Background
Definition and epidemiology
- Heart fails to provide adequate blood flow to meet body's needs.
- Chronic disease with intermittent decompensations (acute HF), and eventually terminal.
- The term 'congestive heart failure' is ill-defined, but typically refers to HF with fluid overload, especially pulmonary oedema.
- Prevalence: 1/70.
Left ventricular failure (LVF)
Heart failure with reduced ejection fraction (HFrEF)
Overview:
- Left ventricular ejection fraction (EF) <40%. A normal EF is ≥50%, with 40-49% a 'mid-range' grey area.
- Also known as systolic heart failure or left ventricular systolic dysfunction (LVSD).
Causes:
- IHD/MI: commonest cause.
- HTN
- Diabetes, usually via IHD.
- Dilated cardiomyopathy.
- Valve disease.
- Arrhythmias
- Drugs or alcohol.
Heart failure with preserved ejection fraction (HFpEF)
Overview:
- LV relaxation failure → inadequate filling → ↓stroke volume despite normal EF (≥50%).
- Also known as diastolic heart failure.
Causes:
- HTN: commonest cause.
- Diabetes
- Constrictive pericarditis.
- Cardiac tamponade.
- Restrictive cardiomyopathy
Right-ventricular failure (RVF)
- Cor pulmonale: primary lung disease (e.g. COPD) → vasoconstriction in poorly ventilated lung tissue to correct ↓V/Q → pulmonary HTN → RVF.
- LVF → pulmonary HTN → RVF.
- Pulmonary valve stenosis (uncommon).
High output heart failure
- Anaemia
- Pregnancy
- Hyperthyroidism
Signs and symptoms
LVF
- SOB
- Orthopnea. Ask how many pillows they sleep with.
- Paroxysmal nocturnal dyspnoea (PND) and nocturnal cough.
- Pink frothy sputum.
- Wheeze
Other symptoms:
- Palpitations
- Poor exercise tolerance.
- Fatigue
- ↓Weight (cachexia) or ↑weight (fluid retention).
Signs:
- Crackles
- S3 heart sound ('gallop rhythm'). S4 is commoner in diastolic HF.
- Murmurs
- Cachexia
- Cold peripheries.
- Displaced apex.
- Pulsus Alternans: Arterial Amplitude strong then weak.
RVF
- Liver congestion leads to nausea, anorexia, early satiety, and right upper quadrant pain.
- Epistaxis
- Nocturia: on lying flat, fluid backs up from legs to kidneys.
Signs:
- ↑JVP
- Peripheral oedema
- Ascites
- Hepatomegaly
- Right ventricular heave due to pulmonary HTN.
NYHA functional classes
- No symptoms.
- Slight limitation, mild symptoms.
- Marked limitation, symptoms with minor activity.
- Severe limitation, symptoms at rest.
Investigations
Basic investigations
- FBC: anaemia may mimic or exacerbate symptoms.
- U+E and LFTs: liver and kidney function can be affected in HF, and are a differential for fluid retention.
- TFT: thyrotoxicosis can cause high output failure, while hypothyroidism may cause symptoms of fatigue and oedema.
- Investigate cardiac RFs: cholesterol, blood glucose.
CXR:
- May show cardiomegaly and pulmonary oedema.
ECG:
- Abnormal in 80%.
- Usually non-specific changes: previous MI or AF (common), or axis deviation (less common). Only 20% have the specific features listed in the following points.
- LVF: Voltage criteria are met if the combined height of {S in V1} + {R in V5 or V6} is at least 35 mm (7 large squares). LV strain pattern is ST depression and T inversion in V5-6; less commonly, there is the mirror image ST elevation in V1-3.
- RVF: Tall R in V1 (>7 small squares or R>S in V1), and large S waves in V4-6. RV strain pattern is ST depression or T inversion in V1-3.
Diagnosis
- Screen with BNP or NT-proBNP, and proceed to transthoracic echo if elevated. Consider going straight to echo if there is a prior history of MI.
- If diagnosis not clear after echo, consider further tests: cardiac MRI, transoesophageal echocardiography.
