Session 10: Heart Failure

Question 1

Define heart failure.

Answer 1

Inability of the heart to meet the demands of the body i.e. deliver a blood volume (carrying oxygen/glucose etc) that allows body tissues to function as required. Clinical syndrome of reduced cardiac output, tissue hypoperfusion, increased pulmonary pressure and tissue congestion.

Question 2

What structures of the heart might be affected leading up to heart failure.

Answer 2

Chamber size + defects in septum, one-way valves and functioning muscles.

Question 3

Most common cause of heart failure. Other causes

Answer 3

Most common is ischaemic heart disease (coronary heart disease) due to myocardial dysfunction like through fibrosis or remodelling of the muscle. Other causes: Hypertension Aortic stenosis Arrhythmias Other valvular or myocardial structural diseases whether acquired or congenital Cardiomyopathies like hypertrophic or dilated heart Pericardial disease Very rarely: Can occur in case of a grossly elevated demand on cardiac output like in sepsis, severe anaemia or thyrotoxicosis (hyperthyroidism) which is called high output heart failure.

Question 4

How is the ability of the heart to meet the demands of the body measured?

Answer 4

By cardiac output: CO = SV x HR SV = EDV - ESV

Question 5

What is stroke volume?

Answer 5

The volume of blood that the heart pumps out per beat. EDV - ESV.

Question 6

What influences stroke volume? In what way?

Answer 6

Increase in Pre-load increases SV Increase in myocardial contractility increases SV Increase in after-load decreases SV

Question 7

What is pre-load? Why does it increase SV?

Answer 7

The volume of the ventricle at the end of diastole which increases the stretch on the ventricle just before contraction.

Question 8

What is after-load? Why does it decrease SV?

Answer 8

The total peripheral resistance. Because the heart has to pump against a higher resistance, which makes it harder to do so.

Question 9

Explain Frank-Starling’s law.

Answer 9

The more ventricular distension during diastole => the greater volume ejected (SV) during systole.

This is due to the intrinsic property of the cardiomyocytes. The greater they are stretched the greater their force of contraction (to a certain point).

Question 10

How does Frank-Starling’s curve vary depending on inotropic state of heart?

What increases contractility?

Answer 10

The contractility of the heart can increase with increased sympathetic activity. This will lead to the curve shifting upwards and to the left which means that there is a greater cardiac output for a given LVEDP/volume.

Question 11

What can reduce cardiac output?

Answer 11

Reduced preload

Reduced contractility

Increased afterload

Question 12

Why might cause a reduced preload (reduced EDV)?

Answer 12

The impared filling of the ventricle during diastole. This means there could be something wrong with the ventricles, they might be too small or too stiff for example.

It can also be caused by a defective valve causing the ventricles to not fill properly.

Question 13

Why would a reduced contractility cause reduced SV?

Answer 13

Whem the muscle isn’t able to produce same force of contraction for a given volume in the ventricle anymore.

Can happen after an MI.

Question 14

Why would an increased afterload cause reduced SV?

Answer 14

The pressure against which the ventricle have to pump will be greater meaning that it will be harder for them to do so as well.

This can happen in e.g. aortic stenosis or chronic severe hypertension.

Question 15

To put it in simple terms. Why might a heart fail?

(2 ways)

Answer 15

Due to a filling problem.

Du to an ejection (contractility) problem.

Question 16

What is a filling problem?
Give example for filling problems.

Answer 16

When the ventricular volume/capacity for blood is reduced so the space available in the ventricle to receive blood is reduced (EDV) so the preload will be reduced. A filling problem is a diastolic problem.

This can happen if the ventricular chambers are too stiff/not relaxing enough or if the ventricular walls hypertrophy.

Can also happen in e.g. mitral valve stenosis.

Question 17

What is an ejection problem?

Give example of ejection problems.

Answer 17

When the heart can’t pump with enough force for a given EDV. The space available in the ventricles is not reduced but poor ventricular contraction so unable to empty as well. Ejection problem is a systolic problem.

This can happen if the muscle wall of the ventricle is too thin or has fibrosed after an MI or chronic ischaemia.
If the chambers have enlarged and have overstretched sarcomeres.
If there is an abnormal or uncoordinated myocardial contraction like in arrhythmias.

Question 18

What is ejection fraction?

Answer 18

(EDV-ESV)/EDV

It is the fraction of blood that is pumped out of the ventricle. Because the ventricle don’t empty all together we are left with a fraction of it which is pumped out.

Question 19

How can heart failure be classified according to ejection fraction?

Answer 19

It can be a heart failure with reduced ejection fraction also called HFrEF (huffruff)

It can be a heart failure with preserved ejection fraction also called HFpEF (huffpuff)

Question 20

Explain HFrEF.

What is the problem in HFrEF?

Answer 20

A reduced ejection meaning that the ventricle fills properly, however it can’t eject the sufficient amount needed.

