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Kin 426 > 5.3: Cardiac Output Regulation > Flashcards

5.3: Cardiac Output Regulation Flashcards

1
Q

cardiac output (CO) definition

A

the total flow of blood out of the left ventricle

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2
Q

cardiac output could be measured in the aorta, except

A

for that a portion of the total output that flows to the heart itself via coronary circulation

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3
Q

cardiac output is the total flow available

A

to perfuse all the tissues of the body (includes coronary circulation: heart)

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4
Q

cardiac output must be able to increase substantially in order to

A

meet the metabolic demands of the body, and maintain arterial pressure

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5
Q

during severe exercise cardiac output

A

can increase 4-to-5 fold

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6
Q

CO increase of 4-to-5 fold during severe exercise is accomplished by

A

increases in heart rate (up to 3-fold, in young adults) and increases in SV (up to 1.5 fold)

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7
Q

what contributes more to CO increases

A

HR
SV contribution is important but not as much as HR

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8
Q

in severe exercise, this increase in CO enables

A

an increase in overall O2 consumption of approximately 12 times

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9
Q

what is CO essential to maintain

A

the mean arterial pressure

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10
Q

Why is the increase in CO essential to maintain mean arterial pressure

A

because total peripheral resistance during exercise decreases to as little as one-third the resting value

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11
Q

what are required to produce the increased cardiac output

A

changes in both the heart and systemic vasculature

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12
Q

why is BP a great measure of cardiac function during exercise

A

if CO doesnt increase BP will decrease
If CO is too increased, BP will drop or not increase

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13
Q

if TPR is not normal and increases

A

then CO must increase greater than that increase

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14
Q

cardiac factors controlling cardiac output

A

heart rate and myocardial contractility

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15
Q

coupling factors controlling cardiac output

A

preload and afterload

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16
Q

what are the cardiac factors (heart rate and myocardial contractility) characteristics of

A

the cardiac tissues, although they are modulated by various neural and humoral mechanisms

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17
Q

why are preload and afterload designated as coupling factors

A

because they constitute a functional coupling between the heart and blood vessels (connections to heart that will affect heart)

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18
Q

to understand the regulation of cardiac output, one must appreciate the

A

nature of the coupling between the heart and the vascular system

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19
Q

how can they show the nature of the coupling between the heart and the vascular system

A

with cardiac and vascular function curves

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20
Q

graphic techniques (cardiac & vascular curves) have been developed to

A

analyze the interactions between the cardiac and vascular components of the circulatory systemt

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21
Q

the graphic analysis (cardiac & vascular function curves involve

A

two simultaneous functional relationships between cardiac output and central venous pressure - preload (i.e. pressure in right atrium and thoracic venae cavae)

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22
Q

the cardiac function curve (CFC) defines

A

one of these relationships

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23
Q

CFC is an expression of the

A

Frank- Starling relationship, and reflects the dependence of CO on preload (i.e., on central venous, or right atrial pressure)

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24
Q

why is pressure in RA a marker of preload

A

pressure in RA connected to volume in RA
more blood coming back, more pressure
directly contributes to volume in LV
as pressure increases in RA, LV EDV will increase

