18. Heart Failure Flashcards
What is the simple definition of heart failure?
inability of the heart to meet the demands of the body
What is the ESC definition of heart failure?
Clinical syndrome of:
- reduced cardiac output,
- tissue hypoperfusion,
- increased pulmonary pressures
- and tissue congestion
What are the most common cause of heart failure?
• Ischaemic Heart Disease(coronary heart disease)
- myocardial dysfunction e.g. through fibrosis (scarring), remodelling of muscle
What are other causes of heart failure?
- myocardial infarction
- Hypertension (increased afterload & accelerates atherosclerosis)
- Arrhythmias
- Aortic stenosis (increased afterload)
- Other valvular or myocardial structural diseases
- Cardiomyopathies (e.g. hypertrophic/dilated)
- Pericardial diseases
• Rarely, can occur if a grossly elevated demand on cardiac output e.g. sepsis, severe anaemia, thyrotoxicosis [high output heart failure]
How do we measure the ability of the heart to meet demands of the body?
Ejection fraction
What is the ejection fraction?
SV/EDV
What influences stoke volume?
- Preload
This refers to the stretch on the ventricle just before contraction in systole. It’s affected by the EDV, the volume in the ventricle at the end of diastole. - Afterload
This refers to the total peripheral resistance - Myocardial contractility
This refers to the myocytes ability to contract
Describe Frank-Starlings Law of the heart
Starling’s law says that the stroke volume of the left ventricle will increase as the left ventricular volume increases.
This is due to increased stretch of the myocytes which causes a more forceful contraction in systole.
Essentially the more the cardiac muscle is stretched the stronger the contraction up to a certain point
Give a factor that can cause the Frank-Starling curve to vary
Frank-Starling curves can vary depending on the inotropic state of the heart.
It can be influenced by sympathetic activity, an increase in synthetic activity can cause an increase in the contractility of the heart.
This causes the curve to shift upwards and to the left.
It means that for an increase in the left ventricular end diastolic pressure should get an increase in CO.
Why is cardiac output reduced in heart failure?
Stroke volume can be reduced due to
– Reduced pre load (reduced EDV)
• Impaired filling of ventricle during diastole
– Reduced myocardial contractility
• Muscle not able to produce same force of contraction for a given volume within ventricle
– Increased afterload
• ↑pressure against which ventricle contracting e.g. aortic stenosis, chronic
What are the 2 reasons that heart can fail?
- A filling problem (diastolic)
Ventricular volume/capacity for blood is reduced
• Ventricular chambers too stiff/not relaxing enough
• Ventricular walls thickened (hypertrophied) - A contractility (ejection) problem (systolic)
Can’t pump with enough force (for a given EDV)
• Muscle walls thin/fibrosed,
• Chambers enlarged (overstretched sarcomeres)
• Abnormal or uncoordinated myocardial contraction
What are the two ways of classifying heart failure according to ejection fracture?
- Heart Failure with reduced Ejection Fraction (HFrEF)
– [systolic dysfunction]
– Contractility problem
– Most common type - Heart Failure with preserved Ejection Fraction (HFpEF)
– [diastolic dysfunction]
– Filling problem
What is the normal ejection fraction?
Normal >50% (typically 60% +)
- abnormal if below 40%
How can a heart be “failing” if EF is maintained…?
“filling problem”..
- Ventricle ejects less volume in a heartbeat (SV reduced) as less volume to begin with
- Fraction of what is available to eject is still >50%
- Hence “Ejection Fraction” is ‘preserved’
Which ventricle is most commonly affected in heart failure?
Left ventricle most commonly involved
• But with subsequent involvement of the right ventricle
What is congestive/biventricular heart failure?
Involvement of both ventricles (biventricular)
What is the most common cause of right ventricular failure?
Left ventricular failure
When might right ventricular heart failure occur in isolation?
Secondary to chronic lung diseases (cor pulmonale)
Explain the presentation circumstances which lead to the development of left ventricular failure,
The left side of the heart receives oxygen-rich blood from the lungs and pumps it forward to the systemic circulation. However failure of the left side of the heart causes blood to back up (be congested) into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood.
Explain the presentation circumstances which lead to the development of right ventricular failure
The most common cause for RV heart failure is LV heart failure.
However right-sided heart failure can also occur in isolation often caused by pulmonary heart disease (cor pulmonale), which is typically caused by difficulties of the pulmonary circulation, such as pulmonary hypertension or pulmonic stenosis.
There’ll be a backward failure of the right ventricle which cause blood to flow back into the venous system.
This leads to congestion of systemic capillaries and generates excess fluid accumulation in the body.
Explain the presentation circumstances which lead to the development of biventricular failure
In biventricular heart failure both ventricles are involved,
It results in the development of symptoms seen for both right and left sided heart failure.
Describe the Frank-Starling’s Curve in Heart Failure
- Increased LV filling in the healthy heart leads to big increase in CO (gradient of curve)
- Increased LV filling in failing heart leads to a very little increase in CO…(gradient of curve)
- Eventually it leads to worsening CO (curve dips)
- Markedly increased LVEDP [in attempts to increase SV] result in falling CO and development of pulmonary congestion
Explain the pathophysiology of heart failure
Heart failure is caused by any condition that reduces the efficiency of the heart muscle,through damage or overloading.
It causes a decrease in CO.
the decreased CO causes a decreased BP (BP = CO x TPR).
This results in the activation of neuro-hormonal systems.
This is an attempt to increase the BP but in this reality culminates in an increased after-load and pre-load which puts even more strain on the failing heart.
Explain the circumstances that results in Heart Failure with reduced Ejection Fraction (HFrEF)
In HFrEF you have systolic dysfunction .
