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SRNACardiacRotation > Determinants and Cardiac basics > Flashcards

Determinants and Cardiac basics Flashcards

1
Q

Determinants of Cardiac Output

A

Heart and Stroke Volume

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2
Q

What is SV?

A

SV is the amount of blood ejected by the ventricle with each contraction.

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3
Q

Preload is the

A

precontractile fiber length of myocardial fiber augmented

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4
Q

Preload can be augmented by

A

End diastolic volume

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5
Q

Venous return is directly proportional to

A

EDV

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6
Q

Some factors that affect venous return

A

Factors that affect venous return include blood volume, venous tone, intrathoracic pressure, pulmonary vascular resistance, and right heart function

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7
Q

What is afterload?

A

Afterload, the force against heart contraction,

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8
Q

What are the 3 determinants of afterload?

A

Ventricular wall stress
Systemic vascular resistance
Blood viscosity.

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9
Q

Afterload and SV relationship is

A

Inversely proportional; As afterload increases, SV decreases.

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10
Q

Contractility is the

A

intrinsic ability of the myocardial fiber to contract.

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11
Q

What is the main role of Intracellular calcium

A

main mechanism which influences the binding strength of actin and myosin filaments that determine the force of myocardial contraction

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12
Q

Cardiac output (CO) is the

A

amount of blood delivered to the tissue in 1 min.

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13
Q

Starling’s law

A

The stronger the stretch, the greater output

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14
Q

Normal CO

A

5-6L/min

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15
Q

What is CI ?

A

CO/BSA

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16
Q

Normal CI

A

2.5 to 3.5⋅L⋅min−1⋅m−2

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17
Q

CO formula is

A

HR x SV

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18
Q

What is the primary determinant of HR?

A

the rate of phase 4 depolarization of the SA node of pacemaker cells

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19
Q

Rate of discharge of SA node is a determinant of HR and determined by

A

humoral and neural (Epi, NE) mechanisms

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20
Q

In children how is the CO determinants different?

A

the myocardium is less contractile and less compliant; therefore HR is critically important for maintenance of CO

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21
Q

How does significant tachycardia affect CO?

A

significant tachycardia can negatively affect CO because increased HR (> 170 beats/min) disproportionately decreases diastolic ventricular filling time relative to decreases in systole, which then contributes to a lower CO.

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22
Q

Heart rhythm also is an important determinant of cardiac output because the atrial contraction inherent in sinus rhythm contributes of _______CO in normal hearts and up to in the case of reduced ventricular compliance or delayed relaxation.

A

20% to 25%; 40% to 50%

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23
Q

What is a normal SV?

A

70-80ml per contraction

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24
Q

What are determinants of SV?

A

Preload, afterload and contractility. and SOMETIMES 4th wall motion abnormalities

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25
Q

What is the formula of SV?

A

EDV - ESV

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26
Q

What are the determinants of EDV?

A

Preload

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27
Q

What are the determinants of ESV?

A

Afterload and contractility

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28
Q

3 determinants of Preload

A

Venous return
Ventricular filling time
Intrathoracic pressure

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29
Q

3 determinants of Afterload?

A

SVR
Wall tension
Blood viscosity

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30
Q

2 determinants of contractility

A

Sympathetic nervous system

Catecholamines drugs.

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31
Q

Preload is directly proportional to

A

end-diastolic myocardial fiber length

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32
Q

Normal EDV

A

120 ml

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33
Q

If no obstruction or loss of volume in circulating pathways is present, venous return should equal

A

CO

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34
Q

Venous return is regulated by according to the formula

A

peripheral venous pressure (Pv), right atrial pressure (Pra), and venous resistance (Rv)

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35
Q

Formula venous return VR =

A

(Pv − Pra)/Rv

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36
Q

Useful estimate of contractility is

A

ejection fraction.

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37
Q

What exerts the most important influence on contractility?

A

The adrenergic nervous system

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38
Q

Provide 95% of resistance to ejection.

A

Systemic vascular resistance (SVR) accounts for approximately

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39
Q

What is the formula of SVR

A

80 x (MAP - RAP ) / CO)

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40
Q

What is afterload defined by?

A

Afterload, as defined by ventricular wall stress, is represented by LaPlace’s law:

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41
Q

Afterload represented by what law?

A

La Place’s Law

42
Q

Laplace law and variable

A

T = P r / 2h
where T is tension in the LV wall
P is pressure
r is ventricular radius, and h is wall thickness.

43
Q

From LaPlace’s law, it is apparent that 3 are primary determinants of afterload.

A

ventricular volume
LV wall thickness, and
systolic intraventricular pressure

44
Q

A failing ventricle effect on afterload and CO.

A

dilate and significantly increase afterload, which significantly reduces CO.

45
Q

Important goal in managing congestive heart failure

A

Reducing afterload

46
Q

A change in contractility is considered to be a change in the

A

contractile force of the heart in the presence of unchanged diastolic dimensions and pressure

47
Q

The sympathetic division of the autonomic nervous system increases the HR via stimulation of

A

Beta-1 adrenergic receptors,

48
Q

Parasympathetic division of the autonomic nervous system decreases the HR by stimulating

A

muscarinic M2 cholinergic receptor

49
Q

Stroke volume and afterload have an _________

relationship

A

inversely proportional

50
Q

What happens to SV and CO when the ventricular

wall tension increases,

A

Decreased SV and CO.

51
Q

Which has the most profound effect on myocardial contractility ? and Why?

A

The sympathetic nervous system as the sympathetic adrenergic fibers release norepinephrine, which stimulates the myocardial beta-1 adrenergic receptors to enhance contractility and CO

52
Q

Inotropism or contractility is affected by the

of SV and CO

A

rate of myofibril shortening as well as by the rate of calcium release from the smooth sarcoplasmic
reticulum.

53
Q

Faster rates of myofibril shortening and
calcium release into the intracellular space contribute
to an

A

increased strength of contractility and augmentation

54
Q

The various degrees of wall motion abnormalities range from 3 different types
toand finally to akinesis, which refers to
the absence of contractility.

A

hypokinesis, dyskinesis, akinesis

55
Q

Refers to the diminished force of contractility,

A

Hypokinesis

56
Q

A paradoxical and asynchronous pattern of contraction,

A

Dyskinesis,

57
Q

How does wall motion abnormalities affect LV?

A

Affect the ability of the left ventricle to adequately fill with the blood volume delivered by the atria, subsequently reducing its SV capacity and CO potential

58
Q

Myocardial contraction occurs as a result of crossbridge

formation between

A

two contractile proteins, actin (thin

filaments) and myosin (thick filaments

59
Q

The intracellular release of calcium from the sarcoplasmic reticulum facilitates the conformational change in what? and what does it allow?

A

two regulatory proteins (troponin and tropomyosin) to allow the cross-bridge formation between actin and myosin

60
Q

Explain the process of calcium release?

A

-Initial calcium release from the sarcoplasmic reticulum is triggered by the electrical depolarization of dihydropyridine, voltage-gated calcium channels.
-As the intracellular calcium concentration increases, it triggers an even greater release of calcium from the sarcoplasmic reticulum via ryanodine, nonvoltagegated
calcium channels

61
Q

What determine the strength as well as rate of the contraction?

A

overall calcium concentration

rate of release from the sarcoplasmic reticulum

62
Q

Calcium regulation and Sympathetic nervous system stimulation (via norepinephrine) activates

A

beta-1 adrenergic receptors, leading to an increase in the intracellular calcium concentration and strength of contraction.

63
Q

In contrast to SNS, calcium regulation of parasympathetic nervous system

A

stimulation (via acetylcholine) activates M2 cholinergic receptors, which enhance the Ca2+- ATPase activity to pump calcium back into the sarcoplasmic reticulum, thus effectively lowering the intracellular calcium
concentration and decreasing the strength and rate of the myocardial contraction.

64
Q

The cardiac cycle can be divided into alternating periods of

A

myocardial contraction, or systole

myocardial relaxation, or diastole.

65
Q

Ventricular SYSTOLIC function is best understood by 2 parameters

A

CO and EF

66
Q

Diastolic function of the ventricle is best understood by

A

ventricular isovolumetric relaxation time

ventricular capacitance during filling

67
Q

Ventricular pressure–volume diagrams:2 main point of interests are

A

EDV and ESV

68
Q

What does EDV really indicates?

A

diastolic function, ability of the ventricular myocardium to relax to fill with blood;

69
Q

What does EDV really indicates?

A

end-systolic volume (ESV), reflects systolic function, including the ability of the ventricular myocardium to contract to eject a fraction of the end diastolic ventricular volume.

70
Q

Generally, as both the right and left ventricle
depolarize in synchronous fashion, the pulmonary and
systemic COs generated are

A

usually equal.

71
Q

The normal range for the left ventricular EF is usually .

A

59%-75%

72
Q

The overall net effect of systolic failure translates into a

A

down and right shift of the pressure–volume loop (negative inotropy)

73
Q

What happens to the EDV and ESV as the systolic function of the ventricle is failing,

A

there is an increase in EDV and ESV because

EF (the ability of the ventricle to eject a fraction of the EDV) is significantly reduced.

74
Q

Systolic augmentation (positive inotropy) shifts the pressure volume loop

A

up and left.

75
Q

The ventricular capacitance can be estimated via

A

transesophageal echocardiography

76
Q

The assess ventricular capacitance you look at those 2 parameters?

A

ventricular isovolumetric relaxation time and the flow velocity across the mitral valve during diastole (ventricular filling).

77
Q

A stiff and less compliant ventricle is indication by 2 things

A

Prolonged isovolumetric relaxation times and high flow velocities across the mitral valve

78
Q

As the diastolic function of the ventricle is failing, the EDV of the ventricle decreases and the less-compliant ventricle becomes

A

unable to accommodate the blood volume delivered by the atrial depolarization.

79
Q

In contrast, a compliant ventricle is

A

able to accommodate a larger EDV and augments SV and CO, thus shifting the loop up and left.

80
Q

Are responsible for the delivery of oxygenated blood to the myocardium.

A

right and left coronary arteries

81
Q

What does the RCA supplies?

A

right atrium, the right ventricle, and the inferior portion of the left ventricle, SA and AV nodes.

82
Q

What does left coronary artery (LCA) includes the

A

left atrium, the interventricular septum, and the anterolateral walls of the left ventricle.

83
Q

Circumflex artery, which supplies the

A

Lateral wall of the left ventricle,

84
Q

Left anterior descending artery (LAD), which supplies the

A

Anterior wall of the left ventricle

Interventricular septum

85
Q

To supply the myocardium with oxygen, the blood flows from the _______ to the _______and then returns to the _______via the _______

A

Epicardial vessels to the endocardial vessels, and then returns to the right atrium via the coronary sinus.

86
Q

The coronary perfusion pressure (CPP) is dependent on the

A

difference between the aortic diastolic pressure (ADP) and the left ventricular end-diastolic pressure (LVEDP),

87
Q

CPP formula

A

CPP = ADP − LVEDP.

88
Q

What is the LVEDP?

A

The LVEDP is an approximation of the resistance to coronary blood flow during diastole

89
Q

CPP is directly proportional to____, but inversely proportional to ______and ______

A

ADP; LVEDP as well as heart rate (HR).

90
Q

CPP increases with:

A

(1) increases in ADP; (2) decreases in LVEDP; and (3) decreases in HR as the diastolic time

91
Q

CPP decreases with:

A

1) decreases in ADP; (2) increases in LVEDP; and

(3) increases in HR.

92
Q

Myocardial oxygen consumption at rest is between

A

7 and 10 mL/100 g tissue/min;

93
Q

CPP ranging from

A

50 to 120 mm Hg, produces coronary blood flows of 60-80 mL/100 g tissue/min

94
Q

Myocardial oxygen consumption increase with

A

exercise

95
Q

In contrast to other organ beds, myocardial arterial oxygen extraction is quite high, about

A

70%-80%, compared to about 25% for the rest of the body.

96
Q

This system has minimal effects on the tone of the coronary vasculature.

A

The parasympathetic nervous system

97
Q

The 4 important factors affecting myocardial oxygen

supply are as follows: CHAC

A

(1) HR (in particular, diastolic time);
(2) CPP (as determined by ADP as well as by LVEDP)
(3) arterial oxygen content (including both oxygen tension as well as hemoglobin concentration); and
(4) coronary vessel diameter.

98
Q

The rate of oxygen supply to the myocardium increases

with

A

ncreases in the diastolic time, increases in CPP, increases in oxygen and hemoglobin concentration, and coronary vasodilation

99
Q

Myocardial oxygen demand is affected by the following

important factors:

A

(1) HR;
(2) ventricular wall tension (as determined by preload, afterload, and wall thickness); and
(3) myocardial contractility

100
Q

The rate of myocardial oxygen consumption (Mv . O2)

increases with

A

increases in HR, increases in wall tension, and

increases in contractility

SRNACardiacRotation (2 decks)

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