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22 spring: Physiology > Test 3: lecture 2 > Flashcards

Test 3: lecture 2 Flashcards

1
Q

action potential curve of skeletal muscle

A

depolarization

repolarization

hyperpolarization

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2
Q

absolute refractory period

A

no additional signal can happen

(waiting for sodium channels to re-set)

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3
Q

relative refractory period

A

second action potential can start but needs to be much stronger

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4
Q

•In reference to the graph below illustrating the contraction of a skeletal muscle fiber over time, what do you think would happen if a second action potential was triggered at the time where the big green arrow is pointing?

A.Nothing because the action potential is still in its refractory period

B.The next contraction would produce a higher tension due to summation

C.The fiber would relax more quickly

D.The next tension/time curve would have a plateau

A

B.The next contraction would produce a higher tension due to summation

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5
Q

____ cardiac cells are not autorhythmic, but do conduct action potentials

A

contractile cardiac cells

(generate force)

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6
Q

___ cardiac cells provide a pathway for spreading excitation through the heart

A

autorhythmic

pacemaker cells

conduction fibers

*don’t generate much contractile force)

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7
Q

the main job of auto-rhythmic cardiac cells is ___

A

pacemaker (create action potential)

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8
Q

how is action potential of fast response action potentials different from skeletal muscles

A

the repolarization phase is much longer (plateau)

2-3 msec

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9
Q

fast response action potentials in the heart are driven by ___

A

voltage gated Na+ channels

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10
Q

slow response AP is driven by __

A

Ca2+ (L-type Ca2+ channels)

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11
Q

what kind of AP do autorhythmic cardiac cells produce

A

slow response AP

(Calcium driven pump)

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12
Q

what kind of AP do contractile cardiac cells produce

A

fast-response AP

Na+ driven

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13
Q

___ potentials lead to spontaneous action potentials

A

•Pacemaker

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14
Q

P acemaker potentials lead to spontaneous action potentials due to hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (funny current) and ___calcium channels

A

T-type

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15
Q

why no hyper-polarization in fast response AP

A

resting at -90

almost at equilibrium potential for potassium (-94)

(normal muscle resting is at 70 so when potassium is repolarizing it is trying to get to its happy place at -94 and causes hyperpolarization)

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16
Q

how do hyperpolarization-activated cyclic nucleotide-gated (HCN) channels work?

A

opened during hyperpolarization

opens and lets sodium into the cell causing a slow depolarization (will get about half way pacemaker potential → other half to threshold by T-type Calcium channels)

“funny current”

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17
Q

how does pacemaker potential work?

A

hyperpolarization-activated cyclic nucleotide-gated (HCN) channels open during hyperpolarization and lets sodium into the cell causing a slow depolarization

about half way, Ttype Ca channels will open and get “pacemaker” cell to threshold

where L-type Ca channels open

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18
Q

___ cause spontaneous depolarization of pacemaker cells

A

hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (sodium channels triggered by hyperpolarization)

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19
Q

how does ANS effect pacemaker potential

A

effects cyclic nucleotide production

which effect hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (sodium channels)

will change slope. very steep → fast HR. low slope → slow HR

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20
Q

what causes plateau for AP in contractile cardiac cells

A

K leaving and Calcium entry are even for a little keeping same charge

calcium channels close but K continues to leave and cell will repolarize

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21
Q

why no summation is contractile cardiac cells

A

AP and contraction same length

(can not receive another AP until contraction is done)

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22
Q

I Kr

A

rapidly activated delayed rectifying potassium current

more potassium leave cell causing repolarization

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23
Q

I Ks

A

slowly activating delayed rectifying potassium current

potassium leave cell cause rapid depolarization

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24
Q

I K1

A

inward rectifying potassium current

potassium trying to get to -94 happy place

(can move potassium in or out)

resting potential for contractile cardiac ell at -90

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25
steps of AP in pacemaker cells
**Phase 4 (pacemaker potential)** * If: funny current, **HCN channel- sodium into cell** (slight depolarization * ICa2+ (T): **calcium current, T-type** voltage gated channel (calcium into cell slowly- slight depolarization) **Phase 0:** •ICa2+ (L): **calcium current, L-type** voltage gated channel (rapid calcium into cell- fast depolarization (not as fast as Na but faster then T type calcium) **Phase 1 and 2 are absent** **Phase 3:** •Ik: **potassiu**m current (K out of cell → repolarization), delayed rectifier potassium (although there are several potassium channels here)• Also important: IKACh: **rectifying potassium** current that is important for parasympathetic regulation of HR
26
explain
4: pacemaker potential : HCN (Na in slowly), T-type Ca (calcium in slowly) hits threshold → stage 0 Ltype Ca (calcium in faster) stage 3: calcium close, K open (K leave cell)
27
intercalated disks
**•****Desmosomes** provide structural strength * Cells are electrically linked through **gap junctions** * The heart behaves as a **functional syncytium** * Anisotropic conduction
28
how is electrical current conducted from cell to cell in the heart
intercalated disks desmosomes (gap junctions)
29
anisotropic conduction
1 direction movement of electrical current
30
functional syncytium means \_\_
heart cells will beat at same time cause electrical signal is passed through gap junctions at intercalated disks
31
conduction through the heart
32
\_\_\_ is the pacemaker of the heart
SA (sinoatrial node)
33
•The ___ is the only pathway through which the signal can pass between the atria and the ventricles
AV node atrioventricular node
34
there is a slight ___ in transmission from SA to AV node
delay | (allow blood to move into ventricles)
35
what causes the delay in transmission from SA to AV node
reduction in gap junctions sending signals reduction in diamter
36
\_\_\_ provides for unidirectional passage of action potential through the atria to ventricles
AV node
37
\_\_\_ act as an auxiliary pacemaker if needed
AV node
38
what is the pathway of the spread of AP through the heart
SA→AV→ bundle of his → perkinji fibers
39
*If any pacemaker/conduction cell can initiate its own action potential, then why is the SA node the heart’s “pacemaker”?*
to keep everything in order unidirectional blood flow ***Because of the hierarchy of normal automaticity and the concept of overdrive suppression!*** SA node will spontaneously fire faster then other places
40
activity of the Na/K pump is dependent on the\_\_ node
SA try to keep up with the 70-80 AP per min if SA stops working, AV node only does 40-60 AP per min but Na/K at same level making cell more negative → hyperpolarization→ makes it harder for the cell to reach threshold → takes longer for pacemaker potential to reach threshold
41
explain overdrive suppression
there are enough Na/K pumps to maintain AP for the SA node at 70-80 AP/min this amount of Na/K makes the cell hyper polarized which makes it harder for other cardiac cells to spontaneously fire
42
abnormally high heart rate
tachycardia •Classified based on site of origin (atrial tachycardia, sinus tachycardia, junctional tachycardia, ventricular tachycardia)
43
abnormally low heart rate
bradycardia
44
dysfunction of the SA node
sick sinus syndrome
45
depolarizations during the refractory period
**Afterdepolarizations**
46
* Early afterdepolarizations (EAD): occur during phase\_\_ * Delayed afterdepolarizations (DAD): occur during phase \_\_
2-3 4
47
early afterdepolarization happens when?
48
what happens with delayed afterdepolarization
49
•a complete block; no atrial action potentials conducted to ventricles
3rd degree block
50
: some atrial action potentials conducted to ventricles
2nd degree block
51
•all atrial action potentials transmitted to ventricles, however the delay at the AV node is abnormally long
1st degree block
52
unidirectional block reentry of AP back into atria
53
abnormal parallel signaling through the heart
reentry unidirectional block * Most common mechanism of arrhythmias * Caused by a block and/or slowed conduction **•****Anatomically defined**•Wolff-Parkinson-White Syndrome •**Functionally defined****•**Ischemia, pH alterations
54
•Length and amplitude of waves of the ECG depend on two factors
:•Size of the sum of potentials•Synchronicity of potentials
55
explain
if you look from A → B the ions closest to you are more positive, then the ions closer to B (1st line) if you look from C→ D the ions have = charge → straight line
56
P wave=
atrial depolarization left to right = more + on right = bump up
57
Q wave
early ventricular depolarization (left side faster then right→ right side not depolarized yet→ from left side = more negative then right → downward bump
58
R wave
ventricular depolarization depolarization from inside to outside, at this time but ventricles not the same width → + deflection toward the apex (left) → left more + then right = positive spike
59
S wave
later ventricular depolarization last bit of ventricles depolarize → from left to right → left negative = small negative spike
60
T wave
ventricular repolarization (repolarization from apex to base, left to right ) repolarization = positive out of the cell = left more + → positive bump
61
QRS=
ventricular depolarization
62
why positive T wave?
repolarization of ventricle = cell becoming more negative = loss + (cell lose K+) the K channels in the apex of the heart faster then the K channels in the base therefore repolarization left → right gives a + bump
63
Einthoven's law
Any two of the three bipolar limb leads determine the third one. Lead I + Lead III = Lead II bipolar limb leads
64
P-Q segment
no bump time after P but before Q
65
intervals vs segments
intervals include wave segments time inbetween wave
66
60 sec/0.75 sec= 80 beats per min
67
draw ECG for tachycardia
short T-P segment
68
draw ECG for bradycardia
long T-P segment
69
draw ECG for 1st degree AV block
•First-degree block: all atrial action potentials transmitted to ventricles, however the delay at the AV node is abnormally long ## Footnote **long P-Q interval**
70
draw ECG for 2nd degree AV block (type 1)
•Second-degree block: some atrial action potentials conducted to ventricles type 1= most AP gets through but each time longer and longer then resets **PR progressively longer** then resets→ eventually AV might take over and there will be a skipped P wave
71
draw ECG for 3rd degree AV block
•Third-degree block: a complete block; no atrial action potentials conducted to ventricles AV node will trigger on its own -40 AP/min, can combine together no obvious pattern, SA on its own, AV on its own
72
ST segment
73
Can atrial repolarization be observed on an ECG if there is a separation between atrial and ventricular depolarization (i.e. during a block?)
in theory yes atrial repolarization occurs during ventricle depolarization (QRS) if there is heart block atria and ventricle beating on there own pace there could be a chance to see the repolarization of atria if timing is correct TA wave -Blue line - wide and shallow and negative = left side more - then right side (same direction as depolarization wave)
74
when on an ECG is the plateau phase in the ventricles occuring?
ST interval
75
can atrial repolarization be observed on an EKG if there is a separation between atrial and ventricular depolarization (i.e during a block)?
yes during 3rd degree heart block, atria and ventricles contract at different patterns, Atria by the SA and ventricles by the AV node. in a normal EKG atria repolarization occurs during the QRS, so you can't see it during block the random rhythm, may allow the repolarization to be seen- (negative wave, **repolarization occurs in same direction as depolarization)**

22 spring: Physiology (34 decks)

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