Chronic Heart Failure

Question 1

What are the 2 types of dysfunction which can be present in HF? What are the associated precipitating events?

Answer 1

Systolic dysfunction= impaired LV contraction
-decreased CO 
-EF< 40%
Causes:
-IHD
-MI
-Cardiomyopathy 

Diastolic dysfunction= impaired LV relaxation due to stiffening 
-increased filling pressures 
-EF> 50%== HFpEF (heart failure with preserved ejection fraction)
Causes:
-ventricular hypertrophy 
-constrictive pericarditis 
-tamponade 
-restrictive cardiomyopathy 

Both lead to state of chronic back pressure

Question 2

How does the heart try to compensate for the dysfunction present in HF to try and maintain CO?

Answer 2

Dilation

Hypertrophy

Increased HR via Ad

RAAS activated

ANP released to decreased BP via diuresis

Question 3

What are the causes of LVF?

Answer 3

IHD

Valvular heart disease- aortic stenosis

MI

Cardiomyopathy

Hypertension

Arrthymias i.e AF

Question 4

How is someone with LVF likely to present?

Answer 4

SOB- worse on exertion i.e. poor exercise tolerance
Fatigue
Cough- producing frothy white/pink sputum
Orthopnoea- ask number of pillows require
PND (paroxysmal nocturnal dyspnoea)
Wheeze= cardiac asthma (bronchiole wall thickening due to increased back pressure into bronchiole veins via LA
Peripheral oedema

Question 5

Why do people with LVF produce frothy white/pink sputum?

Answer 5

Increased pressure in LA causes increased back pressure across pulmonary veins and capillaries. The fenestrated capillaries in lungs are prone to bursting with increased pressure which leads to small amount of blood accumulating in the alveoli

Question 6

What is paroxysmal nocturnal dyspnoea (PND) and why does it occur in people with HF?

Answer 6

Waking up in night with acute SOB, cough and wheeze

Fluid accumulates across large surface area of lungs when person lies flats= reduces area of lung able to work effectively

Resp centre becomes less responsive to resp rate and effort during sleep so person can develop more significant hypoxia before being woken up

Decreased adrenaline circulating when sleeping meaning myocardium is more relaxed= reduces CO

Question 7

How is HF diagnosed?

Answer 7

Clinical diagnoses= evidence of signs and symptoms inline with HF

BNP blood test = elevated
-released in response to volume expansion and increased wall stress of cardiac myocytes

ECG= can indicate the cause i.e. historic MI or hypertrophy

CXR

Echocardiogram
-can assess the ejection fracture to differentiate between the different forms of HF

Question 8

What is the first line medical treatment for HF? What are the aims of this treatment?

Answer 8

ABAL

ACEi= ramipril

• considered in all LV systolic dysfunction
• ARB can be used if patient has problem with cough

Betablocker= bisoprolol/carvedilol
-start slow and go slow (want to be cautious with changes in dosage )

Aldosterone antagonist= spironolactone (when A+B not controlling)

Loop diuretic= furosemide (improves symptoms)

Aim:
-decrease cardiac work but decreasing the rate of the heart with beta-blockers and by decreasing the afterload by removing any excess retained fluid

Question 9

Why do U+Es need to be closely monitored in HF patients?

Answer 9

ACEi and aldosterone antagonists can lead to electrolyte disturbances

Question 10

What signs on examination would be indicative of HF?

Answer 10

Cold peripheries/cyanosis 
Narrow pulse pressure 
Peripheral oedema 
Displaced apex beat due to LV dilation 
RV heave= pulmonary hypertension 
Murmurs associated with valve disease

Question 11

What ECG changes can be found in HF?

Answer 11

Prolonged QRS
Left axis deviation= due to associated LV hypertrophy
Left ventricular hypertrophy= increased height of QRS complexes (>25 combined)
LBBB

Question 12

What signs on CXR would indicated HF?

