CVPR Week 2: Cardiac Muscle Physiology II Flashcards

1
Q

Question

A
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2
Q

Extrinsic regulation of vascular resistance

A
  • Neural / Hormonal control
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3
Q

Intrinsic regulation of vascular resistance

A

Regulation by local factors and mechanisms inherent to cells of the vascular wall

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4
Q

Regulation of vascular resistance

A
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5
Q

Question

A
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6
Q

Extrinsic regulation of Cardiac output

A
  • Neural/Hormonal control
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7
Q

Intrinsic regulation of Cardiac output

A

Starling’s Law of the heart

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8
Q

Objectives

A
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9
Q

How is Heart Rate determined?

A

HR is determined by pacemaker activity

  • Principle control of HR is by the ANS (extrinsic)
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10
Q

How is stroke volume determined?

A

Both intrinsic (Starling’s Law) and extrinsic (ANS) mechanisms regulate SV

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11
Q

Question

A

Sympathetic β1 receptors by Norepinephrine to speed up

Sympathetic α1 receptors vascular constriction

M2 by acetylcholine to inhibit adenylate cyclase???

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12
Q

Sympathetic pathway and parasympathetic pathways

A
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13
Q

What phase of an action potential and what type of action potential is important in determining HR?

A

Phase 4 of slow-response action potentials in the SA node

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14
Q

How HR is increased?

A

Ne increases the slope of SA nodal pacemaker potentials to quicken the ‘pace’ resulting in a decreased interval between action potentials thus increasing HR

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15
Q

How HR is decreased?

A

ACh decreases the slope of the pacemaker potential by hyperpolarizing the SA nodal cells

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16
Q

Identify the effect on HR

A
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17
Q

Identify the effect on HR

A
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18
Q

β1 receptor signal transduction mechanism

A
  • NE stimulation of β1 receptor
  • Gs-coupled activating Adenylate cyclase creating cAMP and activating PKA

Leads to

  1. leads to greater Ca2+ influx
  2. greater CICR from the SR
  3. greater contraction
  4. PKa can phosphorylate Ryanodine receptors and can increase sensitivity to Ca2+ so leads to more CICR and therefore greater contraction
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19
Q

Cardiac Muscarininic receptor signal transduction mechanisms

A
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20
Q

Autonomic tone predominating normal resting individuals

A
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21
Q

During sympathetic stimulation, not only is contractility increased but cardiac myocytes are receiving action potentials more frequently, so how do cardiomyocytes quickly relax

A
  • PKA phosphorylates PL (Phospho Lambda), which regulates (inhibitory) SERCA pump Ca2+ pump and when phosphorylated by PKA, PL disinhibits SERCA.
  • so PKA inhibits PLs inhibition of SERCA
  • ACh would have the opposite effect
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22
Q

Parasympathetic effect on contractility

A

can influence atrial contractility but not really in the ventricles

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23
Q

Effects of NE and ACh on SV

A
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24
Q

Effects of NE on ventricular myocyte contractility

A
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25
Effects of ACh on ventricular myocyte contractility
26
Signal transduction mechanisms associated with β1 receptor and muscarinic receptor stimulation
27
Summary of autonomic control of the heart: HR regulation
28
Summary of autonomic control of the heart: Contractility regulation
29
Starling's Law of the Heart description
30
Starling's Law of the Heart diagram
* ventricular pressure is a function of ventricular end-diastolic volume * when the volume is really high starling's law no longer applies and force of contraction is reduced
31
Thick and thin filament overlap
32
Starling's Law of the Heart: Mechanism
33
Longer fiber lengths ________ spacing between thick and thin filaments.
reduces
34
Starlings law explanation
greater end diastolic volume stretching the heart = greater stroke volume
35
Longer fiber lengths increase the affinity of?
Troponin C for Ca2+
36
Starling Curves altered by stimuli
37
Starling's Law of the heart: Physiological significance
38
Starling's Law of the heart: Physiological significance diagram
sympathetic venous pressure get increased venous return get increased end-diastolic volume get an increased stroke volume
39
What mechanisms lead to increased CO?
* ↑ sympathetic activity to the heart increases HR and contractility * ↑ sympathetic to venous indirectly increase venous constriction and venous return increasing end-diastolic volume (α1 receptors) and thereby increasing cardiac output by starlings law * parasympathetic is the opposite effect on HR and contractility
40
Myocardial response to afterload stress
like lifting a heavyweight, increased BP or afterload impairs myocardial performance contraction velocity and cardiac output
41
What is afterload stress?
the load that cardiac muscle must overcome in order to shorten
42
Afterload is?
Aortic pressure (MABP)
43
Myocardial responses to afterload stress results in?
↑ Arterial pressure and decreased myocardial performance
44
Question
45
Effects of increasing HR on CO
46
Decreased SV associated with high HR (tachycardia) can limit?
CO
47
Decreased SV associated with high HR (tachycardia) can limit? Then what happens with exercise?
so the increased sympathetic tone and venous return helps to mitigate this
48
Summary of intrinsic mechanisms of cardiac regulation
49
Summary of physiologic regulation of myocardial performance
50
Question
51
Question
52
Question
53
chronotropic effects means
time effects in this case HR
54
Cardiac Function Curve AKA
Starling curve
55
typical systole time
300 msec
56
Typical diastole time
500 msec
57
Cardiac cycle typical time
800 msec
58
an increase in HR takes time from?
diastole which will decrease cardiac output
59
Atrial pacing increase reduces
stroke volume
60
Cardiac output to atrial pacing
61
Tachycardia can _______ filling time and thereby can reduce _________ and \_\_\_\_\_\_\_\_\_.
* stroke volume * limit cardiac output
62
What is the principal control mechanism of HR?
Autonomic nervous system (extrinsic)