Chronic Heart Failure: epidemiology, investigation and diagnosis Flashcards

1
Q

<p>What is the definition of heart failure?</p>

A

<p>A clinical syndrome comprising of dyspnoea, fatigue or fluid retention due to cardiac dysfunction, either at rest or on exertion, with accompanying neurohormonal activation</p>

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2
Q

<p>What is the prevalence of heart failure and of asymptomatic LVSD?</p>

A

<p>Heart failure: 0.4 - 2%</p>

<p>Asymptomatic LVSD: 0.4 - 2%</p>

<p>Prevalence and incidence increase with age (mean age 74years)</p>

<p>Estimated 40-60 000 patients with HF/LVSD(left ventricular systolic dysfunction) in Scotland</p>

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3
Q

<p>What is the largest costattached to heart failure</p>

A

<p>Hospital inpatient care</p>

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4
Q

<p>What can be said about re-admission rates for HF?</p>

A

<p>High! and readmission is most likely to happen early.</p>

<p>Length of hospital admission is longer than any other condition.</p>

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5
Q

<p>What are the signs of heart failure?</p>

A

<p>Breathlessness</p>

<p>Fatigue</p>

<p>Oedema</p>

<p>Reduced exercise capacity</p>

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6
Q

<p>What are the signs of heart failure?</p>

A

<p>Oedema</p>

<p>Tachycardia</p>

<p>Raised JVP</p>

<p>Chest crepitations or effusions</p>

<p>3rd Heart sound</p>

<p>Displaced or abnormal apex beat</p>

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7
Q

<p>Is heart failure easy to diagnose based on clinical signs alone?</p>

A

<p>Yes very difficult - diagnosis incorrect in approximately 40-50% of cases</p>

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8
Q

<p>What are the 3 key features that indicate heart failure?</p>

A

<p>Symptoms and signs of HF (rest or at exercise)</p>

<p>Objective evidence of cardiac dysfunction and in (doubtful cases)</p>

<p>Resonse to therapy</p>

<p></p>

<p>(They look like they have it, tests think they have it, and they respond to treatment)</p>

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9
Q

<p>What is objective evidence of cardiac dysfunction?</p>

A

<p>•Echocardiography, Radionuclide ventriculography (RNVG/MUGA), MRI, left ventriculography</p>

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10
Q

<p>What are the screening tests available?</p>

A

<p>12 lead ECG - left ventricular systolic dysfunction is very unlikely if there is a normal ECG but it is still possible (90-95% sensitive)</p>

<p>(Problems with confidence of interpretation in primary care, must be entirely normal or else loses reliability)</p>

<p>BNP(brain (B-type) natriuretic peptide)</p>

<p>Amino acid peptide can be measured easily in bood</p>

<p>–Elevated in heart failure, therefore low BNP effectively excludes heart failure</p>

<p>Potential as diagnostic/ screening test for long time</p>

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11
Q

<p>What does a high / low BNP indicate?</p>

A

<p>•Low BNP effectively rules out heart failure or LVSD, elevated BNP indicates need for an echo/cardiac assessment</p>

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12
Q

<p>What is the common rule as to what will cause heart failure?</p>

A

<p>If sufficiently severe almost any structural cardiac abnormality will cause heart failure</p>

<p>e.g</p>

<p>•LV systolic dysfunction – many causes</p>

<p>•Valvular heart disease</p>

<p>•Pericardial constriction or effusion</p>

<p>•LV diastolic dysfunction/heart failure with preserved systolic function/heart failure with normal ejection fraction</p>

<p>•Cardiac arrhythmias: tachy or brady</p>

<p>•Myocardial ischaemia/infarction (usually via LVSD)</p>

<p>•Restrictive cardiomyopathy eg amyloid, HCM</p>

<p>•Right ventricular failure: primary or secondary to pul hypertension</p>

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13
Q

<p>What are common causes of LV systolic dysfunction?</p>

A

<p><strong>Ischaemic heart disease (usually MI)</strong></p>

<p>•<strong>Dilated cardiomyopathy(DCM): Means LVSD not due to IHD or secondary to other lesion ie valves/VSD</strong></p>

<p>e.g</p>

<p>–Inherited</p>

<p>–Toxins: eg alcohol, catecholamines (phaeochromocytoma or stress cardiomyopathy (takosubo’s cardiomyopathy)</p>

<p>–Viral: acute myocarditis or chronic DCM</p>

<p>–Other infective: HIV, chaga’s disease, Lyme’s disease.......</p>

<p>–Systemic disease: sarcoidosis, haemachromatosis, SLE, mitochondrial dis.</p>

<p>–Muscular dystrophies</p>

<p>–Peri-partum cardiomyopathy (post pregnancy)</p>

<p>–Hypertension</p>

<p>–Isolated non compaction</p>

<p>–Tachycardia related cardiomyopathy</p>

<p>–RV pacing induced cardiomyopathy</p>

<p>–End stage hypertrophic cardiomyopathy</p>

<p>–End stage arrhythmogenic RV cardiomyopathy</p>

<p><strong>Severe aortic valve disease or mitral regurgitation</strong></p>

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14
Q

<p>How do you figure out which type of heart failure is present? IHD, valvular disease or dilated cardiomyopathy</p>

