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year 1 foundations > cardiac drugs > Flashcards

cardiac drugs Flashcards

1
Q

what is an arrhythmia?

A

Describes a condition where there are disturbances in the electrophysiology of the heart as a result of either:

  • Abnormal impulse formation
  • Abnormal impulse conduction
  • Or a combination of the two

= this results in altered rate and/or timing of excitation & contraction and will alter cardiac output (vol by ven per min)

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2
Q

what is inotropy?

A

description of force of contraction (+ = greater force of contraction = increase CO and SV)

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3
Q

what is luisitropy?

A

relaxation ( we want to be able to relax during diastole so it can adequately fill with blood that we can expel)

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4
Q

what is chronotropy?

A

heart rate or speed at which it beats - time (+ = increase heart rate)

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5
Q

what happens when calcium flows through L-type calcium channel?

A
  • during diastole - calcium sequestered into sarcoplasmic reticulum (SR) and interacts with protein, Ryanodine receptor which is a channel in membrane of SR that allows calcium to exit SR and enter cytoplasm of cell→ greater rise of Ca2+ inside cell = causes force generation & contraction (allows actin & myosin to overlap) - ultimately drives ventricular systole
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6
Q

what are 2 different rhythm types due to abnormal impulse formation?

A
  1. trigger rhythm
  2. automatic rhythm
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7
Q

what are causes of triggered rhythms?

A

ectopic foci = action potentials rise from sites other than the SA node

enhanced normal automaticity = increased action potentials from SA node (mostly driven by sympathetic)

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8
Q

what is cause of automatic rhythms? (what does that mean?)

A

early afterdepolarizations
= triggers new action potential before fully returned to resting state - this can start loop

delayed afterdepolarizations
= excessive intracellular calcium can lead to delayed afterdepolarization →increased calcium activates sodium-calcium exchanger which causes small delayed depolarisation - automatic arrhythmias

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9
Q

what are 2 types of abnormal conduction?

A
  1. conduction block = has 3 types and is defined by ECG
  2. re-entry = circus movement & reflection (means continuous re-excitation and we need break to let atria properly fill)
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10
Q

what is each of the 3 degrees of conduction block (degrees of abnormal conduction)?

A
  1. PR interval which exceeds 0.2seconds (200ms) →excitation from atria not making to ventricle quickly
  2. 2 sub types but simple: AV node, PR progressively lengthens until point that there is missing QRS complex (usually happens cyclically)
  3. complete block of conduction through AV node - atria & ventricles work in isolation from each other
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11
Q

what is the aim of drugs for management of arrhythmias?

A

abnormal impulse formation = decrease in slope of pacemaker potential in SA nodal cells and raise threshold

abnormal conduction = decrease conduction velocity (phase 0) and increase in effective refractory period

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12
Q

what is Vaughan-Williams anti-arrhythmic drugs classification system?

A

class I = Na+ channel blockers
a = moderate, b = weak, c = strong

class II = beta adrenoreceptor blockers

class III = potassium channel blockers

class IV = calcium channel blockers

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13
Q

what is the effect of class 1 antiarrhythmic drugs?

A

= Na+ channel blockers (in ventricular myocytes AP)

  • largely affect rapid depolarisation of ventricular AP (phase 0 - the dramatic upstroke) prevent Na+ entering cell
  • depending on which specific drug, might see prolongation of action potential (APD) - may or may not see depending

→slow heart rate and increase AP duration

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14
Q

what is the effect of class 2 antiarrhythmic drugs?

A

= beta adrenoceptors blockers

  • decrease funny current channels
  • funny current channels activated by something (polarisation by PKA due to cAMP) that occurs as result of beta 1 receptor so increase funny current channels mean increase time to reach threshold
  • if block beta 1 then decrease funny current channels = less depolarisation, decrease speed we reach threshold
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15
Q

how are beta adrenoceptors affect the funny current and what effect does that have?

