Heart failure

Question 1

What is normal circulation?

Answer 1

The body has 2 circulations and each pump is linked to the vessels in front and behind.

therefore what happens on one side will affect the other

Question 2

What is cardiac output?

Answer 2

volume of blood leaving either side of the heart per minute - inadequate in heart failure

Question 3

What does stroke volume depend on?

Answer 3

depends on preload, afterload, and contractility

contractility- the intrinsic muscle strength

These three factors will affect cardiac output as well.

Preload- venous return (will be inadequate in heart failure)

After load- resistance (will be excessive in heard failure which will compromise the ejection fraction).

Question 4

How do you calucluate cardiac output?

Answer 4

CO = SV x HR

Question 5

WHat is the ejection fraction?

Answer 5

Stroke volume/ end diastolic volume

(as a %)

>55% normal, 45-54% mildly reduced, 30-44% moderately reduced, <30% severely reduced

Stroke volume= end diastolic volume - end systolic volume

Question 6

How do you measure the ejection fraction?

Answer 6

transthoracic echocardiogram

This is a chest ultrasound

The data you need to use to calculate the ejection fraction comes up on the side.

Question 7

What is heart failure?

Answer 7

clinical syndrome caused by inability of heart to supply blood to tissues. Insufficient to meet metabolic needs, or achieved at expense of filling pressures; causes inadequate organ perfusion and congestion in lungs/legs; often compensate with tachycardia.

The heart cannot keep up with the demand.

Question 8

Why is the heart in a state of tachycardia when it is in heart failure?

Answer 8

It is a compensation mechanism to maintain the cardiac output.

Remember CO= SV x HR

(taccy increases the HR)

Question 9

What is dilated cardiac myopathy?

Answer 9

Thinning of the ventricular walls- they are therefore less able to produce a sufficient pressure to pump.

Question 10

What are the different types of heart failue?

Answer 10

1. Left vs Right heart failure
2. Chronic vs acute heart failure
3. Heart failure with reduced ejection fraction (HFrEF) vs Heart failure with preserved ejection fraction (HFpEF)

Question 11

Left vs right sided heart failure

Answer 11

Left: to do with an issue with the left ventricle. It is a filling or ejection issue. There is congestion. Blood backs up into the lungs ( through the pulmonary veins)- it does not go through the heart. There is increased pressure in the lungs (pulmonary hypertension). Hydrostatic pressure increases in the vessels and fluid leaks out causing oedema. Symptoms: coughing, wheezing, breathlessness

This increases the load on the right ventricle (pulmonary artery) as it needs to contract against a higher load.

Right: similar thing an issue with the right ventricle so that it is not able to fill/ ejection issue. Increased afterload (resistance) because of the pulmonary hypertension. Secondary to left heart failure.

Question 12

Acute vs chronic heart failure

Answer 12

Chronic- slow onset. Due to infection, pulmonary embolism, myocradial infarction or surgery.

Acute: same as chronic but rapid onset

Question 13

Reserved vs preserved ejection fraction

Answer 13

Reduced: abnormal systolic function. Ventricle is unable to contract and pump blood into the aorta and pulmonary artery. Can be due to think ventricle walls, valve issue (stenosis) or damage/destruction of ventricular myocytes. As the systolic volume increases, the stroke volume decreases. Even though there is a increased HR, there is a reduced CO and ejection fraction. Weaker ejection leads to higher diastolic pressure.

Preserved: diastolic dysfunction. The ventricles contract normally but there is a filling issue as the ventricles are more stiff, impaired relaxation or impaired filling. There is a reduced end diastolic volume. Hypertrophies- smaller amount of space for blood fill up. Becuase EDV is inherently reduced, the reduced stroke volume is masked when looking at ejection fraction. it is preserved.

Question 14

Epidemiology of heart failure

Answer 14

Number of heart failure tends to rise above 60 and peaks around 75.

It will tail away again as people die.

Question 15

What are the causes of heart failure?

Answer 15

1. Valve disease- mitral/tricuspid (AV) problems mean ventricles cannot fill with blood, pulmonary/aortic valve means cannot expel blood (systolic issue)
2. IHD (ischaemic heart disease)- narrowing of coronary arteries deprive the heart of oxygen. Less of the heart has to form the same function- it has to work harder and needs more oxygen- this just makes things worse.
3. Myocardial infarction- significant occlusion of the coronary arteries leads to death of the heart muscle.
4. Hypertension- increases afterload to much work harder (need more oxygen which not supplied so die), so muscle grows inward (reducing space for filling). Ventricles will hypertrophy CO decreases
5. Dilated cardiomyopathy- systolic dysfunction- dilated LV reduced generatable pressure, reducing ejection
6. Hypertrophic cardioyopathy- ventricles hypertrophy inwards, increasing thickness of LV. Reduced internal volume and impedes filling.

