Pharm Block 2- Antiarrhythmic Drugs

Front 1

diastolic depolarization

Back 1

-creeping deploarization of RMP caused by funny currents (slow inward Na), dec K+ prem, and opening Ca channels
-SLOW response cells (SA/AV)

Front 2

membrane responsiveness

Back 2

-level of RMP determines the max upstroke (Vmax) of the AP

Front 3

what determines membrane responsiveness in fast response cells

Back 3

-availability of Na+ channels

Front 4

what determines membrane responsiveness in slow response cells

Back 4

-Ca2+ channel availability

Front 5

what does a more neg RMP mean for vmax?

Back 5

-Vmax will be higher bc more channels are in the resting states and available for activation
-higher Vmax--> inc conduction velocity (and vice versa)

Front 6

effective refractory period

Back 6

-minimum interval between two propagating responses

Front 7

ERP in fast response cells

Back 7

-proportional to AP duration
-because recovery from inactivation of Na+ channels is rapid and closely parallels repolarization

Front 8

ERP in slow response cells

Back 8

-delayed
-recovery of Ca2+ channels is time-dep and occurs slowly

Front 9

are fast or slow cells more susceptible to premature stimuli

Back 9

-fast cells
-Na+ channels that mediate AP upstroke recover rapidly from inactivation

Front 10

what kind of drugs inhibit depolarization (and conduction) of fast response cells?

Back 10

-class I antiarrhymthmic agents (ie quinidine)

Front 11

what kind of drugs inhibit depolarization (and conduction) of slow response cells?

Back 11

-calcium entry blockers
-ie verapamil and diltiazem

Front 12

fast response cells

Back 12

-atria, ventricles, His-Purkinje system
-Na+ is main ion for depolarization
-catecholamines and ACh have little effect on depolarization (and conduction)

Front 13

slow response cells

Back 13

-SA and AV nodes
-Ca2+ is major ion for depolarization
-catecholamines enhance depolar
-ACh significantly depresses depolarization

Front 14

three main mech of arrhythmia generation

Back 14

-enhanced automaticity
-triggered automaticity
-re-entry

Front 15

enhanced automaticity

Back 15

-cardiac cell becomes inappropriately excitable and starts firing rapid APs
-depolarizing RMP, inc diastolic depolar, and/or dec threshold

Front 16

triggered automaticity

Back 16

-abnormal depolarization that occurs during an AP
-can trigger abnormal electrical activity
-includes EAD and DAD

Front 17

early afterdepolarization (EAD)

Back 17

-abnormal depolarizations that occur during phase 2 repolarization
-can trigger abnormal beats
-most freq when HR is slow or when cardiac repolarization is prolonged

Front 18

What is EAD thought to be a major cause of?

Back 18

-Torsades de pointes (v fib without pattern)

Front 19

delayed afterdepolarization (DAD)

Back 19

-depolarizations that occur late in the AP configuration (arises from RMP)
-usually during Ca2+ overload from MI, adrenergic stress, or digitalis toxicity

Front 20

when does EAD and DAD occur more frequently

Back 20

-EAD: heart rate slow or when repolar is prolonged (QT)
-DAD: heart rate fast, high Ca2+

Front 21

reentry

Back 21

-abnormal impulse conduction that causes re-entry of an impulse into an area of the myocardium that has already been depolarized
-anatomically or functionally defined

Front 22

anatomically defined re-entry

Back 22

-impulses propagate by more than one pathway btw two points in the heart
-re-entrant conduction loop is established
-prototype: Wolf-Parkinson-White syndrome

Front 23

Wolff-Parkinson-White syndrome

Back 23

-prototype of anatomical re-entry
-rapidly conducting accessory AV pathway is present

Front 24

functionally defined re-entry

Back 24

-requires an area of depressed conduction with unidirectional block AND slow impulse propagation in the retrograde direction
-depressed conduction area is generally from MI

Front 25

sinus tachycardia

Back 25

-HR greater than 100bpm
-dt very active SA node

Front 26

supraventricular tachycardia

Back 26

-HR increased dt early beats origination from an atrial or junctional pacemaker site

Front 27

paroxysmal atrial tachycardia

Back 27

-supraventricular tachycardia that is trasient
-beings and ends rapidly

Front 28

atrial flutter

Back 28

-a stable, well-organized macro-reentrant circuit within RA or LA
-atrial rate>ventric rate

Front 29

atrial fibrillation

Back 29

-atria is sending disorganized electrical signals that are very fast and erratic
-causes ventricle to contract erratically

