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CHAPTER 4

Cardiovascular Physiology

and Support

Mark W. Newton
John R. Gosche
Laura Boomer

Introduction pericardial disease, end diastolic right ventricular filling pressure in the
Failure of the circulatory system leads to organ dysfunction and ulti- right ventricle is equivalent to diastolic atrial pressure and is reflected by
mately to death. A basic understanding of the physiologic principles of central venous pressure. In practice, unfortunately, direct measurements
cardiovascular control is essential for early recognition and appropriate of venous pressure may not always be available. Then indirect indicators
treatment of cardiovascular dysfunction. such as jugular venous distention and changes in blood pressure with
Cardiac Structure and Function changes in patient position (i.e., orthostatic hypotension) should be
looked for, as they may reflect increased or decreased central venous
The force required to pump blood throughout the circulatory system is pressures affecting preload.
generated by the heart. The arrangement of the four chambers of the Afterload is the pressure against which the ventricles must contract
human heart results in two parallel pumping mechanisms (an atrium to eject blood from the heart. Thus, the afterload on the ventricles is
plus a ventricle, each supplying a separate circulation) that are arranged the pressure in the aorta for the left ventricle (or pulmonary main for
in series. Due to this series arrangement, failure of one side of the heart the right ventricle) throughout systole. In the normal heart, changes in
usually ultimately results in dysfunction of the other. The force required systolic pressure over the physiologic range do not significantly affect
to pump blood is provided by the contraction of the cardiac muscle, cardiac output. Only at extremes of pressure does afterload impair
and the valves between the cardiac chambers and at the outflow of the cardiac output in the normally functioning heart. However, congenital
ventricles assure that blood flows in the proper direction. Thus, failure anomalies that result in obstruction of blood flow (e.g., coarctation of the
of any of the cardiac valves due to either acquired or congenital defects aorta, pulmonic stenosis) may create excessive afterload on the heart and
can severely impair cardiac function. impair cardiac output, resulting in heart failure. Furthermore, in patients
Cardiac output is the quantity of blood pumped by the heart per with poor cardiac function (e.g., myocarditis or valvular heart disease),
unit of time. Cardiac output varies with body size and is proportional the judicious use of vasodilators to decrease afterload may significantly
to body surface area. Thus cardiac output is frequently normalised to increase cardiac output.
body surface area, which is referred to as the cardiac index. The normal Contractility refers to the strength of cardiac muscle contraction and
cardiac index per square meter of body surface area for the adult is is measured as the change in ventricular pressure generated per unit of
approximately 3.0 l/min. Normal cardiac index in the newborn infant time. As noted previously, cardiac contractility is affected by preload
is approximately 2.5 l/min. This value rapidly increases during early due to the Frank-Starling relationship. Cardiac contractility is also
childhood to about 4 l/min by 10 years of age. influenced, however, by the autonomic nervous system. Specifically,
Cardiac output is the product of heart rate (contractions per minute) increased sympathetic activity results in increased cardiac contractility,
and average stroke volume (ml per contraction) over a time period. whereas increased parasympathetic activity decreases contractility.
Stroke volume, in turn, is affected by changes in preload, afterload, and Stimuli that increase cardiac contractility are said to have a positive
contractility. During periods of inadequate cardiac output, alterations inotropic effect, and those that decrease contractility are said to be
in all of these variables should be sought and addressed to optimise negative inotropes. Sympathetic stimulation increases contractility by
cardiac function. increasing calcium release during contractions and by increasing the
Preload is the amount of blood in the ventricle at the end of diastole sensitivity of myofilaments to calcium. The negative inotropic effect
and reflects the venous return to the heart. Under normal circumstances, of parasympathetic activity likely primarily results from loss of normal
the heart pumps whatever amount of blood enters the right atrium tonic sympathetic activity. Unfortunately, contractility is a difficult
without a backup of blood in the atria. This physiologic ability to variable to measure in clinical practice. One option for assessing
increase cardiac output is referred to as the Frank-Starling relationship contractile function is to measure ejection fraction by echocardiography.
and reflects improved interdigitation of actin and myosin filaments, The final variable that impacts cardiac output is heart rate. Changes in
resulting in optimal force generation during contraction. This ability heart rate primarily reflect changes in autonomic nervous activity, with
to increase contractile force even occurs in the weakened heart. Thus, sympathetic stimulation increasing heart rate (i.e., positive chronotrope)
increasing blood volume by giving a fluid bolus or transfusion may and parasympathetic stimulation decreasing heart rate (i.e., negative
improve cardiac output and perfusion even in patients with known chronotrope). Heart rate is also affected by intrinsic mechanisms,
cardiac dysfunction. however. For instance, stretch of the right atrial wall during increases in
Of course, there are physiologic limits beyond which increasing end venous return causes an increase in the heart rate by as much as 10–30%.
diastolic volume results in excessive stretch of the myocardial fibres Increases in heart rate generally correlate with increases in cardiac
and decreases contractile force. This circumstance is seldom observed output, but beyond critical levels, further changes in heart rate may have
in patients with normal cardiac function, but may develop in patients the opposite effect on cardiac output. As an example, at very high rates
with cardiac failure due to ischaemia, valvular disease, myocarditis, or above a critical level, stroke volume decreases, thereby limiting cardiac
congenital cardiac anomalies. In the absence of valvular disease and output. Decreased stroke volume at high heart rates results from limited