Suspected heart failure

NICE NG106 (chronic) and CG187 (acute); ACR AC Suspected New-Onset Heart Failure

This pathway is routed by a blood test, not by imaging. NICE NG106 measures NT-proBNP and, if it is raised, buys a transthoracic echocardiogram — the level only sets how quickly. The echocardiogram is unambiguously the first-line imaging study. The chest radiograph is not a cheaper version of it: it answers a different question, which is whether there is pulmonary congestion and whether the breathlessness is something else entirely.

Breathlessness, orthopnoea, fatigue or peripheral oedema in a patient in whom heart failure is being considered — either as a new outpatient referral with a natriuretic peptide result, or acutely in the emergency department.

Referenced decision support — confirm against your local protocol.

Decision support, not a directive. Protocols and timings shown are typical published ones — your local protocol takes precedence, and the vetting radiologist decides.

The request in front of you

Everything is optional. Leave a field alone and the answer assumes nothing — the verdict updates as you go.

Study requested

What the referrer actually asked for. It is evidence of intent, not a constraint on the right answer.

Contrast as written

What the request form says, not what it should say.

Age

Pick a band, or type an exact age if it matters.

years

Pregnancy status

Where is the patient?

Some pathways change in the emergency department — an acutely threatened limb is not an elective work-up.

Renal risk factors

The question a vetter can actually answer from the request. An explicit “none known” is a real answer, and it removes checks rather than deferring them.

Previous contrast reaction

The pathway — tap anything already done

Marking a study complete moves the answer on. A patient arrives partway through a pathway far more often than at the start of one.

Accept as requested

Transthoracic echocardiography — standard adult study

Transthoracic echocardiography

What we'd amend, and why

Heart failure is a syndrome, and the echocardiogram is what turns it into a diagnosis with a treatment attached. It measures the ejection fraction, which is what splits the syndrome into the group with a large evidence base for disease-modifying therapy and the group without; and it gives the mechanism, which is the part that actually changes what happens next — a dilated poorly contracting ventricle, a thick non-compliant one, severe aortic stenosis, a regurgitant mitral valve, a pericardial constriction, right heart failure from pulmonary hypertension. NICE NG106 routes directly here on the natriuretic peptide, and the sequencing is deliberate: the blood test decides who needs imaging, and the imaging then decides what kind of heart failure it is. It takes twenty minutes, uses no ionising radiation and no intravenous contrast, and needs no renal function and no device screening, which is why nothing else on this card competes with it for the first-line position. Its two real limitations are worth stating in the report rather than working around: a poor acoustic window is a genuine result that should trigger a different modality rather than a repeat, and a normal ejection fraction does not exclude heart failure — the preserved-ejection-fraction phenotype requires diastolic indices, left atrial volume and the tricuspid regurgitant velocity to be looked at deliberately.

Nothing needs resolving before this goes ahead. Routine checks below are owned downstream.

How was this decided?

pathwayadult — Adults — suspected chronic heart failure

Decision support only. Local protocol takes precedence.

Worth asking the referrer (3)

None of these hold the request up. They sharpen the protocol or the plan that follows.

What is the NT-proBNP or BNP, in what units, and when was it taken?
It decides both whether echocardiography is indicated and how urgently it should be booked. It is the routing variable for the whole pathway.
Is there a reason to expect a poor acoustic window — obesity, severe airflow obstruction, mechanical ventilation, chest wall deformity or previous thoracic surgery?
It is the commonest legitimate reason for the pathway to hand over from echocardiography to cardiac MRI, and knowing it in advance avoids a wasted appointment.
Has an echocardiogram already been done, and what did it show?
A cardiac MRI request is answerable only against the echocardiographic findings — the MRI is being asked to resolve a specific discrepancy or characterise a specific abnormality.

Pathways

Big forks are separate pathways; the first whose conditions match is the one used.

Acute presentation — suspected acute heart failure

Role	Study & protocol	Why this answers the question
First line	Chest radiograph Chest radiograph — PA (± lateral) usually appropriate	In the acutely breathless patient the radiograph is genuinely first, and for a reason that has nothing to do with diagnosing heart failure: it is the study that can be done in minutes at the bedside and that separates the diagnoses that need opposite treatment. Pneumothorax, lobar consolidation, a large effusion and a lung mass all present as acute breathlessness and all change management immediately, and giving furosemide to a patient with pneumonia is a real harm. What the film adds to the heart failure question itself is congestion — upper lobe blood diversion, septal lines, perihilar alveolar shadowing, effusions — which is useful when present. It is far less useful when absent, and that asymmetry is the whole reason this step is framed as an alternative-diagnosis test rather than as a rule-out.
First line	Transthoracic echocardiography Transthoracic echocardiography — standard adult study usually appropriate	The radiograph and the echocardiogram are both first-line here because they are not competing for the same slot: the film is taken on arrival and the echocardiogram is expected early in the admission — NICE recommends transthoracic Doppler echocardiography within 48 hours in a patient presenting with new suspected acute heart failure. The echocardiogram is what makes the diagnosis and, more importantly in the acute setting, what identifies the mechanism that dictates immediate treatment: severe aortic stenosis, acute mitral regurgitation from a ruptured chord, a large pericardial effusion with tamponade physiology, a right ventricle acutely under strain. Those are different emergencies with different answers, and none of them is distinguishable on the radiograph.

