Session 10 ILOs - Heart Failure Flashcards
Define heart failure
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
Describe the signs and symptoms of heart failure
Left Ventricular HF Signs and symptoms: (7)
- Fatigue/lethary
- Breathlessness on exertion
- Cardiomegaly
-Pulmonary oedema which can manifest as:
- Orthopnoea (shortness of breath lying flat)
- Paroxysmal nocturnal dyspnoea
- Basal pulmonary crackles
Right ventricular HF Signs and symptoms: (5)
- Fatigue/lethary
- Breathlessness
- Peripheral oedema (pitting)
- Raised jugular venous pressure
- Tender, smooth, enlagrged liver
Cause of HF is most likely to be left sided cause, right sided is likely to occur due to left sided failure
Explain the pathophysiology of heart failure
In heart failure, impaired ventricular contractility reduces the cardiac output, and thus BP (BP = CO x TPR). Reduced BP activates the baroceptor and RAAS system:
1) In the short term, Baroreceptors stimulate an increase sympathetic drive that leads to:
- Increased heart rate
- Increased peripheral resistance
2) In the long term, he RAAS system is activated (due to decreased renal perfusion). This causes:
- Increased sodium retention leading to increased water retention (water follows sodium) and this increases the circulating volume
- Anti-Diuretic Hormone release
- Vasoconstriction
- Enhanced sympathetic activity
- This also results in Ang2 (Angiopoietin-2) production
This is all an attempt to increase the BP, as these systems usually do under normal circumstances. However in HF, causes an increased after-load and pre-load, causing a further reduction in stroke volume and cardiac output, which puts even more strain on the failing heart.
Describe the involvement of the renin-angiotensin-aldosterone system and the sympathetic nervous system in heart failure
IIn heart failure, impaired ventricular contractility reduces the cardiac output, and thus BP (BP = CO x TPR). Reduced BP activates the baroceptor and RAAS system:
1) In the short term, Baroreceptors stimulate an increase sympathetic drive that leads to:
- Increased heart rate
- Increased peripheral resistance
2) In the long term, he RAAS system is activated (due to decreased renal perfusion). This causes:
- Increased sodium retention leading to increased water retention (water follows sodium) and this increases the circulating volume
- Anti-Diuretic Hormone release
- Vasoconstriction
- Enhanced sympathetic activity
- This also results in Ang2 (Angiopoietin-2) production
This is all an attempt to increase the BP, as these systems usually do under normal circumstances. However in HF, causes an increased after-load and pre-load, causing a further reduction in stroke volume and cardiac output, which puts even more strain on the failing heart.
Explain the presentation circumstances which lead to the development of left ventricular failure, biventricular failure and isolated right ventricular failure
- The most common cause of HF is ischaemic heart disease / coronary heart disease
- Other causes of HF 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)
- The reason why all these conditions lead to HF is because they result in remodelling of the heart
Remodelling of the heart (most commonly due to ischaemic heart disease) can because 2 things:
- Impairment of ventricular filling (HFpEF)
- Impairment of ventricular ejection (HFrEF)
Heart failure with preserved ejection fraction (HFpEF)
- Issues with filling (Diastolic Dysfunction)
Causes: - hypertrophy/thickened walls which causes reduced ventricular chamber so capacity for blood is reduced
- Chambers are too stiff/fibrosed cardiac tissue so can’t relax enough to allow adequate filling of ventricles
SPACE AVAILABLE REDUCED, EDV reduced
Heart failure with reduced ejection fraction (HFrEF)
- Issues with ejection (Systolic Dysfunction)
Causes - can’t pump with enough force: - Thin or fibrosed muscle walls
- Chambers dilated or enlarged
- Abnormal, uncoordinated myocardial contraction
SPACE NOT REDUCED just POOR contraction - The most common heart failure is left ventricular, and it occurs as a result of remodelling of the heart (loss of cardiac myocyte and replacement with fibrosis)
- Left ventricular failure raises pulmonary arterial pressure leading to additional right-sided heart failure (congestive heart failure = biventricular failure)
- Right sided heart failure rarely occurs on its own but can do in the case of chronic lung disease
Explain the presentation circumstances which lead to the development of heart failure with preserved ejection fraction and heart failure with reduced ejection fraction
Also state some key manifestations in patients with these conditions
Heart failure with preserved ejection fraction (HFpEF)
- Issues with filling (Diastolic Dysfunction)
Causes: - hypertrophy/thickened walls which causes reduced ventricular chamber so capacity for blood is reduced
- Chambers are too stiff/fibrosed cardiac tissue so can’t relax enough to allow adequate filling of ventricles
SPACE AVAILABLE REDUCED, EDV reduced
Heart failure with reduced ejection fraction (HFrEF)
- Issues with ejection (Systolic Dysfunction)
Causes - can’t pump with enough force: - Thin or fibrosed muscle walls
- Chambers dilated or enlarged
- Abnormal, uncoordinated myocardial contraction
SPACE NOT REDUCED just POOR contraction
Key manifestations: - dyspnoea - fatigue (limiting exercise tolerance) • due to tissue hypoperfusion • Plus tissue fluid retention (pulmonary and/or peripheral oedema depending on involved ventricle)
Explain the formation of normal tissue fluid and why oedema can develop in heart failure
Normally, to form tissue fluid, there is a balance in starling’s forces, between hydrostatic pressure and osmotic 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 for fluid return from interstitum to capillary
- Increased volume of tissue fluid accumulates within pulmonary interstitium
= pulmonary oedema
= Peripheral oedema can also be present due to RAAS activation causing water retention
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
- Increased volume of tissue fluid accumulates within interstitial tissues in gravity dependant areas like legs
= peripheral oedema
How do we determine if ‘ejection’ or ‘filling’ cause of HF?
