Heart Failure Flashcards
What is heart failure?
The state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate pressure.
Give some causes of heart failure
Ischaemic heart disease
Hypertension
Dilated cardiomyopathy
High output heart failure - AV fistula or Paget’s disease (extra blood vessels)
Arrhythmia
Restrictive cardiomyopathy e.g. amyloidosis
Valvular/congenital heart disease
What are the stages of heart failure?
I - no symptomatic limitations
II - slight limitations to physical activity, no symptoms at rest
III - limitations with less than normal activity. No symptoms at rest.
IV - can’t carry out physical activity without symptoms. May also have symptoms.
What is normal cardiac output?
5L/min
What is normal stroke volume?
75ml
What is the normal ejection fraction?
Above or equal to 50%
What affects cardiac output?
Venous capacity
Heart rate
Aortic and peripheral impedance
Myocardial contractility
What are the causes of systolic dysfunction?
Increased left ventricular dysfunction
Decreased left ventricular cardiac output
Thinning of the myocardial wall (fibrosis and necrosis, activity of matrix proteinases)
Mitral valve incompetence
Neural-hormonal inactivity
Cardiac arrhythmia
What structural changes can be seen in the heart in heart failure?
Reduced muscle
Uncoordinated or abnormal myocardial contraction
Changes to the ECM (increased collagen/slippage of fibre orientation )
Change in cellular structure and function (myocytolysis/vacuolation)
Myocyte hypertrophy
SR dysfunction
Change to calcium availability
Receptor regulation
Describe how the sympathetic nervous system is activated in heart failure
Baroreceptor mediation.
Instant response
What is the positive short term effect of sympathetic nervous system activation in heart failure
Increases cardiac output by improving contractility, arterial/venous contraction and causing tachycardia.
What are the long term negative effects of sympathetic nervous system activation in heart failure?
Beta-adrenergic receptors downregulated or uncoupled
Noradrenaline increases cardiac hypertrophy and triggers myocyte apoptosis/necrosis via alpha-receptors
Induce upregulation of RAAS
Describe briefly the renin-angiotensin-aldosterone system.
Angiotensinogen to angiotensin I by renin
Angiotensin I to angiotensin II by ACE
AT1R is detrimental
AT2R causes water retention and aldosterone secretion, increases NO production.
What effects does AT1R activation have on the vasculature?
Atherosclerosis
Vasoconstriction
Vascular hypertrophy
Endothelial dysfunction
What effects does AT1R activation have on the heart?
Left ventricular hypertrophy
Fibrosis
Remodelling
Apoptosis