Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular, Pulmonary, and Hepatic Physiology > Cardiac Cycle and Cardiac Output > Flashcards

Cardiac Cycle and Cardiac Output Flashcards

1
Q

what is the cardiac cycle?

A

a single cardiac cycle includes all events associated with one heartbeat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe the atria and ventricles during the cardiac cycle

A

atria and ventricles alternately contract and relax, forcing blood from area of high pressure to areas of low pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what happens as a chamber of the heart contracts?

A

the pressure within that chamber increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

compare and contrast the pressure, expelled blood volume, and pumping pattern on the right side of the heart compared to the left side of the heart

A
  1. pressure on right side of heart is much lower compared to the left side
  2. each ventricle expels the same volume of blood per beat
  3. the same pattern exists for both pumping chambers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how long does the cardiac cycle last when the heart rate is 75 bpm?

A

0.8 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how long does atrial systole contract?

A

about 0.1 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

decribe the ventricles during atrial systole

A

ventricles relaxed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what causes atrial depolarization and what does this look like on a EKG?

A

depolarization of the SA node, is the P wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what causes atrial systole?

A

atrial depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what happens as atria contract? (2)

A
  1. as atria contract, they exert pressure on blood within
  2. this forces blood through open AV valves into the ventricles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does atrial systole contribute to the ventricles?

A

atrial systole contributes the final volume of blood (25mL) to the blood volume already in the ventricles (120ml) for the overall 130mL in the ventricles at the end of systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the end of atrial systole also?

A

end of atrial systole is also the end of ventricular diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is end-diastolic volume? (EDV)

A

the amount of blood in each ventricle as the end of diastole (130mL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what on an EKG marks the onset of ventricular depolarization/systole?

A

QRS complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how long does ventricular systole last and what is happening?

A

lasts about 0.3 seconds; ventricles are contracting and atria are relaxed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what happens to AV valves as ventricular systole begins?

A

pressure rises inside ventricles and pushes blood up against AV valves, forcing them shut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the period of isovolumetric contraction?

A

for about 0.05 seconds at the end of ventricular systole, both SL and AV valves are closed; ventricular volume remains the same

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

why is isovolumetric contraction also called isovolumetric muscle contraction?

A

because cardiac muscle fibers are contracting and exerting force, but not shortening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does the continued contraction of ventricles cause?

A

pressure inside chambers to rise sharply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

when do both SL valves open?

A

when L ventricular pressure surpasses aortic pressure and R ventricular pressure rises above pulmonary trunk pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is aortic pressure?

A

about 80 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is pulmonary trunk pressure?

A

about 20 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what happens after the aortic and pulmonary trunk pressure is surpassed and both SL valves open?

A

ejection of blood begins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is ventricular ejection? how long does it last?

A

the period when SL valves are open, lasts about 0.25 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what happens in the ventricles during ventricular ejection

A

pressure in both ventricles continues to rise
L ventricle rises to about 120 mmHg
R ventricle rises to about 30 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how muhc blood does the L ventricle eject into the aortia during ventricular systole?

A

about 70 mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is end systolic volume?

A

the remaining volume of blood left in each ventricle at the end of systole; about 60 mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is stroke volume?

A

the volume ejected per beat from each ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how do you calculate stroke volume?

A

stroke volume = end diastolic volume - end systolic volume
(SV = EDV - ESV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is stroke volume at rest?

A

about 70mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what marks the onset of ventricular repolarization on EKG?

A

the T wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the relaxation period? how long does it last?

A

when atria and ventricles are both relaxed; lasts about 0.4 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what happens as heart beats faster to relaxation period and atrial and ventricular systole?

A

as heart beats faster, relaxation period becomes shorter, while atrial and ventricular systole shorten only slightly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what causes diastole?

A

ventricular repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what happens as the ventricles relax?

A

pressure within the ventricles falls, and blood in the aorta and pulmonary trunk begin to flow back towards lower pressure in the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what causes the SL valves to close?

