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CVS > Antiarrhythmic drugs > Flashcards

Antiarrhythmic drugs Flashcards

1
Q

Action potential phases

A
  • Phase 0: depolarization by inflow of Na
  • Phase 1: partial repolarization by outflow of K
  • Phase 2: plateau by slow inward Ca
  • Phase 3: repolarization by K outflow
  • Phase 4: resting potential, but in pacemaker cells there is slow Na influx leading to autorhythmicity
  • Refractor period: phases 1-3
  • Drugs will target either phase 0 (prolong depolarization) or phase 3 (prolong depolarization)
  • Targeting phase 0 means affecting Na permeability
  • Targeting phase 2&3 means affecting K permeability (can also target both)
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2
Q

Inhibiting Na permeability

A
  • Slows depolarization (phase 0)
  • Slows conduction, decreases slope and magnitude of AP
  • Prolongs P wave and QRS
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3
Q

Inhibiting K permeability

A
  • Slows repolarization (extends phase 2 and 3)
  • Prolongs AP duration (APD), prolongs refractory period
  • Prolongs ST segment
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4
Q

How ventricular APs relate to ECG

A
  • Phase 0 = QRS
  • Phase 2 = ST segment
  • Phase 3 = T wave
  • Refractory period goes until the peak of the T wave (close to the resting potential in the AP)
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5
Q

Summary of drug effects on AP/ECG

A
  • Inhibiting Na influx: prolongs phase 0 and decreases peak, prolongs P wave and QRS complex (get wider)
  • Inhibiting K efflux: prolongs phase 2 (and 3) which widens the ST segment
  • If you inhibit both K and Na you are prolonging phase 0, 2, and 3 which thus widens the P wave, QRS, and ST segment
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6
Q

Pacemaker cells and latent pacemakers 1

A
  • Normal pacemakers are in the SA node (70/min)
  • Latent pacemakers are in other areas like AV node (50/min) or conduction pathways (30/min) or ventricles (10/min)
  • Latent pacemakers have slower phase 4 depolarization than SA node, thus are depolarized (controlled) by SA node
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7
Q

Pacemaker cells and latent pacemakers 2

A
  • Ectopic pacemakers occur when the SA node does not fire and a latent pacemaker takes control of the rhythm
  • Pacemaker rate is determined by the slope of phase 4 depolarization (larger the slope the greater the rate)
  • Injured cardiac tissue can spontaneously depolarize, due to leaky membrane and less negative resting potential
  • Can convert a pacemaker to latent pacemaker by slowing down phase 4 depolarization or increasing the threshold
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8
Q

Early afterdepolarization (EAD)

A
  • Positive changes in membrane potential during depolarization
  • Occur either in plateau phase (2) or repolarization (3)
  • Prolongation of QT interval is big risk factor
  • Greater risk when on K inhibitors b/c they prolong ST and thus QT
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9
Q

Torsades des pointes

A
  • Wise QT can lead to ventricular tachycardia (torsades) in which each beat has a different morphology
  • The danger is ventricular fibrillation
  • Blocking K efflux increases the chance b/c it widens the QT
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10
Q

Delayed afterdepolarization (DAD)

A
  • Ectopic beat (premature contraction) that occurs after repolarization is complete
  • Occurs @ greater frequency when myocardium has high concentrations of Ca
  • Think digitalis/digoxin (increases Ca)
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11
Q

Altered impulse conduction 1

A
  • Functional: impulse encounters refractory period
  • Fixed: impulse encounters area of scar/fibrosis
  • Can result in brady or tachyarrhythmias
  • Reentry may occur if there is a ring of tissue that does not conduct normally
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12
Q

Altered impulse conduction 2

A
  • Bidirectional block: normal conduction of a ring of tissue, both sides of the ring conduct at equal velocity and cause the two impulses to cancel when they meet (does not form reentrant loop)
  • Unidirectional block: when a ring of tissue does not conduct normally and forms a reentrant loop b/c part of it (fibroses areas) is no longer refractory when the retrograde impulse arrives (from the other side)
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13
Q

Converting unidirectional block to bidirectional block

A
  • Prolonging the refractory period by reducing K permeability
  • Or slowing depolarization by reducing Na permeability (affects ischemic/infarcted areas predominantly)
  • Ectopic pacemakers are more sensitive to anti arrhythmic drugs than SA node
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14
Q

Prolonging refractory period in unidirectional blocks

A
  • Inhibiting K permeability (efflux) will delay repolarization and prolong the refractory period
  • When the retrograde impulse meets the ischemic tissue, the tissue will be in refractory period and unable to fire
  • This creates a bidirectional block and eliminates the arrhythmia
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15
Q

