Acute heart failure and pulmonary oedema

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The first bedside decision is whether the patient is congested, hypoperfused, hypertensive or in shock. Pulmonary oedema with high BP needs rapid unloading and selected vasodilation; cold hypotensive failure needs cause-directed critical-care support rather than automatic escalation of diuretic or nitrate.

NICE makes IV diuresis the routine pharmacological treatment. Oxygen, NIV, nitrates and vasoactive drugs are conditional treatments tied to measured hypoxaemia, respiratory acidosis, severe hypertension/ischaemia or shock.

A new diagnosis needs echocardiography, usually within 48 hours, but immediate bedside imaging is required when shock, tamponade, severe valve disease or a mechanical post-MI complication is suspected.

Key points

Acute heart failure is a syndrome: define congestion, perfusion and blood pressure while searching for ACS, arrhythmia, valve/mechanical disease, infection, uncontrolled hypertension and medicine or renal triggers.
Offer IV loop diuretic therapy for acute heart failure; if the person already takes a loop diuretic, NICE advises an initial IV dose higher than their admission oral dose, then titrate to response.
Give oxygen for hypoxaemia, not routinely to a normoxaemic patient; monitor saturation and blood gases when respiratory failure is severe.
Do not use nitrates routinely in acute heart failure. Consider IV nitrate only in selected severe hypertension, concomitant ischaemia or acute regurgitant valve disease with close BP monitoring.
Do not use NIV routinely; start it without delay when cardiogenic pulmonary oedema causes severe dyspnoea with acidaemia, or when conventional treatment is failing, provided there is no contraindication.
Do not give opiates routinely; respiratory depression, hypotension and delayed recognition of deterioration can outweigh symptomatic benefit.
Inotropes or vasopressors are not routine for congestion; reserve them for potentially reversible cardiogenic shock under critical-care/cardiac monitoring.
Before discharge, ensure clinical stability, an aetiology and management plan, specialist heart-failure input and follow-up by the specialist team within 2 weeks.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Acute coronary ischaemia

Myocardial ischaemia or infarction can abruptly reduce ventricular contractility and compliance. It may also cause papillary-muscle dysfunction or another mechanical complication, rapidly increasing filling pressure and congestion.

Tachyarrhythmia or bradyarrhythmia

A very rapid rhythm shortens filling and raises oxygen demand, while severe bradycardia reduces cardiac output. Either can precipitate pulmonary oedema or shock in a vulnerable heart.

Structural and inflammatory cardiac disease

Acute mitral or aortic valve failure, myocarditis, right-ventricular failure and mechanical post-infarction lesions can cause sudden haemodynamic deterioration, sometimes without preceding peripheral fluid accumulation.

Haemodynamic and systemic precipitants

Marked hypertension, infection, renal decline, anaemia, thyroid disease, treatment non-adherence and medicines that promote retention can upset a previously compensated circulation by increasing afterload, demand or intravascular volume.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Ventricular dysfunction
Impaired contraction or relaxation, or acute valve dysfunction, can prevent the heart from handling venous return effectively. Filling pressures may rise upstream even when the ejection fraction is not known to be reduced.
2
Pulmonary capillary congestion
Raised left-sided filling pressure increases pulmonary capillary hydrostatic pressure. Fluid first enters the interstitium and then the alveoli, reducing lung compliance and impairing oxygen transfer.
3
Respiratory decompensation
Oedematous lungs demand greater work of breathing and create ventilation–perfusion mismatch. Hypoxaemia, fatigue and acidaemia may follow, particularly when extensive alveolar flooding produces frothy sputum.
4
Hypertensive fluid redistribution
An abrupt afterload rise can shift blood into the pulmonary circulation without major total-body fluid gain. This explains flash pulmonary oedema with severe breathlessness but little peripheral oedema.
5
Low-output failure
When forward flow falls, cerebral, renal and peripheral perfusion deteriorate. Cool skin, confusion, oliguria and rising lactate signal progression from congestion towards cardiogenic shock.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Cardiogenic pulmonary oedemaRed flag

Acute severe dyspnoea, orthopnoea, diffuse crackles, hypoxaemia and sometimes pink frothy sputum; marked work of breathing or acidaemia signals imminent ventilatory failure.

