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Pharm 1 - SP19 > 30 - arrhythmic drugs > Flashcards

30 - arrhythmic drugs Flashcards

1
Q

movement or procedure with uniform or patterned

recurrence of a beat, accent, or the like

A

rhythm

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2
Q

Heartbeat is irregular, too fast, or too slow

A

cardiac arrhythmia

in atrial fibrillation, the tracing shows tiny, irregular “fibrillation” waves btw heart beats

the rhythm is irregular and erratic

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3
Q

Contraction of _
ventricle sends O2
depleted (and CO2
rich) blood to the lungs.

Contraction of the _
ventricle sends O2
rich blood to the other tissues.

Electrical signals
coordinate cardiac
muscle contraction

A

right ventricle - O2 depleted and CO2 rich

left ventricle - O2 rich to other tissues

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4
Q

the sum total of action potentials traveling

through the heart creates the _

A

EKG

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5
Q

Diagnostic components of the EKG

_ reflects
depolarization of SA
node

A

P wave

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6
Q

Diagnostic components of the EKG

_describes the time it takes for the
impulse to travel from sinus node through AV node

A

PR interval

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7
Q

Diagnostic components of the EKG

_ reflects
depolarization of right
and left ventricles
(lots of muscle mass,
big signal).
A

QRS complex

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8
Q

Diagnostic components of the EKG

_ segment Ventricles depolarized

A

ST segment.

J point - ventricles depolarized - J point is important because it is the start of the ST segment. The J point must be assessed for:
absolute position: it can be elevated or depressed
shape: it can be notched or slurred

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9
Q

Diagnostic components of the EKG
Repolarization
of ventricles

A

T wave.

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10
Q

Diagnostic components of the EKG

repolarization of
interventricular
septum.

A

U wave

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11
Q 
Four main types of arrhythmias
Extra beats
Supraventricular tachycardias
Ventricular arrhythmias
bradyarrhythmias
A

extra beats - Premature atrial contractions, Premature ventricular contractions

supraventricular tachycardas - Atrial fibrillation
Atrial flutter
Paroxysmal supraventricular tachycardia

ventricular - Ventricular fibrillation
Ventricular tachycardia

bradyarrhythmias - less than 60bpm

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12
Q 
Classification of arrhythmias by _
Atrial
Junctional
Ventricular
AV Heart blocks (atrioventricular node)
A

site of origin

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13
Q

_ arrhythmia

Conduction between the atria and ventricles is blocked or slowed

PR interval lengthened beyond 0.2 seconds

A

primary AV block

200msec or longer

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14
Q

_ arrhythmia

Conduction between the atria and ventricles is blocked or slowed

Disturbance, Delay, Interruption of atrial
impulse conduction through the AV node to the ventricles

PR interval - 0.12-0.2sec

A

secondary AV block

2,3,or 4 P wave before each QRS

PR interval - 0.12-0.2sec - little delay

QRS <0.12s

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15
Q

_ arrhythmia

Conduction between the atria and ventricles is blocked or slowed

aka complete heart block. Impulse generated
in SA node does not propagate to the ventricles.

A

tertiary AV block

none of the pwaves conduct to ventricles (P-P and QRS-QRS are independent)

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16
Q

cardiac arrhythmias result from disorders of impulse _ or impulse_ or both

A

disorders of impulse formation or
impulse conduction or both

causes of arrhythmias
~cardiac ischemia
~excessive discharger or sensitivity to autonomic transmitters
~exposure to toxic substances
~unknown ?
17
Q

_ puts little delay on the wave on Ap’s thru heart

A

AV node

atrial first then ventricles

18
Q

sum total of AP’s traveling thru heart - but at different times

A

ECG/EKG

19
Q

if patient has an arrhythmia

Can always be a secondary problem of _ - when blood isn’t moving smoothly thru system

