Dysrhthmias Flashcards

1
Q

Which ion channel is related to the refractory period of the action potential?

A

Sodium Channels

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2
Q

What is the difference between the Relative Refractory period and the Absolute refactory period.

A

Rel: only a strong signal can depolarize
Abs: No level of stim. can depolarize

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3
Q

What part of the Na channelis responsible for closing the channel during phase 1?

A

Inactivation gate. Intracellular loopH (Ball and Chain)

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4
Q

What effect will changing the action potential duration have?

A

Change the refractory period

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5
Q

What are the steps of cardiac muscle contraction?

A

Ca entry through VOCC
Ca Release from SR
Ca interacts with troponin
=> Contractile shortening of sarcomere

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6
Q

What are the steps of cardiac muscle relaxation?

A

Ca Dissociates from troponin
Ca is taken back up into storage via SERCA
Ca bound to proteins within SR (calsequestrin)
Ca is pumped out of the cell at the cell membrane (NCX, plasma Ca-ATPase)

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7
Q

What are possible changes in E-C coupling that lead to Dysrhythmias?

A

Smaller spark
Fewer RyR open
less Ca released

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8
Q

What is the pacemaker of the heart?

A

SA node (fastest rate of automatic depolarization)

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9
Q

What are possible dysfunctions of phase 4 depolarization of the SA nodal cells?

A

Sinus Tachycardia

Sinud Bradycardia

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10
Q

What ion channels are not present in non-nodal tissue?

A

Funny Current (Hyperpolarization-Activated cyclic nucleotide-gatedchannels) HCN

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11
Q

What are the subsidiary or latent pacemakers?

A

Atrial PM
AV junct. PM
Ventricular PM

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12
Q

What autonomic stimulation will cause Tachy.? Brady?

A

Sympathetic Stim: Enh. Automaticity

Parasympathetic Stim: Reduced Automaticity

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13
Q
How can the following hormones affect phase 4 depolarization?
Ach
Nori?
HypoK
Mild HyperK
Severe Hyper K
A
Ach
Nori?
HypoK
Mild HyperK
Severe Hyper K****
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14
Q

What causes Delayed after Depolarization? DAD

A

Cytosolic and/or SR Ca Overload

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15
Q

What causes Early after Depolarization? EAD

A

Altered ion flux during plateau phase. Prolonged Action potential duration

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16
Q

What can prolonged APD be caused by?

A

Red K current
Inc Ca
Inc Na-Ca exch.
Inc late Na sodium current

17
Q

What effect does a low HR have on Early after Depolarizations?

A

Makes them worse. Anything that lengthes the AP makes them worse.

18
Q

What effect does a high HR have on Delayed after Depolarizations?

A

Makes them worse. anything that shortens the AP. (increased intracellular Ca)

19
Q

What is a Anatomically defined reentrant circuit?

A

Impulses travel more than one pathway in the heart
Wolf-Parkinson-White syn, AVNRT, atrial flutter, PVST

Fixed pathway, Excitable gap

20
Q

What is a Functionally defined Reentrant circuit?

A

Absence of defined anatomical pathway.
Area of inexcitable tissue at the core.
Monomorphic and Polymorphic VT/VF

21
Q

What do Anitomically and Functionally defined Reentrant circuits have in common?

A

Both rely on discrepancy in electrical impulses between cells.

22
Q

What is a circus movement re-entry?

A

Unidirectional block
Wave propagates along a distinct pathway returning to PO origin and following the same path again.
Interruption of the reentrant circuit at any point along the path should terminate circus movement

23
Q

When to DADs take place

A

Phase 4 of myocyte AP

Calcium excess

24
Q

When do EADs take place?

A

Phase 2-3

Sodium or potassium excess

25
Q

What is Wolf-Parkinson-White Syndrome?

A

Accessory Pathway links atrial tissue to ventricular tissue, bypassing AV node

AV node functions to slow conduction, therefore the accessory pathway is abnormally fast.
Seen as a shortened PR interval on ECG

26
Q

Why is there a shortened PR interval in WPW syndrome?

A

There is not slowing by passage through the AV node?

27
Q

What will happen if the refractory period is reduced?

A

Propagating wave front encounters tissue that can be excited and re-enter the initial point of stim (same as reduced cond. velocity)

28
Q

What will happen if the Conduction velocity is reduced?

A

Propagating wave front encounters tissue that can be excited and re-enter the initial point of stim (same as red. refractory period)

29
Q

What precipitates DADs?

A

SR Ca Overload =>Diastolic Ca leak

30
Q

What precipitates EADs?

A

APD prolongation, increased depolarizing currents

SR Ca Overload =>Systolic Ca leak

31
Q

What is the source-sink relationship?

How does non-excitable tissue effect relationship?

A

Source: Strength of impulse
Sink: Amt of tissue source must excite.

Will prolong the Action potential

32
Q

What channel is responsible for the refractory period?

A

Sodium Channel