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Cardiovascular II Final Exam > Drugs for Cardiac Arrhythmias (Konorev) > Flashcards

Drugs for Cardiac Arrhythmias (Konorev) Flashcards

1
Q

Excitation-contraction coupling

A

-Electrical activity controls the rhythm and rate of the heart pump

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2
Q

Ions move in response to their

A

-concentration and electric gradients

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3
Q

Ions move across the membrane at

A

specific times of the cardiac cycle when their specific ION CHANNELS are open

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4
Q

Cardiac action potential

A
  • sequence of ion fluxes through specific ion channels across the cell membrane (sarcolemma)
  • 2 types: Fast and slow (pacemaker) action potential
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5
Q

Fast AP

A
  • Ventricular contractile cardiomyocytes
  • Atrial cardiomyocytes
  • Purkinje fibers
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6
Q

Slow (pacemaker AP)

A
  • SA node cells

- AV node cells

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7
Q

Phase 0 in fast AP

A

-Voltage dependent fast Na+ channels open as a result of depolarization; Na+ enters the cells down its EC gradient

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8
Q

Phase 1 in fast AP

A

-K+ cells exit down its gradient while fast Na+ channels close resulting in some repolarization

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9
Q

Phase 2 in fast AP

A

-plateau phase results from K+ exiting cells offset by and Ca2+ entering through slow voltage-dependent Ca2+ channels

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10
Q

Phase 3 in fast AP

A

-Ca2+ channels close and K+ begins to exit more rapidly resulting in repolarization

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11
Q

Phase 4 in fast AP

A

-Resting membrane potential is gradually restored by Na/K+ ATPase and the Na+/ca2+ exchanger

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12
Q

Depolarizing vs repolarization forces

A
  • Depolarization by Na+ (fast) and Ca+ (slow to open and close)–voltage gated channels
  • Repolarization by K+ (not just one type of K+ channel but many different types)
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13
Q

Phase 4 in pacemaker AP (slow AP)

A
  • Slow spontaneous depolarization
  • Poorly selective ionic influx (Na+, K+) known as pacemaker current (funny current, If)–activated by HYPERPOLARIZATION
  • Slow Ca2+ influx via T-type transient channels (opens and closes very quickly)
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14
Q

Phase 0 in pacemaker AP (slow AP)

A

Upstroke of AP

-Ca2+ influx through the relative slow L-type (long acting) Ca2+ channels

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15
Q

Phase 3 in in pacemaker AP (slow AP)

A
  • Repolarization

- Inactivation of calcium channels with increased K+ efflux

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16
Q

Factors that determine the firing rate or automaticity

A
  • Rate of spontaneous depolarization in phase 4 (slow AP): decreased slope means decreased rate–need more time to reach threshold potential
  • Threshold potential–the potential at which AP is triggered
  • Resting potential- If potential is less negative, less time needed to reach the threshold–firing rate increases
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17
Q

Antiarrythmic Drugs classification according to MOA–Class 1 drugs

A

-Sodium channel blocking drugs

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18
Q

Class 1A drugs

A
  • Quinidine
  • Procainamide
  • Disopyramide
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19
Q

Class 1B drugs

A
  • Lidocaine

- Mexiletine

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20
Q

Class 1C drugs

A
  • Flecainide

- Propafenone

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21
Q

Class 2 drugs are

A
  • Beta Blockers
  • Esmolol
  • Propranolol
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22
Q

Class 3 drugs are

A
  • Potassium channel blocking drugs
  • Amidarone
  • Dronedarone
  • Sotalol
  • Dofetilide
  • Ibutilide
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23
Q

Class 4 drugs

A
  • Cardioactive CCBs
  • Verapamil
  • Diltiazem
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24
Q

Miscellaneous agens

A

-Adenosine

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25
Q

When sodium channel is activated,

A

Na+ current occurs down electric and concentration gradients

26
Q

Resting state of sodium channels

A

-the channel is closed but ready to generate AP (h gates are open but m gates closed)

27
Q

Activated state of sodium channels

A

-depolarization to the threshold opens m gates, greatly increasing sodium permeability

28
Q

Inactivated state of sodium channels

A

-h-gates are closed so inward sodium flux is inhibited; the channel is not available for reactivation–this state is responsible for the refractory period

29
Q

State dependent block of sodium channels

A

drugs may have different affinities towards the ion channel protein while it shuttles through different states of the cycle

30
Q

Most useful Class `1 drugs (Na-channel blockers) block which states of the Na channel?

A

-block open activated or inactivated Na+ channels with very little affinity towards channels in the resting state

31
Q

Kinetics of dissociation

A
  • determines how quickly drugs dissociate from the channel

- Fast, intermediate or slow kinetics

32
Q

If a drug dissociates quickly from the Na channel then how is conductivity of heart affected?

A
  • Conductivity not significantly affected for drugs that dissociate quickly
  • In contrast, drugs that dissociate slowly there is progression of inhibition of conductivity because as the next AP comes, some of the channels will still be blocked due to slow dissociation
33
Q

Features of class 1A drugs

A
  • Block sodium channels

- reduce automatism of latent (ectopic) pacemakers

34
Q

Class 1A drugs–use dependent block

A
  • preferentially bind to OPEN (activated) sodium channels

- Ectopic pacemaker cells with faster rhythms will be preferentially targeted

35
Q

Class 1A dissociation kinetics

A

-dissociate from channel with INTERMEDIATE kinetics

36
Q

In addition to blocking sodium channels, Class I A drugs

A

-Block potassium channels as well causing long QT

37
Q

Effects of Class 1 A drugs on AP and ECG

A
  • prolong AP duration (decreased slope of phase 0)

- Prolong QRS and QT intervals of ECG (widened)

38
Q

Class 1B drugs block what?