A

blood catches the cusps of the SL valves when flowing back into the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

at what pressure does the aortic valve close?

A

about 100 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what does the dicrrotic wave on the aortic pressure curve represent?

A

the rebound of blood off closed cusps of aortic valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is isovolumetric relaxation?

A

the brief interval after SL valves close when ventricular blood volume does not change because all 4 valves are closed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what happens to the ventricles during isovolumetric relaxation and what is the result?

A

ventricles continue to relax and pressure falls quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what happens when ventricular pressure drops below atrial pressure?

A

AV valves open and ventricular filling begins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

when does a majority of ventricular filling occur?

A

just after AV valves open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what happens to the blood that has been flowing into/building up in the atria during ventricular systole when the Av valves open?

A

rushes rapidly into ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

at the end of relaxation period, how full are the ventricles?

A

about 3/4 full

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what happens on an EKG after the relaxation period and what does this signal?

A

P wave appears signaling beginning of another cardiac cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is cardiac output?

A

the volume of blood ejected from the L or R ventricle into aorta or pulmonary trunk each MINUTE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

how is cardiac output calculated?

A

cardiac output (mL/min) = stroke volume (mL/beat) x HR (beats/min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what does cardiac output represent and what is it close to?

A

is close to the total blood volume, so cardiac output represents/ shows that your entire blood volume flows through tthe pulmonary and systemic circulation each minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what normally increases caardiac output?

A

factors that increase stroke volume or heart rate, like exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is cardiac reserve?

A

the difference between a persons max cardiac output and cardiac output at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

compare an average persons cardiac reserve to their resting value

A

the average person has a cardiac reserve 4-5x their resting cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

compare endurance athlete’s max cardiac reserve to their resting cardiac output

A

has a cardiac reserve 7-8x that of resting CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

describe the cardiac reserve of people with severe heart disease

A

may have little to no cardiac reverse; limits simple daily tasks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what happens to stroke volume if more blood returns to the heart during diastole?

A

more blood is ejected during the next systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

describe SV, EDV, and ESv at rest

A

at rest SV is 40-50% of EDV because 40-50% of blood remains in ventricles after each contraction (ESV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what are the 3 factors that regulate stroke volume and ensure that L and R ventricles pump equal volumes of blood? describe

A
  1. preload: the degree of stretch of heart before it contracts
  2. contractility: forcefulness of contraction of individual ventricular muscle fibers
  3. afterload: pressure that must be exceeded before ejection of blood from ventricles can occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what does a greater degree of preload do to muscle fibers?

A

a greater stretch on cardiac muscle fibers prior to contraction increases their force of contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is the frank-starling law?

A

within limits, the more the heart fills with blood during diastole, the greater the forces of contraction during systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is preload proportional to?

A

preload is proportional to EDV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

generally, the greater the EDV, what happens to the next contraction?

A

the greater the EDV, the more forceful the next contraction

61
Q

what 2 key factors determine EDV?

A
  1. duration of ventricular diastole
  2. venous return to R ventricle
62
Q

what 2 things can happen as HR increases in terms of EDV?

A
  1. duration of diastole is shorter and less filling time means smaller EDV so ventricles may contract before adequately filled
  2. when venous return increases, a greater volume of blood flows into ventricles, so EDV may increase
63
Q

when happens to SV when HR exceeds 160 bpm and why?

A

SV typically declines because of short filling time

64
Q

what happens to EDV preload as a result of rapid heart rate?

A

EDV is reduced and preload is lower

65
Q

describe the resting SV of people with slow resting HR and why; include preload in your answer

A

people with slow resting HR usually have large resting SV because filling time is prolonged and preload is larger

66
Q

what does the frank-starling law do?

A

equalized the output of R and L ventricles and keeps the same volume of blood flowing to both systemic and pulmonary circulations

67
Q

according to the frank-starling law, what happens if the L side of the heart pumps a little more blood then the R side?

A

then the volume of blood returning to the R ventricle (venous return) will also increase

68
Q

how does the frank-starling law work?

A

increased EDV causes least full ventricle to contract forcefully on the next beat, bringing both sides back into balance

69
Q

what is contractility?

A

the strength of contraction at any given preload

70
Q

what 2 factors affect stroke volume?

A

exercise and contractility

71
Q

what are positive inotropic agents?

A

substances that increase contractility

72
Q

for a constant preload, what happens to stroke volume when a positive inotropic agent is present?

A

stroke volume increases

73
Q

what do positive inotropic agents usually do to increase contractility?

A

promote Ca2+ inflow during cardiac AP’s, which strengthens the force of the enxt contraction

74
Q

what 3 things have positive inotropic effects?

A
  1. stimulation of the sympathetic division of the autnonomic nervous system hormones such as epinephrine and norepinephrine
    2.increase of Ca2+ levels in interstitial fluid
  2. the drug digitalis
75
Q

where is the drug digitalis extracted from?

A

the foxglove plant

76
Q

what is the active agent in digitalis? what does it do?

A

digoxin; inhibits Na+/K+ ATPase pumps and causes a rise in intracellular [Na+], so Na+ is not flowing out as much and the concentration gradient decrease across the cell membrane; this slows down the Na+/Ca2+ antiport (which usually brings Na+ in and pushes Ca2+ out), which means there is more Ca2+ remainingin cardiac muscle cells to increase contractility

77
Q

what are negative inotropic agents?

A

substances that decrease contractility

78
Q

what 5 things have negative inotropic effects?

A
  1. inhibition of sympathetic ANS
  2. anoxia
  3. acidosis
  4. some anaesthetics
  5. increases K+ levels in interstitial fluid
79
Q

what is anoxia and how does it have negative inotropic effects?

A

reallow low O2; interferes with Na+ channels

80
Q

how does high K+ have negative inotropic effects?

A

interferes with/blocks Na+ channels, slowing depolarization

81
Q

what is afterload?

A

the pressure that must be overcome before the SL valves can open

82
Q

when does ejection of blood from the heart begin?

A

when pressure in the R ventricle exceeds pressure in pulmonary trunk (approx 20mmHg) and when pressure in L ventricle exceeds pressure in aorta (approx 80mmHg) and the higher pressure in the ventricles can push open SL valves

83
Q

what does and increase in afterload cause? what is the result?

A

increases in afterload cause stroke volume to decrease, so more blood remains in the ventricles at the end of systole

84
Q

what 2 conditions can increase afterload?

A
  1. hypertension (electaed blood pressure)
  2. narrowing of arteries by atherosclerosis
85
Q

what is congestive heart failure?

A

loss of pumping efficiency by heart

86
Q

give 5 causes of congestive heart failure

A
  1. CAD
  2. congenital defects
  3. long term high blood pressure (increases afterload)
  4. MI (regions of dead heart tissue)
  5. valve disorders
87
Q

what happens as the pumping of the heart becomes less effective in congestive heart failure? (2)

A
  1. more blood remains in ventricles at the end of each cycle
  2. gradually EDV (preload) increases
88
Q

what happens initially in cingestive heart failure due to the Frank Starling law?

A

initialy, increased prelaod may promote increased force of contraction

89
Q

describe the potentially lethal feedback loop of congestive heart failure

A

as preload increases further, the heart is overstretched and contracts less forcefully, and the less effective pumping leads to even lower pumping capability

90
Q

what is the result of congestive heart failure?

A

one side of the heart usually fails before the other

91
Q

what happens if the left ventricle fails first in congestive heart failure?

A

the heart can’t pump out all the blood it receives and as a result, blood backs up in the lungs and causes pulmonary edema

92
Q

what is pulmonary edema?

A

fluid accumulation in the lungs that can cause suffocation if untreated

93
Q

what happens if the right ventricle fails first in congestive heart failure?

