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
what 2 ways can cardiac arrhythmias arise?
heart block | abnormal pacemaker
26
explain heart block
impulse blocked between SAN and ventricles | ventricles beat slowly
27
how can heart block be treated
pacemaker
28
explain arrhythmias caused by abnormal pacemaker
abnormal pacemaker arises outside SAN firing impulses and overriding SAN causes discoordination and decrease in CO
29
define supraventricular arrhythmia
abnormal pacemaker has origin in atrial tissue/AV node
30
define ventricular arrhythmia
abnormal pacemaker has origin in ventricle
31
what can cause development of abnormal pacemaker?
ischaemia | structural abnormalities
32
what are the 2 basic strategies for arrhythmic drugs
1. increase refractory period so less signals can be fired | 2. suppress conduction in the zone of abnormal conduction
33
when is supressing conduction of abnormal pacemaker especially effective?
supraventricular tachycardia