Acute or worsening heart failure is a common reason for hospitalization which carries a high mortality. Prompt diagnosis or exclusion of HF and its cause and precipitating factors can improve the quality and efficiency of care, shorten hospital stay, reduce readmission and improve prognosis. While the clinician remains central to reaching a clinical diagnosis of heart failure, the use of traditional and novel diagnostic technologies will improve the specificity and sensitivity of the diagnosis of heart failure diagnosis and provide insights into its pathophysiogical profile and help tailor therapy to individual patient need. Chest X-rays and electrocardiograms are generally available; echocardiograms less so. Novel technologies include both invasive and non-invasive methods to detect increases in intrathoracic fluid, pulmonary congestion, left ventricular filling pressures, cardiac output and vascular function. However, few of these technologies have been subjected to randomised controlled trials investigating their ability to improve patient management.
Heart failure (HF) is common and as longevity increases its incidence and prevalence will rise [
Surprisingly, the epidemiological data on the precise presentation of acute heart failure is remarkably difficult to come by. Most authorities assume that breathlessness is the main presenting symptom and that most patients are acutely distressed by it at rest. Recent data from a National Audit of England & Wales has called this assumption into question. Many patients present with worsening exertional breathlessness and peripheral oedema but are comfortable at rest [3,7] Also, recent reports suggest that many patients have worsening symptoms and evidence of congestion for several days prior to presentation suggesting that technologies, such as home telemonitoring, might be deployed for early detection and that redesign of services might prevent a large proportion of admissions [8-10].
There is often also a great initial uncertainty about whether HF is the cause of symptoms. Many patients are treated with diuretics without the clinician making a conscious diagnosis of HF, leading to deficiencies in investigation and treatment. Unfortunately, such patients, who may be far more common than those labelled as CHF, will not be picked up by most audits of heart failure [
Early assessment and prompt diagnosis or exclusion of HF will improve the quality and efficiency of care, shorten hospital stay, reduce readmission and improve prognosis [
Patients with breathlessness or oedema or those treated with loop diuretics for uncertain cause should be assessed to identify a) Whether they have heart failure and whether it is the cause of their symptoms and signs;
b) Other medical conditions (e.g.: atrial fibrillation, acute coronary syndrome, infection, anaemia or chronic kidney disease) that should be considered as a differential diagnosis, exacerbating factors or co-morbidity;
c) Their dominant acute problem (breathlessness or peripheral oedema);
d) Their cardiac phenotype (e.g.: left ventricular ejection fraction, valve disease) that will determine what treatment they should receive;
e) Their heart rate and rhythm and blood pressure that will also guide treatment.
Patients with the acute onset of severe dyspnoea often present in the early morning hours. In many healthcare systems, this is when the most junior and least experienced staff will be available. Although experts may be able to manage patients without the reassurance of technical support, less experienced staff may welcome investigations that provide them with the confidence they might otherwise lack. However, experienced staff also need to critically review their practice. The outcome of acute heart failure both in hospital and after discharge is often poor and this may be due, in part, to the persistence of outmoded concepts and practice in the care of these patients.
Exacerbations of heart failure cover a wide spectrum of presentations with two distinctly different clinical phenotypes as shown in
reasons. These patients generally have neither a raised venous pressure nor peripheral oedema. Their problem is fluid in the wrong place (the lungs). Other relatively specific symptoms of heart failure are orthopnoea, and paroxysmal nocturnal dyspnoea. There are many other nonspecific features that may be due to heart failure, such as fatigue, disturbed sleep pattern, skeletal muscle wasting and depression, but these are generally unhelpful for its diagnosis.
Examination of the lungs may reveal fine crepitations indicating pulmonary oedema. Crepitations are not an accurate guide to left ventricular filling pressure in patients with chronic heart failure, but may be clinically useful in the setting of acute heart failure for instance after a myocardial infarction. The Killip classification is a powerful prognostic tool in this clinical setting [
A third heart sound may be normal in young people but indicates left ventricular dysfunction in people aged > 40 years. The pulmonary component of the second heart sound (P2) will be increased in pulmonary hypertension, which may be secondary to left atrial hypertension. However, detection of these signs by auscultation has poor inter-observer reproducibility and is usually only obvious in patients with severe decompensation who are in sinus rhythm. Jugular venous pressure is one of the most specific signs of heart failure but often difficult to elicit, especially in a patient who is acutely breathless and using their accessory muscles of respiration. It reflects right atrial pressure and therefore will only be increased if there is a problem on the right side of the heart, which is a late manifestation of left sided heart disease [
The initial investigations performed in the acute setting are useful to assist in diagnosis, to identify precipitating factors and for risk stratification and triage for escalation to a high-dependency unit or transfer to a general ward or to an observation unit and same-day discharge (
optimal. For instance, respiratory rate is probably the best method by which to quantify dyspnoea and yet it is often overlooked. Many authorities would consider it medical negligence not to order a chest X-ray for a patient with severe breathlessness to exclude pulmonary disease. Taking arterial gases is often painful for patients and entirely unnecessary. Trancutaneous oxygen saturations combined with venous gases provide all the necessary information. On the other hand, internationally, rather few acute medical receiving units have echocardiography available 24 hours a day, seven days per week.
Natriuretic peptides can be considered cardiac stress hormones. Increases in natriuretic peptides are non-specific with respect to the nature of the stress but when normal are reassuring that the patient’s cardiovascular system is not under great threat and when elevated that the patient has a problem requiring clarification. In the acute setting, measurement of natriuretic peptides may improve diagnostic accuracy by ruling out heart failure (NT-proBNP < 300 ng/L or BNP <100 ng/L) or by increasing the certainty of a clinical diagnosis (NT-proBNP > 2000 ng/L or BNP >500 ng/L). However, accurate interpretation requires experience and many patients will have a value in the diagnostic grey-zone [19,20]. The two main reasons for a substantial elevation in natriuretic peptides other than ventricular dysfunction are atrial fibrillation and renal dysfunction with sex (women have higher levels) and body mass index (fat people have lower levels) having a modest effect. Older people have higher levels but this reflects the decline in renal function and diastolic left ventricular function that occur with age. Older people have higher natriuretic peptides and a worse prognosis because their cardiac and renal function is worse. It is inappropriate to correct natriuretic peptides for age [
Whether natriuretic peptides can be used to guide therapy in the setting of acute or chronic heart failure remains controversial [24,25].
In the BACH study, MR-proANP (>120 pmol/ml) was not inferior to BNP (>100 pg/ml) for identifying patients with heart failure and MR-pro ADM was superior to BNP and NT-proBNP for predicting 90-day mortality [
Most patients with heart failure will have coronary artery disease as a cause or co-morbidity of heart failure and acute coronary syndromes (ACS) may often be a precipitating factor for exacerbations [
Clinical guidelines recommend early echocardiography in acutely dyspnoeic patients who are suspected of having heart failure. This is a mostly unrealised ideal situation that rarely happens in clinical practice. Indeed, international research protocols in AHF have learnt to avoid requiring an immediate echocardiogram because that would preclude getting substantial numbers of patients into studies. There are too few adequately trained staff and little access to equipment to provide 24 hour cover seven days per week in most hospitals where these patients are seen (i.e. not University teaching hospitals!).
Ideally, prompt echocardiography should be part of the diagnostic work-up of all patients with suspected heart failure in the emergency setting, especially if a structural cause is suspected that might be amenable to intervention (e.g.: aortic stenosis, ruptured mitral chordae). Echocardiography will identify patients with heart failure and a reduced ejection fraction (HF-REF), although the severity of ventricular dysfunction is prone to substantial observer error. Ultrasound may also be used to assess lung oedema [36,37]. However, echocardiography is a highly inaccurate method of diagnosing heart failure with a preserved left ventricular ejection (HF-PEF) with the single most helpful echocardiographic measure being the left atrial volume or size. Natriuretic peptides are commonly grossly elevated in patients with HF-PEF and a fairly unremarkable looking echocardiogram. These patients respond symptomatically to treatment for heart failure and have a poor prognosis; so who are they if not patients with heart failure? Beware the false-negative echocardiogram in heart failure! Doppler echocardiography is complex to interpret, subject to many measurement errors and has failed the multi-centre clinical study test on many occasions. Regional wall motion abnormalities or thinning may indicate myocardial ischaemia or infarction but is usually unable to distinguish between acute and chronic ventricular dysfunction. Echocardiography is very useful for diagnosing valve problems and assessing RV function (tricuspid annular plane systolic excursion or TAPSE), pulmonary artery systolic pressure, inferior vena cava dilatation (indicating increased right atrial pressure), pericardial effusion and, with less confidence, constrictive pericarditis.
From Ohms law, “when an electrical current is passed through human tissue, the voltage difference between two points on the body is proportional to impedance” [
Bio-impedance can be measured using external electrodes placed on wrists and ankles rather like a standard ECG or by electrode configurations that seek to measure thoracic impedance only (
Using an implanted system, the MIDHeFT study reported that impedance monitoring could detect volume overload and predict the risk of hospitalisation with some success in a small single centre experience [
monitoring was more sensitive than weight gain in predicting future heart failure events (76% vs 23%) [
There are too few data on the use of non-invasive bioimpedance to evaluate its diagnostic utility in the emergency setting or its usefulness for subsequent monitoring during the recovery phase. [
This technology uses either a wearable patch or implantable device that emits low-power electromagnetic signals into the chest [50,51]. Tissues reflect the signal according to their fluid content and this can be used to measure lung water. This might be used to predict deterioration or monitor resolution of lung oedema to identify the patient’s optimal “dry” weight and timing of discharge.
Pulse wave reflections can affect LV afterload and coronary perfusion [
Although the third heart sound (S3) may be specific for increased left ventricle filling pressure in adults and can
predict outcome, it is often clinically difficult to detect in acute settings due to ambient noise, body habitues and tachypnoea. Expertise in auscultation will also vary greatly. Modern technological innovations now make it possible to capture information about S3 at the same time as the ECG recording (
FPP can be used to measure the blood pressure (and heart rate) continuously, beat-to-beat (
and new vasodilator agents that may cause profound hypotension [
This was the classic instrument for assessing and monitoring heart failure in the latter part of the 20th Century. Many people doubted its utility. A large randomized trial demonstrated no advantage to direct measurement of pressures with treatment tailored to haemodynamic targets [
In acute HF, current US guidelines recommend urgent cardiac catheterization and attempt to revascularization when prolonged meaningful survival is expected in patients with known or suspected myocardial ischaemia, especially when there are clinical features of hypoperfusion [
The management of AHFS is often poor and this may explain, in part, its dire prognosis. Despite of limitations, clinical evaluation remains the primary tool for initial assessment and monitoring the response to therapy. A single measurement of plasma concentrations of a natriuretic peptide provides reassurance that a clinical diagnosis of AHFS is correct; normal concentrations alert the clinician to rare diagnoses, such as constrictive pericarditis, or alternative diagnoses mimicking heart failure. However, natriuretic peptides are not diagnostic when used alone, nor has it been established that serial measurement of natriuretic peptides adds value to clinical monitoring. Further studies are required to assess the practical clinical value of applying novel technologies to the management of AHF to monitor the response to treatment, discharge readiness and the risk of readmission. However, monitoring will not help patients unless it changes management. Ultimately, novel technologies need to show that they change decisions about care made by clinicians and/or patients, leading to more favourable outcomes including better symptom control, less disability and a longer life. If, as a by-product, they can also reduce the frequency or shorten the duration of hospitalisation, a surrogate measure of patient well-being and health-service costs, then so much the better.