Cardiac Cycle Flashcards by Charlie Simpkin

Isovolumetric contraction

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

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EDV

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

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Right heart cath

inserted thru vein

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

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Left heart cath

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

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Stroke Volume

SV=EDV-ESV

the amount of blood ejected in a beat

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Left ventricular ejection fraction

EF=SV/EDV

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

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Heart sounds: L R comparison

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

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S2 splitting: Right heart

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

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S2 Splitting: left heart

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

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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”

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

“Ten-nessee”

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Palpable pulse

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

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a wave

RA contraction (diastole) = increased atrial pressure

highest pressure felt in jugular vein

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C wave

RV pressure in early systole (bulging of tricuspid into RA

small bump in jugular pressure

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V wave

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

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elevated a wave

tricuspid stenosis

R heart failure

Cannon a waves

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

no a waves

a fib

large v wave

tricuspid regurgitation

Kinetic energy

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

Tension heat

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

2 main determinants of myocardial O2 demand

Ventricular wall stress
HR
contractility

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

Wall stress

directly proportional to systolic ventricular pressure, radius of ventricular chamber

inversely proportional to ventricular wall thickness

Factors impacting SV

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

passive tension

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

Active tension

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

Frank starling law

increased preload (EDV)= increased force of contraction increased EDV=increased SV

Frank Starling: systolic failure

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

force velocity relationship

Increased afterload--->decreased outflow velocity increased EDV--->increased outflow velocity

Afterload

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

Contractility (inotropy)

measure of contractile strength that is independent of sarcomere length and EDV increased contractility---> increases SV at the same EDV

vascular funciton curve

increased RAP=decreased venous return as RAP becomes more negative--->increased VR due to increased DRIVING FORCE

Shifts in vascular function curve

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