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
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
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
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
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
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
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
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
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
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
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
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
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
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
- CXR findings in HF
-
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
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
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
