Heart Failure is not a diagnosis in itself, rather a collection of symptoms which require investigation to find the underlying cause.

Heart failure syndrome is the term used to describe the collection of symptoms such as; breathlessness and fatigue, and signs such as fluid retention.

As an FY1 you will likely encounter patients with heart failure across all wards/specialties. You may also be involved in medical take/A+E where you will clerk these patients in.

NB: Acute pulmonary oedema is covered elsewhere & will not be covered in detail here

Causes
Primary (cardiac):
ACS, valve disease, arrhythmia, cardiomyopathy, pericardial disease, diastolic dysfunction, pulmonary HTN

Secondary:
COPD, sepsis, anaemia, hypertension, renal failure, endocrine (e.g. thyroid), nutritional deficiencies (including alcohol), hypoventilatory syndromes (obesity, OSA, neuromuscular)

Clerking a patient with suspected Heart Failure:
Following an ABCDE assessment:

History:
  • shortness of breath (rest/exertion)
  • orthopnoea (pillows at night)
  • paroxysmal nocturnal dyspnoea (wake up gasping for air)
  • fatigue/reduced exercise tolerance
  • Associated history of causes above (including medication non-concordance)
Examination
  • Oedema (pedal - extent e.g. up to calf, sacral)
  • Elevated JVP (see tips)
  • Pleural effusion (reduced air entry, dull to percussion)
  • hepatomegaly/ascites
  • murmurs - Gallop rhythm (s3/4 due to ventricular overload), AS/valvular (causal)
  • NB – Can also be useful to document if Cold/Warm (peripheral) and Wet/Dry (congested) - simple extension of the examination can help stratify patient prognosis, of which cold and wet is least favourable.
Assessing JVP
  • Most important part of clinical examination in heart failure, as this is an indirect observation of right atrial pressure. (Correlating with fluid status/overload status).
  • Method to assess; Patient 45 degrees, tilt head slightly to one side (usually LHS) without causing too much contraction of sternocleidomastoid as this will obscure JVP, observe for double pulsation of JVP (palpate if unsure arterial). Then measure height of JVP horizontally and cross with the measurement up vertically from angle of Louis. Add 5cm (RA is 5cm below sternal angle). Normal is 6-8cm. Use good lighting, hepatojugular reflux can help make it more visible.
  • In practice measuring as above is not often performed and shortcuts such as assessing the JVP as being raised to angle of jaw and up to the ear are used as reference points of overload.
Investigations

Bloods:
  • FBC – (anaemia), LFT (hypo-albuminemia), U+E (renal function for diuresis, cardiorenal syndrome)
  • BNP
    • HF considered unlikely if 
      • BNP less than 100 ng/litre
      • NT‑proBNP less than 300 ng/litre
  • TFTs (causal - can be missed)
  • Trop I (if clinical suspicion of ACS as causal)
  • ABG if acute pulmonary oedema/hypoxia (serial alongside interventions)
Imaging & others:
  • ECG (for arrhythmias and ACS)
  • CXR – DDx (exclude other causes of SOB) & confirm features of heart failure
    • A Alveolar Oedema (bat wings hilar region) 
    • B Kerley B lines (horizonal lines peripheries)
    • C Cardiomegaly
    • D Dilated Pulmonary Vessels (Upper lobe diversion)
    • E Pleural Effusion (typical is Bilateral).
  • Echocardiogram - (Cardiomyopathy, Valves, Ejection Fraction)
Initial treatment
  • Sitting position
  • Oxygen if hypoxic (be careful in those at risk of type 2 respiratory failure)
  • Diuresis to offload – Usually IV furosemide is preferred
    • If diuretic naive consider stat 40mg IV initial and re-assess
    • If already on diuretic, use up to 2x usual dose in this instance (be careful they may already have had their usual diuretics)
    • Furosemide can be given in AM/Noon BD dosing or via 24hr infusion - max 240mg/24hr for both methods
    • Consider their mobility & ability to pass urine with a consideration of a catheter if need be. In the US furosemide is called Lasix because it lasts 6h. Giving it late can lead to inpatient falls (or an annoyed patient). 
NB – furosemide 40mg PO equivalent to 1mg bumetanide PO.

