Ch 20

Front 1

cardiac cycle

Back 1

includes alternate periods of contraction and relaxation

Front 2

Systole

Back 2

contraction

Front 3

diastole

Back 3

relaxation

Front 4

atrial systole

Back 4

when the atria contracts

Front 5

end-diastolic volume (EDV)

Back 5

prior to contraction: the maxium amount of blood that it will hold in this cardiac cycle, typically 130 ML

Front 6

stroke volume

Back 6

during the ventricular ejection, each ventricle will eject 70-80 ml

Front 7

ejection fraction

Back 7

the stroke volume at rest is about 60 % of the end-diastolic volume

Front 8

end-systolic volume (ESV)

Back 8

the amount of the blood remaining in the ventricle when the semilunar valve closes: volume of 50 ml, about 40 % of the end- diastolic volume

Front 9

auscultation

Back 9

a technique for listening to the heart

Front 10

stethoscope

Back 10

an instrument used to listen for normal and abnormal heart sounds

Front 11

Lubb

Back 11

The first heart sound, last a little longer than the second, which marks the start of ventricular contraction, produced as the AV valve closes

Front 12

Dubb

Back 12

the second heart sound, occurs at the beginning of ventricular filling when the semi-lunar valves close

Front 13

heart murmur

Back 13

the surges, swirls, and eddies that accompany regurgitation create a rushing, gurgling sounds

Front 14

cardiodynamics

Back 14

refers to the movements and forces generated during cardiac contraction: end-diastolic volume, end-systolic volume, stroke volume, ejection fraction

Front 15

cardiac output

Back 15

the amount of blood pumped by the left ventricle in one minute
CO (ML/min)=
HR(beats/min) x SV (mL/beat)

Front 16

what can adjust the heart rate

Back 16

activities of the autonomic nervous system or by circulating hormones

Front 17

what can change the stroke volume

Back 17

adjusting the end-diastolic volume (how full the ventricles are when they start to contract), the end- diastolic volume (how much blood remains in the ventricle after it contracts

Front 18

abnormal conditions affecting cardiac output

Back 18

various drugs, abnormal variations in concentrations, and changes in body temperature can alter the basi rhythm of contraction established by the SA nodem caffeine and nicotine are stimulants to the nervous system

Front 19

cardioacceleratory center

Back 19

controls the sympathetic neurons that increase the heart rate

Front 20

cardioinhibitory center

Back 20

controls the parasympathetic neurons that slow the heart rate

Front 21

the sympathetic and parasympathetic divisions alter the heart rate by

Back 21

changing the ionic permeabilities of cells in the conducting system

Front 22

when NA is released by the sympathetic neurons

Back 22

they bind to beta-1 receptorsm leading to the opening of sodium-calcium ions channels

Front 23

The subsequent influx of positively charged ions increases

Back 23

the rate of depolarization and shortens the period of repolarization and the nodal cells reach threshold more, quickly and the heart rate increases

Front 24

the atrial reflex

Back 24

Baunbridge reflex, involves adjustments in the heart rate in response to an increase in the venous return, when the rate of the venous return to the heart increases, the heart rate, and hence the cardiac output, rises as well

Front 25

hormones

Back 25

Epinephrine, norepinephrine, and thyroid hormone increases heart rate by their effect on the SA node

Front 26

EDV

Back 26

end-diastolic volume is the amount of blood a ventricle contains at the end of diastole, just before contractions begin

Front 27

Two things that effect EDV

Back 27

1) the filling time 2) venous return

Front 28

filling time

Back 28

is the duration of ventricular diastole

Front 29

venous return

Back 29

is the rate of blood flow over this period

Front 30

preload

Back 30

the degree of stretching experienced by the ventricular muscle cells during ventricular diastole, directly proportional to the EDV. the greater the EDV the larger the preload

Front 31

the relationship between the amount of ventricular stretching and contractile force means that

Back 31

within normal physiological limitsm increasing the EDV results in a corresponding increase in the stroke volume

Front 32

Frank-Starling principle

Back 32

the relationship between the amount of ventricular streching and contractile force: more in and more out

Front 33

ESV is effected by 3 factors

Back 33

preload, the contractibility of the ventricle, and the afterload

Front 34

contractibility

Back 34

is the amount of force preduced during contractionm at a given preload

Front 35

positive inatropic action

Back 35

positive factors that increases contractibility, stimulates the entry of Ca2+ into the cardiac muscle cells, increasing the force and duration of ventricular contractions

Front 36

negative inotropic action

Back 36

decrease contractility, often block ca+2 movement or depress cardiacmuscle metabolism

Front 37

afterload

Back 37

is the amount of tension the contracting ventricle must produce to force open the semilunar valve and eject blood, afterload is increased by any factor that restricts blood flow through the arterial system

Front 38

why can't cardiac output increase indefinitely

Back 38

because the available filling time shortens as the heart rate increases. cardiac output first plateaus and then declines