Pathophysiology, Investigation and Management of Heart Failure

Question 1

What is heart failure?

Answer 1

A state in which the heart fails to maintain adequate circulation for the needs of the body, despite adequate filling pressure (failure of the heart to pump), with a characteristic pattern of haemodynamic, renal, neural and hormonal responses.

Question 2

Describe the aetiology of heart failure?

Answer 2

Ischaemic heart disease is the primary cause of systolic heart failure. Others include: hypertension, arrhythmias, dilated/restricted/hypertrophic cardiomyopathy (idiopathic, pregnancy, bugs, drugs) and pericardial disease.

Question 3

What may Heart failure progress from and to?

Answer 3

There may be progression with classification from class I - no symptomatic name limitation of physical activity, to class IV - no physical activity without symptoms, with it discomfort increases, but it may exist at rest.

Question 4

Basic physiology of the heart:
Cardiac output/CO = __ L/min
Left ventricular end systolic volume/LVESV =___ml
Left ventricular end diastolic volume/LVEDV=___ml, so the ejection fraction is ___+%.
The heart has a mass ~_____g.

Answer 4

5
75
150
50
330

Question 5

List some factors influencing cardiac output.

Answer 5

Heart rate, venous capacity (LV preload), aortic and peripheral impedance (afterload) and myocardial contractility.

Question 6

Explain Starling’s Law of the heart.

Answer 6

The force developed in a muscle fibre depends on the degree to which it’s stretched (cardiac output vs. end diastolic pressure - whole curve moves with change in contractility - congestive symptoms).

Question 7

Left ventricular systolic dysfunction is a main type of heart failure.
Increased left ventricular __________, reducing the left ventricular cardiac ________. There’s __________ of the myocardial wall - fibrosis and _________ of myocardium/activity of matrix _________. Mitral valve ____________, neuro-hormonal ___________ and cardiac ____________.

Answer 7

Capacity
Output
Thinning
Necrosis
Proteinases
Incompetence
Activation
Arrhythmias

Question 8

With left ventricular systolic dysfunction, the loss of muscle may lead to uncoordinated/abnormal myocardial contraction, but what changes are occurring at a cellular level initially?

Answer 8

Changes to the extracellular matrix: increased collagen I and III, slippage of myocardial fibre orientation, change of cellular structure and function - myocytolysis, vacuolation of cells, myocytes hypertrophy, SR dysfunction, changes to calcium availability/receptor regulation.

Question 9

Describe the role of global remodelling in the pathophysiology of heart failure over time.

Answer 9

Global remodelling may occur days to months after acute infarction and a hypertrophied heart (diastolic HF), e.g. From hypertension, may result in global thinning and a dilated heart, as thickening can’t be sustained. Necrosis and atrophy in cardiomyocytes.

Question 10

The baroreceptor reflex (controlled by the SNS, so part of the neuro-hormonal response), is an early compensatory method to improve cardiac output (cardiac contractility, vasoconstriction and tachycardia), but can have long term deleterious effects, how?

Answer 10

Beta-adrenergic receptors become down regulated/uncoupled and noradrenaline induces cardiac hypertrophy/myocyte apoptosis and necrosis via alpha-receptors and induce up regulation of the RAAS. Reduction in heart rate variability.

Question 11

Myocardial damage –> activation of the ____ –> myocardial ____________, decreased ____________ and myocyte ____________.

Answer 11

SNS
Hypertrophy
Contractility
Damage

Question 12

RAAS is commonly activated in heart failure.

What does Angiotensin II act on, to what affect?

Answer 12

Angiotensin II works on AT1R for vasoconstriction and retention leading to pathology and abnormality.
Also AT2R, which along with the bradykinin system, increases NO (vasodilatory).

Question 13

Angiotensin II plays a key role in organ damage, what can in cause in the body?

Answer 13

Stroke, hypertension, heart failure/MI, renal failure and death.

