Heart Failure

Complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation

Aetiology

• The main causes are ischaemic heart disease, dilated cardiomyopathy and hypertension

• Other causes include other forms of cardiomyopathy, valvular disease, arrhythmias, pericardial disease, infections, alcohol, diabetes and congenital heart disease

Pathophysiology

Underlying mchanism of reduced cardiac output

• Ejection fraction: the percentage of blood that is pumped out of the heart during each beat (SV/EDV x 100)

• Ejection fraction <40%

• Reduced contractility → systolic ventricular dysfunction → decreased LVEF → decreased cardiac output

• Commonly caused by ischaemic heart disease, can also occur with valvular heart disease and hypertension

• Consisting of symptoms and signs of heart failure with an ejection fraction of >50%

• Decreased ventricular compliance → diastolic ventricular dysfunction → reduced ventricular filling and increased diastolic pressure → decreased cardiac output

• Causes include increased stiffness of the ventricle (e.g. in long-standing hypertension with ventricular wall hypertrophy), and impaired relaxation of the ventricle (e.g. constrictive pericarditis)

• Increased left ventricular afterload - increased mean aortic pressure (e.g. arterial hypertension) or by outflow obstruction (e.g. aortic stenosis)

• Increased left ventricular preload - left ventricular volume overload (e.g. backflow into the left ventricle caused by aortic insufficiency)

• Increased right ventricular afterload - increase in pulmonary artery pressure (e.g. pulmonary hypertension)

• Increased right ventricular preload - right ventricular volume overload (e.g. tricuspid valve regurgitation)

Compensation mechanisms

• Increased adrenergic activity - increases heart rate, blood pressure and ventricular contractility

• Increase of RAAS - activated following decrease in renal perfusion secondary to reduction of stroke volume and cardiac output
• Increased angiotensin II secretion results in:
• Peripheral vasoconstriction which increases systemic BP which increases afterload
• Vasoconstriction of the efferent arterioles which decreases renal blood flow and increases intraglomerular pressure, which maintains GFR
• Increased aldosterone secretion results in increased renal Na+ and H2O resorption, which increases preload

• Secretion of BNP - predominantly secreted by the ventricles in response to increased myocardial wall stress, works to decrease blood pressure

Consequences of decompensated heart failure

• Forward failure - reduced cardiac output results in poor organ perfusion leading to organ dysfunction (e.g. hypotension, renal dysfunction)

• Backward failure:
• Left ventricle - increased left ventricular pressure leads to backup of blood into the lungs, increasing pulmonary capillary pressure which causes pulmonary oedema
• Right ventricle - increased pulmonary artery pressure from left ventricular failure decreases right-sided cardiac output, resulting in systemic venous congestion which produces peripheral oedema and progressive congestion of internal organs e.g. liver, stomach
• Biventricular HF - in clinical practice, biventricular heart failure with features of left and right heart failure is more likely than isolated failure of one ventricle

Clinical presentation

Symptoms

• Exertional dyspnoea

• Orthopnoea

• Paroxysmal nocturnal dyspnoea

• Fatigue

Signs

• Tachycardia

• Elevated jugular venous pressure

• Cardiomegaly

• Third and fourth heart sounds

• Bi-basal crackles

• Pleural effusion

• Peripheral ankle oedema

• Ascites

• Tender hepatomegaly

NYHA Classification

• Class I - no limitation of physical activity, activity doesn’t cause SOB

• Class II - slight limitation of physical activity, comfortable at rest but normal activity causes SOB

• Class III - marked limitation of physical activity, comfortable at rest but less than normal activity causes SOB

• Class IV - unable to carry out any activity without symptoms, can be symptomatic at rest

Investigations

Diagnostic algorithm

• Signs on CXR of HF:
• Pulmonary oedema - haziness in perihilar region, Kerley B lines, bat-wing shadowing
• Cardiomegaly

• Additional diagnostic tests (if needed) may include: angiogram, MRI

• PND/Orthopnea

• Neck Vein Distention

• Rales

• Positive Hepatojugular Reflex

• Cardiomegaly

• S3/S4 Gallop

Management

General measures

• Education

• Dietary modification - salt restriction, fluid restriction

• Smoking cessation, alcohol reduction

• Low intensity exercise - rehabilitation and home based

• Keep vaccines up to date

• Lorry/bus drivers need to notify the DVLA if they are symptomatic

• Consider antiplatelet and statin

HFpEF

• Loop diuretic e.g. furosemide to relieve symptoms of fluid overload

• Manage cause/precipitating factors

HFrEF - ABAL

• ACE inhibitor (e.g. ramipril)

• β blocker (e.g. bisoprolol)

• Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone)

• Loop diuretics improves symptoms (e.g. furosemide)

• Other add ons if symptoms not controlled with above measures:
1. Sacubitril/valsartan - stop ACEi/ARB, continue β-blocker and spironolactone
2. Ivabradine - sinus rhythm ≳75 bmp
3. Digoxin
4. Hydralazine + nitrates

Acute HF presentation - LMNOP

• Lasix (furosemide) IV → 1 mg/kgBB bolus → if dyspnoe persist, increase to 2 mg/kgBB bolus

• Morphine IV → 2-4 mg bolus lambat

• Nitrates - sublingual or oral

• Oxygen 2-4 L/min via NK

• Position - sit patient up

• Treat cause of decompensation (MI, arrythmia, myocarditis)

• β-blockers contraindicated

Complications

• Arrythmias - most commonly AF and ventricular arrhythmias

• Depression

• Cachexia

• Chronic kidney disease

• Sudden cardiac death