There’s a problem with heart contraction and therefore the heart can’t pump with enough force. This means you have a contractility problem.
Causes include:
Thin/ fibrosed walls, enlarged chambers , abnormal/ uncoordinated contraction.
This is the most common type of heart failure
Explain the circumstances that results in Heart Failure with preserved Ejection Fraction (HFpEF)
In HFpEF you have diastolic dysfunction.
There’s a problem with the heart where it doesn’t fill properly.
This means that the heart will operate at a lower point in the Starling curve reducing stroke volume and hence cardiac output.
The main cause of this is hypertrophy.
This is because the chambers become stiff and cannot relax enough to allow adequate filling if the ventricles.
What physiological mechanisms does the body use to increase CO?
- Baroreceptors: increased sympathetic activity.
- Reduced renal perfusion leads to activation of RAAS pathway
What effect do physiological mechanisms to try and correct CO have on heart failure?
Whilst these mechanisms aim to help they ultimately lead to an increased cardiac demand and a further reduction in stroke volume (further deterioration in cardiac output and the condition).
Describe the involvement of the renin-angiotensin-aldosterone in heart failure
A reduction in cardiac output causes a reduction in blood pressure, this will be seen as a reduction in renal perfusion.
This causes an activation of the renin-angiotensin-aldosterone (RAAS) pathway.
The enzyme renin is released from the kidneys, it catalyses the conversion of angiotensin to angiotensin I.
Angiotensin I will then be converted to angiotensin II by ACE (angiotensin converting enzyme).
Angiotensin II is a powerful vasoconstrictor causing an increase in the contraction of the blood vessels.
As well as this angiotensin II will cause the release of aldosterone this promotes an increase in the retention of sodium and water.
This will cause an increase in the circulating blood volume.
It also causes the secretion of ADH which promotes water retention by the kidney and it also cause vasoconstriction.
There’ll be an increased pre-load due to increased volume of blood and there’ll be increased afterload due to vasoconstriction
Describe the involvement of the sympathetic nervous system in heart failure
When there’s a reduction in cardiac output from the heart you’ll get a fall in blood pressure.
Baroreceptors will detect this change and stimulate sympathetic drive.
This leads to an increase in heart rate and peripheral resistance.
This will result in an increase in afterload (pressure that the ventricle has to pump against).
This means that there’ll be increased cardiac work
What are the symptoms of heart failure?
– Fatigue/ lethargy,
– Breathlessness
– +/- leg swelling
What are the relative hydrostatic and oncotic pressures on the arterial and venous end of capillary beds?
Arterial end: Higher hydrostatic pressure (net flow out)
Venous end: higher oncotic pressure (net flow in)
Explain the formation of normal tissue fluid
In normal formation of tissue fluid, the oncotic pressure in the capillaries from arterial end to venule end stays the same, whereas the hydrostatic pressure in the capillaries decrease from arterial to venule. Therefore, at the venule end, the hydrostatic pressure is less than the oncitic pressure, so fluid moves back into the venule. The hydrostatic pressure at arterial end being greater than oncotic pressure initially pushes the fluid out of the capillaries to form tissue fluid.
Explain why oedema can occur in heart failure
If failing right or left ventricle –> higher pressures in venous circulation –> increased hydrostatic pressure at venule end of capillary beds –>Gradient between
Hydrostatic and Oncotic pressures at venule end less favourable for fluid returning to capillary –> fluid remains in interstitium –> oedema
Explain where oedema occurs in right sided heart failure
PERIPHERAL OEDEMA
Failure of the right side of the heart to pump effectively raises venous pressure(as blood backs up into the veins) and therefore capillary pressure.
An increased capillary hydrostatic pressure favours the movement of water out of the capillaries.
Explain where oedema occurs in left sided heart failure
PULMONARY OEDEMA
left sided heart failure raises left atrial pressure and thus the pressure of vessels in the pulmonary system increases as blood back up into the blood vessels of the lungs.
What are the signs and symptoms of right sided heart failure?
- Fatigue/lethargy
- Breathlessness
- Peripheral oedema (pitting)
- Raised jugular venous pressure
- Tender, smooth enlarged liver (liver congestion)
What are the signs and symptoms of left sided heart failure?
- Fatigue/lethargy
- Breathlessness (exertional)
- Orthopnoea
- Paroxysmal nocturnal dyspnoea
- Basal pulmonary crackles
- Cardiomegaly (displaced apex beat-indicating enlarged LV)
What is orthopnoea?
Breathlessness when lying flat
What is paroxysmal nocturnal dyspnea?
Sudden awakening from sleeping with shortness of breath
How can you directly measure the pressures in the right side of the heart
Measurement of the pressure in the right internal jugular vein can be used as a direct reflection of pressures in the right side of the heart.
An increase in pressure in the right internal jugular vein can suggest an increase in pressure in the right ventricle which indicates heart failure.
Describe the function of:
- ACE inhibitors
- Diuretics
- Natriuretic peptides
ACE inhibitors are drugs used to treat heart failure.
They prevent the production of angiotensin II which is a powerful vasoconstrictor. They also prevent the formation of aldosterone.
They have an indirect vasodilatory and diuretic effect.
Diuretics reduce blood volume and the formation of oedema.
Impaired contractility of the ventricles leads to increased volume in the atria. The natriuretic peptides, ANP and BNP are released as the atria are stretched. These peptides cause natriuresis (loss of sodium and water at the kidneys) as well as promoting vasodilation and inhibiting renin secretion.Unfortunately the beneficial effects are not usually sufficient to overcome the deleterious effects of the other systems.
