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Cardiovascular Phys Flashcards

1
Q

cardiac output

A

the volume of blood the heart pumps out per minute

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2
Q

what is CO at rest

A

5 L/min

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3
Q

what is CO at max exercise

A

25 L/min

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4
Q

how do you solve for CO/Q

A

HR * SV = Q

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5
Q

stroke volume

A

the amount of blood ejected in each beat

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6
Q

what is the variable that changes the most

A

stroke volume

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7
Q

what is stroke volume most affected by

A

exercise through
- blood flow
- blood volume
- vascular changes
- cardaic morphology (the shape of the heart)
- muscle function
- hormones
- nervous system

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8
Q

what is HR affected by

A

intrinsic and extrinsic factors

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9
Q

extrinsic factors affecting HR

A

hormones (+), PNS (-), SNS (+)

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10
Q

intrinsic control of HR

A

SA node, AV node, Perkinjie fibers, etc.

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11
Q

what normally changes before the other regarding cardiac output factors

A

SV normally changes before HR but the initial change will will cause the other variables to change as well

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12
Q

what is the role of the heart and how does blood keep flowing through the system

A

to pump blood into a closed system while pressure differences keep blood flowing throughout the system

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13
Q

what are the 3 factors that control the heart

A

central command
arterial baroreceptors
muscle metaboreceptors

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14
Q

central command

A

“feed forward system” explains that changes first occur w/ decrease in parasympathetic activity then sympathetic activity begins

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15
Q

arterial baroreceptors

A

pressure sensors in walls of carotid sinus and aortic arch
- sense levels of arterial pressure
- depending on situation can initiate vasodilation if BP increases

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16
Q

what is the primary short term controller of arterial pressure

A

arterial baroreceptors

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17
Q

role of muscle metaboreceptors

A
  • sense metabolic activity
  • capable of eliciting profound increase in sympathetic activity + arterial pressure
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18
Q

what does the muscle metaboreceptors do in response to change

A
  • senses Co2, pH (chemoreceptors), size of blood vessels (mechanoreceptors)
  • can increase HR, ventricular performance, CO, peripheral vasoconstriction, central blood volume mobilization
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19
Q

does each factor work independently in responding to changes?

A

yes, but they can also work together at some points
- rapid increase in HR can be due to central command, resistance of the arterial baroreflex, activation of skeletal muscle mechanoreceptors

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20
Q

preload

A

the degree of tension on the ventricle prior to contraction, related to the amount of blood in the ventricle

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21
Q

what causes increased tension and what is the outcome

A

more blood in ventricle = greater preload = more forceful contraction = increased SV and Q

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22
Q

afterload

A

resistance the heart must overcome in order to eject blood into systemic circulation

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23
Q

why is afterload important

A

increased BP or arterial pressure may lead to increased afterload which could result in myocardial hypertrophy and MI
- the pressure is too great to overcome so the ventricles get bigger in order to increase contraction strength

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24
Q

equation for SV

A

EDV- ESV

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25
EDV
end-diastolic volume - the amount of blood in the ventricles prior to contraction
26
ESV
end systolic volume - the amount of blood that remains in the ventricles after contraction
27
blood volume
change in hematocrit and or plasma
28
how does chronic training affect blood volume
it increases blood volume by about 15-20%
29
what is the normal blood volume in an untrained individual
80 ml/kg
30
what is the blood volume in a trained individual
90-100 ml/kg
31
how does the increased blood volume affect the cardiovascular system
increase preload, and also the efficienty of cardiovascular system - increase venour return which leads to greater Q increased BV = increased VR = increased preload = increase SV = increased Q
32
what are clinical concerns regarding blood and exercise
hypovolemia hypervolemia dehydration
33
hypovolemia
decreased BV = increased HR due to sympathetic tone like adrenaline
34
hypervolemia
increased BV = increased efficiency
35
dehydration and blood
decreased BV bv sweating takes fluid from blood = increased viscosity = increased HR
36
how does blood flow distribution get affected by exercise
blood flow focuses on areas of working tissue - heart always receives 4% of total flow - brain always has the same amount of blood flow (750ml/min)
37
how does plasma volume change throughout exercise
- plasma volume increases rapidly at first then begins to die down as time goes on - hematocrit doesn't actually change until about 2 weeks into exercise due to delayed response in kidneys to release EPO and for erythropoiesis to occur in the bones
38
explain the HR vs VO2 graph
- comparing a trained and untrained individual HR may be the same but VO2 is greater in the trained individual - this is due to the increased SV (probs larger heart) - HR * SV = Q if HR is the same then the only thing that changes is SV in order to have the larger Q
39
how is the parasympathetic tone used to detect issues within the heart
post exercise there should be immediate withdrawl of symptoms, if there is longer time to return to rest, then there may issues within the heart
40
concerns of heart transplant and HR during exercise
- heart transplant = so parasympathetic and sympathetic input - HR can only be affected via hormones - takes a while to return back to rest and more time to reach target HR
41
concerns with cardiac deinnervation and HR during exercise
- disruption of autonomic regulation - similar results to the heart transplant
42
training induced changes in HR
- increased sympathetic tone, increased AcH release at the heart - decreased sympathetic tone following exercise (can occur faster or just less in general, decreased release of adrenaline) - reduced sensitivity to catecholamines - changes in cardiac morphology
43
what are the types of changes in cardiac morphology
- myocardial hypertrophy - dilated cardiomyopathy
44
myocardial hypertrophy
- pathologic hypertrophy due to chronic high load of BP/BV - can cause MI - weight training induces similar effects but not super thick compared to when involved with high BP
45
dilated cardiomypoathy
- thinner myocardium, resulting in weaker walls that cant push as hard - "enlarged heart" - commonly seen after chemotherapy or alcoholic disorders
46
can myocardium regrow
no
47
how does training affect HR contractility
via frank starling mechanism
48
what is the frank starling mechanism
increase in preload = increase in Q and an increase in HR will increase contractility
49
how does an increase in HR increase contractility
via the Bodwitch effect - as HR increases there's less time for Ca2+ to be pumped out of the cells and they also enter cells at a faster rate - the remaining Ca2+ can be used for increased actin and myosin overlap = increase in contractility - increase in systolic phase with a decrease in diastolic phase
50
when is the frank starling mechanism good until
aroudn 160 bpm - SV is mazed out bc EDV cannot increase anymore bc there's not enough time to fill the chambers
51
what is the normal SV
60 - 100 mL/beat - Women 60 - Male 100
52
what is the normal exercise SV
100-140 mL/beat
53
what happens to SV during exercise
it doesnt change, but EDV and ESV decrease at the same rate to maintain the same SV
54
ejection fraction
percentage of blood ejected from the ventricles/beat into systemic circulation
55
at rest how much percent of the blood is ejected
50-70%
56
what happens to ejection fraction as exercise intensity increases
it will increase up to 80-85% - due to increase in contractility, increase in preload, decrease in afterload
57
what does a lower EF indicate
heart is struggling to pump blood - could be due to heart failure, result of chemotherapy (dilated cardiomyopathy)
58
what are signs of heart failure
fatigue, dyspnea, edemaca
59
cardiac index
CO/body surface area
60
why is cardiac index used
creates a standardized assessment of heart function
61
what is the normal value of CI
3.33
62
what is the best measure of the capacity of a cardiovascular system
whole body oxygen consumption
63
ficks equation
CO * AVoO2 diff = VO2
64
what does ficks equation tell us
- since AVO2 diff is a fixed value besides in males between age 18-22 CO is the main influence on VO2
65
what does the PV loop illustrate
how CO is related to ESV and EDV and how exercise shifts/changes the drawing
66
how does the PV loop change with heart disease
the loop gets smaller - this is due to decreases SV - decreased venous return = decreased preload (decreased EDV) - increased BP/arterial stiffness = increased afterload
67
how does the PV loop change with lower BP
loop gets shorter - decreased pressure in the ventricles, and decreased contractility
68
how does the pV loop change with exercerse
shifts towards the right (getting wider) - SV will have a slight increase in width due to increase in preload (increasing EDV)
69
how does the PV loop change with prolonged exercise
width would stay the same while shifting towards the y axis - decrease EDV and ESV rates keeps SV the same but less volume fills the chambers
70
cardiac contractility
as HR increases (frequency) there is also more force within each contraction - aided by sympathetic input like EPI and NE
71
how does BP respond to exercise
theres a linear increase in systolic BP during exercise
72
how much does the systolic BP increase by during exercise
8-12 mmHg for every 1 MET increase
73
1 MET
(metabolic equivalence) - the amount of energy required to keep someone alive in a laying position in a dark room
74
how is TPR affected by exercise
decreases bc vasodilation in working muscles = decreased resistance in the systemic circulation
75
what happens to diastolic BP during exercise
should remain relatively the same bc of the change in TPR it offsets the increase in CO
76
what affects arterial BP
(all increases) - Blood volume - heart rate - stroke volume - blood viscosity - Total peripheral resistance
77
what is the number 1 regulator of short term BV
renin-angiotensin - aldosterone system
78
what is the mechanism of the renin-angiotensin-aldosterone system
decrease BV = baroreceptors in kidney sense change = release of renin = combines with angiotensinogen = angiotensin I = combines with AVE (angiotensin converting enzyme) = angiotensin II = aldosterone release (fluid retention via sodium reabsorption) and vasoconstriction
79
what is the resting rate of blood flow
70mL/100 g of cardiac tissue
80
what is total cardiac blood flow
250 mL/min
81
what is O2 extraction in coronary blood flow
around 80%
82
what are the clinical conerns surrounding coronary blood flow
as heart size increases harder to supply blood everywhere = innerside of heart becoming hypoxic and ischemic
83
what is the primary driver of coronary blood flow
aortic pressure (since the coronary arteries branch off of the aorta)
84
what are controllable risk factors
things that can be affected by lifestyle
85
what are uncontrollable risk factors
genetics, things that cant be changed
86
hypoxia
- reduced oxygen supply to the tissues - can have normally blood flow just reduced O2 content
87
ischemia
- reduced ozygen supply accompanied by inadequate supply of nutrients or removal of waste - blood flow is reduced or absent due to a clot - can lead to necrosis
88
atherosclerosis
- hardening and narrowing of blood vessels - results in increased TPR
89
myocardial infarction
when coronary blood flow is reduced to a critical level
90
what are the types of MI
slow onset: ischemia or blockage slowly builds up sudden onset: plaque ruptures or sudden near complete blockage
91
what are the three areas of injury with MI
necrosis (tissue death) area of ischmeia (contractile function) secondary area of ischemia (depressed functions, the cells are still alive)
92
stable AMI/angina
reproduceable chest pain/tightness
93
unstable AMI/angina
not reproduceable, heart may randomly become hypoxic
94
how does aerobic exercise help heart blood flow
increases capillary density = better outcomes bc more passageways for blood flow

Ex Phys (12 decks)

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