Congested but perfused

Raised JVP, peripheral oedema, ascites, weight gain and pulmonary congestion with maintained BP/perfusion; IV diuresis is central.

Hypertensive acute heart failure

Abrupt pulmonary oedema with markedly elevated BP may reflect afterload-driven fluid redistribution rather than massive total-body fluid excess.

Low-output or cardiogenic shockRed flag

Hypotension with cool peripheries, confusion, oliguria and rising lactate; rapidly assess ACS, mechanical disease, RV failure and arrhythmia.

High-risk precipitant

ACS, rapid/slow arrhythmia, acute valve lesion, myocarditis, PE, infection, anaemia, thyroid disease, non-adherence, NSAIDs or renal decline may be the treatable driver.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
ABCDE observations, continuous ECG and 12-lead ECGFirst step
Why
Grade severity and detect ACS or arrhythmia.
Interpretation and limitations
Hypotension, ischaemic change, malignant rhythm or worsening consciousness drives immediate escalation.
02
Chest X-ray
Why
Look for pulmonary congestion, pleural effusions and alternative pulmonary disease.
Interpretation and limitations
A normal film does not exclude acute HF; asymmetric oedema can mimic pneumonia.
03
Natriuretic peptide
Why
Help rule out new acute HF when the diagnosis is uncertain.
Interpretation and limitations
Low BNP/NT-proBNP makes HF less likely; renal dysfunction, AF and age raise levels, while obesity and prior HF treatment may lower them.
04
Transthoracic echocardiography
Why
Define ventricular function, valves, filling, pericardial disease and mechanical complications.
Interpretation and limitations
For new suspected acute HF, obtain early imaging, generally within 48 hours; use immediate bedside echo for shock or structural emergency.
05
FBC, U&E/eGFR, potassium, magnesium, LFT, glucose, CRP and thyroid tests as indicated
Why
Find precipitants, treatment risk and end-organ injury.
Interpretation and limitations
Trend renal function and electrolytes during diuresis; interpret changes alongside congestion and perfusion rather than in isolation.
06
Arterial or venous blood gas with lactate
Why
Assess acidaemia, carbon dioxide retention and hypoperfusion in severe illness.
Interpretation and limitations
Acidaemia with severe pulmonary oedema supports urgent NIV when appropriate; rising lactate suggests inadequate perfusion.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Asthma or COPD exacerbation

Prominent wheeze, prolonged expiration and an obstructive respiratory history favour airways disease. Raised venous pressure, pulmonary congestion and relevant cardiac or natriuretic-peptide findings support heart failure, although both conditions can coexist.

Pneumonia

Fever, focal bronchial breathing, inflammatory markers and lobar consolidation favour infection. Cardiogenic oedema is usually more diffuse, but asymmetric oedema can resemble pneumonia and infection may precipitate heart failure.

Pulmonary embolism

Pleuritic pain, haemoptysis, venous thromboembolic risk and disproportionate hypoxaemia suggest pulmonary embolism. Right-heart strain without typical left-sided congestion strengthens that alternative diagnosis.

ARDS or sepsis-related lung injury

A clear systemic insult, inflammatory shock and bilateral infiltrates without dominant cardiac filling-pressure features support non-cardiogenic pulmonary oedema. Echocardiography and the overall haemodynamic pattern help separate or identify coexistence.

Renal fluid overload

Advanced renal dysfunction, reduced urine output and widespread volume accumulation may drive pulmonary congestion without primary cardiac deterioration. Renal and cardiac causes frequently overlap, so echocardiography and serial assessment are useful.

