Page 217 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Regulation of Stroke Volume Venous Return
Frank–Starling mechanism (FSM): The heart Blood from the capillaries is collected in the
autonomously responds to changes in ventric- veins and returned to the heart. The driving
ular volume load or aortic pressure load by ad- forces for this venous return (! B) are: (a) vis a
justing the stroke volume (SV) in accordance tergo, i.e., the postcapillary blood pressure (BP)
with the myocardial preload (resting tension; (ca. 15 mmHg); (b) the suction that arises due
! p. 66ff.). The FSM also functions to maintain to lowering of the cardiac valve plane in sys-
an equal SV in both ventricles to prevent con- tole; (c) the pressure exerted on the veins
gestion in the pulmonary or systemic circula- during skeletal muscle contraction (muscle
tion. pump); the valves of veins prevent the blood
Preload change. When the volume load from flowing in the wrong direction, (d) the in-
(preload) increases, the start of isovolumic creased abdominal pressure together with the
Cardiovascular System stroke volume (SV), cardiac work and end-sys- venous dilatation and suction (! p. 206).
contraction shifts to the right along the passive
lowered intrathoracic pressure during inspira-
tion (P pl; ! p. 108), which leads to thoracic
P–V curve (! A1, from point A to point A 1).
This increases end-diastolic volume (EDV),
Orthostatic reflex. When rising from a
tolic volume (ESV) (! A).
supine to a standing position (orthostatic
change), the blood vessels in the legs are sub-
Afterload change. When the aortic pressure
jected to additional hydrostatic pressure from
load (afterload) increases, the aortic valve will
raises blood volume in the leg veins (by ca.
has risen accordingly (! A2, point D t). Thus,
8 not open until the pressure in the left ventricle the blood column. The resulting vasodilation
the SV in the short transitional phase (SV t) will
0.4 L). Since this blood is taken from the central
decrease, and ESV will rise (ESV t). Con- blood volume, i.e., mainly from pulmonary ves-
sequently, the start of the isovolumic contrac- sels, venous return to the left atrium
tion shifts to the right along the passive P–V decreases, resulting in a decrease in stroke
curve (! A2, point A 2). SV will then normalize volume and cardiac output. A reflexive in-
(SV 2) despite the increased aortic pressure crease (orthostatic reflex) in heart rate and pe-
(D 2), resulting in a relatively large increase in ripheral resistance therefore occurs to prevent
ESV (ESV 2). an excessive drop in arterial BP (! pp. 7 E and
Preload or afterload-independent changes 212ff.); orthostatic collapse can occur. The drop
in myocardial contraction force are referred to in central blood volume is more pronounced
as contractility or inotropism. It increases in when standing than when walking due to
response to norepinephrine (NE) and epineph- muscle pump activity. Conversely, pressure in
rine (E) as well as to increases in heart rate (! 1- veins above the heart level, e.g., in the cerebral
adrenoceptor-mediated, positive inotropic ef- veins, decreases when a person stands still for
fect and frequency inotropism, respectively; prolonged periods of time. Since the venous
! p. 194). This causes a number of effects, par- pressure just below the diaphragm remains
ticularly, an increase in isovolumic pressure constant despite changes in body position, it is
peaks (! A3, green curves). The heart can referred to as a hydrostatic indifference point.
therefore pump against increased pressure The central venous pressure (CVP) is
levels (! A3, point D 3) and/or eject larger SVs measured at the right atrium (normal range:
(at the expense of the ESV) ( ! A3, SV 4). 0–12 cm H 2O or 0–9 mmHg). Since it is mainly
While changes in the preload only affect the dependent on the blood volume, the CVP is
force of contraction (! p. 203 B1), changes in used to monitor the blood volume in clinical
contractility also affect the velocity of contrac- medicine (e.g., during a transfusion). Elevated
tion (! p. 203/B2). The steepest increase in CVP (! 20 cm H 2O or 15 mmHg) may be patho-
isovolumic pressure per unit time (maximum logical (e.g., due to heart failure or other dis-
dP/dt) is therefore used as a measure of con- eases associated with cardiac pump dysfunc-
tractility in clinical practice. dP/dt is increased tion), or physiological (e.g., in pregnancy).
204 E and NE and decreased by bradycardia
(! p. 203 B2) or heart failure.
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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