University of Virginia Health System

Basic Cardiovascular Physiology

  This section is a review of some basic tenets of cardiovascular physiology which are relevant to invasive cardiac monitoring.  How these principles apply to the specific catheters will be discussed on other pages in greater detail.

Some Basic Review:

Circulatory System:  The circulatory system consists of the heart, the blood vessels, (arteries, arterioles, and blood) and its purpose is to carry oxygen and nutrients to tissues in the body, and to carry away the byproducts of metabolism.

Contractility:  Contractility is the intrinsic ability of cardiac muscle to develop force for a given muscle length.  It is also referred to as inotropism.

Preload:  Preload is the muscle length prior to contractility, and it is dependent of ventricular filling (or end diastolic volume.)  This value is related to right atrial pressure.  The most important determining factor for preload is venous return.

Afterload:  Afterload is the tension (or the arterial pressure) against which the ventricle must contract.  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 most often in 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 a series, and are therefore interdependent; in normal physiology, the right and left ventricle will have the same output.   

   Remember from physiology second year that cardiac function is the volume of blood pumped each minute, and is expressed 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

HR is the number of beats per minute

1. Heart Rate (HR)

    Heart rate is directly proportional to cardiac output; an adult HR is normally 80-100 beats per minute (bpm.)  Heart rate is an intrinsic factor if 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 three factors: 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 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.)

• 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 fiber length is also increased, resulting in an increased ‘tension’ of the muscle.  
• In this way, cardiac output is directly related to venous return, the most important determining factor of preload.  When heart rate is constant, cardiac output is directly related 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.
• 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.

• Cardiac Function Curve : This is simply the Frank-Starling curve for the ventricle showing the relationship of cardiac output as a function of end diastolic volume. 
• Venous Return Curve :  This is the relationship between blood flow in the vascular system (venous return) and right atrial pressure.
• Mean Systemic Pressure :  This is the point where the venous return curve intersects the X axis. The mean systemic pressure reflects the right atrial pressure when there is ‘no flow’ in the system.  At this point the pressure is equal throughout the circulatory system. 
• Equilibrium:  This is the steady-state where the two curves intersect; it reflects the point where cardiac output is equal to venous return. 

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.  Changes in the mean systemic pressure will shift the vascular function curve left or right. 

• Mean systemic pressure is increased 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 C.O. and right atrial pressure.

2.  Inotropic Changes : Contractility is determined by various autonomic mechanisms and certain drugs (such as digitalis). Inotropic changes will alter the slope of the cardiac curve up or down (as discussed above).

• Positive inotropic agents, such as digoxin, will increase contractility and therefore increase the cardiac output (as shown above).  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).

3.  Total Peripheral Resistance Changes : TPR is 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.

• 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 a result of this simultaneous change, both the cardiac output and the venous return are decreased, however the right atrial pressure remains 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 will remain the same .         

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