Heart failure Flashcards
The most common cause of heart failure
MI
More people survive it now and consequently are living with heart failure
Causes of heart failure aside from MI
Pressure overload - hypertension, aortic stenosis
Volume overload - valve regurgitation
Contractile dysfunction - ischemic heart disease, congenital cardiomyopathy, pregnancy, cardiomyopathies
Symptoms of right-sided heart failure?
tiredness and weakness, urinating less, peripheral oedema (up to thighs, sacrum, abdominal wall), ascites, nausea, anorexia, facial engorgement, epistaxis
The treatment for an MI
Percutaneous coronary intervention
Pass a wire through the clot and put a stent in to allow return of blood
What heart failure does to the Starling curve
curve is shallower and doesn’t reach same peak
Why do patients with HF have chronically high plasma catecholamines (adrenaline, NA)?
Baroreceptor response to a decrease in BP –> increase SNS activity to adrenal glands –> adrenaline (mainly) & NA act on B1 receptors in heart, supplementing SNS nerves
Consequence of persistent adrenergic stimulation of the heart
Initially - good, increase inotropy and SV
later - contractile dysfunction in myocytes leads to ectopic activity and arrhythmia, internalisation of adrenoreceptors leads to exercise intolerance, also get pathological hypertrophy
Why are baroreceptors stimulated in HF
Decreased ventricular function means decreased SV and CO so decreased ABP which is detected
Baroreceptors detect decreased ABP –> less afferent activity to CNS –> CNS action on the kidney?
increases sympathetic activity to the kidneys (vasoconstriction of renal artery - lower GFR - more renin release)
Renin effect on blood pressure
RENIN RAISES BP
Why do patients with HF have chronically high angiotensin II
- Low ABP detected by baroreceptors –> CNS acts on kidneys
- Low ABP detected directly by the kidneys (macula densa, arterioles)
Result is to RAISE RENIN
the initial consequence of increased blood volume in (early stage) heart disease
increased EDV allows SV to be maintained at rest along with increased contractility (ejection fraction maintained)
the later consequence of increased blood volume in (late stage) heart disease
increased EDV goes beyond the plateau of the Starling curve and so SV can no longer be maintained (reduced ejection fraction)
How does left sided HF cause pulmonary oedema
mis-match in LV and RV CO due to failing heart causes blood to accumulate in pulmonary circulation –>
Increased capillary hydrostatic pressure –> increased capillary filtration
What classic symptom of HF is caused by pulmonary oedema
SOB