Heart Physiology Flashcards

(71 cards)

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
cardiac muscle cells have a very long absolute refractory period which
prevents wave summation and tetany that would halt pumping action of heart
26
an electrocardiogram (ECG or EKG) is
a graphic recording of the electrical changes that accompany a heartbeat
27
a P wave is
a small unpward wave produced by depolarization of the atria following the spontaneous initiation of an action potential in the SA node
28
atrial contraction occurs
about .1 second after P wave begins
29
the QRS comples is produced when
the AV node fires and the ventricles depolarize as the impulse travels through the Purkinje fibers
30
complicated shape of the QRS complex is due to
the fact that the left ventricle is larger than the right ventricle and depolarizes at a slightly different rate
31
ventricle contraction occurs during
the S-T segment
32
atrial repolarization also occurs during the S-T segment but is
masked by depolarization of ventricles
33
a T wave is produced when
the ventricles repolarize before they start to relax
34
both atria contract (atrial systole) while
both ventricles relax (ventricular diastole)
35
both ventricles contrace (ventricular systole) while
both atria relax (atrial diastole)
36
heart sounds occur because of
blood turbulence while valves are closing
37
"lubb" sound of heartbeat occurs when
the AV valves are closing-soon after ventricular systole begins
38
"dupp" sound of heartbeat occurs when
the semilunar valves snap shut-at begining of ventricular diastole
39
ventricular filling occurs after
the AV valves open | -begins rapidly, slows down, finishes by time atrial systole occurs
40
end-diastolic colume (EDV) is
30 mL but only 30% is due to atrial systole
41
isovolumetric contraction occurs when
the ventricles start to contract but dont eject any blood because all 4 valves are closed
42
ventricular ejection occurs when
ventricular pressure increases enough to open the semilunar valves and force blood into the aorta and the pulmonary trunk
43
end-systolic volume (ESV)
after ventricular ejection is about 60 mL
44
isovolumetric relaxation occurs when
the ventricles start to relax but don't fill with blood because all 4 valves are closed
45
cardiac output (CO)
describes the volume of blood ejected from each ventricle each minute and it is calculated from stroke volume and heart rate
46
stroke volume (SV)
is the amount of blood ejected by each ventricle during ventricular systole (about 70 mL)
47
heart rate (HR)
averages 75 beats per minute
48
average cardiac output for a resting adult is
about 5.25 liters/minute
49
stroke volume is governed by three factors
1. preload 2. contractility 3. afterload
50
preload is
the degree to which cardiac muscle cells stretch just before they contract
51
increasing preload is
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
Frank-Sterling law of the heart
greater EDV will cause cardiac muscle to stretch more and generate greater contractile force
53
contractility is
the contractile force that gets developed for a particular preload
54
increasing contractility will
increase stroke volume
55
positive inotropic agents
increase contractility by making more calcium available, increases length of plateau and allows more contractile force to develop
56
negative inotropic agents
(potassium, calcium channel blockers) will produce contractility by reducing amount of calcium that gets released
57
afterload is
the pressure that is needed to open the semilunar valves
58
increasing afterload will
decrease stroke volume
59
heart rate is regulated by
the cardiac center in the medulla oblongata
60
autonomic nervous system doesn't
initiate a heartbeat, but it does modulate the heart rate
61
impulses transmitted along sympathetic cardiac accelerator nerves
release norepinephrine which binds to adrernergic receptors to increase heart rate and exert positive chronotropic effect
62
iimpulses transmitted along vagus nerve to heart
release acetylcholine which binds to cholinergic receptors to decrease heart rate and exert negative chronotropic effect
63
cardiac center receives input from
the cerebral cortex, limbic system, hypothalamus, and from various receptors in order to regulate heart rate
64
proprioceptors in muscles and joints
detect changes in physical activity
65
baroreceptors in the aorta and carotid arteries
monitor changes in blood pressure
66
chemoreceptors in the aorta, carotid arteries, and the medulla oblongata
monitor changes in blood pH, carbon dioxide, oxygen
67
certain chemicals in the body have chronotropic effects on heart rate
epinephrine and norepinephrine, caffeine, nicotine, calcium, potassium
68
epinephrine and norepinephrine
increase heart rate (positive agent)
69
caffeine and nicotine
increase heart rate
70
calcium
prolongs the plateau of a cardiac muscle action potential
71
potassium
reduces the strength of a cardiac muscle action potential by making myocardium less excitable