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Overview of Circulation

 The function of circulation :

o Transport nutrients to tissues
o Transport waste products away
o Transport hormones
o In general  maintain an appropiate environment in all the tissue fluid

 The circulation is divided into

o Systemic circulation / greater circulation / peripheral circulation
o Pulmonary circulation

 Role of each part of the circulation

o Arteries  transport blood under high pressure to the tissues, so it has strong vascular walls, and blood flow
with high velocity
o Arterioles  the last small branches, act as control conduits, have strong muscular walls that can close the
arterioles completely or can dilate several fold, so that can alter blood flow in response to tissues need.
o Capillaries  exchange fluid, nutrient, electrolytes, hormones and other subtances via capillary pores
o Venules  collect blood from capillary
o Veins  as conduits for transport back to the heart

 Blood volume (nice to know) :

o 84 % in systemic circulation ( 64 % in veins, 13 % in arteries, 7 % in the systemic arterioles and capillaries )
o 16 % in heart and lungs ( 7 % in heart and 9 % in lungs )

 Basic principles of circulatory function :

o The rate of the blood flow to each tissue of the body is almost always precisely controled in relation to tissue
o The cardiac output is controlled mainly by the sum of all the local tissue flows
o Arterial pressure regulation is generally independent of either local blood flow control or cardiac output

 Blood Flow  the quantity of blood that passes a given point in the circulation in a given period time
 Interrelationships of pressure, flow, and resistance :
o Blood flow is determined by pressure difference of blood between the two end vessels / pressure gradient,
and the impediment to blood flow through the vessel / vascular resistence
o The blood flow is directly proportional to the pressure gradient, but inversely proportional to the resistance
o In formula called Ohm’s law  F (Flow) = ΔP / R

 There are two type of blood flow :

o Laminar flow / streamline flow, blood flowing to 1 direction.
o Turbulent flow, blood flowing in all direction in the vessels and continually mixing withing the vessels
Roles of the Kidney in Long-Term Control of Arterial Pressure
 Long-term control of arterial pressure is closely intertwined with homeostasis of body fluid volume, which is
determined by the balance between the fluid intake and output.


 The renal-body fluid system for arterial pressure control acts slowly but powerful as follows :
 If blood volume increases and vascular capacitance is not altered, arterial pressure will also increase.
 The rising pressure in turn causes the kidneys to excrete excess volume thus returning the pressure back
toward normal.
 Indeed, increase in arterial pressure only by few mmHg can double renal output of water, which is called pressure
diuresis ; as well as double the output of salt, which is called pressure natriuresis.
 Tabel
 In the human, at an arterial pressure of 50 mmHg urine output is essentialy zero, at 100 mmHg output is normal,
and at 200 mmHg output about 6-8 times normal

“Near Infinite Feedback Gain”

 There are 2 curves :
o The renal output curve for water and salt in response to rising arterial
o The line that represents the net water and salt intake
 When 2 curves intersect is called equilibrium point, where input equals intake.
 If the arterial pressure rises, will causes the renal output increases, body loses
fluid, blood volume decreases, and arterial pressure decreases, furthermore
this will not cease until the pressure eventually returns exactly to the
equilibrium point.
 If the arterial pressure falls, will causes the renal output decreases, body fluid
volume increases, blood volume increases, and the arterial pressure rises.
 This return of arterial pressure called “near infinitive feedback gain”

