or ischaemia exists under senior supervision. Pulmonary oedema with respiratory failure may need continuous positive airway pressure or non-invasive ventilation.
Treat COPD exacerbation with short-acting bronchodilators delivered by a device the person can use; nebulisers require a gas source and oxygen strategy appropriate to carbon dioxide risk. NICE recommends prednisolone 30 mg orally daily for five days for most hospitalised exacerbations when no contraindication alters the plan. Use antibiotics only when sputum purulence, severity and risk support likely bacterial benefit under NICE NG114.
For persistent hypercapnic respiratory failure despite optimal treatment, non-invasive ventilation is the treatment of choice when consistent with clinical context and goals. Explain mask, monitoring and likely burdens. Deteriorating consciousness, secretion, haemodynamic instability or inability to protect the airway needs critical-care reassessment, not repeated NIV without an escalation decision.
Review precipitating and competing disease: pneumonia, aspiration, pulmonary embolism, acute coronary syndrome, arrhythmia, anaemia, thyroid disease, sleep apnoea, renal failure and medicine non-adherence. Dysphagia, dental problems and breathlessness during meals contribute to malnutrition; diuretic-related urgency and night-time oxygen tubing contribute to falls.
After acute treatment, optimise chronic therapy. Heart-failure treatment follows ejection fraction, symptoms, pressure, kidney function, potassium and goals, with specialist MDT support and careful titration. COPD treatment follows symptoms and exacerbations, smoking support, inhaler technique and eosinophil or asthma features. Do not withhold disease-modifying therapy solely because of age, but simplify and monitor for frailty-related adverse effects.
Assess practical delivery. Observe inhaler technique with the actual device and consider spacer, breath-actuated or nebulised alternatives only when clinically appropriate. Check who weighs, manages diuretic variation, orders oxygen and recognises deterioration. Oxygen is a prescribed treatment requiring fire and smoking safety, equipment support and a target; it is not a generic response to dyspnoea.
Rehabilitation is treatment. Offer pulmonary rehabilitation after relevant COPD admission and cardiac rehabilitation where indicated, adapting transport, cognition, oxygen, balance and strength. Include nutrition, anxiety, pacing, energy conservation and advance-care planning. At transition provide one reconciled regimen, rescue plan, follow-up, weight or symptom thresholds and contacts.
Key points
Do not label all breathlessness as COPD or all oedema as heart failure; identify physiology, baseline and the precipitating cause.
First-line acute assessment is ABCDE, controlled oxygen, ECG, chest examination, blood gas when indicated, chest radiograph and targeted cardiac, infection and renal tests.
In people at risk of hypercapnic respiratory failure, target oxygen saturation is usually 88% to 92% pending blood gases and individual prescription.
Acute heart failure with congestion requires IV loop diuretic and close urine, weight, renal, electrolyte, pressure and symptom monitoring.
A creatinine rise during effective decongestion does not automatically mean fluids are needed; examine perfusion and residual congestion.
COPD exacerbation treatment uses increased short-acting bronchodilators, prednisolone 30 mg orally daily for five days when indicated, and antibiotics only under sputum and severity criteria.
Non-invasive ventilation is the preferred escalation for persistent hypercapnic ventilatory failure during COPD exacerbation despite optimal medical therapy, when appropriate.
After stabilisation, optimise guideline-directed heart-failure treatment and inhaled therapy, but check renal function, pressure, inhaler technique, cognition and practical administration.
Aetiology
01
Heart-failure decompensation
Ischaemia, arrhythmia, infection, hypertension, renal decline, medicine omission and excess sodium or fluid precipitate congestion and reduced cardiac reserve.
02
Obstructive lung exacerbation
Viral or bacterial infection, pollution, inhaler failure and comorbid cardiac disease worsen airflow obstruction and gas exchange.
03
Mixed cardiorespiratory disease
COPD, heart failure, pulmonary hypertension, sleep-disordered breathing and deconditioning frequently coexist and amplify symptoms during a single acute presentation.
04
Frailty and treatment disruption
Cognitive, dexterity, swallowing, social and transition barriers cause missed inhalers, diuretics, oxygen or monitoring despite an accurate prescription.
Pathophysiology
1
Pulmonary congestion
Elevated cardiac filling pressure drives fluid into interstitial and alveolar spaces, reducing compliance and oxygen diffusion.
2
Airflow obstruction and trapping
Airway inflammation, bronchoconstriction and mucus impede expiration, causing dynamic hyperinflation, respiratory muscle load and ventilation mismatch.
3
Gas-exchange failure
Ventilation-perfusion mismatch causes hypoxaemia, while severe obstruction or fatigue reduces alveolar ventilation and raises carbon dioxide.
4
Cardiorenal-respiratory interaction
Venous congestion and low output impair kidneys, while fluid, renal dysfunction and anaemia worsen pulmonary and cardiac workload.
5
Reserve and deconditioning
Low muscle strength and endurance make ordinary activity exceed cardiopulmonary capacity, with bed rest further lowering the threshold.