Nothing in this fork defers the echocardiogram — it sequences the radiograph ahead of it in time, not instead of it. A patient who is admitted with new suspected acute heart failure and discharged without an echocardiogram has not completed the pathway.
A portable AP film in a semi-recumbent patient exaggerates the cardiothoracic ratio, redistributes the pulmonary vessels by gravity alone and hides small effusions. The projection must be stated, and cardiomegaly should not be called from it.
Where the patient is too unwell for a formal study, focused bedside echocardiography by the treating team answers the immediate questions — effusion, gross ventricular function, inferior vena cava filling — and is a legitimate bridge, not a substitute for a full study later.

Adults — suspected chronic heart failure

Matches your inputsDefault

Role	Study & protocol	Why this answers the question
First line	Transthoracic echocardiography Transthoracic echocardiography — standard adult study usually appropriate	Heart failure is a syndrome, and the echocardiogram is what turns it into a diagnosis with a treatment attached. It measures the ejection fraction, which is what splits the syndrome into the group with a large evidence base for disease-modifying therapy and the group without; and it gives the mechanism, which is the part that actually changes what happens next — a dilated poorly contracting ventricle, a thick non-compliant one, severe aortic stenosis, a regurgitant mitral valve, a pericardial constriction, right heart failure from pulmonary hypertension. NICE NG106 routes directly here on the natriuretic peptide, and the sequencing is deliberate: the blood test decides who needs imaging, and the imaging then decides what kind of heart failure it is. It takes twenty minutes, uses no ionising radiation and no intravenous contrast, and needs no renal function and no device screening, which is why nothing else on this card competes with it for the first-line position. Its two real limitations are worth stating in the report rather than working around: a poor acoustic window is a genuine result that should trigger a different modality rather than a repeat, and a normal ejection fraction does not exclude heart failure — the preserved-ejection-fraction phenotype requires diastolic indices, left atrial volume and the tricuspid regurgitant velocity to be looked at deliberately.
Second line	Cardiac MRI Cardiac MRI — function and late gadolinium enhancement usually appropriate	Cardiac MRI enters this pathway for two distinct reasons, and a good request says which. The first is measurement: ventricular volumes and ejection fraction come from direct planimetry of a short-axis cine stack with no geometric assumption, so where the echocardiographic window is poor, or where the echocardiographic ejection fraction is discordant with the clinical picture, or where a device decision turns on which side of a threshold the number falls, MRI is the reference method. The second is aetiology, which is the larger contribution: gadolinium is an extracellular agent, so it accumulates wherever interstitial space has expanded and washes out of it slowly, and late imaging with the inversion time set to null normal myocardium turns that into a map of abnormal muscle. The distribution is what names the disease — subendocardial or transmural enhancement in a coronary territory means infarction, mid-wall enhancement suggests a non-ischaemic process, a global subendocardial pattern with abnormal gadolinium kinetics suggests amyloid — and mapping and extracellular volume extend that to diffuse disease that has no focal scar at all. What MRI is not is a first test for breathlessness: booked before the echocardiogram, it usually restates it at many times the cost and with a device screen, a cannula and a breath-hold requirement attached.
Problem solving	Chest radiograph Chest radiograph — PA (± lateral)	The radiograph belongs on this card, but not on the diagnostic ladder, and the honest description of it is a study that answers a neighbouring question. It detects pulmonary congestion and pleural effusions, and it is very good at producing the alternative diagnosis — pneumonia, a mass, a pneumothorax, hyperinflation pointing at airways disease — which in a breathless outpatient is a real contribution. What it cannot do is diagnose or exclude heart failure. A substantial minority of patients admitted with decompensated heart failure have no radiographic congestion at all, particularly in chronic disease where lymphatic drainage has adapted, so a clear film in a breathless patient with a raised natriuretic peptide changes nothing. Cardiomegaly is neither sensitive nor specific, and on an AP or supine film the cardiothoracic ratio is not interpretable at all. Requested as a companion to the echocardiogram it is useful; requested instead of it, it is the commonest way this pathway goes wrong.

