cardiac output Flashcards
What determines Cardiac output
1) Preload: Directly related to venous return
2) Contractility: inotropic agents, heart rate, condition/state of the heart (ex. heart failure)
3) Afterload
4) Heart rate
–> #1-3: relate to stroke volume
–> #4 = heart rate
Cardiac output = HR x Stroke volume
What occurs in the Frank-Starling Curve if you decrease HR
Decreased HR = Increase filling time = Increase End diastolic volume = increased Stroke volume
CO (cardiac output) = (lower) HRxSV (higher) = cardiac output is maintained despite lowering or raising HR!!!!
Define Preload
end diastolic pressure when ventricle has become filled (what has been dumped into ventricle (Venous return)
Define Afterload
aortic pressure
- total peripheral resistance
- the pressure that the heart has to pump into/against
What are the effects of Increasing END DIASTOLIC VOLUME (Preload)
- INCREASES STOKE VOLUME (all other variables equal (graph gets wider/fatter but stays equally tall)
- -> occurs during dumping more stuff into the system (fluid replacement overkill)
- -> More coming in, more going out
What are the effects of increasing after load
- REDUCE stroke volume (all other variables equal
- -> Graph gets skinnier AND taller
- -> Harder to open aortic valve so requires more pressure
- ex: Increasing arterial pressure
Describe the effects of Increasing Contractility
- Positive inotropic agent shifts the AFTERLOAD “curve” upward
- results in an INCREASE in STROKE VOLUME
- Pumping more efficiently
Describe the effects of Decreasing Contractility
- In the same way, a negative Inotropic agent (decrease in contractility) shifts the developed tension curve downward
- -. Results in DECREASE IN STROKE VOLUME
- CALLED SYSTOLIC DYSFUNCTION
- ex: myocardial infarction, ischemia, dilated cardiomyopathy, volume overload
Describe the effects of DIASTOLIC Dysfunction
Diastolic dysfunction indicates impairment in the “relaxation capacity” of the ventricle (ventricle becomes stiffer or less compliant)
–> ex: remodeling of matrix, hypertrophy, transient ischemia, restrictive cardiomyopathy
Describe Frank-Starlings law of the heart
Stretch of sinus node directly increases heart rate
- plateau caused by collapse of large veins under high negative pressure in chest
- Mean systemic filling pressure (Psf) = pressure driving blood BACK to heart.
- -> if Right atrial pressure = Psf, venous return is ZERO
What occurs when Blood volume changes?
Less blood in the circulation REDUCES the Psf
- More blood will INCREASE Psf
- *Shifts the venous return curve
What occurs when you constrict or dilates your vessels?
Changes in Arteriolar TONE causes changes in what is coming back to the heart BUT NOT the overall Psf (overall volume stays the same) (rate of return changes but the total volume stays the same)
- Vasoconstriction reduces venous return
- Vasodilation increases venous return
Describe the effects of sympathetic control on the Heart
Increases HR
- Innervation of SA/AV node
- Increaes FORCE of contraction via innervation of muscle cells which alters the Ca++ permeability in the myocytes to increases contraction
Describe the effects of Parasympathetic control on the Heart
Decreases HR
- Innervation of SA/AV nodes
Describe the Autonomic Control of the HEART during ACUTE Exercise
Changes during Systole
- Increase GlycogenoLYSIS (more energy, enhanced contraction
- Increase cellular permeability to calcium (increase contractile efficiency)
- Increase HR (reduced filling time)
- OVERALL INCREASE IN CARDIAC OUTPUT
Changes during DIASTOLE:
- Increase HR (reduced filling time)
- Enhanced Ca++ uptake (increases Ca+ efflux and increases Ca++ sequestration
- SHORTER RELAXATION time but more EFFICIENT and faster FILLING