Additional chapter-specific clues

Alternative diagnosis

COPD/asthma, pneumonia, PE, ARDS, renal fluid overload and sepsis can mimic or coexist; natriuretic peptides and imaging support but do not replace clinical integration.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-lineImmediate stabilisationFirst stepFirst lineSuspected acute heart failure

1Sit upright, start ABCDE, cardiac monitoring, IV access and targeted oxygen only if hypoxaemic; obtain ECG, bloods and imaging without delaying treatment.
2Identify the haemodynamic phenotype and urgent precipitant, especially ACS, arrhythmia, acute valve/mechanical disease or infection.
3Offer IV loop diuretic and measure urine output, symptoms, BP, renal function and electrolytes.
4EscalationSeek early specialist heart-failure input; escalate immediately if shock, severe respiratory failure or a structural emergency is present.

02Second-linePulmonary oedema not settlingSecond linePersistent severe dyspnoea, hypoxaemia or acidaemia

1Reassess diagnosis, BP, perfusion, diuretic delivery/response and precipitant; avoid reflex fluid or opioid administration.
2Start NIV without delay for cardiogenic pulmonary oedema with severe dyspnoea and acidaemia, using a monitored setting and an intubation plan.
3Consider IV nitrate only for selected severe hypertension, myocardial ischaemia or acute regurgitant valve disease with frequent BP checks.
4EscalationEscalate to invasive ventilation when NIV is contraindicated, not tolerated or failing and this matches goals of care.

03Third-lineDiuretic resistanceThird linePersistent congestion despite an appropriate IV loop-diuretic strategy

1Confirm congestion, adherence, renal perfusion and actual urine response; review NSAIDs and other sodium-retaining medicines.
2Increase the IV loop-diuretic dose or use an infusion under specialist oversight; add sequential nephron blockade only with close electrolyte/renal monitoring.
3Do not use routine ultrafiltration; consider it only for confirmed diuretic resistance after specialist assessment.
4Discuss renal input when severe AKI, refractory electrolyte disturbance or dialysis indication coexists.

04EscalationShock or refractory deteriorationEscalationHypoperfusion, hypotension, rising lactate or multi-organ injury

1Call critical care and cardiology, obtain urgent echo and invasive haemodynamic monitoring as appropriate.
2Correct the cause urgently: revascularise ACS, treat unstable arrhythmia, drain tamponade or repair acute structural disease.
3Use inotrope/vasopressor support only for potentially reversible cardiogenic shock with continuous monitoring.
4Refer selected refractory patients early to a centre capable of temporary mechanical support, advanced HF therapy or transplantation.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

First-line relief of congestion and pulmonary oedema.

Furosemide IV

If loop-diuretic naive, the cited SmPC starts 20–40 mg IV for pulmonary oedema; if diuresis does not increase, it permits a repeat after 30–60 minutes, if necessary at twice the dose. If already taking a loop diuretic, NICE advises an initial IV dose higher than the pre-admission oral dose, followed by response- and renal-function-led adjustment.

Monitor BP, urine output, creatinine, sodium, potassium and magnesium. Give IV furosemide slowly—this SmPC limits injection to 4 mg/min, or 2.5 mg/min in advanced renal failure (serum creatinine above 442 micromol/L); rapid/high dosing increases hypotension, electrolyte-loss and ototoxicity risk.

Selected severe hypertension, concomitant ischaemia or acute regurgitant valve disease; not routine acute-HF treatment.

Glyceryl trinitrate IV

When specifically selected for unresponsive congestive/acute left-sided heart failure, the cited SmPC starts 20–25 micrograms/min IV by infusion pump; reduce to 10 micrograms/min or increase by 20–25 micrograms/min every 15–30 minutes to response. Its usual overall range is 10–200 micrograms/min.

Avoid in hypotension, RV infarction/preload dependence or recent PDE5-inhibitor use; severe aortic stenosis requires specialist haemodynamic judgement. Continuous BP monitoring is required.

