Systemic Vascular Resistance

SVR refers to the resistance to blood

flow offered by all of the systemic
vasculature, excluding the pulmonary
vasculature.
 Regulation of systemic vascular
resistance
sympathetic stimulation
responsiveness of the vasculature
number of involved vascular beds
 Vascular tone
Vascular tone refers to the degree of constriction
experienced by a blood vessel relative to its maximally
dilated state.
Regulation of vascular tone
 Regulation of vascular tone
 Vascular tone is determined by many different competing
vasoconstrictor and vasodilator influences acting on the blood vessel.
 Extrinsic factors that originate from outside of the organ or tissue in
which the blood vessel is located
 Intrinsic factors that originate from the vessel itself or the
surrounding tissue.
 Extrinsic factors regulate arterial blood pressure by altering
systemic vascular resistance
 Intrinsic mechanisms are important for local blood flow regulation
within an organ.
Vascular tone at any given time is determined by the balance of
competing vasoconstrictor and vasodilator influences.
 In general, extrinsic factors
(neurohumoral) such as sympathetic
nerves and circulating angiotensin II
increase vascular tone (i.e., cause
vasoconstriction); however, some
circulating factors (e.g., atrial natriuretic
peptide) decrease vascular tone.
Intrinsic factors include:

Myogenic mechanisms (originating from vascular smooth muscle), which

increase tone.

Endothelial factors such as NO and endothelin can either decrease or increase

tone, respectively.

Local hormones/chemical substances (e.g., arachidonic acid metabolites,

histamine and bradykinin can either increase or decrease tone.
 Metabolic by-products or hypoxia, which generally
decrease tone.

The mechanisms by which the above influences either

constrict or relax blood vessels involve a variety of
signal transduction mechanisms that ultimately
influence the interaction between actin and myosin
in the smooth muscle.
 CVP
The term "central venous pressure" (CVP)
describes the pressure in the thoracic vena
cava near the right atrium.
Therefore CVP and right atrial pressure are
essentially the same.
ΔCVP = ΔV / Cv
 CVP
Venous compliance and venous volume are
not static, but dynamic
Many factors influences these two variables:
cardiac output, respiratory activity,
contraction of skeletal muscles (particularly
legs and abdomen), sympathetic
vasoconstrictor tone, and hydrostatic forces
(i.e., gravity)
 Compliance of blood vessels

• Compliance is a slope

• At low pressures, veins

have a greater compliance
than arteries

• At high pressures,
compliance is similar in
C = V/ P
veins and arteries (but
C = compliance (mL/mm Hg) volume is much greater in
V = volume (mL) veins)
P = pressure (mm Hg)
Cardiovascular Physiology Concepts
http://www.cvphysiology.com/Blood%20Pressure/BP004.htm
Compliance changes related to vasocontraction or aging

With vasocontraction:
• Venous volume
decreases and pressure
increases

• Venous compliance
decreases

Similar effects in arteries with aging

Venous pressure and compliance
 A decrease in cardiac output either due to
decreased heart rate or stroke volume (e.g.,
in ventricular failure) results in blood
backing up into the venous circulation
(increased venous volume) as less blood is
pumped into the arterial circulation. The
resultant increase in thoracic blood volume
increases CVP.
 An increase in total blood volume as
occurs in renal failure or fluid retention
through activation of the renin-angiotensin-
aldosterone system increases venous
pressure.
Venous constriction caused by sympathetic
activation of veins, or by circulating
vasoconstrictor substances (e.g.,
catecholamines, angiotensin II) decreases
venous compliance, which increases CVP.
A shift in blood volume into the thoracic
venous compartment that occurs when a
person changes from standing to supine
position increases CVP.
 Arterial dilation as occurs during withdrawal of
sympathetic tone or with arterial vasodilator drugs causes
increased blood flow from the arterial into the venous
compartments. This increases venous blood volume and
CVP. This is what occurs when the heart is functioning
normally. It is important to note, however, that arterial
dilation in ventricular failure leads to a decrease in CVP
instead of an increase. This occurs because the arterial
dilation decreases afterload on the ventricle leading to
an increase in stroke volume. Ventricular stroke volume
is more strongly influenced by afterload when the
ventricular is in failure than when it has normal function.
CVP is also increased during a force expiration,
particularly against a high resistance (as occurs with a
Valsalva maneuver) due to external compression of the
thoracic vena cava as intrapleural pressure rises. This
mechanical compression of the vena cava functionally
reduces the compliance of the vena cava.
Muscle contraction, particularly of the limbs and
abdomen, compresses the veins (i.e., decreases
compliance) and forces blood into the thoracic
compartment, thereby increasing thoracic blood volume
and CVP.
Gravity effects on CVP
Muscle pump
Respiratory pump