A
  • sodium channels only! (decreases slope of phase 0)

- More specific action on sodium channels–do not block K channels!

39
Q

Class 1B use dependent block (bind to what state of sodium channel?)

A
  • bind to inactivated state
  • preferentially bind to depolarized cells
  • so only affects damaged cells like in ischemia leading to arrhythmias because damaged cells are usually partially depolarized–does NOT affect normal tissue!!!
40
Q

Class 1B kinetics

A

-FAST dissociation kinetics–no effect on conduction in normal tissue

41
Q

Effects of 1B drugs on AP and ECG

A
  • may shorten AP

- do NOT prolong QT duration or AP because potassium channel is not blocked

42
Q

Class 1B useful in treating

A

-ventricular arrhythmias secondary to acute myocardial ischemia

43
Q

Class 1C drugs block

A
  • sodium channels, slow impulse conduction

- also block CERTAIN K+ channels but not ones that repolarize!!

44
Q

Class 1C drugs preferentially bind to

A

-open (activated) sodium channels

45
Q

Class 1C drugs dissociation kinetics

A

-SLOW

46
Q

Class 1C drugs effects on AP, and ECG changes

A
  • Do NOT prolong AP and QT interval duration of ECG

- Prolong QRS interval duration

47
Q

what causes long QT syndrome by class 1A drugs?

A

-decreased outward K flux

48
Q

Sympathetic innervation of pacemaker activity

A
  • Pacemaker cells express B1 receptors
  • B1 receptors are GPCRs that are coupled to Gs proteins
  • Activates adenylyl cyclase leading to increase cAMP
  • > Activates protein kinase A
  • PKA phosphorylates Funny channel protein so that it opens faster
  • PKA also phosphorylates T and L type Ca channels–which will make them open at a more negative AP inducing a stronger Ca2+ current (more Ca2+ flux into cell)
49
Q

Sympathetic effect on the pacemaker AP

A
  • Increased slope due to effects on If and T-type Ca channels–tachycardia
  • Reduced threshold due to effect on L-type Ca channel (more robust flux of Ca ions)
50
Q

Beta Blockers effect on slow AP

A
  • Decreased slope due to effects on If and T-type Ca channels–slows HR
  • -SA node–slows HR (increase RR interval)
  • -AV node–decrease AV conductance (Increase PR interval)
  • Increased threshold due to effect on L-type Ca channel
51
Q

Beta Blockers effect on ventricular myocardium

A

-Decrease Ca2+ overload, prevent delated after depolarizations

52
Q

Types of potassium channels

A
  • Calcium activated–activated by Ca channel in cytosol; increase in Ca due to opening of Ca+ channel activates this channel will contribute to repolarization
  • Inwardly rectifying
  • Tandem pore domain
  • Voltage gated–contributes to repolarization
53
Q

Why is sodium channel considered “fast” while K channel is not?

A
  • Because both the electrical and chemical gradient of sodium are in the same direction (out to in)
  • In contrast, K+ is higher inside the cell so its chemical gradient wants to go outside but electrically, its positive so wants to go inside the negatively charged cell
54
Q

Regulation of RESTING potential by Class 3 drugs (potassium blocking)–what kind of potassium channels??

A
  • Inward (electric) gradient is in equilibrium with the outward (concentration) gradient in the resting cell
  • Inwardly rectifying K+ channels are open in the resting state
  • No current occurs in these channels because of this equilibrium
  • If EC K+ concentration changes, membrane potential will have to readjust to reach new equilibrium
55
Q

Regulation of AP by class 3 drugs

A
  • VOLTAGE gated K+ channels contribute to the regulation of AP
  • Repolarization of cell membanre during AP
  • Limit fréquency of AP (regulate duration of REFRACTORY PERIOD)
56
Q

Class 3 drugs effects on AP and ECG

A
  • Block potassium channel
  • So QT interval is prolonged and AP is prolonged as well
  • Prolong REFRACTORY PERIOD
57
Q

APD prolongation by class 3 drugs is

A

-RATE dependent with the most marked effect at SLOW heart rate

58
Q

Class 4 drugs blocks ____ channels; what are the different staes of this channel?

A
  • Ca channel
  • Resting closed state
  • Activated state (voltage dependent gate is open)
  • Inactivated state
59
Q

Mechanisms of Ca channel inactivation by class 4 drugs

A
  • VDI–voltage dependent inactivation
  • CDI–calcium dependent inactivation

**In cardiac tissue, Ca contributes to inactivation state by negative feedback; As Ca comes in and conc of Ca in cytosol builds up too much, Ca binds to Calmodulin and Ca-calmodulin complex binds to C-terminal domain of L-type Ca channel and blocks the Ca entry leading to the inactivated state

60
Q

Class 4 drugs block what state of Ca channels?

A
  • Both the activated and inactivated L type calcium channels

- Active in slow response cells–decrease the slope of phase 0 depolarization

61
Q

Class 4 drugs names, effects on AP, ECG

A
  • Verapamil, Diltiazem
  • Slow sinoatrial node depolarization, cause bradycardia
  • Prolong AP duration and refractory period in AV node
  • Prolong AV node conduction time
  • May suppress delayed afterdepolarizations–may be effective in DAD-induced ventricular arrhythmias

Cardiovascular II Final Exam (13 decks)

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