Heart failure Flashcards
describe the normal circulation
body has 2 circulations
each pump linked to vessels in front and behind - so what affects one side will automatically affect the other side
what is cardiac output
the vol of blood leaving wither side of the heart per minute - usually from the L ventricle
preload
stretch cardiac myocyte
inadequate venous return affect SV
afterload
force have to contract against
excessive resistance compromises venous return
contractility
extrinsic muscle strength
inadequate contractility can compromise SV
what is EDV
volume in ventricles when the heart is relaxed
ESV
vol in vent when the heart is contracted
EF =
100* (sv/EDV)
ranges of EDV
=/>55% normal
45-54% mildly reduced
30-44% moderately reduced
<30% severely reduced
how do you measure an EF
use transthoracic echocardium - ultrasound of the chest
what is heart failure
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
reason for tachycardia
compensation of heart failure - maintain CO
can also beat harder - +ve inotropy
what is dilated cardiomyopathy
thinner wall
heart cant generate enough pressure
3 types of heart failure
left v right
chronic v acute
HF with reduced EF v HF with preserved EF
left HF
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
R HF
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
chronic HF
slow onset
caused by infection, pul embolism, MI or surgery
acute HF
rapid onset
caused by similar things to chronic and viral myocarditis
symptoms similar to chronic but timing onset and worsening are worse
HFrEF
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
what causes HFrEF
dilated cardiomyopathy
aortic stenosis
valve not eject blood into aorta
HFpEF
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
cause of HFpEF
hypertrophy inwards = smaller space to fill
reduced EDV and reduced SV means EF the same
what is the relation of HF with age
peak age at 75-84
decrease from here as people die of it/other comorbidities
6 causes of heart failure
valve disease ischemic heart disease MI hypertension dilated cardiomyopathy hypertrophic cardiomyopathy
valve disease
mitral/tricuspid = cant fill
aortic/pulmonary = systolic issue
hardening of valve
cause congestion in the lungs/legs
IHD
less heart to perform function
work harder
O2 not available because of narrow arteries
MI
myocyte die from occlusion
hypertension
increased afterload so ventricles have to work harder
hypertrophy inwards
less space for blood in diastole
less blood ejected to the body - CO down
dilated cardiomyopathy
wall thinner - reduced generatable pressures
more blood but not enough force to eject it
systolic disfunction
hypertrophic cardiomyopathy
less blood ejected to body
reduced ventricular volume
diastolic issue
main cause of heart failure
coronary artery disease - occlusion of arteries, less O2 to the myocytes
patient clinical features
exertional breathlessness
fatigue - because beat harder and faster
orthopnoea
paroxysmal nocturnal dyspnoea - wake up coughing and out of breath
anorexia
weight loss
clinical features
tachycardia reduced pulse pressure pitting oedema increased JVP hepatomegaly ascites
investigations
x-ray - enlarged heart ECG - measure EF ambulatory ECG - arrhythmia, heart not pumping efficiently exercise test angiogram BNP
raised jugular venous pressure
JVP measure of pressure in RA
increased pressure R side of heart
pressure back up in systemic veins - especially jugular
rise in pressure = HF
pitting oedema
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
ascites
fluid accumulation in peritoneal cavity from rise in hydrostatic pressure = leakage of fluid
Brain (B) type natriuretic peptide
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
3 types of treatment for anything
conservative, medical, surgery
conservative treatment for HF
weight loss
exercise
stop smoking
less alcohol
medication
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
sequence of medical treatment
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
overall effect of diuretics and ACE inhibitors
reduction in afterload
overall effect of B blockers
slow heart
so need less energy and O2
types of fluid control
haemofiltration
peritoneal dialysis
haemodialysis
devices used in HF
intra-aortic balloon pumping
resynchronisation
VAD/total artificial heart
surgical procedures
coronary artery bypass graft - to bypass the blockage
valve surgery
transplantation
how does the law of Laplace affect HF
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
what is the law of LaPlace
(pressureradius)/2wall thickness
(pressure*vol)/LV mass
beneficial physiological response to damage
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
pathophysiological response to damage
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
what happens when there is an imbalance between beneficial physiological and pathological
worsens heart failure
other functions of RAAS
cardiac hypertrophy and fibrosis
renal parenchymal fibrosis
SNS other functions
increase vasopressin
increase HR
increase contractility
cardiac fibrosis
effect of osmotic and non-osmotic stimuli
vasopressin made
free water retention
HF for the patient
breathless and tired heart damaged and less effective pump marked neurohormonal activation poor QOL reduced life expectancy
classification of heart failure
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
progression of HF
diagnosis [sudden death] mild moderate severe death [coronary events speed up process eg MI]
normal EDV
130ml
normal ESV
48ml
normal SV
81mm
normal EF
62%
what sided HF causes pitting oedema
R
what sided HF causes congestion in the lungs
L
