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CVS II > Drugs on heart > Flashcards

Drugs on heart Flashcards

1
Q

What does high HR do?

A
  • Increases myocardial O2 consumption
  • Reduces coronary circulation perfusion time (only perfuses during diastole)
  • Increases arrhythmia risk
  • Linked to atherosclerosis/coronary artery plaque disruption
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2
Q

What HR shows greater risk to CVD?

A

Resting rate > 70 bpm

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3
Q

What’s the central treatment for angina, heart failure, post-MI treatment, arrhythmias?

A

drugs that lower HR

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4
Q

Why lower HR

A

High HR is predictor of morbidity + mortality from CVD

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5
Q

How to lower HR?

A

Decrease initiation + frequency of pacemaker potentials by:

  • Inhibit vgcc: reduce phase 0, slower upstroke
  • Inhibit If channels: increase Phase 4, slower diastolic depolarisation before reaches threshold, slower to activate vgcc
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6
Q

What are Ca2+ channel blockers (CCB)?

A

Drugs that site in channel pore blocking Ca2+ entry into SA cells reducing HR

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7
Q

Why do CCB need to selectivity target Ca2+ channels in SAN?

A

Ca2+ channels also in cardiac myocytes (phase 2, plateau phase) + vascular smooth muscle
providing Ca2+ influx for contraction

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8
Q

Subtypes of CCB?

A 
vascular = Dihydropyridines
cardiac = Diphenylalkyamines
vascular+cardiac = Benzothiazepines
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9
Q

What’s Amlodipine?

A

Dihydropyridine

vascular selective CCB

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10
Q

What’s Verapamil?

A

Diphenylalkyamine

cardiac selective CCB

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11
Q

What’s Diltiazem?

A

Benzothiazepine

vascular+cardiac selective CCB

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12
Q

How can CCBs cause heart block?

A

Non-selective blocking actions on:
Ca2+ channels in cardiac myocytes for contractility
AVN for conduction

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13
Q

What’s Ivabradine?

A

Selective inhibitor of If channel in SAN
Decreases pacemaker potential frequency
Decreases HR to reduce myocardial O2 demand
Used in heart failure, angina

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14
Q

Describe how If channel blockers work?

A
  • inhibits If
  • inhibits diastolic depolarisation
  • slows unstable membrane potential from reaching threshold
  • slower to activate vgcc
  • slower upstroke of phase 0
  • reduction in pacemaker frequency potentials
  • decrease HR
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15
Q

How sympathetic increases HR?

A

NA binds to β1 adrenoceptor (Gs) - stimulate adenyl cyclase producing cAMP from ATP which increases If channel activity

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16
Q

How para decreases HR?

A

Ach binds to M2 (Gi) - inhibit adenyl cyclase so no cAMP from ATP which decreases If channel activity

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17
Q

Affect of β1-adrenoceptor blockers (antagonists)?

A

reduce sympathetic NA/A on SAN reducing HR

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18
Q

What’s Atenolol?

A

β1-adrenoceptor blockers (antagonists)

reduce sympathetic NA/A on SAN so increase in HR/contractility subdued which reduces work / O2 demands on heart

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19
Q

Why isn’t β1-adrenoceptor blockers used with CCB?

A

reduce contractility too much + produce too much bradycardia

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20
Q

Why isn’t β1-adrenoceptor blockers used on asthmatic patients?

A

can affect β2 on lungs so less bronchial dilation

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21
Q

Why can β1-adrenoceptor blockers cause fatigue?

A

can’t increase HR enough, less blood flow

22
Q

Affect of Mus receptor blockers (antagonists)?

A

reduce para vagus/Ach on SAN so removal of inhibitory influence on HR – vagal tone which increase HR

23
Q

What treatments are Mus blockers used for?

A

COPD, IBS, overactive bladder

24
Q

What’s Atropine?

A

Mus receptor blockers (antagonists)

increase HR creating stable CO

25
Q

Adverse effect of Mus blockers?

A

tachycardia increases O2 demands on heart

Important in patients w co-morbidities (COPD + angina)

26
Q

What happens during heart failure?

A

CO unmaintained – poor blood flow so end organs poorly perfused

27
Q

How to maintain CO in heart failure?

A

Increase: contractility, ejective force, SV - CO = HR x SV

28
Q

eg of acute heart failure?

A

cardiac arrest, anaphylaxis, sepsis

29
Q

eg of chronic heart failure?

