Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > 13) Arrhythmia & Anti-Arrhythmic Drugs > Flashcards

13) Arrhythmia & Anti-Arrhythmic Drugs Flashcards

1
Q

Pacemaker cells function

A
  • Intrinsically generate rhythmic action potentials in the absence of external stimuli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Sinoatrial (SA) node

A
  • The pacemaker

- Normal initiation site of the heartbeat/impulse (the action potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The impulse spreads from the SA node to the

A
  • Atrioventricular (AV) node

- Then to the bundle of His and the Purkinje system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The SA node excites

A
  • The right atrium

- Impulse travels through Bachmann’s bundle to excite left atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Arrhythmia

A
  • Abnormality in cardiac rhythm (heart beats)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Types of cardiac cells

A
  • Pacemaker (SA node)

- Non-pacemaker (cardiac myocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pacemaker (SA node) cell characteristics

A
  • Exhibit Automaticity
  • Intrinsically generate
    APs and stimulate the heart beats without External Stimuli
  • Leaders/Initiators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Non-pacemaker (cardiac myocyte) cell characteristics

A
  • Do NOT exhibit automaticity
  • Receive impulses from pacemakers to generate action potential and induce contraction
  • Followers/Executers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cardiac myocyte Phase 4 (resting)

A
  • Cardiomyocyte is −90 mV

- Maintained by slow outward leak of K+ currents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cardiac myocyte Phase 0 (depolarization)

A
  • An AP triggered by an impulse from pacemaker cell
  • Fast Na+ channels start to open
  • Na+ leaks into the cell causing depolarization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cardiac myocyte Phase 1 (early repolarization)

A
  • Some K+ channels open briefly

- Allow an outward flow of K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cardiac myocyte Phase 2 (plateau)

A
  • L-type Ca2+ channels are open, inward current of Ca2+
  • K+ leaks out
  • Countercurrents are electrically balanced
  • Transmembrane potential (TMP) is maintained at a plateau
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cardiac myocyte Phase 3 (repolarizaton)

A
  • Persistent outflow of K+, now exceeding Ca2+ inflow
  • Brings TMP back towards resting potential of −90 mV
  • Prepares the cell for a new cycle of depolarization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

The action potential in cardiomyocytes is composed of

A
  • 5 phases (0-4)

- Begins and ends with phase 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SA node Phase 4 (spontaneous depolarization)

A
  • Membrane potential is -60 mV
  • Ion channels open and conduct slow, inward (depolarizing) Na+ currents called “funny” currents (If)
  • Transient (T-type) Ca++ channel starts to open
  • Inward Ca++ currents further depolarize the cell to about -40 mV
  • Second type of Ca++ channel opens (long-lasting/L-type) to depolarize the cell until AP threshold is reached (usually between - 40 and -30 mV)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

SA node Phase 0 (depolarization phase of the action potential)

A
  • Primarily caused by increased Ca++ conductance through the L-type Ca++ channels
  • If and T- Ca++ currents are closed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SA node Phase 3 (repolarization)

A
  • Occurs as K+ channels open
  • At the same time, L-type Ca++ channels closes
  • Once the cell is completely repolarized at about -60 mV, the cycle is spontaneously repeated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mechanisms of arrhythmia

A
  • Disorders in impulse formation

- Conduction block or delay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Disorders in impulse formation

A
  • Altered automaticity

- Abnormal automaticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Altered automaticity

A
  • Specialized heart cells (like SA and AV nodes) possess the property of automaticity
  • An increase or decrease in the activity of these cells may lead to arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Abnormal automaticity

A
  • Arrhythmia occurs when cardiac sites other than the SA node shows enhanced automaticity which should not possess automaticity
  • Thereby, Non-Pacemaker cells exhibit abnormal automaticity “ectopic foci” and may may generate competing impulse and arrhythmia may occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Conduction abnormalities (block or delay)

A
  • Occur when the propagating impulse fails to conduct or conduct at slower rate
  • When an impulse arrives at tissue that is still refractory, it will not be conducted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Antiarrhythmic drugs classification (Vaughan Williams Classification based on MOA)

A
  • Class I = Na channel blockers (IA, IB, IC)
  • Class II = B-blockers
  • Class III = K channel blockers
  • Class IV = Ca channel blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Class IA sodium channel blockers MOA

A
  • During phase 0
  • Greater degree of blockade in tissues that are frequently depolarizing
  • Can inhibit potassium channels (Class III activity)
  • Proarrhythmic
  • Can slow down the conduction velocity and induce QT prolongation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Class IB sodium channel blockers MOA

A
  • During phase 0
  • Shorten phase 3 repolarization and the duration of AP
  • Reduction inward Na without affecting outward K shortens AP duration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Class IC sodium channel blockers MOA

A
  • During phase 0
  • Dissociate slowly
  • Minor effect on the duration of AP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Class IA drugs (names)

A
  • Quinidine
  • Procainamide
  • Disopyramide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Quinidine (class IA) properties

A
  • Alpha-adrenergic blocking activity

- Anticholinergic actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Quinidine (class IA) special characteristics

