Session 10 ILOs - Heart Failure

Question 1

Define heart failure

Answer 1

Heart Failure is the inability of the heart to meet the demands of the body - in simple terms

Clinical definition = clinical syndrome of reduced output, tissue hypoperfusion, increased pulmonary pressures and tissue congestion arising from an impairment of ventricular filling and/or emptying

Question 2

Describe the signs and symptoms of heart failure

Answer 2

Left HF Signs and symptoms:

• Fatigue/lethary
• Breathlessness on exertion
• Orthopnoea (shortness of breath lying flat)
• Paroxysmal nocturnal dyspnoea
• Basal pulmonary crackles

Right HF Signs and symptoms:

• Fatigue/lethary
• Breathlessness
• Peripheral oedema (pitting)
• Raised jugular venous pressure

Cause of HF is most likely to be left sided cause, right sided is likely to occur due to left sided failure

New York Health Association Functional Classification:
Class 1: No symptomatic limitation on physical activity
Class 2: Slight limitation on physical activity, no symptoms at rest
Class 3: Marked limitation on physical activity, no symptoms at rest
Class 4: Inability to carry out physical activity without symptoms, may have symptoms at rest

Question 3

Explain the pathophysiology of heart failure

Answer 3

The most common cause of HF is ischaemic heart disease / coronary heart disease, which causes remodelling of the heart

Other causes include:

• Hypertension
• Valvular disease e.g. aortic stenosis
• Cardiomyopathy
• Arrythmias etc.
• Very rarely due to increased demand on cardiac output (e.g. high output HF)

Remodelling of the heart (most commonly due to ischaemic heart disease) can because 2 things:

1. Impairment of ventricular filling (HFpEF)
2. Impairment of ventricular ejection (HFrEF)

HFpEF:
- Chambers are too stiff/fibrosed
- Thickened ventricular walls
HFrEF:
- Thin or fibrosed ventricle walls
- Dilated/enlarged chambers
- Abnormal/uncoordinated contraction

Question 4

Explain the normal relationship between central venous pressure (or end diastolic pressure) and cardiac output and how that relationship alters with increasing severity of heart failure due to impaired contractility

Answer 4

Under normal physiologic conditions, the right and left ventricular output are equal.

• If the cardiac output decreases due to decreased left ventricle output, this increases the pressure in the pulmonary circulation which increases hydrostatic pressure and less fluid can return, which then increases central venous pressure (due to increased fluid in system)
• In addition, central venous pressure can influence cardiac output, decreases in central venous pressure can lead to changes in the filling pressures of the left heart

With increasing heart failure, these affects are exacerbated and can result in pulmonary oedema and/or peripheral oedema

Question 5

Explain the presentation circumstances which lead to the development of heart failure with preserved ejection fraction and heart failure with reduced ejection fraction

Answer 5

Heart failure with preserved ejection fraction (HFpEF)
- Issues with filling
Causes - reduced ventricular chamber:
- Fibrosed cardiac tissue (inability to stretch)
- Smaller cavity due to fibrosis (thickened walls)

Heart failure with reduced ejection fraction (HFrEF)
- Issues with ejection
Causes - can’t pump with enough force:
- Thin or fibroses walls
- Dilated chambers
- Inability to contract in coordinated manner

Question 6

Explain the presentation circumstances which lead to the development of left ventricular failure, biventricular failure and isolated right ventricular failure

Answer 6

Left ventricular = common
- Increased pressures in the left ventricle due to failure to eject
- Increased pulmonary pressures
- Increased hydrostatic pressures, so less fluid return to capillaries
- Increased volume of tissue accumulates within pulmonary interstium
= pulmonary oedema

Right ventricular = NOT common
Only really occurs when someone has a primary lung condition
- Increased pressures in the right ventricle due to failure to eject
- Increased systemic venous pressures (increased jugular venous pressure)
- Increased central venous pressure, so less fluid return to capillaries
- Increased volume of tissue accumulates within tissue
= peripheral oedema

Right ventricular failure generally occurs as a result of left ventricular failure

Question 7

Describe the involvement of the renin-angiotensin-aldosterone system and the sympathetic nervous system in heart failure

Answer 7

In normal circumstances, the RAAS system helps to increase blood pressure - which normally is a correct physiological mechanism

Impaired ventricular contractility reduces the cardiac output, which activates baroceptosr and RAAS system
HOWEVER, these mechanisms lead to increased cardiac demand and actually a further reduction in stroke volume and cardiac output

• In the SHORT term, baroceptors increase sympathetic stimulation, increased HR and peripheral resistance = increased afterload and increased cardiac work
• In the LONG term, the RAAS system is activated (due to decreased renal perfusion), this results in Ang2 production and the effects of this = increased preload and afterload, further increases in cardiac work

Question 8

Explain the formation of normal tissue fluid and why oedema can develop in heart failure

Answer 8

Normally there is a balance in starling’s forces, between hydrostatic pressure and oncotic pressure on both inside and outside of the capillary

In LEFT HF:
- Increased LV pressure increases the hydrostatic pressure at the venule end of the pulmonary capillary beds which disrupts the balance
- Therefore the gradient is less favourable to fluid return from interstitum to capillary
= pulmonary oedema

In RIGHT HF:
- Increased RV pressure increases the hydrostatic pressure at the venule end of the capillary beds in systemic circulation which disrupts the balance
- Therefore the gradient is less favourable to fluid return from interstitum to capillary
= peripheral oedema

Question 9

Identify targets for drug action to manipulate cardiac output

Answer 9

Treatment for HFpEF (preserved)

• IV Furosemide, works by inhibiting luminal Na/K/Cl transporter in thick ascending limb, causing Na/K/Cl loss in urine
• This reduces blood volume os reduces preload and helps to clear fluid from the lungs (onset quickly in 30 mins)

Treatment in general:

• RAAS blockers (ACE inhibitor or ARB) to decrease preload
• Beta blocker (blocks affects of adrenaline on heart, reduce HR)
• Mineralocorticoid receptor antagonist
• Biventricular implantable cardioverter defibrillator (ICD)

Question 10

Describe the principles involved in the general management of heart failure, and the categories of drugs used in its therapy

Answer 10

General investigations:

• ECG
• Chest x-ray
• Bloods (NTpro-BNP, FBC, U and Es)
• Transthoracic echocardiogram

General management:

• HFpEF = use IV Furosemide to control BP
• Valvular/structual HF = surgery!
• RV failure = usually secondary to LV HF so needs specialist assessment

General treatments:

• IV Furosemide, works by inhibiting luminal Na/K/Cl transporter in thick ascending limb, causing Na/K/Cl loss in urine (HFpEF ONLY)
• RAAS blockers (ACE inhibitor or ARB) to decrease preload
• Beta blocker (blocks affects of adrenaline on heart, reduce HR)
• Mineralocorticoid receptor antagonist
• Biventricular implantable cardioverter defibrillator (ICD)

Question 11

Describe the role of intervention and device therapy in managing patients with heart failure

Answer 11

Biventricular implantable cardioverter defibrillator (ICD)

Theory:

• Stimulate both sides of the heart simultaneously and restore the synchrony of the LV
• Patients with LV dysfunction are at an increased risk of sudden cardiac death secondary to ventricular tachyarrhythmias
• An ICD is used for heart-failure treatment when the person is considered to be a high risk of dying from an abnormal heart rhythm