DIT review - Cardiology 4 Flashcards
1
Q
Describe what part of the action potential each class of Anti-arrhythmics works on (which electrolyte channel and which phase)
A
THINK: No Bad Boy Keeps Clean
- Class I
- Na+ channel blockers
- Phase 0 of myocytes
- Class II
- Beta blockers
- Phase 4 of pacemakers
- Class III
- K+ channel blockers
- Phase 2 and 3 of myocytes
- Class IV
- Ca2+ channel blockers
- Phase 0 of pacemakers
2
Q
Describe the different effects on Phase 0 slope and effective refractory period of Class IA, IB, and IC antiarrhythmics
A
- Class IA:
- Intermediate Na+ channel binding – moderately decreased phase 0 slope
- Also block K+ channels – prolonged refractory period
- Class IB:
- Weakest Na+ channel binding – minimally decreased phase 0 slope
- Cause shortened refractory period
- Class IC:
- Strongest Na+ channel blocking – significantly decreased phase 0 slope
- No effect on refractory period
3
Q
What is the effect of Class I antiarrythmics on QRS complex
A
Widened QRS due to decreased AP conduction velocity
- Because drug is state-dependent and effect is stronger on channels with more depolarization (rapid heart rate), QRS will be even WIDER in patients with tachycardia
4
Q
What is the order of binding affinity for Na+ channels in the different Class I antiarrhythmics
A
IC > IA > IB
5
Q
What are the Class IA antiarrhthmics
A
-
Quinidine
- = dining prom queen
-
Procainamide
- = prom king
-
Disopyramide
- = “prom queen DISAPPEARS” headline
6
Q
Uses of Class IA antiarrhythmics
A
- Supraventricular and ventricular arrhythmias
- = top and bottom of IA sign are lit up
- Wolff-Parkinson-White (WPW) syndrome (a type of SVT)
- = white wolf pack sign
7
Q
Adverse effects of Quinidine
A
Cinchonism (a syndrome of tinnitus, HA, and dizziness)
8
Q
Adverse effects of Procainamide
A
Drug-induced lupus
9
Q
Adverse effects of Disopyramide
A
Exacerbation of heart failure (has negative inotropic effects at toxic concentrations)
10
Q
Adverse effects of all Class IA antiarrythmics
A
QT interval prolongation (precipitates torsades) due to prolonged AP (effects on K+ channel)
11
Q
What are the Class IB antiarrhythimcs
A
-
Lidocaine
- = “you lied”
-
Mexiletine
- = Mexican flag
-
Phenytoin (anti-epileptic)
- = tow truck driver
12
Q
What are the effects of Class IB on QT interval/torsades
A
- No chance of prolonged QT and torsades
- Shorten phase 2 and 3 of cardiac AP, leading to shortened refractory period (speed up AP duration)
- = pulling curtain closed
- Shorten phase 2 and 3 of cardiac AP, leading to shortened refractory period (speed up AP duration)
13
Q
Uses of Class IB antiarrhythmics
A
- Ventricular arrhythmias (especially in ischemic tissue)
- = illuminated cracked (ischemic) bottom of heart
- = “you’re DEAD to me” = ischemia induced ventricular arrhythmias
14
Q
Adverse effects of Class IB antiarrhythmics
A
- Neuro (e.g. Parasthesias, tremor, convulsions)
- = brain-shaped trucker hat
15
Q
What are the Class IC anti-arrhythmics
A
-
Flecainide
- = flakes cereal
-
Propafenone
- = purple phone
16
Q
Uses of Class IC antiarrhythmics
A
- Supraventricular and ventricular arrhythmias
- = illuminated top and bottom of heart sign
- Atrial fibrillation (and flutter)
- = irregularly irregular signal on TV
- First goal is control of ventricular rate (accomplished by beta-blockers)
- Class IC can then restore and maintain normal sinus rhythm
17
Q
Adverse effects of Class IC antiarrhythimcs
A
- Contraindicated in patients with history of structural ischemic heart disease (due to proarrhythmic effects)
- = “healthy heart only” cereal
18
Q
What drugs are Class II antiarrhythmics
A
Beta blockers (“-olol”)
19
Q
MOA of Class II antiarrhythmics
A
- Do not directly modify ion channel function
- Block sympathetic input to the SA and AV node
- Beta blocker decrease cAMP
- Decreased cAMP leads to closure of membrane calcium channels (needed for upstroke of nodal action potential)
- Beta blockers lead to prolonging of phase 4 (slow depolarization) of the nodal action potential
- In the SA node this leads to decreased sinus rate, suppressing abnormal pacemaker activity
- In the AV node, this causes a dramatic prolongation of AV conduction time and effective refractory period
20
Q
Uses of Class II antiarrhythmics
A
- Supraventricular arrhythmias (e.g. atrial fibrillation with RVR)
- = top of neon heart is illuminated
- IV beta blockers (e.g. Esmolol) can be used for acute supraventricular arrhythmias
- = ivy
- Atrial fibrillation (and flutter)
- = Irregularly irregular signal on TV
- BB can accomplish the first goal of treatment which is to control rate of the ventricles
- = rate-controlling metronome under the TV
- This does not fix the atrial fibrillation though (accomplished by Class IC)
21
Q
Adverse effects of beta-blockers
A
- Heart block
- = top of Luis Armstrong hat is a shield held up to heart
