heart failure Flashcards

1
Q

what is heart failure

A

inability of the heart to maintain tissue perfusion at normal filling pressure

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2
Q

what does the frank starling curve show

A

as we increase the end diastolic pressure of the left ventricle the stroke volume in systole increases

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3
Q

what does increased adrenaline do to the heart

A

increases heart rate and force of contraction to increase stroke volume

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4
Q

why does heart failure decrease starlings curve

A

heart does not have enough force to pump blood around the body but there is a high LV end diastolic pressure

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5
Q

what is systolic dysfunction

A

impaired ventricular contraction/ inotropy

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6
Q

what is diastolic dysfunction

A

impaired ventricular relaxation

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7
Q

what are the physiological effects of heart failure

A
  • ventricle walls don’t meet
  • bigger LV than LA
  • decreased contractility
  • increased chamber dimension
  • decreased wall thickness
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8
Q

what is preload

A

volume of blood in the ventricles after diastole

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9
Q

what is afterload

A

resistance left ventricle overcomes to overcome circulating blood

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10
Q

what are neurohormonal changes in heart failure

A

compensation for the lack of oxygen that is reaching the body so increases neuronal and hormonal firing

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11
Q

what is the maladaptive remodelling in heart failure

A

issues are not helped or corrected then they become worse and cycle starts again

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12
Q

what are the electrophysical changes in heart failure

A
  1. decrease in Ca2+ in the cytosol
  2. decrease Ca2+ binding to troponin-C
  3. decreases force of contraction
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13
Q

what causes an increase in heart contraction

A
  • increased sympathetic activity
  • more calcium in cytosolic space
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14
Q

why is digoxin used in heart failure

A
  • inhibits Na, K and ATPase
  • increase cytosolic ca concentration
  • increases force of contraction
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15
Q

why is dobutamine used in heart failure

A
  • increases sympathetic activity in the heart
  • increases cytosolic ca
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16
Q

why is milrinone used in heart failure

A
  • inhibits PDE2
  • increases cytosolic ca
17
Q

why don’t inotropic agents not always work

A

heart works faster as stimulation increased but is less efficient

18
Q

what are the pro-arrhythmogenic changes in heart failure

A

increase inward current + decreased outward current = action potential prolongation causing arrhythmias

19
Q

what causes an increase in sympathetic overactivity in heart failure

A
  1. baroreceptors detect decrease in blood pumped
  2. baroreceptors signal to medullary cardiovascular centre
  3. increase HR and contractility
  4. renin release
  5. cutaneous arterial vasoconstriction
  6. adrenalin release
20
Q

how is beta1 adrenergic signalling altered in heart failure

A
  1. sympathetic overdrive
  2. beta adrenergic signalling downregulated by antagonist
  3. decreases cardiac reserve
21
Q

what are the beta 1 adrenergic mediated effects

A
  • increases heart rate
  • increases force of contraction
  • increases renin release
  • decreases cardiac efficiency
  • increase hypotrophic signalling
22
Q

how is the RAAS system activated

A
  1. reduced cardiac output B1-AR activated in juxtaglomerular cells
  2. renin released
  3. angiotensin released from liver
  4. renin and angiotensin make angiotensin I
  5. ACE convert angiotensin I to angiotensin II
  6. aldosterone production for Na reabsorption, vasoconstriction, sympathetic activity
23
Q

stages of vasoconstriction as neurohormonal signalling compensation

A
  1. Alpha1 and angiotensin 2 type 1 receptors on smooth muscle
  2. increase the calcium in the cell
  3. leads to contraction
  4. increases the total peripheral resistance
  5. increase arterial BP
  6. increase tissue perfusion
  7. increases afterload
24
Q

how does Na+ and H2O retention increase preload

A
  1. increase RAAS signalling
  2. angII activates, increasing sodium retention
  3. aldosterone binds to receptors, more sodium retained
  4. increases circulating volume and tissue perfusion
25
Q

fluid overload from heart failure compensatory mechanism in

A
  • 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
26
Q

what medication is used to counteract the fluid overload

A
  • ACE inhibitors
  • angII receptor antagonist in PCT and collecting ducts
  • loop diuretic ins thick ascending limb
27
Q

what effect do natriuretic peptides cause

A
  • relax smooth muscle (vasodilation)
  • inhibit sodium reabsorption
28
Q

what is concentric hypertrophy

A
  • systolic function maintained and diastolic impaired
  • big thick LV
  • heart contracts well but is stiff
29
Q

what is the result of stiff contraction

A
  • decreases passive relaxation
  • less volume at end of diastole
  • decrease in stroke volume
30
Q

ejection fraction calculation

A

EF = stroke volume/ end diastolic volume

31
Q

what are the stages of the heart failure cycle

A
  1. injury to heart
  2. decreased cardiac output
  3. decrease in renal perfusion
  4. increase sympathetic activation and increased RAAS
  5. vasoconstriction, increase TP, increased blood volume
  6. increased after and preload
  7. structural remodelling