Decreasing AP peak in unidirectional blocks 1

A
  • Inhibiting Na influx will decrease the peak of phase 0 (depolarization) in ischemic/infarcted tissue (preferentially)
  • Ischemic/infarcted tissue has fewer functioning Na channels, thus the resting potential is less negative, the slope of AP is decreased, and the magnitude of the AP is decreased
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16
Q

Decreasing AP peak in unidirectional blocks 2

A
  • Further blocking Na influx results in a greatly reduced depolarization and prevents the damaged area from reaching threshold when the retrograde impulse arrives
  • Since the retrograde impulse cannot cause the damaged area to depolarize to threshold (Na channels blocked) the retrograde impulse cannot continue and a unidirectional block is transformed into a bidirectional block
17
Q

Antiarrhythmic drug (AADs) functions

A
  • Decrease automaticity of ectopic pacemakers more than SA node
  • Either decrease excitability/AP magnitude (Na inhibition) or increase refractory period (K inhibition) in more depolarized (ischemic/infarcted) tissue
  • Other types of AADs: Ca blockers (nodes use Ca to depolarize, so these will mostly affect AV node arrhythmias), and BBs
18
Q

Classes of AADs: Ia-c (1)

A
  • Class Ia: blocks Na influx (moderate) and K efflux, thus slows depolarization/conduction (and reduces peak) in atria and ventricles, and prolongs repolarization (refractory) time (APD)
  • Widens P, QRS, and ST segment
  • Includes Quinidine, procainamide, disopyramide
  • Class Ib: blocks Na influx (mild) only, and it shortens AP peak and repolarization time (in normal cells) but prolongs refractory period/APD (repolarization time) in ischemic cells (still inhibits phase 0 depolarization)
19
Q

Classes of AADs: Ia-c (2)

A
  • Class Ib works only in ischemic areas and only in ventricles, and in these areas has the same effect as class Ia (widens P, QRS, and ST segment)
  • Includes lidocaine, mexilitine, tocainide
  • Type Ic: blocks Na influx (strong) only, but does not change repolarization time
  • Only prolongs phase 0 and lowers AP peak (prolongs P and QRS)
  • Includes Fecanide and propafenone
20
Q

Classes of AADs: II-misc. (1)

A
  • Type II are BBs: diminsh phase 4 depolarization in pacemakers, thus reduce automaticity of ectopic pacemakers
  • Type III block K efflux and markedly prolong repolarization time (ST segment)/APD/refractory period
  • Works for both ventricular tachycardia and SVTs
  • Type III includes amiodarone, sotalol, and ibutilide
21
Q

Classes of AADs: II-misc. (2)

A
  • Type IV are Ca influx blockers that work on the AV node mostly
  • Prolongs depolarization (phase 4) and repolarization time in AV node, thus decreasing conduction time thru AV node
  • Works only in SVTs
  • Type IV includes verpamil and diltiazem
  • Misc: adenosine and digoxin
22
Q

Similarity btwn class I drugs

A
  • All class I drugs slow depolarization of ectopic pacemaker cells by 2 ways
  • They increase the threshold for AP (make threshold potential more positive- harder to reach)
  • They also decrease the slope of phase 4 depolarization (increase the time to reach threshold)
  • Both accomplished by blocking Na channels
23
Q

Class Ia drugs 1

A
  • These drugs block Na influx moderately, and K efflux
  • They prolong phase 0 (and reduce AP magnitude) and prolong APD/refractory period (widens P, QRS, ST segment)
  • All have some degree of vagolytic action (prevent Ach release from vagus)
  • Quinidine: effective for atrial and ventricular arrhythmias, not used much due to side effects (toxic)
24
Q

Class Ia drugs 2

A
  • Most common negative side effects (NSE) of quinidine: GI disturbances (anorexia, nausea, vomiting, etc) and cinchonism (syndrome of headaches, tinnitus, dizziness)
  • Increases risk of torsades de pointes (almost all AADs do this) b/c it increases ST segment (and thus QT interval)
25
Q

Class Ia drugs 3

A
  • Procainamide: Effective mostly for ventricular arrhythmias, also avoided due to toxic side effects
  • NSEs of procainamide: lupus-like syndrome and tosades are most important
  • Disopyramide: approved only for ventricular arrhythmias, but avoided due to NSEs
  • NSEs: depression of cardiac conduction can precipitate heart failure, also torsades
26
Q

