Heart Failure Flashcards

1
Q

What are the symptoms of heart failure?

A

Breathlessness, exercise intolerance, fatigue, swelling in the extremities

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2
Q

what is acute Heart Failure the result of?

A

Sudden circulatory collapse - sudden drop in CO during AMI

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3
Q

what is systolic dysfunction and diatolic dysfunction and which is most common?

A

Systolic dysfunction = inability of the heart to contract and eject blood - THIS IS THE MOST COMMON
Diastolic dysfunction = lack of compliance to filling e.g. left ventricle thining or thickening = isn’t able to fully relax

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4
Q

Which is most common, left or right sided HF?

A

Left is most common and the cause of right sided usually

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5
Q

What is the difference between compensated and decompensated HF?

A

Compensated = managed and controlled with pharmacological help
Decompensated = having several episodes, not managed - will lead to death
Symptoms =worsening breathlessness, coucg with frothy bloody sputum, dizziness, fatigue, coldness NEED HOSPITAL ADMISSION

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6
Q

What compensatory measure is seen in HF patients when trying to meet oxygen demands?

A

We see an increase in ventricular end diastolic volume = increase in Preload. The more the ventricle is fills, the more it will stretch (like an elastic band) so it will contract with more force to try and reach desired stroke volume. This mechanism will work at rest but will never be able to reach demands at exertion.

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7
Q

What happens during cardiogenic shock?

A

Blood volume drops e.g. artery has been cut so will never meet hearts needs without pharmacological help to increase contractility = fatal

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8
Q

What are the symptoms at different stages of HF?

A
  1. ) asymptomatic but see very early signs of ventricular dysfunction
  2. ) Breathlessness and fatigue during moderate exercise
  3. )Breathlessness and fatigue during mild exercise
  4. ) Symptoms even at rest
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9
Q

HF is usually caused by some form of cardiomyopathy (disease of the myocardium is associated with cardiac dysfunction). What are the main causes?

A

Inherited:
1.) Congenital hypertrophic cariomyopathy (thickening of ventricles)
3.)Arrhythmic RV Cardiomyopathy (fatty deposits between muscle fibres of the heart = inefficient contractility)
Aquired:
1.) Pressure overload = increased afterload (due to HT - systemic/pulmonary, aortic/pulmonary valve stenosis)
2.) Ischaemic cardiomyopathy e.g. MI, coronary artery disease
3.) Valvular disease (structural damage due to HT or valve stenosis)
4.) Infection/Inflammation myocarditis - can be due to bacteria, viruses, alcohol or chemotherapy

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10
Q

How does HR progression lead to decrease in cardiac function

A

1.) reduced myocyte contractility = ventricles start to fail
2.) This leads to less CO
3.) this leads to less tissue pefusion as the main organs are prioritised
4.) The body compensated by trying to increase blood volume by retaining water = oedema
5.) Get reduced venous return = less is pumped out from left side to body = less is returned to the right side via the lungs.
BREATHLESSNESS, FATIGUE, OEDEMA

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11
Q

What are the symptoms of reduced cardiac output?

A

Fatigue, low tolerance to extertion

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12
Q

What are the symptoms of reduced skeletal muscle blood?

A

Blood is diverted to the major organs causing muscle weakness, fatigue, low tolerance to exertion.
Eventually will see muscle wasting and weigh loss (bc blood not being perfused to gut)

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13
Q

What are the symptoms of LV failure?

A

Pulmonary oedema = blood isn’t being pumbed into circulation = backlog into lungs = breathlessness, paroxymal nocturnal dyspnoea (fluid moving in lungs in the night = panick)

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14
Q

What are the symptoms of RV failure?

A

Increase in venous pressure, blood can’t be returned to the lungs to be oxygenated = backlog - will see swelling in the jugular vein that brings blood back down from the brain, will also get hepatic congestion (backlog in abdomen) and peripheral oedema (swelling in arms and legs)

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15
Q

What are baroreceptors part in the neurohormonal axis?

A

Following a heamorhage there will be a decrease in the firing of the baroreceptors. The medulla senses this and stimulates the SNS to release noradrenaline to act on the beta receptors in the heart and tha alpha receptor in the vasculature. Nad causes an increase in heart rate, peripheral vasoconstricion and contractility (SV) all of which lead to an increase in CO.

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16
Q

How is renal perfusion a part of the neurohormonal axis?

A

Decrease CO = decrease renal perfusion. This is sensed by the juxtaglomerular apparatus which increases the production of renin = increase production of angiotensin 2 = more ADK secretion from the posterior pituitary gland and an increase in aldosterone sectretion from the adrenal cortex. Both of these lead to water retention through different mechanisms. This is an attempt to increase Blood volume

17
Q

The neurohromonal response is a self perpetuating spiral when it comes to remodelling, why?

A

Heart failure causes dilation of the ventricles = ventricles become thicker or thinner = REMODELLING = inability to contract during systoli = decreased CO. This triggers the neurohormonal axis which increases heart rate, vasoconstriction and blood volume in an attempt to increase Preload to meet the problem with demand. This causes further ventricular dilation and therefore further remodelling

18
Q

Why do b-type natriuretic proteins, adrenomedullin and NO help in diagnosis of heart failure?

A

These compounds are released in hte body to try and conteract the effect of the neurohormonal axis = reduce swelling and stimulates vasodilation

19
Q

What are the aims of HF treatment?

A
  1. ) Improve symptoms
  2. ) Reduce exacerbations
  3. ) Increase exercise tolerance (qol)
  4. ) Decrease mortality
20
Q

What do we target when treating HF?

A

The neurohormonal axis - this is what drives the progression of the condition.
Particularly the renin-aldosterone system and the SNS

21
Q

Name a drug class that targets the renin-aldosterone system, will treat LV dysfunction but might cause a dry cough as a side effect?

A

ACE inhibitors - given as a low initial dose to reduce the risk of a rapid decrease in BP - rise dose over 2-3 weeks
*be aware of hyperkalaemia

22
Q

What can be added to an ACE inhibitor if swelling and fluid in pulmonary persists?

A

Loop or thiazide diuretic

23
Q

Why should we be extra careful if a dry cough presents in patients with HF?

A

Could be a sign of pulmonary oedema

24
Q

If ACE is contraindicated, what is the alternative used to target the renin aldosterone system?

A

AT1 receptor antagonist - directly inhibit Ang2

25
Q

What class of drugs will target the SNS and stop noradrenaline’s effect on heart rate?

A
B-blockers
Certain ones (not the ones used in HT) e.g. bisoprolol, carvedilol are given at low dose and titrated as not to overly slow down heart rate. Give once started ACE/ARB treatment
26
Q

How will b-blockers lowering HR help in HF>

A

slower HR = longer diastolic filling period = better filling = increased cardiac output
Might also stabilise electrical conduction = reducing arrhythmias

27
Q

After the addition of an ACE/ARB +B-blocker (to max dose), what is the 3rd step in the treatment of HF?

A

aldosterone recetor antagonist e.g. spirinolactone at low dose
be aware of hyperkalaemia

28
Q

What additional therapies are there?

A
  1. )loop/thiazide related diuretic - oedema
  2. ) Digoxin
  3. ) Ivabradine (funny current blocker slows down HR)
  4. ) Hydralazine/nitrate combo