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Cardiac output (CO)

-Volume of blood pumped by the left ventricle (LV) in one minute
-Coronary blood flow is regulated by metabolic factors only (no neural control)
-CO = SV x HR


Factors controlling EDV

-Effective filling pressure: venous pressure
-Ventricular compliance
-Heart rate (diastolic interval)


Factors controlling ESV

-Contractility: length-tension (ideal overlap of sarcomeres) and force-velocity (pre-load vs after-load and sympathetic stimulation)
-Aortic pressure: affected by TPR, SV, and aortic compliance


Ventricular compliance

-High compliance means the ventricle can be stretched with ease, low compliance means stiffer walls
-This interacts w/ the HR and venous pressure to give the EDV
-At equal venous pressures, low compliance walls do not fill as well and lead to low EDV
-High compliance walls fill more effectively and generate greater EDV


Heart rate on EDV

-When HR is increased, the expense is at diastolic time (systolic time remains relatively fixed)
-At higher HR, diastolic time shortens so much that the ventricles cannot fill fully and the EDV can drop
-At low HRs atrial contraction adds little blood to the EDV
-But at these high HRs, the atrial contraction becomes crucial to achieve max EDV, and if there is disturbance in atrial rhythm the CO may be affected due to low EDV


Length-tension on ESV (frank-starling): increased venous pressure 1

-2 things to consider: increased venous pressure and increased aortic resistance, both can affect the ESV/CO
-With increase venous pressure there is more filling of the ventricles thus EDV goes way up
-With a higher EDV there is more stretch on the ventricles and greater overlap of the sarcomeres, which results in a stronger force of contraction (up to a point- beyond ideal overlap force of contraction goes down)


Length-tension on ESV (frank-starling): increased venous pressure 2

-Therefore the increased EDV leads to increased SV and thus CO w/ the same arterial BP
-Since the EDV is increased greatly we will also see a small increase in the ESV
-This is because not all of the excess blood will be pumped so the residual volume (ESV) will also increase


Length-tension on ESV (frank-starling): increased aortic resistance 1

-If the aortic (arterial) resistance is increased there is at first a reduction in SV as the ventricle cannot empty as effectively against the resistance
-Thus ESV increases and since the venous pressure is the same (diastolic inflow equal) the increase in ESV will lead to an increase in EDV (blood builds up in ventricle)


Length-tension on ESV (frank-starling): increased aortic resistance 2

-Once this has happened a new steady-state is reached in which the increased EDV increases stretch on the ventricle walls and increases force of contraction
-Since the heart is working against increased aortic pressure, the increased force of contraction does not increase SV or CO
-Thus you seen increased ESV and EDV, with unchanged SV and CO, from increased aortic pressure


Positive vs negative inotropes

-Positive inotropes enhance the contractile properties of the cardiac muscle (NE)
-Negative inotropes diminish the contractile properties of cardiac muscle (Ach)
-Both of these play a role in the force-velocity curves, by either increasing Vmax (+ inotropes) or decreasing Vmax (- inotropes)


Force-velocity 1

-Pre-load: the force that determines the initial fiber length (overlap of sarcomeres)
-Pre-load is the EDV as determined by the venous pressure
-Increasing pre-load helps the cardiac cells reach maximum force of contraction against the after-load, or the force the heart is contracting against
-Therefore higher pre-load w/ same after-load increases the velocity of contraction (an indication of effectiveness of actin-myosin cross-bridges, number of open binding sites, and Ca availability)


Force-velocity 2

-The after-load is the aortic resistance (aortic pressure), which is largely determined by TPR (also a little by SV and aortic compliance)
-Increasing after-load will do 3 things: increases tension before shortening, decrease degree of shortening, and decrease velocity of shortening


Force-velocity 3

-Overall, increasing pre-load w/ constant after-load: velocity increases (Vmax doesn't change)
-Increasing after-load w/ constant pre-load: velocity decreases (Vmax doesn't change)


Changing Vmax

-The velocities can change due to venous pressure (pre-load) or aortic pressure (after-load), but the main way we increase or decrease the velocities is by changing Vmax
-Vmax can only be changed by + or - inotropes, via neural activation
-NE release from sympathetic stimulation is a + inotrope, thus making cross-bridges more efficient and stronger at all lengths (no matter the pre/after loads)
-Ach from parasympathetic stimulation has the opposite effect (- inotrope) and decreases Vmax regardless of pre/after loads


Effects of contractility and aortic pressure on ESV

-Increasing contractility (primarily by + inotropes) leads to decreased ESV (most of the blood in LV is expelled) and thus increases SV-> increases CO
-Increasing aortic pressure (by increasing TPR) leads to increases ESV (more resistance for the LV to work against-> doesn't move as much blood) and thus decreases SV-> decreases CO


Force-velocity effects in an intact heart

-In an intact heart the force-velocity effects dominate the length-tension effects (which are simply a safety net)
-Length-tension only operates during heart failure, as a reserve mechanism to preserve CO
-Length-tension aspects of force-velocity (changing muscle fiber lengths) do not matter so much as the neural inputs (changing cross-bridge dynamics)
-Changing the sympathetic nerve supply is the dominant way to affect the force-velocity in an intact heart
-Therefore, changing after load and preload have relatively small influences on cardiac function, whereas changing neural input has large effects


Energy requirements of the heart

-Use the PTI (pressure-time index) to measure the amount of O2 consumption in the heart
-PTI = HR x BP
-Worth noting that CO can be increased w/o increasing O2 consumption only if cardiac pressure doesn't increase (in response to BP increase)


Ventricular function curves

-Plot CO against right atrial pressure (RAP, the same as venous pressure)
-At rest the curve is sinusoidal, and with maximum activation there is increased CO at the same RAP
-This indicates a positive inotrope is increasing the contractility of the muscles, and it is not the RAP affecting length-tension
-As opposed to the failing heart, which has greatly reduced CO at any given RAP
-Positive inotropes: moves curve up and to left
-Negative inotropes: moves curve down and to right


Neural affecters of CO

-For EDV: sympathetic input can affect HR (increasing HR very slowly increases EDV up to a point around 150 b/m, at which the EDV drops due to incomplete filling)
-Circulating agents and temp also affect the HR
-Increasing HR increases CO (CO = SV x HR)
-For ESV: sympathetic input increases contractility (length-tension and force-velocity) and increases Vmax
-The increased contractility results in less blood in ventricle after systole (decreases ESV) and thus increases SV, increasing CO
-Sympathetic stimulation to peripheral arterioles increases TPR (TPR affect on CO to be discussed in guyton model)


Cardiac cycle

-Starting at diastole, the AV valves open and the ventricles fill with blood
-The ventricles start with ESV and end w/ EDV (increase in volume), at which point AV valves close and systole begins
-There is isovolumetric contraction (both valves closed) which increases the pressure, followed by opening of the semilunar valves and ejection (reduction in volume)
-At ESV the semilunar valves close and there is isovolumetric relaxation (with both valves closed)
-Once pressure drops the AV valves open and diastole begins again