This means that that there is a systolic dysfunction i.e. contractility problem.

This is the most common type.

Question 21

Explain HFpEF.

What is the problem in HFpEF?

Answer 21

There is a preserved ejection fraction. This means that the fraction will still be the same so it might not look like there is any problem with the heart, however the fraction only tells you how much of the blood was emptied out of the ventricle. So if you start out with a smaller amount of blood in the ventricle at EDV and the fraction is still around 60% the stroke volume might still be much lower (EDV-ESV) where as (EDV-ESV)/EDV is still fine.

E.g. 60/120 is a fraction of 50% where as 40/80 is also.

It means there is a problem with the filling of the ventricle and a diastolic dysfunction.

Question 22

How can you classify heart failure depending on the ventricles involved?

What is most common?

Answer 22

Whether it is a left ventricle heart failure or if it is right ventricle.

It could also be both.

Most common is left ventricle heart failure.

Question 23

Most common cause of right ventricular heart failure.

Answer 23

Left ventricular heart failure.

This means that the most common cause of biventricular would also be left ventricular heart failure.

Question 24

What is biventricular heart failure called in a more common manner?

Answer 24

Congestive heart failure.

Question 25

Can right ventricular heart failure occur in isolation (without involvement of LV HF)? If so, how?

Answer 25

Yes. It might occur as secondary to chronic lung diseases (cor pulmonale).

Question 26

How would Frank-Starling's Curve change in heart failure of contractility impairment? (Left ventricle). How would an increased LV filling impact the curve? Consequence of increased filling (LVEDP).

Answer 26

Increased left ventricle filling in a healthy heart leads to a big increase in cardiac output. However in a failing heart it leads to a very little increase and will much sooner lead to a worsening cardiac output as the curve dips due to impaired contractility. This means that an attempt to increase LVEDP can result in falling cardiac output and lead to pulmonary congestion.

Question 27

Explain how the body can react to a failing heart.

Answer 27

A reduction in cardiac output leads to a fall in blood pressure. This will either stimulate the sympathetic nervous system, or the RAAS.

Question 28

Explain how heart failure and the sympathetic nervous system work together.

Answer 28

Decrease in cardiac output leads to a decrease in blood pressure. This causes baroreceptor in e.g. carotid sinus to react and increase the sympathetic drive. This causes an increase in heart rate and in peripheral resistance which will increase the afterload. This also increases cardiac work.

Question 29

Expain how heart failure and RAAS work together.

Answer 29

Decreased cardiac output leads to a decrease in blood pressure. Renal perfusion decreases which makes the juxtaglomerular cells in the kidneys to think that the blood pressure is too low and we need the heart to beat more. The juxtaglomerular cells release renin which activates RAAS. Angiotensin II is eventually formed and this increases circulating volume due to NA+ and water retention via aldosterone. It also stimulates ADH to increase water retention. Also causes vasoconstriction. Also enhances sympathetic activity. All of these together causes an increase in preload and in afterload and will increase cardiac work.

Question 30

Why might the activation of RAAS and the sympathetic nervous system be helpful in a heart failure?

Answer 30

This is because there is an increase in cardiac demand and this leads to further reduction in stroke volume and further deterioration.

Question 31

What effects might a long-term activation of the sympathetic nervous system and angiotensin II have on the heart?

Answer 31

Cardiotoxic effects.

Question 32

General signs and symptoms of heart failure.

Answer 32

Fatigue/lethargy Breathlessness (Leg swelling in some cases) Oedema (pulmonary and peripheral (lower limbs))

Question 33

Symptoms depending on left vs right HF.

Answer 33

Question 34

Explain why a patient with heart failure might experience oedema.

Answer 34

This is because of the formation of tissue fluid. It is dependent on the gradient between the hydrostatic and the oncotic pressure. In a normal healthy person the hydrostatic pressure would be high in the arterial circulation and the arterial end of the capillaries meaning the net movement of fluid will be into the interstitium as the hydrostatic pressure \> oncotic pressure. As the blood travels to the venous end of the capillaries and to the venules the hydrostatic pressure will be much lower and oncotic pressure \> hydrostatic pressure meaning that fluid will move back into the venule end and fluid will not be retained. In a failing heart the venous pressure can increase and therefore also increase the hydrostatic pressure at the venule end. If the hydrostatic pressure increases this means that the difference between the hydrostatic pressure and the oncotic pressure will be much smaller. Since the oncotic pressure doesn't change. This means that there is less fluid coming back into the venules and instead stay in the interstitium. This causes oedema.

Question 35

What is an indication of raised jugular venous pressure? How can it be examined.

Answer 35

You examine the right internal jugular vein and see if it protruding any. If there is a distention of the right internal jugular this can be used as a direct reflection of the pressure in the right side of the heart. This means that raised jugular venous pressure is an indication of right ventricular heart failure.