Heart failure Flashcards

1
Q

What is heart failure?

A

Combination of symptoms and signs resulting from impaired function of the heart - heart cannot meet the demand for blood

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2
Q

How can heart failure be classified?

A
  • Time (acute/ chronic HF)
  • Anatomy (right/ left sided HF)
  • Physiology (systolic vs diastolic function)
  • Cause (ischaemic vs non-ischaemic)
  • Genetics
  • Cardiac vs non-cardiac cause
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3
Q

Discuss ejection fraction in heart failure

A
  • Ejection fraction is the volume ejected with each heartbeat expressed as a % of the EDV
  • Echo is used to calculate ejection fraction – divide stroke volume by the EDV
  • EF should be >50% in a healthy person
  • HF can occur with preserved or reduced ejection fraction
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4
Q

Classical presentation of heart failure

A
  • Nocturnal breathlessness and swollen legs + cough
  • SOB: important to know when it happens, on exercise? Only at night? Any wheeze?
    • Differentials: COPD, PE, ischaemic heart disease
  • Bilateral swollen legs: suggests systemic issue
  • Cough: when? Productive?
    • Classic in HF is white frothy sputum
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5
Q

What is chronic heart failure?

A

Collection of symptoms and signs caused by impairment to the pumping function of the heart

  • Ventricular contraction impairment causes systolic dysfunction and reduced ejection fraction = HF with reduced ejection fraction
  • Impairment of ventricular filling/ relaxation causes diastolic impairment = HF with preserved ejection fraction
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6
Q

What is the pathway of management of a patient who is acutely unwell with heart failure?

A

Depends on patient’s haemodynamic state and clinical stage

  • Patient sent to coronary care unit/ HDU
    • Loop diuretic to remove excess fluid
    • IV morphine to reduce stress
    • IV GTN to accommodate fluid
  • Initial, non-pharm treatment:
    • Sit patient upright to improve ventilation-perfusion
    • Oxygen if hypoxic (<94%)
    • Non-invasive ventilation if patient has pulmonary oedema + significant dyspnoea and hypoxia
    • Monitor urine production, U&E for kidney function
    • Weight patients daily
    • Restrict fluid intake
    • Invasive ventilation may be needed
  • Once stable: commence on chronic HF medication
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7
Q

Outline the American heart association stages of HF

A
  • A: high risk without structural heart disease or symptoms
  • B: structural heart disease without signs or symptoms
  • C: Structural heart disease with current or prior symptoms
  • D: refractory heart failure requiring specialist intervention
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8
Q

Epidemiology of heart failure

A
  • Affects 1% in Europe
  • 5yr survival 50%
  • Most common cause of hospitalisation in those 65+
  • Takes up 2% annual NHS budget
  • Average hospital stay is 7 days
  • Average age diagnosis = 76
  • Reduced ejection = more common in men
  • Preserved ejection fraction = more common in women
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9
Q

Causes of heart failure

A
  • Ischaemic heart disease = most common cause of reduced ejection fraction
  • HTN = most common cause of reduced ejection fraction
  • Mechanical/ structural cardiac defects
  • Diseases which increase demand on heart e.g., haem conditions, inflammation, infection, malignancy
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10
Q

How can heart failure be prevented?

A
  • Encourage patients to improve lifestyle
  • Primary prevention of HF
    • Early recognition of CV risk factors to reduce ischaemic heart disease which leads to HFREF and LV hypertrophy which causes HFPEF
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11
Q

Discuss the pathogenesis of heart failure

A
  • Different mechanisms depending on whether ejection fraction is preserved or not

HFREF – poor pump ability

  • Caused by an abnormality of systolic contraction
  • MI >> cell death and necrosis >> scar formation
    • Scar tissue doesn’t contribute to pumping action so stroke volume is reduced
  • Increasing venous return stretches the myocardium beyond optimum tension-length relationship and this reduces the contractile force of the heart

HFPEF – stiff heart that won’t fill, doesn’t relax

  • Caused by abnormality of cardiac relaxation
  • Chronically increased afterload as a consequence of HTN leads to compensatory LV hypertrophy
  • Hypertrophy = thick ventricular wall which causes stiffness and reduced compliance meaning to myocardium doesn’t relax during diastole
  • Stiffness can also be caused by microvascular ischaemia which results in increased LV end-diastolic pressure, inadequate filling of the ventricle and reduced stroke volume

Both HFREF and HFPEF reduce CO

  • This causes up-regulation of sympathetic NS and RAAS because they try to increase venous return and CO by increasing peripheral resistance
  • At first this is beneficial but eventually speeds decline in function
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12
Q

Clinical features of heart failure

A
  • Ankle swelling
  • Light-headedness
  • Lethargy
  • Weight loss + cachexia
  • Lung crepitations
  • Tender hepatomegaly
  • Low mood

Right sided heart failure symptoms

  • Failure to clear blood coming from the systemic circulation = rise in systemic venous pressure = peripheral oedema and raised JVP