Question 14

Why is the RAAS commonly activated in heart failure and what does this mean?

Answer 14

Reduced renal blood flow and renin induction from the macula dense by the SNS. Elevated AII leads to vasoconstriction (increase afterload), promotes left ventricular hypertrophy and myocytes dysfunction. Aldosterone release promotes sodium/water retention and stimulates thirst by central action.

Question 15

Natriuretic hormones:
ANP - predominate renal action - ___________ afferent and _______________ efferent arterioles. Decreased resorption by the ___________ ______ inhibits _______ and ____________ secretion. There’s systematic arterial and venous vascular ___________. BNP has a similar effect and there is C type from the CNS and epithelium, with ___________ effects.

Answer 15

Constricts
Vasodilates
Collecting ducts
Renin and aldosterone
Dilation
Limited

Question 16

What is the main overall effect of natriuretic peptides?

Answer 16

Balance vascular tone and sodium/water balance of the RAAS and they have a role as a sensitive HF marker. A stretch of an increase in cardiac chamber volume leads to their release.

Question 17

What is another name for Vasopressin?

Answer 17

Anti-diuretic hormone (ADH).

Question 18

What is hyponatraemia?

Answer 18

Water in excess of sodium retention and from increased water intake / action of ADH on V2 receptors in the collecting duct.

Question 19

What is the change in the effect hyponatraemia/osmolality has on ADH release normally, compared to in cases of heart failure and what is the deleterious effect of this?

Answer 19

Normally, hyponatraemia/osmolality inhibits ADH release, but it causes an increased release with heart failure - more water retention and increased systemic resistance means a reduced cardiac output.

Question 20

Endothelin is secreted by vascular ____________ cells - it causes systemic and renal _____________, by activating the _____ system via autocrine activity. There are ____________ levels in some heart failure; it correlates with indices of ___________.

Answer 20

Endothelial
Vasoconstriction
RAAS 
Increased 
Severity

Question 21

What are the 5 main neuro-hormonal responses to heart failure?

Answer 21

The baroreceptor reflex,
The renin angiotensin aldosterone system,
Natriuretic peptides,
Anti-diuretic peptide and 
Endothelin.

Question 22

______________ E1 and I2 are stimulated by noradrenaline and the ______ system. It ____________ renal arterioles to attenuate their effects. _________ block its de novo synthesis.

Answer 22

Prostaglandins
RAAS
Vasodilate
NSAIDs

Question 23

Nitric oxide is a _____________ made by nitric oxide ____________ of endothelial cells and this is blunted in heart failure, so there’s a ______ of vasodilation balance.

Answer 23

Vasodilator
Synthase
Loss

Question 24

Bradykinin __________ the natriuesis and vasodilation. It also stimulates __________ production.

Answer 24

Promotes

Prostaglandin

Question 25

Tissue necrosis factor ____________ in heart failure and depresses myocardial __________, stimulates ____ synthase and may have a role in _________ (weakness/wasting).

Answer 25

Increases
Function
NO
Cachexia

Question 26

What is oedema?

Answer 26

An excessive volume of fluid within the tissues - interstitial and intracellular.

Question 27

How can heart failure cause oedema?

Answer 27

There are changes to capillary dynamics. The RAAS means fluid retention, so this is exacerbated.
Net filtration pressure = hydrostatic pressure - osmotic pressure.

Question 28

Vascular endothelium -
_____________ peripheral arterial resistance (due to increased endothelin, RAAS, reduced NO and the SNS) and alterations in vascular _____ exacerbate clinical deterioration, which can lead to …(3).

Answer 28

Increased
Tone
Skeletal muscle changes
Renal effects
Anaemia

Question 29

How can vascular changes involved with heart failure lead to skeletal muscle changes?

Answer 29

Reduced blood flow leads to reduced muscle mass (cachexia) - affecting all muscles limbs to diaphragm. Abnormalities of structure and function contribute to fatigue and exercise intolerance.