Vasopressor for selected hypotensive, potentially reversible cardiogenic shock.

Noradrenaline

The cited ready-to-use SmPC, licensed for adults weighing over 50 kg, starts noradrenaline base at 0.05–0.15 micrograms/kg/min by central IV infusion pump and titrates in 0.05–0.1 micrograms/kg/min steps to perfusion/MAP; its maintenance range is 0.05–1.5 micrograms/kg/min.

For this cited product use a central venous catheter and preferably arterial BP monitoring; other preparations have different concentrations and labels. Watch for arrhythmia, ischaemia and extravasation, and correct the cause concurrently.

Selected low-output cardiogenic shock with inadequate contractility, often alongside a vasopressor if BP is low.

Dobutamine

Most adults respond to 2.5–10 micrograms/kg/min by continuous IV infusion; titrate to monitored perfusion and cardiac output.

Tachyarrhythmia, myocardial ischaemia and hypotension; ICU/cardiology supervision only and use the lowest effective duration.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Respiratory failure

Progressive alveolar flooding causes severe hypoxaemia, respiratory muscle fatigue and acidaemia. Non-invasive or invasive ventilatory support may be needed when work of breathing remains high despite initial treatment.

Cardiogenic shock

Inadequate forward flow produces hypotension and tissue hypoperfusion, with confusion, cool peripheries, oliguria and rising lactate. This phenotype requires urgent cause-directed cardiac and critical-care support.

Acute kidney injury

Reduced renal perfusion and venous congestion can impair filtration, while diuresis alters fluid and electrolyte balance. Trends should be interpreted alongside congestion, perfusion and response to treatment rather than as isolated laboratory values.

Myocardial ischaemia and arrhythmia

Raised wall stress, hypoxaemia and sympathetic activation increase myocardial oxygen demand and electrical instability. Ischaemia or a malignant rhythm can then worsen ventricular function and create a self-perpetuating decline.

Persistent congestion and readmission

Residual pulmonary or systemic congestion after apparent improvement increases the likelihood of early deterioration and readmission. Discharge planning should confirm clinical stability, a working aetiology and precipitant plan, and specialist follow-up.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Respiratory rate, work of breathing, oxygen saturation and repeat blood gas after NIV or worsening.
Continuous rhythm, frequent BP and perfusion markers; invasive arterial monitoring in shock or vasoactive therapy.
Strict fluid balance, urine output and daily weight during decongestion.
Creatinine/eGFR, sodium, potassium and magnesium at least daily during active IV therapy, more often if unstable.
Symptoms, JVP, oedema and lung findings to judge decongestion rather than weight or creatinine alone.
Before discharge: stable oral regimen, precipitant addressed, education/care plan and specialist follow-up within 2 weeks.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Treat the phenotype

A hypertensive wet patient and a cold hypotensive patient can look equally breathless but need very different haemodynamic treatment.

NIV has a defined trigger

NICE reserves immediate NIV for severe dyspnoea with acidaemia in cardiogenic pulmonary oedema, or failure of medical therapy—not routine use in every congested patient.

Renal change needs context

A modest creatinine rise during successful decongestion may not mean treatment failure; persistent congestion itself worsens renal function and outcome.

Flash oedema can be structural

Acute MR, ischaemia or marked afterload may cause severe pulmonary oedema without large peripheral oedema or weight gain.

Discharge is an intervention

Residual congestion and an untested follow-up plan predict readmission; stability, education, medicines and early specialist review must be explicit.

11Common pitfallsFrequent interpretation and management errors.

01
Giving oxygen to every patient regardless of saturation.
02
Using nitrates, morphine or NIV routinely instead of tying them to a defined indication.
03
Giving the same low IV furosemide dose to a patient already taking high-dose oral loop diuretic.
04
Stopping decongestion solely for a small creatinine change without reassessing congestion and perfusion.
05
Missing ACS, acute MR or another reversible cause by labelling the episode simply 'fluid overload'.