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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
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2
Q

Sinoatrial (SA) node

A
  • The pacemaker

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

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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

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4
Q

The SA node excites

A
  • The right atrium

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

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5
Q

Arrhythmia

A
  • Abnormality in cardiac rhythm (heart beats)
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6
Q

Types of cardiac cells

A
  • Pacemaker (SA node)

- Non-pacemaker (cardiac myocytes)

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7
Q

Pacemaker (SA node) cell characteristics

A
  • Exhibit Automaticity
  • Intrinsically generate
    APs and stimulate the heart beats without External Stimuli
  • Leaders/Initiators
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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
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9
Q

Cardiac myocyte Phase 4 (resting)

A
  • Cardiomyocyte is −90 mV

- Maintained by slow outward leak of K+ currents

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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
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11
Q

Cardiac myocyte Phase 1 (early repolarization)

A
  • Some K+ channels open briefly

- Allow an outward flow of K+

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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
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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
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14
Q

The action potential in cardiomyocytes is composed of

A
  • 5 phases (0-4)

- Begins and ends with phase 4

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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)
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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
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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
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18
Q

Mechanisms of arrhythmia

A
  • Disorders in impulse formation

- Conduction block or delay

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19
Q

Disorders in impulse formation

A
  • Altered automaticity

- Abnormal automaticity

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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
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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
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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
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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
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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
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25
Class IB sodium channel blockers MOA
- During phase 0 - Shorten phase 3 repolarization and the duration of AP - Reduction inward Na without affecting outward K shortens AP duration
26
Class IC sodium channel blockers MOA
- During phase 0 - Dissociate slowly - Minor effect on the duration of AP
27
Class IA drugs (names)
- Quinidine - Procainamide - Disopyramide
28
Quinidine (class IA) properties
- Alpha-adrenergic blocking activity | - Anticholinergic actions
29
Quinidine (class IA) special characteristics
- Can cause cinchonism blurred vision, tinnitus, headache, disorientation, and psychosis
30
Quinidine (class IA) metabolism
- Substrate of CYP3A4 | - Inhibitor of CYP2D6
31
Procainamide (class IA) properties
- Anticholinergic actions | - NO alpha-adrenergic activity
32
Procainamide (class IA) metabolism
- Acetylated in the liver to N-acetyl procainamide (NAPA) - Prolongs duration of the AP (QT prolongation) - Proarrhythmic
33
Disopyramide (class IA) properties
- Most anticholinergic effect of this class | - NO alpha-adrenergic activity
34
Disopyramide (class IA) metabolism
- Substrate of CYP3A4
35
Disopyramide (class IA) special characteristics
- Negative inotropic effects - May precipitate HF - Should not be used in patients with HF
36
Properties shared by all class IA drugs
- Proarrythmic - Can induce QT prolongation - Anticholinergic adverse effects (ex: dry mouth, urinary retention, blurred vision, and constipation)
37
Class IB drugs (names)
- Lidocaine | - Mexiletine
38
Lidocaine (class IB) metabolism
- First pass so only given IV
39
Lidocaine (class IB) characteristics
- High safety profile - Least cardiotoxic agent among sodium channel blockers - No negative inotropic effect
40
Lidocaine (class IB) side effects
- CNS side effects that often limit the duration of continuous infusions - Nystagmus (early indicator of toxicity) - Drowsiness - Slurred speech - Paresthesia - Agitation - Confusion - Convulsions
41
Mexiletine (class IB) metabolsim
- Oral | - Narrow therapeutic index
42
Mexiletine (class IB) most common side effecs
- Nausea - Vomiting - Dyspepsia
43
Class IC drugs (names)
- Flecainide | - Propafenone
44
Flecainide (class IC)
- Substrate of CYP2D6 | - Well tolerated
45
Flecainide (class IC) side effects
- Blurred vision - Dizziness - Nausea
46
Propafenone (class IC)
- Substrate of CYP2D6 | - B-blocking effects
47
Propafenone (class IC) side effects
- Blurred vision, dizziness, and nausea - Bronchospasm due to its β-blocking effects - Should be avoided in patients with asthma
48
β-Blockers reduce arrhythmia by
- Blocking B-adrenergic receptors | - Antagonizing the increased sympathetic tones and high levels of circulating catecholamines (NE and epinephrine)
49
β-Blockers reduce phase 4 spontaneous depolarization through
- Reducing automaticity at SA node and decreasing the heart rate - Reducing AV nodal conduction
50
Metoprolol is a selective β-1 receptor blocker widely used in
- Treatment of cardiac arrhythmias - Reduces the risk of bronchospasm compared to nonselective β-blockers - CYP2D6 substrate
51
Esmolol is a very-short-acting selective β-1 receptor blocker used for
- IV administration in acute arrhythmias that occur during surgery or emergency situations
52
Esmolol has a fast onset of action and a short half-life, making it ideal for
- Acute situations | - Limiting its adverse effect profile
53
Class III drugs diminish
- Outward potassium current during the repolarization phase
54
Class III drugs prolong
- Duration of AP without altering phase 0 of depolarization or the resting membrane potential
55
All class III drugs have the potential to
- Induce arrhythmia
56
Amiodarone and dronedarone
- 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
Sotalol
- Class III antiarrhythmic agent | - Also has potent nonselective β-blocker (class II) activity
58
Ibutilide MOA
- Reduces repolarization (phase 3) | - Prolongs the duration of action potential through
59
Ibutilide prolongs the duration of action potential through
- Inhibiting/blocking potassium channels | - Activating the slow inward sodium current during phase 2
60
Class III K channel blockers (names)
- Amiodarone - Dronedarone - Sotalol - Dofetilide - Ibutilide
61
Amiodarone (class III) metabolism
- Prolonged half-life of several weeks | - Distributes extensively in adipose tissue
62
Amiodarone (class III) is a substrate of
- CYP3A4
63
Amiodarone (class III) is an inhibitor of
- CYP1A2 - CYP2A4 - CYP2C9 - CYP2D6
64
Amiodarone (class III) characteristics
- Iodine moiety in its structure (structurally related to thyroxine) - May cause thyroid dysfunction (hypo or hyperthyroidism)
65
Amiodarone (class III) drug interactions
- 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
Dromedarone (class III) metabolism
- First pass effect - Bioavailability increased by food - Less lipophilic, has lower tissue accumulation, and has a shorter serum half- life than amiodarone
67
Dromedarone (class III) is a substrate of
- CYP3A4
68
Dromedarone (class III) is an inhibitor of
- CYP3A4 | - CYP2D6
69
Dromedarone (class III) side effects
- Liver injury | - QT prolongation
70
Dromedarone (class III) drug interactions
- 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
Solatol (class III) metabolism
- Not metabolized - Not inhibited or induced any CYP450 enzymes - Excretion of sotalol is predominantly via the kidney unchanged
72
Solatol (class III) side effects
- Life threatening arrhythmia | - QT prolongation
73
Solatol (class III) drug interactions
- 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
Dofetilide (class III) metabolism
- Excreted unchanged in the urine
75
Dofetilide (class III) side effects
- Box warning proarrhythmia serious arrhythmia (torsade de pointe)
76
Ibutilide (class III) metabolism
- First-pass metabolism | - Not used orally
77
Ibutilide (class III) side effecs
- High risk of QT prolongation and proarrhythmia
78
Ibutilide (class III) characteristics
- Does NOT have sodium blocking (class I), antiadrenergic (B- blocking, class II) or calcium blocking (class IV) activities
79
Class IV CA channel blockers
- 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
Class IV Ca channel blockers activity lead to
- Reduction in automaticity in SA node | - Reduction in AVN conduction and prolongation the effective refractory period
81
Class IV drugs (names)
- Verapamil | - Diltiazem
82
Verapamil and Diltiazem (class IV) metabolism
- Substrates and inhibitors of CYP3A4
83
Verapamil and Diltiazem (class IV) drug interactions
- 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
Verapamil and Diltiazem (class IV) side effects
- Peripheral vasodilatation, ‘negative inotropic effects | - Extracardiac effects include constipation, lassitude, nervousness and peripheral edema
85
Digoxin increases
- Vagal efferent activity to the heart | - Mechanism that is not understood
86
Parasympathomimetic action of digoxin
- Reduces sinoatrial (SA) firing rate (decreases heart rate; negative chronotropy) - Reduces conduction velocity of electrical impulses through the atrioventricular node
87
Increase in vagal tone in the heart induced by digoxin will reduce
- Automaticity in SA node | - Conductivity in AV node
88
Digoxin increases the vagal tone in the heart, and consequently this will
- Reduce automaticity in SA node (SA node) - Reduce the AV nodal conduction (AV node) - Correct for arrhythmia
89
Digoxin is often used in the treatment of patients with
- 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
Adenosine
- Nucleoside that occurs naturally throughout the body | - Half-life in the blood is less than 10 seconds
91
Adenosine MOA
- 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
Given as an IV bolus dose, Adenosine directly
- Inhibits AV nodal conduction | - Has lesser effects on the SA node
93
Magnesium sulfate
- Slows the rate of SA node impulse formation | - Prolongs conduction time along the myocardial tissue

Pharmacology (27 decks)

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