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Pharmacology > Agents used in cardiac arrhythmias > Flashcards

Agents used in cardiac arrhythmias Flashcards

1
Q

Principal effects of stimulation of sympathetic nerves to the heart

A

Activation of beta-1-adrenoreceptors

  1. increase rate –> + chronotropic effect
  2. increase automaticity –> + bathmotropic effect
  3. increase AV conduction –> + dromotropic effect
  4. increase contractile force –> + inotropic effect
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2
Q

Principal effects of stimulation of parasympathetic nerves to the heart

A

Activation of M2- cholinoreceptors

  1. decrease rate –> - chronotropic effect
  2. decrease automaticity –> - bathmotropic effect
  3. decrease AV conduction –> - dromotropic effect
  4. contractile force –> NO EFFECT
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3
Q

Places in the heart where parasympathetic innervation is present

A

ONLY IN THE ATRIA

NOT IN THE VENTRICLES

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4
Q

Cardiac arrhythmia

-Cause

A

Deactivation of cardiomyocytes is not synchronized

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5
Q

The cardiac action potential

-phases and what happens in each one

A

Phase 0 –> depolarization, Na+ ions go to inside of the cell. Cell charge becomes +
Phase 1 –> very short phase, Na+ stops to flow and K+ channels open
Phase 2 –> plateau phase, calcium flows to inside
Phase 3 –> Ca2+ flow stops, K+ leaves the cell. This happens in order to make cell negative again
Phase 4 –> back to resting potential, cell is negative

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6
Q

SA node action potential (3)

A
  • it is different
  • only 0,3,4 phases
  • less K+ leaves the cell, more positive ions will be left intracellularly
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7
Q

Effective refractory period (ERP)

A

time needed to restore capability of Na+ channels

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8
Q

Cardiac rate and rhythm

A
  1. electrical impulse originates in the SA node
  2. Atria
  3. Atrioventricular node - conduction is slow
  4. His-Purkinje system
  5. Ventricles
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9
Q

The cardiac action potential

  1. Refractory period of sodium-dependent cardiac cells depends on:
  2. Refractory period of calcium-dependent AV node depends on:
A
  1. the membrane potential, extracellular potassium concentration, actions of drugs that bind to the sodium channel
  2. on the rate of recovery from inactivation of calcium channels
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10
Q

Effect of potassium

A

Hyperkalemia –> arrthythmia, bradycardia, may cause total asystole –> increase K+ will increase K+ conduction during phase 3 = K+ going out, it will leave the cell with a very negative charge

Hypokalemia –> prolonged action potential duration, increased pacemaker rate, increased pacemaker arrhythmogenesis –> decrease K+ extracellularly –> it will leave the cell with a positive charge

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11
Q

Types of arrhythmias

A
  1. disturbances in impulse formation –> abnormal automaticity
    - ectopic pacemaker activity, delayed after-depolarization
  2. disturbances in impulse conduction –> abnormal conduction
    - re-entry, heart block
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12
Q

Delayed after-depolarization (5)

A
  • prolongation of the QT interval in the ECG
  • occur in late phase 3 or early phase 4 - something wrong with K+ flow channels
  • abnormally high amounts of Ca2+ intracellulary
  • increase Ca2+ levels –> pump becomes more active –> sodium-calcium pump brings 1 additional charge to the INSIDE –> influx of + charges = membrane depolarization

SOLUTION: beta blockers

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13
Q

Re-entry (5)

A
  • might occur in small bifurcating branches of the Purkinje system
  • an area of unidirectional block develops in one of the branches
  • 1 branch is damaged –> signals go through the other side –> signals come back through the damaged zone, it cannot go up but goes in circle –> causes tachycardia
  • refractory period is shorter than conduction time

SOLUTION: drugs that extend ERP –> class 1a or class 3

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14
Q

Anti-arrhythmic drug classification

A

Class 1 - sodium channel block
Class 2 - sympatholytic - inhibit transmission of nerve impulse to sympathetic nervous system
Class 3 - prolong action potential duration
Class 4 - block cardiac calcium current

