Cardiac PV Loops Flashcards
cardiac output
CO
total volume of blood pumping into the aorta and pulmonary artery in 1 minute
equation for CO
CO = SV x HR
is cardiac output in the RV >< or = LV
equal
stroke volume
amount of blood ejected with each beat
cardiac index
cardiac output indexed to body size
what are measures of cardiac performance
volume
pressure
flow (echocardiogram)
right vs left heart pressure
right: lower pressure system b/c PA is lower pressure than aorta
left: higher pressure system b/c aorta is higher pressure than PA
pressure volume loops
shows the relationship between pressure and volume during 1 cardiac cycle
PV Loop: marker A
end-systolic volume; volume remaining after contraction
AV: open (begins filling)
SL: closed
PV Loop: marker B
end-diastolic volume; volume in ventricles after filling
AV: close (allows pressure to rise)
SL: closed
PV Loop: marker C
pressure generated in ventricle prior to contraction
AV: closed
SL: opens –> ejection of blood
PV Loop: marker D
pressure remaining after emptying ventricle
AV: closed
SL: close –> prevent regurg
diastole on PV loop
ventricular relaxation and filling
A (early) –> B (late)
volume INCREASES
pressure NO CHANGE
low pressure phase allows for passive filling (atrial > ventricular contraction)
what is compliance
stretch of the ventricle walls that allows for minimal change in pressure during filling
isovolumetric contraction on PV loop
closing of AV valves
B (EDV) –> C
volume NO CHANGE
pressure INCREASES
moderate pressure phase - ventricular pressure rises until it exceeds aortic pressure
systole on PV loop
ventricular contraction nad ejection
C –> D
volume DECREASES
pressure INCREASES
high pressure phase (ventricular > aortic to allow for blood flow out of ventricles, then ventricular decreases until < aortic)
isovolumetric relaxation on PV loop
closing of SL valves
D (ESV) –> A
volume NO CHANGE
pressure DECREASES
does the ventricle completely empty after systole
NO - always some blood remaining in ventricle (end systolic volume)
equation for stroke volume
SV = EDV - ESV
ejection fraction
fraction of blood in the ventricles that gets ejected with every beat
equation for ejection fraction
EF = stroke volume / EDV
EF = (EDV - ESV) / EDV
what are the two determinants of cardiac output
- heart rate
- stroke volume
how does HR affect SV
increase HR = increase CO BUT only up to a point
once HR gets too high –> reduced time to fill during diastole –> less blood available to eject –> decreased CO
also effected by contractility
what 4 components of stroke volume affect CO
- preload
- afterload
- contractility (inotropy)
- relaxation (lusitropy)
preload
diastolic wall stress - the stress put on the ventricular walls by blood entering during diastole
how does preload affect cardiac output
increase preload = increase CO
heart wants to return to the same ESV –> must get rid of more blood if preload increases –> increases CO
what is the main determinant of preload
blood volume/venous return
afterload
systolic wall stress - the pressure required to generate a strong enough contraction to push blood out against aortic pressure
“impedance to ejection”
how does afterload affect cardiac output
increase afterload = decrease CO
too much pressure in aorta –> heart can’t push out as much blood –> decrease CO
what is the main determinant of afterload
systemic vascular resistance/blood pressure
(hypertension –> high pressure in aorta –> high afterload –> low CO)
Laplace’s law
measures the amount of wall stress
wall stress = (pressure x radius) / (2 x wall thickness)
what does Laplace’s law show
the heart can accommodate to increased wall stress by increasing wall thickness to lower wall stress back to baseline
proven by L ventricle wall being thicker than R ventricle
contractility (inotropy)
degree that muscle fibers shorten
how does contractility affect cardiac output
increase inotropy = increase CO
stronger contraction results in more blood being ejected per beat
how does inotropy affect the PV loop
increases the slope of the ESPVR curve
results in a lower ESV (because more blood ejected)
does NOT affect load
does inotropy depend on load
NO - regulated by ANS to alter Ca influx and sensitivity
relaxation (lusitropy)
ventricular compliance and diastolic function
how does lusitropy affect cardiac output
increase lusitropy = increase cardiac output
increased compliance allows for greater filling (increase EDV) –> increased CO
how does diastolic dysfunction affect CO
decreases relaxation –> decreased compliance –> decreased CO
equation for ventricular compliance
deltaV / deltaP
equation for ventricular stiffness
deltaP / deltaV
myocardial oxygen demand
MVO2; the amount of oxygen required by the myocardium to function
what is MVO2 dependent on
- heart rate (inc HR = inc MVO2)
- wall stress/pressure (inc pressure = inc MVO2)
- contractility (inc inotropy = inc MVO2)
when do the coronary arteries delivery oxygenated blood to the heart
during diastole