Left sided heart failure symptoms

  • Increased pressure in the LA and pulmonary circulation causing pulmonary congestion with dyspnoea, orthopnoea and paroxysmal nocturnal dyspnoea
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13
Q

Classification of heart failure based on breathlessness: NYHA

A
  • Class I: no symptoms
  • Class II: mild symptoms, breathless while climbing hill/ stairs
  • Class III: mild symptoms, comfortable at rest
  • Class IV: severe symptoms, breathless at rest
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14
Q

Diagnosis of chronic heart failure

A
  • ECG, CXR, bloods and echo
  • Bedside
    • ECG: evidence of ischaemic heart disease: Q waves, T wave inversion, BBB
    • LV hypertrophy – esp. HFPEF
    • Prolonged QRS
    • Rhythm abnormalities: AF. Paroxysmal ventricular arrhythmias
    • Normal ECG makes HF diagnosis unlikely
  • Bloods
    • BNP: concentrations increase with severity and fall with successful treatment
    • Rule out anaemia as a cause of dyspnoea
    • U&E: assess renal function
    • LFTs: right sided failure = congestion = abnormal LFTs
    • Lipids: hyperlipidaemia causes ischaemic heart disease
    • Glucose: check for DM
  • Imaging
    • CXR findings in HF
      • Kerley B lines: pulmonary oedema
      • Batwing shadowing
      • Pleural effusions
      • Increased heart size
  • Special tests
    • Echo: transthoracic
    • Measure ejection fraction
    • Look for valve disease
    • Measure chambers
    • Identify LV hypertrophy
  • 6 min walk test to assess functional capacity
  • Exercise testing
  • Coronary angiography to assess coronary artery disease
  • Cardiac MRI to assess ventricular volumes and wall thickness, chamber dimensions and look for ischaemia, may show presence of scar tissue
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15
Q

Management of chronic heart failure

A
  • Aims:
    • Treat cause
    • Improve prognosis
    • Improve QoL
    • Reduce symptoms
    • Reduce aggravating factors
  • Lifestyle: exercise, smoking, salt and water restriction in advanced cases, vaccination against flue, driving implications (have to tell DVLA if any symptoms which can affect driving or if you’re an HGV/ bus driver the DVLA need to be informed and patient must stop driving while DVLA investigate)
  • Medication:
    • RAAS antagonists – ACEi and ARBs
    • HFPEF: no medication that improves prognosis, nothing that promotes the heart to relax in a way that would be beneficial because we can’t only promote relaxation during diastole…
      • Treating the underlying cause – HTN, DM, weight loss, statins, diuretics to remove fluid, beta blockers to reduce HR and increase diastole/ filling time
    • HFREF
      • 1st line = b-blockers and ACEi
    • Symptomatic:
      • Loop + thiazide diuretics
      • Digoxin to control ventricular rate in patients with AF
      • Avoid all calcium channel blockers other than amlodipine because they depress cardiac function and worsen symptoms
      • Treat depression – 3x more common in HF
  • Devices
    • Implantable cardioverter defibrillator for HFREF patients at risk of ventricular arrhythmias
  • Surgery: valve repair/ replacement
    • CABG
    • LV restoration
    • Insertion of LV assist device
    • Heart transplant: only curative option
      • Contraindicated in renal failure, elderly, pulmonary arterial HTN
  • Prognosis
    • Poor: 35% die within 12 months
    • 50% die within 5 years
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16
Q

Discuss acute heart failure

A
  • Sudden onset of symptoms and signs as a result of impaired cardiac function
  • Typically affects patients in 70s, 30% have no heart hx, 60% have known ischaemic heart disease

Causes

  • De novo: MI, acute valve dysfunction, arrhythmia, cardiac tamponade
  • Chronic HF > acute on chronic HF where mechanisms maintaining CO become overwhelmed
    • Negatively inotropic drugs
    • Poor adherence to medication
    • Significant illness – heart has to work harder and eventually cannot compensate
    • Thyroid dysfunction: mainly hypothyroidism
17
Q

How can acute heart failure be prevented?

A
  • Frequent monitoring of disease progression
  • Encourage medication adherence
  • Manage illnesses that can exacerbate HF
18
Q

What are the clinical features of acute heart failure?

A
  • Fatigue, oedema, cough, SOB with significant orthopnoea
  • Signs; tachypnoea, tachycardia, HTN, 3rd heart sound
  • Severe presentations are usually due to left sided failure which causes pulmonary oedema >> reduced sats and added sounds on chest auscultation
  • Patients often have signs of right-sided decompensation inc. raised JVP and peripheral oedema
  • ECG changes non-specific
  • CXR: pulmonary oedema
  • Urgent echo to identify cause esp. if new-onset HF
19
Q

Are calcium channel blockers used for heart failure?

A

Calcium channel blockers, with the exception of amlodipine, should be avoided in heart failure as they can further depress cardiac function and exacerbate symptoms