Heart failure


Definition

  • any structural or functional disorder that impairs the ability of the heart to function as a pump to support physiological circulation


Most common causes:

  • ischaemic heart disease, CHD, CAD

  • Cardiomyopathy

  • Hypertension


Pathophysiological changes:

  • ventricular dilation

  • Myocyte hypertrophy

  • Salt and water retention

  • Peripheral vasoconstriction

  • Sympathetic stimulation


Different types of heart failure:

  • right or left ventricular

  • Systolic or diastolic (70%/30%)


systolic heart failure - impaired contractility/ejection

Diastolic heart failure - impaired filling/relaxation


Right ventricular heart failure:

  • Pressure/volume overload

  • Usually caused by lung disease: chronic hypoxemia (low levels of O2 in blood), vasoconstriction and impaired smooth muscle relaxation, elevation of pulmonary vascular resistance, increase RV work so RV enlargement

  • As a result - tricuspid regurgitation, venous system congestion, decreased RV systolic function, decreased pulmonary delivery of LV preload, decreased CO


What happens with venous system congestion:

  • jugular venous distension

  • Hepatomegaly

  • Ascites - accumulation of fluid in peritoneal cavity, can cause fluid pushing on small and large intestine causing nausea/vomiting

  • Calf oedema (pitting)

  • Spleenomegaly


Hepatojugular reflex test - similar to measuring JVP normally, pressure on liver to see if distension caused


Left ventricular heart failure:

  • fluid build up

  • Increased fluid and pressure in PVs, increased pressure in pulmonary capillaries, pulmonary oedema, decreased ventilation, decreased blood oxygenation which leads to hypoxeamia


heart failure:

  • most common type is LVSD

  • Triggers sympathetic hyperactivity - tries to compensate for low cardiac output with neurohormonal mechanisms

  • At start of mechanisms, increased LV end-diastolic volume and pressure

  • LV end-diastolic volume and pressure causes: decreased cardiac output/stroke volume/mean arterial bp and increased myocardial wall stress - activation of SNS

  • SNS leads to RAAS activation, vasoconstriction, adrenaline release - so increased hr and contractility and direct cardiotoxicity (muscle damage or heart electrophysiology dysfunction)


Activation of RAAS - Na and fluid retention which increases preload and afterload

Increased vasoconstriction - wall stress so increased afterload


Increased afterload causes:

  • Myocardial dilation

  • Negative remodelling and decreased contractility

  • Myocyte necrosis, fibrosis and apoptosis


Starling’s law:

  • increased pre load + increase contraction force

  • Overstretched heart

  • Reduced ability to form cross bridges

    • Heart contracts less forcefully`


HFpEF:

  • The heart pumps normally but the muscle is too stiff so cannot properly fill wit blood

  • heart failure with preserved ejection fraction

  • Caused by:

— anaemia

— pregnancy

— thiamine deficiency


AHF presents suddenly, CHF presents more insidiously


HFREF and HFPEF are the 2 types of LVEF heart failures


HFREF:

  • classified by ejection fraction <40%

  • Usually caused by ischaemic and valvular heart disease and hypertension

  • 3 requirements to diagnose: symptoms and signs of typical and reduced LV ejection fraction


HFPEF:

  • Classified by symptoms and signs of hf with ef >50%

  • Signs - decreased LV compliance, increase wall thickness and LA size, abnormal LV relaxation but normal volume

  • Aka diastolic heart failure/dysfunction

  • 4 requirements to diagnose - symptoms and signs of heart failure, mildly reduced LV ef and LV not dilated and relevant structural heart disease and or diastolic dysfunction


HFmrEF - patients in midzone with 40-50% ef


Signs of heart failure:

  • hypotension

  • Tachycardia

  • Elevated JVP - greater than 3cm

  • Displaced apex beat

  • Third heart sound

  • Ascites

  • Oedema

  • Hepatomegaly

  • Spleenomegaly

  • Firm, smooth, tender and pulsatile liver edge - specific sign for right sided heart failure

