Cardiac Cycle Flashcards
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
EDV
the highest volume of blood held in the ventricles during isovolumetric relaxation
Right heart cath
inserted thru vein
-3 tips: RA, RV, pulmonary wedge (index of LA pressure)
Left heart cath
inserted into artery advanced into left heart measures flow (ventricular volume changes,)
Stroke Volume
SV=EDV-ESV
the amount of blood ejected in a beat
Left ventricular ejection fraction
EF=SV/EDV
how much of the blood that you could have ejected, did you actually eject
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
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
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
S3
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”
S4
late diastole, just before next S1
associated with an unusually strong atrial contraction-ventricular wall stiffness and decreased compliance assocaited with hypertrophy
“Ten-nessee”
Palpable pulse
radial pulse occurs nearly simultaneous with heart beat, pressure wave travels faster than flow of blood
a wave
RA contraction (diastole) = increased atrial pressure
highest pressure felt in jugular vein
C wave
RV pressure in early systole (bulging of tricuspid into RA
small bump in jugular pressure
V wave
RA filling (TC closed) fill atria from IVC/SVC at beginning early diastole
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
