Pathophysiology of Cardiac Failure Flashcards

1
Q

what 3 factors affect SV?

A
  • preload
  • afterload
  • contractility
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2
Q

what is afterload?

A
  • force contracting heart must generate to eject blood from heart
  • heart is pumping against tension in the ventricle wall and the pressure in the aorta
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3
Q

What will happen if the heart can’t generate sufficient wall tension?

A

decreased SV since not enough force to overcome the afterload

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4
Q

how is heart failure graded?

A

1,2,3 and 4

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5
Q

what is class 1 heart failure?

A
  • no limitation of physical activity

- ordinary physical activity does not cause undue fatigue, palpitations or dyspnea

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6
Q

what is class 2 heart failure?

A
  • slight limitation to exercise

- ordinary exercise results in palpitations, dyspnea and fatigue

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7
Q

what is class 3 heart failure?

A
  • marked limitation of exercise

- less than ordinary exercise= fatigue, palpitations and dyspnea

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8
Q

what is class 4 heart failure?

A
  • cant exercise, experience symptoms at rest also

- discomfort increases by doing activity

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9
Q

what is ejection fraction?

A

proportion of blood you can eject from your ventricle

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10
Q

Describe the features of systolic ventricular dysfunction?

A
  • impaired cardiac contractility
  • ejection fraction decreased because heart muscle just doesn’t contract as well as it should
  • the EDV is the same however
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11
Q

describe the features of diastolic ventricular dysfunction?

A
  • normal ejection fraction
  • decreased filling occurring or impairment of ventricular relaxation
  • EDV lower
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12
Q

what is the overall similarity between diastolic and systolic ventricular dysfunction ?

A

lower SV and hence cardiac output is falling

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13
Q

What conditions affect systolic dysfunction of the ventricle?

A
  • contractility: ischaemic heart disease, cardiomyopathy
  • volume overload- overstretched leading to problems with subsequent contractions
  • pressure overload- valvular stenosis means you can’t push out as much blood, not ejecting same volume each stroke
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14
Q

what can lead to impairments of relaxation which result in diastolic dysfunction?

A
  • impedance of ventricular expansion
  • extreme hypertrophy of chamber wall
  • ischaemia of heart can reduce the hearts ability to relax during diastole and fill
  • increased heart rate
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15
Q

what is the effect of long term heart failure on the heart?

A

usually both sides of the heart eventually become affected

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16
Q

where does blood come from to the right side of the heart? what effect does right heart failure therefore have?

A
  • blood comes from the veins and peripheral tissues

- if unable to clear the blood it will accumulate downstream in tissues and organs= leads to oedema

17
Q

how does oedema arise as a result of R side heart failure?

A

increase in pressure in the veins since blood is not cleared therefore leads to an increase in hydrostatic pressure in vein.
more fluid pushed out along the entire length of the capillaries and this accumulates in soft tissue

18
Q

what effect does R heart failure have on the GI system?

A

problems with congestion in capillaries hence can’t absorb nutrients effectively from the GI tract: weight loss, anorexia

19
Q

what is the effect of liver congestion as a result of R sided heart failure?

A

liver is the site of detoxification= congestion of fluid and toxins in the liver will result in damaging the liver

20
Q

where does L heart pump blood? what is the effect of left heart failure on the body? what clinical signs are visible?

A
  • systemic circulation
  • decreased tissue perfusion since cable to provide the output to supply the tissues
  • cyanosis and hypoxia signs become visible
21
Q

what congestion effect does L heart failure have?

A

pulmonary congestion since left side can’t beat to meet the demand of the R side which is normal

22
Q

what affect does pulmonary congestion have on the patient as a result of L heart failure?

A
  • cough with a frothy sputum
  • orthopnea- in recumbent position patient struggles to breath
  • PND
23
Q

what is orthopnea?

A
  • postural related
  • in recumbent position the patient has issues with breathing
  • lie down gravity effect lessened hence massive fluid return from legs to heart and backs up in lungs due to L heart failure
24
Q

what is PND?

A
  • waking up gasping for breath in middle of night
  • gravity effect=accumulation of fluid in ankles
  • lie down fluid re-distributes back to heart but L can’t cope due to failure and fluid starts to accumulate in the pulmonary circulation
25
Q

how does left heart failure lead to right heart failure?

A
  • blood not cleared from lungs
  • increases resistance to flow in the pulmonary circulation
  • R side has to work harder and will eventually lead to failure of R side since it can’t cope
26
Q

What causes R ventricular dysfunction?

A
  • pulmonary hypertension
  • valve damage, stenosis, incompetence
  • cardiomyopathies, infarction affecting the pumping abilities of the R ventricle
  • L knock on affect to right
27
Q

What leads to left ventricular dysfunction?

A
  • hypertension- elevated total peripheral resistance, afterload increased
  • acute MI
  • aortic or mitral stenosis or regurgitation
28
Q

what are the compensatory mechanisms of the body trying to achieve during heart failure?

A

keep mean arterial blood pressure high.

29
Q

how can compensatory mechanisms worsen heart failure?

A

if heart is damaged it can’t meet the O2 and energy demands and can’t cope with further stress
long term compensatory mechanisms put stress of heart up to meet demand

30
Q

what detects the heart failing and the cardiac output dropping?

A

decreased renal blood flow hence decreased volume getting filtered out into the urine

31
Q

how do kidneys respond to decreased CO? What effect does this have?

A
  • renin release triggered= angiotensin 2 produced + aldosterone leading to sodium and therefore water retention
  • vascular volume increased to increase venous return increasing frank starling mechanism
32
Q

what other sensors detect drop in CO? what is their response to the drop?

A
  • baroreceptors in aortic and carotid bodies
  • increase sympathetic nervous system increasing HR and TPR via vasoconstriction= increasing afterload in order to increase contractility of the heart
33
Q

how does the effect of the frank starling mechanism result in worsening heart failure?

A
  • increased vascular volume increases EDV therefore increasing muscle stretch and O2 consumption
  • overstretching sarcomeres you start to see a decrease in force generated
  • increasing EDV only results in a slight increase in SV however increases the force on the heart
34
Q

How does sympathetic activity worsen heart failure?

A
  • initially helpful= increased HR and contractility increases CO
  • increases heart workload and energy demand of the suffering heart tissue
  • increases TPR which heart pumping against
  • increases renin release
35
Q

what happens as a result of desensitisation of beta and adrenoreceptors?

A
  • effects of sympathetic activity start to decrease
  • iontropy starts diminishing
  • cardiac activity drops
36
Q

how does the renin angiotensin system worsen heart failure?

A
  • decreased blood flow through kidneys increases release of renin
  • angiotensin 2 results in increasing TPR and blood volume
  • deposition of fibroblasts and collagen in ventricles increase stiffness altering its contractility
37
Q

what is the strategy to treat heart failure?

A
  • decrease preload and afterload to decrease cardiac work demand
  • relax smooth muscle
  • inhibit RAAS, prevent accumulation of fluid exasperating oedema
  • prevent inappropriate increase in HR