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ESA2 > CVS Heart Failure > Flashcards

CVS Heart Failure Flashcards

1
Q

Define heart failure

A

A state in which the heart fails to pump enough blood to meet the needs of the tissues/organs of the body, despite adequate filling pressure

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2
Q

What is the primary cause of HF?

A

Ischaemic heart disease

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3
Q

How many classes of HF are there?

A

4

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4
Q

Which class HF do you get symptoms at rest?

A

IV

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5
Q

What 4 things affect cardiac output?

A

Preload
Afterload
Contractility
Heart rate

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6
Q

Why does End diastolic filling pressure have to be almost perfect for maximised CO in HF?

A

Because normally the force developed by muscle fibre depends on the degree to which the fibre is stretched. In gross HF, higher filling pressure actually has a negative effect on CO as the filling pressures are already higher than a normal heart so on the frank starling curve any further stretch will reduce cardiac fibre contraction

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7
Q

Why is the preload increased in heart failure?

A

It is an early mechanism to help sustain CO - with worsening HF an increase in preload will then have a negative effect on CO (frank starlings curve).

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8
Q

Broadly, what three changes occur in HF in the heart/body?

A
  • Structural changes - muscle mass to increase CO
  • Functional changes - increase preload to increase CO
  • Neurohumoral changes - to increase CO
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9
Q

What structural changes occur as a result of chronic wall stress leading to HF?

A

Initially:

1) Hypertrophy of myocytes
2) Death/apoptosis of cells
3) Regeneration

Eventually leads to:

1) Remodelling - wall thinning
2) Myocytolysis and vacuolation of cells (loss of contractile machinery gives appearance of empty cell)
3) Increase in collagen
4) Slippage of myocardial fibre orientation (due to dilation of chamber)

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10
Q

What functional changes occur in the myocyte?

A

1) Uncoordinated/abnormal contraction
2) SR dysfunction
3) Changes to Ca availability and/or receptor regulation

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11
Q

What is global thinning and when does it occur?

A

Thinning of the wall of the myocardium of the LV -

After MI there is thinning (due to necrosis) in an infarcted area - the rest of the heart compensates by thinning too - to spread pressure and prevent rupture in the infarcted area.

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12
Q

What happens in concentric vs eccentric vs dilated heart remodelling?

A

Concentric - new sarcomeres are added in parallel in response to pressure overload - hypertrophy - leads to reduced compliance and reduced ability to fill - diastolic failure

Eccentric hypertrophy - due to volume (and pressure) overload - new sarcomeres are added in parallel - so heart

Dilated heart - many causes e.g. dilated cardiomyopathy, aortic regurg or post hypertrophy e.g. in hypertension as hypertrophy cannot be sustained (increased need for blood to muscle but no increase in blood flow so cells die)

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13
Q

What is the ejection fraction like for systolic vs diastolic HF?

A

Systolic - Low <50% - thinned

Diastolic - ‘preserved’ - hypertrophied

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14
Q

What are the 6 groups of neurohumoral HF compensatory mechanisms?

A

1) Sympathetic NS
2) RAAS
3) ANP/BNP
4) ADH
5) Endothelin
6) Others - prostaglandins, NO, kallikrien system, TNF-alpha

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15
Q

What are the early (2) and late (3) sympathetic nervous system mechanisms to compensate for HF?

A

Early - 1) Baroreceptor reflex to increase
2) sympathetic increase in HR, contractility, and arterial and venous vasoconstriction

Late - 1) Downregulation and uncoupling of beta-adrenoceptors

2) NA - stimulates hypertrophy of myocytes and activates RAAS system
3) Increased SNS and reduced ParaSNS reduces HR variability (which predisposes to arrhythmias)

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16
Q

What two compensatory mechanisms occur in HF and why are these actually deleterious?

A

SNS and RAAS are activated in response to reduced CO, but in turn these eventually reduce CO and have a negative effect on HF

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17
Q

What do the 3 late SNS mechanisms lead to eventually?

Effect of: RAAS increasing fluid, increased O2 demand by increased HR and contractility, direct effect of SNS

A

1) Myocardial hypertrophy (due to RAAS vasoconstriction increasing wall stress and RAAS fluid retention increasing wall stress)
2) Decreased contractility (increased O2 demand needed for hypertrophy and also by increased HR and contractility - with no added perfusion leads to ischaemia within the myocardium myocyte death and reduced contractility)
3) Direct cardiotoxicity of SNS - myocyte damage

These three all interlink and affect eachother too.

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18
Q

How and why is RAAS activated in HF (4)? Which receptor does AngII primarily work at?

A
  • Reduced CO leads to reduced renal flow - stimulates renin
  • SNS stimulates renin
  • Reduced Na at the distal convoluted tubule
  • Also endothelin - renal vasoconstrictor - activates RAAS

Attempts to compensate to increase cardiac output

AT1Receptor

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19
Q

What negative effects can RAAS have longterm on HF? Name 4 major organs and how it affects them

A
  • Angiotensin II big role in organ dysfunction (increased wall stress from vasoconstriction, increased hypertrophy of myocytes, atherosclerosis, reduced kidney function

Stroke, HF/MI, renal failure, Hypertension - leads to LVH and myocyte dysfunction

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20
Q

What 5 effects does AngII have that can affect HF?

A 
Increased Na reabsorption 
Increased H2O absorption
ADH - Thirst 
Vasoconstriction - Hypertension - LVH/myocyte dysfunction
Aldosterone release
21
Q

What effects do ANP and BNP have? Same or opposite to RAAS? How is it used clinically?

A

Opposite to RAAS

Released in response to stretch - predominantly kidney action

1) Constricts afferent and vasodilators efferent arterioles
2) Decreases Na+ reabsorption in collecting duct
3) Inhibits Renin and Aldosterone
4) ?Systemic arterial and venous vasodilation

Pro NT BNP/BNP marker for HF - low -ve predictive value so is a sensitive test

22
Q

What is the role of ADH in HF?

A

ADH is increased in HF in response to RAAS

Increased H2O reabsorption in collecting duct of kidney
Increased thirst

Leads to hyponatraemia, increased H2O retention and increased systemic resistance = reduced CO

23
Q

Which substance correlates with poor prognosis in research? What does it do?

A

Endothelin

Activates RAAS as is a renal vasoconstrictor (autocrine)

24
Q

Prostaglandins E2/I2, NO and Bradykinin do what in HF?

What does alpha-TNF do?

A

PGs - oppose RAAS
NO - vasodilates - opposes RAAS but blunted in HF
Bradykinin - natriuresis and vasodilation - stimulates PGs

Alpha-TNF depresses myocardial function

25
Q

Define oedema

A

Excessive fluid build up in interstitium and intracellularly

26
Q

What are some causes of oedema?

A

HF
Lymphoedema
Kwashiorkor

27
Q

How does HF cause oedema?

A

Increased venous blood due to poor cardiac function increases hydrostatic pressure along with RAAS increasing fluid vol so increasing hydrostatic pressure further

28
Q

What 4 effects/mechanisms occur on vasculature to increase the peripheral arterial resistance in HF?

A
  • SNS
  • RAAS
  • Endothelin
  • Reduced NO
29
Q

What do changes in skeletal muscle flow in HF lead to?

A

Reduced flow leads to muscle wasting (cachexia) and reduced exercise tolerance which adds to symptoms

30
Q

What late changes happen to the kidney in severe HF?

A

Reduced GFR due to reduced CO - leads to increased urea and creatinine in blood. Lose nephrons lose kidney function, kidney shrinks. This can be exacerbated by treatments inhibiting the actions of AngII

31
Q

What is the relevance of anaemia in HF? What causes it?

A

Often concomitant and exacerbates symptoms

Multifactorial - one reason increased plasma vol, anaemia of chronic disease, iron malabsorption, chronic renal failure

32
Q

What is HF with preserved ejection fraction AKA? What are key factors, and features of the HF? Is it more or less severe than systolic HF?

A

Diastolic failure

Female, elderly
Often - HTN, diabetes, obesity

Normal ejection fraction with concentric remodelling
Hospitalisation and mortality similar to systolic HF

33
Q

What leads to impaired relaxation in diastolic HF?