Clinical features and red flags
Congested heart-failure pattern
Orthopnoea, raised venous pressure, oedema, weight gain and crackles support elevated cardiac filling pressures.
Obstructive exacerbation pattern
Wheeze, prolonged expiration, increased dyspnoea and sputum change suggest COPD exacerbation after competing diagnoses are assessed.
Hypercapnic failureRed flag
Drowsiness, headache, tremor or acidosis with raised carbon dioxide requires controlled oxygen and ventilatory assessment.
Acute pulmonary oedemaRed flag
Severe distress, diffuse crackles, frothy sputum and hypertension or shock requires emergency cardiac treatment.
Mixed cardiorespiratory disease
Congestion, obstruction, infection and deconditioning coexist, so response to one treatment does not exclude another process.
Functional treatment failure
The prescription is correct but cognition, dexterity, supply or support prevents inhaler or diuretic administration.
Red flags requiring action
New severe hypoxia, exhaustion, reduced consciousness or worsening acidosis indicates impending respiratory failure.
Pink frothy sputum, diffuse crackles, hypertension or shock with acute breathlessness suggests pulmonary oedema and requires emergency treatment.
Investigations
01ECG and continuous rhythm assessmentFirst step
Why
Identify ischaemia and arrhythmic precipitants.
Interpretation and limitations
Relate rhythm, rate and ischaemic change to symptoms, pressure, troponin and previous ECG rather than treating one abnormality in isolation.
02Chest radiograph
Why
Assess congestion, infection and alternative thoracic disease.
Interpretation and limitations
Pulmonary oedema, effusion or infiltrate supports but does not independently establish cause; compare with prior imaging and hydration.
03Arterial or venous blood gas
Why
Define ventilatory and metabolic failure.
Interpretation and limitations
Use pH and carbon dioxide to guide controlled oxygen and NIV; repeat after treatment and worsening consciousness or work.
04Renal, electrolyte and blood profile
Why
Guide diuresis and identify precipitating disease.
Interpretation and limitations
Trend creatinine, sodium, potassium, FBC and inflammation with urine, congestion and medicines, not a single reference result.
05Natriuretic peptide and echocardiography
Why
Confirm and phenotype suspected heart failure.
Differential diagnosis
01
Pneumonia or aspiration
Focal or systemic infection may coexist with wheeze or oedema and requires imaging and antimicrobial assessment.
02
Pulmonary embolism
Disproportionate hypoxia, pleuritic pain, haemoptysis or thrombotic risk requires structured PE investigation rather than diagnostic anchoring.
03
Acute coronary or arrhythmic disease
Ischaemia and rapid or slow rhythm can present as breathlessness, weakness or delirium without classic chest pain.
04
Anaemia and metabolic disease
Anaemia, acidosis, thyroid disease and renal failure produce breathlessness and fatigue without primary airway or fluid decompensation.
05
Deconditioning or anxiety
Low fitness and panic can amplify dyspnoea but are diagnoses after acute physiological and structural danger is assessed.
Management
01First-line breathlessness routeSupport gas exchange and distinguish mechanismsFirst stepFirst lineFrailty is accompanied by acute dyspnoea, hypoxia or oedema.+
1Use ABCDE, controlled oxygen, ECG, chest and congestion examination, blood gas and targeted laboratory and imaging tests.
2Treat pulmonary oedema, obstructive exacerbation, infection, ischaemia, arrhythmia or thromboembolism according to the dominant physiology.
3EscalationReassess response, renal function and gas exchange early and escalate respiratory or circulatory failure without diagnostic anchoring.
02Acute heart-failure routeDecongest while protecting perfusion and kidneysClinical and imaging findings support fluid congestion.+
1Give IV loop diuretic at an exposure appropriate to prior treatment and monitor urine, weight, symptoms and pressure.
Complications
01
Respiratory failure
Hypoxaemia, hypercapnia and muscle fatigue can require controlled oxygen, non-invasive ventilation or invasive support during acute deterioration.
02
Kidney and electrolyte injury
Congestion, low perfusion, diuretics, infection and renin-angiotensin treatment can alter renal function and potassium during decompensation.
03
Delirium and falls
Hypoxia, carbon dioxide retention, hypotension, nocturia and medicines cause acute confusion and unsafe mobility during unfamiliar care.
04
Cachexia and sarcopenia
Inflammation, breathlessness during meals and low activity produce weight, muscle and functional loss that worsens prognosis.
05
Repeated admission and carer crisis
Complex monitoring, oxygen, breathlessness and night symptoms can overwhelm community support and fragment medicine plans across repeated transitions.
Monitoring and follow-up
Trend respiratory rate, work, oxygen delivery and target, consciousness and blood gases during acute failure.
Record urine, daily weight, oedema, JVP, breathlessness and lying or standing pressure during diuresis.
Monitor creatinine, sodium, potassium and glucose after diuretic, steroid and chronic-treatment changes.
Review sputum, fever, imaging and culture response and reassess antimicrobial need and duration.
