30 - arrhythmic drugs Flashcards

(35 cards)

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

19
Q

if patient has an arrhythmia

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

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
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.
class 1 C increase QRS duration most
26
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.
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
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
class 1 B Shorten duration of action potential. Bind primarily to inactivated state of the channel. Dissociate from the channel with rapid kinetics
28
which ABC of class 1 antiarrhythmic drugs Flecainide and Propafenone. Used to treat supraventricular arrhythmias
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
class _(1-4) of antiarrhythmic drugs diminish phase 4 depolarization, thus depressing automaticity, prolonging AV conduction and decreasing HR and contractility
class 2 beta-adrenergic antagonists beta 2 atagonist if heart is beating too fast
30
how do class 2 betablockers work they can diminish both _ and _ currents
diminsh both Na and Ca phase 4 of the cardiac AP
31
which receptor | - increase force of heart contraction, increase rate of contraction, excessive stimulation leads to arrhythmias
beta 1
32
what kind of beta adrenergic drug do we use if that patients heart is beating too fast
beta 2 antagonist
33
class _ antiarrhythmic drugs block potassium K+ channels and thus prolonging AP delayed repolarization
class 3 K+ channel blockers
34
in contrast to the sodium-channel blockers, _ and _ drugs are increasing in use
class 2 - Beta blockers and class 3 K channel blockers
35
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
class IV blocking Ca channels major systemic effects though slow conductiong and increase refractory period verapamil