Front 30

premature ventricular contraction

Back 30

-electrical signal originates from within ventricles
-results in ventricular contractions before signal from atria is received

Front 31

ventricular tachycardia

Back 31

-very fast, steady electrical signal
-originates from within ventricles

Front 32

ventricular fibrillation

Back 32

-very fast and erratic signal
-originates from within ventricles
-results in the inability of ventricles to fill with blood and pump
-life threatening

Front 33

4 mech by which antiarrhythmic drugs reduce spontaneous discharge in automatic tissues

Back 33

-dec phase 4 slope
-inc threshold for AP firing
-inc max diastolic potential (make more neg)
-inc AP duration

Front 34

Class I antiarr drugs

Back 34

-Na+ channel blockers in fast response cells
-fewer Na ch--> dec membrane responsiveness --> dec conduction velocity --> dec phase 4 slope

Front 35

class IA antiarr drugs

Back 35

-quinidine and disopyramide
-inc AP threshold, dec Vmax, inc ERP

Front 36

quinidine on K+ channels

Back 36

-blocks them
-inc ERP
-sets stage for afterdepolarizations and fatal triggered arrhythmias

Front 37

quinidine as a vagolytic

Back 37

-anticholinergic effects
-can inc conduction vel through AV node
-use with B-blocker or CCB to prevent this with atrial flutter

Front 38

quinidine uses

Back 38

-atrial flutter or fib
-prevention of ventric tachy and v fib
-dec usage dt vagolytic and GI side effects

Front 39

disopyramide

Back 39

-like quinidine (class IA antiarr)
-fewer GI effects
-greater anticholinergic effects
-neg ionotrop-- c/i in CHF

Front 40

class IB drugs

Back 40

-lidocaine
-dec membrane responsiveness in rapidly firing cells
-use-dependent block in diseased myocardium
-inc threshold
-dissociates rapidly

Front 41

lidocaine effect on ERP

Back 41

-shortens it (opposite of quinidine)

Front 42

lidocaine uses

Back 42

-v-tachy and digitalis-induced arrhythmias
-safe for pts with long QT syndrome

Front 43

class 1C antiarr

Back 43

-Flecainide (very potent)
-marked dec membrane responsiveness
-inc threshold
-dissociates slowly --> most potent
-variable effect on ERP

Front 44

flecainide uses

Back 44

-ONLY in life-threatening situations of supraventricular of ventricular arrhythmias are unresponsive to other interventions

Front 45

class II anti-arr

Back 45

-B-blockers: propanolol
-slow phase 4 depolar
-prolong repoalr at AV node--> increase ERP but don't affect repolar in ventricles
-profound effect when symp stim is high

Front 46

can pts with long QT use propanolol?

Back 46

-YES
-it prolongs repolarization in AV node but doesn't affect repolarization in ventricular tissue

Front 47

propanolol s/e

Back 47

-bronchospasm
-neg ionotropic effect
-heart block
-bradycardia

Front 48

b-blocker use

Back 48

-atrial and ventricular tachy and fib

Front 49

Class III antiarr

Back 49

-K+ ch blockers: amiodarone and sotalol
-prolong repolarization (and ERP)
-Na, Ca, a, b blocker (moderate)
-overall: dec diastolic depolar, dec membrane responsiveness Vmax, inc ERP

Front 50

class III s/e

Back 50

-amiodarone and satolol
-triggered arrhythmias (torsades de pointes)
-pulm fibrosis and altered thyroid function, hypotenision

Front 51

class III uses

Back 51

(sotalol and amiodarone)
-ventric tachy and fib
-prevents ventric arrhythmias in pts with HF or hx of MI
-prevents recurrent paroxysmal a-fib or flutter

Front 52

class IV antiarr

Back 52

-CCBs
-act primarily on slow response cells
-diltiazem and verapamil
-dec membrane responsiveness and inc threshold

Front 53

combining digitalis and CCB

Back 53

-verapamil and diltiazem increase plasma digitalis by competing for renal excretion
-combo= severe heart block

Front 54

CCB uses

Back 54

-re-entant paroxysmal supraventricular tachycardia

Front 55

digitalis for antiarr

Back 55

-enhances efferent vagal parasymp activity to dec conduction at AV node
-used for afib and supraventricular tachy

Front 56

adenosine

Back 56

-activates K+ channels at AV node (slows phase 4 at AV node)
-used for supraventricular tachycardias