Because all organs can fail…some failing organs are just more important than others.
Definition: cardiac output is inadequate for the body’s requirements
Can be divided into systolic and diastolic failure, left and right sided failure, acute and chronic failure and low output and high output failure.
Acute Heart Failure: new acute onset heart failure or decompensation of chronic heart failure characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypoperfusion.
Chronic heart failure: develops or progresses slowly. Venous congestion is common but arterial pressure is well maintained until very late.
Aetiology/ risk factors:
Systolic failure: inability of the ventricle to contract normally, resulting in decreased cardiac output and an ejection fraction (EF) < 40%. (Normal LVEF is ~ 50-75%)
= ischaemic heart disease, MI, cardiomyopathy
Diastolic failure: inability of the ventricle to relax and fill normally causing increased filling pressures (EF > 50%).
= constrictive pericarditis, cardiac tamponade, restrictive cardiomyopathy, hypertension
-Systolic and diastolic failure usually coexist.
Left ventricular failure: causes include IHD, MI, hypertension, cardiomyopathy, aortic valve disease, mitral regurgitation
Right ventricular failure: causes include left ventricular failure, infarction, cardiomyopathy, pulmonary hypertension, pulmonary valve disease, pulmonary embolus, chronic lung disease (cor pulmonale), tricuspid regurgitation, constrictive pericarditis/ pericardial tamponade.
Biventricular failure: arrhythmia, cardiomyopathy (dilated or restrictive), myocarditis, drug toxicity
-Left and right ventricular failure may occur independently or together as Congestive Cardiac Failure (CCF).
Low-output heart failure (most HF): cardiac output is low and fails to increase normally with exertion
= pump failure: (causes of systolic and diastolic failure), decreased heart rate (beta blockers, heart block, post-MI), negatively inotropic drugs (antiarrhythmics)
= excessive preload: fluid overload (impaired renal excretion, iatrogenic), mitral regurgitation
=chronic excessive afterload: aortic stenosis, hypertension
High-output failure (rare): cardiac output is normal or increased but needs are increased to an extent which the heart fails to meet. Occurs with a normal heart but even earlier if there is heart disease.
=anaemia, thyrotoxicosis, pregnancy, arteriovenous malformation, Paget’s disease (arteriovenous connections form in bone), beri beri (thiamine deficiency).
Epidemiology: prevalence 1-3% of the general population, ~10% among elderly patients
-poor exercise tolerance
-orthopnoea (do you get breathless when you lie flat? how many pillows do you sleep with?)
-paroxysmal nocturnal dyspnoea (do you wake up in the middle of the night gasping for breath?)
-nocturnal cough +/- pink frothy sputum (sputum characteristic of pulmonary oedema)
-wheeze (cardiac ‘asthma’)
Right ventricular failure: (blood backed up to the systemic circulation)
-pulsation in neck and face (if cause is tricuspid regurgitation)
-In congestive cardiac failure there is both right and left ventricular failure and so patients will present with a combination if both sets of symptoms.
-In acute cardiac failure there is pulmonary and/or peripheral oedema with or without signs of peripheral hypoperfusion. E.g. Dyspnoea, wheeze, cough and pink frothy sputum.
-In high-output heart failure there are initially features of right ventricular failure and later left ventricular failure becomes evident.
Left ventricular failure:
-cool peripheries, cyanosis
-hypotension, narrow pulse pressure
-displaced apex beat (LV dilation)
–pulsus alternans = alternating strong and weak beats (suggests LVF-also cardiomyopathy or aortic stenosis)
-murmurs of mitral or aortic valve disease (e.g. AS -Ejection Systolic Murmur- as a cause of heart failure, MR- Pansystolic Murmur- as a consequence of LV dilation in heart failure)
-S3 gallop = third heart sound, low pitched and best heard with bell of stethoscope. Occurs in a dilated left ventricle with rapid ventricular filling or poor LV function.
-bilateral basal fine crackles
-pleural effusion (stony dull percussion note and reduced breath sounds)
-wheeze (cardiac asthma)
–S3 gallop = third heart sound, low pitched and best heard with bell of stethoscope. Occurs in a dilated left ventricle with rapid ventricular filling or poor LV function.
Right ventricular failure:
-right ventricular heave (pulmonary hypertension)
-murmurs of pulmonary or tricuspid valve disease (functional tricuspid regurgitation due to RV dilation)
-elevated JVP, hepatojugular reflux (pressing on the abdomen produces a rise in JVP that persists throughout a 15sec compression, a sign of right ventricular failure, reflecting inability to eject the increased venous return)
-peripheral oedema, ascites, ankle/sacral pitting oedema
-Framingham Criteria can be used to make a diagnosis of CCF.
Framingham criteria for congestive cardiac failure (CCF)
-Diagnosis of CCF requires at least 2 major criteria or 1 major + 2 minor criteria.
-Paroxysmal Nocturnal Dyspnoea
-Crepitations (pulmonary oedema)
-S3 gallop =
-Cardiomegaly (on CXR)
-Increased central venous pressure (> 16cmH2O at right atrium)
-Weight loss > 4.5kg in 5 days in response to treatment
-Neck vein distention
-Acute pulmonary oedema
-Bilateral ankle oedema
-Dyspnoea on ordinary exertion
-Tachycardia (HR > 120/min)
-Decrease in vital capacity by 1/3rd from maximum recorded
-FBC (anaemia?), U&Es, LFTs, CRP, glucose, lipids, Thyroid Function Tests
Alveolar shadowing (diffuse fluffy opacification = alveolar oedema)
Kerley B lines (septal lines = interstitial oedema)
Cardiomegaly (cardiothoracic ratio > 50%)
Dilated prominent upper lobe vessels (upper lobe Diversion)
-peribronchial cuffing (bronchial wall thickening)
-classic perihilar ‘bat’s wing’ shadowing (oedema)
-fluid in fissures
–ECG-may indicate cause. Look for evidence of ischaemia (Q waves, T wave inversion), MI (ST changes) or ventricular hypertrophy.
It is rare to get a completely normal ECG in chronic heart failure.
-BNP = molecule secreted mainly form ventricular myocardium. Plasma BNP reflects myocyte stretch and is closely related to left ventricle pressure. Can be released in large quantities in MI and left ventricular dysfunction.
As a biomarker of heart failure- sensitivity > 90%, specificity 80-90%
If BNP > 100ng/L this suggests heart failure.
If BNP < 50ng/L this ‘rules out’ heart failure.
According to NICE, if ECG and BNP are normal, heart failure is unlikely. If either is abnormal, an echo is required.
-Echocardiography– key investigation. May indicate cause (MI, valvular disease) and can confirm the presence or absence of ventricle dysfunction. Measures ejection fraction.
Endomyocardial biopsy– rarely needed
Chronic Heart Failure:
Conservative: stop smoking, eat less salt, and optimise weight and nutrition.
-treat cause (e.g. dysrhythmias, valve disease)
-treat exacerbating factors (anaemia, thyroid disease, infection, hypertension)
-avoid exacerbating factors (NSAIDs = fluid retention, verapamil/diltiazem = -ve inotrope)
Loop diuretics to relieve symptoms e.g. furosemide (40mg/24h PO) or bumetanide (1-2mg/24h PO)
Add K-sparing diuretic- spironolactone– if hypokalaemia (S/E of loop diuretic), predisposition to arrhythmias or if on digoxin (hypokalaemia increases digoxin toxicity).
Consider adding a thiazide e.g. metolazone (5-20mg/24h PO) if refractory oedema.
Consider in all those with left ventricular systolic dysfunction.
Angiotensin Receptor Blockers (ARBs) can be used as substitutes if cough is a problem.
⇒Beta blocker e.g. carvedilol
Initiate after diuretic and ACE inhibitor. Start at low dose and build up.
⇒Spironolactone (25mg/24h PO)
-use in those still symptomatic despite optimal therapy as listed above
⇒Digoxin (e.g. 125 mcg/24h PO if sinus rhythm)
Helps symptoms, even in those with sinus rhythm.
Consider for patients with left systolic dysfunction who have signs or symptoms of heart failure while receiving standard therapy, including ACE inhibitors and beta blockers, or in patients with AF (+/- warfarin).
Maintain K+ at 4-5mmol/L.
Hydralazine + isosorbide dinitrate– if intolerant to ACE-I and ARBs. Reduced mortality when added to standard therapy (including ACE-i) in Black patients with heart failure.
Intractable heart failure:
-Re-assess cause and compliance with medications. Switching furosemide to bumetanide might help.
-Consider admitting for:
-strict bred rest +/- salt and water restriction (~< 1.5L/24h)
–Metolazone (thiazide diuretic) and IV furosemide
–Opiates and IV nitrates may relieve symptoms.
-Monitor daily weight and U&Es, keeping an eye on potassium (loop and thiazide diuretics can cause hypokalaemia)
-DVT prophylaxis: heparin + TED stockings
⇒ In extremis- try IV inotropes
⇒ Consider cardiac resynchronisation (pacemaker), LV assist device, or transplantation.
Management of acute heart failure: EMERGENCY
-Sit the patient upright
–Oxygen (100% if no pre-existing lung disease)
-IV access and monitor ECG.
-Treat any arrhythmias e.g. AF
-Investigations whilst continuing treatment: CXR, ECG, U&Es, troponin, ABG, consider echo, plasma BNP (helpful if diagnosis in question)
–Diamorphine 1.25-5mg IV slowly (caution in liver failure and COPD)
–Furosemide 20-80mg IV slowly (larger doses needed in renal failure)
–GTN spray, 2 puffs or 2 x 0.3mg tablets sublingual (don’t give if SBP < 90 mmHg as nitrates are vasodilators)
-If SBP ≥ 100mmHg, start a nitrate IV infusion e.g. isosorbide dinitrate 2-10mg/h. Keep SBP ≥ 90 mmHg.
-If patient is worsening:
-More furosemide 40-80mg
-Consider CPAP (continuous positive airway pressure- improves ventilation, drives fluid out of alveolar spaces and into vasculature)
-Increase nitrate infusion if able do so without dropping SBP < 100 mmHg
→If SBP < 100 mmHg, treat as cardiogenic shock and refer to ICU. Patient will require inotropes e.g. dobutamine.
Monitor progress: BP, pulse, cyanosis, resp rate, JVP, urine output, ABG
Once stable and improving, similar to chronic heart failure management:
-daily weights, aim reduction of 0.5kg/day (less fluid overloaded)
-change to oral furosemide or bumetanide
-if on large doses of loop diuretic (furosemide) consider addition of thiazide e.g. bendroflumethiazide or metalazone 2.5-5mg daily PO).
–ACE inhibitor if LV ejection fraction < 40%. If contraindicated, consider hydralazine and nitrate.
-Consider beta blocker and spironolactone (if LVEF < 35%)
-Patient may be suitable for biventricular pacemaker or cardiac transplantation
-Consider digoxin +/- warfarin, especially if AF.
Complications: respiratory failure, cardiogenic shock, death
Prognosis: prognosis is poor with ~25-50% of patients dying within 5 years of diagnosis
If admission is needed, 5yr mortality ~ 75%.
The higher the BNP, the higher the cardiovascular and all-cause mortality.