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Physiology Part 1 > Lec 11-12 Cardiac electrical activity at tissue/organ > Flashcards

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
Q

Why is there no signal from an orthogonal wave?

A

V2 - V1 = AP1 - AP2

since AP1 and AP2 occur at same time in this instance, AP1 - AP2 = 0

26
Q

What is requirement for seeing ECG deflections?

A
  • when voltages in the heart are changing with respect to location
27
Q

What 2 things determine strength of signal?

A
  1. propagation direction

2. mass of tissue contributing to signal

28
Q

How do you get V1, VII, VIII?

A 
VI = VLa - VRa
VII = VLL - VRa
VIII = VLL - VLa

La = left arm, Ra = right arm, Ll = left leg

29
Q

What are angles of aVR, aVL, lateral, VII, aVF, VIII

A 
lateral = 0
II = +60
aVF = +90 [vertical down]
III = +120
aVR = -150
30
Q

What are precordial leads?

A

placed in transverse plane, provide info about activity along anterior-posterior direction

31
Q

What does P wave represent?

A

atrial depolarization

32
Q

What does QRS complex represent?

A

ventricular depolarization

33
Q

What does T wave represent?

A

ventricular repolarization

34
Q

Why is there no signal from conducting tissues?

A

not enough tissue mass

35
Q

What is there no signal from atrial repolarization?

A

not strong enough signal, depolarization signal is much stronger

36
Q

What does QT interval represent?

A

AP duration = from ventricular depolarization to repolarization

37
Q

What does PR interval represent?

A

propagation through AV node = atrial depolarization to ventricular depolarization

38
Q

What is time of QT interval?

39
Q

What is time of PR interval?

A

120-200 ms

40
Q

What is time of QRS complex?

41
Q

Why is AV node propagation slower than ventricular propagation?

A

AV: propagation via L-type Ca current is slower than Na
Ventricle: propagation via fast Na upstroke

42
Q

What happens with parasympathetic to AV node? mech?

A
  • 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
Q

What happens with sympathetic to AV node? mech?

A
  • positive dromotropy = faster than normal conduction
  • activation B adrenergic [Gs] –> activates AC –> increased cAMP –> more PKA activation –> more phosphorylation Ltype Ca –> increased upstroke
44
Q

What is regular HR?

A

60-100 bpm

45
Q

How do you count ECG boxes – what is a small box? a large box? how many boxes to 1 s?

A

small box = 40 ms
large box = 200 ms
5 large boxes = 1 s

46
Q

How do you determine electrical axis of heart?

A
  • from lead that produces the largest QRS [depolarization] signal
47
Q

3 things to estimate electrical axis

A
  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
Q

What is normal for dominant axis?

A

0 to +90, [0 to -30 is borderline]

49
Q

What is axis in LV hypertrophy?

A
  • shift toward negative values
50
Q

What is axis in RV hypertrophy?

A
  • right axis deviation [shift toward positive values > 90]
51
Q

How does cellular physiology explain the phases of QRS complex [ie the shape]

A
  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
Q

In what conditions do you get wide QRS?

A

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
Q

How many squares wide for QRS to be considered slow?

54
Q

What do P waves that are not always followed by QRS indicate?

A

AV failure/block since conduction is not always getting through

55
Q

What are signs of monomorphic ventricular tachycardia?

A

monomorphic = all complexes are similar
wide QRA = ventricles are exciting themselves
shortened R-R interval

56
Q

What is reentry?

A
  • 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
Q

2 causes of VT

A
  1. ventricular focus

2. reentry

Physiology Part 1 (37 decks)

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