Cardiac Cycle

Question 1

Isovolumetric contraction

Answer 1

part of systole when blood volume stays the same with in the ventricle, but tension is building rapidly
-followed by ejection phase
Aortic and pulmonary valves are closed
Mitral and tricuspid valves are closed

Question 2

EDV

Answer 2

the highest volume of blood held in the ventricles during isovolumetric relaxation

Question 3

Right heart cath

Answer 3

inserted thru vein

-3 tips: RA, RV, pulmonary wedge (index of LA pressure)

Question 4

Left heart cath

Answer 4

inserted into artery advanced into left heart
measures flow (ventricular volume changes,)

Question 5

Stroke Volume

Answer 5

SV=EDV-ESV

the amount of blood ejected in a beat

Question 6

Left ventricular ejection fraction

Answer 6

EF=SV/EDV

how much of the blood that you could have ejected, did you actually eject

Question 7

Heart sounds: L R comparison

Answer 7

LV contracts before RV
Mitral closes before Tricuspid
unusual to hear S1 split
Pulmonary valve opens before aortic (Shorter isovolumetric contraction in RV)
RV has longer ejection phase
Aortic valve close before pulmonary ( due to lower pressure)
normal to hear S2 split: A2 P2

Question 8

S2 splitting: Right heart

Answer 8

due to negative thoracic pressure upon inspiration—>greater venous return to RA–>increased EDV—>increased RV ejection volume—>delayed closure of of Pulmonary valve–>Delays P2 closure—>enhances splitting

Question 9

S2 Splitting: left heart

Answer 9

Negative thoracic pressure–>retention of blood in pulmo vv.—>reduced VR to LA/LV—>decreased LV EDV and ejection—>less time for LV ejection accelerates aortic valve closure—>more splitting

Question 10

S3

Answer 10

early in diastole, after normal S2
during rapid ventricular filling phase (may indicate ventricular enlargement associated with heart failure, reduced distensibility/compliance)

“Ken-tuck-y”

Question 11

S4

Answer 11

late diastole, just before next S1
associated with an unusually strong atrial contraction-ventricular wall stiffness and decreased compliance assocaited with hypertrophy

“Ten-nessee”

Question 12

Palpable pulse

Answer 12

radial pulse occurs nearly simultaneous with heart beat, pressure wave travels faster than flow of blood

Question 13

a wave

Answer 13

RA contraction (diastole) = increased atrial pressure

highest pressure felt in jugular vein

Question 14

C wave

Answer 14

RV pressure in early systole (bulging of tricuspid into RA

small bump in jugular pressure

Question 15

V wave

Answer 15

RA filling (TC closed)
fill atria from IVC/SVC at beginning early diastole

Question 16

elevated a wave

Answer 16

tricuspid stenosis

R heart failure

Question 17

Cannon a waves

Answer 17

complete heart block (third degree AV- no association b/w atria and ventricles, so your atria contracts against closed AV valves—>increased pressure in atria)

Very large A waves

Question 18

no a waves

Answer 18

a fib

Question 19

large v wave

Answer 19

tricuspid regurgitation

Question 20

Kinetic energy

Answer 20

generated by the heart that helps eject blood through SL valves
use to calculate total external work
-small component of the entire work done by heart

Question 21

Tension heat

Answer 21

greatest determinant of ATP utilization (energy cost)
amount of work that is being performed by heart during isovolumetric phases (NO WORK BEING DONE, but still splitting ATP)

determined by ventricular wall tension (AFTERLOAD), time spend in systole, k

Question 22

2 main determinants of myocardial O2 demand

Answer 22

Ventricular wall stress
HR
contractility

if you want to decrease O2 demand–>decrease wall stress, decrease heart rate

Question 23

Wall stress

Answer 23

directly proportional to systolic ventricular pressure, radius of ventricular chamber

inversely proportional to ventricular wall thickness

Question 24

Factors impacting SV

Answer 24

Preload=EDV
Afterload= what heart has to work against: increased afterload–>increased leftover blood after systole (ESV)
Contractility: independent of preload (regulated by Ca concentrations

Question 25

passive tension

Answer 25

increases at a shorter sarcomere length vs skeletal muscle (skeletal muscle does not begin to generate tension until 2.6um)

cardiac muscle is less distensible elastic elements (think titan), therefore it will break if stretched past 2.6um due to

Question 26

Active tension

Answer 26

determined by preload (EDV)
increased preload—>increased tension
**determined by increased Ca affinity, increased Ca influx, increased RYR affinity to Ca

Question 27

Frank starling law

Answer 27

increased preload (EDV)= increased force of contraction

increased EDV=increased SV

Question 28

Frank Starling: systolic failure

Answer 28

increased EDV—>insignificant increase in SV

LV backup–>increased LA pressure (wedge pressure)–>increased LA pressure–>increased Pulmonary vv. pressure —>inc Pc—>pulmonary edema—> increased RV pressure—>RV failure—>RA failure—>venous distension—>hepatomegaly, ascites, peripheral edema

Question 29

force velocity relationship

Answer 29

Increased afterload—>decreased outflow velocity

increased EDV—>increased outflow velocity

Question 30

Afterload

Answer 30

Increased afterload (increased aortic pressure)–> greater time of systole spent in isovolumetric contraction–>decreased SV and ejection fraction—>increased ESV

Most direct measure is peak systolic pressure

Question 31

Contractility (inotropy)

Answer 31

measure of contractile strength that is independent of sarcomere length and EDV

increased contractility—> increases SV at the same EDV

Question 32

vascular funciton curve

Answer 32

increased RAP=decreased venous return

as RAP becomes more negative—>increased VR due to increased DRIVING FORCE

Question 33

Shifts in vascular function curve

Answer 33

shifts up with increased blood volume (increased x intercept (MSFP)

shifts down with decreased blood volume-hemorrhage or dehydration(decrease MSFP)

no changes in slope