Anti Arrhythmic Drugs - Konorev Flashcards
1
Q
Fast action potential is seen in ?
A
- Ventricular Contractile cardiomyocytes
- Atrial Cardiomyocytes
- Purkinje Fibers
2
Q
Slow action potential is seen in…?
A
- Sinoatrial Node
- Atrioventricular Node cells
3
Q
What is the order of Action potential in Fast AP? What is Phase 0
A
- 0, 1, 2, 3, 4
- Phase 0 is the upstroke and is voltage-dependent fast Na+ channels opening from depolarization as Na+ enters the cell down its chemical gradient
4
Q
What is the order of action potential in Slow AP? what is Phase 0?
A
- Phase 4, 0, 1, 2, 3
- Phase 0 is upstroke the Ca2+ influx throughout relatively slow L type (long acting) Ca 2+ channels
- Phase 4 consists of poorly selective in flux of Na+ and K+ pacemaker current If that is activated by hyper polarization and slow Ca2+ influx through T type Ca2+ channels
5
Q
What are the class 1A antiarrythmics? (3)
A
- Quinidine
- Procainamide
- Disopyramide
6
Q
What are the class 1B anti arrhythmic drugs?
A
- Lidocaine
- Mexiletine
7
Q
What are the class 1C antiarrythmic drugs
A
- Flecainide
- Propafenone
8
Q
What is the action of Class 1A antiarrhythmics?
A
- Block sodium channels (slow impulse conduction and reduce automatism of pace makers0 –> Reduce phase 0 and Prolong QRS in ECG
- Block potassium channels –> prolong action potential duration and prolong QT interval ECG
9
Q
What does Procainamide do?
A
- Class 1A
1. Blocks Sodium Channels
2. Antimuscarinic Activity
3. Hypotension–> ganglion-blocking properties that reduce peripheral vascular resistance
10
Q
Is Procainamide used frequently?
A
No, needs a frequent dose and has lupus-related side effects
11
Q
What is the clinical use of procainamide?
A
- not first choice
- used in sustained ventricular tachycardias and arrhythmias associated with myocardial Infarctions
12
Q
What are the adverse effects of Procainamide?
A
- QT interval prolongation –> induction of Tornado de pointes arrythmias
- syncope
- Lupus with Arthritis, pleuritic, pulmonary disease, hepatitis, fever
- hypotension
13
Q
What are the actions of quinidine?
A
Class 1A
-Sodium channel blocker
- antimuscarinic effect on heart–> can enhance AV conductance
- Hypotension–> Tachycardia
14
Q
Is quinine used often?
A
no, there are better antiarrhythmics
- has cardiac and extracardiac adverse effects
15
Q
What are the adverse effects of quinidine?
A
- QT interval prolongation–> induction of torsade de pointes, arrhythmia, and syncope
- GI side effects (diarrhea, nausea, vomiting)
- Tinnitus, hearing loss, confusion, delirium, disturbances in vision, and psychosis (cinchonism)
- Thrombocytopenia, hepatitis, fever
16
Q
What is the action of Disopyramide?
A
- Sodium channel block
- antimuscarinic on heart
17
Q
What is the clinical use of Disopyramide
A
Recurrent ventricular arrhythmias
18
Q
What are the adverse effects of Disopyramide?
A
- Prolonged Qt, induction or torsades de pointes arrythmia and syncope
- Negative inotropic effect –> may precipitate heart failure
- Atropine-like symptoms - tachycardia, urinary retention, dry mouth, blurred vision, constipation, exacerbation of glaucoma
19
Q
What is the mechanism of class 1B drugs
A
- block sodium channels -> decreased phase 0 slope
- more specific and do not potassium channels –> do not prolong action potential or QT duration on ECG
20
Q
How is class 1B lidocaine administered?
A
only IV because extensive first pass metabolism
21
Q
What is the the clinical use of lidocaine?