Question 30

Explain the effect heart failure can have on the kidneys.

Answer 30

GFR(glomerular filtration rate) is maintained initially by haemodynamic changes at the glomerulus - neurohormonal activation leads to increased sodium/water retention, but in severe heart failure renal blood flow falls, so there is reduced GFR, so a rise in serum urea and creatinine - exacerbated by treatments limiting Angiotensin II actions.

Question 31

Anaemia may contribute to heart failure symptoms. It is common and easily treated, with a multifactorial aetiology, what are some causes?

Answer 31

Chronic inflammatory disease, expanded plasma volume, drug therapy, iron malabsorption, chronic renal failure (kidneys are the source of erythropoietin).

Question 32

Left ventricular systolic heart failure (LVSHF), involves a reduced ejection fraction (EF). What is the type of heart failure with preserved ejection fraction?

Answer 32

HFpEF - heart failure preserved ejection fraction - diastolic.

Question 33

Almost ___% of heart failure patients have HFpEF - they are frequently _________ and elderly and often will have a history of ____________/__________/_________. It involves normal ____ function, with ____________ remodelling.

Answer 33

50
Female
Hypertension, diabetes, obesity
LV
Concentric

Question 34

How do collagen deposition, hospitalisation, mortality and diagnosis compare in HFpEF and LVSHF?

Answer 34

Hospitalisation and mortality are similar, with a less clear diagnosis and more collagen deposition with HFpEF.

Question 35

HFpEF:
Impaired diastolic LV _________ (increased left atria and _____________ ________ pressure). Filling is dependent on the high left atrial pressure. A right __________ dysfunction may result - it triggers neurohormonal activation as per __________ heart failure.

Answer 35

Filling
Pulmonary artery
Ventricle
Systolic

Question 36

What are the different types of heart failure?

Answer 36

Left sided, right sided or biventricular (congestive) heart failure. LVSHF ‘pump failure’ or HFpEF ‘failure of LV relaxation).

Question 37

What are the signs/symptoms of left sided heart failure?

Answer 37

Fatigue, exertional dysponea, Orthopnoea (well lying down) and paroxysmal nocturnal dyspnoea (PND), which can wake the patient up. If mild, there may be few clinical signs, but as it progresses: tachycardia, cardiomegaly, 3rd/4th heart sounds, functional murmur of mitral regurgitation, basal pulmonary crackles and peripheral oedema.

Question 38

What is the aetiology of right sided heart failure?

Answer 38

The result of long standing LVHF or chronic disease, pulmonary embolism/hypertension (pulmonary/tricuspid valvular disease, left to right shunts, isolated RV cardiomyopathy).

Question 39

Describe the signs/symptoms of right sided heart failure.

Answer 39

Related to distension and fluid accumulation in areas drained by the systemic veins: fatigue, dyspnoea, anorexia, nausea, increased JVP, tender smooth hepatic enlargement, pitting oedema and ascites/pleural effusion.

Question 40

Why does heart failure on the whole have a profound effect on quality of life?

Answer 40

The heart fails to discharge its contents properly, leading to congested lungs and later congested peripheries. There’s a characteristic response of renal, neural and hormonal responses.

Question 41

What may provide successful treatment for heart failure?

Answer 41

Neurohormonal blockade.

Question 42

List some potential causes of heart failure.

Answer 42

Diseased myocardium - IHD, abnormal loading conditions (hypertension), toxic damage (cytotoxic drugs-chemotherapy).

Question 43

Describe some chronic clinical signs and symptoms of heart disease.

Answer 43

Pulmonary congestion, venous congestion, dependent oedema.

Dyspnoea, lethargy, orthopnoea.

Question 44

Heart failure is more malignant than some cancers, with 50% dead within ___ years.
~______ml of fluid is needed to make pleural effusion visible, so it’s a sign of longevity.
The path of the IJV is straight up from the _________ between the sternal head of the ___________________ (SCM) and part of the EJV.
To check for __________ oedema, press 1 finger in 1 place (check both legs-more likely on left).