A
  • Can cause cinchonism blurred vision, tinnitus, headache, disorientation, and psychosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Quinidine (class IA) metabolism

A
  • Substrate of CYP3A4

- Inhibitor of CYP2D6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Procainamide (class IA) properties

A
  • Anticholinergic actions

- NO alpha-adrenergic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Procainamide (class IA) metabolism

A
  • Acetylated in the liver to N-acetyl procainamide (NAPA)
  • Prolongs duration of the AP (QT prolongation)
  • Proarrhythmic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Disopyramide (class IA) properties

A
  • Most anticholinergic effect of this class

- NO alpha-adrenergic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Disopyramide (class IA) metabolism

A
  • Substrate of CYP3A4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Disopyramide (class IA) special characteristics

A
  • Negative inotropic effects
  • May precipitate HF
  • Should not be used in patients with HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Properties shared by all class IA drugs

A
  • Proarrythmic
  • Can induce QT prolongation
  • Anticholinergic adverse effects (ex: dry mouth, urinary retention, blurred vision, and constipation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Class IB drugs (names)

A
  • Lidocaine

- Mexiletine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Lidocaine (class IB) metabolism

A
  • First pass so only given IV
39
Q

Lidocaine (class IB) characteristics

A
  • High safety profile
  • Least cardiotoxic agent among sodium channel
    blockers
  • No negative inotropic effect
40
Q

Lidocaine (class IB) side effects

A
  • CNS side effects that often limit the duration of continuous infusions
  • Nystagmus (early indicator of toxicity)
  • Drowsiness
  • Slurred speech
  • Paresthesia
  • Agitation
  • Confusion
  • Convulsions
41
Q

Mexiletine (class IB) metabolsim

A
  • Oral

- Narrow therapeutic index

42
Q

Mexiletine (class IB) most common side effecs

A
  • Nausea
  • Vomiting
  • Dyspepsia
43
Q

Class IC drugs (names)

A
  • Flecainide

- Propafenone

44
Q

Flecainide (class IC)

A
  • Substrate of CYP2D6

- Well tolerated

45
Q

Flecainide (class IC) side effects

A
  • Blurred vision
  • Dizziness
  • Nausea
46
Q

Propafenone (class IC)

A
  • Substrate of CYP2D6

- B-blocking effects

47
Q

Propafenone (class IC) side effects

A
  • Blurred vision, dizziness, and nausea
  • Bronchospasm due to its β-blocking effects
  • Should be avoided in patients with asthma
48
Q

β-Blockers reduce arrhythmia by

A
  • Blocking B-adrenergic receptors

- Antagonizing the increased sympathetic tones and high levels of circulating catecholamines (NE and epinephrine)

49
Q

β-Blockers reduce phase 4 spontaneous depolarization through

A
  • Reducing automaticity at SA node and decreasing the heart rate
  • Reducing AV nodal conduction
50
Q

Metoprolol is a selective β-1 receptor blocker widely used in

A
  • Treatment of cardiac arrhythmias
  • Reduces the risk of bronchospasm compared to nonselective β-blockers
  • CYP2D6 substrate
51
Q

Esmolol is a very-short-acting selective β-1 receptor blocker used for

A
  • IV administration in acute arrhythmias that occur during surgery or emergency situations
52
Q

Esmolol has a fast onset of action and a short half-life, making it ideal for

A
  • Acute situations

- Limiting its adverse effect profile

53
Q

Class III drugs diminish

A
  • Outward potassium current during the repolarization phase
54
Q

Class III drugs prolong

A
  • Duration of AP without altering phase 0 of depolarization or the resting membrane potential
55
Q

All class III drugs have the potential to

A
  • Induce arrhythmia
56
Q

Amiodarone and dronedarone

A
  • Both have beta blocker (class II) and calcium channel blocker (class IV) actions on the SA and AV nodes
  • Decreases the heart rate and conduction
57
Q

Sotalol

A
  • Class III antiarrhythmic agent

- Also has potent nonselective β-blocker (class II) activity

58
Q

Ibutilide MOA

A
  • Reduces repolarization (phase 3)

- Prolongs the duration of action potential through

59
Q

Ibutilide prolongs the duration of action potential through

A
  • Inhibiting/blocking potassium channels

- Activating the slow inward sodium current during phase 2

60
Q

Class III K channel blockers (names)

A
  • Amiodarone
  • Dronedarone
  • Sotalol
  • Dofetilide
  • Ibutilide
61
Q

Amiodarone (class III) metabolism

A
  • Prolonged half-life of several weeks

- Distributes extensively in adipose tissue

62
Q

Amiodarone (class III) is a substrate of

A
  • CYP3A4
63
Q

Amiodarone (class III) is an inhibitor of

A
  • CYP1A2
  • CYP2A4
  • CYP2C9
  • CYP2D6
64
Q

Amiodarone (class III) characteristics

A
  • Iodine moiety in its structure (structurally related to thyroxine)
  • May cause thyroid dysfunction (hypo or hyperthyroidism)
65
Q

Amiodarone (class III) drug interactions

A
  • Drugs that induce QT prolongation, class I (quinidine)
  • Concomitant use of drugs that have depressant effects on the heart (B-blockers (propranolol), verapamil (CCB)) can precipitate bradycardia and cardiac arrest, sinus arrest and AV block
  • CYP3A4 inhibitors (ketoconazole, grapefruit juice, verapamil), increase plasma concentration of amiodarone, and consequently can precipitate arrhythmia
66
Q

Dromedarone (class III) metabolism

A
  • First pass effect
  • Bioavailability increased by food
  • Less lipophilic, has lower tissue accumulation, and has a shorter serum half- life than amiodarone
67
Q

Dromedarone (class III) is a substrate of

A
  • CYP3A4
68
Q

Dromedarone (class III) is an inhibitor of

A
  • CYP3A4

- CYP2D6

69
Q

Dromedarone (class III) side effects

A
  • Liver injury

- QT prolongation

70
Q

Dromedarone (class III) drug interactions

A
  • Drugs that induce QT prolongation
  • Verapamil (CCBs) and B-blockers can cause Cardiac block
  • Digoxin increases risk of arrhythmia and cardiac arrest
  • Digoxin potentiate the dronedarone induced decrease in AV node conduction
  • CYP3A4 inhibitors/inducers affect dronedarone
71
Q

Solatol (class III) metabolism

A
  • Not metabolized
  • Not inhibited or induced any CYP450 enzymes
  • Excretion of sotalol is predominantly via the kidney unchanged
72
Q

Solatol (class III) side effects

A
  • Life threatening arrhythmia

- QT prolongation

73
Q

Solatol (class III) drug interactions

A
  • Antiarrhythmics drugs (e.g., Amiodarone)
  • May precipitate arrhythmia and QT prolongation. Calcium channel blockers (e.g., verapamil) and B- blockers (e.g., propranolol)
  • AV conduction block, bradycardia, cardiac arrest and hypotension adverse effects associated with β-blockers
74
Q

Dofetilide (class III) metabolism

A
  • Excreted unchanged in the urine
75
Q

Dofetilide (class III) side effects

A
  • Box warning proarrhythmia serious arrhythmia (torsade de pointe)
76
Q

Ibutilide (class III) metabolism

A
  • First-pass metabolism

- Not used orally

77
Q

Ibutilide (class III) side effecs

A
  • High risk of QT prolongation and proarrhythmia
78
Q

Ibutilide (class III) characteristics

A
  • Does NOT have sodium blocking (class I), antiadrenergic (B- blocking, class II) or calcium blocking (class IV) activities
79
Q

Class IV CA channel blockers

A
  • Block L-type calcium channels in firing cells
    SA/AV nodes
  • Slow down phase 0 depolarization rate
  • Slow down the spontaneous depolarization of phase 4
80
Q

Class IV Ca channel blockers activity lead to

A
  • Reduction in automaticity in SA node

- Reduction in AVN conduction and prolongation the effective refractory period

81
Q

Class IV drugs (names)

A
  • Verapamil

- Diltiazem

82
Q

Verapamil and Diltiazem (class IV) metabolism

A
  • Substrates and inhibitors of CYP3A4
83
Q

Verapamil and Diltiazem (class IV) drug interactions

A
  • B-blockers (e.g., propranolol, sotalol)
  • Cardiac block
  • Statins (simvastatin) and other CYP3A4 substrates
  • Plasma concentration increased
  • Grapefruit juice may increase plasma levels of verapamil
84
Q

Verapamil and Diltiazem (class IV) side effects

A
  • Peripheral vasodilatation, ‘negative inotropic effects

- Extracardiac effects include constipation, lassitude, nervousness and peripheral edema

85
Q

Digoxin increases

A
  • Vagal efferent activity to the heart

- Mechanism that is not understood

86
Q

Parasympathomimetic action of digoxin

A
  • Reduces sinoatrial (SA) firing rate (decreases heart rate; negative chronotropy)
  • Reduces conduction velocity of electrical impulses through the atrioventricular node
87
Q

Increase in vagal tone in the heart induced by digoxin will reduce

A
  • Automaticity in SA node

- Conductivity in AV node

88
Q

Digoxin increases the vagal tone in the heart, and consequently this will

A
  • Reduce automaticity in SA node (SA node)
  • Reduce the AV nodal conduction (AV node)
  • Correct for arrhythmia
89
Q

Digoxin is often used in the treatment of patients with

A
  • Heart failure who have arrhythmia
  • Most other drugs that can be used to achieve this goal have undesirable negative inotropic side effects (e.g. beta blockers and calcium channel blockers
90
Q

Adenosine

A
  • Nucleoside that occurs naturally throughout the body

- Half-life in the blood is less than 10 seconds

91
Q

Adenosine MOA

A
  • Activation of K+ current
  • Inhibition of calcium current
  • Results in a marked hyperpolarization
    and suppression of calcium dependent action potentials in SA & AV nodes
92
Q

Given as an IV bolus dose, Adenosine directly

A
  • Inhibits AV nodal conduction

- Has lesser effects on the SA node

93
Q

Magnesium sulfate

A
  • Slows the rate of SA node impulse formation

- Prolongs conduction time along the myocardial tissue

Pharmacology (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions