Heart failure Flashcards

1
Q

describe the normal circulation

A

body has 2 circulations

each pump linked to vessels in front and behind - so what affects one side will automatically affect the other side

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2
Q

what is cardiac output

A

the vol of blood leaving wither side of the heart per minute - usually from the L ventricle

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3
Q

preload

A

stretch cardiac myocyte

inadequate venous return affect SV

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4
Q

afterload

A

force have to contract against

excessive resistance compromises venous return

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5
Q

contractility

A

extrinsic muscle strength

inadequate contractility can compromise SV

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6
Q

what is EDV

A

volume in ventricles when the heart is relaxed

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7
Q

ESV

A

vol in vent when the heart is contracted

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8
Q

EF =

A

100* (sv/EDV)

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9
Q

ranges of EDV

A

=/>55% normal
45-54% mildly reduced
30-44% moderately reduced
<30% severely reduced

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10
Q

how do you measure an EF

A

use transthoracic echocardium - ultrasound of the chest

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11
Q

what is heart failure

A

inability of heart to keep up with demand
inadequate perfusion of organs - brain, liver and kidneys
congestion in lungs and legs - fluid builds up
collection of signs and symptoms

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12
Q

reason for tachycardia

A

compensation of heart failure - maintain CO

can also beat harder - +ve inotropy

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13
Q

what is dilated cardiomyopathy

A

thinner wall

heart cant generate enough pressure

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14
Q

3 types of heart failure

A

left v right
chronic v acute
HF with reduced EF v HF with preserved EF

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15
Q

left HF

A

disfunction with the LV
ejection problem with getting blood out /filling
blood back into lungs through pul vein= congestion -cause pulmonary hypertension - increase hydrostatic pressue - the fluid leaks into the airspace - this is pul oedema
cause breathlessness, coughing and wheezing - respiratory symptoms and dizziness and cyanosis

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16
Q

R HF

A

dysfunction in R ventricle
ejection/filling problem
increased afterload from pul circulation because of pul hypertension that was caused by L HF
heart pumps more
needs more O2 but don’t have it - cell death - HF

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17
Q

chronic HF

A

slow onset

caused by infection, pul embolism, MI or surgery

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18
Q

acute HF

A

rapid onset
caused by similar things to chronic and viral myocarditis
symptoms similar to chronic but timing onset and worsening are worse

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19
Q

HFrEF

A

abnormal systolic function - vent not pump into aorta
impaired contraction of v, despite of high HR = low CO
caused by damage of v myocytes
reduced EF = higher diastolic vol - lower SV and higher/same EDV
ESV high - because less is ejected therefore SV decrease and EF decrease

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20
Q

what causes HFrEF

A

dilated cardiomyopathy
aortic stenosis
valve not eject blood into aorta

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21
Q

HFpEF

A

abnormal diastolic volume
normal contraction of the ventricles
increased stiffness of ventricle - impaired relaxation/filling FILLING ISSUES
EDV reduced therefore reduced SV masked and so is preserved

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22
Q

cause of HFpEF

A

hypertrophy inwards = smaller space to fill

reduced EDV and reduced SV means EF the same

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23
Q

what is the relation of HF with age

A

peak age at 75-84

decrease from here as people die of it/other comorbidities

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24
Q

6 causes of heart failure

A
valve disease 
ischemic heart disease 
MI 
hypertension 
dilated cardiomyopathy 
hypertrophic cardiomyopathy
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25
Q

valve disease

A

mitral/tricuspid = cant fill
aortic/pulmonary = systolic issue
hardening of valve
cause congestion in the lungs/legs

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26
Q

IHD

A

less heart to perform function
work harder
O2 not available because of narrow arteries

27
Q

MI

A

myocyte die from occlusion

28
Q

hypertension

A

increased afterload so ventricles have to work harder
hypertrophy inwards
less space for blood in diastole
less blood ejected to the body - CO down

29
Q

dilated cardiomyopathy

A

wall thinner - reduced generatable pressures
more blood but not enough force to eject it
systolic disfunction

30
Q

hypertrophic cardiomyopathy

A

less blood ejected to body
reduced ventricular volume
diastolic issue

31
Q

main cause of heart failure

A

coronary artery disease - occlusion of arteries, less O2 to the myocytes

32
Q

patient clinical features

A

exertional breathlessness
fatigue - because beat harder and faster
orthopnoea
paroxysmal nocturnal dyspnoea - wake up coughing and out of breath
anorexia
weight loss

33
Q

clinical features

A
tachycardia 
reduced pulse pressure
pitting oedema 
increased JVP 
hepatomegaly 
ascites
34
Q

investigations

A
x-ray - enlarged heart 
ECG - measure EF 
ambulatory ECG - arrhythmia, heart not pumping efficiently 
exercise test 
angiogram 
BNP
35
Q

raised jugular venous pressure

A

JVP measure of pressure in RA
increased pressure R side of heart
pressure back up in systemic veins - especially jugular
rise in pressure = HF

