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CVS > Drugs and the heart > Flashcards

Drugs and the heart Flashcards

1
Q

What are the different ways drugs can affect the heart

A

Direclety
- can actually affect cardiomyocytes
- Can affect rate/rhythm
- force of contraction

Indirectly

  • can influence by vasculature
  • Blood volume and the composition of blood
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2
Q

What are arrythmias

A

when the heartbeat’s rhythm is irregular or abnormal

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3
Q

what can be the difference disorders of rate or rhythm

A
  • rhythm could be too fast or slo
  • abnormal generation/conduction
  • disruption of how cardiac action potentials
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4
Q

What are the causes of arrhythmias?

A
  • Pathology (is it due to nodes or conducting tissue)
  • Drug-induced (taking particular drugs for therapeutic or recreational)
  • Congenital
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5
Q

How do we name arrhythmias

A

Classify based on where the origin is from (so is it atrial, ventricular or nodal)

and the effect it has on heart rate (normal HR, tachycardia bradycardia)

for example ventricular tachycardia

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6
Q

How do anti-arryhtmatic drug work?

typically how do they target the heart

A

can focus on cardiac action potential

they act on different parts of the action potential graph

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7
Q

How many classes of antiarrhythmic drugs work

A

4

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8
Q

Name a drug in class 1

A

lidocaine, flecainide

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9
Q

How do class 1 drugs work

A

they target voltage-gated sodium channels
which….
increase the refractory period →which reduce the general exictbity of cardiomyocytes
-so the cells are less likley to fire

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10
Q

Name some class 2 antiarryhmic drugs

A
  • beta blockers
  • Eg metoprolol, propanolol
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11
Q

How do class 2 anti-arrhythimcs work

A
  • decreases sympathetic effect by blocking beta 1 receptors
    • increases slope of the action potential
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12
Q

Name some class 3 antiarrhytmics

A

amiodarone (Idoine molecule, used in thyroid action), sotalol (has some beta blocker action)

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13
Q

How do class 3 antiarrhytmics work

A
  • they prolong the action potential
  • by blocking potassium channels involved in repolarisation (primary for antiarrhythmics )
  • but these drugs do act on other receptors
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14
Q

Name a class 4 anti-arrhythmic

A

Verapamil

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15
Q

How do class 4 anti-arrhythmics work

A
  • they are calcium ion channel blockers
  • they specfically block the L-type calcium channels
    • found in muscle cells to determine intracellular calcium levels
  • this decreases the rate of depolarisation (targets AVN)
  • so blocks how fast deporlrisation happens
  • ## can slow conduction increasing the refraction period, so stops some APs in atria from being translated to the ventricles

these drugs have relative cardomyocselectivity

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16
Q

Non classifeid drugs

Name some anti-arrhythmics that aren’t part of the classification

A

adenosine
cardiac glycosides

17
Q

How does adenosine work

A
  • Acts on adenosione receptors on SA/AV → causes opening of k+ channel
  • this causes the membrane to hyperpolarise
  • so we get a delay in the next action potential, so the membrane potential is further away from threshold
  • so binding of adenosine causes an increase in the refractory period
  • and nodal condition is slowed

caffine is an anatgonist for adensoine receptors

so drining caffine my cause heart palpatations, so the nodal cells are closer to threshold hold, so they are more likley to fire -> so HR increases

18
Q

Name a cardiac glycosides

A

digoxin

most commonly used

19
Q

How do cardiac glycosides usually work

A

They have some CNS action → Increases vagal activity,
-means there’s an increase in PNS activity
-therefore, we get a decrease in AV conduction rate
-and decreases ventricular rate too

20
Q

What are the general side effects of antiarrhythmic drugs

A
  • Can cause arrhythmias
    • when fiddling with ion levels can make things work
      -They have -ve inotropic action
    • can affect contraction, so if you decrease force of contraction, it wont help if somoen is has cardiac compromise
21
Q

Why might we need drugs to affect the force of contraction?

A
  • Anaphylaxis
    • massive reduction in blood pressure
  • Heart failure
    • Cardiac Output is insufficient for the metabolic needs of the body
22
Q

How is he force of contraction normally determined

what ion is involved

A

intracellular calcium i

23
Q
A
24
Q

How can drugs work to increase the contractility?

generally what can they do

A
  • Inotropic effects
  • change muscle fibres
25
Q

What do negtative ionotropic drugs do usually

A

decreases intracelluar calcium
so they decrease force of contraction

26
Q

What classes of drugs cause a positive ionotropic effect

A
  • Sympathomimetics
  • Cardiac glycosides
  • Phosphodiesterase inhibitors
27
Q

How do poisitive ionotropic drugs work generally

A

they increase intracelluar calcium, which increases force of contraction

28
Q

How does digoxin work

A

-Digoxin binds to and results in the partial inhibition of Na+/K+ ATPase
-when we inhibit the Na+/k+ ATPase there is an acculmation of intracelluar sodium
-if that happens this impacts the sodium calcium exchnager,
-think about it, if theres more sodium inside the cell, the conc gradient is not gradienting, so it will be worse at letting sodium in, and worse at letting calcium out,
-which means well get an acculmation of extrecelluar calcium (since there;s less activity)
which increases the force of contraction

Na+/K+ ATPase normally maintains ion concentration gradient inside/outside cells.

29
Q

What will happen if we fully inhibit the Na+/K+ ATPase

A

if we fully inhibit the sodium pottassum atpase we will die

30
Q

What are the Side effects of cardiac glycosides

A
  • can cause Ionic disturbance
  • this can affect excitability
    • potentially cause arrhythmias -neuronal disturbances
    • and smooth muscles might manifest in GIT
  • Rare complication: gynecomastia (breast growth)
    • digoxin can fool estrogen receptors, which can cause breast growth

Digoxin can cross the BBB and therefore impact neurones in CNS in a similar way. At a high toxic level, Digoxin can cause neurological disturbance

31
Q

What are the clinical use of digoxin

A

-heart failure patients

wrong dose of digoxin ca cause arrhmias

32
Q

What drugs can interact with digoxin

A
  • Diuretics
  • this is bad because diruretics decreases K+
  • so these potassium ions bind to the sodium-potassium ATPase, at the same place that digoxin does
  • so they compete with each other
  • so all in all, if theres less pottasium ions, its easier for digoxin to bind
  • which means your more likley to get adverse effects
33
Q

Name some Phosphodiesterase inhibitors (PDEs)

A

Eg milrinone, enoximone

34
Q

How do Phosphodiesterase inhibitors (PDEs) work

A

-typically phosphodiesterase causes cAMP/cGMP breakdown
-If we inhibit this enxyme we can increase cAMP/cGMP
- if we inhibit PDE we can increase cAMP, which means increase in calcium levels, which increases force of contraction
- this is a positive iontropic effect

35
Q

What are the side effects of PDE inhibitors

A

-increased excitability as PDE type 3 inhibition adjust Ca2+ levels in cardiac myocytes
-may result in arrhythmias at the wrong doses

36
Q
A
36
Q

What are the other drugs not mentioned that can be used for cardiac failure

A
  • You can decrease Heart rate
    • for example beta blockers
    • ivabradine
    Can be used, but don’t affect the heart
  • Diuretics (decreases blood volume)
  • Vasodilators (increases systemic volume)
  • ACE inhibitors

CVS (4 decks)

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