Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

semester 4 - CPT & Prescribing > 10. Antiarrhythmics > Flashcards

10. Antiarrhythmics Flashcards

1
Q

what must occur for the heart to contract efficiently?

A
  • To function efficiently, heart needs to contract sequentially (atria, then ventricles) and in synchronicity
  • Relaxation must occur between contractions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what do each part of the ECG rhythm show?

A

p wave - atrial contraction
qrs complex - ventricular contraction
t wave - repolarisation of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what conditions may Result in rate and/or timing of contraction of heart muscle that may be insufficient to maintain normal cardiac output (CO)?

A

Heart condition where disturbances in
– Pacemaker impulse formation
– Contraction impulse conduction
– Combination of the two

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the resting membrane potential and what is it maintained by?

A

• A transmembrane electrical gradient (potential) is maintained, with the interior of the cell negative with respect to outside the cell
• Caused by unequal distribution of ions inside vs. outside cell
– Na+ higher outside than inside cell
– Ca+ much higher outside than inside cell
– K+ higher inside cell than outside
• Maintenance by ion selective channels, active pumps and exchangers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the fast and slow action potential?

A

Fast: in normal cardiac myocytes - atrium and purkinje fibres included
Slow: in SA and AV nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

WHat are the different parts of the Fast action potential?

A

0: Na+ in (depolarisation)
1: K+ out (partial repolarisation)
2: Ca++ in (plateau)
3: K+ out (repolarisation)
4: resting potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are class 1 drugs and what are their general effects on the fast action potential?

A

Na channel blockers

  • Marked slowing conduction in tissue (phase 0) - depolarisation not as rapid - stop rhythm moving across tissue
  • Minor effects on action potential duration (APD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are class 2 drugs and what are their general effects on the fast action potnetial?

A

Beta blockers

- reduced calcium influx in phase 2 therefore diminish phase 4 depolarisation and automaticity (??)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are class 3 drugs and what are their general effects on the fast action potnetial?

A

Potassium channel blockers

  • stops efflux of potassium
  • Increase action potential duration (APD) (increased refractory period)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are class 4 drugs and what are their general effects on the fast action potnetial?

A

Calcium channel blockers

  • Calcium channel blockers decrease inward Ca2+ currents resulting in a decrease of phase 4 spontaneous depolarization
  • affect plateau phase of action potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the different parts of the slow cardiac action potential?

A

0: Ca++ in (depolarisation)
3: K+ out (repolarisation)
4: funny current - slow spontaneous depolarisation (slow Na+ in)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the effect of CCBs on the slow action potential?

A

Decreases rate of depolarisation
slope of phase 0 = conduction velocity so therefore conduction velocity decreased
- increases refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What drugs affect automaticity of cardiac action potentials?

A 
steeper slope of depolarisation:
- beta agonists
shallower slope of depolarisation:
- muscarinic agonists
- adenosine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are 2 mechanisms of arrhythmogenesis?

A
  • abnormal impulse generation

- abnormal impulse conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the different types of abnormal impulse generation? (3)

A

Automatic rhythms:
- enhanced normal automaticity (increased AP from SA node)
- ectopic focus (site other than SA node)
Triggered rhythms:
- early/delayed after depolarisations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the different types of abnormal impulse conduction?

A 
Conduction block:
- 1st, 2nd, 3rd degree
Reentry:
- circus movement (reentrant tachycardia)
- reflection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give 3 examples conditions that cause reentry tachycardia.

A
  • Wolf parkinson white syndrome
  • AV nodal reentry tachycardia
  • Area of ischaemia can also cause reentry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Wolf-Parkinson White?

A

Abnormal conduction between the atria and ventricles leading to tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe what happens in reentry pathways?

A

two pathways for electric conduction down AVN - slow and fast - conduction usually goes down fast pathway but in some conditions that pathway can be blocked so go down slow pathway and then back up into atria via fast pathway - AVNR tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In case of abnormal generation, what is the purpose of drugs? Which drugs do this?

A
  • Decrease of phase 4 slope (in pacemaker cells)
  • raises threshold for depolarisation
    Beta blockers and CCBs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In case of abnormal conduction, what is the purpose of drugs? Which drugs do this?

A
  • ↓conduction velocity (remember phase 0) (Na+ blockers)

- ↑Effective refractory period (so the cell won’t be reexcited again) (K+ blockers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

summarise what arrhythmia’s occur due to?

A

– Automatic or triggered activity

– Re-entry due to scar, anatomy of AV node slow and fast pathway/ WPW

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

summarise aim of antiarrhythmic drugs?

A

– Reduce abnormal impulse generation
– Slow conduction through tissue
– Block AV node to terminate some rhythms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Give examples of class 1B drugs.

