Heart Failure

Question 1

What is the most common cause of heart failure? [1]

Answer 1

Coronary arterial disease

Question 2

What are the 3 different classifications / types of heart failure?

Answer 2

1. Left ventricular systolic dysfunction (LVSD, known as HFrEF): where EF is less than 40%
The EF is low enough to not require further signs or symptoms for diagnosis

2. Heart failure with mildly reduced LV function (HFmrEF): Where EF is 40-49%
Also requires:
Elevated naturietic peptides
One of: structural heart disease OR diastolic dysfunction

3. Heart failure with mildly reduced LV function (HFmrEF): Where EF is >50%
Also requires:
Elevated naturietic peptides
One of: structural heart disease OR diastolic dysfunction
.

Question 3

What are 4 causes of heart failure? [4]

Answer 3

Coronary artery disease: myocardial ischaemia or MI (as that part of the heart wont be working)

Hypertension: get left ventricular hypertrophy (LV stiffened and can’t relax)

Cardiomyopathy: dilated cardiomyopathy: reduces EF, hypertrophic cardiomyopathy leads to LV thickening, inflammatory disorders of LV, tachyarythmias (e.g. chronic afib will lead to heart failure)

Valvular heart disease: aortic and mitral regurgitation lead to LV dilatation and LV failure.

Question 4

Why might a patient develop acute decompensation heart failure and therefore present with significant symptoms? [4]

Answer 4

Cardiac arrhythmias (e.g., AF):

Hypertension

Anaemia

Infections

Question 5

What symptoms would someone with heart failure present with? [3]

What else do you need to do if suspect heart failure and why? [1]

Answer 5

Shortness of breath

Ankle oedema

Fatigue

Also need to conduct an ECHO as the above are very non-specific

Question 6

Explain why heart failure causes the following symptoms:
1. Sweating
2. Ankle oedema
3. Fatigue

Answer 6

1. Sweating: increased sympathetic activity & tachycardia
2. Ankle oedema: Left heart failure causes fluids in the lungs: oedema. Right heart failure causes back flow to rest of body: JVP; ankle oedema; ascites

3.Fatigue: reduced cardiac output means can’t perfuse organs and periphery very well. causes cool skin and peripheral cyanosis

Question 7

Which investigations may you undertake to ID heart failure?

Answer 7

Detailed history and exam

If previous MI: Echo: Ventricles should appear the same size, if not suggests heart failure (systolic or diastolic). If appear ok, heart failure unlikely.

If no previous MI: Check BNP levels.
If raised: have an Echo and repeat above.
If not raised, heart failure unlikely

CXR: Look for pulmonary oedema pulmonary congestion (upper lobe blood diversion)

ECG

Question 8

Explain why heart failure increase BNP levels and how BNP works [3]

Answer 8

BNP: B-type natriuretic peptide

Secreted by myocardial cells in response to raised left atrial pressure. [1]

Works by promoting natriuresis (lose Na: lose H20) & vasodilatation; both reduce fluid in heart [1]

This occurs by inhibiting ADH and aldosterone release [1]

Question 9

What are the two different physiological mechanisms that drugs target when treating heart failure?

Answer 9

Sympatho-adrenal activation

RAAS

Question 10

How does targeting sympatho-adrenal activation and RAAS systems cause an increase in contractile function?

Answer 10

Question 11

Which drugs would you use to treat:

a) systolic and diastolic failure?

b) systolic failure

Answer 11

Systolic and diastolic failure
Treat aetiological and aggravating factors (e.g. MI / anaemia etc / CAD)
Treat fluid retention with diuretics (want net loss of fluid)

Systolic failure (reduced EF)
- ACE-Is (all grades of heart failure). Can cause dry cough.
- ARBs (if ACE-Is cannot be tolerated)
- beta-blockers (all grades of heart failure)
- spironolactone (NYHA grade III and IV only) treats oedema
- cardiac resynchronization therapy (CRT) (pacemaker: causes two sides of heart to pump together – increases EF)
- ± ICD (implanted cardiac defib: monitors heart rhythm – if goes into VF or VT, will give a shock into normal rhythm)
- ARB/neprilysin inhibitor (neprilysin inhibits breakdown of BNP)
- SGLT-2 inhibitors (ESC guidelines 2021).