A

Thicker and shorter myocytes
Increased collagen deposition
Less compliance so relies on high LA pressure to fill ventricle

34
Q

Why can RV dysfunction occur with diastolic HF?

A

Because increased LA pressure, increases PA pressure which in turn increases RV workload

35
Q

Does it trigger the same neurohormonal response as systolic HF?

A

Yes

36
Q

What is congestive HF?

A

Biventricular

37
Q

What are some symptoms of Left heart failure? Clinical signs of HF?

A

Fatigue
Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea

Tachy
Cardiomegaly
Strong apex beat (V5)
Crackles in lung on auscultation
3rd or 4th heart sound - Gallop rhythm - indicative
Functional murmur of mitral regurg (due to poor pump action)
Peripheral oedema - if severe (normally pulm oedema first with LSHF)

38
Q

What is a major cause of RHF, and some other ones? What are symptoms and signs of Right HF?

A

Most frequent cause is bivent failure from LSHF

Chronic lung disease e.g. COPD. Also PE/pulm HTN can cause, swell as pulm/tricuspid valve disease, L->R shunts, right ventricular cardiomyopathy.

Increased JVP
Peripheral pitting oedema - ascites
Enlarged liver and spleen 
Fatigue, dyspnoea, nausea etc
Pleural effusion
39
Q

What is the difference in causes and pathophys of concentric, eccentric and dilated HF?

A

Concentric - pressure overload - HTN/aortic stenosis - new sarcomeres added IN PARALLEL - increased myocardium size = increased O2 demand that heart can’t supply - myocyte death and dysfunction –> HF –> loss of compliance so get diastolic failure (increased filling pressure but reduced filling as reduced relaxation). Preserved ejection fraction. Increased collagen

Dilated - volume overload - e.g. in mitral/aortic regurgitation - new sarcomeres added IN SERIES –> sarcomere slippage and increased O2 demand needed –> myocyte death and dysfunction –> HF –> LV systolic failure as can’t pump blood out, increased compliance but reduced ejection fraction due to elevated wall stress.

Eccentric - mix of volume and pressure overload e.g. systolic heart failure with hypertension can cause this.

40
Q

Can hypertrophied heart become dilated?

A

yes e.g. hypertension - myocytes die - remodelling - becomes dilated as cannot maintain the compensatory hypertrophy

41
Q

Do medicines for HF directly cause the heart contraction to increase?

A

No

42
Q

Which side are you more likely to see peripheral oedema on first?

A

LHS

43
Q

Major cause of HF?

A

Ischaemic heart disease

44
Q

Is Class I or Class III evidence of European Society of Cardiology more reliable?

A

Class I most reliable evidence for treatment

45
Q

Name 4 types of drugs that are helpful in HF and how?

A

B blockers - antag to SNS activation - reduce HR reduce reduce force of contraction so reduce O2 demand on heart

then either:

ACEi - block angiotensin converting enzyme so prevent effects of Ang II

or

Ang II antags - prevent effects of Ang II

then

Aldosterone antagonists - K+ sparing diuretic acts on NaKATPase in distal convoluted tubule, increasing Na and H2O excretion whilst sparing potassium - important to help combat hypokalaemia which can cause arrhythmias in heart failure (effect of aldosterone).

46
Q

Name one other type of treatment that isn’t a drug? When would you consider this type of management?

A

CRT - bivent pacemaker/defibrillator that attempts to coordinate contraction of ventricles to increase efficiency and ability of heart to pump blood

With increased QRS length and LBBB on ECG

47
Q

What are sacubritril/valsartan?

A

New drugs that can be used instead of ACEi in heart failure

48
Q

What major outcomes are we looking for with treatment?

A 
Reduced hospitalisation
Reduced mortality
Reduced mobility
Increase in cardiac function/reduced symptoms
Increase in QuALYs
49
Q

How would you assess/test for HF in clinic?

A

History - e.g. of hypertension/ischaemic heart disease, symptoms/exposure to anything toxic e.g. chemo drugs

Clinical examination - JVP/crackles in lungs/oedema/murmur

ECHO

ECG

Blood test: BNP/Pro NT-BNP (not done if go straight to echo in cardiac clinic - but done more in community)

ESA2 (37 decks)

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