heart failure Flashcards

1
Q

cardiac output

A

stroke volume x hr

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2
Q

preload

A

force that stretches cardiac muscle prior to contraction - volume filling heart from venous return

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3
Q

afterload

A

pressure heart must exert to eject blood during ventricular contraction

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4
Q

how to reduce preload

A

furosemide diuretics

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5
Q

how to reduce afterload

A

increase diameter and increase contractility

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6
Q

vasodilators used in heart failure

A

ACEi, ARBs, nitrates, PDEIs (afterload)

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7
Q

diuretics in heart failure

A

furosemide (preload)

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8
Q

positive inotropes in heart failure

A

B agonists, PDEIs, digoxin

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9
Q

cardio-inhibitors in heart failure

A

b-blockers

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10
Q

ACEi MOA

A
  • Prevents angiotensin i → angiotensin ii

- Increase in peripheral vascular resistance = increased afterload

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11
Q

side effects ACEi

A

dry cough and angioedema, hypotension, hypekalaemia

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12
Q

diuretics in HF

A

Loop diuretics act on aLOH to block NaKCC channels → increased sodium excretion and decreased ECF volume

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13
Q

side effects loop diuretics

A

hypokalaemia, deafness, renal toxicity

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14
Q

mineralocorticoid receptor antagonists in HF

A

Act in DCT to block aldosterone receptors - limited expression of sodium and potassium channels -> reduced preload

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15
Q

side effects mineralocorticoid antagonists

A

hyperkalameia and gynaecomastia

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16
Q

b agonists in HF

A

e. g. dobutamine

- B1 is cardiac specific and increases force of contraction

17
Q

what would a1 do to heart

A

increase after load

18
Q

side effects b agonists

A

tachycardia and no benefit in chronic disease

19
Q

PDEIs in HF

A
  • B1 adrenoreceptor

- Increase 2nd messengers intracellularly by preventing breakdown

20
Q

side effects PDEIs

A

hypotension, tachycardia and arrythmias

21
Q

what leads to increase heart contractility

A

b1 action

22
Q

what leads to increased vasodilatation

A

b2 action

23
Q

cardiac glycosides in HF MOA

A
  • Ion exchange in myocytes
  • Na/K pump inhibited
  • Secondary inhibition of calcium/sodium exchange
  • Rise in intracellular calcium = increased ionotropicity
  • Lows AV conduction - used in AF
24
Q

cardiac glycoside e.g.

A

digoxin

25
Q

side effects cardiac glycosides

A

arruthmias, contraindicated in hypokalaemia/renal impairment

26
Q

B-blocker MOA in chronic HF

A
  • Sympathetic nervous system
  • Activation of sympathetic nerves during HF can cause arterioconstriction, venoconstriction, tachycardia and renin release
  • That is why we block with B blockers
27
Q

side effects b blockers

A

bronchospasm in asthmatics, cold hands and feet

28
Q

treatment for HF

A

Loop diuretics (all patients) +/- oxygen (94-98%) +/- vasodilators (nitrates, don’t give if pt hypotensive)

29
Q

how to treat pt with HF in respiratory failure

A

CPAP

30
Q

how to treat hypotensive HF pt

A

If pt in hypotension (+ve inotropic agents) +/- vasopressor agents

31
Q

ongoing treatment for HF

A

ACEi and B blockers

32
Q

what to give if pt low tolerance to ACEi

A

ARBs