heart failure Flashcards
what is heart failure
inability of the heart to maintain tissue perfusion at normal filling pressure
what does the frank starling curve show
as we increase the end diastolic pressure of the left ventricle the stroke volume in systole increases
what does increased adrenaline do to the heart
increases heart rate and force of contraction to increase stroke volume
why does heart failure decrease starlings curve
heart does not have enough force to pump blood around the body but there is a high LV end diastolic pressure
what is systolic dysfunction
impaired ventricular contraction/ inotropy
what is diastolic dysfunction
impaired ventricular relaxation
what are the physiological effects of heart failure
- ventricle walls don’t meet
- bigger LV than LA
- decreased contractility
- increased chamber dimension
- decreased wall thickness
what is preload
volume of blood in the ventricles after diastole
what is afterload
resistance left ventricle overcomes to overcome circulating blood
what are neurohormonal changes in heart failure
compensation for the lack of oxygen that is reaching the body so increases neuronal and hormonal firing
what is the maladaptive remodelling in heart failure
issues are not helped or corrected then they become worse and cycle starts again
what are the electrophysical changes in heart failure
- decrease in Ca2+ in the cytosol
- decrease Ca2+ binding to troponin-C
- decreases force of contraction
what causes an increase in heart contraction
- increased sympathetic activity
- more calcium in cytosolic space
why is digoxin used in heart failure
- inhibits Na, K and ATPase
- increase cytosolic ca concentration
- increases force of contraction
why is dobutamine used in heart failure
- increases sympathetic activity in the heart
- increases cytosolic ca
why is milrinone used in heart failure
- inhibits PDE2
- increases cytosolic ca
why don’t inotropic agents not always work
heart works faster as stimulation increased but is less efficient
what are the pro-arrhythmogenic changes in heart failure
increase inward current + decreased outward current = action potential prolongation causing arrhythmias
what causes an increase in sympathetic overactivity in heart failure
- baroreceptors detect decrease in blood pumped
- baroreceptors signal to medullary cardiovascular centre
- increase HR and contractility
- renin release
- cutaneous arterial vasoconstriction
- adrenalin release
how is beta1 adrenergic signalling altered in heart failure
- sympathetic overdrive
- beta adrenergic signalling downregulated by antagonist
- decreases cardiac reserve
what are the beta 1 adrenergic mediated effects
- increases heart rate
- increases force of contraction
- increases renin release
- decreases cardiac efficiency
- increase hypotrophic signalling
how is the RAAS system activated
- reduced cardiac output B1-AR activated in juxtaglomerular cells
- renin released
- angiotensin released from liver
- renin and angiotensin make angiotensin I
- ACE convert angiotensin I to angiotensin II
- aldosterone production for Na reabsorption, vasoconstriction, sympathetic activity
stages of vasoconstriction as neurohormonal signalling compensation
- Alpha1 and angiotensin 2 type 1 receptors on smooth muscle
- increase the calcium in the cell
- leads to contraction
- increases the total peripheral resistance
- increase arterial BP
- increase tissue perfusion
- increases afterload
how does Na+ and H2O retention increase preload
- increase RAAS signalling
- angII activates, increasing sodium retention
- aldosterone binds to receptors, more sodium retained
- increases circulating volume and tissue perfusion
fluid overload from heart failure compensatory mechanism in
- increased circulating volume increases hydrostatic pressure
- fluid in peripheral circulation causes pitting oedema, increasing JVP
- fluid in bronchi and alveoli
- accumulation of blood cause vascular distension decreasing lung compliance to dysponea
what medication is used to counteract the fluid overload
- ACE inhibitors
- angII receptor antagonist in PCT and collecting ducts
- loop diuretic ins thick ascending limb
what effect do natriuretic peptides cause
- relax smooth muscle (vasodilation)
- inhibit sodium reabsorption
what is concentric hypertrophy
- systolic function maintained and diastolic impaired
- big thick LV
- heart contracts well but is stiff
what is the result of stiff contraction
- decreases passive relaxation
- less volume at end of diastole
- decrease in stroke volume
ejection fraction calculation
EF = stroke volume/ end diastolic volume
what are the stages of the heart failure cycle
- injury to heart
- decreased cardiac output
- decrease in renal perfusion
- increase sympathetic activation and increased RAAS
- vasoconstriction, increase TP, increased blood volume
- increased after and preload
- structural remodelling
