Intro to CV physiology Flashcards

1
Q

What is bathmotropy?

A

Excitability or threshold of excitation

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2
Q

What is chronotropy?

A

AP emission frequency or HR

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3
Q

What is dromotropy?

A

AP conduction speed or conductibility

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4
Q

What is inotropy?

A

Muscular contraction force or contractility

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5
Q

What is lusitropy?

A

Diastolic relaxation

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6
Q

What is tonotropy?

A

Distensibility

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7
Q

What is the average range for a cardiac muscle AP?

A

200 to 400 msec

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8
Q

What is the significance of the long refractory period of cardiac muscle?

A

Cannot be tetanized
Prevents fatigue
Allows time for heart chambers to fill

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9
Q

What are the 10 steps of cardiac excitation-contraction coupling?

A
  1. AP enters from adjacent cell
    2.Voltage-gated Ca++ channels open
  2. Ca++ induced Ca++ release from SR through RyR channels
  3. Local Ca++ release causes Ca++ sparks
  4. Summed Ca++ sparks creates a Ca++ signal
  5. Ca++ binds to troponin C initiating contraction
  6. Ca++ unbinds from troponin initiating relaxation
  7. Ca++ is pumped back into SR through SERCA channels
  8. Ca++ is exchanged for Na by NCX antiporter
  9. Na gradient is maintained by Na/K ATPase
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10
Q

What occurs during phase 0 of cardiac muscle AP?

A

Opening of voltage gated Na channels
Transient influx of Na

Rapid depolarization

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11
Q

What occurs during phase 1 of cardiac muscle AP?

A

Closure of voltage gated Na channels - Na influx stops
Opening of voltage-gated transient K channels
K efflux - tiny repolarization

Initial rapid repolarization

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12
Q

What occurs during phase 2 of cardiac muscle AP?

A

Opening of voltage gated L-type Ca channels
Ca influx balances K efflux and triggers Ca release from SR
Contraction

Plateau

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13
Q

What occurs during phase 3 of cardiac muscle AP?

A

Ca channels inactivate slowly - decreasing Ca influx
Increased K efflux through delayed rectifying K channel
Repolarization

Late repolarization

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14
Q

What will occur during phase 3 is Ach is present?

A

Ach activates IKAch and increases K efflux
Increases hyperpolarization

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15
Q

What occurs during phase 4 of cardiac muscle AP?

A

RMP is reestablished at -85 mV

Resting membrane potential

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16
Q

What are the 4 types of K channels in heart muscle?

A

Inward rectifying K+ channel (Ik1)
Transient outward K+ channel (It0)
Delayed rectifying potassium channel (Iks, Ikr, and Ikur)
G-protein activated inward rectifying K current (Girk or IkAch)

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17
Q

What is the inward rectifying K channel?

A

Leaky K channel which closes near the end of depolarization and reopen during repolarization

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18
Q

What is the transient outward K channel?

A

Opens transiently at the end of phase 1 and closes during the middle of plateau/phase 2

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19
Q

What is delayed rectifying K channel?

A

Open slowly during the plateau and then more rapidly near the end of phase 2 to initiate repolarization

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20
Q

What is G-protein activated inward rectifying K current?

A

Channel opens in response to Ach release
Efflux of K to cause further hyperpolarization
Reduces effects of If and Ca channels

21
Q

What occurs during phase 0 of SA node AP?

A

Decreased Ca influx through T-Ca channels
Increased Ca influx through L-Ca channels

22
Q

What occurs during phase 3 of SA node AP?

A

Increased K efflux through voltage-gated K channels

23
Q

What occurs during phase 4 of SA node AP?

A

K channels close
Funny Na channels open – Na influx
Slow depolarization of cell
Near threshold funny channels close and T-Ca channels open
L-Ca channels open at threshold

24
Q

What will occur with selective inhibition of funny Na channels?

A

Decreased HR
No effect on contractility

25
What causes extra systole?
A sufficiently strong stimulus during relative refractory period
26
What is the compensatory pause?
Missed normal systole from the presence of an extra systole
27
What is post-extra systolic potentiation?
Extra volume of blood collected in ventricle during compensatory pause resulting in an increased force of contraction
28
What results in the staircase phenomenon?
When stimuli of same strength are applied at short intervals resulting in increase in height of contraction
29
What is the intrinsic firing rate of the SA node?
70-80 bpm
30
What is the intrinsic firing rate of the AV node?
40-60 bpm
31
What is the intrinsic firing rate of the AV bundle?
40 bpm
32
What is the intrinsic firing rate of the Purkinje fibers?
15-20 bpm
33
What causes the AV nodal delay?
Narrow fiber diameter Relatively few gap junctions Slow depolarization due to slow voltage-gated Ca channels
34
What is the purpose of AV nodal delay?
Allows time for complete ventricular filling Maintains ventricular contraction rate in case of A fib
35
What is the conduction rate of the SA node?
0.5 m/s
36
What is the conduction rate of the atrial pathways and ventricular muscle?
1 m/s
37
What is the conduction rate of the AV node?
0.05 m/s
38
What is the conduction rate of the AV bundle?
1 m/s
39
What is the conduction rate of Purkinje fibers?
4 m/s
40
How does SyNS influence conduction?
Increases
41
How do beta blockers influence conduction?
Decrease
42
How does PsNS influence conduction?
Decrease
43
How does ischemia or hypoxia of the heart decrease conduction?
Decrease
44
How does digoxin influence conduction?
Decrease
45
How to Ca channel blockers influence conduction?
Decrease
46
How does norepinephrine from SyNS work in cardiac muscle?
Binds to Beta-1 receptors Adenyl cyclase increases cAMP increasing PKa Phosphorylation of membrane Ca channels - increases contractility Phospholamban stimulates SERCA reuptake into SR - increases HR Troponin I releases Ca bound to troponin C - quicker relaxation
47
How does Ach from PsNS work in cardiac muscle?
Binds to M2 receptors in atria Inhibits adenyl cyclase Closure of membrane Ca channels - decreases contractility Inactivation of SERCA channels - decreases HR Increases K permeability - hyperpolarization
48
How does ischemia in heart affect conduction?
Katp channels open - increased extracellular K Depolarization Decreases slope of phase 0 Reduced AP conduction velocity
49
How does acidosis effect myocardial function?
Inhibits myofibrillar responsiveness to Ca Decreases binding of Ca to troponin C Decreases force of contraction