Heart failure 1

Question 1

What is the definition of heart failure?

Answer 1

An inability of the heart to deliver blood (and oxygen) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increases cardiac filling pressures.

Question 2

What is the cause of a majority of heart failure cases.

Answer 2

Left ventricular systolic dysfunction - usually because of a prior heart attack.

Question 3

What is the group of heart failure patients who have normal ejection fractions

Answer 3

HFPEF heart failure with preserved ejection fraction. This is instead due to diastolic failure. During the ralaxation of the heart, the energy dependent relaxation of the heart muscle is impaired.

Question 4

What drug type gives the most benefit to patients with left ventricle systolic dysfunction?

Answer 4

Vasodilator therapy via a neurohumoral blockade (RAAS-SNS) and not via direct left ventricle stimulants.

Not LV stimulants because: After acute heart failure, CO is reduced. This activates the SNS and RAAS to try and support circulation. But this response is not beneficial to these patients.

Question 5

How does LVSD lead to excersise intolerance.

Answer 5

Reduced cardiac output means muscles are not perfused sufficiently.

Question 6

How does LVSD lead to a pulmonary odoema?

Answer 6

If CO is impaired, filling pressures begin to increase. The heart starts to dilate and there is backward pressure upstream of the ventricles. If there’s back pressure in the left ventricle there will be increased pressure in the left atria. As the left atria is connected to the pulmonary vein, this pressure will also increase, disrupting the balance of pressure across the lungs, potentially leading to a pulmonary odoema. More commonly, it causes breathlesness after exercise.

Question 7

What is the result of high right atrial pressure

Answer 7

This is connected to our venous system. It can cause jugular venous pressure increases (superior vena cava) and you are visually able to see the jugular vein.

When venous pressure increases as a result; the liver can grow from congestion, as well as ankle odoema.

Question 8

What effect does heart failure have on the frank starling curve.

Answer 8

As LVEDP increases there is very little benefit to CO

Question 9

What is the role of diuretics and venodilators in patients with HF

Answer 9

To dilate the veins and reduce LVEDP away from the point of pulmonary congestion, whilst maintaining CO above the level of hypotension.

Question 10

Which groups of diuretics are used for the treatment of heart failure

Answer 10

Loop diuretics and aldosterone antagonists.

Question 11

Give two examples of loop diuretics

Answer 11

Furosemide - huge diuresis

and Bumetanide - can be better absorbed when swelling of the gut is present in patients.

Question 12

Give two examples of potassium sparing diuretics

Answer 12

Spironolactone - has an oestrogen like effect and can cause enlargement/ pain in breast tissue. If that’s the case swith them to …. Eplerenone

Question 13

What are some adverse effects of diuretics

Answer 13

Hypovolaemia

Hypotension

Low serum K, Na, Mg, Ca

Erectile dysfunction

Raised uric acid

Imparied glucose tolerance.

Question 14

Give two examples of vasodilator therapies

Answer 14

Hydralazine and isosorbide di-nitrate

Both of these reduce mortality and improve LVEF

Question 15

Describe how the cardiac and systemic systems are in place to respond to heart failure

Answer 15

Draw out image.

Question 16

How does the body react to heart failure

Answer 16

As if the body was losing blood

1. Tachy cardia (increase CO)
2. Positive inotropic effect (increase CO)
3. Vasoconstriction (increase BP)
4. Sodium and water retention (Increase circulatory volume)

Question 17

What are the problems with the response in place to heart failure/ blood loss

Answer 17

1. Tachycardia - increased workload and oxygen demand on an already failing heart.
2. Positive inotropic effect - Increased workload and oxygen demand on an already failing heart
3. Vasoconstriction - Increased afterload and work/ oxygen demand
4. Na and water retention - Increased preload and odoema
5. Chronic adrenergic stimulation - myocyte toxicity and arrhythmia

Question 18

Give an example of an aldosterone antagonist

Answer 18

Spironalactone

Question 19

What drugs are used to prevent the conversion of angiotensin 1 into angiotensin II

Answer 19

ACE inhibitors

Ramipril, Perindopril, Trandolapril

Question 20

What are the 2 main advers effects of ACE inhibitors

Answer 20

Those related to reduced angiotensin II and those related to increased kinins (ACE metabolise kinins)

Reduced angiotensin II = hypotension, acute renal failure as angiotensin II maintains GFR pressure. Hyperkalaemia (aldosterone removes K), Teratogenic effects in pregnancy.

Kinins because ACE is mainly found in the lungs, therefore kinins are found in the lungs at a greater conc and can cause a cough. Rash and anaphalactoid reactions. Angio-odoema (swelling of the larynx).

Question 21

Give three examples of Angiotensin II receptor blockers

Answer 21

Candesartan

Valsartan

Losartan

The adverse effects of these include symptomatic hypotension (especially in volume depleted patients), hyperkalaemia, renal dysfunction and angi-odoema

Question 22

Give three examples of beta blockers used in HF

Answer 22

Carvedilol, Bisoprolol and metoprolol

Question 23

What is the role of digosin in HF treatment

Answer 23

No effect on mortality but does reduce hospitalisations due to HF. Therefore it is used as an add on to treatment.

Question 24

What is the role of Ivabradine in HF

Answer 24

It blocks the If current in the sinus node which slows the sinus node rate.

It’s used in HF when B blockers are not adequate. This suggests that the SNS is still active and overriding the other treatment, then Ivabradine is used.

Question 25

What is the role of Sacubitril/Valsartan therapy in HF

Answer 25

Sacubitril is a neprilysin inhibitor which increases the conc of natriuretic peptide.

Valsartan is an angiotensin II blocker

Together they reduce mortality associated to HF

Question 26

How does acute heart failure present and how is it initially treated

Answer 26

Pulmonary odoema, pale, sweaty (SNS overide)

Treated with oxygen, diamorphine, nitrates, loop diuretics. These can turn the patient around within 30 minutes.

Question 27

What are the uses of inotropes in HF

Answer 27

Adronergic agonists

PDE III inhibitors - The breakdown of cAMP is prevented - potentiating SNS stimulation

Question 28

What are the two types of adronergic agonists

Answer 28

Given intravenously for short term use only.

1. Inoconstrictors - norepinephrin, epinephrin have their effect on alpha one receptors
2. Inodilators - Dobutamine, Isoproterenol act on B1/2 which vasodilate in muscle.

Question 29

What is the result of prescribing the PDE III inhibitor - Milrinone

Answer 29

When given to HF patients mortatlity rate is increased compared to placebo, stim of a failing heart sees no benefit. Can be used in acute treatment but not long term.