Heart Failure Introduction HF is a due to abnormality of cardiac structure and/or function with constellation of symptoms (orthopnoea, dyspnoea, etc)

) and signs (oedema, rales, etc) Prevalence is 2% of overall population (5-10% of above 65) Types o Systolic dysfunction (EF < 40%) o Diastolic dysfunction (EF > 40%) Classification New York Heart Association (NYHA) NYHA class I No limitation of physical activity NYHA class II Slight limitation of physical activity NYHA class III Marked limitation of physical activity NYHA class IV Symptoms at rest American College of Cardiology/American Heart Association (ACC/AHA) Heart Failure Stages Stage A high risk of HF but nil structural heart disease or symptoms Stage B Structural heart disease but nil symptoms Stage C Structural heart disease with symptoms Stage D refractory HF requiring intervention Aetiology Coronary artery disease o Myocardial ischemia and infarction Valvular disease o Obstructive disease aortic stenosis o Regurgitant disease aortic and mitral regurg Dilated cardiomyopathy o Alcohol o Infiltrative disorders (amyloidosis or sarcoidosis) o Genetic disorders Becker and Duschenne (lack of or no functional dystrophin respectively) Arrhythmia o Chronic brady or tachyarrhytmia Metabolic o Hypertension o Anaemia high volume output o Thyrotoxicosis o Beri-beri Infective o Viral can cause myocarditis (coxsackie, HIV, parvovirus B19) o Chagas disease protozoan (Trypasonoma cruzi) infection spread by insect vectors. Pseudocysts and acute myocarditis can occur o Rheumatic fever strep pyogenes Pulmonary hypertension Aetiology (Diastolic Dysfunction) Hypertrophy o Primary Hypertrophic cardiomyopathy o Secondary hypertension or valvular lesion Restrictive cardiomyopathy

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Infiltrative disorders (amyloidosis or sarcoidosis) Haemachromatosis

Pathogenesis Impairment of cardiac myocytes can occur either suddenly or slowly o Myocardial infarcts (sudden) or hypertension (slow) Patients remain asymptomatic or minimally symptomatic for up to years due to compensatory mechanisms via neurohormonal activation o Activation of Renin-Angiotensin-Aldosterone-System (RAAS). This maintains high cardiac output by increasing salt and water retention o Increased cardiac contractility via adrenergic pathway (noradrenaline) o Vasodilatory molecules reduce afterload such as ANP, BNP, prostaglandins (PGE2 and PGI2) and nitric oxide (NO) Neurohormonal activation also results in left ventricular (LV) remodelling o Myocyte hypertrophy and alteration of its contractile properties o Progressive loss of myocytes through necrosis and apoptosis o -adrenergic desensitisation o Abnormal collagen weaving surrounding myocytes and myocardial metabolism LV remodelling results in impairment of heart contractility o There is increased LV end-diastolic volume due to poor contractions leads to poor stroke volume (Frank-Starling mechanism) o This also leads to LV wall thinning and dilation of LV o Dilatation of LV leads to increased afterload as more contractility is needed to displace the higher volume of diastolic blood (Laplaces Law) o This causes increased backflow due to lower EF (more blood retained in diastole) and arisal of HF symptoms Diastolic Dysfunction o Impaired myocardial relaxation due to delayed calcium uptake by myocyte sarcoplasmic reticulum leads into reduction in ATP concentration o Alternatively, there is delayed LV filling due to increased wall stiffness (hypertrophy or fibrosis) o Elevated LV end-diastolic pressure leads to increased pulmonary capillary pressures Clinical features Dyspnoea on exertion Orthopnoea redistribution of fluid from the splanchnic circulation that increases the pulmonary capillary pressure Paroxysmal Nocturnal Dyspnoea Nocturnal cough often missed symptom Cheyne-Strokes respiration cyclical apnoea and hyperventilation. Periods of apnoea causes hypercapnia that stimulates the depressed respiratory centre Raised JVP more than 8cm (3cm from sterna angle) Investigation ECG LVH or Q waves (past MI) CXR posteroanterior view. ABCDE o Alveolar bat wing o B-lines (Kerley) o Cardiomegaly o Diaphragmatic blunting

o Effusion Echocardiogram o Able to assess LV size, contractility, EF, wall movements and valvular defects o Diastolic dysfunction L atrial dilatation and LV hypertrophy with abnormality of diastolic filling (pulse-wave) o Cor pulmonale RV size o Ejection Fraction = Blood Markers o Brain Natiuretic Peptide (both B-type and N-terminal) are good markers for HF but not recommended as guide to HF therapy Nuclear Imaging o Gated pool scan or Multiple-Gated Acquisition (MUGA) scan assesses LV, RV and EF Cardiac MRI (cMRI) o Gold standard of RV imaging but highly expensive

Treatment Treat co-morbidities o HTN, CAD, T2DM, anaemia, etc Activity o Routine modest exercise is beneficial in NYHA I-III Diet o Low-salt diet (2-3g/d) helps reduce retention of fluid Fluid restriction o Evidence is only seen in patients with hyponatremia (<130mmol) Diuretics o First line treatment in patients with fluid retention. o Benefits: reduces symptoms, fluid retention but doesnt improve mortality o Loop diuretics (Frusemide 20mg OD) act on Loop of Henle by inhibiting Na-K-2Cl co-transporter (also inhibits Mg and Ca reabsorption too). Increases fractional excretion of sodium (FeNa) by 25% and has to be slowly titrated up. Adverse effects include hypokalemia, hyperuricaemia (gout) and volume depletion o Thiazide diuretics (HCT 25mg qid) and metalazone (5mg BD) inhibits Na-Cl symporter at the distal convoluted tubules with FeNa of 10%. ACE inbhibitors o First line in preventing disease progression (even asymptomatic patients) o Benefits: improves mortality, stabilizes LV remodelling, LOS and symptoms o Interfere with RAAS by inhibiting conversion of angiotensin I to angiotensin II o Enalapril/ramipril 2.5mg BD need to be started at low doses and slowly titrated o Adverse effects: hypotension, hyperkalaemia, cough (bradykinin upregulation) and angioedema (1%) Angiotensin Receptor Blockers o Alternatives to ACEi if intolerable o Evidence showing that addition of ARB to ACEi is beneficial in chronic HF due to alternative pathways (ARBs blocks the effects of Angiotensin II) o If used in conjuction with BB, ARBs can reverse LV remodelling and improve mortality o Candesartan 4mg OD or valsartan 40mg BD BetaBlockers (BB) o Benefits: reversing LV remodelling (with ACEi or ARB), symptomatic relief and improved mortality

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Proven via research: start Bisoprolol 1.25mg OD , Carvedilol 3.125mg BD, or metoprolol CR 23.75mg OD. Start low and only double every 2-4 weekly as increasing doses can increase fluid retention due to reduction of sympathetic system Target dose: Bisoprolol 10mg OD, Carvidolol 25mg BD or metoprolol CR 190mg. >70y: Nebivolol 1.25mg OD with a target of 10mg OD reduces all-cause mortality Adverse effects: hypotension, bradycardia, heart block, lethargy, impotence and bronchospasm

Digoxin o Recommended for symptomatic patients with AF or as an adition to standard therapy o A cardiac glycoside with positive inotropic effect by inhibiting Na-K ATPase thus increasing intracellular calcium. Also delays conduction through the AV node Loading ( ) Daily dosing of 62.5-250mcg daily (serum digoxin of 0.5-1ng/ ml) Adverse effect: electrolyte imbalance, arrhythmia (VF/VT), heart block, CNS (xanthopsia yellow vision) Alternative vasodilator therapy o Hydralazine 50mg TDS is an arterial vasodilator that reduces afterload o Isosorbide mononitrate 20mg TDS is a venodilator that reduces preload o Hydralazine + Isosorbide mononitrate has to be used concurrently and has proven mortality benefit. Caution with use of NO-based drugs (Viagra) o GTN patch (5-15mg OD) reduces pulmonary and systemic blood pressure so it can reduce sysmptoms of orthopnoea and PND Anticoagulation (read AF) o Reduces risk of thromboembolic disease as depressed LV function promotes blood stasis o Warfarin (target INR of 2-3 ) or aspirin o o o