When to escalate
  • Acute pulmonary oedema (wheeze, frothy sputum, clammy)
  • Cardiogenic shock (peripherally shutdown, hypotensive)
  • ACS (chest pain, significant raised troponin, ischaemic ecg changes)
  • Syncope
  • Arrythmia (not corrected with initial measures)
  • Unable to tolerate diuresis due to hypotension/renal function
Management on the wards:
  • Daily clinical assessment of fluid status – (as above for examination, JVP)
  • Daily weight (aim 0.5kg/day loss) - essential to guide diuresis success.
  • Daily U+E whilst on IV diuretic (monitor eGFR and serum potassium, sandoK commonly prescribed)
  • Fluid restriction – (1.5ltr usual restriction)
  • Echo - To assess if LV systolic dysfunction (reduced EF)/Not LVSD (preserved EF)
  • Converting to oral diuretics
    • Usually when stable, showing good diuresis progress, usually to same dose (e.g. 80mg IV BD to 80mg PO BD).
    • IV furosemide is up to 50% more potent than oral due to bioavailability (even less when overloaded). However, the dose is usually kept the same as after the initial diuresis they usually need less for maintenance. Be careful though of rebound pulmonary oedema after you switch.
When monitoring U&Es expect a small rise in Creatinine/drop in eGFR. Diuresis often needs to continue & the renal function may improve if renovascular congestion is present. Discuss worsening renal function with seniors and be very wary of IV fluids in a stable patient which could cause them harm of worsening overload.

If they are not achieving 0.5kg loss per day & renal function allows, discuss with seniors the possibility of one off thiazide doses e.g. metolazone

Further options include dobutamine, but this is highly specialist & requires a cardiac monitor and CCU.

Medication optimisation:
  • If LVSD/reduced EF – commence on: ACEi/arb, beta blockers once euvolaemic only (as negatively inotropic and can worsen acute HF), aldosterone agonist (e.g. spironalactone)
  • If not LVSD/preserved EF – diuresis and comorbidity management is mainstay (no evidence that medications above benefit in HF-pEF sub-group)
  • Continue diuresis until JVP normalises, they able to manage at home and on oral regimen
  • Manage their comorbidities: BP control, angina, renal function, AF rate control (digoxin usually preferable), diabetes, OSA, anaemia, BMI and if cor pulmonale - optimise O2
Follow up/information for discharge letters:
  • Cardiac rehabilitation
  • Community Heart Failure Team
  • Instructions for GP – usually asked to up titrate HF medications to tolerated BP. Also usually asked to repeat UEs (as patients have been on IV diuretic or new ACE etc).
  • Patients weight should be included on discharge
  • Lifestyle: reduce salt, avoid excess fluid, smoking cessation
To be aware
  • Heart Failure is not a diagnosis. A patient may present with symptoms of heart failure syndrome.
    • An example diagnosis on discharge may be: Heart Failure with Reduced Ejection Fraction secondary to hypertensive heart disease
  • In your clerking assessment look for signs and symptoms of Heart Failure Syndrome and aim also to look for a potential underlying cause.
  • Gain practice assessing JVP, observing seniors to become confident at assessing fluid status.
  • When using diuretics small drop in eGFR/rise in Cr can be expected, in this case continue. If continued/significant drop - use clinical assessment of fluid status to guide continuation and discuss with a senior.
  • Aim for >0.5kg weight loss per day.
  • Avoid beta blockers in initial presentation/during acute decompensation as they are negatively inotropic and can worsen situation if used at this point. Introduce when euvolemic.
  • Heart failure with reduced EF needs treatment like any other condition, commence on medications as above to maximum tolerated alongside diuresis to improve patient outcome.
References & Further Reading
Written by Dean Manning FY3