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