A

clotting

20
Q

4 classes of drugs for arrhythmic drugs

Class 1 - block Na channels

Class 2 - beta anatagonists

Class 3 - prolong AP and refractory period

Class 4 - Ca channal antagonist

which phase of heart

A

1 - phase 0, depolarization Na coming in

2 - phase 4 - resting potential K+

3 - between phase 1 and 3 - working on K channels

4 - phase 2 - blocking Ca

21
Q

phases of cardiac AP

0-4

A 
0- Na coming in steep rise
1 - K+ and Cl- out 
2 - Ca++ in K+ out
3 - K out
4- resting potential
22
Q

Class 1 antiarrhythmic drugs block _

A

block Na channel

Drugs with intermediate lengths bind to Na channels - not shutting down but tweaking enough to cause little change
When injecting Lidocaine - we block entire Na channel and prevent AP all

We are tweaking the depolarization (Na channel) and changing AP stop

23
Q

Class 1 Na channel blockers

Lengthen duration of action potential.

Bind more selectively to the open state of the channel.

Dissociate from channel with intermediate kinetics.

A

class 1 A

increase QRS and QT

24
Q

Class 1 Na channel blockers

Shorten duration of action potential.

Bind primarily to inactivated state of
the channel.

Dissociate from the channel with rapid kinetics.

A

class I B

decrease QT

25
Q

Class 1 Na channel blockers

Minimal effect on duration of action potential.

Bind more selectively to the
open state of the channel.

Dissociate from channel with slow kinetics.

A

class 1 C

increase QRS duration most

26
Q

which ABC of class 1 antiarrhythmic drugs

Procainamide. Effective against atrial and ventricular arrhythmias.
Frequent dosing (t1/2 = 3 hrs) limits its utility. Can produce lupus like
symptoms.

A

class 1 A

Lengthen duration of action potential.

Bind more selectively to the open state of the channel.

Dissociate from channel with intermediate kinetics

27
Q

which ABC of class 1 antiarrhythmic drugs

Lidocaine. One of the less toxic antiarrhythmic drugs. Used in
conjunction with arrhythmias associated with myocardial
infarctions. Very short t1/2. Administered by infusion

A

class 1 B

Shorten duration of action potential.

Bind primarily to inactivated state of
the channel.

Dissociate from the channel with rapid kinetics

28
Q

which ABC of class 1 antiarrhythmic drugs

Flecainide and Propafenone. Used to treat supraventricular arrhythmias

A

class I C

Minimal effect on duration of action potential. Bind more selectively to the
open state of the channel. Dissociate from channel with slow kinetics.

29
Q

class _(1-4) of antiarrhythmic drugs diminish phase 4 depolarization, thus depressing automaticity, prolonging AV conduction and decreasing HR and contractility

A

class 2

beta-adrenergic antagonists

beta 2 atagonist if heart is beating too fast

30
Q

how do class 2 betablockers work

they can diminish both _ and _ currents

A

diminsh both Na and Ca

phase 4 of the cardiac AP

31
Q

which receptor

- increase force of heart contraction, increase rate of contraction, excessive stimulation leads to arrhythmias

A

beta 1

32
Q

what kind of beta adrenergic drug do we use if that patients heart is beating too fast

A

beta 2 antagonist

33
Q

class _ antiarrhythmic drugs

block potassium K+ channels and thus prolonging AP

delayed repolarization

A

class 3 K+ channel blockers

34
Q

in contrast to the sodium-channel blockers, _ and _ drugs are increasing in use

A

class 2 - Beta blockers and class 3 K channel blockers

35
Q

Class _ antiarrhythmic drugs

block Ca++ channels

decrease inward Ca current, decreasing rate of phase 4 spontaneou depolarization

slow conduction in tissues dependent on Ca current (AVnode)

MAJOR EFFECTS ON VASCULAR SM AND HEART THOUGH

A

class IV blocking Ca channels

major systemic effects though

slow conductiong and increase refractory period

verapamil

Pharm 1 - SP19 (26 decks)

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