L20: Heart Failure investigation and management

Question 1

How is heart failure classified in functional terms?

Answer 1

Class I–> no symptomatic limitation in physical activity

Class II–> Slight limitation of physical activity

• -> Ordinary physical activity result in symptoms
• -> No symptoms at rest

Class III–> Marked limitation of physical activity

• -> Less than ordinary physical activity result in symptoms
• -> No symptoms at rest

Class IV

• -> Inability to carry out any normal physical activity without symptoms
• -> May have symptoms at rest
• -> Discomfort increases with any degree of physical activity

Question 2

What are the key questions to ask yourself when investigating heart failure?

Answer 2

Does the patient have heart failure? 
--> History and clinical examination?
--> Differential diagnosis?
What sort of heart failure does the patient have?
--> HFrEF (LVHD)
--> HFpEF 
--> Valvular/ structural defect
--> Right ventricular failure 
--> High output cardiac failure (anaemia or thyrotoxicosis)
What is causing the heart failure?
--> Ischaemic heart disease?
--> Hypertension?
--> Viral? 
--> Alcohol (ETOH)

Question 3

Why is it important we discover the cause of the heart failure?

Answer 3

Directs treatment

Symptomatic treatment the same but prognosis treatment different

Question 4

What is the symptomatic treatment of heart failure?

Answer 4

IV Furosemide

Question 5

What is the treatment for heart failure with reduced ejection fraction?

Answer 5

Cardiac rehabilitation/ community heart failure team
ACE/ARB
Beta blockers
Mineralocorticoid receptor antagonists (MRA) spironolactone
Sacubitril valsartan - (angiotensin receptor blockers–> vasodilation–> makes blood flow easier)
ICD/ Biventricular pacemaker (keeps HR normal)
Ivabradine (HR regulator), hydralazine (vasodilator), nitrate, IV iron, Coronary artery bypass graft

Question 6

What effect does IV furosemide have?

Answer 6

Causes venodilatory effects–> immediate–> reduced preload–> reduced work on heart–> clear fluid in the lungs–> symptomatically improves quickly
Also diuretic effects
Onset diuretic action 30 mins peaking at 60 to 90 minutes
Higher doses required in renal failure and reduced CO
–> Perfusion to the kidneys is reduced so need more drug to have the same effect
–> CO reduced also means more furosemide (affect over longer period of time) is needed to increase urine output

Question 7

What is it important to do when you give furosemide?

Answer 7

Monitor patient
Don’t want to over do it and release too much fluid
Don’t want to under do it
Monitor–> HR, BP, RR, pO2%, CXR
-Fluid balance, hourly urine output
- Daily weight (aim for 1kg weight loss per day)

Question 8

What other investigation will you want to carry out to determine the cause of heart failure?

Answer 8

ECG–> determine the cause of the heart failure
Chest x-ray–> show pulmonary oedema–> needs offloading
Echocardiogram–> see whats going on in the heart
Often difficult to determine if heart failure has caused decompensation or decompensation has caused heart failure

Question 9

What are the markers of left ventricular hypertrophy?

Answer 9

No methods are completely sensitive or specific
QRS complexes invading neighbouring complexes
R wave in V5 added to S wave in V3–> >70mV (good indicator)

Question 10

What blood tests would you want to carry out when investigating potential heart failure? Why?

Answer 10

1. NTpro-BNP–> naturetic peptide–> released in response to atrial/ventricle stretch due to fluid overload
   - -> Normal range varies with age and gender, in atrial fibrillation it can triple
2. FBC–> patient with HF often anaemic, may explain the symptoms
3. U and Es–> renal function often deteriorate in HF, Na+/K+ levels important for medication
4. LFTs–> May be elevated due to hepatic congestion
5. Clotting–> Important if considering anticoagulants
6. Thyroid function, vitamin D level–> alternative explanation for symptoms
7. CRP–> look for infection/ inflammation

Question 11

What is the most important blood test?

Answer 11

NTpro-BNP >2000 indicate HF, <400 probably not
Released in response to stretch in atrial and ventricles due to fluid overload
Neagtive predictive value 97% (probability that subjects with a negative screening test don’t have the disease)

Question 12

What is the negative impact of heart failure?

Answer 12

Body recognises that there is decreased in BP
Doesn’t recognise heart is weak
Automatic response to make the heart pump heart (increase contractility) and increase heart rate to increase the BP –> (neurohumoral response)
Kidneys also increase absorption of salt and fluid to increase BP (via RAAS)–> pt with HF reduce intake of salt and fluid

Question 13

What is the positive impact in heart failure?

Answer 13

Only kicks in when really high ANP and BNP–> too late
Increase excretion of Na+ and fluid
Reduce sympathetic nervous system activation–> increase vasodilation
Decrease RAAS

Question 14

How do you manage HF in a patient with a weak heart?

Answer 14

ACEI /ARB
Beta blocker- Ca2+
Mineralocorticoid receptor antagonist
Biventricular ICD

Question 15

Why don’t we commonly do coronary artery bypass surgery?

Answer 15

10 year data shows improvement

But earlier years not really any improvement (no real reduction in mortality)

Question 16

How do ACE inhibitors and angiotensin receptor blockers work?

Answer 16

Stop the conversion of angiotensin 1 to angiotensin 2
Prevents
–> aldosterone release–> reduced Na+ and H20 resorption
–> Prevents vasoconstriction–> reduces preload
–> Prevents enhances sympathetic activity–> stops heart rate increasing and force of contraction increasing

Question 17

How does sympathetic activation lead to myocardial damage?

Answer 17

Increase RAAS
Increases vasoconstriction
Increase heart rate and contractility
Increases direct toxicity on the heart

Question 18

Why is the sympathetic system employed?

Answer 18

Early compensatory mechanisms–> increase CO by increase contractility, vasoconstriction and increased heart rate (tachycardia)
Long term deleterious effects–> beta-adrenergic receptors down regulated/uncoupled
Increased NA–> cardiac hypertrophy, myocyte apoptosis and necrosis via alpha-receptors
Induce up-regulation of the RASS
Reduction in heart rate variability

Question 19

How do beta blockers work?

Answer 19

1. Reduce heart rate (cardiac beta receptor)
2. Reduce BP (reduce cardiac output)
   - -> reduce myocardial oxygen demand
3. Reduce mobilisation of glycogen
4. Negate unwanted effects of catecholamines

Question 20

Why do beta blockers have to be prescribe cautiously?

Answer 20

Failing myocardium maybe dependent on heart rate–> may cause decompensation
Initiate at low dose, titrate slowly, alter other medication

Question 21

What would a biventricular pacemaker do?

Answer 21

Pacemaker in right ventricle and left ventricle to restore synchronicity
Important in Left bundle branch block LBBB

Question 22

What is the best approach to take for people with heart failure due to a reduced ejection fraction?

Answer 22

Patient education–> help patient to understand what is wrong with them etc…
Multi-disciplinary team–> Dr, Nurses, consultants, physiotherapists
Cardiac rehabilitation
Evidence based treatment–> ACE/ARB, Beta blockers, MRA, ICD/ CRT-D
Pallative care and heart transplants (under 65s without co-morbidities)

Question 23

What is a key aspect to treating/ managing patients with heart failure?

Answer 23

Exercise

Patient should be getting moderately out of breath everyday