Answer 44

5
500
Clavicle
Sternocleidomastoid

Question 45

Why can heart failure be described as a viscous cycle?

Answer 45

Impaired LV function, leads to decreased SV and CO, so there’s neurohormonal activation, increasing the systemic vascular resistance and so the outflow resistance.
The decrease in SV and CO also leads to deuces renal perfusion so increased sodium/water retention, so an increase in blood volume, increasing the preload/filling pressure, which leads to ventricular dilation and increased wall stress, reducing SV and CO.

Question 46

Why is heart failure described as a state of neurohormonal imbalance?

Answer 46

There is decreased vasodilator/natriuretic/anti-mitotic mediators and an increase in the opposite.

Question 47

Overreaction of the RAAS and SNS is detrimental in HFpEF; how does this underpin the basis of therapy?

Answer 47

Beta-blockers and RAAS inhibitors.

Question 48

Heart failure is very prevalent with >=___% in those over 70. At age 55, the lifetime risk factor of heart failure is 33% in men and ___% in women. ________ to the NHS relate largely to hospitalisation - medium length stay in the UK is __ days. Patients are usually hospitalised more than once per ______. ___________ rates remain high - more men till 85+. Patients are likely to fare better if placed in a ______________ setting and if a HF nurse follows up after ___________ and if HF team saw them/gave input.

Answer 48

10
28
Cost
9
Year
Mortality
Cardiology
Discharge

Question 49

Evidence for treatment is reflected in guidelines. What type of drugs are ideal to use?

Answer 49

Class I recommended drugs with a level of evidence of A.

Question 50

What time of drugs are used to inhibit the RAAS?

Answer 50

ACEI (Angiotensin converting enzyme inhibitors),
ARB (Angiotensin receptor blockers) and
MRA (muscarinic receptor agonists).

Question 51

IA recommendation for treating heart disease is ACEI, __________________ and MRA at different times of need (add on) and sacubitril/valsartan is IB to replace _____.

Answer 51

Beta blockers

ACEI

Question 52

What help does evidence show that ACE inhibitors give?

Answer 52

Consistent improvement in cardiac function, symptoms and clinical status, a decrease in mortality and hospitalisation - evidence for use in types I (asymptomatic) to IV (immobilised).

Question 53

What potential issue do you need to be careful of when using ACE inhibitors alongside MRA?

Answer 53

They may retain potassium.

Question 54

Recent paradigm shifts in the treatment of HF call for ACEI (or ARB) + beta-blocker + mineralocorticoid receptor agonist, what is LCZ696?

Answer 54

2 drugs in 1, with 1:1 bioavailability - sacubitril and valsartan - simultaneously inhibits neprilysin and blocks AT1 receptors, leading to more excretion of sodium and reducing death from cardiovascular causes/1st hospitalisation for HF. There is a therapeutic algorithm for symptomatic HFpEF.

Question 55

What may a heart failure patient’s ECG show?

Answer 55

A wide QRS, as there’s interruption to the conduction down the normal, fast His-Purkinje system. The heart may not be in sinus rhythm - the ventricles aren’t synchronised and so are inefficient.

Question 56

Cardiac dyssynchrony in HF can have a deleterious prognostic impact, what must be done?

Answer 56

Resynchronise with biventricular pacemaker leads.

Question 57

For heart failure, guidelines suggest specialists, access to diagnostic tests and pathways to management, what may a cardiac MRI show?
Non invasive investigations are recommended first, what may be seen on an echocardiogram?

Answer 57

An MRI may show a scar and an echocardiogram could show a dilated left ventricle with a thin wall.

Question 58

Heart failure had effective evidence based treatments, but despite this, due to its high mortality and morbidity, how is it unique compared to other coronary artery diseases?

Answer 58

It is the only manifestation of coronary artery disease with increasing prevalence.