Class Ib drugs 1

A
  • On normal cells these drugs shorten APD (repolarization) and prolong depolarization (also decrease AP peak)
  • But these effects are not significant b/c these drugs only work on ischemic/infarcted tissue and in the ventricles
  • In infarcted tissues Ib drugs have the same action as class Ia drugs: decrease AP peak and prolong depolarization, and prolong repolarization/APD (widen P, QRS, ST segment)
  • Lidocaine: effective for acute ventricular arrhythmias during acute MI (no effect in atria)
27
Q

Class Ib drugs 2

A
  • Lidocaine is rapidly redistributed to peripheral tissues, and undergoes extensive 1st pass metabolism (cannot be taken orally)
  • Reduced liver flow (HF) will increase serum concentrations
  • Serum levels must be monitored, toxicity (neurologic) depends on serum levels, and routine use is contraindicated
  • Other type Ib drugs (tocainide, mexiletine) are similar to lidocaine but are resistant to 1st pass metabolism and thus can be administered orally
28
Q

Class Ic drugs 1

A
  • Powerful inhibitors of Na influx, they greatly slow phase 0 depolarization and lower AP peak, w/o affecting repolarization/APD
  • Prolong only P and QRS
  • Flecainide: only approved for use of supra ventricular arrhythmias in normal hearts
  • Is pro arrhythmic in setting of structural heart disease and ventricular arrhythmias
29
Q

Class Ic drugs 2

A
  • Flecainide is used in WPWS, since flecainide preferentially blocks conduction thru accessory pathways in setting of tachyarrhythmias
  • Other adverse effects of flecainide: CNS (blurred vision, nausea, tremor, metallic taste), heart failure
  • Propafenon: similar indications to flecainide (supra ventricular arrhtyhmias)
  • Adverse effects: metallic taste, constipation, proarrhtyhmic
30
Q

Class II drugs

A
  • BBs, diminish phase 4 depolarization in nodes and decrease ectopic pacemaker depolarization
  • Prolong AV conduction, decrease HR and contraction force
  • Used in SVAs and ventricular ectopy, also prevent sudden cardiac death in acute MI
  • Adverse effects: fatigue, lethargy, hyperglycemia, hypotension, bradycardia
31
Q

Class III drugs 1

A
  • Prolong APD by inhibiting K efflux, no change on phase 0
  • Prolongs ST segment, APD, refractory period
  • Amiodarone: widely used for atrial and ventricular arrhythmias
  • Low toxicity (less risk of torsades), but slow hepatic metabolism and inhibits CYP450
32
Q

Class III drugs 2

A
  • NSEs of amiodarone: dose-dependent toxicity of pulmonary fibrosis, hyper or hypothyroidism, and hepatocellular necrosis
  • Therefore need to have baseline PFT (pulm function tests), TFT (thyroid function test), and LFT (liver function test)
  • Dronedarone: less toxic than amiodarone, so better for long-term use, but can increase mortality in those w/ HF
33
Q

Class III drugs 3

A
  • Dofetilide: oral only, used during Afib, but can lead to excessive QT prolongation and thus increases risk for torsades
  • Ibutilide: IV only, otherwise same as dofetilide (contraindicated in those w/ LVH)
  • Sotalol: oral only, used for atrial and ventricular arrhythmias, less QT prolongation so less risk of torsades
34
Q

Class IV drugs

A
  • Ca channel blockers (verapamil and diltiazem)
  • They prolong AV nodal conduction and refractory time
  • Decrease HR and contractility
  • Only are affective in SVAs (no ventricular arrhythmia use)
  • NSEs: contraindicated in those w/ LV dysfxn (HF)
35
Q

Adenosine

A
  • Binds to receptor and inhibits AC, thus inhibits the inward Ca current
  • Since AV node utilizes Ca for depolarization adenosine slows conduction thru AV node and inhibits AV node reentry arrhythmias
  • NSEs: flushing, dyspnea, chest pain, transient arrhythmias
  • Contraindicated in asthma, heart block
36
Q

Digoxin

A
  • Cardiac glycoside, blocks Na/K ATPase
  • This increase Na levels and in turn leads to deactivation of Na/Ca channel (brings Na in for Ca out)
  • As Na levels rise there is less of a gradient for Na to enter via the Na/Ca channel so more Ca remains in the cell
  • Digoxin increase cardiac contraction and slows AV conduction by increasing AV node refractory period
  • Used in control of ventricular rate during Afib or atrial flutter
  • Improves Sx from CHF exacerbations
  • Narrow therapeutic index

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