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Cardiology > Cardiac Function > Flashcards

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
Q

Stretch activated Ca2+ channels increase Ca2+ release from the

A

Sarcoplasmic Reticulum (SR)

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26
Q

Increasing volume increases the

A

Maximal pressure

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27
Q

Increasing the ventricular volume regulates the

A

Contractile force

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28
Q

Does not change when preload is decreased

A

ESPVR

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29
Q

The Frank-Starling law of the heart is that the SV is determined by the

A

LVEDV

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30
Q

Increasing the PRELOAD (EDV) increases the

A

Force of contraction

31
Q

Increasing the force of contraction increases the

A

Stroke Volume (and thus CO)

32
Q

Increases as cardiac filling increases

A

SV

33
Q

Altering the preload DOES NOT affect the

A

ESPVR

34
Q

Increased venous return raises

A

EDV

35
Q

HR and atrial contraction are two factors which regulate the

A

Ventricular Preload

36
Q

Ventricular filling varies with

A

HR

37
Q

Atrial contraction is only an important component of ventricular filling when

A

HR is high or we have decreased ventricular compliance

38
Q

In the normal heart, PRELOAD correlates with

A

End-Diastolic Pressure (EDP)

39
Q

Affects the relationship between EDP and EDV

A

Compliance of the heart

40
Q

How easily the heart expands when it is filled with a volume of blood

A

Compliance

41
Q

The slope of the volume vs pressure plot is the

A

Compliance

42
Q

Ventricular compliance can be altered by

A

Disease

43
Q

Reflects stiffness of the ventricle

A

End-Diastolic Pressure-Volume Relationship (EDPVR)

44
Q

An increased EDPVR shows a

A

Stiff ventricle

45
Q

A stiff ventricle is harder to

A

Fill

46
Q

With a stiff ventricle, we have a higher pressure for any given

A

Volume

47
Q

With a stiff ventricle, we have a lower volume for any given

A

Pressure

48
Q

Under conditions of decreased compliance, the left ventricle does not

A

Relax

49
Q

When we have a stiff ventricle, we will have an increase in LVEDP, this leads to an increase in

A

Pulmonary capillary pressure

50
Q

Heart failure with preserved ejection fraction

A

“Diastolic” Heart Failure

51
Q

We can see concentric hypertrophy with

A

Hypertension and valvular disease

52
Q

Amyloidosis, glycogen storage diseases, hemochromatosis, and mutations in sarcoma result proteins can all result in

A

Restrictive cardiomyopathy

53
Q

Blood pressure in the thoracic vena cava near the right atrium

A

Central Venous Pressure (CVP)

54
Q

A major determinant of filling of the right ventricle

A

CVP

55
Q

CVP determines the

A

Preload

56
Q

The load against which the heart must contract to eject blood

A

Afterload

57
Q

A larger afterload causes

A

Decreased SV

58
Q

Makes the ventricle work harder to eject blood

A

Increased afterload

59
Q

Increasing the afterload DOES NOT affect the

A

ESPVR

60
Q

Decreases velocity and extent of fiber shortening

A

Increased afterload

61
Q

We can see chronic elevations in afterload with

A

Hypertension and aortic stenosis

62
Q

What are three examples of afterload reducing agents?

A

ACE inhibitors, Hydralazine, Sympathomimetics

63
Q

Determined by cellular mechanisms that affect the intrinsic contractility

A

Inotropy (contractility)

64
Q

Will INCREASE stroke volume independent of changes in preload or afterload

A

Increased inotropy

65
Q

Inotropy alters the slope of the

A

ESPVR

66
Q

Increases the intrinsic contractility

A

Inotropy

67
Q

The maximal pressure generated for any specific volume

A

Intrinsic contractility

68
Q

Inotropy causes the slope of the ESPVR to

A

Increase

69
Q

Sympathetic nervous system inner action of the heart influences

A

Inotropy

70
Q

Inotropy is also influenced by increased circulating

A

Catecholamines

71
Q

What is the effect on inotropy of sympathetic nervous system stimulation?

A

Increases inotropy

72
Q

Heart failure with reduced ejection fraction

A

Systolic Heart failure

73
Q

Activation of muscarinic ACh receptors decreases

A

cAMP

74
Q

What are three examples of positive inotropic agents for the heart?

A

Beta-agonists, phosphodiesterase-3 inhibitors, Digoxin

Cardiology (27 decks)

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