Antidysrhythmics

Question 1

Condition where spontaneous depolarizations occur due to abnormal impulse generation in sinus or ectopic foci

Answer 1

Automaticity cardiac dysrhythmias

Question 2

explain the patho of re-entry cardiac dysrhythmias

Answer 2

impulses propagate more than one pathway.

i.e WPW

Question 3

what type of cardiac dysrhythmias are Seen more with volatile anesthetics because of suppression of SA node and conduction pathway

Answer 3

re-entry dysrhythmias

Question 4

8 factors that promote dysrhythmias

Answer 4

electrolyte imbalance
hypoxemia
acid base imbalance
ischemia
bradycardia 
increased mechanical stretch
SNS 
drugs

Question 5

what type of acid base balance is more prone to dysrthymias?

Answer 5

alkalosis

Question 6

antidysrhythmic drugs mechanisms of action [basic]

Answer 6

Most work directly or indirectly by blocking various ion channels
[remember: there are different parts of action potential that we manipulate]

Question 7

Blocking Na+ affects what part of action potential?

Answer 7

velocity of AP upstroke

Question 8

Blocking K+ affects what part of action potential?

Answer 8

refractory

Question 9

Blocking Ca+ affects what part of action potential

Answer 9

slope of phase 4 in nodal tissue

Question 10

Newly developed brady or tachydysrhythmias resulting from chronic antidysrhythmic therapy

Answer 10

Prodysrhythmias

Question 11

what is Torsades de Pointes

Answer 11

Polymorphic ventricular tachycardia

Ventricular Fibrillation

Question 12

what causes Incessant Ventricular Tachycardia

Answer 12

Antidysrhythmic drugs that slow conduction can allow re-entrant impulses (Ia & Ib)

Question 13

Wide Complex Ventricular Rhythm is usually seen with?

Answer 13

with class Ic drugs due to slow conduction.

Question 14

phase 0 of action potential represents

[initial upstroke]

Answer 14

rapid depolarization from opening of Na channels and closing of K channels

Question 15

phase 1 of action potential represents

[slight downstroke before plateau]

Answer 15

initial repolarization resulting from opening of K channels and closure of Na channels

Question 16

phase 2 of action potential represents

[plateau]

Answer 16

plateau phase resulting from sustained Ca current

Question 17

phase 3 of action potential represents

[downstroke]

Answer 17

repolarization from closure of Ca channels and opening of K channels

Question 18

phase 4 represents

[resting, baseline]

Answer 18

resting potential - K channel open, Ca/Na channels closed

Question 19

how do conduction myocytes (ventricular) differ from pacemaker cells?

Answer 19

“fast” action potentials that are dependent on Na for phase 0 (depolarization)
lower resting membrane potential

Question 20

how do pacemaker (nodal) cells differ from conduction myocytes?

Answer 20

“slow” action potentials that rely on Ca for phase 0 (depolarization), leaky Na
less negative resting membrane potential

Question 21

what does changing the rate of phase 4 depolarization do to the heart rate?

Answer 21

pns (ACh) stimulation elongates phase 4 which results in slower HR while sns (norepi) shortens phase 4 with causes an increase in the HR

Question 22

Drug Classification I

Answer 22

membrane stabilizers

inhibit fast Na channels

Question 23

Drug Classification II

Answer 23

beta adrenergic antagonists

decrease rate of depolarization

Question 24

Drug Classification III

Answer 24

refractory prolongers

inhibit K

Question 25

Drug Classification IV

Answer 25

calcium channel blockers | slow Ca channels

Question 26

Decrease depolarizations & conduction velocity | **Blocking Na+ moves the threshold potential farther away from the resting potential

Answer 26

class I

Question 27

describe Beta Adrenergic Antagonist and its effect on electrolytes

Answer 27

Decrease magnitude of Ca+ influx current | Decreases K+ current (Na+/K+ pump)

Question 28

Useful in ischemic related dysrhythmias, reduces mortality

Answer 28

Beta Adrenergic Antagonist because it slows everything down | [slower phase 4, slower automaticity, slower AV node conduction]

Question 29

these Interact with Beta Blockers

Answer 29

Refractory Prolongers, Class III r/t reduced automaticity and prolonged action potential duration (slows)

Question 30

Useful in rate control for rapid ventricular response situations with A fib and A flutter, PSVT Useful in ventricular tachycardia

Answer 30

Class IV, Cardiac Ca+ channel blockers

Question 31

Have not been shown to reduce mortality after MI

Answer 31

Class IV, ca channel blockers

Question 32

Class Ia & Ib do what to mortality and ventricular dysrythmias?

Answer 32

↑ mortality and vent dysrhythmias

Question 33

Amiodarone & β Blockers do what to mortality post MI

Answer 33

decrease

Question 34

which can complicate CHF?

Answer 34

Class Ia & Ic

Question 35

what does Lidocaine do post MI?

