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Phase 1 - S2 Cardiovasular System > Session 9 - Heart Failure > Flashcards

Session 9 - Heart Failure Flashcards

1
Q

Define heart failure

A

A state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure

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2
Q

What is the primary cause for heart failure

A

Ischaemic heart disease

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3
Q

Name some causes of heart failure

A

Hypertension, alcohol, pregnancy, valvular disease, collagen deposition, arrhythmia

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4
Q

What is class I heart failure

A

No symptomatic limitation of physical activity

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5
Q

What is class IV heart failure

A

Inability to carry out physical activity without symptoms, with symptoms coming at rest

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6
Q

What the ejection fracture

A

50% plus

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7
Q

In heart failure what 4 things can affect the cardiac output

A
  • heart rate
  • LV preload
  • after load
  • myocardial contractility
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8
Q

what is left ventricular systolic dysfunction

A

where theres increase LV capacity but reduced LV cardiac output

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9
Q

how des LVSD affect the mitral valves

A

it pulls the cusps apart due to the widening of the LV

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10
Q

what are the structural changes of the heart in LVSD

A
  • loss of muscle
  • abnormal contraction
  • increase in collagen
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11
Q

why does LVSD result in thinning of the walls

A

there is fibrosis and necrosis as well as activity of proteinases

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12
Q

true or false - LVSD causes neuro-hormonal activation

A

true - it activates the sympathetic NS, RAAS, natuiretic hormones, endothelin, prostaglandins and TNF

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13
Q

how does activation of the sympathetic NS affect LVSD

A
  • compensatory mechanisms to improve cardiac output including increasing contractility, vasoconstriction and tachycardia
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14
Q

what are the detrimental affect of the sympathetic NS being activated in LVSD

A
  • beta adrengeric receptors become down regulated as they are being over used
  • noradrenaline induces cardiac hypertrophy and necrosis and there is an up-regulation of the RAAS system
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15
Q

what does RAAS do in LVSD

A

causes fluid retention increasing the stress on the walls of the ventricles leading to decreased contractility and hypertrophy

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16
Q

outline RAAS

A

angiotensinogen from the liver is converted into angiotensin I by renin (from the kidney). this is then converted to angiotensin II by ACE enzymes. angiotensin I can act on type 1 and 2 receptors

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17
Q

what does angiotensin II cause when it binds to type 1 receptors

A

vasoconstriction and an increase in salt and water retention and causes aldosterone release

18
Q

what does angiotensin II cause when it binds to type 2 receptors

A

increasing amounts of nitric oxide

19
Q

what causes an increase in nitric oxide

A

bradykinin

20
Q

why is nitric oxide advantageous in LVSD

A

it is a vasodilator

21
Q

why is RAAS often activated in LVSD

A

there is reduced renal flow from the reduced cardiac output so the sympathetic nervous system induces the production of renin from the macula densa

22
Q

what do natriuretics do

A

they inhibit renin and aldosterone, decrease sodium absorption in the kidneys and causes vasodilation

23
Q

when are natriuretic hormones released

A

when the increasing volume to the heart causes it to stretch

24
Q

what is anti-diuretic hormone

A

causes salt and water retention

25
Q

what is endothelin

A

a hormone secreted by endothelial cells which activates RAAS by acting as a renal vasoconstrictor

26
Q

what do prostaglandins do in LVSD

A

vasodilate renal arterioles to reverse the affects of NA/RSSA

27
Q

what does nitric oxide do

A

vasodilator produced by endothelial cells

28
Q

what does TNF do

A

depresses myocardial function

29
Q

what causes an increase in peripheral arterial resistance

A
  • SNS
  • RAAS
  • reduced NO
  • increased endothelin
30
Q

why are there skeletal muscle changes in LVSD

A

as there is less skeletal muscle blood flow - this gives fatigue and exercise intolerance

31
Q

what happens to the kidneys in severe heart failure

A

they shrink as renal blood flow falls

32
Q

what is heart failure with preserved ejection fraction

A

where the ejection fraction still remains normal
the LV relaxation decreases
this leads to impaired LV filling

33
Q

what are risk factors for HFpEF

A

obesity, elderly, female, diabetes, hypertension

34
Q

what does the heart look like in HFpEF

A

there are thicker and shorter myocytes

increased collagen deposition

35
Q

what is congestive heart failure

A

where both the right and left side of the heart fail

36
Q

what are the signs and symptoms of left heart failure

A

fatigue, dyspnoea, orthopnea, tachycardia, cardiomegaly, mumur, pulmonary crackles, peripheral oedema

37
Q

what is dyspneoa

A

breathlessness

38
Q

what is orthopnoea

A

breathlessness when lying flat

39
Q

why may there be a heart murmur in left heart failure

A

as the cusps of the mitral value are pulled apart as the LV dilates allowing blood to flow through

40
Q

why is peripheral oedema seen in L heart failure

A

there is an increase pressure in the vessels

41
Q

what causes right sided heart failure

A

chronic lung disease, pulmonary embolism and pulmonary hypertension

42
Q

what are the signs and symptoms of right sided heart failure

A

fatigue, dyspnoea, anorexia, nausea, increased JVP, oedema

Phase 1 - S2 Cardiovasular System (16 decks)

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