Observe inhaler and oxygen use and check device supply, charging, fire safety and carer support.
Track walking, chair rise, falls, nutrition, dyspnoea confidence and rehabilitation participation.
After transition, confirm early heart-failure or respiratory review and who manages rescue and diuretic plans.
Special situations
Wheeze can be cardiac
Airway narrowing during pulmonary oedema means wheeze does not establish COPD as the sole mechanism.
Creatinine needs congestion context
Renal numbers may worsen during successful decongestion, and reflex fluid can recreate pulmonary oedema.
Oxygen has a target
Both untreated hypoxaemia and excessive oxygen can harm a person susceptible to carbon dioxide retention.
The device is part of the dose
An effective inhaled medicine delivers nothing when inspiratory flow, seal, coordination or cognition is inadequate.
Rehabilitation treats both organs
Stronger peripheral muscle reduces ventilatory demand and improves function across cardiac and respiratory diagnoses.
Common pitfalls
01
Calling every wheeze a COPD exacerbation without assessing pulmonary oedema.
02
Giving uncontrolled high-concentration oxygen to a person at risk of hypercapnic failure.
03
Giving fluid for a creatinine rise despite persistent congestion.
04
Prescribing antibiotics for every COPD exacerbation without bacterial criteria.
05
Writing continue inhalers without observing the actual device technique.
06
Withholding disease-modifying heart-failure therapy solely because of chronological age.
07
Discharging oxygen tubing and diuretic urgency without falls and toilet planning.
08
Providing separate heart and lung rescue plans that give conflicting instructions.
Offer pulmonary or cardiac rehabilitation adapted to frailty, with progressive strength, nutrition, anxiety and breathlessness support.
Create one deterioration plan covering daily symptoms or weight, diuretic actions, inhaler rescue, oxygen target, antibiotics or steroids, and when to seek urgent care.
Chest pain, ischaemic ECG change, sustained arrhythmia or syncope requires an acute coronary and rhythm pathway.
Unilateral pleuritic pain, haemoptysis or unexplained tachycardia raises pulmonary embolism despite coexisting COPD or heart failure.
Fever, focal chest signs, new infiltrate or sepsis physiology requires infection assessment and source-appropriate antimicrobials.
Abrupt decline after a sedative, opioid, beta-blocker omission, diuretic change or inhaler failure requires immediate medication reconciliation.
Interpretation and limitations
Peptide thresholds guide referral, while echocardiography defines ventricular, valvular and pressure abnormalities for treatment selection.
06Spirometry after stability
Why
Confirm persistent airflow obstruction in the right setting.
Interpretation and limitations
Do not rely on acute-exacerbation spirometry; post-bronchodilator testing supports COPD while symptoms and imaging assess alternatives.
07Observed medicine and device use
Why
Detect practical treatment and administration failure.
Interpretation and limitations
Watch inhaler, spacer, oxygen, diuretic and weighing routines with cognition, dexterity, vision and carer support assessed.
2Treat precipitating ischaemia, arrhythmia, infection or hypertension and avoid routine fluid solely for a creatinine rise.
3Review residual congestion, renal and electrolytes daily and transition to an oral regimen with monitoring and self-care ownership.
03COPD exacerbation routeRelieve obstruction and identify failureIncreased breathlessness, cough or sputum occurs in established or suspected COPD.+
1Use short-acting bronchodilators, controlled oxygen and prednisolone when indicated and assess bacterial criteria for antibiotics.
2Repeat gas and clinical assessment and use NIV for persistent hypercapnic ventilatory failure despite optimal treatment when appropriate.
3Before discharge optimise inhalers, technique, smoking support, pulmonary rehabilitation and an individual rescue and follow-up plan.
04Frailty recovery routeMake chronic treatment usableAcute physiology improves but symptoms, weakness or administration burden remain.+
1Reconcile and optimise heart and lung medicines with renal, pressure, cognition, dexterity and swallowing modifiers.
2Begin progressive cardiac or pulmonary rehabilitation, nutrition and falls-safe oxygen and toileting planning.
3Coordinate specialist, primary, pharmacy, therapy, oxygen and carer follow-up around goals and deterioration thresholds.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Shortens recovery and improves lung function during a clinically significant obstructive exacerbation.
Prednisolone for COPD exacerbation
Give 30 mg orally once daily for five days for an acute COPD exacerbation when systemic corticosteroid treatment is indicated under NICE guidance.
Review glucose, delirium, infection, fluid retention and gastrointestinal or psychiatric risk; extend beyond five days only for a separate specialist indication.
Relieves pulmonary and systemic congestion during acute heart-failure decompensation.
Intravenous loop diuretic for acute heart failure
Give intravenous loop diuretic by bolus or infusion; if the person already takes a loop diuretic, use an initial dose higher than the admission oral dose and titrate to clinical response under the acute-heart-failure protocol.
Monitor urine, weight, pressure, creatinine, sodium and potassium closely; persistent congestion may justify continued decongestion despite a modest creatinine rise, whereas hypotension requires reassessment.