[box type=”download”] Relation of cardiac output (CO), heart rate (HR) and stroke volume (SV) Frank – Starling relation between stroke volume and end diastolic volume Starling curve (knowledge of the detail of this curve is required) Implications of imbalance in the Starling relationship – pulmonary odema Baroreceptors as a determinant of CVP upon standing to correct the Starling relationship Implications of the Starling relationship for increased afterload[/box]
Cardiac output (CO) = heart rate (HR) X stroke volume (SV).
SV is influenced by the filling pressure (preload), cardiac muscle force, and the pressure against which the heart has to pump (afterload).
Both the heart rate and force are modulated by the autonomic nervous system (ANS).
Filling pressure and Starling’s law
The right ventricular end diastolic pressure (EDP) is dependent on central venous pressure (CVP) and left ventricular EDP is dependent on pulmonary venous pressure.
EDP and the compliance of the ventricle determine the end diastolic volume (EDV).
As EDP (and so EDV) increases, the force of systolic contraction and thus SV also increases.
This is called the Frank–Starling relationship, and the graph relating SV to EDP is called a ventricular function curve.
The Starling’s law states: ‘The energy released during contraction depends on the initial fibre length’.
Cardiac muscle has a much steeper relationship between stretch and force than skeletal muscle, because stretch also increases the Ca2+ sensitivity of troponin, so more force is generated for the same intracellular Ca2+.
The ventricular function curve is therefore steep, and small changes in EDP lead to large increases in SV.
Importance of Starling’s law
The most important consequence of Starling’s law is that SV in the left and right ventricles is matched.
If, for example, right ventricular SV increases, the amount of blood in the lungs and thus pulmonary vascular pressure will also increase.
As the latter determines left ventricular EDP, left ventricular SV increases due to Starling’s law.
This represents a rightward shift along the function curve.
Starling’s law thus explains why an increase in afterload (e.g. hypertension) may have little effect on CO.
More blood is left in the left ventricle after systole, and as a result, blood accumulates on the venous side and filling pressure rises.
Cardiac force therefore increases according to Starling’s law until it overcomes the increased afterload and, after a few beats, CO is restored at the expense of an increased EDP.
Autonomic nervous system
Sympathetic stimulation increases heart rate and cardiac muscle force.
The ventricular function curve therefore shifts upwards.
Parasympathetic decreases HR.
Sympathetic nerves also activate arterial and venous vasoconstriction.
Arterial vasoconstriction increases total peripheral resistance (TPR) and impedes blood flow.
Venoconstriction reduces the compliance of veins and hence their capacity – CVP increases.
Sympathetic stimulation therefore increases CO by increasing heart rate, contractility and CVP.
Postural hypotension.
On standing from a prone position, gravity causes blood to pool in the legs and CVP falls.
This in turn causes a fall in CO (due to Starling’s law) and thus a fall in blood pressure.
This postural hypotension is normally rapidly corrected by the baroreceptor reflex, which causes venoconstriction (partially restoring CVP) and an increase in heart rate and contractility, so restoring CO and blood pressure.
Even in healthy people it occasionally causes a temporary blackout (fainting or syncope) due to reduced cerebral perfusion.
Venous return and vascular function curves
Venous return will be impeded by a rise in central venous pressure CVP.
CVP is only altered by changes in blood volume or its distribution (e.g. venoconstriction).
Venous return is maximum when CVP is zero.
Conversely, venous return will be zero if the heart stops, ~ CVP will equal mean circulatory pressure (PMC)at this point.
Raising blood volume or venoconstriction increase PMC causing a parallel shift of the vascular function curve. Arterial vasoconstriction has insignificant effects on PMC.
Guyton’s analysis (graph)combines vascular and cardiac function curves into one graph.
The only point where CO and venous return are equal is the intersection of the curves (A); this is thus the
operating point.
If blood volume is now increased, the shift in the vascular function curve leads to a new operating point (B) where both CO and CVP are increased; blood loss does the opposite (C).
In exercise, sympathetic stimulation causes both increased cardiac contractility and venoconstriction, but TPR falls due to vasodilation in active muscle.
Thus both cardiac and vascular function curves shift up, but because of the fall in TPR the latter has a steeper slope.
The new operating point (D) shows that in exercise CO can be greatly increased with only minor changes in
CVP.