Lecture 1 Flashcards

1
Q

Stroke volume

A

volume of blood ejected by the left ventricle after one contraction. SV=EDV-ESV

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2
Q

Pericardium

A

composed of two layers, the fibrous pericardium and the serous pericardium.

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3
Q

fibrous pericardium

A

dense, irregular connective tissue that protects and anchors the heart which prevents overstretching.

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4
Q

serous pericardium

A

thin, delicate membrane that consists of the parietal layer (outer layer), pericardial cavity that’s filled with pericardial fluid and the visceral layer.
Other functions include prevention of displacement, providing physical barrier against infection and inflammation, and having pain and mechanoreceptors to elicit changes.

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5
Q

EDV

A

volume of blood in the right and/or left ventricle at end load or filling in diastole

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6
Q

Ejection fraction

A

measurement of the percentage of blood leaving your heart each time it contracts, which is usually 55 to 75%.
EF=SV/EDV

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7
Q

Cardiac index

A

better indicator of cardiac function.

CI= CO L/min /body surface area

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8
Q

Cardiac output

A

normally 3.5 to 8 L per min, maximum is 20 to 30 L per min.

CO = HR X SV

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9
Q

Frank Starling’s law

A

increase in EDV increases stretching (Preload) which increases stroke volume.

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10
Q

Factors that affect stroke volume

A

preload, contractility, and afterload

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11
Q

Myocardial contractility

A

increase in strength of contraction that increases stroke volume. Epinephrine and calcium ions increase contractility.

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12
Q

Preload

A

dependent on EDV and 2 facts effect EDV. First, venous return or venous pressure and second, the duration of diastole.

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13
Q

Afterload

A

ventricular wall tension

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14
Q

La Place formula

A

Wall Tension = (Intraventricular pressure x Radius)/ Ventricular wall thickness

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15
Q

How does arterial pressure affect afterload?

A

Increase in arterial pressure increases resistance to ventricular ejection

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16
Q

relationship between ventricular function curve and contractility

A

Curves can shift upward when cardiac performance is enhanced or shift downward when cardiac performance is depressed.

17
Q

enhanced cardiac performance

A

increased inotropy, increased heart rate, and reduced afterload ie sympathetic stimulation, epinephrine, digitalis, caffeine

18
Q

depressed cardiac performance

A

decreased inotropy, decreased heart rate, and by increased afterload ie hypoxia, acidosis, hypercapnia, CHF, barbiturates

19
Q

mechanism of action of digitalis

A

digoxin inhibits the Na/K pump
Na builds up in the cell
low gradient for Na to run Na/Ca transporter.
calcium ions increase in cell and therefore force of contraction will increase.

20
Q

parasympathetic ns

A

connected the vagus nerves
slows down heart rate, parasympathetic tone is 40 bpm
under resting conditions parasympathetic NS predominates.

21
Q

Sympathetic activity and epinephrine

A

fight or flight response
speeds up heart rate and stroke volume
Sympathetic tone can increase heart rate up to 180-200 bpm
increase force of contraction
reduce systole period
people with heart disease sym. NS predominates.