L15 - drug effects on the heart Flashcards

1
Q

define myocardial infarction

A

heart attack

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2
Q

define heart failure

A

insufficient CO to match body’s needs

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3
Q

in what ways can drugs act to improve heart function

A
  1. act on heart muscle (pacemaker)
    2 act on coronary arteries
  2. act on other arteries and veins (reduce cardiac work)
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4
Q

how does PNS decrease HR

A
  1. releases ACh which acts on M2 receptors in SA node
  2. causes opening of K+ channels and hyperpolarisation
  3. also inhibits funny current
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5
Q

give example of drug that can increase HR

A
  1. muscarinic (M2) antagonists (atropine)
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6
Q

give example of drug that can decrease HR

A

anticholinesterases (ACEs) - increase [ACh] in synapse

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7
Q

what does ivabradine do

A

inhibits funny current slowing HR

independent of ANS

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8
Q

why is ivabradine a good treatment of angina & heart failure

A

decreases cardiac O2 demand

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9
Q

how does the SNS increase HR

A
  1. NA acts on B1 adrenoreceptors causing cAMP release, which activates PKA causing :
    • increased HR (funny current)
    • increased contractility (and SV, and therefore CO)
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10
Q

what is the effect of the SNS on funny current

A
  1. NA binding to B1 causes release of cAMP 2nd messenger

2. cAMP activates HCN channels (funny current is HCN channel)

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11
Q

does PNS or SNS dominate heart rate at rest?

A

PNS

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12
Q

describe the process of B1 activation increasing HR

A

processes lead to PKA release

  1. PKA phosphorylates Ca2+ channels opening them
  2. PKA phosphorylates phospholamban which causes increase Ca2+ uptake into SR
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13
Q

give examples of B1 agonists at the heart

A

dopamine/dobutamine (B1)

ispoprenaline (B1 & B2)

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14
Q

name the cardiac glycosides

A

digoxin

digitoxin

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15
Q

what do digoxin and digitoxin do

A

treat severe heart failure and atrial fibrillation by increasing contractility

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16
Q

describe digoxin mechanism of action on heart cells

A
  1. partially blocks Na/K ATPase pump which increases intracellular Na+
  2. means less Ca2+ is pumped out via antiport mechanism (of Na in, no gradient)
  3. increased Ca2+ uptake into SR
  4. during AP more Ca2+ can be released
  5. increased contractility
17
Q

what is the late Na current? (late/Na)

A

the late / incomplete inactivation of Na channels after depolarisation
(more channels left open)

18
Q

what causes late Na current

A

ischaemia / hypoxia causes increased [reactive oxygen species]
these act on /Na so it doesn’t fully inactivate

19
Q

describe the effect of the late Na current

A
  1. increases [Na] due to more channels being open
  2. less Ca2+ out via Na antiport (no gradient for Na in)
  3. increases intracellular Ca2+
  4. leads to :
    - myocardial stunning
    - diastolic stiffness
20
Q

what is diastolic stiffness

A

ventricles dont fully relax
less ventricular filling
-decreases CO
-increases cardiac work

21
Q

what is myocardial stunning

A

when cardiac cells dont contract correctly

22
Q

what does ranolazine do?

A

blocks late Na current

23
Q

examples of Ca2+ blockers for heart

A

verapamil & diltiazem

24
Q

effects of Ca2+ blockers on heart

A

decrease contractility, HR, cardiac work

vasodilation

25
Q

what 2 ways can cardiac arrhythmias arise?

A

heart block

abnormal pacemaker

26
Q

explain heart block

A

impulse blocked between SAN and ventricles

ventricles beat slowly

27
Q

how can heart block be treated

A

pacemaker

28
Q

explain arrhythmias caused by abnormal pacemaker

A

abnormal pacemaker arises outside SAN firing impulses and overriding SAN
causes discoordination and decrease in CO

29
Q

define supraventricular arrhythmia

A

abnormal pacemaker has origin in atrial tissue/AV node

30
Q

define ventricular arrhythmia

A

abnormal pacemaker has origin in ventricle

31
Q

what can cause development of abnormal pacemaker?

A

ischaemia

structural abnormalities

32
Q

what are the 2 basic strategies for arrhythmic drugs

A
  1. increase refractory period so less signals can be fired

2. suppress conduction in the zone of abnormal conduction

33
Q

when is supressing conduction of abnormal pacemaker especially effective?

A

supraventricular tachycardia