36
Q

pitting oedema

A

fluid accumulation in tissue from rise in pressure = fluid leakage - in lower extremities
pitting effect when physically depressed
indentation visible for a short period
caused by R heart failure - blood backs in the legs
not to RA/RV

37
Q

ascites

A

fluid accumulation in peritoneal cavity from rise in hydrostatic pressure = leakage of fluid

38
Q

Brain (B) type natriuretic peptide

A

natriuresis = sodium excretion
BNP is released from v myocytes in response to stretch
BNP causes vasodilation of microvessels (reduces afterload so ventricles don’t work as hard) , reduced aldosterone secretion = no Na reabsorption = no water reabsorption and reduced renin secretion - all reduce extra cellular fluid - reduces pressure

39
Q

3 types of treatment for anything

A

conservative, medical, surgery

40
Q

conservative treatment for HF

A

weight loss
exercise
stop smoking
less alcohol

41
Q

medication

A

ACE inhibitor - reduce aldosterone production
B blocker - slow heart down, need less energy and so O2
diuretic - reduce excess fluid eg spironolactone ivabradine - work in funny channels = vasodilation
sacubital/valsartan - valsartan is angiotensin receptor blocker sacubital - inhibit enzyme that breaks down BNP
cardiac resynchronisation therapies - heart beat more efficiently eg v beat together

42
Q

sequence of medical treatment

A

new diagnosis
ACE inhibitor - titrate upwards /angiotensin receptor blocker if ACE intolerant
B blocker and titrate upwards (no contraindications and patient stable)
spironolactone (diuretic) - if still moderately to severly symptomatic
specialist advice

43
Q

overall effect of diuretics and ACE inhibitors

A

reduction in afterload

44
Q

overall effect of B blockers

A

slow heart

so need less energy and O2

45
Q

types of fluid control

A

haemofiltration
peritoneal dialysis
haemodialysis

46
Q

devices used in HF

A

intra-aortic balloon pumping
resynchronisation
VAD/total artificial heart

47
Q

surgical procedures

A

coronary artery bypass graft - to bypass the blockage
valve surgery
transplantation

48
Q

how does the law of Laplace affect HF

A

pressure and vol govern cardiac function
in compensatory hypertrophy - thickness i9ncrease = stress decrease but less space for blood to pool in v - treatment is to reduce stress
in dilated cardiomyopathy - wall thickness decrease = more stress = unable to eject blood because not enough force

49
Q

what is the law of LaPlace

A

(pressureradius)/2wall thickness

(pressure*vol)/LV mass

50
Q

beneficial physiological response to damage

A

NP system - BNP produced (from increased ventricular wall stress), ANP from increased atrial stress
causes vasodilation - reduce blood pressure, sympathetic tone, aldosterone levels
natriuresis, diuresis, antifibrotic effects
reduce afterload

51
Q

pathophysiological response to damage

A

RAAS activated because heart beat is less effective so there is less renal perfusion
make ANG2
bind to AT1 receptor
cause vasoconstriction - increase bp, increase sympathetic tone, increase aldosterone, increase sodium fibrosis
also: high and low mechanoreceptor = SNS activation - vasoconstriction and Na and water retention

52
Q

what happens when there is an imbalance between beneficial physiological and pathological

A

worsens heart failure

53
Q

other functions of RAAS

A

cardiac hypertrophy and fibrosis

renal parenchymal fibrosis

54
Q

SNS other functions

A

increase vasopressin
increase HR
increase contractility
cardiac fibrosis

55
Q

effect of osmotic and non-osmotic stimuli

A

vasopressin made

free water retention

56
Q

HF for the patient

A
breathless and tired
heart damaged and less effective pump 
marked neurohormonal activation 
poor QOL 
reduced life expectancy
57
Q

classification of heart failure

A
functional classification - based on New York Heart Association: 
class 1 - no limitation physical, ordinary physical activity doesn't cause fatigue, palpitation, dyspnoea 
2 - slight physical activity limitation, comfortable at rest - ordinary physical activity = fatigue etc
3 - marked limitation activity, comfortable rest, less ordinary activity = fatigue 
4 - unable to do any physical activity without discomfort, symptoms at rest, any physical activity undertaken - discomfort is increased
58
Q

progression of HF

A
diagnosis
[sudden death] 
mild 
moderate 
severe 
death 
[coronary events speed up process eg MI]
59
Q

normal EDV

A

130ml

60
Q

normal ESV

A

48ml

61
Q

normal SV

A

81mm

62
Q

normal EF

A

62%

63
Q

what sided HF causes pitting oedema

A

R

64
Q

what sided HF causes congestion in the lungs

A

L