Cardiac Function Flashcards

1
Q

Required for the Ca2+ release from the SR that leads to Contraction

A

Influx of Ca2+

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2
Q

In the heart, what is required for contraction?

-Distinguishing feature between cardiac and skeletal muscle

A

Extracellular calcium

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3
Q

The mechanism by which an AP initiates Ca2+ release in cardiac muscle is called

A

Calcium-Induced Calcium Release (CICR)

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4
Q

In a cardiac myocyte, increased intracellular Ca2+ is sensed by the Ca2+-sensitive

A

Ryanodine Receptors (RYR)

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5
Q

Does NOT have CICR

A

Skeletal muscle

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6
Q

SR calcium release in skeletal muscle is independent of

A

Ca2+

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7
Q

In cardiac muscle, relaxation requires removal of Ca2+ from the cytoplasm. This occurs via

A

SERCA (back to SR) and NCX (out of cell)

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8
Q

Returns Ca2+ to the Sarcoplasmic Reticulum (SR)

A

SERCA

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9
Q

Calcium is removed from the cardiac cell via

A

NCX

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10
Q

The intrinsic ability of myocardial cells to develop force at a given muscle length

A

Contractility (inotropy)

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11
Q

Most mechanisms that affect inotropy affect how

A

Ca2+ is handled by the cell

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12
Q

What are the three measures of ventricular function?

A

Stroke volume, Ejection fraction, and Cardiac Output

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13
Q

The volume of blood ejected per contraction

-difference between EDV and ESV

A

Stroke Volume (SV = EDV - ESV)

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14
Q

A way to look at the efficiency of ventricular contraction

A

Ejection fraction

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15
Q

Determines the percent EDV ejected with each beat

A

Ejection Fraction

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16
Q

The total volume of blood ejected by the heart in one minute

A

Cardiac Output (CO)

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17
Q

How do we calculate Cardiac Output (CO)?

A

CO = SV x HR

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18
Q

The biggest contributor to increased CO during exercise is

A

Increased HR

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19
Q

In order for CO to increase, we also need some increase in

A

SV

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20
Q

An increase in HR alone can cause CO to

A

Fall

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21
Q

Which three factors influence stroke volume?

A

Preload, afterload, inotropy

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22
Q

A cardiac myocyte can generate more force when it is

A

Stretched

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23
Q

This stretch-induce inotropy is related to

A

Ca2+

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24
Q

Increases TN-C Ca2+ affinity and stretch-activated Ca2+ channels

A

Stretch

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25
Stretch activated Ca2+ channels increase Ca2+ release from the
Sarcoplasmic Reticulum (SR)
26
Increasing volume increases the
Maximal pressure
27
Increasing the ventricular volume regulates the
Contractile force
28
Does not change when preload is decreased
ESPVR
29
The Frank-Starling law of the heart is that the SV is determined by the
LVEDV
30
Increasing the PRELOAD (EDV) increases the
Force of contraction
31
Increasing the force of contraction increases the
Stroke Volume (and thus CO)
32
Increases as cardiac filling increases
SV
33
Altering the preload DOES NOT affect the
ESPVR
34
Increased venous return raises
EDV
35
HR and atrial contraction are two factors which regulate the
Ventricular Preload
36
Ventricular filling varies with
HR
37
Atrial contraction is only an important component of ventricular filling when
HR is high or we have decreased ventricular compliance
38
In the normal heart, PRELOAD correlates with
End-Diastolic Pressure (EDP)
39
Affects the relationship between EDP and EDV
Compliance of the heart
40
How easily the heart expands when it is filled with a volume of blood
Compliance
41
The slope of the volume vs pressure plot is the
Compliance
42
Ventricular compliance can be altered by
Disease
43
Reflects stiffness of the ventricle
End-Diastolic Pressure-Volume Relationship (EDPVR)
44
An increased EDPVR shows a
Stiff ventricle
45
A stiff ventricle is harder to
Fill
46
With a stiff ventricle, we have a higher pressure for any given
Volume
47
With a stiff ventricle, we have a lower volume for any given
Pressure
48
Under conditions of decreased compliance, the left ventricle does not
Relax
49
When we have a stiff ventricle, we will have an increase in LVEDP, this leads to an increase in
Pulmonary capillary pressure
50
Heart failure with preserved ejection fraction
“Diastolic” Heart Failure
51
We can see concentric hypertrophy with
Hypertension and valvular disease
52
Amyloidosis, glycogen storage diseases, hemochromatosis, and mutations in sarcoma result proteins can all result in
Restrictive cardiomyopathy
53
Blood pressure in the thoracic vena cava near the right atrium
Central Venous Pressure (CVP)
54
A major determinant of filling of the right ventricle
CVP
55
CVP determines the
Preload
56
The load against which the heart must contract to eject blood
Afterload
57
A larger afterload causes
Decreased SV
58
Makes the ventricle work harder to eject blood
Increased afterload
59
Increasing the afterload DOES NOT affect the
ESPVR
60
Decreases velocity and extent of fiber shortening
Increased afterload
61
We can see chronic elevations in afterload with
Hypertension and aortic stenosis
62
What are three examples of afterload reducing agents?
ACE inhibitors, Hydralazine, Sympathomimetics
63
Determined by cellular mechanisms that affect the intrinsic contractility
Inotropy (contractility)
64
Will INCREASE stroke volume independent of changes in preload or afterload
Increased inotropy
65
Inotropy alters the slope of the
ESPVR
66
Increases the intrinsic contractility
Inotropy
67
The maximal pressure generated for any specific volume
Intrinsic contractility
68
Inotropy causes the slope of the ESPVR to
Increase
69
Sympathetic nervous system inner action of the heart influences
Inotropy
70
Inotropy is also influenced by increased circulating
Catecholamines
71
What is the effect on inotropy of sympathetic nervous system stimulation?
Increases inotropy
72
Heart failure with reduced ejection fraction
Systolic Heart failure
73
Activation of muscarinic ACh receptors decreases
cAMP
74
What are three examples of positive inotropic agents for the heart?
Beta-agonists, phosphodiesterase-3 inhibitors, Digoxin