A

Lidocaine (IV only), mexiletine (oral only)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what is the action of class 1B drugs?
Weak sodium channel blockade | – slows impulse conduction (phase 0) in abnormal/ischaemic and fast beating tissue
26
What are the effects of class 1B on cardiac activity?
• Fast binding offset kinetics • No change in phase 0 in normal tissue (no tonic block) • APD slightly decreased (normal tissue) ↑ increase threshold (Na+) tachycardia ↓ phase 0 conduction in fast beating or ischaemic tissue,
27
What are the effects of class 1B drugs on ECG?
None in normal, in fast beating or ischaemic ↑ QRS
28
What are class 1B drugs used for?
acute : Ventricular tachycardia (esp. during ischaemia) Not used in atrial arrhythmias or AV junctional arrhythmias
29
why is lidocaine given iv?
due to extensive first pass metabolism§
30
adverse effects of class 1B drugs?
CNS effects – drowsiness, dizziness, nausea and vomiting
31
warnings, contraindications of class 1B drugs?
Other antiarrhythmic agents that may compound bradycardia and negative inotropy
32
important drug interactions of class 1B drugs?
active metabolites require CYP activity – caution with many CYP inhibitors/inducers
33
Give 2 examples of class 1C drugs?
Flecainide | - oral or IV
34
action of class 1C drugs?
Marked sodium channel blockade | – slows impulse conduction (phase 0) and decrease automaticity
35
What are the effects of class 1C on cardiac activity?
- Substantially ↓↓ phase 0 (Na+) in normal - ↓ automaticity (↑threshold) - ↑ APD (K+) and ↑refractory period, esp in rapidly depolarizing atrial tissue.
36
What are the effects of class 1C drugs on ECG?
Increases PR, QRS, QT
37
What are class 1C drugs used for?
- Used for supraventricular arrhythmias (fibrillation and flutter) - Premature ventricular contractions (caused problems) - Wolff-Parkinson-White syndrome
38
adverse effects of class 1 C drugs?
CNS effects – drowsiness, dizziness, nausea and vomiting increase ventricular response to SVT - flutter - Proarrhythmia and sudden death especially with chronic use (CAST study) and in structural heart disease
39
warnings, contraindications of class 1C drugs?
Other antiarrhythmic agents that may compound negative inotropy Should be prescribed alongside AV node blocking drug (beta blocker) to prevent 1:1 AV conduction in AF and flutter
40
important drug interactions of class 1C drugs?
drugs that also prolong QT interval
41
When are class 1C drugs not used?
Structural heart disease or ischaemic heart disease
42
Give 3 examples of class II drugs.
- propranolol (oral or IV), - bisoprolol (oral), - metoprolol (oral) and
43
action of class II drugs?
Beta receptor antagonists – reduce rate of spontaneous depolarisation of SA and AV node and slow conduction velocity – increase refractory period - remember can also be used in resistant hypertension
44
What are the cardiac effects of class II drugs?
- Increase APD (action potential duration) and refractory period in AV node to slow AV conduction velocity - decrease phase 4 depolarization (catecholamine dependent)
45
What are the effects of class II drugs on ECG?
- increase PR | - decrease heart rate
46
What are the uses of class II drugs?
- treating sinus and catecholamine dependent tachycardia - converting reentrant arrhythmias at AV node - protecting the ventricles from high atrial rates (slow AV conduction) in atrial flutter or atrial fibrillation
47
adverse effects of class 1 C drugs?
hypotension, fatigue, bronchospasm
48
warnings, contraindications of class 1C drugs?
asthma, ACUTE heart failure, partial AV block
49
important drug interactions of class 1C drugs?
beta agonists, verapamil and diltiazem – specialist care only
50
Give 2 examples of class III drugs.
amiodarone (oral or IV), sotalol (oral)
51
action of class III drugs?
``` Inhibit potassium channel activity - increase refractory period decrease AV conduction (class II/IV activity) ```
52
What are the cardiac effects of amiodarone?§
- ↑ increase refractory period and ↑APD (K+) - ↓ phase 0 and conduction (Na+) - ↑ threshold - ↓ phase 4 (β block and Ca++ block) - ↓ speed of AV conduction
53
What are the effect of amiodarone on ECG?
↑ PR,↑ QRS, ↑ QT, ↓ HR
54
What are the uses of amiodarone?
Very wide spectrum: effective for most arrhythmias
55
What are the adverse effects of amiodarone
pulmonary fibrosis, hypo/hyperthyroidism, photosensitivity, hepatitis,
56
warnings, contraindications of class III drugs?
active thyroid disease, heart block
57
important drug interactions of class III drugs?
amiodarone - Lots! Increases [plasma] of digoxin, warfarin, verapamil
58
What are the cardiac effects of sotalol?
- ↑ APD and refractory period in atrial and ventricular tissue - Slow phase 4 (β blocker) - Slow AV conduction
59
What are the effects of sotalol on ECG?
↑ QT, ↓ HR
60
What is sotalol used for?
Wide spectrum: supraventricular and ventricular tachycardia
61
What are the side effects of sotalol?
Proarrhythmia, fatigue, insomnia
62
Give 2 examples of class IV drugs.
verapamil (oral/IV) and diltiazem (oral)
63
why does amioidarone have long time for complete elimination once stopped?
