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CVS 2023 > heart failure - treatment and management > Flashcards

heart failure - treatment and management Flashcards

1
Q

Classification of heart failure

A

NYHA functional classification (class 1-4)

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2
Q

Class 1 heart failure

A

No symptomatic limitation of physical activity

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3
Q

Class 2 heart failure

A

Slight limitation to physical activity

  • Ordinary physical activity gives symptoms
  • No symptoms at rest
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4
Q

Class 3 heart failure

A

Limitation to physical activity

  • less than ordinary activity = symptoms
  • no symptoms at rest
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5
Q

Class 4 heart failure

A

Inability to carry out any physical activity without symptoms

  • may have symptoms at rest
  • discomfort increases with any degree of physical activity
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6
Q

Investigations heart failure

A

Do they have heart failure (history, examination, investigations)

What sort of heart failure do they have? (HFrEF, HFpEF, valvular, RV heart failure, high output heart failure)

What is causing heart failure? (ischaemic heart disease, hypertension, viral ETOH (ethanol alcohol))

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7
Q

What is HFrEF? usually

A

Left ventricular systolic dysfunction

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8
Q

What is HFpEF? usually

A

Stiff left ventricular (diastolic - not called this anymore)

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9
Q

Symptomatic treatment heart failure

A

Furosemide (reduce fluid levels)

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10
Q

Which heart failure is prognosis treatment effective for?

A

HFrEF

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11
Q

Prognosis treatments (drugs)

A 
ACE inhibitors
Angiotensin receptor blockers
Beta blocker 
Mineralocorticoid receptor antagonist (eg spironolactone)
SGLT2 inhibitors (diabetes)
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12
Q

New prognosis drugs treatment

A

Sacubitril valsartan

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13
Q

Other prognosis treatment (no drugs)

A

Implantable cardioverter defibrillator (control arrhythmias)

Biventricular pacemaker - make rhythm better speed if heart too slow

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14
Q

Immediate treatment heart failure presentation

A

Furosemide
O2 (if hypoxic)
Respiratory support - if needed eg CPAP
IV nitrates, morphine

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15
Q

Problem with beta blockers

A

Slow heart rate in already low cardiac output situation

If heart rate is keeping alive (ie stroke volume is very small) = BAD

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16
Q

What drugs may be needed in atrial fibrillation?

A

Anti-coagulants (high risk of thrombus forming in atria)

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17
Q

What can CXR show in heart failure?

A 
Cardiomegaly
Upper lobe diversion (pulmonary veins dilated)
Fluid in fissure (boundaries of lung)
Pleural effusions
Kerley B lines (horizontal white lines)
18
Q

Furosemide

A

Immediate effects 30 mins peaking 60-90 mins

Higher doses needed in renal failure

19
Q

Monitoring furosemide

A

HR, BP, O2 CXR
Fluid balance (in vs out)
Hourly urine output
Daily weights (1kg weight loss per day)

20
Q

Left ventricular aneurysm ECG and Xray

A

Broad QRS lines (V shape)

Boot shaped heart x-ray

21
Q

Blood tests heart failure gold standard

A

NTpro-BNP

natriuretic peptide released in response to atrial/ventricular stretch from fluid overload
range varies with age/gender (atrial fibrillation can increase)

22
Q

Other blood tests heart failure

A

FBC (anaemic?)
U&E’s (renal function deteriorates in HF, Na+ K+ levels needed for medications)
LFT’s (hepatic congestion? = elevated)
Clotting (need anticoagulants?)
Thyroid, Vit D, CRP (is it heart failure from heart)

23
Q

Why do we get heart failure?

A

2 sides:
Dark side, makes things worse - RAAS system and baroreceptor sympathetic stimulation

Light side - Increase ANP and BNP (doesnt activate until TOO LATE)

24
Q

What does increase ANP and BNP cause?

A

Increase natriuresis - sodium excretion
Increase diuresis
Vasodilation
Decrease RAAS activity

25
Q

Sacubitril valsartan how does it work

A

Slows breakdown of natriuretic peptides - helps

26
Q

Key history questions heart failure

A 
Recent viral illness
Anabolic steroids
ETOH (alcohol)
Smoking
Family history
27
Q

Investigations heart failure

A

Echocardiogram

Stress Cardiac MRI/coronary angiogram (ischaemia?)

28
Q

What does RAAS do in heart failure?

A

Angiotensin 2 =
vasoconstriction
enhanced sympathetic activity
salt and water retention

29
Q

Drugs targeting RAAS

A 
ACE inhibitors (no angiotensin 2 produced)
ARB - blocks angiotensin acting on receptors
30
Q

What does RAAS and sympathetic activation overall result in?

A

Increased myocardial oxygen demand
Myocardial hypertrophy
Decreased contractility
Myocyte damage (direct cardiotoxicity of long term SNS activation)

31
Q

What does short term activation of SNS do?

A

Tachycardia
Increase cardiac contractility
Vasoconstriction

32
Q

What does long term activation of SNS do?

A

B adrenergic receptors are down regulated/uncoupled (no longer sensitive)

Noradrenaline then induces hypertrophy/myocyte apoptosis via a-receptors
Upregulates RAAS

33
Q

What do B blockers do?

A

Reduce HR
Reduce BP (and CO)
= reduced myocardial oxygen demand

Resensitise receptors (stop unwanted catacholamine effects)
Reduce mobilisation of glycogen
34
Q

Problem with Beta blockers?

A

Failing myocardium may be dependent on HR for cardiac output
If lowered could be detrimental

start low dose

35
Q

What is spironolactone (aldosterone receptor antagonist) used for?

A

When using ACE inhibitor and ARB therapy, aldosterone can ‘escape’ and return to normal concentrations
Blocks effects on receptor

36
Q

Biventricular pacemaker location

A

Lead in coronary sinus vein

Right atrium ventricle

37
Q

Biventricular defibrillator X-ray

A

Bright white coil/worm base of heart

38
Q

What is needed when treating HFrEF?

A 
Cardiac rehab
Multidisciplinary team
Patient education
Pallative care/transplant 
evidence based treatments
39
Q

Summary all investigations

A

Bloods (NTpro-BNP, FBC)
ECG
CXR
Transthoracic echocardiogram

Cardiac MRI (ischaemia/myopathy)
Coronary angiography (x-ray vessels)
Cardiomyopathy blood test screen (eg haemachromatosis)
Genetics

40
Q

HFpEF treatments

A

Control BP

Limited evidence spironolactone ?

41
Q

Valvular/structural treatments

A

Surgery to repair valve/replace

42
Q

When does RV failure occur?

A

Usually secondary to LV failure

If isolated could be chronic lung condition - refer to specialist

CVS 2023 (26 decks)

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