A

activation of beta 1 by adrenaline - activation of beta 1 which is Gs →stimulates adenylyl cyclase →increases ATP to cAMP →cAMP →increased PKA →phosphorylates stuff (like funny current channels) to increase positive lusitropy, inotropy, chronotropy (increase SV & CO as heart beats stronger & faster)

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16
Q

what is the effect of class 3 antiarrhythmic drugs?

A

= K+ channel blockers

  • largely affect repolarization in SA node and cardiac myocytes
  • prolong time it takes to re-polarize cells →increase in AP duration
  • risky as can increase QT elongation which can lead to lethal arrhythmias if not managed effectively
17
Q

what is the effect of class 4 antiarrhythmic drugs?

A
  • block Ca2+ channels which means slow conduction of atrium
  • affects plateau by decreasing amount of calcium entering cell
18
Q

what are the 3 cycles of voltage gated Na+ channels?

A
  • open, closed, inactive = cycles these 3 states in action potential
  • they can’t go from inactive →open they need to go inactive→closed and that’s only triggered by repolarisation
19
Q

what can Class I antiarrhythmics be used to manage? (when prescribed?)

A

used to manage atrial fibrillation, fast beating (life threatening ventricular arrhythmias), ischaemic tissue, inherited long QT syndrome etc

  • Use-dependent block – these drugs bind preferentially to open and inactive sodium channels
20
Q

what are examples of Class I antiarrhythmics?

A

Flecainide, Lidocaine and Mexilitine

21
Q

what is atrial fibrillation?

A

the most common cardiac arrhythmia – characterised by chaotic electrical excitation of the atria which can cause irregular and rapid heart rate and ineffective atrial contraction

  • typically first experience low frequency and severity then progress
22
Q

what drugs are often used in atrial fibrillation?

A

Flecainide & propafenone
- used as pill in pocket strategy, given early in progression and usually very effective

23
Q

what are some examples of non selective beta blockers?

A

propranolol, sotalol

24
Q

what are some examples of selective beta blockers?

A

atenolol, bisoprolol, carvedilol

25
Q

when would you prescribe beta blockers?

A

for hypertension - also non sustained ventricular arrhythmias, atrial tachycardia, angina etc

beta blockers = decrease open of funny current = slow rate we achieve threshold in SA = reduce action potentials in same unit of time

26
Q

what is an example of a potassium channel blocker?

A

amiodarone

27
Q

when would you prescribe potassium channel blockers?

A

they’re effective for managing arrhythmias where other classes of drugs have failed (they do have increased risk of adverse drug effects like hyperthyroidism and pulmonary toxicity)

28
Q

what is big problem of K+ channel blockers?

A

absolute refractory period = time where we can’t trigger another excitation

K+ = increase time of refractory period →can be big problem

29
Q

what are examples of calcium channel blockers?

A

verapamil & diltiazem

30
Q

what is angina?

A

a mismatch between myocardial perfusion and oxygen demand. Can be stable or unstable and is characterised by retrosternal chest pain which may radiate to jaw and left arm

31
Q

what drug type (classification) is used in management of hypertension, angina and supraventricular arrhythmias?

A

calcium channel blockers

32
Q

what is atropine?

A

= a muscarinic antagonist that binds to & blocks muscarinic acetylcholine receptors therefore, antagonizing the effects of acetylcholine

  • used in management of beta blocker induced-bradycardia & bradycardia after MI
33
Q

what is ivabrodine?

A

= inhibits funny current in SA node cells and can reduce heart rate and useful in patients who poorly tolerate beta blockers

  • used in management of angina & heart failure
34
Q

what is digoxine?

A

= acts as positive inotrope to increase contractility and thus cardiac output

  • used in management of atrial fibrillation or flutter & heart failure
35
Q

what is adenosine?

A

= natural nucleoside which binds to adenosine A1 receptors in AV primarily

  • useful for terminating re-entrant supraventricular tachycardia

year 1 foundations (36 decks)

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