Heart Physiology Flashcards

1
Q

cardiac muscle has

A

short, thick branching cells (fibers), each one with one central nucleus

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2
Q

sarcoplasmic reticulum is

A

less developed that in skeletal muscle, but contains larger T-tubes to admit more calcium ions from extracellular fluid

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3
Q

cardiac muscle fibers are

A

joined end to end by intercalated discs

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4
Q

desmosomes

A

hold muscle fibers together

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5
Q

gap junctions allow

A

action potentials to spread from one cardiac fiber to the next fiber

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6
Q

cardiac muscle contains more ___________ than skeletal muscle

A

myoglobin and more mitochondria than skeletal muscle

-because it utilizes aerobic respiration almost exclusively it is less prone to fatigue

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7
Q

cardiac muscle fibers are autorhythmic and can

A

depolarize automatically to generate action potentials

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8
Q

excitation of cardiac muscle begins in

A

the sinoatrial (SA) node

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9
Q

SA node is located

A

in the right wall of the atrium just below the opening from the superior vena cava

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10
Q

SA node functions as

A

a pacemaker of the heart to initiate each heartbeat and set sinus rythym for entire heart

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11
Q

cardiac action potential spreads from

A

SA node throughout both atria by way of gap junctions which causes both atria to contract simultaneously

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12
Q

the nerve siglnal spreads to the

A

atrioventricular (AV) node in the interatrial septum

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13
Q

`as the nerve signal passes through the AV node there is a

A

brief time delay (0.1 second)

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14
Q

The nerve signal passes into the atriocentricular bundle (bundle of His), which is

A

a tract of conducting fibers that is only electrical connection between atria and the ventricles

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15
Q

the atrioventricular bundle divides into

A

right and left bundle branches, which carry the nerve signal along either side of the interventricular septum toward the heart’s apex

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16
Q

Large diameter conduction myofibers (Purkinje fibers) conduct

A

the nerve signal from the bundle branches into the ventricular myocardium

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17
Q

cells in the SA node gradually

A

depolarize due to slow inflow of sodium ions and minimal outflow of potassium ions, generating a pacemaker potential

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18
Q

when this pacemaker potential reaches its threshold of

A
  • 40 mV,voltage regulated “fast calcium channels”open and calcium ions rush in to trigger action potential
  • the influx of calcium is what produces the action potential
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19
Q

when nerve signal has concluded

A

pacemaker potential starts over to produce next heartbeat

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20
Q

it takes about 50 milliseconds for the nerve signal to reach the

A

AV node wher it is momentarily delayed to allow the ventricles to fill prior to contracting

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21
Q

signals travel fastest through

A

the Av bundle and the Purkinje fibers and trigger the myocardial contractions that begin at the apex of the heart

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22
Q

cardiac muscle cells depolarize

A

very rapidly because voltage-regulated Na+ channels open and close very quickly

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23
Q

voltage-regulated calcium channels open and close

A

slowly to admit calcium ions, prolongs depolarization and creates a plateau when muscle cells contract

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24
Q

voltage-regulated potassium channels open and

A

potassium ions rush out which returns membrane resting potential

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25
Q

cardiac muscle cells have a very long absolute refractory period which

A

prevents wave summation and tetany that would halt pumping action of heart

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26
Q

an electrocardiogram (ECG or EKG) is

A

a graphic recording of the electrical changes that accompany a heartbeat

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27
Q

a P wave is

A

a small unpward wave produced by depolarization of the atria following the spontaneous initiation of an action potential in the SA node

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28
Q

atrial contraction occurs

A

about .1 second after P wave begins

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29
Q

the QRS comples is produced when

A

the AV node fires and the ventricles depolarize as the impulse travels through the Purkinje fibers

30
Q

complicated shape of the QRS complex is due to

A

the fact that the left ventricle is larger than the right ventricle and depolarizes at a slightly different rate

31
Q

ventricle contraction occurs during

A

the S-T segment

32
Q

atrial repolarization also occurs during the S-T segment but is

A

masked by depolarization of ventricles

33
Q

a T wave is produced when

A

the ventricles repolarize before they start to relax

34
Q

both atria contract (atrial systole) while

A

both ventricles relax (ventricular diastole)

35
Q

both ventricles contrace (ventricular systole) while

A

both atria relax (atrial diastole)

36
Q

heart sounds occur because of

A

blood turbulence while valves are closing

37
Q

“lubb” sound of heartbeat occurs when

A

the AV valves are closing-soon after ventricular systole begins

38
Q

“dupp” sound of heartbeat occurs when

A

the semilunar valves snap shut-at begining of ventricular diastole

39
Q

ventricular filling occurs after

A

the AV valves open

-begins rapidly, slows down, finishes by time atrial systole occurs

40
Q

end-diastolic colume (EDV) is

A

30 mL but only 30% is due to atrial systole

41
Q

isovolumetric contraction occurs when

A

the ventricles start to contract but dont eject any blood because all 4 valves are closed

42
Q

ventricular ejection occurs when

A

ventricular pressure increases enough to open the semilunar valves and force blood into the aorta and the pulmonary trunk

43
Q

end-systolic volume (ESV)

A

after ventricular ejection is about 60 mL

44
Q

isovolumetric relaxation occurs when

A

the ventricles start to relax but don’t fill with blood because all 4 valves are closed

45
Q

cardiac output (CO)

A

describes the volume of blood ejected from each ventricle each minute and it is calculated from stroke volume and heart rate

46
Q

stroke volume (SV)

A

is the amount of blood ejected by each ventricle during ventricular systole (about 70 mL)

47
Q

heart rate (HR)

A

averages 75 beats per minute

48
Q

average cardiac output for a resting adult is

A

about 5.25 liters/minute

49
Q

stroke volume is governed by three factors

A
  1. preload
  2. contractility
  3. afterload
50
Q

preload is

A

the degree to which cardiac muscle cells stretch just before they contract

51
Q

increasing preload is

A

anything that increases volume of blood that returns to heart (i.e. slow HR) or speed with which blood returns to heart will increase pre-load

52
Q

Frank-Sterling law of the heart

A

greater EDV will cause cardiac muscle to stretch more and generate greater contractile force

53
Q

contractility is

A

the contractile force that gets developed for a particular preload

54
Q

increasing contractility will

A

increase stroke volume

55
Q

positive inotropic agents

A

increase contractility by making more calcium available, increases length of plateau and allows more contractile force to develop

56
Q

negative inotropic agents

A

(potassium, calcium channel blockers) will produce contractility by reducing amount of calcium that gets released

57
Q

afterload is

A

the pressure that is needed to open the semilunar valves

58
Q

increasing afterload will

A

decrease stroke volume

59
Q

heart rate is regulated by

A

the cardiac center in the medulla oblongata

60
Q

autonomic nervous system doesn’t

A

initiate a heartbeat, but it does modulate the heart rate

61
Q

impulses transmitted along sympathetic cardiac accelerator nerves

A

release norepinephrine which binds to adrernergic receptors to increase heart rate and exert positive chronotropic effect

62
Q

iimpulses transmitted along vagus nerve to heart

A

release acetylcholine which binds to cholinergic receptors to decrease heart rate and exert negative chronotropic effect

63
Q

cardiac center receives input from

A

the cerebral cortex, limbic system, hypothalamus, and from various receptors in order to regulate heart rate

64
Q

proprioceptors in muscles and joints

A

detect changes in physical activity

65
Q

baroreceptors in the aorta and carotid arteries

A

monitor changes in blood pressure

66
Q

chemoreceptors in the aorta, carotid arteries, and the medulla oblongata

A

monitor changes in blood pH, carbon dioxide, oxygen

67
Q

certain chemicals in the body have chronotropic effects on heart rate

A

epinephrine and norepinephrine, caffeine, nicotine, calcium, potassium

68
Q

epinephrine and norepinephrine

A

increase heart rate (positive agent)

69
Q

caffeine and nicotine

A

increase heart rate

70
Q

calcium

A

prolongs the plateau of a cardiac muscle action potential

71
Q

potassium

A

reduces the strength of a cardiac muscle action potential by making myocardium less excitable