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25
cardiac function curve is a characteristic of the
heart itself it has been studied in hearts that have been completely isolated from the rest of the circulatory system
26
vascular function curve defines the
dependence of the central venous pressure on the cardiac output
27
the relationship between the central venous pressure and the cardiac output depends only on
certain vascular system characteristics, namely peripheral resistance, arterial and venous compliances, and blood volume
28
the vascular function curve is entirely independent of the
characteristics of the heart, and can be evaluated even if heart was replaced by a mechanical pump
29
the greater the preload of the heart
the greater the cardiac output (greater filling, greater EDV)
30
in the intact circulation, what constitutes the preload of the heart
the pressure in the great veins (i.e., the central venous pressure)
31
in the whole heart, what determines preload
the stretch of the ventricles prior to systole will determine the strength of the subsequent contraction (bigger EDV, bigger SV)
32
The CO is the
output of left ventricle
33
even though CO is output of LV, what ultimately determines the CO
preload of the right ventricle
34
SV of RV is same as
SV of LV
35
Why does right ventricle determine CO of LV
because during periods when CO is constant, and within limits, the LV will pump whatever volume of blood comes to it, from the right side of the heart
36
what ultimately determines the output of the left side of heart
filling pressure on the right side of the heart
37
the filling pressure of the right side of the heart is functionally equal to
the central venous pressure
38
in the intact circulation, what is the preload considered to be
central venous pressure
39
in intact circulation, the preload is considered to be the CVP, and this is approximately equal to
mean of right atrial pressure, which when tricuspid valve is open, is approx. equal to the RV pressure
40
the relationship between what and what is shown in the cardiac function curve
preload or filling pressure and stroke volume (or CO)
41
cardiac function curves are also known as
"starling curves" or ventricular function curves
42
how are partial curves obtained in human subjects
through the use of intracardiac pressure and volume transducers
43
the cardiac function curve is a manifestation of the
Frank-Starling relationship or length-dependence of cardiac contraction (as preload increases, increase in SV)
44
for cardiac function curve what does steeper slope mean
greater contractility
45
decreased RA pressure (preload)
decreased LV volume (EDV)
46
increased RA pressure (preload)
increased LV volume (EDV)
47
as RA pressure decreases, SV
decreases
48
as RA pressure increases, SV
increases
49
in the pressure loop what is happening when right atrial pressure increases and SV (CO) increases
diastolic filling is longer, mitral valve open for longer, increased LV volume
50
in pressure loop what is happening as RA pressure decreases and SV (CO) decreases
diastolic filling is shorter, decreased LV volume
51
right atrial pressure (preload) and SV are
directly proportional
52
decreased preload is associated with
decreased EDV
53
increased preload is associated with
increased EDV
54
What is the straight line on top of the volume pressure loop
ESPVR (end systolic pressure volume loop relationship) indicates the max pressure pressure the ventricle can produce at a given volume (indication of contractility)
55
the contractility of the ventricle has not changed in graph and thus
the ESPVR has not changed and therefore the ESV does not change when preload changes
56
because of ESV not changing the increased preload results in
increased SV and decreased preload results in decreased SV
57
When different stroke volumes are then plotted against the preload pressures at which they occurred (fig 1b)
the entire relationship yields the Cardiac function curve (CFC)
58
as ESDVR changes,
the slope of the line will change
59
In fig 2b, 3 different curves at 3 different SVs but have same
preload (EDV)
60
In fig 2a when preload stays same but ESV changes
increase contractility, ESV increases, larger width and SV increases decrease contractility, ESV decreases, smaller width, decreased SV
61
more contractility means
more pressure and steeper slope
62
increases in cardiac contractility are produced by
actions of norepinephrine or epinephrine on heart
63
what is primary way in which cardiac output is increased physiologically
increase contractility produced by norepinephrine and epinephrine
64
norepinephrine and epinephrine act to
increase contractility by the cellular mechanisms and have the effect of raising the peak pressure that can be developed at a given left ventricular volume
65
increases in contractility are reflected in an
ESPVR that is shifted upward and to the left (increased slope) and vice versa for decreases in contractility
66
when can decreases in contractility occur
cardiac damage
67
what can you not have on same curve
decreased contractility with increased ESV
68
increases in contractility thus
increased SV by decreasing ESV
69
at each preload, SV is increased with
increased contractility and entire cardiac function curve is increased upwardly (fig 2b)
70
decreased contractility results in
decreased stroke volume at all preloads
71
with a change in contractility, the heart will be
characterized by a completely new cardiac function curve
72
even with completely new cardiac function curve with change in contractility it still reflects the
frank-starling relationship or the length-dependence of the cardiac contraction
73
factors that change the cardiac function curve
contractility afterload
74
increase and decrease in afterload causes
changes in ESV
75
in changing afterload graphs what does not change
contractility preload
76
increased afterload
volume at end of systole is higher and higher pressure
77
decreased afterload
volume at end systole is lower and lower pressure, aortic valve open for ejection at a lower pressure
78
in Fig 3b preload is
held constant, EDV the same
79
afterload is the
load experienced by the LV after the aortic valve opens (ending the isovolumic contraction phase)
80
afterload is related to the
arterial blood pressure and hemodynamic properties of the arterial system
81
hemodynamic properties of the arterial system influence the
dynamics of the arterial blood pressure during ejection of the SV into the arterial system
82
increases in afterload are represented on
left ventricular P-V loop as a higher pressure throughout ejection phase (3a)
83
when diastolic arterial blood pressure is elevated
the isovolumic contraction must then develop a higher pressure in the LV (compared to normal basal state) before aortic valve can be forced open
84
if ventricular contractility is constant, the
ESVPR is not altered and therefore SV is reduced
85
why is SV reduced when ventricular contractility is constant
because heart is not able to achieve a lower ESV (does not have increased ability to "squeeze down" against elevated pressure)
86
decreases in afterload result in
increased SV because heart is able to squeeze down more, achieving a lower ESV
87
A change in afterload places the LV
on a completely new function curve (3b) which still displays the length-dependence of cardiac contraction
88
both systolic heart failure and diastolic heart failure have
severe reduction in VO2 (exercise intolerant)
89
Systolic heart failure
HF with reduced ejection failure (Hfref)
90
Hfref is secondary to
myocardial infarction
91
why does Hfref have a rightward shift
due to increase in EDV (bcuz heart enlarging) and walls are getting thinner with poorer squeeze (decreased contraction)
92
why does Hfref have increased EDV
to offset SV
93
When does death occur for Hfref
when EDV cannot increase anymore (eventually ESPVR decreases)
94
Ejection fraction
SV(EDV-ESV/EDV)
95
Hfref is
thin walled, dilated and ballooned
96
diastolic failure is more prominent in
females
97
diastolic failure
Heart failure with preserved ejection fraction (Hfpef)
98
Hfpef has pressure
higher at any given volume
99
Hfpef is associated with
hypertension
100
Hfpef generally has
normal squeeze function (contractility) but very poor relaxation and decreased compliance
101
diastolic used to not be
thought of as heart failure just diastolic failure
102
diastolic failure's heart is
thick
103
aortic stenosis has
high EDP
104
why does aortic stenosis have high EDP
owing to heart contracting against very small opening less area for blood to leave pressure rises in LV
105
Any benefit from exercise training in Hfpef is derived from
peripheral adaptations specifically increase in AVO2 diff
106
benefits from exercise in Hfref include
increase in heart function increase in A-vo2 diff decrease in heart chamber size

Kin 426 (12 decks)

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