Amiodarone has very lard Vd and very long half life
64
action of class IV drugs?
``` Calcium channel blockers -slow conduction of action potential through AV node non-dihydropyridine class – more selective for cardiac tissue than vascular smooth muscle (remember non-dihydropyridine class have no effect on heart) ```
65
What are the cardiac effects of class IV drugs?
- slow conduction through AV (Ca++) - ↑ refractory period in AV node - ↑ slope of phase 4 in SA to slow HR
66
What are the effects of class IV drug on ECG?
↑ PR, ↑↓ HR (depending of blood pressure response and baroreflex)
67
What are class IV drugs used for?
- control ventricles during supraventricular tachycardia | - convert supraventricular tachycardia (re-entry around AV)
68
What are the adverse effects of class IV drugs?
Constipation (verapamil), bradycardia, heart block
69
warnings, contraindications of class IV drugs?
Caution in partial AV block, unstable angina, hypotension and HF
70
important drug interactions of class IV drugs?
beta-blockers – specialist care only
71
which drugs are included in class V "others" drugs?
adenosine ivabridine digoxin atropine
72
What is the mechanism of action of adenosine?
A1 receptor agonist – activate K+ channels enhancing flow out of cells causing hyperpolarisation → ↓ HR - ↓ Ca++ currents - ↑ refractory period in AV node - slows AV conduction – no effect on ventricles
73
how is adenosine administered?
rapid i.v. bolus, very short T1/2 (seconds)
74
What are the cardiac effects of adenosine?
Slows AV conduction
75
What is adenosine used for?
- convert re-entrant supraventricular arrhythmias | - diagnosis of coronary artery disease (scans)
76
adverse effects of adenosine?
bradycardia and asystole – remember feeling of “impending doom” when used for converting re-entrant SV arrhythmia – half life v. short so not long lasting sensation but can feel unpleaseant
77
warnings, contraindications of adenosine?
Should be avoided in patients that wont tolerate transient bradycardia, bronchospasm in asthma and COPD
78
important drug interactions of adenosine?
caution with dipyridamole which prevents cellular reuptake of adenosine prolonging its effects, adenosine antagonists such as theophylline
79
action of ivabridine?
• If (funny) channel blocker in SA node slows conduction through SA node but does not affect BP • Useful where lowering BP is a concern
80
How is ivabradine administered ?
orally in 2.5mg bd dosing up to 10mg bd
81
adverse effects of ivabradine?
vision disturbance, headache and dizziness
82
warnings, contraindications of ivabridine?
caution in acute coronary syndromes where heart rate is low
83
important drug interactions of ivabridine?
other antiarrhythmic drugs that cause bradycardia
84
What is ivabradine used for?
- reduce inappropriate sinus tachycardia - reduce heart rate in heart failure and angina (avoiding blood pressure drops)
85
What is the MOA of digoxin?
Cardiac glycoside - for AF and flutter its action is indirect via increased parasympathetic vagal tone (↑ K+ currents, ↓ Ca++ currents, ↑refractory period ) - In heart failure direct action by inhibiting Na+/K+ ATPase
86
What is digoxin used for?
treatment to reduce ventricular rates in atrial fibrillation and flutter
87
adverse effects of digoxin?
bradycardia, GI disturbance | low therapeutic index – risk of digoxin toxicity
88
warnings, contraindications of digoxin?
Heart block, renal failure, hypokalaemia (increased digoxin activity)
89
important drug interactions of digoxin?
Diuretics that can cause hypokalaemia, amiodarone
90
What is the MOA of atropine?
* Antimuscarinic – blocks M2 receptors (vagal activity) increasing firing of SA node and conduction through AV node * Particularly useful where bradycardia results from increased vagal tone
91
What is atropine used for?
treat vagal bradycardia
92
adverse effects of atropine?
dry mouth, dizziness, headache, anxiety
93
warnings, contraindications of atropine?
where antimuscarinic action unwanted – urinary retention, glaucoma, GI obstruction
94
important drug interactions of atropine?
caution with other antimuscarinic agents
95
Which drugs in AF?
Rate control(slow conduction through AV node to reduce heart rate back to normal levels): Bisoprolol, verapamil, diltiazem + digoxin Rhythm control: Sotalol, flecainide with bisoprolol, amiodarone
96
Drugs for VT?
- Metoprolol/bisoprolol - Lignocaine/mexiletine - Amiodarone
97
Should flecainide be used alone in atrial flutter?
No - Give AV nodal blocking drugs to reduce ventricular rates in atrial flutter - can be given in atrial fibrillation
98
Best treatment for WPW?
Flecainide (or amiodarone)
99
Drugs for re-entrant SVT?
• Acutely (IV) - Adenosine - Verapamil - flecainide • Chronic (repeated episodes, orally) - Bisoprolol, verapamil - sotalol - Flecainide - amiodarone
100
Which drugs for ectopic beats?
* Bisoprolol first line * Calcium channel blockers * Flecainide, sotalol or amiodarone
101
Drugs for sinus tachycardia?
* Ivabradine (no drop in blood pressure) | * Bisoprolol, verapamil

semester 4 - CPT & Prescribing (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions