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A&P 2 Lecture > Chapter 18 Part 1 (Lecture) [The Heart] > Flashcards

Chapter 18 Part 1 (Lecture) [The Heart] Flashcards

1
Q

The 2 Factors that Contribute to Cardiac Output

A
  • Heart Rate
  • Stroke Volume
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2
Q

Cardiac Output

A
  • Cardiovascular regulation is all about maintaining adequate blood flow to vital tissues.
  • Best indicator of peripheral blood flow.
  • It is the amount of blood pumped by the left ventricle in one minute.
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3
Q

The Calculation of Cardiac Output

A

CO= HR x SV

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4
Q

Heart Rate

A
  • Heart muscle contracts on its own
  • The heart is controlled indirectly by signals from the brain & by hormone, mostly in form of adjusting heart rate.
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5
Q

Stroke Volume

A

The amount of blood that leaves the ventricles in one pump.

SV= EDV-ESV

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6
Q

Systole

A
  • Contraction
  • The chamber contracts & pushes blood into an adjacent chamber.
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7
Q

Diastole

A
  • Relaxation
  • The chamber relaxes & fills with blood.
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8
Q

Sinoatrial (SA) Node

A
  • Each heart beat begins with an action potential from this node.
  • This is also known as the “pacemaker”
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9
Q

Atrioventricular (AV) Node

A
  • Contaisn pacemaker cells, but does not generally affect heart rate.
  • Can take over for SA node if it fails, though it only generates beats at 40-60 beats a second.
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10
Q

Can you survive with damage to SA node?

A

Yes, the AV node takes over but it results in a slower heart rate.

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11
Q

Properties Unique to Cardiac Muscle

A
  • Intercalated Discs
  • Branched
  • 1-2 nuclei
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12
Q

Why does cardiac muscle need to be richly supplied with capillaries?

A
  • High neeed for O2
  • Highly active
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13
Q

What is the importance of the intercalated discs and gap junctions?

A

Spread depolarization rapidly

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14
Q

Why is the heart in such a confined space in the chest? What are the advantages? What are the disadvantages?

A
  • Small space for protection.
  • Disadvantage: In the case of an accident the space can become even smaller, not allowing the heart to function fully.
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15
Q

Flow of Blood

A
  1. Right Atrium
  2. Tricuspid (Right AV) Valve
  3. Right Ventricle
  4. Pulmonic (Semilunar) Valve
  5. Lungs
  6. Left Atrium
  7. Bicuspid (Left AV) Valve
  8. Left Ventricle
  9. Arotic (Semilunar) Valve
  10. Body
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16
Q

Why is the wall of the left ventricle thicker than the wall of the right ventricle?

A

The left ventricle pumps to the body, so it needs more power (thicker muscles)

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17
Q

Steps of the Cardiac Cycle

A
  1. Atrial Systole
  2. Isovolumetric Contraction
  3. Ventricular Ejection
  4. Isovolumetric Relaxation
  5. Ventricular Filling
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18
Q

Atrial Systole

A
  • AV valves
    • Open
  • Semilunar valves
    • Closed
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19
Q

Isovolumetric Contraction

A
  • AV Valves
    • Closed
  • Semilunar Valves
    • Closed
20
Q

Ventricular Ejection

A
  • AV Valves
    • Closed
  • Semilunar Valves
    • Open
21
Q

Isovolumetric Relaxation

A
  • AV Valves
    • Closed
  • Semilunar Vlaves
    • Closed
22
Q

Ventricular Filling

A
  • AV Valves
    • Open
  • Semilunar Valves
    • Closed
23
Q

Sounds of the Heart

A
  • S1 (Lubb)
  • S2 (Dubb)
  • S3
  • S4
24
Q

S1

A
  • Lubb
  • Start of ventricular contraction, produced when the AV valves close
25
Q

S2

A
  • Dubb
  • End of ventricular contraction, produced when semilunar valves close
26
Q

S3

A

Very faint, sound of blood flowing into ventricles

27
Q

S4

A

Very faint, sound of atrial contraction

28
Q

Internodal Pathways

A

Conduct APs to atria as it continues toward the ventricles.