Answer 35

increases bradydysrhythmias & mortality after and MI

Question 36

Prevent Supraventricular dysrhythmias, PVCs | Maintain sinus rhythm in Afib, Aflutter

Answer 36

Quinidine

Question 37

Mechanism of Action: quinidine

Answer 37

Decreases phase 4 slope, prolongs conduction | Blocks Na+ K+, alpha block, vagal inhibition

Question 38

SE of what drug? Prolongs QRS, QT, PR, hypotension, may increase NMB

Answer 38

quinidine

Question 39

quinidine has a Depressant effect on myocardial contractility

Answer 39

but may offset this by an increase in HR

Question 40

indicated for Ventricular and atrial tachydysrhythmias | Premature ventricular contractions

Answer 40

Procainamide (Procan)

Question 41

Mechanism of Action: procainamide

Answer 41

Blocks Na+, K+ channels | Decreases automaticity, increases refractoriness

Question 42

Slowed conduction times Prolongs QRS, QT, Hypotension due to myocardial depression Lupus-like symptoms

Answer 42

side effects procainamide

Question 43

indicated for Atrial & Ventricular Tachydysrhythmias | Maintain sinus rhythm in Afib, Aflutter

Answer 43

Disopyramide(Norpace)

Question 44

Mechanism of Action: disopyramide

Answer 44

Na+ channel block, anticholinergic actions | Slowed conduction

Question 45

adverse effects of what drug? Myocardial depressant Depresses contractility, aggravate CHF Prolonged QT

Answer 45

Disopyramide(Norpace)

Question 46

indicated for: Ventricular dysrhythmias Little effect on supraventricular dysrhythmias Re-entry cardiac dysrhythmias (PVCs, Vtach)

Answer 46

Lidocaine

Question 47

Non-dysrhythmic use lidocaine?

Answer 47

ERAS - multimodal pain control

Question 48

Mechanism of Action: lidocaine

Answer 48

delays phase 4

Question 49

side effects lidocaine

Answer 49

May increase mortality after MI Myocardial depressant Neurologic, Seizures Prolonged PR, QRS

Question 50

why use lidocaine?

Answer 50

More rapid than quinidine or procainamide | Easily titrated

Question 51

list Class I drugs

Answer 51

lidocaine disopyramide (norpace) procainamide (procan) quinidine

Question 52

Beta Adrenergic Antagonists are effective in dysrhythmias

Answer 52

r/t increases in SNS

Question 53

Mechanism of Action: Beta Adrenergic Antagonists

Answer 53

Decrease spontaneous phase 4 depolarization | Decreased conduction through AV node

Question 54

Adverse effects Beta Adrenergic Antagonists

Answer 54

Prolonged PR, depressed myocardium | Bradycardia, hypotension, Bronchospasm

Question 55

Beta Adrenergic Antagonists are contraindicated for what patients?

Answer 55

CHF, RAD, AV block patients.

Question 56

Amiodarone (Cordorone) is what class?

Answer 56

class III

Question 57

indications of what drug: Resistant V-tach, V-fib, A-fib, WPW Acute termination of V-tach, V-fib (1st line treatment)

Answer 57

Amiodarone (Cordorone)

Question 58

Mechanism of Action amio?

Answer 58

Blocks Na+, reduces currents of K+, Ca+ | Prolongs AP, refractory and conduction

Question 59

Alpha and beta antagonist of amio causes

Answer 59

vasodilation

Question 60

amio helps with chest pain how?

Answer 60

Dilates coronary arteries (antianginal)

Question 61

Adverse effects: amio

Answer 61

``` Hypotension r/t vasodilation, LV depression Pulmonary toxicity (lipophilic, slow elimination) Altered thyroid function (resembles thyroid hormone) ```

Question 62

more side effects amio

Answer 62

Marked QT prolongation, bradycardia, AV block Resistant to catecholamines, Reduce oxygen concentrations

Question 63

Derivative of amiodarone | Prevents return to afib/flutter

Answer 63

Dronedarone (Multaq)

Question 64

dronedarone is Only for patients

Answer 64

currently in sinus rhythm which have been converted from afib/flutter

Question 65

side effect of dronedarone?

Answer 65

increase of heart failure

Question 66

these are indicated for Paroxysmal SVT, re-entrant tachy Ventricular rate control in A-fib, A-flutter Not effective in reducing ventricular ectopy

Answer 66

Verapamil and Diltiazem

Question 67

Mechanism of Action: verapemil, dilt

Answer 67

Block Ca+ in cardiac cells Decreases spontaneous phase 4 depolarization Vasodilation or coronary and peripheral arteries Depress AV node, negative chronotropic SA node

Question 68

adverse effects verap, dilt

Answer 68

AV block, aggravates reduced LV fxn Hypotension Myocardial depression NMB may be exaggerated

Question 69

Treat atrial tachydysrhythmias. Slow AV node conduction which slows ventricular response in A-fib. * Enhance assessory pathway conduction

Answer 69

Digitalis

Question 70

how does digitalis increase contractility?

Answer 70

Cardiac glycosides ultimately increase Ca+ which increases cardiac contractility. Can cause any cardiac dysrhythmia.

Question 71

slows sinus rate and conduction through AV node, Not effective in A-fib, A-flutter, V-tach

Answer 71

adenosine (asystole <5 seconds)

Question 72

useful in ventricular but not atrial dysrhythmias, digitalis toxicity induced ventricular dysrhythmias, Can depress sinus node

Answer 72

Phenytoin

Question 73

Useful in preventing Torsades de Pointes, Digitalis-induced dysrhythmias and ventricular ectopy.

Answer 73

Magnesium

Question 74

other use for magnesium

Answer 74

eras - Anesthetic- and analgesic-sparing effect by enhancing the analgesic actions of opioids

Question 75

moves threshold potential further away from resting potential. Useful in hyperkalemia where resting potential is closer to threshold potential.

Answer 75

calcium

Question 76

Muscarinic antagonist prevents Ach from producing negative chronotropic, inotropic and dromotropic (conduction velocity) effects.

Answer 76

Robinul

Question 77

produces negative lusitropic (myocardial relaxation) effects and potent coronary vasoconstriction

Answer 77

vaso