A

blood backs up in systemic ceins and over time the kidneys cause increase in blood volume resulting in peripheral edema noticeable in the feet and ankles

94
Q

what does cardiac output depend on? (2)

A
  1. heart rate
  2. stroke volume
95
Q

what is important in short term control of cardiac output and blood pressure?

A

adjustments in heart rate

96
Q

what happens in terms of cardiac output and why during exercise?

A

cardiac output increases to supply working muscles and other tissues with oxygen and nutrients

97
Q

if the ventricular myocardium is damaged or if blood volume is reduced by bleeding, what may happen to stroke volume?

A

stroke volume may fall

98
Q

in cases of exercise or decreased stroke volume, how do homeostatic mechanisms maintain adequate cardiac output? (2)

A
  1. increasing heart rate
  2. increase heart contractility
99
Q

what are the 2 (of many) most important factors that contribute to heart rate regulation?

A
  1. ANS (sympathetic and parasympathetic)
  2. hormones released by adrenal medulla
100
Q

where does nervous system regulation of the heart originate?

A

in the cardiovascular center of the medulla oblongata

101
Q

what is the medulla oblongata?

A

a region of the brain stem that receives input from various sensory receptors and from the higher brain centers like the limbic system and the cerebral cortex

102
Q

describe what the limbic system and cerebral cortex do

A

limbic system: emotional brain
cerebral cortex: analytical and logical

103
Q

how does the cardiovascular center of the brain direct appropriate output?

A

by increasing or decreasing frequency of nerve impulses in sympathetic and parasympathetic branchers of ANS

104
Q

why does your heart rate rise before physical activity begins in competitive situations?

A

limbic system sends nerve impulses to CV center

105
Q

what takes over from the limbic system during exercise to keep heart rate up?

A

proprioceptors send nerve impulses at increased frequency to cardiovascular center

106
Q

what ia a major stimulus for the fast increase in heart rate that occurs a the onset of exercise?

A

proprioceptor input

107
Q

other than proprioceptors, what 2 other receptors send provide input to the cardiovascular center?

A
  1. chemoreceptors
  2. baroreceptors
108
Q

where are important baroreceptors located? what do they do?

A

in the arch of the aorta and carotid arteries; detect changes in blood pressure and provide input to the cardiovascular center when it changed

109
Q

what are the 4 E situations that increase sympathetic ANS stimulation?

A
  1. Excitement
  2. Emergency
  3. Exericse
  4. Embarassment
110
Q

where do sympathetic neurons extend?

A

from the medulla into the spinal cord

111
Q

what are the sympathetic neurons that extend from the thoracic region of the spinal cord called?

A

called cardiac accelerator nerves

112
Q

where do cardiac accelerator sympathetic nerves extend to? (3)

A
  1. SA node
  2. AV node
  3. most portions of myocardium
113
Q

what do impulses in cardiac accelerator nerves trigger?

A

release of norepinephrine that binds to beta-1 receptors on cardiac muscle fibers

114
Q

what are the 2 effects of release of norepinephrine that binds to beta-1 receptors on cardiac muscle fibers?

A
  1. speeds rate of spontaneous depolarization in SA and AV nodes cause the pacemaker to fire more rapidly so HR increases
  2. in contractile fibers, enhanced Ca2+ entry through voltage-gated slow Ca2+ so contractility increases
115
Q

why does a moderate increase in heart rate not cause stroke volume to decline?

A

the increased contractility offsets the decreased preload

116
Q

under maximal sympathetic stimulation, what can HR reach in a young adult?

A

220 bpm

117
Q

how do you calculate max heart rate?

A

220-age

118
Q

what happens to stroke volume at max heart rate and why?

A

stroke volume decreases because of reduced filling time

119
Q

what does max heart rate decline with?

A

age

120
Q

how do parasympathetic nerve impulses reach the heart?

