Heart failure Flashcards
what is heart failure?
failure of the heart to meet bodily demands
what factors affect SV (and therefore CO)?
increased contractility + pre-load = increased SV
increased after-load = decreased SV
what is the relationship between pre-load and SV?
increased blood vol in ventricle at end of dyastole causes ventricles to stretch more during systole so greater force of contraction = increased SV
what factors increase contractility of ventricular myocytes?
greater stretch of ventricle = increased contractility
greater sympathetic activity = increased contractility
what are the causes of heart failure?
most common = ischaemic heart disease
other causes = hypertension, arrhythmias, valvular disease
how does ischaemic heart disease cause heart failure?
remodelling 2 types:
ventricular hypertrophy = reduced filling = decreased pre load = decreased SV = decreased CO
ventricular walls are thinner but cant contract well = decreased contractility = decreased SV = decreased CO
what are the 2 broad types of heart failure?
HFpEF = heart failure where filling of the heart is the issue
HFrEF = heart failure where emptying of heart is the issue
how do we measure ejection fraction?
using echocardiogram
SV / EDV
normal = > 50%
how does ejection fraction differ in HFpEF and HFrEF?
HFrEF = < 40%
HFpEF = > 50%
what are the common symptoms of heart failure?
dyspnoea (breathlessness)
fatigue (reduced exercise tolerance)
pulmonary or peripheral oedema
what is the most common type of heart failure?
left ventricular systolic dysfunction (left ventricular HFrEF)
* ventricle size is normal or thinner but decreased contractility
what is the impact of increasing pre-load in a failing heart?
(first think about why it would be good in a healthy heart)
1. increased pre-load has little effect on increasing CO
2. eventually increasing pre-load decreases CO
3. increased fluid in ventricles = increased pressure
4. increased pressure in pulmonary circulation = pulmonary congestion
what happens when the CO decreases?
CO = BP x TPR
1. decreased CO = decreased BP
2. decreased BP activates 2 pathways
3. detected by baroreceptors or decreased renal perfusion
* detected by baroreceptors = increased HR and increased TPR
* decreased renal perfusion activates RAAS = increased Na+ and fluid retention in kidney = increased pre-load
how does left ventricular systolic dysfunction cause pulmonary oedema?
- increased pressure in LV
- increased pressure in pulmonary circulation
- increased hydrostatic pressure in venule end
- less favourable gradient between hydrostatic and oncotic pressure
- increased interstitial fluid accumulation = pulmonary oedema
although less common, how can left ventricular systolic dysfunction cause peripheral oedema?
- reduced renal perfusion = activation of RAAS
- increased Na+ and H20 retention
- accumulates in lower extremeties due to gravity