14. Cardiac Output & Contractility Flashcards
what is preload
- amount of blood ready to be pumped at the end of diastole = end diastolic volume
- wall tension in ventricle just before contraction is initiated
- fiber length at the end of diastole
how is preload related to venous return
more blood returning → greater preload
- in a steady state, venous return = CO
- frank starling: volume of blood ejected depends on the volume present at end of diastole
what is afterload
force opposing contraction, pressure required to eject blood (i.e. open aortic/pulmonary valve)
- increase in vessel pressure causes and increase in afterload
how does afterload effect the velocity of muscle fiber contraction?
when is velocity the greatest?
- velocity of shortening decreases as afterload increases (inverse relationship)
- greatest if afterload were 0
what effect does preload have on contractility and CO?
afterload?
↑ preload → ↑ CO and contractility
↑ afterload → ↓ CO
Heart must then ↑ contractility or HR to overcome
Describe the relationship between heart rate and contractility in terms of the positive staircase effect.
↑ HR (+ chronotropic effect) → ↑ contractility (+ ionotropic effect)
Positive staircase effect: ↑ force of contraction in a stepwise manner d/t cumulative increase in intracellular Ca; more Ca enters cell and more is taken up into SR
also seen with premature or out of synch beat; weak beat will be followed by stronger beats
how do you calculate SV and what is normal
SV: volume of blood ejected by ventricles with each beat
= HR x CO = EDV - ESV
Normal = 70 mL
how do you calculate EF% and what is normal
Ejection fraction: fraction of EDV ejected in each SV, measures efficiency and contractility
= SV / EDV
Normal = 55%, reduced in heart failure patients
how do you calculate CO and what is normal
CO: total volume of blood ejected by ventricle per minute
= SV x HR
Normal = 5L/min
what effects does the sympathetic system have on contractility?
how?
positive ionotropic effect through B1 adrenergic activation → ↑ in contractility
Activation causes phosphorylation of…
- Sarcolemmal Ca channels → ↑ inward ICa during phase 2
- Phospholamban (stimulatory) → ↑ activity of Ca pump so more Ca is accumulated in the SR
- Troponin I (inhibitory, inhibition of inhibitor)
what effect do cardiac glycosides have on contractility?
how?
Cardiac glycosides: ↑ contractility
Done by inhibiting Na-K-ATPase → ↑ in intracellular Na, diminishing gradient used by Na-Ca exchanger (more Ca stays in)
what effect does the parasympathetic system have on contractility?
how?
negative ionotropic effect in atria only via muscarinic activation → ↓ in contractility
- ↓ inward ICa during phase 2
- ACh ↑ outward IK via K-ACh channel
what is happening between points 1 and 2 on pressure volume loop?
1 → 2: isovolumetric contraction, all valves closed
- 1: EDV (preload), marks the end of diastole, pressure is low (EDV = 140 mL)
- 2: afterload, marks point where ejection of blood begins, aortic valve open
what is happening between points 2 and 3 on pressure volume loop?
2 → 3: ventricular ejection
- max pressure between points 2 and 3
- SV = 70 mL (measured by width of loop)
- 3: ESV
what is happening between points 3 and 4 on pressure volume loop?
3 → 4: isovolumetric relaxation
- 3: systole ends (ESV) and ventricles relax
- Pressure falls quickly by volume remains constant
- 4: AV valve opens
what is happening between points 4 and 1 on pressure volume loop?
4 → 1: ventricular filling
what effect does increased preload have on pressure volume loop?
↑ venous return, ↑ blood volume → ↑ EDV
Shifts point 1 and 2 to the right
Compensation: ↑ contractility
what effect does increased afterload have on pressure volume loop?
↑ in aortic pressure (ventricle must eject blood against higher pressure) → ↓ SV, ↓ EF%
↓ SV → ↑ ESV
Shifts point 2 and 3 up
d/t aortic stenosis, hypertension
what effect does increased contractility have on pressure volume loop?
greater tension in ventricle → ↑ SV, ↑ EF% (↑ SV → ↓ ESV)
Shifts points 3 and 4 to the left, 2 → 3 gets higher
d/t adrenergic stimulation
what is stroke work and how does it effect function of the heart?
= SV x pressure work (aortic pressure)
Area within the pressure-volume loop
Heart has to work harder to overcome aortic pressure → cardiomegaly
how does pressure work effect LV?
what does this have to do with O2 consumption?
how do you calculate CO based on O2 consumption
- LV must proportionally work harder than RV despite CO being similar because systemic pressure is greater than pulmonary pressure.
- Pressure work (fighting aortic pressure) requires the most O2 consumption
- CO = O2 consumption / ([O2] pulmonary a - [O2] pulmonary v)
Aortic stenosis and HTN increase LV pressure work
describe the cardiac function curve
↑ venous return → ↑ RA pressure → ↑ EDV and end diastolic fiber length
describe the vascular function curve
relationship between venous return and RA pressure
what is the equilibrium point between the cardiac and vascular function curve
CO = 5 L/min
RA pressure = 2 mm Hg
what effect will increased inotropy have on the cardiac fxn curve?
decreased?
↑ ionotropy → ↑ HR → ↓ afterload
↓ ionotropy → ↓ HR → ↑ afterload
what is mean systemic pressure
pressure in atria when there is no blood flow
CO and VR are zero, pressure is equal throughout cardiovascular system
how would mean systemic pressure be increased and what effect would this have on the graph?
decreased?
↑ MSP by ↑ in blood volume or ↓ in venous compliance
- shifts curve to the right
↓ MSP by ↓ in blood volume or ↑ in venous compliance
- shifts curve to left
what effect does + inotropy have on cardiac fxn and how would this appear on the graph?
- inotrophy?
+ inotropic effect: ↑ contractility and CO
- slope of cardiac fxn curve ↑
- e.g. digitalis
- inotropic effect: ↓ contractility and CO
- slope of cardiac fxn curve ↓
what effect does increased TPR have on cardiac fxn and how would this appear on the graph?
decreased TPR?
Increased: ↓ CO and venous return
- Shifts intersection point ↓
Decreased TPR: ↑ CO and venous return
- Shifts intersection point ↑
***No change in atrial pressure
what effect does increased blood volume have on cardiac fxn and how would this appear on the graph?
decreased blood volume?
↑ blood volume: ↑ MSP, ↑ CO and RA pressure
- cardiac function curve moves up
↓ blood volume: ↓ MSP, ↓ CO and RA pressure
- cardiac function curve moves down
what happens to inotropy, vascular compliance, blood volume, and TPR in heart failure?
↓ inotropy and vascular compliance
↑ blood volume and TPR