29
Q

AV Bundle & Branches

A

Connection between atria & ventricles, also inervates the ventricles

30
Q

Purkinje Fibers

A

Final link in network, responsible for depolarization of ventricluar muscle cells & trigger ventricular systole

31
Q

Steps of Cardiac Muscle Stimulation

A
  • Rapid Depolarization
  • Plateau
  • Repolarization
32
Q

Rapid Depolarization

A
  • Similar to that in skeletal muscle fiber
  • When threshold of -70mV is reached, fast sodium channels open to allow a massive & quick influx of sodium
  • This causes sarcolemma to depolarize
33
Q

Plateau

A
  • Membrane Potential stays near 0mV
  • As the membrane approaches 30 mV, sodium gates close
  • However, voltage-gated slow calcium channels open
  • The release of Ca ions balance the loss of Na ions, & the membrane potential stays near 0Mv
  • This is to protract the contraction (lasts about 175 milliseconds)
34
Q

Repolarization

A

Ca channels will begin closing, slow K channels open to bring muscel back to resting potential.

35
Q

Advantage of longer contractions?

A

Pump as much blood as possible out of the ventrcle.

36
Q

To slow heart rate

A
  • Parasympathetic neurons open K channels in plasma membrane
  • Thus, the membrane takes longer to reach threshold, thereby slowing heart rate
37
Q

To increase heart rate

A
  • Norepinephrine binds to beta-1 receptors
  • This leads to opening of ion channels that increase rate of depolarization thereby increasing rate
38
Q

End-Diastolic Volume (EDV)

A

Amount of blood in ventricle after diastole

39
Q

End-Systolic Volume (ESV)

A

Blood left in ventricle after systole

40
Q

Venous Return

A
  • Amount of venous blood delivered to the heart each minute
  • Factors: blood volume, muscular activity & rate of blood flow through peripheral capillaries
  • When blood volume goes down, venous return reduces
  • When skeletal muscle contract & compress adjacent veins, peripheral tissues increase activity, venous return increases
41
Q

Filling Time

A
  • The duration of ventricular diastole
  • If venous return remains constant, slowing heart rate increases EDV
  • Increasing heart rate decreases EDV
42
Q

Preload

A
  • The amount of myocardial stretching
  • The greater the EDV, thew greater the preload
  • If EDV is very small, the sarcomeres are too short to develop much power
  • As EDV increases, then sarcomeres reach optimum length leading to more powerful & efficient contractions
  • Greater EDV= greater stroke voume
43
Q

Contractility

A
  • The amount of force during a contraction at a given amount of preload
  • Sympathetic stimulation increases contractility (epinephrine, thyroid hormones, glucagon)
  • Beta blockers reduce contracility
44
Q

Afterload

A
  • The amount of tension the contracting ventricle must produce to force open the semilunar valve and eject blood
  • As afterload increases, stroke volume decreases
  • The greater the afterload, the longer the period of isovolumetric contraction, the shorter the period of ventricular ejection, & thus the larger the ESV
  • Afterload is increased by any factor that restricts blood flow through the arterial system
45
Q

Factors that Affect Heart Rate

A
  • Sympathetic Stimulation/parasympathetic stimulation
  • Rising body temp. will increase heart rate
  • Lowering body temp. will decrease heart rate
  • Many hormones increase heart rate (epinephrine & thyroxine)
46
Q

Comparing & Contrasting Skeletal & cardiac Muscle Contractions

A
  • Cardiac twitch lasts longer, Ca ions continue to enter for extended period
  • Thus period of active muscle contraction is longer
  • The refactory period of cardiac continues until relaxation is well underway
  • This prevents summation from occuring & thus tetany is impossible

A&P 2 Lecture (7 decks)

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