A

cardiomyopathy, chronic hypertension, valve disease

30
Q

What are drug targets to increase contractility (inotropic agents)?

A

Gs coupled receptor agonists - bind to receptors linked to Gs (β1, glucagon receptor)
PDE inhibitors - less cAMP -> AMP, build up of cAMP driving PKA
Other Ca2+ rising processes

31
Q

What’s phosphodiesterase (PDE)?

A

cause breakdown cAMP -> AMP

32
Q

What are β1-adrenoceptor agonists + eg?

A

Gs coupled receptor agonists
A, dobutamine, dopamine
Used in acute heart failure

33
Q

eg of other Gs coupled agonist?

A

Glucagon – glucagon receptors in heart muscle

34
Q

What’s used for acute heart failure when the patient is on β blockers?

A

Gs coupled agonist GLUCAGON

A, dobutamine, dopamine won’t work

35
Q

Why isn’t Gs coupled agonists used in chronic heart failure?

A

increase: HR (proarrhythmic), myocardial work, O2 demand

36
Q

What are PDE inhibitors + eg?

A

Gs coupled receptor agonist
Amrinone – phosphodiesterase III inhibitor (PDE3 is heart specific)
Used in severe + chronic cases - waiting for heart transplant

37
Q

Describe how PDE inhibitor Amrinone work

A

build up of cAMP, activates PKA, increase vgcc + Ca2+ influx

38
Q

What are cardiac glycosides + eg?

A

other Ca2+ rising process : increases contractility
by reducing Ca2+ extrusion - but high toxicity
Digoxin

39
Q

Describe how cardiac glycosides Digoxin work

A
  • Digoxin inhibits Na+/K+ ATPase on cardiomyocyte surface
  • No 3Na+ out , 2K+ in
  • build up of Na+
  • less Ca2+ out, 3Na2+ in by Na/Ca exchanger (NCX)
  • more Ca2+ uptake into stores so greater CICR
  • greater contraction
40
Q

What are Ca2+ sensitizers + eg?

A

other Ca2+ rising process
used in decompensated heart failure - condition w poor outcome
Levosimedan, Omecamtiv

41
Q

Disadvantage of Gs coupled agonist + alternative?

A

induced rise in Ca2 requires Ca2+-ATPase for reuptake into stores so more O2 consumption, stresses heart, increase HR - pro-arrhythmogenic
Ca2+ sensitizers

42
Q

Describe how Ca2+ sensitizers work

A
  • no effect on Ca2+
  • increase contractile sensitivity (troponin) to Ca2+
  • contraction at lower Ca2+
  • no increase O2 consumption or pro-arrhythmogenic
43
Q

Describe how Levosimedan works

A

Ca2+ sensitizer

  • bind to troponin C
  • increase binding of Ca2+ to TnC
44
Q

Describe how Omecamtiv works

A

Ca2+ sensitizer

-increases actin-myosin interactions

45
Q

Why use β blockers in chronic heart failure?

A

To prevent:

  • overworking by slowing HR increases diastolic time - increases coronary perfusion
  • overworking by reducing contractility reduces O2 demand
  • desensitization of βadrenoceptors caused by excess compensatory sympathetic in heart failure - so available for contractility
  • βadrenoceptor associated arrhythmias
46
Q

Describe how Diuretics work

A

-excrete more fluid
-reducing blood volume
-reducing central venous pressure + SV (via Starling’s law)
-reduces CO
-reduces BP
BP=CO (blood volume) x TPR (blood vessel constriction)

47
Q

What are Diuretics + eg?

A

reduces afterload

loop, thiazide, K+ sparing

48
Q

What are ACEi, ARB + eg?

A

reduces afterload

ramipril, losartan

49
Q

Describe how ACEi, ARB work

A
  • reduce Ang II-induced vasoconstriction : reduces TPR

- reduce Ang II-induced aldosterone : reduces blood volume - reduces CO

50
Q

What’s the cardiac pain in angina caused by?

A

occlusion of coronary arteries, poor perfusion of heart, produces acid, stimulates sensory nerves

51
Q

What’s a nitrate donor + eg?

A

dilates coronary arteries to increase blood flow, relieves cardiac pain from angina
Glyceryl tri-nitrate (GTN) : spray under tongue

52
Q

What’s nitric oxide (NO)?

A
  • continually produced/released

- lipophilic, soluble gas, freely diffusible out of endothelium into surrounding VSMCs

CVS II (19 decks)

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