Pathophysiology Of Heart Failure

Question 1

What is heart failure?

Answer 1

“The inability of the heart to meet the demands of the body.” -i.e. deliver a blood volume (carrying oxygen / glucose ect.) that allows body tissues to function as required..

OR

“A clinical syndrome of reduced cardiac output, tissue hypoperfusion, increased pulmonary pressure and tissue congestion.” - see oedema / increased tissue fluid.

Question 2

What enables the heart to work as an effective pump?

Answer 2

Input

One-way valves - competent and not stenosed

Chambre size - if small, not very much blood

Functioning muscle -cardiac myocytes much be normal and contract normally need adequate blood supply and normal muscle arrangement.

Output

Question 3

What is the most common cause of heart failure?

Answer 3

Ischaemic heart disease (coronary heart disease).

• myocardial dysfunction e.g. through fibrosis (scarring), remodelling of muscle.

Question 4

What are other causes of heart failure?

Answer 4

• Hypertension - increased afterload on ventricle and accelerates athlerosclerosis (inc. in coronary arteries). This leads to hypertrophy.
• Aortic stenosis - increased afterload on ventricles.
• Cardiomyopathies - e.g. hypertrophic / dialated.
• Arrhythmias
• Pericardial disease
• Other valvular myocardial structural diseases (acquired or congenital).

Rarely, can occur if a grossly elevated demand on cardiac output. E.g. sepsis, severe anaemia, thyrotoxicosis. This is high output. heart failure.

It is important to identify the underlying cause as this will direct the sebsequent treatment options.

Question 5

How do we measure the ability of the heart to meet demands of the body?

Answer 5

CO = SV x HR

CO = volume delivered / min (expelled per ventricle/min)

SV = Volume ejected by a ventricle in a single beat

A normal heart will only eject about 2/3rds of its EDV.

​

Question 6

What is the ejection fraction?

Answer 6

This is SV / EDV = fraction ejected.

So, it is the proportion ejected by the ventricles.

SV is only a fraction of the total volume within the ventricle at the end of diastole (EDV).

Question 7

What three things affect stroke volume?

Answer 7

Pre-load - (Volume in ventricles at the end of diastole = EDV) ..this is the stretch on the ventricles just before comtraction.

After-load - Total peripheral resistance.

Myocardial contracility.

Question 8

What is Frank-Starling’s Law?

Answer 8

More ventricular distension during diastole = greater volume ejected (SV) during diastole.

The bigger the venous return, the better the contraction as greater cardiac output.

Intrinsic property of cardiac myocytes… the greater they are stretched the greater their force of contraction.. up to a certain point…

Question 9

How does the Frank-Starling Law change depending on the inotropic state of the heart?

Answer 9

Contractility of the heat can increase with increased sympathetic activity (curve shifted upwards and to the left)

Greater CO for a given LVEDP (more volume is forced out)

Question 10

How can stroke volume be reduced?

Answer 10

Reduced preload (reduced EDV) Impaired filling of the ventricles during diastole

Reduced myocardial contractility - heat muscle is no longer able to produce same force of contraction for a given volume at the end of diastole.

Increased afterload - Increased pressure against the ventricles is contracting against. E.g. secondary aortic stenosis, chronic severe hypertension.

Question 11

Why can the heart fail?

Answer 11

• A filing problem (diastole) -‘Space’ available in ventricle to receive blood is reduced…EDV (pre-load) therefore reduced.
  
  • Ventricular chambers too stiff / not relaxing enough
  • Ventricular walls thickened (hypertrophied)
• A contractility (ejection) problem (Systole) - ‘Space’ available in ventricles not an issue but poor ventricular contraction so unable to empty it as well.
  
  • Can’t pump with enough force (for a given EDV)
  • e.g. muscle walls thin / fibrosed, chambers enlarged (overstretched sarcomeres), abnormal or uncoordinated myocardial contraction.

Question 12

What is HFrEF?

Answer 12

Heart failure with reduced ejection fraction.

Systolic dysfunction

More common

Question 13

What is HFpEF??

Answer 13

Heart failure with preserved ejection fraction.

• Diastolic dysfunction.
• Nearly 50% patients

Question 14

Types of heart failure

Answer 14

The..

Question 15

What ventricle is most commonly involved in heart failure?

Answer 15

Most commonly involves the left ventricle - But, with subsequent involvement of the right ventricle.

Question 16

When does right ventricular heart failure occur?

Answer 16

• Right ventricular heart failure can occur isolation, secondary to chronic lung disease (cor pulmonale)

This is much less common than left ventricular heart failure

The most common cause for right ventricular heart failure is left ventricular heart failure.

Question 17

Frank-starling Curve in Heart Failure..

Answer 17

CO does not increase much even though increased left ventricular filling (pre-load). This means that pre-load keeps increasing and it eventually leads to worsening CO.

Markedly increased LVEDV (in an attempt to increase stroke volume) results in pulmonary congestion (Oedema).

Question 18

What gets triggered as a result of CO Decrease?

Answer 18

1. Damaged ventricular tissue.
2. Reduction in efficiency of ventricular contraction
3. Reduced stroke volume
4. Reduced cardiac output
5. Neuro-hormonal activation

The compensatory mechanisms, however, ultimately lead to an increased cardiac demand and a further reduction in stroke volume (this further deteriorates cardiac output and condition)

Question 19

What are the neurological consequences of heart failure?

Answer 19

1. Decrease in cardiac output
2. Decrease in blood pressure
3. Baroreceptors e.g. in the carotid sinus detect this
4. Increased sympathetic drive
   
   • Increased heart rate
   • Increased peripheral resistance
5. Increases afterload

These things all increase cardiac work.

Question 20

What are the hormonal conseqeunces of heart failure?

Answer 20

1. Decrease cardiac output
2. Decrease in blood pressure
3. This decreases renal perfusion
4. Activation of the renin-angiotensin-aldosterone (RAAS) pathway
5. Production of angiotensin II leads to:
   
   1. Increase of circulating volume due to Na+ and water retention (via aldosterone)
   2. This stimulates ADH (which causes more increase in volume)
   3. Vasoconstriction
   4. Enhances sympathetic activity

These things increase pre-load and afterload which cause an increased cardiac work.

Question 21

What are the clinical signs and symptoms of HF?

Answer 21

• Fatigue / Lethargy
• Breathlessness
• +/- leg swelling

Many signs arise as a result of increased interstitial fluid (oedema) either in pulmonary or peripheral (lower limb) tissues

Question 22

Why does tissue oedema form in heart failure?

Answer 22

If failing right ir left ventricle - higher pressue in venous circulation - this increases hydrostatic pressue at the venule end of the capillary beds.

Increased capillary hydrostatic pressures loads to less fluid being draen back intravascularly at the venule end.

Question 23

What are the differences in symptoms from LV and RV heart failure?

Answer 23

Although, patietns often present with symptoms of both left and right ventricular heart failure.

Question 24

What does a raised jugular venous pressure tell you?

Answer 24

Measurement of the pressure in the right internal jugular vein can be a direct reflection of pressures in the right side of the heart. -Pulsations will go up with RV heart failure.