Question 16

Majority of heart failure is caused by?

Answer 16

Coronary heart disease- occulsion of the coronary arteries

Question 17

Clinical features of heart disease

Answer 17

Patient: breathlessness, fatigue, weight loss, anorexia, orthopnoea

Clinical- tachycardia, pitting oedema, increased jugular venous pressure, ascites (Increased fluid in peritoneal cavity)

Investigations- chest x-ray will see an enlarged heart, ECG to measure ejection fraction

Question 18

Hallmark signs of heart failure

Answer 18

• Raised jugular venous pressure- increased pressure in the right side of the heart therefore pressure backs up into systemic veins (especially jugular vein) JVP rises and there is pulsation in the neck
• Pitting oedema- fluid accumulation in tissues (lower extremities), leads to a pitting effect when physically depressed) WIll be visible fro a short period
• Ascites- fluid build up in the peritoneal cavity

Question 20

What is B-type natriuretic peptide (BNP)?

Answer 20

natriuresis- sodium excretion

BNP is released from the ventricular myocytes in response to stretch. It is a marker for heart failure.

If it is greater than 100 for people under 70 years of age, there is indication that they have heart failure. (greater than 300 for over 70)

BNP causes vasodilation of vessels, and it will reduce BP 9reduced aldosterone secretion), reducing afterload and ventricles don’t have to work as hard.

It also reduces aldosterone secretion- reduces sodium absorbtion, therefore reduce in water absorption less fluid accumulation. It does this by inhibiting renin secretion (RAAS).

All of this results in reduced extracellular fluid

And a reduced pressure :)

Question 21

Lifestyle changes to reduced risk of HF?

Answer 21

1. Weight loss
2. Stop smoking
3. Less alcohol
4. More exercise

Question 22

Medication for HF

Answer 22

First line: ACE Inhibitors (reduce afterload and block aldosterone production) and Beta Blockers (bisoprolol/carvedilol NOT atenolol/metoprolol - reduce HR but don’t change afterload). Beta blockers slow the heart down so it requires less energy and oxygen to function.

Diuretics can also lead to fluid loss to reduce BP- it is also an aldosterone antagonist.

Second line: ivabradine (if HR>70) to cause vasodilation. It also inhibits the enzyme that breaks down BNP.

Sacubitril (inhibits enzyme to break down BNP)/valsartan (stops aldosterone being produced)

Last thing- cardiac resynchronisation therapy for more efficient contraction

Question 23

The timeline for medication with HF

Answer 23

Question 24

what do diuretics and ace inhibitors do?

Answer 24

They reduce the load so the heart has to put less effort into pumping

Question 25

Why are beta blockers good?

Answer 25

They slow the heart rate down, reducing the speed saves energy makes it easier

Question 26

Non-pharmacological treatments

Answer 26

1. Fluid control- haemofiltration, peritoneal dialysis and haemodialysis
2. Devices- intra-aortic balloon pumping, resynchronisation, total artificial heart (TAD)
3. Surgical- coronary artery bypass graft, valve surgery, transplantation

Question 27

What is the law of LaPlace?

Answer 27

It’s to do with wall stress.

Pressure x Radius / 2 x wall thickness

If the wall thickness increases, the wall stress decreases

This is seen in the compensatory mechanism of ventricular hypertrophy. Reduces wall stress in response to acute load, but then leads to dilated cardiomyopathy as ventricle volume has reduced - increasing wall stress; thin wall can no longer contract with enough force to eject blood. Its not a good cycle. The hypertrophy is only a SHORT TERM SOLUTION.

Question 28

Neural and hormonal changes

Answer 28

There is a benefical physiological and pathophysiological response.

Benefical to do with BNP- allows for vasodiation and lowers BP, decreases aldosterone levels. BNP is good stuff.

Pathophysiological response0 reduced renal perfusion as the heart is beating less effectively. This activates RAAS which will increase BP.

Question 29

Living with heart failure

Answer 29

• Breathlessness
• Fatigue

This is becuase the heart is damaged and is a less effective pump.

There is marked neurohormonal activation

Quality of life is poor

Life expectancy is reduced.

Question 30

What is the NYHA classifcation of HF?

Answer 30

New York Heart association. Functional. HF based on patient physical limitations.

Question 31

Progression of HF

Answer 31

Becomes more severe till death, and coronary events (e.g. MI) speeds up process of dying