Many of clinical signs and symptoms in the patient will be the same…
So we measure the stroke volume and end diastolic volume on echocardiogram
Do SV/EDV to give percentage
Normal is over 50%, given that the values for SV and EDV are normal
SV = EDV-ESV
EF = HFrEF ‘ejection problem’
• EF <40%
EF = HFpEF: ‘filling problem’
• EF≥50%
Describe the principles involved in the general management of heart failure, and the categories of drugs used in its therapy
General investigations: (5)
- ECG
- Chest x-ray
- Bloods (NTpro-BNP (natriuretic peptide, tells us about whether it is heart failure or not), FBC, U and Es)
- Transthoracic echocardiogram
- Further tests depending on clinical picture:
General management:
1) Symptomatic treatment:
- IV Furosemide for all causes of HF, (HFpEF) This causes diuresis (water loss/wee) to reduce the volume of fluid in the circulation.
This will reduce the after-load and increase the cardiac output. - Giving a diuretic also helps to reduce oedema.
2) Prognosis treatment: (most effective for HFrEF)
Drug treatment:
- (RAAS blockers) ie ACE inhibitors and Angiotensin receptor blockers (M)
- Beta blocker (M)
- Mineralocorticoid receptor antagonist (eg spironolactone) (M)
Non-drug treatment:
- Implantable cardioverter defibrillator (control arrhythmias) (M)
- Biventricular pacemaker - speed up heart rhythm if too slow
M = one of the 4 main treatments that lecturer said to remember
Immediate/acute treatment:
- Give oxygen if they are hypoxic
- Give an IV loop-diuretic, Furosemide. This causes diuresis (water loss) to reduce the volume of fluid in the circulation. This will reduce the after-load and increase the cardiac output.
- Giving a diuretic also helps to reduce oedema.
- Give heparin to reduce the risk of venous clots forming or to prevent propagation of those which have formed.
- The management may require additional ventilator support and IV nitrates.
Identify targets for drug action to manipulate cardiac output
Treatment for HFpEF (preserved)
- IV Furosemide, for all causes of HF, (HFpEF)
- Onset diuretic action within 30 mins of IV admin (makes you wee more) to reduce the volume of fluid in the circulation.
This will reduce the preload and thus workload of the heart and increase the cardiac output. - Giving a diuretic also helps to reduce oedema.
- Immediate venodilatory effect, which clears fluid from lungs
Treatment for HFrEF:
- RAAS blockers (ACE inhibitor or ARB) to decrease preload
- Beta blocker (blocks affects of adrenaline on heart, reduce HR)
- Mineralocorticoid receptor antagonist ie spironolactone block the effects of a hormone produced naturally by your adrenal glands which can cause your heart failure to get worse. They help lower blood pressure, reduce congestion and thus protect the heart.
Describe the role of intervention and device therapy in managing patients with heart failure
Intervention:
Multi-disciplinary approach to HF:
1) Cardiac rehabilitation:
- Help you improve your health and recover from a heart attack/heart disease/heart surgery
- Involves exercise training, emotional support and education about lifestyle changes
- establishing a plan to help you regain strength, prevent your condition from worsening, reduce your risk of future heart problems, and improve quality of life.
2)Patient education ie advise given to: Reduce salt and alcohol intake and increase aerobic exercise
Used to treat HFrEF
Device therapy:
1) Biventricular pacemaker - speed up heart rhythm heart too slow
2) Implantable cardioverter defibrillator (control arrhythmias) (M)
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
The role of it in summary:
- To provide cardiac resynchronisation therapy (CRT) or to prevent sudden cardiac death (SCD) by acutely treating ventricular tachycardia (VT) or fibrillation
Be able to draw and 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
Normally, increased filling/increased CVP/EDV leads to a big increase in CO (gradient of the curve)
In HF:
- Increased LV filling in failing heart (heart failing due to impaired contractility) leads to a very little increase in CO…(gradient of curve)
- Eventually it leads to worsening CO (curve dips) (as the cardiac contractile filaments are no longer overlapping)
- In some cases of HF, due to falling CO, mechanisms kick in to try and increase preload and thus increase EDV/CVP.
But instead result, these mechanisms result in falling CO and development of pulmonary congestion/oedema