A

<p>Take a detailed history - may provide answer</p>

<p>Esculde renal failure, anaemia, thyroid function tests</p>

<p>Serology to check for viruses and autoantibodies</p>

<p>Consider to exclude phaechromocytoma (cancer in the adrenal gland)</p>

<p>Consider other causes such as thyroid, muscular dystrophy</p>

<p><strong>ECG, ECHO and sometimes a CXR</strong></p>

<p><b>Consider coronary angiography in patients with chest pain who are over 70.</b></p>

<p><b>Cardiac MRI</b>looking for infarction, inflammation and fibrosis</p>

<p></p>

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15
Q

<p>Why is echocardiography always an essential investigation?</p>

A

<p>Assesses:</p>

<p>–LV systolic dysfunction</p>

<p>–Valvular dysfunction</p>

<p>–Pericardial effusion / tamponade</p>

<p>–Diastolic dysfunction</p>

<p>–LVH</p>

<p>–Atrial/ventricular shunts / complex congenital heart defects (ventral septal defects)</p>

<p>–Pulmonary hypertension / Right heart dysfunction</p>

<p>•May not identify constriction / may miss shunts (but you will see atrial dilatation)</p>

<p></p>

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16
Q

<p>What changes LVEF?</p>

A

<p>•Disease / physiological changes can both decrease and increase the LVEF - it is however a continuous biological variable like haemoglobin / anaemia</p>

17
Q

<p>Can LV ejection fraction be calculated by echo?</p>

A

<p>Yes but it is difficult to quantify accurately and reproducably</p>

<p>Depends on:</p>

<p>–Quality of images</p>

<p>–Experience of operator</p>

<p>–Calculation method –</p>

<p>•M-mode</p>

<p>•Simpson’s biplane</p>

<p>–Use of contrast agents</p>

<p>–Time-consuming to perform accurately</p>

<p>–Normal range is centre specific, but LVEF not routinely measured and NR not routinely established</p>

18
Q

<p>What are the normal, mild, moderate and severe LVEF?</p>

A

<p>•normal (50-80%)</p>

<p>•mild (40-50%)</p>

<p>•moderate (30-40%)</p>

<p>•severe (<30%)</p>

19
Q

<p>What is LVEF MUGA?</p>

A

<p>•Much easier to obtain an accurate figure for the LVEF</p>

<p>•Greater reproducibility</p>

<p>•Ionising radiation</p>

<p>•No additional structural information</p>

<p>•centre specific normal range</p>

20
Q

<p>What is a potent predictor of death in hospitalized heart failure patients?</p>

A

<p>Left ventricular systolic function</p>

21
Q

Classification of Heart Failures

A
22
Q

<p>Does heart failure always reduce cardiac output?</p>

A

<p>NO - very complex problem</p>

23
Q

<p>Why is HF considered a systemic disorder?</p>

A

<p>Because it involves cardiac dysfunction, renal dysfunction, skeletal muscle dysfunction, systemic inflammation and neurohormonal activation</p>

24
Q

<p>How is the renin - angiotensin - aldosterone system affected by systemic HF?</p>

A

<p>Causes salt and water retention (by reduced blood flow to the kidneys)</p>

<p>Adverse haemodynamics</p>

<p>Causes an increase in blood volume - causes LY hypertrophy / remodelling and fibrosis (of LV)</p>

<p>Hypokalaemia and hypomagnesaemia</p>

25
Q

<p>How does neurohormonal activation affect the sympathetic nervous system?</p>

A

<p>It is arrythmogenic, adverse haemodynamics, increase in renin etc</p>

26
Q

<p>What is Left ventricular injury a result of?</p>

A

<p>Coronary artery disease</p>

<p>Hypertension</p>

<p>Cardiomyopathy</p>

<p>Valvular heart disease</p>

<p>Neurohormonal activation - for example renin-angiotensin-aldosterone system)</p>

27
Q

<p>What is the result of left ventricular injury?</p>

A

<p>Left ventricular dysfunction - leading to pump failure, arrythmia, heart failure and even death</p>

28
Q

<p>What are the outcomes of neurohormonal activation?</p>

A

<p>Vasoconstriction</p>

<p>Endothelial dysfunction</p>

<p>Renal sodium retention</p>

29
Q

<p>What are the resultant symptoms of neurohormonal ativation?</p>

A

<p>Dyspnoea</p>

<p>Fatigue</p>

<p>Oedema</p>

<p></p>

<p>HEART FAILURE</p>

30
Q

<p>What is modern pharmacological treatment of heart failure?</p>

A

<p>–Diuretics</p>

<p>–ACE inhibitors</p>

<p>–Betablockers</p>

<p>–Aldosterone receptor blockers</p>

<p>–ARBs</p>

<p></p>

<p>In some patients, ACEI or ARB are now replaced by</p>

<p>ARNI’s: angiotensin receptor neprilysin inhibitor – makes use of beneficial neurohormonal systems (BNP?)</p>