Heart failure

Question 1

Define afterload.

Answer 1

The pressure the chamber of the heart has to generate in order to eject blood out of the chamber.

Question 2

What is afterload equal to?

Answer 2

Afterload is equal to the total peripheral resistance or systemic vascular resistance, which is the force required to push blood around the circulatory system and create blood flow.
Specific to afterload this is the amount of resistance the heart must overcome in order to open the aortic valve and push blood into the systemic circulation.

Question 3

Considering afterload is equal to the systemic vascular resistance, what conditions may lead to an increase in afterload?

Answer 3

Hypertension
Aortic stenosis (narrowing of the aortic value)
Chronic lung disease

Question 4

In relation to the three conditions that cause an increase in afterload, which would lead to left ventricular failure and which would lead to right?

Answer 4

The left side of the heart is responsible for pumping oxygenated blood from the lungs and to the rest of the body via the aorta (coronary artery).
The aortic valve is present on this side and divides the left ventricle and the aorta so aortic stenosis would cause increase in afterload leading to left ventricular heart failure.

Hypertension where there is increased blood pressure in vessels would have a more direct consequent on the left side of the heart which is pumping blood to the rest of the body, increasing afterload and causing left ventricular heart failure.

However the right side of the body is pumping deoxygenated blood from the body into the lungs via the pulmonary artery, when there is chronic lung disease this causes pulmonary hypertension, meaning there is increased pressure within this artery meaning there must be an increase in afterload, causing right sided heart failure.

Question 5

Define preload.

Answer 5

The volume of blood present in the ventricle after diastole (passive filling of the heart and atrial contraction).

Question 6

What is preload also known as?

Answer 6

Left ventricular end diastolic volume

Question 7

What are some of the causes of excessive pre-load?

Answer 7

It is caused by hypervolemia which can be caused by:
Fluid retention (renal failure, increased aldosterone levels)
Excessive IV fluids
Polycythaemia (over production of red blood cells)
Drugs - NSAIDs and Steroids

Question 8

Compare the two types of heart failure.

Answer 8

Systolic heart failure:
Insufficient force of contraction in order to eject blood from the ventricles during systole

Diastolic heart failure:
When there is reduced ventricular volume- there is a problem refilling the heart during diastole

Question 9

Explain how systolic and diastolic heart failure are linked.

Answer 9

Systolic and diastolic heart failure are linked regarding Starling’s Law of the heart which states:
Increased pre-load (the blood volume present in the left ventricle during diastole) increases the stretch of the cardiac muscle, which increases the contraction and therefore the volume of blood that is ejected per contraction (the stroke volume).

Think of a rubber band, expanding the rubber band (representing increased volume), increases the pressure and force that the band snaps back when you let go.

Question 10

What is cardiac output?

Answer 10

Cardiac output is the volume of blood ejected/pumped from the heart each minute.

Question 11

What is stroke volume?

Answer 11

Stroke volume is the volume of blood ejected from the heart per contraction (beat)

Question 12

What is the equation for cardiac output?

Answer 12

Heart rate (beats/min) x Stroke volume (ml/beat)

Question 13

What is ejection fraction and what would you expect it to be in a healthy patient and one with HF?

Answer 13

Ejection fraction is the volume of blood that is ejected from the ventricle per contraction (stroke volume) as a fraction of the total volume of blood that fills the ventricle during diastole.

In a healthy patient ejection fraction is between 50-70%:
Stroke volume is about: 70mL
Ventricular volume during diastole: 130mL

(70/130) x 100 = 64%

In patients with heart failure, they can have any of the following depending on what type of heart failure they have and this can progress:
Preserved ejection fraction (over 50%)
Midline ejection fraction (between 41-50%)
Reduced ejection fraction (below 40%)

Question 14

In which type of heart failure are you likely to see a reduced ejection fraction?

Answer 14

Systolic heart failure where there is insufficient force of contraction in order to eject blood from the ventricles and into the arteries.

