Download Basic Cardiovascular Physiology

Basic Cardiovascular Physiology
This section is a review of some basic tenets of cardiovascular physiology.
Some Key Words:
Contractility: Contractility is the intrinsic ability of cardiac muscle to develop force at a given muscle length
(ie independent of thick/thin filament overlap). It is also referred to as inotropism.
Preload: Preload relates to the muscle length (and, therefore, the strength of contraction) just prior to
systole, and so it is dependent of ventricular filling (or end diastolic volume.) The most important
determining factor for preload is venous return. Preload is sometimes thought of in terms of right atrial
pressure (since RAP can be measured, and the higher the pressure the greater is the filling of the atrium, and
the greater is the filling of the ventricle, and the greater is the stretch of the cardiac muscle, and the greater
is the force of contraction).
Afterload: Afterload is the force that the ventricle must overcome when it contracts in order to pump blood;
it is, effectively, the end-diastolic arterial pressure trying to push blood back into the ventricle. If arterial
pressure increases, afterload also increases. Afterload for the left ventricle is determined by aortic pressure,
afterload for the right ventricle is determined by pulmonary artery pressure.
Determinants of Cardiac Performance:
When we discuss ventricular dysfunction, it is usually with reference to the left ventricle; however, it is
important to understand that the same basic principles apply to the right ventricle. The left and right sides of
the heart exist in series, and are therefore interdependent; in normal physiology, the right and left ventricles
have exactly the same output.
Cardiac output is the volume of blood pumped each minute, and is determined by the following equation:
CO = SV x HR
Where:
CO is cardiac output expressed in L/min (normal ~5 L/min)
SV is stroke volume per beat (about 0.07 L/beat)
HR is the number of beats per minute (about 70 beats/min)
1. Heart Rate (HR)
Cardiac output is directly proportional to heart rate; an adult HR is normally 70-90 beats per minute (bpm).
Heart rate is an intrinsic property of the SA (pacemaker) node in the heart, and it is modified by autonomic,
humoral, and local factors. For example:
1. An increase in vagal activity, via M2 cholinergic receptors in the heart, will decrease the heart rate.
2. An increase in sympathetic activity, via B1 and B2 adrenergic receptors throughout the heart, will
increase the heart rate.
2. Stroke Volume (SV)
Stroke Volume is determined by the three factors mentioned at the top of the page: preload, afterload,
and contractility. The preload gives the volume of blood that the ventricle has available to pump, as well as
the end diastolic length of the muscle. The contractility is the force that the ventricular muscle can create at
the given length, and the afterload is the arterial pressure against which the muscle will contract. These
factors establish the volume of blood pumped with each heart beat. Valvular dysfunction and ventricular
geometric form can also affect stroke volume, depending on the pathology of the valves or the ventricle.
How Determinants of Cardiac Function Interact:
Here we will examine two ways of looking at the relationship between the multiple determinants of cardiac
function, and how changes in the separate factors affect the overall cardiac output.
1. Frank – Starling Principle :
This principle illustrates the relationship between cardiac output and left ventricular end diastolic
volume (or the relationship between stroke volume and right atrial pressure.)
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The Frank Starling principle is based on the length-tension relationship within the ventricle. If
ventricular end diastolic volume (preload) is increased it follows that the ventricular fibre length is also
increased; this results in an increased ‘tension’ generated by the muscle and, therefore, increased
stroke volume.
In this way, cardiac output is determined by venous return, since venous return is the most important
determining factor of preload. When heart rate is constant, cardiac output is directly proportional to
preload (up to a certain point.)
An increase in preload will increase the cardiac output until very high end diastolic volumes are
reached. At this point cardiac output will not increase with any further increase in preload, and may
even decrease after a certain preload is reached (basically due to ‘overstretching’ the muscle fibres).
Also, any increase or decrease in the contractility of the cardiac muscle for a given end diastolic
volume will act to shift the curve up or down, respectively.
2. Cardiac and Vascular Function Curves:
These are simultaneous plots of cardiac output and venous return as a function of end diastolic
volume (or right atrial pressure.)
Figure 2: Simultaneous Plots of the cardiac and vascular function curves. The two curves cross at the point of
equilibrium for the cardiovascular system.
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Cardiac Output Curve : This is simply the Frank-Starling curve for the ventricle showing the
relationship of cardiac output as a function of end diastolic volume (or RAP).
Venous Return Curve : This is the relationship between blood flow in the vascular system (venous
return) and right atrial pressure. The curve as plotted implies that high EDV or RAP decreases VR but
increases CO; these effects are obviously not sustainable as CO needs to equal VR on a minute to
minute basis. However, one can imagine that if RAP or EDV is high, then it becomes more difficult for
blood to flow back into the heart, so VR will be less.
Equilibrium point: This is the steady-state where the two curves intersect; it reflects the RAP or
EDV where cardiac output is equal to venous return (ie where we are most of the time).
Mean Systemic (Filling) Pressure : The mean systemic pressure equates to the right atrial
pressure when there is no ‘flow’ in the system (ie VR is 0). So, this is the point where the venous
return curve intersects the X axis (ie VR = 0). The RAP at this point represents the pressure
throughout the circulatory system (since blood is not flowing). You can think of the MS(F)P as being
the single pressure you would record in the vascular system if you tied off all of the vessels leading
into and out of the heart.
Cardiac output can increase or decrease by altering the Frank-Starling curve, the venous return curve, or
both; some predictions can be made by examining how the curves shift as the variables change.
1. Mean Systemic Pressure Changes: The mean systemic pressure is affected by blood volume as well as
venous compliance (which determines how much blood is present in the venous side of the circulation).
Changes in the mean systemic pressure will shift the vascular function curve left or right.
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Mean systemic pressure is incrased by an increase in blood volume and/or a decrease in venous
compliance (as shown above). This will act to shift the vascular function curve to the right, illustrating
an increase in both cardiac output and right atrial pressure.
Conversely, mean systemic pressure is decreased by a decrease in blood volume and/or an increase
in venous compliance (not shown). This will shift the vascular function curve to the left, illustrating a
decrease in both CO and right atrial pressure.
2. Inotropic Changes : Contractility is determined by various autonomic mechanisms and certain drugs
(such as digitalis). Inotropic changes alter the slope of the cardiac curve up or down (as mentioned earlier).
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Positive inotropic agents, such as digoxin, will increase contractility and therefore increase the cardiac
output (as shown above); ie greater SV at any given HR and EDV (ie emptying the ventricle more
means less pressure is needed to refill it). This new equilibrium point now reflects an increased
cardiac output and a lower right atrial pressure (more blood is now being ejected from the heart with
each beat).
Negative inotropic agents have the opposite effect, decreasing contractility and cardiac output, and
increasing right atrial pressure (not shown); thus, reducing SV leaves more blood behind in the
ventricle, requiring a higher pressure to refill it.
3. Total Peripheral Resistance Changes : TPR is mainly determined by the resistance of the arterioles.
Changes in TPR will change the slope of both the cardiac function curve and the venous return curve.
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An increase in TPR (shown above) will cause blood to be retained on the arterial side of circulation and
will increase the aortic pressure against which the heart must pump. This will act to shift both slopes
downward as less blood is pumped and less flows back to the heart as VR. As a result of this
simultaneous change, both the cardiac output and the venous return are decreased, so the right
atrial pressure remains about the same.
A decrease in TPR (not shown) will allow more blood to flow to the venous side of circulation and will
lower the aortic pressure against which the heart must pump. This will shift both slopes upward.
Both cardiac output and venous return will be simultaneously increased; again, right atrial pressure
remains about the same.