3- Mechanisms of Dysrhythmias Flashcards

(43 cards)

1
Q

what phases correspond to the absolute refractory period?

A

phase 0,1, and2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

time that the cell is unable to respond to another incoming impulse

A

absolute refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

relative refractory period phase

A

phase 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

sustained inability to respond to an incoming impulse under normal conditions

A

relative refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

why doesn’t the heart tetanize like skeletal muscle?

A

extended absolute refractory period due to calcium channels

AND

no recruting

*everything is all or none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

define calcium spark

A

calcium-induced(voltage) calcium release(SR calcium channels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

name of calcium release channels

A

ryanodine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

increased activity of SERCA by SNS =

A

calcium taken away to increase relaxation faster ALSO SNS increases rate of calcium release from ryanodine.
Together = increased contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

classify: abnormal or enhanced automaticity

A

active arrhytmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

classify: triggered activity

A

active arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

classify: reentrant circuits

A

active arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

slower than normal

A

sinus bradycardia

faster (>100) would be sinus tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

effect of hypokalemia

A

decreases phase 4 K availabale –> easier depolarization and less time between AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

effect of mild hyperkalemia

A

increased AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

effect of severe hyperkalemia

A

unexcitable, no AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

“triggered activity”

A

delayed or early afterdepolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

arrhythmia is generated at a time when the cell is fully repolarized

A

DAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

arrhythmia generated during phase 2 or phase 3 depending

19
Q

characteristically extended action potential duration indicates…

20
Q

reduced potassium current –>

A

repolarization takes longer than normal –> prolonged APD

21
Q

increased intracellular calcium –>

A

extended plateau phase and extra calcium can activate an additonal sodium current –> prolonged APD

22
Q

mutation of NCX to increase current during the end of phase 2 –>

A

prolonged APD

23
Q

when can EADs be accentuated..

A

at lower heart rates due to the physiologically natural longer APDs at this point

24
Q

exacerbated by higher HR…

A

DADs

because ther is not sufficient time to reduce intracellular calcium between successive beats

25
a fixed pathway exists which connects atrial tissue to ventricular tissue and in doing so, bypasses the AV node
wolff-parkinson-white syndrome
26
how does wolff parkinson white syndrome manifest on ECG
shortened PR interval (because the bypass impulse travels faster to ventricles than normally conducted signal)
27
core of inexciteable tissue would be..
functional reentract obstacle
28
associated with spiral wae
anatomical-define reentrant circuit
29
stable spiral wave originating from one position within the ventricular mass
monomorphic ventricular tachycardia
30
meandering or drifting spiral waves throughout the ventricular mass
polymorphic tachycardia
31
rely on the principles of electrical anisotropy and spatial inhomogeneities
reentrant circuits
32
conduction abnormality as a result of tissue structure
passive arrhythmia
33
"source sink"
a smaller sink will increase APD and a larger sink will reduce APD and conduction velocity contributes to anisotropy and inhomogeneity in the propogating wavefront
34
true or false: changing the AP duration will change the refractory period
true
35
vagal stimulation would have what effect on HR
vagal is parasympathetic so it would derease automaticity and decrease HR --> sinus brady cardia sympathetic would be the opposite: sinus tachyccardia
36
if both para and symp are stimulate who will win for HR?
para
37
how does Ach change automaticity
slower by increasing potassium current
38
how does NE change automaticity
faster by increasing calcium and funny current
39
how do hypokalemia and ischemia change automaticity
faster becasue of a decreased potassium current
40
what 4 things could cause a prolonged APD?
1. reduced potassium current 2. increased calcium 3. increased sodium-calcium exchanger activity 4. increased late sodium current
41
true or false: only anatomically defined reentrant circuits rely on electrical anisotropy and tissue inhomogeneiteies
FALSE both anatomical and cuntionally defined reentrant ircuits rely on electrical anisotropy and tissue inhomogeneiteies
42
spiral wave
functioanlly defined reentrant circuit
43
fixed pathway with excitable gap
anatomically defined reentrant circuit