Answer 12

A= alveolar oedema (looks like bat wings)

B= Kerley B lines due to interstitial oedema

C= cardiomegaly (globular heart)

D= dilated prominent upper lobes veins (upper lobe diversion)

E= pleural effusion

Question 13

What does low-output mean in context of HF? What are the causes of low-output heart failure?

Answer 13

Decreased CO without ability to increase CO with normal exertion

Excessive preload

• mitral regurgitation
• fluid overload i.e renal failure

Pump failure

• systolic +/- diastolic HF
• decreased HR when on beta blockers or post-MI
• negative ionotropic antiarrhythmics

Chronic excessive afterload

• aortic stenosis
• hypertension

Question 14

What is the different consequences for excessive preload and excessive afterload on heart failure?

Answer 14

Preload= ventricular dilatation
-leads to exacerbation of pump failure

Afterload= ventricular hypertrophy
-leads to stiffening of ventricle wall which leads to diastolic dysfunction

Question 15

When is digoxin used in treatment of heart failure?

Answer 15

In patients with LVSD who are still symptomatic after treatment with ACEi and beta blockers or in patients who have AF

Question 16

Where is BNP secreted from and what is it’s role? Why is it investigated in suspected HF? What is the diagnostic criteria for BNP?

Answer 16

Secreted by ventricular myocardium (secretion closely related to ventricular pressure)

Role:

• increase GFR and decreased renal absorption of Na+ which reduces the preload
• relaxation of SM to decreased preload

Sensitive bio-marker to distinguish heart failure from the other possible causes of dyspnoea

>100ng/L= indicates HF
<50ng/L= “rules out” HF

Question 17

Apart from heart failure, what other conditions can cause a rise in BNP?

Answer 17

Tachycardia 
Cardiac ischaemia 
COPD
PE
Renal disease 
Sepsis 
Diabetes 
Hepatic cirrhosis

Question 18

Why is it important to monitor Hb levels in HF patients?

Answer 18

Need to determine if have anaemia:

• anaemia can induce high output state which can exacerbate HF
• associated with high mortality if untreated/managed

TX:
-iron infusion

Question 19

How is the management of HF adjusted when patient has CKD?

Answer 19

Need to change form which diuretics administered to reduce the strain on the kidneys:
-move from oral furosemide to infusion

Question 20

How is ARNI used in HF alongside the 1st line treatment (ABAL)? What are the possible SE?

Answer 20

ARNI= Entresto= contains 2 active components= Valsartan + Sacubitril

• valsartan= angiotensin blockers
• sacubitril= neprilysin inhibitor= prevents the breakdown of natriuretic peptides (BNP) (i.e. inhibits normal action of neprilysin) = increases Na+ and H2) excretion to reduce blood volume and reduce blood pressure

Therefore= decreases strain on heart

Use:
-used in chronic HF with reduced ejection fraction or NYHA II, III, IV

SE:

• renal impairment
• hypotension

Question 21

How can SGTL2 drugs be used in HF management along side 1st line treatment?

Answer 21

Have been found to decreased mortality of HF patients

• block glucose reabsorption in PCT
• glucose absorption paired with sodium absorption so decreasing glucose absorption leads to increased sodium excretion which can lead to increased water loss= can act to lower BP and decreases strain on heart

Question 22

What is the NYHA scoring system used in HF?

Answer 22

New York Heart Association classification of severity of chronic HF

I= no physical limitation of ADL
II= slight limitation of ADL i.e. mild SOB when walking
III= marked limitation in ADL i.e. breathless when getting dressed, cleaning, putting the bins out 
IV= breathless at rest

Question 23

What is CRT and what role does it have in management HF?

Answer 23

Cardio re-synchronisation therapy

Used in patients with left ventricular systole dysfunction= the dysfunction in contraction can lead to symptoms such as breathlessness (patients with congestive HF)

It is placed in the coronary sinus in HF