Control of Cardiac Output/Cardiac Cycle Flashcards
7 phases of cardiac cyce
(Systole 2,3,4)(Diastole 5,6,7,1)
2- Isovolumetric contraction
3- Rapid ejection
4- Reduced ejection
5- Isovolumetric relaxation
6- Rapid filling
7- Diastasis
1- Atrial systole
Phase 1
Atrial systole
NOT REQUIRED
20-40% of LV filling
LVEDV=120ml
Possible s4
When are all valves closed?
Phase 2- isovolumetric contraction
S1= mitral valve closes
ALSO
Phase 5- isovolumetric relaxation
S2= pulmonic and aortic valves close
When are pulmonic and aortic valves open?
Phase 3- rapid ejection
No heart sounds
What percent ejects during phase 3?
70%
LVESV
50ml
Phase 6
Rapid ventricular filling
Possible S3
Phase 7
Reduced ventricular filling
Diastasis
Frank sterling law
The bigger the preload, the bigger the force of contraction and thus bigger SV (within limits)
When the sarcomere length is increased, more actin and myosin can bind, causing bigger contraction
Cardiac SV responds more to preload than nuerohormonal mechanisms like the intrincsic heart nodes
Matching venous return to cardiac output in BOTH ventricles
Changes force in contraction and SV in response to venous return
Increase volume increases contraction
What is the more independent flow?
Arterial is less controlled by blood flow and CO
What is CO? Not the equation
Quantity of blood pumped into the aorta each minute
Venous return
The amount of blood coming into the RA each minute
What controls CO normally?
Venous return, the heart is not the primary controller of CO
SV formula
EDV- ESV
EF
SV/EDV
What controls heart pumping?
ANS
SNS can double CO
ANS can decrease CO to almost 0 by vagal
What is more important for changing CO? HR or SV
HR
Bowditch (Treppe) Effect
“staitway effect”
Increase in Hr also increases inotropy
Due to an increase in intracellular CA with higher HR
NaK-ATPase cant keep up with influx of Na, so Na/Ca pump doesnt work well
Values for SV, EDV, ESV
70ml
120ml
50ml (wont close all the way like alveoli wont), but can decrease to 20 under high inotropy effect, EDV increases, which bumps sv to 150ml
Preload and how its measured
Tension of cardiac myoctyes
Related to sarcomere length
LVEDV
LVEDP
PCWP
CVP
Frank starling curve
Looks like small s curve with the same starting point but different end points
Shift right and down- means increased afterload or decreased inotropy
Shift left and up, means increased inotropy or decreased afterload
Laplace law
T(Wall stress)= P(pressure) R(Radius) /H(thickness
What does increased afterload do to LVESV and SV?
Increases LVESV, decreases SV
What can and cant change heart force?
Can:preload- dependent activation, inotropy-independent activation
Cant: recruitment like other skeletal muscles
When does CA influx to increase inotropy, what phase?
Phase 2
What (physiologic) 3 ways to stimulate inotropywith calcium
CA influx phase 2 during AP
Increasing CA by SR
Sensitizing Trop-C to CA
What does SNS effect mostly in the heart?
Inotropy, ventricular and atrial inotropy
What does PNS affect mostly in the heart?
Negative effect on atria, minimal on ventricles
Anrep affect
Sudden increase in afterload will increase inotropy
Increasein afterload increases LVEDP, frank starling causes increased inotropy
Only lasts for 15 minutes
Primary- frank starling, trop c sensitize
delayed- SR release of CA
What increases afterload?
Aortic pressure
SVR
AV Stenosis
Ventricular dilation
What is responsible for the increased CO that follows an increase in afterload? (Primary and delayed)
- Frank sterling mechanism/Troponin C sensitivity to calcium
- CA increase by SR