- HFrEF diagnosis: {signs and symptoms of HF} plus {echo or MRI evidence of EF <40%}.
- HFpEF diagnosis: {signs and symptoms of HF} plus {EF ≥50%} plus {↑BNP/NT-proBNP} plus {structural or functional heart disease such as left ventricular hypertrophy or left atrial enlargement}.
- HFmrEF (HF with mid-range EF): as for HFpEF but EF 40-49%.
B-type natriuretic peptide (BNP):
- Pro-BNP is synthesised in the ventricular wall when it is stressed. Then circulates as BNP and N-terminal Pro-BNP – either of which can be used to help diagnose HF – and serves to lower peripheral resistance.
- Levels can be increased by: IHD, AF, PE, kidney failure, cirrhosis, and sepsis. Levels also naturally rise with age, so a high reading under 60 is more concerning than in someone very elderly.
- Levels can be lowered by cardiac meds (ACEi, ARBs, β-blockers, spironolactone) and obesity.
- ↑↑BNP is a poor prognostic factor, although ongoing BNP monitoring to guide treatment does not appear to be useful.
Management
Overview
- Can be mostly managed in primary care, but specialist referral is needed for initial diagnosis, NYHA class 4 HF, treatment-resistant HF, or HF associated with pregnancy or valve disease.
- Specialist nurses should be involved if available.
- Follow-up at least every 6 months, including U+E and weighing.
Lifestyle and preventative measures
- Refer all stable patients to cardiac rehab.
- Stop smoking.
- Flu and pneumococcal vaccination.
- Monitor weight and fluid balance, advising moderate fluid restriction. Get help if rapid gain e.g. 2 kg in 3 days. Evidence for salt restriction is limited, and some studies say it may be harmful.
- Treat co-morbidities such as IHD, AF, and dyslipidaemia.
HFrEF
Pharmacalogical
Most patients are on four agents, all of which except diuretics have a mortality benefit:
- ACEi – any one (though enalapril has most evidence) – should be offered to all, and titrated to evidence-based dose. ARB if intolerant.
- β-blockers – bisoprolol, metoprolol, or carvedilol – should also be offered to all, and titrated to evidence-based dose.
- Diuretics – loop (furosemide, bumetanide) or thiazides – if there is fluid overload (pulmonary or peripheral oedema), which is usually the case.
- Mineralocorticoid receptor antagonists (MRA) – spironolactone or eplerenone – should be added if patient remains symptomatic. Given to block effects of aldosterone on heart as opposed to diuretic effect.
Further options if symptoms persist:
- Digoxin, especially if there is AF. Reduces admissions but not mortality.
- Sacubitril-valsartan (Entrestro) combines a neprilysin inhibitor – which prevents breakdown of vasodilators – and ARB (hence replaces existing ACEi or ARB). Consider if EF ≤35%. Reduces admissions and mortality.
- Ivabradine inhibits the sinus node If ('funny') channel – the mixed Na+ and K+ channel whose opening initiates depolarization – slowing the heart. Consider if EF ≤35% and sinus rhythm with HR ≥75.
- Hydralazine plus nitrate, especially if African or Caribbean ethnicity.
Interventional and surgical
- Cardiac resynchronisation therapy (CRT) (aka biventricular pacing) if {NYHA 2-4 with EF ≤35%} and {QRS ≥150 ms or LBBB}.
- Implantable cardioverter defibrillator (ICD) if there is a history of VF or VT, or a high risk of it. Can be combined with CRT in CRT-D.
- LV assist devices (LVAD) as a bridge towards transplant.
- Transplant if end-stage and no other options.
Drug contraindications in HF
- NSAIDs, especially diclofenac. Low-dose aspirin is OK.
- Steroids
- Most CCBs, especially rate-limiting.
- Pioglitazone
- TCAs
- β-agonists.
RVF and HFpEF
- There is little evidence-based treatment for RVF or HFpEF, except for symptomatic relief with diuretics, management of co-morbidities, and lifestyle changes.