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15
Q

Class 1 drugs

  • mechanism of action
  • classes and names
A

-reduce phase 0 and 4 sodium currents

Class 1a - QUINIDINE

Class 1b - LIDOCAINE

Class 1c - PROPAPHENONE

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16
Q

Unwanted effects of class 1 drugs

A

LIDOCAINE

- CNS actions –> drowsiness, disorientation, convulsions

17
Q

Class 2 drugs

  • mechanism of action
  • indications
  • names
  • unwanted effects
A
  • reduce b-adrenergic activity in the heart
  • decrease inward ions currents during phase 2 and 4
  • pacemaker depolarization is slowed, conduction velocity is slowed in AV node, RP is prolonged
  • prevent recurrence of tachy-arrhythmias, reduce mortality following myocardial infarction
  • PROPRANOLOL, METOPROLOL, ESMOLOL
  • worsening bronchospasms (asthma), negative inotropic effects, bradycardia, fatigue
18
Q

Class 3 drugs

  • mechanism of action
  • name
A
  • block K+ channels
  • prolong action potential duration by reducing outward phase 3 K+ current –> prolongs plateau
  • prolong ERP –> decrease the ability of the heart to response to rapid tachycardias

-AMIODARONE

19
Q

AMIODARONE

  • class
  • mechanism of action
  • indication
  • pharmacokinetics
  • unwanted effects
A
  • class 3
  • prolong cardiac action potential, increases refractory period
  • supraventricular and ventricular tachyarrhythmias, Wolf-Parkinson-White syndrome
  • high volume of distribution - so initially a high dose is necessary
  • microcrystalline deposits in cornea and skin, thyroid dysfunction, paresthesia’s, tremor, pulmonary fibrosis, QT interval prolongation
20
Q

Class 4

  • names
  • mechanism of action
  • indication
  • contraindication
  • unwanted effects
A

-VERAPAMIL, DILTIAZEM

  • decrease inward calcium in phase 2 and 4 –> slow conduction in SA and AV nodes,
  • act on L-type channels causing a state and use dependent selective depression of calcium current,
  • shorten plateau and reduce force of contraction
  • reduce ventricular rate, prevent recurrent of paroxysmal supra-ventricular tachycardia
  • Wolf-Parkinson-white syndrome
  • headache, negative effects –> constipation, ankle edema
21
Q

Verapamil vs. Diltiazem

A

V –> mainly acts on the heart

D –> has a balanced effect on heart and blood vessels

22
Q

Adenosine

  • mechanism of action
  • indications
  • dosing,metabolism
  • unwanted effects
A
  • produce endogenously
  • act on cardiomyocytes –> decrease CAMP –> increase amount of K+ channels open –> causes a much stronger repolarization
  • hyperpolarizes tissue and slows the rate of rise of the pacemaker potential
  • supraventricular tachycardia
  • effects last 20-30s, metabolized by enzymes on the luminal surface of vascular endothelium
  • related to parasympathetic system activation –> chest pain, shortness of breath, dizziness, nausea
23
Q

Volume of distribution

A
  • ability of the drug to bind to different tissues in our body
  • high VOD –> higher dose is needed in order to fulfill all of the compartments and so the concentration remains in a good level
24
Q

Classification of the drugs is based on:

A
  1. how class affects action potential duration
  2. how it affects the refractory period
  3. based on association and dissociation to Na+ channels
  4. to which stage Na+ channels it has the highest affinity
25
Q

Class 1A drugs

  • name
  • function
  • indication
A

-QUINIDINE

  • prolong action potential duration = prolong ERP,
  • dissociate from the channel with intermediate kinetics,
  • block Na+ channels in open state,
  • affect conduction velocity

-Indications : for atrial problems –> fibrillation, flutter, extrasystole

26
Q

Class 1b drugs

  • name
  • function
  • indication
A

-LIDOCAINE

  • Shorten APD = short ERP,
  • dissociate from the channel with rapid kinetics,
  • block Na+ channels in inactive state,
  • no effect on conduction velocity

-Indications: for ventricular problems –> fibrillation, tachycardia, extrasystole

27
Q

Class 1c

  • name
  • function
  • indication
A

-PROPAPHENONE

  • minimal effects on APD,
  • dissociate from the channel with slow kinetics,
  • block Na+ channels in all states,
  • affect conduction velocity

-Indications: for atrial problems –> fibrillation, flutter, extrasystole

Pharmacology (29 decks)

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