Increased Fluid Volume Can Elevate Arterial Pressure by Increasing Cardiac

Output or Total Peripheral Resistance
 The sequential events are :
 What is autoregulation? Whenever excess amount of blood flows
through a tissue, the local tissue vasculature constricts and decreases the blood
flow back toward to normal.
 The process if arterial pressure decreases :
 Renin is synthesized and stored in an inactive form caled prorenin in the
juxtaglomerular cells (JG cells) of the kidney.
 When arterial pressure decrease, intrincsic reactions in the kidney
cause many prorenin to split and release renin and most of it enter the
renal blood.
 Renin act enzymatically on another plasma protein (angiotensinogen) to
release angiotensin I.
 Within a few second angiotensin I form angiotensin II, occur to a great
extent in the lungs, catalized by angiotensin converting enzyme.
 Angiotensin II can elevate arterial pressure by :
o Vasoconstriction in many area of the body
o Decrease excretion of both salt and water by kidneys in two major
ways :
 Acts on kidneys to cause salt and water retention; by constrict the
renal arterioles  diminishing blood flow  reduce the pressure
in the peritubullar capillaries  rapid reabsorption of fluid
 Causes the adrenal gland to secrete aldosterone, and aldosterone
in turn increases salt and water reabsorption by kidney tubules
 The process if arterial pressure increases :

Cardiac Output, Venous Return, and

Their Regulation
 Cardiac output  the quantitiy of blood pumped into the aorta each
minute by the heart. It is the sum of the blood flows to all of the tissues
in the body
 Venous return  the quantity of blood flowing from the veins into the right atrium each minute.
 Cardiac output and venuos return must equal.
 Factors that affect directly the cardiac output :
o The basic level of body metabolism
o Whether the person is exercising
o Person’s age
o Size of the body
 For young healthy men, resting cardiac output averages about 5,6 L/min. For women 4.9 L/min. While for resting
adult is about 5 L/min.
 Cardiac output is regulated throughout life almost directly in proportion to the overal bodily metabolic activity.
Therefore the declining cardiac index is indicative of declining activity or declining musce mass with age.

Control of Cardiac Output by Venous Return – Role of the Frank-Starling Mechanism of the Heart
 When one states that cardiac output is controlled by venous return  not the heart as primary as the primary
controller, it is the various factor of the peripheral circulation that affect flow of blood into the heart from the
veins, called venous return that are primary control.
 That because heart has a built-in mechanism that normally allows it to pump automatically whatever amount of
blood that flows into the right atrium from the veins  Frank-Starling law of the heart.
 In this law : when increased quantity of blood flow to heart  streches the walls of heart chambers  cardiac
muscle contract with increased force.
 Another important : streching the heart causes heart to pump faster – at an increase heart rate; causes by strech
of the sinus node and bainbridge reflex (a nervous reflex, passing first to the vasomotor center of the brain and
then back to the heart by way of the simpatetic nerves and vagi).

Cardiac Output Regulation is Sum of Blood Flow Regulation in All the Local Tissues of the Body – Tissue
Metabolism Regulates Most Loca Blood Flow.
 Venous return is the sum of all the local blood flows through all the individual tissue segments of the peripheral
circulation, and so does cardiac output.
 The long-therm cardiac output level also varies reciprocally with changes in total peripheal resistance, as long as
arterial pressure is unchanged.
 For instance, any time the long term of total peripheral resistance changes, the cardiac output changes
quantitively in exactly the opposite direction.

The Heart has Limits for the Cardiac Output That it Can Achieve
 Cardiac Output Curve  to show the amount of blood that heart can pump; there are definitive limits.
 The plateau level is about 13 L/min (while normal about 5 L/min) means that the normal human heart without
any special stimulation can pump an amount of venous return up to about 2.5 times the normal venous return
before the heart becomes a limiting factor.
 The upper most  hypereffective heart, the lowermost  hypoeffective hearts.
 Factor causes a hypereffective heart
o Effect of nervous excitation to increase heart pumping, by sympathetic stimulation and parasimpathetic
o Increased pumping effectiveness caused by heart hypertrophy.
 Factor causes a hypoeffective heart :
o Increased arterial pressure
o Inhibition of nervous excitation of heart
o Pathological factors
o Coronary artery blockage
o Valvular heart disease
o Congenital heart disease
o Myocarditis
o Cardiac hypoxia

Factor That Affect Venous Return

 There are 3 principles factors that affect venous return to the heart from the systemic circulation :
o Right atrial pressure ; which exerts a backward forces on the veins to impede flow of blood from the veins into
the right atrium
o Degree of filling of the systemic circulation ; which forces the systemic blood toward the heart
o Resistance to blood flow between the peripheral vessels and the right atrium