A
termination of ventricular tachycardia in the setting of acute myocardial ischemia
22
Q
What are the adverse effects of lidocaine
A
- least toxic of class 1 drugs-> pro arrhythmic effects are uncommon
- may cause hypotension in heart failure patients->inhibit cardiac contractility
- Neuro side effects -> paresthesias, tremor, slurred speech, convulsions
23
Q
What is the mechanism of mexiletine?
A
orally active congener of lidocaine
- has electrophysiological and antiarrhythmic effects similar to lidocaine
24
Q
What are the adverse effects of mexiletine?
A
- tremor
- blurred vision
- nausea
- lethargy
25
What are the actions of Class 1 C drugs
- block Sodium channels-> slow impulse conduction
- block certain potassium channels
- do not prolong Qt interval
- Prolong QRS interval
26
What class is flecainide?
Class 1C
27
What are the clinical uses of Flecainide?
- Normal patients that have supra ventricular arrhythmias
| - Refractory ventricular arrhythmias that are life threatening
28
What are the adverse effects of Flecainide?
Ventricular arrhythmia exacerbation in paths with preexisting ventricular tachyarrhythmias
- Patients with a previous MI
- patinets with ventricular ectopic rhythms
- contraindicated with hx of structural or ischemic heart disease (healthy hearts only)
29
What class is propafenone?
- sodium channel blocking kinetics similar to flecainide
| - possesses weak beta blocking activities
30
What is the clinical use of propafenone
supra ventricular arrhythmias in patients without structural disease
*Healthy Hearts only*
31
What are the adverse effects of Flecainide and propafenone?
exacerbation of ventricular arrhythmias
-esp pass with preexisting tachyarrhythmias, MI, or ventricular ectopic rhythms
32
What are the class 1C antiarrhtymic drugs?
Propafenone and Flecainide
33
What are class 2 anti arrhythmic drugs?
Beta Blockers
34
What are the antiarrhytmic actions of beta blockers?
SA node--> decrease HR and increase RR interval
AV node-->Decrease AV conductance and increase PR interval
There is a decreased response to polarization
- increased threshold from the effect on L-type Ca2+ channels
- decreased slope from the effects on Funny sodium and T-type Ca channels
35
What beta blocker is used for
- arrhythmias from stress/thyroid storm
- atrial fibrillation and flutter
- paroxysmal supraventricular arrhythmias
- arrhytmias associated with MI--> to decrease Motality in patients with MI
Propanolol
36
What are the properties of esmolol?
It is a short acting selective beta 1 blocker
- has a short half life
- used in IV form--> rapid onset followed by response termination
37
What are the clinical uses of esmolol?
IV Class 2 beta blocker
- supraventricular arrhythmias
- arrhythmias associated with thyrotoxicosis
- myocardial ischemia or acute myocardial infarction with arrhythmias
- Used with general anesthesia to control arrhythmias in preoperative period
38
What are the adverse effects of Beta blockers
1. Reduced Cardiac Output
2. Bronchoconstriction
3. Impaired glucose mobilization
4. increased VLDL and decreased HDL (BAD)
5. Sedation, depression,
6. Withdrawal syndrome associated with sympathetic hyperresponsivness
39
What are the contraindications of beta blockers?
1. Asthma
2. Peripheral vascular disease
3. Raynauds
4. Type 1 diabetics on insulin
5. Bradyarrhythmias and AV conduction abnormalities
6. Severe depression of Cardiac function
40
What are the class 3 Antiarrhytmic drugs?
1. Amiodarone
2. Sotalol
3. Dofetilide
4. Ibutulide
41
How do class 3 anti arrhythmic drugs affect action potential?
1. block potassium channels
2. prolong AP
3. Prolong QT interval
4. Prolong refractory period
42
What is the clinical uses of Class 3 amiodarone?
1. Recurrent ventricular tachycardia
| 2. Atrial fibrillation
43
What are the pharmacodynamic properties of Class 3 Amiodarone
- blocks potassium channels
- prolongs QT interval and APD
- blocks inactivated sodium channels
- has adrenolytic activity
- has calcium channel blocking activity
- causes Brady cardia and slows AV conduction
44
What are the adverse side effects of amiodarone?
