Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PPE - Pharmacology > Cardiac Arrhythmia Drugs > Flashcards

Cardiac Arrhythmia Drugs Flashcards

1
Q

What is an arrhythmia?

A

A heart condition where there is a disturbance in:
Pacemaker impulse formation
Contraction impulse formation
Combination of the two

Results in rate and/or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output (CO)

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

How is a normal heartbeat conducted?

A

Sinus node sends out a signal (Higher rate that any other)
This spreads across the atria making it contract
It then reaches the AV node, and then spreads down the bundle of HIS, down the right or left bundle branch
Then spreads across the bottom of the ventricles and spreads across the ventricles, making them contract from the bottom upwards

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

Describe the PQRST segment of an ECG

A

P - Contraction of atria
Q - small down - depolarisation of ventricular septum
R - large up - depolarisation of main mass of ventricles
S - small down - final depolarisation of ventricles
T - Repolarisation of ventricles

PR interval - first deflection of P to first deflection of Q

QRS Complex - Contraction of ventricles

ST segment - time between end of QRS and start of T

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

How is the resting cell membrane potential kept?

A

A transmembrane electrical gradient is maintained, with the interior of the cell negative with respect to outside the cell

Caused by distribution of ions:

  • Na+ higher outside cell
  • Ca2+ much higher outside cell
  • K+ higher inside cell

Maintenance by ion selective channels and pumps

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

Describe the fast cardiac potential.

A

4 phases (5 really)
0 - Na+ influx - sharp rise in potential
1 - as Na+ channels close, Ca2+ opens, influx of Ca2+
2 - Efflux of K+ as well, Ca2+ influx still
(1+2 result in slow repolarisation of action potential, more of a plateau)
3 - Just efflux of K+ - sharp drop in K+
4 - Na+/K+ATPase opens, returns cell to normal

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

What is the effect on the fast cardiac action potential if you block Na channels?

A

Marked slowing conduction in tissue (phase 0)

Minor effects on action potential duration (APD)

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

What is the effect on the fast cardiac action potential of beta-blockers?

A

Diminish phase 4 depolarisation and automaticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the effect on the fast cardiac action potential if you block K channels?

A

Increase refractory period

Increase action potential duration (APD)

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

What is the effect on the fast cardiac action potential if you block Ca channels?

A

Decrease inward Ca2+ currents
Decrease of phase 4 spontaneous depolarisation
Effects plateau phase of action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does a slow cardiac action potential look like?

A

4 phases
0 - slow increase in potential - Ca2+ influx
2 - peak - Ca2+ influx
3 - sharp decrease in action potential - efflux of K+
4 - Slow rise threshold - slow influx of K and Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the effect on the slow cardiac action potential if you block Ca2+ channels?

A

Slow the depolarisation, increase refractory period

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

Which drugs affect automaticity?

A

Beta agonists - increase phase 4 slow slope
Increase pacemaker

Muscarinic agonists, adenosine - slow phase 4
Decrease pace

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

What are the two main categories of mechanisms of arrythmogenesis? (And how are they broken up?)

A 
Abnormal impulse generation
Automatic rhythms
- Enhanced normal automaticity
- Ectopic focus
Triggered rhythms
- Delayed afterdepolarisation
- Early afterdepolarisation
Abnormal conduction
Conduction block (not conducted from atria to ventricles)
- 1st degree
- 2nd degree
- 3rd degree
Re-entry
- Circus movement
- Reflection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the main actions of arrhythmia drugs?

A

In case of abnormal generation:

  • Decrease of phase 4 slope (in pacemaker cells)
  • Raises the threshold

In case of abnormal conduction:

  • Decrease conduction velocity (phase 0)
  • Increase ERP (so the cell won’t be re-excited again)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tell me about class 1A agents.

A

Procainamide, quinidine, disopyramide

Effect sodium channels

Effects on cardiac activity:

  • \/ conduction (decrease phase 0 of AP)
  • /\ refractory period (^APD (K+) and ^Na inactivation)
  • \/ automaticity (\/ slope of phase 4, fast potentials)
  • /\ increase threshold (Na+)

Effects on ECG:
/\ QRS, +/-PR, /\QT

Uses
Wide spectrum:
Quinidine:
- maintain sinus rhythms in AF and flutter
- Prevent recurrent tachycardia and fibrillation
Procainamide:
- Acute treatment of supraventricular and V arrhythmias

Side effects:

  • Hypotension, \/CO
  • Proarrhythmia (generation of new arrhythmia)
  • Dizziness, confusion, insomnia, seizure (high dose)
  • Gastrointestinal effects (common
  • Lupus-like syndrome (esp. procainamide)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tell me about class 1B agents

A

Lidocaine, mexiletine, phenytoin

Sodium channels

Effects on cardiac activity:

  • No changes in phase 0 in normal tissue (no tonic block)
  • APD slightly decreased (normal tissue)
  • /\ increase threshold (Na+)
  • \/ phase 0 conduction in fast beating tissue

Effect on ECG:
- None in normal, in fast beating or ischaemic /\QRS

Uses:
- Acute: Ventricular tachycardia and fibrillation
- (esp. during ischemia)
- Not used in atrial arrhythmias or AV junctional
arrhythmias

Side effects:

  • Less proarrhythmic then class 1A
  • CNS effects: dizziness, drowsiness
17
Q

Tell me about class 1C agents.