  • Basal crepitation - popping and crackling sound

  • Pleural effusion - no crackling, dull resonance, flat percussion


Symptoms of heart failure:

  • dysponoea

  • Orthopnoea

  • PND

  • Palpitations

  • Chest pain

  • Fatigue

  • Reduced exercise tolerance

  • Ankle swelling

  • Weight loss

  • Wheeze


Classes of heart failure:

  • I, II, III, IV

  • New York heart association

  • Asymptomatic, mild, moderate, severe

  • Diagnosis based on - detailed history, clinical findings, np levels, reduced LV ejection fraction

  • Usually stay in hospital 5-10 days when diagnosed


Class I:

  • asymptomatic

  • No limitation of ordinary physical activity due to breathlessness, fatigue or palpitations

  • Evidence of LVSD


Class II:

  • mild

  • Slight limitation on physical activity

  • Comfortable at rest but activities like climbing up stairs results in symptoms


Class III:

  • moderate

  • Marked limitation

  • Mild exertion like walking can provoke symptoms


Class IV:

  • severe

  • Symptoms at rest

  • Symptoms increase with physical activity


Natriuretic peptides:

  • ANP from atria and BNP from ventricles

  • Measured because released in response to volume expansion/pressure overload

  • Counter regulate RAAS by vasodilation and increased urinary Na+ excretion

  • Test tool is NT-proBNP

  • More than or equal to 400 unlikely

  • 400-2000 6 weeks wait and echo

  • More than 2000 2 weeks wait and echo


Ejection fraction:

  • explored by echo/MRI

  • Stroke volume/end diastolic volume x 100

  • The fraction of blood pumped out of ventricle in one beat

  • Normal range - 50-70%

  • For heart failure less than 55%


Management:

  • based on; relieving symptoms, delaying disease progression, improving quality and length of life, trying to find factors aggravating HF to be treated

  • General lifestyle advice - education, dietary modification, quit smoking, physical activity and rehabilitation, driving, vaccinations against pneumococcal disease and flu


Monitoring of hf:

  • functional capacity

  • Fluid status

  • Cardiac rhythm


ICD:

  • used for heart failure

  • Shocks heart back into sinus rhythm whenever it detects fibrillation

  • 1 or 2 leads, on RV and RA


CRT-D:

  • crt and icd

  • Can also detect and resolve faster hr


CRT-P:

  • pacemaker


CRT - sends small electrical impulses to get L and R ventricles pumping at the same time, 3 leads (3rd on the LV), criteria - LBBB on ECG, LVEF <30%, NYHA class III


Signs of L sided heart failure:

  • pulmonary oedema

  • Orthopnoea

  • Frothy white and pink sputum

  • Pulsus alternans - alternating strong and weak pulses


Signs of R sided heart failure:

  • ascites

  • Peripheral oedema

  • Raised JVP

  • Cardiomegaly

  • Hepatsplenomegaly


Signs of HF on chest x ray:

  • alveolar oedema

  • Cardiomegaly

  • Dilated uber lobe vessels

  • Pleural effusion


Indications of heart failure:

  • ABCDEF

  • Alveolar oedema

  • Kerley B lines

  • Cardiomegaly

  • Dilation of upper lobe vessels

  • Pleural effusion

  • Fluid in horizontal fissure


Ejection fraction:

  • % of blood that is expelled from heart per beat

  • Ventricles don’t normally eject all blood from its chambers on contraction

  • Normal = 55-65% ejection

  • HF = <40%


Classification of HF:

  • acute vs chronic

  • Right sided vs left sided

  • HFrEF vs HFpEF (systolic vs diastolic)

  • High output vs low output


Acute HF:

  • rapid onset of symptoms and/or signs of HF usually life-threatening

  • Urgent evaluation and treatment

  • Acute myocardial dysfunction, acute pericardial, pericardial tamponade

  • May present suddenly with cardiogenic shock or sub-acutely with decompensation of chronic HF


Chronic HF:

  • progressive cardiac dysfunction from structural and/or functional cardiac abnormalities

  • Reduction in cardiac ouput and/or elevated intra cardiac pressure at rest/on stress

  • Usually precipitated by conditions that affect muscle, vessels, valves, conduction

  • Progressive symptoms with episodes of acute deterioration


Systolic HF:

  • HFrEF

  • Reduction in left ventricular EF < 40%

  • Heart pumping out a reduced proportion of blood that fills ventricles during diastole

  • Increase in blood at end of systole leads to ventricular street, dilation, eccentric remodelling - commonly caused by IHD


Diastolic HF:

  • HFpEF

  • Impaired ventricular relaxation or filling

  • Ventricular hypertrophy tends to develop and diastolic HF characterised by concentric remodelling (shown on echo)

  • Increased stiffness in wall, decreased compliance

  • Impairment of diastolic ventricular filling = decreased cardiac output


LVSD:

  • heart incapable of maintaining a cardiac output thats adequate for metabolic demand

  • Triggers sympathetic hyperactivity

  • Failing heart tries to compensate for low CO with compensatory neurohormonal mechanisms but just makes HF worse and produces additional symptoms

  • Sustained sympathetic stimulation activates RAAS + neurohormones, greater preload and afterload increased nA concs, progressive retention of Na and H2O, Myocyte apoptosis


RVSD:

  • lung disease causes chronic hypoxemia - leads to chronic vasoconstriction and impaired smooth muscle relaxation

  • Elevation of pulmonary vascular resistance

  • Pulmonary artery pressure rises

  • RV work increases leading to thickening and dilation of RV

  • RV eventually fails becoming more spherical, tricuspid regurgitation so venous system congestion

  • Depressed RV systolic function decreases pulmonary delivery of LV preload = diminished CO


Cardiac remodelling:

  • changes in size, shape and function in response to cardiac injury or increased load e.g. exercise

  • Pathological remodelling - may occur after conditions such as MI or cardiomyopathy

  • May predispose to systolic or diastolic hF


Low output HF:

  • traditional heart failure as heart cannot maintain adequate CO to meet demands

  • Increased systemic vascular resistance in attempt to maintain mean arterial pressure

  • Weak pulse, cool peripheries, low bp


High output HF:

  • Normal or higher CO

  • Unable to meet increased demand for perfusion despite normal cardiac function

  • Reduced systemic vascular resistance to diffuse arteriole vasodilation or shunting

  • Increased metabolic demand, reduced vascular resistance, significant shunting


Diagnosis:

  • history and clinical findings

  • ECG

  • BNP levels

  • Further blood tests, CXR, urinalysis, lung function testing

  • Echocardiography


BNP:

  • protein released by heart muscles in response to excessive stretching

  • Used to assess likelihood of HF

  • Has good negative predictive value therefore good at excluding HF

  • Negative test warrant further investigations into causes of symptoms

  • Could be caused by diabetes, sepsis, old age, kidney disease, liver cirrhosis, hypoxaemia


Diagnose HFrEF:

  • symptoms of typical

  • Signs of typical

  • Reduced LV EF


Diagnose HFpEF:

  • symptoms of typical

  • Signs of typical

  • Normal or mildly reduced LV EF and LV not dilated

  • Relevant structural heart disease and or diastolic dysfunction


TTE:

  • transthoracic echocardiography

  • Main investigation for confirmation

  • Should be completed in patients with elevated BNP

  • If clinical exam reveals murmur or ECG abnormal

  • Looks at EF

  • HFrEF = <40%

  • HFmrEF = 40-49%

  • HFpEF = >50%


Investigations:

  • observations

  • Bp

  • ECG

  • Urinalysis

  • FBC

  • U&Es

  • LFT

  • Cholesterol and HbA1c

  • TFT

  • BNP

  • Cardiac enzymes

  • Echocardiogram

  • CXR

  • Chest MRI

  • Coronary angiogram

  • Right heart catheterisation

  • 24hr ECG

  • Lung function tests


Lifestyle management:

  • education

  • Diet = salt restriction, avoid alcohol

  • Smoking cessation

  • Physical activity, exercise training, rehab

  • Influenza and pneumococcal disease vaccine


Monitoring HF:

  • important because HF can fluctuate

  • Monitor functional capacity

  • Monitory fluid status

  • Monitor cardiac rhythm


Stages of HF:

  • stage A - high risk with no symptoms

  • Stage B - structural heart disease, no symptoms

  • Stage C - structural disease, previous or current symptoms

  • Stage D - refractory symptoms requiring special intervention


Treatment for HFrEF:

  • beta blockers and ace inhibitors

  • Diuretics

  • Mineralocorticoid receptor antagonists


Treatment for HFpEF:

  • loop diuretics


Treatment for systolic HF:

  • diuretics - furosemide 20mg once daily, symptomatic relief of dysponoea

  • Ace inhibitors - rampiril 1.25mg once daily, improve symptoms

  • Angiotensin II receptor antagonists - intolerant to ACE inhibitors

  • Beta blockers - Bisoprolol 1.25 once daily, reduce mortality, improve functional status, nebivolol used in treatment of stable mild to moderate HF in patients over 70

  • Aldosterone antagonists - eplerenone 25mg once daily or spironolactone, improve survival, contraindications: hyperkalaemia, hyponatraemia, acute kidney injury

  • Angiotensin receptor nephrilysin inhibitor

  • Cardiac glycosides - digoxin, add-on therapy, atrial fibrillation

  • Vasodilators and nitrates - reduces preload and afterload, intolerant to ace/ARAs

  • Inotropic and vasopresor agents - acute HF


Acute heart failure:

  • rapid onset of symptoms and signs of HF secondary to abnormal cardiac function

  • Elevated cardiac filling pressures

  • Severe dysponoea and fluid accumulates in interstitium and alveolar spaces of lung (pulmonary oedema)


Poor prognosis indicators of acute HF:

  • high pulmonary capillary wedge pressure

  • Low serum sodium concentration

  • Increased left ventricular end-diastolic dimension on echo

  • Low oxygen consumption


Causes of acute HF:

  • IHD

  • Valvular heart disease

  • Hypertension

  • Acute and chronic kidney disease

  • Atrial fibrillation


Types of acute HF:

  • acute decompensated HF - mild features of HF e.g. dyspnoea

  • Hypertensive AHF - high BP, preserved LV function, pulmonary oedema

  • Acute pulmonary oedema - Tachypnoea, Orthopnoea, pulmonary crackles, pulmonary oedema

  • Cardiogenic shock - systolic bp <90

  • High-ouput HF - warm peripheries, pulmonary congestion, bp may be low

  • Right HF - low CO, elevated JVP, Hepatomegaly, hypotension


Pathophysiology of acute HF

  • activation of RAAS and SNS

  • Prolonged ischaemia

  • Exacerbation of myocardial dysfunction

  • Myocardium may exhibit hibernation


Investigations of acute HF:

  • 12 lead ECG

  • CXR

  • Blood investigations

  • Plasma BNP or NT-proBNP

  • TTE


Management of AHF:

  • arterial gas sampling

  • Central venous cannulation

  • Pulmonary artery catheterisation

  • Patients with AHF managed in high dependency area with regular measurement of temp, HR, bp and cardiac monitoring

  • Prophylactic anticoagulation with low molecular weight heparin


Initial treatment for AHF:

  • oxygen and IV loop diuretics

  • GTN infusion if needed

  • Regular medication for HF continued (beta blockers stopped if HR less than 50 bpm/2nd or 3rd degreee AV block or shock

  • If doesn’t work, inotropic support with dobutamine, phosphodiesterase inhibitors and levosimendan


Vasodilators:

  • not be given routinely to all

  • Contraindication is hypotension

  • May have role in severe hypertension/mitral valve disease


Opiates:

  • not offered routinely

  • Increased morbidity in patients