- AV block and bradycardia
- incidence of torsades (lower risk than other class 3 drugs)
- hepatits
- fatal pumonary fibrosis
- Photodermatits -> glue/grey skin discoloration
- optical neuritis
- blocks peripheral conversion of thyroid hormones--> hyper or hypothyroidism
45
What class is sotalol?
```
Class 2 non selective beta blocker
- class 3 agent--> prolongs action potential duration
```
46
What is the clinical use of sotanlol?
- life threatening ventricular arrhythmia
| - maintenance of sinus rhythm in patients with afib
47
What are the adverse side effects of sotalol
- depression of cardiac function
| - provoke torsades de pointes
48
How do class 3 dofetilide and ibutilide work?
block there rapid component of delayed rectifier potassium current (repolarization)
49
What is the clinical use of dofetilide
maintain sinus rhythm after cardio version in patients with Afib
50
What are the adverse effects of Dofetilde and Ibutilide
QT interval prolongation and increased risk of ventricular arrhythmias
51
What are the clinical uses of defetilide and ibutilide
- restore sinus rhythm in patients with a fib
52
What type of cells to class 4 drugs act on?
Cells that exhibit pacemaker potential -->
- decrease slope of phase 0
- increase L-type Ca2+ channel threshold potential
53
How do Class 4 anti arrhythmic drugs work?
- Block L type calcium channels
- Slow sinoatrial node depolarization to reduce heart rate
- prolong conduction and refractory period in the AV node
54
What are the 2 class 4 drugs ?
Verapamil and diltiazem
55
What are the clinical uses of class 4 verapamil and diltiazem?
1. termination and prevention of paroxysmal supraventricular tachycardia cardia
2. Ventricular rate control in A fib and flutter
56
What are the Adverse effects of Verapamil and diltiazem?
1. Cardiac--> Negative inotropy, Av block, sinoatrial node arrest, Bradyarrhythmias, hypotension
2. constipation (verapamil)
57
What anti arrhythmic is used to provide rapid relief of paroxysmal supraventricular tachycardia?
adenosine -> brings it to sinus rhythm rapidly and is given intravenously
58
What are the adverse effects of adenosine?
-SOB
-Bronchoconstriction
-chest burning
-AV block
Hypotension
59
How does adenosine work as an anti arrhythmic?
activates A1 adenosine receptor (GPCR Gi)
- enhances potassium current and inhibits Ca2+ and funny currents--> causes hyperpolarization and suppression of pacemaker cell AP
- Inhibits AV conduction and increases AV nodal refractory period
60
What was the result of CAST (cardiac arrhythmia suppression trial) trial with Flecainide and other Class 1 C drugs
trial was stopped because it increased mortality by 2.5 fold
- is a proarrhythmia because it induced a significant new arrhythmia or worsened an existing one
61
What is a proarrhythmia?
drug induced siginificant new arrhythmia or worsening of an existing arrhythmia
62
What is the clinical approach to treating arrhythmias?
1. Eliminate the cause
2. Make a firm diagnosis
3. Consider underlying cardiac conditions and comorbidities
4. Consider nonpharmacological therapy of arrhythmias
63
What are non pharmacological approaches to cardiac Arrhythmia treatment?
1. Catheter ablation
2. implantable cardioverter-defibrillator
3. artificial cardiac pace maker
4. direct current cardioversion
64
How can class 1A and class 3 drugs trigger fatal arrhythmias?
Class 1A and Class 3 excessively slow repolarization--> can cause torsades de pointes
65
How do class 1A and 1C drugs trigger fatal arrhythmias?
cause excessive conduction slowing--> persistent ventricular tachycardias
66
When should pharmacotherapy be used for cardiac arrhythmias?
