Control of Cardiac Output Flashcards
What is cardiac output ? Give a formula for it.
“effective volume of blood expelled by either ventricle of the heart per unit of time”
Cardiac Output = Stroke volume x heart rate
What is the average stroke volume ? average heart rate ? Deduce the average cardiac output from this information.
70 mL
70 bpm
5 L/min
If the demands of tissues increase, what is the maximum stroke volume the heart can produce ? maximum heart rate ? maximum cardiac output ?
140 mL
200 bpm
30 L/min
Describe the main ways in which stroke volume can be controlled.
INTRINSIC (Self-Regulating)
1) FRANK STARLING MECHANISM (change in pre-load)
↑EDV and ↑force of contraction (Increased pre-load results in an increased EDV due to increased amount of blood flowing to ventricles. Increased EDV results in a direct increase in force of contraction (because different EDVs, walls achieve different levels of stretch) which increases stroke volume through increase in ejection fraction (an increase in force of contraction results in an increase in ejection fraction even if EDV does not increase)
2) CHANGES IN AFTERLOAD
“If afterload is increased (e.g., increasing aortic pressure by increasing systemic vascular resistance; red loop in figure), the stroke volume is reduced and the end-systolic volume increased. The increased end-systolic volume, however, leads to a secondary increase in end-diastolic volume because more blood is left inside the ventricle following ejection and this extra blood is added to the venous return, thereby increasing ventricular filling. This secondary increase in preload enables the ventricle to contract with greater force (Frank-Starling mechanism), which partially offsets the reduction in stroke volume caused by the initial increase in afterload (Consequently, in a normal heart, changes in aortic pressure have relatively little affect on stroke volume.)”
EXTRINSIC Sympathetic nerves (increase force of contraction and thus stroke volume/ejection fraction)
Define pre-load and afterload.
PRELOAD = Venous pressure or venous return to heart (If increase EDP, increase amount of blood flowing to ventricles)
AFTERLOAD = Aortic/pulmonary artery pressure (Force heart is exerting against when it contracts, main components being vascular resistance and ventricular wall tension)
Show, in graphical form, EDV, ESV and stroke volume in normal conditions, with intrinsic control, and with extrinsic control.
Refer to slide 4 in lecture on “Control of Cardiac Output”
State Frank Sterling’s Law of the Heart. Explain its role in balancing between L and R sides of the heart.
” strength of the heart’s systolic contraction (i.e. stroke volume) is directly proportional to its diastolic expansion” (hence, by increasing pre-load increase force of contraction and vice versa when decreasing pre-load)
“Hence, this allows for automatic balancing between CO from left-side of heart to volume returning to right-side because:
-increase in stroke volume leads to an increase in cardiac output and arterial pressure; therefore, the afterload on the ventricle increases. This partially offsets the increased stroke volume by increasing the end-systolic volume. The reason for this is that the increased afterload reduces the velocity of fiber shortening and therefore the ejection velocity. “
VICE VERSA “a decrease in preload reduces stroke volume, but this reduction is partially offset by the decreased afterload (reduced aortic pressure) so that the end-systolic volume decreases slightly”
Show Frank Sterling’s Law of the Heart in graphical form (as muscle force as a function of muscle length), including lines denoting total force, active force and resting force, explaining what each of these stands for.
Refer to slide 5 in lecture on "Control of Cardiac Output" Total force = Resting force + Active force Resting force (diastolic) = Recoil resulting from natural elasticity of heart Active force (systolic) = Force generated by muscle contracting itself
Can extrinsic and intrinsic controls of cardiac output work together ?
Yes they can (both can contribute at the same time to increased force of contraction), but it’s mainly just the SNS and intrinsic control (not the PSNS)
Graph the effect of SNS control on force of contraction, comparing it to “normal” force of contraction and a theoretical negative inotropic control of force of contraction.
Refer to slide 6, lecture on “Control of Cardiac Output”
Summarise the main ways in which cardiac output may be altered.
Three main things:
- Increase EDV (intrinsic control, through preload) results in increased force of contraction, and hence stroke volume
- Increase Sympathetic activity (as well as increase in adrenaline) increase force of contraction and hence stroke volume + increase heart rate
- Decrease parasympathetic activity increases HR (chronotropic effect)
Anything that changes either stroke V or heart rate will change cardiac output since
CO = HR x SV
Draw an illustrating showing the oscillation in pressure in the different vessels and heart chambers. Explain the shape of the graph.
Refer to slide 8, lecture on “Control of Cardiac Output”
Overall pattern: Properties of vascular tree means oscillation gets dampened the further
you go in CVS tree so by time you get to capillaries, near continuous fluid flow going through rather than stop start in ventricles
1) In ventricle, push at high degree of P to get aortic valve to open to get blood into aorta
2) Pressure in aorta (non-compliant vessel) means get peak systolic pressures. However, downstream resistance of CV tree that aorta is trying to get blood into resists that flow (aorta still squeezing to push blood further) hence oscillation where P in diastole settles in region of 80.
3) Large arteries thick and very elastic (hard to stretch) so big peaks of pressure because no compliance
4) As go gown vascular tree (e.g. small arteries, arterioles), start distributing pressure because cross sectional area of vascular tree starts increasing (so pressure starts dropping and pulsatile flow starts to diminish into something that’s fairly low P and continuous)
5) (Then same in pulmonary system but at lower magnitude pressure)
Describe the main features of transmission of Pressure Pulses to the Peripheral Arteries.
In systole, arterial system expands to accommodate full ventricular stroke volume. BUT arterial system has limited capacity so SVR limits how fast blood can escape
In diastole, energy stored in arterial walls during systole drives blood forward (without ventricular push)
Describe the main causes of the dampening of pressure pulses in smaller Arteries, arterioles, and capillaries.
(1) “resistance to blood movement in the vessels (because a small amount of blood must flow forward at the pulse wave front to distend the next segment of the vessel; the greater the resistance, the more difficult it is for this to occur)”
(2) “compliance of the vessels (the more compliant a vessel, the greater the quantity of blood required at the pulse wave front to cause an increase in pressure)”
Define a compliant vessel, giving examples of compliant vessels.
Tube with elastic walls which will stretch easily with increasing volume, with little changes in pressure.
Arteries, veins