A

by L and R vagus nerve

121
Q

where do vagal axon terminals terminate? (3)

A
  1. SA node
  2. AV node
  3. some in atrial myocardium
122
Q

how do vagal axon terminal contribute to autonomic regulation of the heart rate?(3)

A
  1. release acetylcholine which decreases the HR by slowing the rate of spontaneous depolarization in autorhythmic fibers
  2. acetylcholine increases permeability of fiber membranes to potassium ions
  3. this causes hyperpolarization of cell
123
Q

describe the balance of atunomic regulation of HR

A

continually shifting balance between sympathetic and parasympathetuc stimulation of the heart

124
Q

at rest, what part of the ANS dominates?

A

parasympathetic

125
Q

what 3 things are involved in chemical regulation of the heart rate?

A
  1. hypoxia, acidosis, alkalosis
  2. hormones
  3. ionic imbalances
126
Q

how do hypoxia, acidosis, and alkalosis chemically regulate the heart rate?

A

all depress cardiac activity

127
Q

what hormones are involved in chemical regulation of HR and where do they come from?

A

epinephrine and norepinephrine from the adrenal medulla

128
Q

what do epinephrine and norepinephrine do to HR and contractility?

A

increase HR and contractility

129
Q

what 3 things can cause the adrenal medulla to release more hormones? (epi and norepi)

A
  1. exercise
  2. stress
  3. excitement
130
Q

what do thyroid hormones do to contractility and HR?

A

thyroid hormones enhance contractility and increase HR

131
Q

what is a sign of hyperthyroidism?

A

tachycardia

132
Q

how is the thyroid gland involved in chemical regulation of HR?

A

involved in overall metabolsim; affects receptors for epinephrine and norepinephrine and more receptors means more availability and a greater effect on the heart

133
Q

what do ionic imbalances do?

A

can compromise the pumping effectiveness of the heart

134
Q

what 3 ions in particular have large effects on the heart?

A
  1. K+
  2. Ca2+
  3. Na+
135
Q

what do elevated blood concentrations of K+ or Na+ do to heart rate and contractility?

A

elevated blood concentrations of K+ or Na+ decrease HR and contractility

136
Q

how does elevated blood concentrations of Na+ decrease contractility?

A

excess Na+ blocks Ca2+ infow during cardiac action potential, decreasing the force of contraction

137
Q

how does elevated blood concentrations of K+ slow heart rate?

A

excess K+ blocks generation of action potential due to hyperpolarization making it hardder for the cell to reach the threshold to generate an action potential

138
Q

what does a moderate increase in intersitital Ca2+, and therefor intracellular Ca2+ do to HR and contractility?

A

speeds HR and strengthens HR (increases contractility)

139
Q

what is high Na+ called?

A

hypernatremia

140
Q

what is high K+ called?

A

hyperkalemia

141
Q

what is high Ca2+ called?

A

hypercalcemia

142
Q

other than chemical regulation and ANS, give 4 factors in HR regulation

A
  1. age
  2. gender
  3. fitness
  4. body temperature
143
Q

what is a newborn baby’s avg resting HR and why?

A

high, around 120 due to high metabolic rate and more sympathetic influence because have to grow a lot and real fast

144
Q

why do adult females tend to have slightly higher resting heart rates than men?

A

females tend to have smaller hearts that have to beat faster

145
Q

in a physically fit person, what can occur and why?

A

bradycardia (below 50bpm) because a slowly beating heart is more efficient

146
Q

what does increased body temp do to HR and how?

A

increases heart rate because a higher temperature causes the SA node to discharge more quickly in an attempt to move blood and heat to the periphery away from the core

147
Q

what does a decreased body temp dp to HR and contractility?

A

decreased body temp decreases HR and contractility because trying to keep the core warm

148
Q

what is done to a person’s HR during heart surgery and why?

A

slow HR by hypothermia to slow metabolism to reduce the O2 need of tissues

Cardiovascular, Pulmonary, and Hepatic Physiology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions