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Vascular resistance
Vascular resistanceis the resistance to flow that mustbe
overcome to pushbloodthrough thecirculatory sys-tem. The resistance
offered by the peripheral circu-lation is known as the systemic
vascular resistance(SVR), while the resistance offered by the
vasculatureof the lungs is known as the pulmonary vascular
re-sistance (PVR). The systemic vascular resistance mayalso be
referred to as the total peripheral
resistance.Vasoconstriction(i.e., decrease in blood vessel
diameter)increases SVR, whereasvasodilation(increase in diame-
ter) decreases SVR.Units for measuring vascular resistance are
dynscm5,pascal seconds per cubic metre (Pas/m) or, for easeof
deriving it by pressure (measured in mmHg) andcardiac
output(measured in l/min), it can be given inmmHgmin/l. This is
numerically equivalent to hybridreference units (HRU), also known
as Wood units, fre-quently used by pediatric cardiologists. To
convert fromWood units to MPas/m3 you must multiply by 8, or
todynscm5 you must multiply by 80.[1]
1 Calculation of resistance
The basic tenet of calculating resistance is that flow isequal
to driving pressure divided by resistance.
The systemic vascular resistance can therefore be calcu-lated in
units of dynscm5 as
80 (mean arterial pressure mean right atrial pressure)
cardiac output
where mean arterial pressure is 2/3 of diastolic blood
pressure plus 1/3 of systolic blood pressure (or Diastolic+
1/3(Systolic-Diastolic).
The pulmonary vascular resistance can therefore be cal-culated
in units of dynscm5 as
80 (mean pulmonary arterial pressure mean pulmonary artery wedge
pressure)
cardiac output
where the pressures are measured in units of millimetresof
mercury (mmHg) and the cardiac output is measuredin units of litres
perminute (L/min). The pulmonaryartery wedged pressure(also called
pulmonary artery oc-
clusion pressure or PAOP) is a measurement in whichone of the
pulmonary arteries is occluded, and the pres-sure downstream from
the occlusion is measured in order
to approximately sample the left atrial pressure.[4] There-fore
the numerator of the above equation is the pressuredifference
between the input to the pulmonary blood cir-cuit (where the hearts
right ventricle connects to the pul-monary trunk) and the output of
the circuit (which is theinput to the left atrium of the heart).
The above equationcontains a numerical constant to compensate for
the unitsused, but is conceptually equivalent to the following:
R=
P
Q
where R is the pulmonary vascular resistance (fluid
re-sistance), P is the pressure difference across the pul-monary
circuit, and Q is the rate of blood flow throughit.
As an example: If Systolic pressure: 120 mmHg,Diastolic
pressure: 80 mmHg, Right atrial mean pressure:3 mmHg, Cardiac
output: 5 l/min, Then Mean ArterialPressure would be: (2 Diastolic
pressure + Systolic pres-sure)/3 = 93.3 mmHg, and Systemic vascular
resistance:(93 - 3) / 5 = 18 Wood Units. Or Systemic vascular
re-
sistance: 18 x 80 = 1440 dyns/cm5. These values are inthe normal
limits.
2 Determinants of vascular resis-
tance
The major determinant of vascular resistance issmall
ar-teriolar(known as resistancearterioles) tone. These ves-sels are
from 450mdown to 100 m in diameter. (Asa comparison, the diameter
of acapillaryis about 3 to 4m.)
Another determinant of vascular resistance is the
pre-capillaryarterioles. These arterioles are less than 100 min
diameter. They are sometimes known as autoregula-tory vessels since
they can dynamically change in diame-ter to increase or reduce
blood flow.
Any change in theviscosityof blood (such as due to achange in
hematocrit) would also affect the measured vas-cular
resistance.
3 Regulation of vascular resistance
There are many factors that alter the vascular resis-tance. Many
of theplatelet-derived substances, includ-
1
https://en.wikipedia.org/wiki/Platelethttps://en.wikipedia.org/wiki/Hematocrithttps://en.wikipedia.org/wiki/Viscosityhttps://en.wikipedia.org/wiki/Arterioleshttps://en.wikipedia.org/wiki/Capillaryhttps://en.wikipedia.org/wiki/Micrometrehttps://en.wikipedia.org/wiki/Arteriolehttps://en.wikipedia.org/wiki/Diastolic_pressurehttps://en.wikipedia.org/wiki/Systolic_pressurehttps://en.wikipedia.org/wiki/Pulmonary_wedge_pressurehttps://en.wikipedia.org/wiki/Pulmonary_wedge_pressurehttps://en.wikipedia.org/wiki/Minutehttps://en.wikipedia.org/wiki/Litrehttps://en.wikipedia.org/wiki/MmHghttps://en.wikipedia.org/wiki/Cardiac_outputhttps://en.wikipedia.org/wiki/MmHghttps://en.wikipedia.org/wiki/Dynehttps://en.wikipedia.org/wiki/Vasodilationhttps://en.wikipedia.org/wiki/Vasoconstrictionhttps://en.wikipedia.org/wiki/Total_peripheral_resistancehttps://en.wikipedia.org/wiki/Circulatory_systemhttps://en.wikipedia.org/wiki/Circulatory_systemhttps://en.wikipedia.org/wiki/Blood
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2 7 SEE ALSO
ingserotonin, are vasodilatory when theendotheliumisintact and
are vasoconstrictive when the endothelium isdamaged.
Cholinergic stimulationcauses release ofendothelium-derived
relaxing factor(EDRF) (later it was discovered
that EDRF was nitric oxide) from intact endothelium,causing
vasodilation. If the endothelium is damaged,cholinergic stimulation
causes vasoconstriction.
3.1 Role of adenosine
Adenosineprobably doesn't play a role in maintainingthe vascular
resistance in the resting state. However,it causes vasodilation and
decreased vascular resistanceduring hypoxia. Adenosine is formed in
the myocar-dial cells during hypoxia, ischemia, or vigorous
work,due to the breakdown of high-energy phosphate com-pounds
(e.g.,adenosine monophosphate, AMP). Most ofthe adenosine that is
produced leaves the cell and acts asa direct vasodilator on the
vascular wall. Because adeno-sine acts as a direct vasodilator, it
is not dependent on an
intact endothelium to cause vasodilation.
Adenosine causes vasodilation in the small and mediumsized
resistance arterioles (less than 100 m in diameter).When adenosine
is administered it can cause a coronarystealphenomenon,[5] where
the vessels in healthy tissuedilate as much as the ischemic tissue
and more blood isshunted away from the ischemic tissue that needs
it most.This is the principle behind adenosinestress testing.
Adenosine is quickly broken down byadenosine deami-nase, which
is present inred cellsand the vessel wall.
4 Coronary vascular resistance
The regulation of tone in the coronary arteries is a com-plex
subject. There are a number of mechanisms for reg-ulating coronary
vascular tone, including metabolic de-mands (i.e.: hypoxia),
neurologic control, and endothelialfactors (i.e.:
EDRF,endothelin).
Local metabolic control (based on metabolic demand) isthe most
important mechanism of control of coronaryflow. Decreased tissue
oxygen content and increased tis-sue CO2 content act as
vasodilators. Acidosis acts as adirect coronary vasodilator and
also potentiates the ac-tions ofadenosineon the coronary
vasculature.
5 References
[1] Fuster, V.; Alexander, R.W.; O'Rourke, R.A. (2004)
Hursts the heart, book 1. 11th Edition, McGraw-Hill
Pro-fessional, Medical Pub. Division. Page 513. ISBN
978-0-07-143224-5.
[2] Table 30-1 in: Trudie A Goers; Washington UniversitySchool
of Medicine Department of Surgery; Klingen-smith, Mary E; Li Ern
Chen; Sean C Glasgow (2008).The Washington manual of surgery.
Philadelphia: WoltersKluwer Health/Lippincott Williams &
Wilkins.ISBN 0-7817-7447-0.
[3] Derived from values in dyns/cm5
[4] University of Virginia Health System.The
Physiology:Pulmonary Artery Catheters
[5] Masugata H, Peters B, Lafitte S, et al. (2003).Assessment of
adenosine-induced coronary stealin the setting of coronary
occlusion based on theextent of opacification defects by myocardial
con-trast echocardiography. Angiology 54 (4):
4438.doi:10.1177/000331970305400408.PMID 12934764.
6 Literature
1. Grossman W, Baim D. Grossmans Cardiac Catheter-ization,
Angiography, and Intervention, Sixth Edition.Page 172, Tabe 8.1ISBN
0-683-30741-X
2.Heart information: Systemic vascular resistance
7 See also
Adenosine
Perfusion
Cardiac output
Vasoconstriction
Vasodilation
https://en.wikipedia.org/wiki/Vasodilationhttps://en.wikipedia.org/wiki/Vasoconstrictionhttps://en.wikipedia.org/wiki/Cardiac_outputhttps://en.wikipedia.org/wiki/Perfusionhttps://en.wikipedia.org/wiki/Adenosinehttp://booktine.com/systemic-vascularresistancehttps://en.wikipedia.org/wiki/Special:BookSources/068330741Xhttps://www.ncbi.nlm.nih.gov/pubmed/12934764https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.1177%252F000331970305400408https://en.wikipedia.org/wiki/Digital_object_identifierhttp://ang.sagepub.com/cgi/pmidlookup?view=long&pmid=12934764http://ang.sagepub.com/cgi/pmidlookup?view=long&pmid=12934764http://ang.sagepub.com/cgi/pmidlookup?view=long&pmid=12934764http://ang.sagepub.com/cgi/pmidlookup?view=long&pmid=12934764http://www.healthsystem.virginia.edu/internet/anesthesiology-elective/cardiac/pacphys.cfmhttp://www.healthsystem.virginia.edu/internet/anesthesiology-elective/cardiac/pacphys.cfmhttps://en.wikipedia.org/wiki/Special:BookSources/0-7817-7447-0https://en.wikipedia.org/wiki/Special:BookSources/0-7817-7447-0https://en.wikipedia.org/wiki/International_Standard_Book_Numberhttps://en.wikipedia.org/wiki/Special:BookSources/9780071432245https://en.wikipedia.org/wiki/Special:BookSources/9780071432245https://en.wikipedia.org/wiki/Adenosinehttps://en.wikipedia.org/wiki/Endothelinhttps://en.wikipedia.org/wiki/Red_blood_cellhttps://en.wikipedia.org/wiki/Adenosine_deaminasehttps://en.wikipedia.org/wiki/Adenosine_deaminasehttps://en.wikipedia.org/wiki/Cardiac_stress_testhttps://en.wikipedia.org/wiki/Coronary_stealhttps://en.wikipedia.org/wiki/Coronary_stealhttps://en.wikipedia.org/wiki/Adenosine_monophosphatehttps://en.wikipedia.org/wiki/Adenosinehttps://en.wikipedia.org/wiki/Nitric_oxidehttps://en.wikipedia.org/wiki/Endothelium-derived_relaxing_factorhttps://en.wikipedia.org/wiki/Endothelium-derived_relaxing_factorhttps://en.wikipedia.org/wiki/Endotheliumhttps://en.wikipedia.org/wiki/Serotonin
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