- Heart block manifests as a prolonged PR interval on EKG
- = Public Relations microphones
22
Q
MOA of Class III antiarrhythmics
A
- Class III anti-arrhythmics block K+ channels of the myocardium, prolonging phase 2 and phase 3, and allowing myocardium to be depolarized for longer (prolonged refractory period)
23
Q
What drugs are Class III anti-arrhythmics
A
-
Amiodarone
- = Amigos
- “-tilide” suffix (e.g. Dofetilide and Ibutilide)
- = “til I die” note
-
Sotalol
- = soda
- Is also a beta blocker (-lol suffix)
- Muted bugle
24
Q
MOA of Amiodarone
A
- Shares properties of class I, II, III, and IV anti-arrhythmics
- = uno, dos, tres, quatro
- Blocks inactivated Na+ channels (class I), weak beta-adrenergic effects (class II), blocks K+ channels (class III), and weak Ca2+ blocking effects (class IV)
25
Uses of Class III antiarrhythmics
* Both supraventricular and ventricular arrthmias
* = Heart illuminated on top and bottom
* Atrial fibrillation
* = irregularly irregular signal on TV
* Useful for restoring and maintaining normal sinus rhythm (along with Class IC)
26
Adverse effects of Amiodarone
* Neuro side effects (e.g. tremor, ataxia, peripheral neuropathy, sleep disturbances)
* = skull brains on amigos hats
* Gray corneal micro deposits (usually asymptomatic)
* = gray sunglasses
* Hyper- or hypothyroidism
* = big and small bowties on amigos
* Pulmonary fibrosis (restrictive lung disease)
* = fibrotic lung embroidery
* = tight button = restrictive
* Heart block (due to Class II and IV depressing conduction through AV node
* = hat shield held against chest
* Heart failure
* = trampled failing heart balloon
* Hypersensitivity hepatitis
* = liver spot on cow
* Gray-blue skin discoloration
* = gray-blue outfits
* Photodermatitis
* = flash photo
* Is an inhibitor of CYP450
* = broken chrome bumper
* Widening of QT interval (can induce torsades) – caused by **_Sotalol, Dofetilide,**_ and _**Ibutilide_**
* = twisted streamer near soda and “til I die” note
27
What drugs are Class IV antiarrhythmics
Non-dihydropyridine calcium channel blockers:
* **_Verapamil_** = very vanilla
* **_Diltiazem_** = Delicious dark chocolate
28
Uses of Class IV antiarrhythmics
* Supraventricular arrhythmias (e.g. atrial fibrillation with RVR)
* = illuminated top of heart neon sign
* Atrial fibrillation
* = irregularly irregular signal on TV
* CCB will control ventricular rate, preventing rapid ventricular response (“rate control”)
* = metronome
* This does not fix the atrial fibrillation though
29
Adverse effects of Class IV antiarrhythmics
* Prolonged PR interval on EKG because conduction from atrial P-wave to ventricular QRS is delayed
* Heart block
30
Describe Digoxin's MOA as an anti-arrhythic
* Exerts direct parasympathomimetic effects via direct stimulation of the vagus nerve, leading to AV inhibition
* Similar effect of beta-blockers (Class II) and Ca2+ blockers (Class IV)
31
Uses of Digoxin as an anti-arrhythmic
* Atrial arrhythmias, including A-fib
* = irregularly irregular signal on light board behind DJ
* Controls ventricular rate, preventing rapid ventricular response
* = metronome with Vegas sign on top
32
Uses of Magnesium as an anti-arrhythmic
* Useful for the treatment of certain arrhythmias (e.g. torsades)
33
Describe the effects of hyper- and hypo-kalemia on EKG
* Both hyper- and hypokalemia can induce arrhythmias
* = male banana dancer pointing up and female banana dancer pointing down
* Hyperkalemia can cause peaked T waves with shorted QT interval
* = peaked streamer above hyperkalemia banana dancer
* Hypokalemia can cause U waves at the end of the T wave
* = streamer that hypokalemia banana dancer is pointing to
34
Describe the MOA of Adenosine as an anti-arrhythmic
* Adenosine is a purine nucleotide
* = purine shaped gate
* Activates inhibitor A1 receptors on the myocardium and at the SA and AV nodes
* = A1 written on gate
* Activation of A1 receptors increases potassium outward conduction and suppresses calcium inward current
* = banana flying out of cup
* = falling calci-yum ice cream
* This causes membrane potential to remain negative for a longer period and calcium-dependent action potentials (at nodes) are suppressed
* = note-shaped dance floor
* This decreases AV conduction, leading to prolonged AV refractory period
* = disconnected bottom of neon heart
35
Uses of Adenosine as an anti-arrhythmic
* First line agent for acute treatment of supraventricular arrhythmias
* = illuminated top of neon heart with #1 ribbon
* Coronary dilation (mediated by A2 receptors)
* = dilated coronary crown
36
Adverse effects of Adenosine
* High-grade AV block
* = hat blocking heart of swing dancer
* Shortness of breath, chest pain, major flushing, and sense of impending doom
* = flushed dancer clutching chest
* Hypotension (due to vasodilation) and HA
* = fainting dancer
37
What substances inhibit the action of Adenosine
Caffeine and Theophylline
