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CVPR > CVPR Week 2: Cardiac Muscle Physiology II > Flashcards

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
Q

Effects of ACh on ventricular myocyte contractility

A
26
Q

Signal transduction mechanisms associated with β1 receptor and muscarinic receptor stimulation

A
27
Q

Summary of autonomic control of the heart: HR regulation

A
28
Q

Summary of autonomic control of the heart: Contractility regulation

A
29
Q

Starling’s Law of the Heart description

A
30
Q

Starling’s Law of the Heart diagram

A
  • 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
Q

Thick and thin filament overlap

A
32
Q

Starling’s Law of the Heart: Mechanism

A
33
Q

Longer fiber lengths ________ spacing between thick and thin filaments.

A

reduces

34
Q

Starlings law explanation

A

greater end diastolic volume stretching the heart = greater stroke volume

35
Q

Longer fiber lengths increase the affinity of?

A

Troponin C for Ca2+

36
Q

Starling Curves altered by stimuli

A
37
Q

Starling’s Law of the heart: Physiological significance

A
38
Q

Starling’s Law of the heart: Physiological significance diagram

A

sympathetic venous pressure get increased venous return get increased end-diastolic volume get an increased stroke volume

39
Q

What mechanisms lead to increased CO?

A
  • ↑ 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
Q

Myocardial response to afterload stress

A

like lifting a heavyweight, increased BP or afterload impairs myocardial performance contraction velocity and cardiac output

41
Q

What is afterload stress?

A

the load that cardiac muscle must overcome in order to shorten

42
Q

Afterload is?

A

Aortic pressure (MABP)

43
Q

Myocardial responses to afterload stress results in?

A

↑ Arterial pressure and decreased myocardial performance

44
Q

Question

A
45
Q

Effects of increasing HR on CO

A
46
Q

Decreased SV associated with high HR (tachycardia) can limit?

A

CO

47
Q

Decreased SV associated with high HR (tachycardia) can limit? Then what happens with exercise?

A

so the increased sympathetic tone and venous return helps to mitigate this

48
Q

Summary of intrinsic mechanisms of cardiac regulation

A
49
Q

Summary of physiologic regulation of myocardial performance

A
50
Q

Question

A
51
Q

Question

A
52
Q

Question

A
53
Q

chronotropic effects means

A

time effects in this case HR

54
Q

Cardiac Function Curve AKA

A

Starling curve

55
Q

typical systole time

A

300 msec

56
Q

Typical diastole time

A

500 msec

57
Q

Cardiac cycle typical time

A

800 msec

58
Q

an increase in HR takes time from?

A

diastole which will decrease cardiac output

59
Q

Atrial pacing increase reduces

A

stroke volume

60
Q

Cardiac output to atrial pacing

A
61
Q

Tachycardia can _______ filling time and thereby can reduce _________ and _________.

A
  • stroke volume
  • limit cardiac output
62
Q

What is the principal control mechanism of HR?

A

Autonomic nervous system (extrinsic)

CVPR (93 decks)

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