Lec 11-12 Cardiac electrical activity at tissue/organ Flashcards

1
Q

Through what do action potential propagate cell to cell?

A

through gap junction

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2
Q

What does PVC stand for?

A

premature ventricular contraction

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3
Q

What does VT stand for?

A

ventricular tachycardia

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4
Q

What are you recording with ECG?

A

extracellular voltages

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5
Q

What stain to find intercalated disks?

A

connexin 43 protein

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6
Q

What is connexon vs connexin?

A

connexon: complete multimeric channel, 6 subunits from each cell
connexin: each subunit, or category of protein in general

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7
Q

What 2 diseases are gap junctions/connexons disrupted in?

A
  • heart failure

- arrhythmogenic cardiomyopathy

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8
Q

What 2 things determine how fast APs propagate?

A
  1. # gap junctions between cells [altered in disease]

2. inward current responsible for AP upstroke

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9
Q

What ion current is main determinant of conduction velocity?

A

Na current = speed of upstroke

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10
Q

What 2 effects of decreased Na current on AP?

A
  1. slower upstroke [so slower individual AP]

2. longer delay between APs = slower propagation

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11
Q

Does excitement go endo –> epi cardium or vice versa?

A

propagates endo to epi

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12
Q

What is voltage difference measured in AP vs ECG?

A

AP: Vin - Vout
ECG: V2 - V1
V1 = endocardium, V2 = epicardium

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13
Q

How do you get voltage outside from voltage inside?

A

Voltage outside is negative of voltage inside

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14
Q

Whats an easy way to calculate V2 - V1 [pseudo-ECG]?

A

V2 - V1 = AP1 - AP2 = dV/dt

V1 = endocardium, V2 = epicardium

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15
Q

What is weird about one dimensional pseudo-ECG

A

T wave is negative but should be positive

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16
Q

What is cellular basis of upright T wave?

A
  • cells are no identical across ventricular wall, stronger phase 1 in epicardium than endocardium
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17
Q

Difference between epicardial and endocardial ventricular cells? What is cause of these differences?

A
  • more pronounced phase 1 in epicardial cells
  • shorter APs in epicardial

different expression of K channels

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18
Q

What is cellular basis for positive T wave?

A
  • endocardium activated before and re-polarized after epicardium
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19
Q

What do electrodes measure?

A

differences between voltages NOT absolute voltages

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20
Q

What kind of deflection do you get from a depolarization wave moving toward a positive electrode [V2]?

A

upward/positive deflection

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21
Q

What kind of deflection do you get from a repolarization wave moving toward a positive electrode [V2]?

A

negative/down deflection

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22
Q

What kind of deflection do you get from an orthogonal depolarization/repolarization wave?

A

None – no signal

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23
Q

What kind of deflection do you get from a repolarization wave moving away from a positive electrode [V2]?

A

positive deflection

24
Q

What kind of deflection do you get from a depolarization wave moving toward a positive electrode [V2]?

A

negative deflection

25
Why is there no signal from an orthogonal wave?
V2 - V1 = AP1 - AP2 | since AP1 and AP2 occur at same time in this instance, AP1 - AP2 = 0
26
What is requirement for seeing ECG deflections?
- when voltages in the heart are changing with respect to location
27
What 2 things determine strength of signal?
1. propagation direction | 2. mass of tissue contributing to signal
28
How do you get V1, VII, VIII?
``` VI = VLa - VRa VII = VLL - VRa VIII = VLL - VLa ``` La = left arm, Ra = right arm, Ll = left leg
29
What are angles of aVR, aVL, lateral, VII, aVF, VIII
``` lateral = 0 II = +60 aVF = +90 [vertical down] III = +120 aVR = -150 ```
30
What are precordial leads?
placed in transverse plane, provide info about activity along anterior-posterior direction
31
What does P wave represent?
atrial depolarization
32
What does QRS complex represent?
ventricular depolarization
33
What does T wave represent?
ventricular repolarization
34
Why is there no signal from conducting tissues?
not enough tissue mass
35
What is there no signal from atrial repolarization?
not strong enough signal, depolarization signal is much stronger
36
What does QT interval represent?
AP duration = from ventricular depolarization to repolarization
37
What does PR interval represent?
propagation through AV node = atrial depolarization to ventricular depolarization
38
What is time of QT interval?
300 ms
39
What is time of PR interval?
120-200 ms
40
What is time of QRS complex?
120 ms
41
Why is AV node propagation slower than ventricular propagation?
AV: propagation via L-type Ca current is slower than Na Ventricle: propagation via fast Na upstroke
42
What happens with parasympathetic to AV node? mech?
- negative dromotropy = slower than normal conduction through AV - slower upstroke, longer delays between APs - muscarinic activated [Gi] --> inhibit AC --> less cAMP --> less PKA --> less phosphorylation L-type Ca current --> decreased upstroke
43
What happens with sympathetic to AV node? mech?
- positive dromotropy = faster than normal conduction - activation B adrenergic [Gs] --> activates AC --> increased cAMP --> more PKA activation --> more phosphorylation Ltype Ca --> increased upstroke
44
What is regular HR?
60-100 bpm
45
How do you count ECG boxes -- what is a small box? a large box? how many boxes to 1 s?
small box = 40 ms large box = 200 ms 5 large boxes = 1 s
46
How do you determine electrical axis of heart?
- from lead that produces the largest QRS [depolarization] signal
47
3 things to estimate electrical axis
1. look for max positive R with no negative, this is the closest 2. look for closest WRS to integral of zero, axis is perpendicular to this 3. If two R waves are equally tallest, axist is between the two
48
What is normal for dominant axis?
0 to +90, [0 to -30 is borderline]
49
What is axis in LV hypertrophy?
- shift toward negative values
50
What is axis in RV hypertrophy?
- right axis deviation [shift toward positive values > 90]
51
How does cellular physiology explain the phases of QRS complex [ie the shape]
1. get very small: primary direction of propagation L -->R across septum, mostly perpendicular but pointed slightly toward the negative electrode --> get slightly negative wave 2. traveling down purkinje, many parts of endocardium in apex of heart excited at once, net excitation pointing at lead 2 --> get very big wave since pointing directly at it 3. No vectors pointing directly at lead 2 anymore, going L -->R and a little toward lead 2, still positive but less so 4. Not much tissue at top of ventricle so weak signal, also pointing slightly away to negative
52
In what conditions do you get wide QRS?
In DAD normal: depolarization via conduction is fast abnormal: depolarization starts outside of conduction system so goes via ventricular propagation and is much slower
53
How many squares wide for QRS to be considered slow?
3 squares
54
What do P waves that are not always followed by QRS indicate?
AV failure/block since conduction is not always getting through
55
What are signs of monomorphic ventricular tachycardia?
monomorphic = all complexes are similar wide QRA = ventricles are exciting themselves shortened R-R interval
56
What is reentry?
- depressed region causes forward impulse to be obstructed and extinguished - allows retrograde impulse - premature stimulus encounters refractory tissue and blocked on right side, it will propogate slowly on left. by the time it propagates around the bottom, right side has recoveres [this is confusing to me]
57
2 causes of VT
1. ventricular focus | 2. reentry