A

Flecainide and propafenone

Sodium channel

Effects on cardiac activity:

  • Substantially \/\/ phase 0 (Na+) in normal
  • \/ automaticity (/\ threshold)
  • /\ APD (K+) and /\ refractory period

Effects on ECG
- /\ PR, /\ QRS, /\ QT

Uses:

  • Wide spectrum
  • Used for supraventricular arrhythmias (Fib + flutter)
  • Premature ventricular contractions
  • Wolff-Parkinson-White syndrome

Side effects:

  • Proarrhythmia and sudden death especially chronic use
  • /\ ventricular response to supraventricular arrhythmia
  • CNS and GI effects
18
Q

Tell me about class II agents

A

Propranolol, acebutolol and esmolol

Cardiac effects:
- /\ APD and refractory period in AV node to slow AV
conduction velocity
- \/ phase 4 depolarisation (catecholamine dependant)

Effects on ECG:
- /\ PR, \/HR

Uses:
- Treating sinus and catecholamine dependant
tachycardia arrhythmias
- Converting re-entrant arrhythmia in AV
- Protecting the ventricles from high atrial rates
- (slow AV conduction)

Side effects:

  • Bronchospasm
  • Hypotension
  • Don’t use partial AV block or ventricular failure
19
Q

Name some class III agents

A

Amiodarone, sotalol, ibutilide, dofetilide

20
Q

Tell me about amiodarone.

A

Cardiac effects:

  • /\ increase refractory period and /\ APD (K+)
  • \/ phase 0 and conduction (Na+)
  • /\ threshold
  • \/ phase 4 (beta block and Ca2+ block)
  • \/ speed of AV conduction

Effects on ECG
/\ PR, /\ QRS, /\ QT, \/HR

Uses:
- Very wide spectrum: effective for most arrhythmias

Side effects: (many serious that increase with time)

  • Pulmonary fibrosis
  • Hepatic injury
  • Increase LDL cholesterol
  • Thyroid disease
  • Photosensitivity
21
Q

Tell me about sotalol.

A

Cardiac effect:

  • /\APD and refractory period in atrial and ventricles
  • Slow phase 4 (beta blocker)
  • Slow AV conduction

ECG effect
/\ QT, \/HR

Uses:
- Wide spectrum: supraventricular and ventricular
tachycardia

Side effects:

  • Proarrhythmia
  • Fatigue
  • Insomnia
22
Q

Tell me about class IV agents.

A

Verapamil, Diltiazem

Cardiac effects:

  • Slow conduction through AV (Ca2+)
  • /\ refractory period in AV node
  • /\ slope of phase 4 in SA to slow HR

Effects on ECG
- /\ PR, \//\ HR (depending of bp response and baroreflex)

Uses:

  • Control ventricles during supraventricular tachycardia
  • Convert supraventricular tachycardia

Side effects:

  • Caution when partial AV block is present.
  • Can get asystole if beta blocker is on board
  • Caution when hypotension, decreased CO or sick sinus
  • Some gastrointestinal problems
23
Q

Tell me about adenosine in the treatment of arrhythmias.

A

Mechanism:

  • Natural nucleoside that binds A1 receptors
  • Activates K+ currents in AV and SA node
  • \/ APD, hyperpolarization
  • \/ HR
  • \/ Ca2+ currents
  • /\ refractory period in AV node

Cardiac effects:
- Slows AV conduction

Uses:

  • Convert re-entrant supraventricular arrhythmias
  • Hypotension during surgery, diagnosis of CAD
24
Q

Tell me about Digoxin.

A

Mechanism:

  • Enhances vagal activity
  • (/\K+ currents, \/ Ca2+ currents, /\ refractory period)

Uses:
- Treatment of atrial fibrillation and flutter

25
Q

Tell me about atropine.

A

Mechanism:
- Selective muscarinic antagonist

Cardiac effects:
- Block vagal activity to speed AV conduction and
increase HR

Uses:
- Treat vagal bradycardia

26
Q

What is magnesium used for in arrhythmic treatment?

A

Treatment for tachycardia resulting from QT

PPE - Pharmacology (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions