Unit 2 Lecture 5: Cardiac Output Flashcards
What is the formula for cardiac output?
SV x HR
SV indicates how much volume the left ventricle has to pump out
HR is how fast our heart is beating
What factors regulate SV?
Sympathetic Nervous System (SNS) & EDV (end-diastolic volume)
Which factors that help regulate CO are extrinsic? Intrinsic?
Extrinsic: PNS (HR), SNS (HR & SV) & Venous Return (SV)
Intrinsic: EDV (SV)
How does venous return increase?
Via SNS which will also increase EDV since venous return affects how much blood the ventricles will stretch out to hold & therefore the SV as well
Why is SV not dependant on action potentials?
SV is more reliant on downstream processes like excitation-contraction coupling & changes in Ca2+
How can you change pacemaker potential?
By changing pacemaker activity
* PNS to decrease pacemaker activity (decrease HR)
* SNS to increase pacemaker activity (increase HR)
How does the membrane potential change when it comes to pacemaker potential?
Must change the ion permeability of the membrane to have an impact on pacemaker potential
Must adapt to different ion fluxes
During PNS when acetylcholine is released what happens to pacemaker activity and what causes it to change?
Pacemaker activity decreases; negative effect on HR
* Changes are due to increased K+ efflux
* Changes are due to decreases Na+ and Ca2+ efflux
* Resting membrane potential decreases
NOTE: T-type calcium channels dictate pacemaker membrane potential so decreasing that will result in decreased pacemaker potential
What happens to threshold potential when SNS and PNS are involved?
Threshold potential of pacemaker potential is -40mV (same)
During SNS when epinephrine and norepinephrine are released what is happening to pacemaker activity?
Increases HR
* Increase in Na+ and Ca2+ influx into the cell via the channels
* Threshold potential stays the same
* K+ is not affected & resting membrane potential does not change
What is a key regulator of SV? What predominantly dictates SV?
- Key regulator is cardiac muscle cell as they contract to push blood out
- EDV (end-diastolic volume) dictates how much SV there will be
What do the X and Y-axis of the Frank-Starling Mechanism represent?
- Y-axis represents SV; increased SV means more blood is being pumped out of the heart
- X-axis represents EDV; increased EDV means more blood is passively filling into the ventricles & actively filling via atrial contraction
REMEMBER: Increasing SV is by stretching the ventricles & increasing Venous return
How does cardiac muscle work during the descending limb of the length-tension curve
Trick question; it does not actually operate once the length-tension curve begins to drop because that indicates the heart is being overly stretched and is not producing enough force
What causes the rise on the Frank-Starling Mechanism
- Increasing EDV and SV; SV means more blood will be pumped out and that means venous return is higher & therefore, muscle tension increases
- EDV relates to length so more EDV means greater length & venous return
NOTE: Ventricles stretch out more which allow for more muscle tension which makes sense since greater SV means more blood moving through ventricles so it needs to be able to withstand the pressure
What if we were to only change the SV and keep the EDV the same? What happens to the Frank-Starling curve?
SV indicates increase in tension but how this is done is through SNS.
- SNS control gives us greater SV; depends on calcium release inside every cardiac muscle cell
- Dictating the release of calcium inside every single cardiac muscle cell is the L-type channel of the plateau phase in cardiac action potential
