L20 - Heart failure pathophysiology Flashcards
Definition of heart failure
Summarise some causes
heart unable to pump enough blood to meet demands of body.
could be caused by:
- abnormalities in structure, function of heart
- underlying CAD
- previous MI
Summarise the pathophysiology of heart failure (2)
- structural/cardiac abnormality
- reduced cardiac output
- elevated intracardiac pressures (rest/exercise) - myocardial injury
- changes in myocytes
- changes in ECM
- –> pathological ventricle remodelling
- –> ventricular dilation
- –> impaired ventricular contractility
Describe systolic dysfunction? (4)
- decreased stroke vol
- higher that normal end systolic vol
- incomplete emptying
- higher than normal end diastolic vol and pressure
What occurs in diastolic dysfunction? (3)
- reduced chamber compliance
- higher than normal diastolic filling pressure
- incomplete filling
Summarise factors precipitating oedema?
- increased capillary hydrostatic pressures (HF)
- decreased plasma oncotic pressure (hypoproteinemia)
- increased capillary permeability (pro-inflam mediators)
Describe the vicious cycle of heart failure with reduced ejection fraction? (6)
- Myocardial injury, maladaptive LV remodelling
- decreased ventricular function
- decreased cardiac output
- over-activation of neurohormonal signalling pathways
- –> RAAS
- –> SNS
- –> reduced natriuretic peptide sensitivity - increase in cardiac work
- myocardial injury!
Describe the effects of signalling pathways on the heart? (4)
- v.constriction, apoptosis, hypertrophy, fibrosis
- –> afterload increases - sodium and water retention, increase intravascular vol
- –> preload increases - overall increase in cardiac work
- myocardial injury, maladaptive LV remodelling
What role do natriuretic peptides play in protection of heart?
- decreased BP
- reduced CO
- reduced ventricular remodelling
- v.dilation
- VSMC proliferation
What is an important biomarker in heart failure?
As heart failure progresses
- –> SNS activation
- –> RAAS
- increased BV
- sustained myocardial stretch
- elevated levels of circulating BNP
Summarise the components of the RAAS system
Functions of RAAS
- angiotensinogen (liver)
- angiotensin I
- angiotensin II
- AT1 receptor
V.CONSTRICTION
- increase bp
- increase symp tone
- increase [aldosterone]
- increase fibrosis
- increase hypertrophy
- decreases natriuresis/diuresis
Summarise the action of natriuretic peptides
Opposes RAAS
V. DILATION
- decrease bp
- decrease symp tone
- decrease [aldosterone]
- decrease fibrosis
- decrease hypertrophy
- increases natriuresis/ diuresis
Progression of HF can be attributed to 2 main mechanisms
- myocyte death
- decline in systolic function —> activation of neurohormonal signalling pathways
NPS
- v.dilation
SNS
- andrenaline
- noradrenaline
- v.constriction a1,b1,b2
RAAS
- angiotensin II
- AT1 receptor
- v. constriction
Frank-Starling mechanism
recap what happens in HF
ventricular output increases in relation to preload.
i.e. with greater stretch of myocardial fibres, greater force of contraction generation
HF: decreased SV —> reduced chamber emptying with higher than normal diastolic volume.
summarise LEFT heart failure
retrograde pressure transmission to pulmonary circulation.
Heart unable to pump blood into circulation to meet demands
- increased pressure within heart
- blood backs up into pulmonary circulation
- LA, through open mitral, pulmonary vein then capillaries
LHS HF
describe systolic heart failure?
- LV muscle wall contraction fails
- compromised pumping
- decreased ejection fraction
- enlargement of ventricle
