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A&P 2 > Electrical Activity of the Heart > Flashcards

Electrical Activity of the Heart Flashcards

1
Q

how are cardiac muscle cells in comparison to skeletal muscle cells?

A

short, mono or bi nucleated rather than multi-nucleated

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2
Q

what do cardiac muscles have at cell linkages

A

intercalated discs

  • gap junctions
  • desmosomes (macula adherens) anchor actin filaments at the end of the sarcomere
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3
Q

what do desmosomes have to prevent adjacent cells from being pulled apart

A

mechanical couplings

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4
Q

what are pacemaker cells features of

A

cardiac muscle and autostimulatory cells

-non contractile cardiac muscle

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5
Q

what are fast response action potentials

what are slow response action potentials

A

muscle and purkinje fibers

SA and AV nodes

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6
Q

what happens when an AP triggers an electical dischange

A

travels rapidly across the atrial and ventricular muscles regardless of whether its origin was fast or slow

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7
Q

for APs, what goes in and out

A

Na in

K out

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8
Q 
what happens in phase 0 of cardiac muscle action potential 
phase 1?
phase 2?
phase 3?
phase 4?
A

0-depolarization due to Na influx
1-initial repoloarization bc of K outflux
2-plateau bc transient increase, K outflux slows, Ca channel now open and flattens curve
3-repolarization: decrease influx Ca and incrase outflux K
4-resting potential/stead state of ion flow

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9
Q

what does an abs refractory period do?

A

ensures that cardiac muscle cells can’t be tetanized

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10
Q

what does a relative refractory period do

A

period in which an action pot can be elicited w/ an increased inward current

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11
Q

why can an effective tetanic (muscle spasm) contraction not be produced

A

bc of the duration of the action pot, cardiac muscles relax b4 it can be activated again

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12
Q

what do catecholamines do

A

enhance ca movement and increase size of AP
by binding to B1 receptor
-also increase of phase 3 K conductance (norepinephrine)

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13
Q

what do B2 catecholamine receptors do

what do B1 receptors do

A

mediate relaxation of smooth muscle

receptors in the heart

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14
Q

you dont want to extend plateau phase too far in an increase of phase 3 K conductance or else it will interfere w/ waht

A

refractory period

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15
Q

what are ca channel blockers used to treat

A

arrhythmias and high bp by slowing the heart

-depress ca movement => smaller action pot

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16
Q

in SA node AP what is phase 1, 3, 4

A

0-depolarization due to ca influx
3-repolarization due to K outflux
4-accounts for the pacemaker activity; due to slow influx Na, which is turned on by repolarization

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17
Q

in phase 4 in SA node AP, why is it not flat

A

slow influx of Na

-will reach threshold and fire on its own

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18
Q

what happens after repoloarization of phase 4

A

starts immediately heading towards threshold again “unstable resting pot”

19
Q

what happens when phase 4 of SA node reaches threhshold

A

Ca generates AP

20
Q

what nerve hyperpolarizes the resting pot and decreases the slope and heart rate of phase 4
what increaes the slope and heart rate?

A 
vagus nerve (acetylcholine)
sympathetic nerves (norepinephrine)
21
Q

what does the electrocardiogram do

A

measure of the heart’s electrical activity
-can detect abnormality in heart rhythm, size of heart, electrolyte imbalances, myocardial ischemia and infarction, drug effects

22
Q

what does an ECG not sure

A

direct info about contractile performance

23
Q

why is ECG called a dipole

A

bc whenever there is a discharge, there will be a separation of charges across the heart

24
Q

what is the electrical pathway

A

SA => AV => bundle of His => bundle branches => post fascicles

25
Q

what is the p wave of the ECG

A

rep depolarization of the SA node and atria

when atria repolarize, the wave is hidden in the QRS complex

26
Q

what is the QRS complex in the ECG
PR interval?
QT interval?

A

rep ventricular depolarization

  • time it takes AP to get from SA node through the atria and just beyond the AV not but not yet the ventricles
  • contraction of ventricles
27
Q

what is teh T Wave of ECG

U wave?

A

rep repolarization of the ventricles

dunno, sometimes seen after T wave

28
Q

an ECG may run by having electrods in only 3 positions, what are tehy

A

right arm, left arm, leg

29
Q

what potential change are you measuring btwn locations in einthoven’s triangle

A

lead 1: RA to LA
lead 2: RA to leg
lead 3: LA to leg

30
Q

what is einthoven’s law

A

if the electrical potentials of any 2 of the 3 bipolar limb ECG leads are known, the 3rd can be determined mathematically from the 1st two by simply summing the 1st 2 (signs of leads must be observed)

31
Q

where are chest leads connected to

A

the positive terminal of the ECG and the negative electrode is attached at the same time to the right arm, left arm, and left leg

32
Q

for a standard 12 point, how many electrodes involved

A

10, only 6 across the chest
right and left arm
right and left leg

33
Q

how many scenarios are there clinically where a cardiologist would be interested in analyzing a full ECG

A

12

34
Q

what are some heart abnormalies detected with ECG X____X

A 
1. right or left ventricle hypertophy 
2 respiratory sinus arrythmia
3. sinus tachycardia
4. premature ventricular or atrial contraction
5. atrial fibrillation
6. ventricular fibrillation
7. heart block
8. right or left bundle branch block
35
Q

what is the first sign of a myocardial infarction

A

inversion of T wave

36
Q

what does a progression of ischemia in a myocardial infarction result in

A

elevation of S-T segment

-ST segment elevation myocardial infarction (STEMI)

37
Q

what does a myocardial infarction lead to

A

development of Q waves in front of elevated S-T

38
Q

waht is ischemia

A

restriction of blood flow

39
Q

what is an infarct

A

an area of necrosis in a tissue or organ resulting from obstruction of the local circulation by a thrombus (blood clot) or embolus (blockage in blood vessel)

40
Q

what is an inotropic modification

A

somethign with a + inotropic effect increases the contractile force of cardiac muscle

41
Q

what is the treppe/bowditch phenomenon

A

gradual increase in muscular contraction follwoing rapidly repeated stimulation

  • seen w/ rapid heart contractions
  • each peak back to baseline b4 another
42
Q

why do contractions gets stronger w/ time in treppe/bowditch phenomenon

A

ca doesnt have time to get sequestered back into the sarcoplasimc ret so overall concentration gets higher in cytosol
-results in a “positiive inotropic mod” or cardiac muscle contraction

43
Q

what is digitalis

what does it inhibit

A

cardiac flycoside found in the foxglove plant

Na/K ATPase inhibitor => increased intracell Ca which gives a + inotropic effect

44
Q

what is s1 and s2 and s3 and s4 in the cardiac cycle

A

s1- the 1st heart sound, due to the clower of mitral and tricuspic valves
s2-due to closure of pulmonary and aortic semilunar valves
s3 and s4-abnormal heart sounds for the gen pop

A&P 2 (8 decks)

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