This would reduce the stroke volume - the volume of blood per contraction ejected from the heart, whilst the volume of of blood filling the ventricle during diastole would be unaffected.

Instead of 70/130 may become only 40/130 which has a EF of 31%.

In diastolic heart failure the stroke volume might also only be 40mL however there is a reduced re-filling of the heart during diastole so this is also reduced:

40/70 has a EF of 58%

Question 15

What are some of the causes of cardiac remodelling?

Answer 15

Acute myocardial infarction
Pressure overload (increased afterload) - aortic stenosis, hypertension
Inflammation of the heart muscle- myocarditis
Idiopathic dilated cardiomyopathy
Volume overload (Hypervolemia)

Question 16

Explain how heart failure can occur after a myocardial infarction.

Answer 16

During a myocardial infarction, there is an occlusion of a major coronary artery due to an atherosclerotic plaque rupture. This reduces the coronary perfusion and blocks oxygen supply to the myocardium. The heart has a high demand for oxygen due to its continuous pumping of blood around the body (contraction and relaxation). Cardiomyocytes are very sensitive to changes in oxygen levels and therefore inadequate oxygen supply during an MI leads to:
Myocardium necrosis
Reduced myocardial contractility
Reduced cardiac output

Question 17

What is the primary goal, when damage to the cardiomyocytes has occurred after an MI?

Answer 17

To compensate for the reduced cardiac output. The heart goes into compensatory heart failure which involves mechanism to try and improve the cardiac output.
The mechanisms often work at first but have long-term implications.

Question 18

What is decompensated heart failure?

Answer 18

When compensatory mechanisms the heart has adapted are no longer sufficient to maintain cardiac output often following an event which required an increased demand such as infection, sepsis, fluid overload, anaemia.

Question 19

What is the difference between acute and chronic heart failure?

Answer 19

Acute HF is a sudden drop in contractility and cardiac output and the heart develops compensatory mechanisms (compensatory heart failure) to try and maintain the cardiac output.
Chronic heart failure is a progressive reduction in cardiac output, it also remains in compensatory HF until an event happens requiring an increased demand causing decompensated HF.

Question 20

Would you expect post MI a patient to develop acute or chronic heart failure?

Answer 20

Either can occur and is largely dependent on the extent of infarction, remodelling processes. Chronic heart failure post MI is due to diffuse fibrosis.
It is possible if there is a very large infarction size for a patient to immediately enter decompensated heart failure.

Question 21

Define ischaemia.

Answer 21

Occurs due to reduced blood flow, when insufficient oxygen supply causes hypoxia of cells.

Question 22

Define infarction.

Answer 22

When blood flow is completely blocked, leading to an absence of oxygen and necrosis of cells.

Question 23

How quickly does cardiac remodelling occur post MI?

Answer 23

Within 30 minutes of ischaemia there are changes in the cardiomyocyte structure, within 3 hours there is progressive cardiomyocyte death.

Question 24

What are the two aspects of cardiac remodelling?

Answer 24

Thickening of the LV wall (hypertrophy)
Stiffness of the LV wall (fibrosis)

Question 25

Explain the two types of fibrosis that occur post MI?

Answer 25

Replacement fibrosis - hypoxia induced cardiomyocyte cell death is replaced with a fibrinolytic scar (produced by fibroblasts) to prevent rupturing of the LV wall
Reactive fibrosis - mechanical stress, hormonal and paracrine mediators induces the expansion of connective tissue in areas remote to the infarction area which causes increased stiffness of myocardium, reduced contractility and reduced cardiac output.

Question 26

How does myocardial fibrosis lead to increased stiffness of the myocardium?

Answer 26

Increased accumulation of collagen deposited in the ECM

Question 27

What are the causes of left sided systolic heart failure?

Answer 27

Damage to the myocardium (post MI)
Long standing hypertension
Dilated cardiomyopathy

Question 28

What are the causes of left sided diastolic heart failure?

Answer 28

Long standing hypertension
Aortic stenosis
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy

Question 29

What are the four compensatory mechanisms the heart employs in attempt to try and increase cardiac output?