Question 12

How would you decide who gets cardiac resynchronisation therapy?

Answer 12

Optimal medical therapy before consideration of devices. E.g adapt doses. Need continuous monitoring at heart failure clinics (in the community)
Sinus rhythm
LVEF less than 35%
NYHA III/IV symptoms (bad symptoms)
QRS prolongation – if prolonged suggests that L/R ventricle aren’t synchronous (probably due to R or L BBB)
less than 150msec
less than 120msec + mechanical dyssynchrony on echo.

Question 13

How would you treat someone with acute failure?
a) immediately?
b) after stabilisation?
c) ongoing management?

Answer 13

Immediately:
Pharmalogical: O2 & duiretic
Non Pharmalogical: ventilation; ultrafiltration

After stabalisation: ACE-I/ARB, beta-blocker, aldosterone inhibitor

Ongoing management: Valve surgery; revasc; transplant

Question 14

Name 4 complications of heart failure

Answer 14

Intravascular thrombosis
pulmonary embolism
systemic embolism

Infection
chest infection
ulcerated cellulitic legs

Functional valvular dysfunction
MR, TR

Multi-organ failure
renal failure
liver failure

Cardiac Arrhythmias
AF
VT VF

Sudden death

PROB. OF SURVIVAL ASSOCIATED WITH NHYA CLASS SYMPTOMS

Question 15

Name 4 risk factors for heart failure [4]

Answer 15

Risk factors:

65 and older African descent
Men (due to lack of protective effect provided by oestrogen resulting in the early onset of IHD in men
Obesity
Previous MI
Arrythmias
Liver damage
Toxins (fags / alcohol / cocaine)

Question 16

Explain how the RAAS system usually works

Answer 16

Angiotensinogen is converted to angiotensin I under the action of renin

Angiotensin I is then converted to angiotensin II under the act of angiotensin converting enzyme (ACE)

Angiotensin II then:

i) proximal tubule: Increases Na+ reabsorbtion, which increases blood flow, which increases BP
ii) adrenal cortex: increases aldosterone, which causes increase Na+ & H20 reabsorbtion in distal tubule, increase bloodflow and BP
iii) systemic arterioles: binds to GPCR = artriolar vasoconstriction = increases BP
iv) brain: stimules release of ADH = increase Na reabsorbtion

This results in the increased volume of the blood which in turn increases blood pressure and thus venous pressure which in turn increases pre-load thereby increasing the stretching of the heart and thus force of contraction and thus stroke volume and thus cardiac output

Question 17

How does RAAS system work in heart failure?

Answer 17

RAAS increases force of contraction the cardiac myocytes, which requires more energy and thus more blood.

However in heart failure (which is most commonly caused by ischaemic heart disease) there will be no increase in blood and thus the cardiac myocytes will die resulting in a decrease in force of contraction and thus a decrease in stroke volume and a decrease in cardiac output

Question 18

How does sympathetic system work to increase BP under normal conditions?

Answer 18

When baroreceptors (located in the** arterial wall of the aorta, carotid and in the heart walls and major veins**) detect a drop in arterial pressure or an increase in venous pressure (due to back flow of blood) they stimulate **sympathetic activation **

This increases the force of contraction (positively inotropic) of the heart (which increases stroke volume) as well as heart rate - both resulting in an increase in cardiac output

Question 19

How does sympathetic system work to increase BP under heart failure?

Answer 19

Heart failure there is chronic sympathetic activation which results in the receptors being acted on by the sympathetic system to down regulate.

Causes overall less receptors to be acted on, meaning the effect of sympathetic activation is diminished and cardiac output stops increasing in response to sympathetic activation