The order on this pathway is not a ranking of quality — it is a ranking of what answers the question asked. The radiograph is listed last because it does not diagnose heart failure, not because it is unhelpful; in an undifferentiated breathless patient it may well be the first film taken.
Where the echocardiogram shows unexplained ventricular impairment or hypertrophy, the question has moved on and the cardiomyopathy card carries the tissue-characterisation pathway, including the coronary assessment that new ventricular impairment needs before it can be called a cardiomyopathy.
Rate and rhythm decide whether a cardiac MRI will be diagnostic. Uncontrolled atrial fibrillation degrades the cines and the enhancement imaging the study depends on, and is worth addressing before the appointment rather than at it.

Pitfalls

Treating the chest radiograph as a rule-out. A meaningful proportion of patients admitted with decompensated heart failure have no radiographic congestion, so a clear film in a breathless patient with a raised natriuretic peptide excludes nothing.
Calling cardiomegaly from an AP or supine film. Magnification and projection make the cardiothoracic ratio uninterpretable, and the projection has to be stated for the film to be read at all.
Booking cardiac MRI as the first cardiac imaging test, or without saying what the echocardiogram showed. The MRI is asked to resolve a specific problem that the echocardiogram defines.
Reading a normal ejection fraction as excluding heart failure. Preserved-ejection-fraction disease is roughly half of all heart failure, and it is diagnosed from diastolic indices, left atrial volume and the tricuspid regurgitant velocity — which have to be asked for.
Accepting a raised natriuretic peptide at face value in atrial fibrillation, advanced age or renal impairment, all of which raise it independently; and dismissing heart failure in an obese patient whose natriuretic peptide is falsely low.
Requesting a CT chest "to look at the heart". A non-gated acquisition cannot measure ventricular function, its chambers are motion-blurred, and it will not answer the question at a dose and contrast cost the echocardiogram does not impose at all.
Comparing an echocardiographic ejection fraction with an MRI one across time. The two methods systematically differ, and a device decision taken at a threshold should rest on one method used consistently.
Stopping at the diagnosis. A new impaired ventricle needs the reason established — ischaemia, valve disease, infiltration, alcohol, chemotherapy, tachycardia-mediated — because several of those have specific treatments and one of them is reversible by rate control alone.
Missing high-output failure. Severe anaemia, thyrotoxicosis and a large arteriovenous fistula all produce congestion with a normal or hyperdynamic ventricle, and the echocardiogram report will not volunteer the cause unless the request asks.

Priors — what to pull first

Find the previous echocardiogram before booking anything. A known ejection fraction with a date turns "suspected heart failure" into a question about change, which is a different and usually easier question.
Compare the current radiograph with an old one taken when the patient was well — the heart size that matters is the one that has changed, and a single film cannot show that.
Where a cardiac MRI is requested, retrieve the device card and any prior imaging of the same device: artefact seen once is artefact that will be seen again.

What makes a good request

NICE NG106 sets the sequence and the urgency: an NT-proBNP above roughly 2000 ng/L earns specialist assessment and transthoracic echocardiography within two weeks, a level between roughly 400 and 2000 ng/L within six weeks, and a level below about 400 ng/L makes untreated heart failure unlikely. Confirm the local thresholds and units, because BNP and NT-proBNP assays are not interchangeable and neither are their cut-offs.
The natriuretic peptide is not a clean signal. Age, atrial fibrillation, renal impairment, pulmonary hypertension and sepsis all raise it independently, so a raised value in an 85-year-old in atrial fibrillation is much weaker evidence than the same value in a 50-year-old in sinus rhythm. Obesity lowers it, so a normal result in a markedly obese breathless patient does not exclude the diagnosis. Sacubitril-valsartan raises BNP but not NT-proBNP.
A good request states the natriuretic peptide with its units and date, the rhythm and rate, the body habitus or any reason to expect a poor acoustic window, and — where cardiac MRI is being asked for — what the echocardiogram already showed.
Where the request is for cardiac MRI as the first cardiac imaging test, the answer is nearly always the echocardiogram. MRI on this pathway is a problem-solving study for a problem the echocardiogram has to define first.
Once heart failure is confirmed, the question stops being "is this heart failure" and becomes "why", and that is the cardiomyopathy pathway — ischaemic assessment, tissue characterisation, infiltrative disease.

Scoring this once it is done

The classification and risk tools this question ends in.

eGFR (CKD-EPI 2021 Creatinine)

How these studies are acquired

Contrast, phases and timing for every study on the pathways above.

Chest radiograph — PA (± lateral)Transthoracic echocardiography — standard adult study Cardiac MRI — function and late gadolinium enhancement

Confirm locally

Transthoracic echocardiography — standard adult study: timings are typical — confirm against local protocol.
Timings, contrast volumes and rates above are typical published values. Your department's protocol, scanner and patient population decide the actual numbers.
Safety thresholds and premedication policy follow local policy where it differs from the cited guidance.

References

Implemented from the cited published sources. Educational and workflow support only; confirm against current guidelines and local policy before clinical use.