Answer 29

Left ventricular hypertrophy in attempt to increase contraction
Arterial vasoconstriction diversion to essential organs
Sympathetic nervous system activation to increase blood pressure and perfusion
Na+ and water retention to increase blood pressure and perfusion

Question 30

Briefly outline how post MI leads to left sided systolic heart failure.

Answer 30

Reduced coronary perfusion during MI, leads to hypoxia induced cardiomyocyte death.
This results in reduced contractility short and long term.
Short term:
Reduced cardiac output due to cell death, Drop in blood pressure, SNS activation, RAAS activation resulting in vasoconstriction (Angiotensin 2 and Catecholamines) and aldosterone secretion (salt and water retention).
Increased systemic vascular resistance, increased afterload and increased pre-load due to increased fluid retention

Long-term leads to cardiac remodelling:
Left ventricular hypertrophy
Myocardium fibrosis
Long-term increased stiffness of the myocardium, reducing contractility

Question 31

Briefly outline how long standing hypertension leads to left sided systolic and diastolic heart failure.

Answer 31

Systolic HF:
Hypertension increases the systemic vascular resistance and therefore this increases the afterload.
To compensate for the increased afterload demand, the muscle is larger to compensate for the increased afterload demand. However this ventricular hypertrophy can cause ischaemia as there is an increased oxygen demand for a larger muscle and also the larger muscle squashes the coronary arteries decreasing the oxygen supply. This overall reduces the efficiency of the hypertrophic left ventricle and contractility of the myocardium.

Diastolic HF:
Left ventricular hypertrophy formed as a result of hypertension and increase afterload requirements reduces the space available for blood filling during diastole.

Question 32

Briefly outline how dilated cardiomyopathy leads to left sided systolic heart failure.

Answer 32

In order to compensate for an increased pre-load, the left ventricle myocardium dilates increasing volume of blood available to enter the ventricle during diastole. Whilst initially this is a good compensatory mechanism, eventually the myocardium becomes thinner and thinner and is unable to provide a force of contraction sufficient to the volume of blood present in the ventricles.

Question 33

Briefly outline how aortic stenosis leads to left sided diastolic heart failure.

Answer 33

Aortic stenosis is the narrowing of the valve that separates the left ventricle from the aorta. As a result the afterload increases due to being an increased pressure to overcome the narrowed aortic valve. Left ventricular hypertrophy occurs and again reduces the space available within the left ventricle for blood filling during the diastole.

Question 34

Briefly outline how hypertrophic cardiomyopathy leads to left sided diastolic heart failure.

Answer 34

Hypertrophic cardiomyopathy, is a congenital condition that results in a thickened myocardium (left ventricular hypertrophy) which limits the space with the ventricle for filling of blood during diastole.

Question 35

Briefly outline how restrictive cardiomyopathy leads to left sided diastolic heart failure.

Answer 35

In restrictive cardiomyopathy, diastolic dysfunction occurs as a result of stiffness of the myocardium and the inability for it recoil and stretch after contraction and hence there is limited re-filling during diastole, leading to a reduced pre-load.

Question 36

What do symptoms of heart failure arise from?

Answer 36

Hypoperfusion (inadequate forward perfusion)
Congestion/oedema (backward component)

Question 37

What are the symptoms of hypoperfusion?

Answer 37

These effects are independent from which side of the heart is failing:

Peripheral vasoconstriction
Fatigue and exercise intolerance
Cold and pale extremities
Fluid and electrolyte retention
Tachycardia and tachypnoea

Question 38

What are symptoms suggestive of Right sided heart failure?

Answer 38

Peripheral oedema
Hepatomegaly
Raised jugular venous pressure
Peripheral cyanosis
Fluid and electrolyte retention

Question 39

What are symptoms suggestive of left sided heart failure?

Answer 39

Pulmonary oedema
(Dyspnoea, Orthopnea, Paroxysmal nocturnal dyspnoea)
Cough/wheeze
Central cyanosis
Tiredness
Breathlessness