- alleviate weakness and fatigue--> improve quality of life
- prevent deterioration of hemodynamics -> low cardiac output, hypotension, and syncope
- minimize risk of sudden cardiac death associated with certain types of arrhythmias
67
What is atrial fibrillation?
organized atrial contraction is lost--> reduced left ventricular filling
68
What are the sx of Afib?
- fatigue, weakness, decreased exercise tolerance
- hypotension
- pulmonary congestion
- exacerbation of heart failure
69
What is renentry?
type of arrhythmia in which one impulse enters and excites areas of the heart more than once
70
How would you describe the electrical impulse conduction in Afib?
rapid irregular erratic rhythm with a disorganized atrial activation 350-600bpm
- ventricular rate is 120-180 bpm depending on AV conductivity
71
What is rhythm control in A fib tx?
rhythm control is conversion to sinus rhythm through cardioversion (direct or chemical -Class 1C or 3)
72
What drugs help to maintain sinus rhythm in AF patients with minimal heart disease
1. Catheter ablation
2. Sotalol
3. Amiodarone
4. Dofetilide
5. Flecainide
6. Propafenone
Class 1C and Class 3
73
What tx maintains sinus rhythms in AF pts with structural disease
1. Cateter ablation
2. Sotalol
3. Amiodarone
4. Dofetilide
Class 3
74
If a patient with AFib can not be treated with direct cardio conversion and has no HF and LVEF greater than 40%, what are the treatment options?
1. Amiodarone
2. Dofetilide
3. Flecainide
4. Ibutilide
5. Propafenone
75
If a patient with AFib can not be treated with direct cardio conversion and has HF and LVEF less than 40%, what are the treatment options?
Amiodarone
Dofetilide
Ibutilidte
76
What is the tx strategy for someone with Paroxysmal/persistent AF without HF, and LVEF >40%
1. CCB or beta blocker
2. CCB and dioxin or beta blocker and digoxin
3. Amiodarone
77
What is the Tx strategy for pt with paroxysmal or persistent AF with HF and LVEF <40%
1. beta blocker
2. Beta blocker and digoxin
3. Amiodarone
78
What is Paroxysmal supraventricular tachycardia mechanism?
- dual properties in AV node have heterogenous electrophysiologic properties (fast and slow conducting_ to allow for rentry circuit formation
79
What are the symptoms of Paroxysmal supraventricular tachycardia?
abrupt onset of palpitations
- dizziness
- lightheadedness
- dyspnea
- chest pain
80
What forms a reentry circuit?
Anterograde conduction through the slow pathways
| retrograde conduction through the fast pathways
81
What does the egg look like for Paroxysmal supraventricular tachycardia? (PSVT)
Narrow QRS complex tachycardia, P wave inverted or not seen because atrial depolarization occurs simultaneously with ventricular depolarization
82
How do you treat Paroxysmal supraventricular tachycardia initially?
1. vagal maneuvers
| 2. Adenosine
83
How do you treat PSVT with LVEF > 40% or no hx of HF
1. Diltiazem or verapamil
2. Beta blocker
3. Digoxin
84
How do you treat PSVT with LVEF<40%/ HF
1. Digoxin
2. Amiodarone
3. Diltiazem
85
What is used to prevent PSVT episodes?
1. Catheter ablation
2. CCB ( Verapamil and Diltiazem)
3. Betablocker (Metoprolol, Atenolol, Propanlol)
86
What is Torsade de Pointes?
-Rapid for of polymorphic VT that occurs in setting of prolonged ventricular depolarization (long QT)
87
What are the clinical manifestations of Torsades?
-HR 160-250
-Palpitations, dizzy, light headed
-hypotension, hemodynamic collapse, syncope
sudden cardia death
- egg looks like twisting of points
88
What causes acquired long QT syndrome?
1. Prolonged AP duration ( slow HR- sinus Brady or AV block and Electrolyte abnormalities hypokalemia and hypomagnesium)
2. Drugs (especially 1A and 3
89
What does QT interval represent?
The time it takes the ventricle to contract in systole
90
What does PR interval represent?
The time between atrial and ventricular depolarizaiton