- Long term O2 therapy is beneficial in cor pulmonale.
Prognosis
- Usually due to arrhythmia or pump failure.
- 30% in 1 year, 50% in 5 years.
Acute pulmonary oedema
Causes
Cardiogenic pulmonary oedema
Aka acute heart failure.
- Decompensated HF or cardiomyopathy.
- Hypertension
- MI: flash pulmonary oedema (acute), ventricular septal rupture (days later).
- Valve disease: AR, AS, MR, infective endocarditis.
- Arrhythmias
- Kidney failure.
- Others: myocarditis, aortic dissection, hypothyroidism, high-output failure (anaemia, hyperthyroidism).
Non-cardiogenic pulmonary oedema
Altered capillary membrane permeability, due to:
- Acute respiratory distress syndrome (ARDS), secondary to pneumonia, sepsis, aspiration, or severe trauma.
- Rarely: neurogenic (seizures, trauma, SAH), PE.
- It is almost never due to reduced oncotic pressure.
Signs and symptoms
- Respiratory: SOB, orthopnea, cough ± pink frothy sputum, sat up and leaning forward.
- Sweaty, pale, anxious, nauseated.
- Fluid overload: bilateral fine crackles, peripheral oedema.
- CV signs: cool peripheries, ↓BP, ↑HR, ↑JVP, S3 heart sound, murmur, cardiac wheeze.
Investigations
- ABG: may show ↓O2.
- ECG: arrhythmias, ischaemic changes.
- POCUS: bilateral B-lines, pleural effusions.
Bloods:
- Basics: FBC (↓Hb as cause), U+E (investigate renal cause and as giving furosemide), LFT (RVF).
- Extras: troponin (MI), TFT (high or low as cause), BNP (only if diagnosis unclear).
CXR:
- Alveolar oedema: bilateral patchy shadowing which may be in bat's wings distribution. More diffuse patchiness in ARDS.
- Other signs of heart failure e.g. cardiomegaly, Kerley B lines. See CXR findings in heart failure.
Echo:
- Heart failure, valve disease.
Management
- Supplementary O2 to treat hypoxia. Noninvasive ventilation (CPAP or BiPAP) if persistent hypoxia, acidosis, or respiratory distress despite this.
- Furosemide IV to reduce fluid overload. If already on PO long-term, double the dose by using the 'same' dose for IV (as IV is double the potency of PO). Monitor fluid balance, and consider fluid restriction and placing urinary catheter.
- Nitrate IV infusion if BP >140 to reduce cardiac preload. Can be given as SL spray initially.
If poor response:
- Critical care options: intubation if refractory to NIV, dobutamine and/or noradrenaline if cardiogenic shock.
- Further diuretic options: thiazide, spironolactone, metolazone.
- Salbutamol if there is cardiac wheeze.
Continued management:
- Fluid balance: fluid restriction, daily weights. If there is fluid overload, aim for ~1 kg loss per day.
- Switch to furosemide PO.
- DVT prophylaxis.
- Start on HFrEF medication before leaving hospital if this is a first presentation.
Baby check at birth and 6 weeks Check notes and get equipment ready: Measuring tape. Ophthalmoscope Sats probe. In notes, look at full details of pregnancy and birth, including Apgar scores at 1 and 5 minutes. Observation: Colour: pink/red, pale, jaundiced. Any rash? Erythema toxicum is a self-limiting rash of red papules and vesicles, surrounded by red blotches which sometimes give a halo appearance. Usually occurs between 2 days and 2 weeks. Behaviour and mood. Movements. Face: dysmorphism? Head: Feel fontanelle (bulging? sunken?) and sutures. Note that posterior fontanelle closes at 1-2 months, and anterior at 7-19 months. Measure circumference at widest point; take the highest of 3 measurements. Looking for hydrocephalus and microcephaly. Eyes: check red reflex with ophthalmoscope. Feel inside top of mouth with little finger for cleft palate. Also gives you the sucking reflex. Inspect ears to see if they are low-set (below eye level), have any tags or lumps, and check behind the
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