AntiArrythmics Intro - Nordgren Flashcards

1
Q

Name the three factors that if deviated will lead to a cardiac arrhythmia:

A

Rate of Impulse
Site of impulse origin
Conduction of the impulse

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2
Q

Describe the status of the gates of a sodium channel when it is “resting”, “activated”, and “inactivated.”

A

Resting: Activation gate is closed - Inactivation gate is open
Activated: Both activation/inactivation gates are open
Inactivated: Activation gate is open - inactivation gate closed

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3
Q

Atrial, purkinje, and ventricular cells differ from SA and AV nodal cells in the channel that is responsible for their depolarization. What ion channel is responsible for each?

A

Atrial, purkinje, and ventricular = Na Current

SA and AV = Ca Current

(Remember that the Ca channels are inactivated and activated in much the same way as Na channels BUT the transitions occur more slowly and at more positive potentials)

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4
Q

In all heart cell types, what is responsible for the occurrence of phase 3 of the action potential?

A

Phase 3 is final repolarization.

This results fromt he completion of Na/Ca inactivation and the growth of K permeability.

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5
Q

The time period between Phase 0 and the point in Phase 3 where Na channels have recovered to allow another Action Potential is known as:

A

The refractory period!

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6
Q

What happens to the number of available Na channels under optimal and suboptimal resting membrane potential conditions when a Na-blocking drug is given?

A

Optimal Conditions (very negative potential) = Number of available channels is decreased

Suboptimal Conditions (less negative potential) = Number of channels will increase at a sharper slope because of drug blockade and inactivation gate closures

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7
Q

How will depolarization of membrane potential affect the recovery time of Na channels?

A

Depolarized cells recovery more SLOWLY.

Refractory period will increase
Na channel blockade is going to prolong the recovery time a ton more also

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8
Q

What happens to Na currents when the cell’s resting membrane potential is depolarized to -55mV?

A

Na currents are abolished (inactivated)

SA and AV nodal cells don’t have the same effect because their normal resting membrane potential is -50 to -70. Much more depolarized than normal cardiac cells.

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9
Q

Disturbances of impulse formation and impulse conduction leads to:

A

Arrhythmias

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10
Q

Afterdepolarizaton are one of the disturbances of impulse formation. What are the differences between early and delayed afterdepolarizations?

A

Early:
Occur during the AP
Exacerbated at SLOW heart rates
Another spike during the normal plateau phase

Delayed:
Occur just after AP
Exacerbated at fast heart rates
Spike from resting potential

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11
Q

A heart block occurs when the electrical signal is slowed or disrupted as it moves through the heart.
What’s the difference between a partial and complete block?

A

Partial: Electrical signals are delayed and/or occasionally blocked

Complete: Electrical signals completely blocked

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12
Q

What is reentry?

A

Impulses reenter and excite areas of the heart more than once.

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13
Q

Explain Wolf-Parkison-White Syndrome:

A

In this REENTRY syndrome, an abnormal anatomical connection between the atria and ventricle called the Bundle of Kent is present.
This bundle allowed for an impulse to be conducted from the ventricles back into the atria (reentry) or cause the ventricles to contract prematurely.

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14
Q

What kinds of anti-arrhythmic drugs use a mechanism of prolonging the effective refractory period?

A

Class 3 drugs - The K channel blockers

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15
Q

What is the method of action of Class 1 drugs?

A

Na Channel blockers

They alter the action potential duration and change the Na channel kinetics

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16
Q

How do class 2 drugs work?

A

Beta-adrenoceptor blockade

-Block SNS effects in the heart

17
Q

How do class 4 drugs work?

A

Ca Channel blockers

-Slow conduction where depolarization is Ca dependent

18
Q

What is the advantage of “use” or “state-dependent” drugs?

A

Ideally you want to bind well to activated/inactivated channels and poorly to rested channels.

These drugs will then block activity in fast tachycardia and loss of resting potential when there are many inactivated channels during rest

19
Q

What do you have to be careful with as you increase the dose of Na channel blockers?

A

At higher doses, the lack of specificity increases - can also block K channels.

20
Q

What kind of arrhythmia do you have if you are getting early extra beats originating int he atria?

A

Premature atrial contractions

Subtype of Supraventricular

21
Q

Rapid, unusual regular rhythm originating above the ventricles.
Name that arrythmia:

A

Paroxysmal Supraventricular Tachycardia

22
Q

Name that arrythmia:
Extra abnormal pathway between ventricles and atria.
(you get a slurred upstroke to QRS)

A

Accessory pathway tachycardia

23
Q

Rapid heart rate due to more than one path through the AV node:
Name that arrythmia:

A
AV nodal reentrant tachycardia.
-Could be:
Atrial tachycardia
Atrial fibrillation (disorganized, rapid, irregular)
Atrial flutter (organized and regular
24
Q

Early extra beats beginning in the atria:

Name that arrythmia:

A

Premature ventricular contractions

25
Q

Rapid ventricular rhythym:

A

Ventricular tachycardia

26
Q

What do you gotta do if someone has ventricular fibrillation?

A

CPR and defibrillation, FAST!

27
Q

IF the time it takes the heart to contract and then recover is prolonged…
Name that arrythmia:

A

Long QT syndrome

kind of ventricular arrhythmia

28
Q

Arrhythmia can be broadly categorized as ventricular, supraventricular, or ?

A

Bradycardia!