Chapter 10

The Blood Vessels and Blood Pressure

Some organs receive blood flow in excess of their own needs. They are the digestive organs, kidneys, and skin.

• Blood is constantly reconditioned. This maintains a relatively constant composition in the blood.

• Large percentages of the cardiac output are distributed to the digestive tract, kidneys, and skin. They are reconditioning organs. They can withstand temporary reduction in blood flow.

• The blood flow distributed to other organs is less, supplying their metabolic needs and adjusted to their level of activity. These organs (e.g., brain) do not have an extra margin of blood supply. They do not tolerate significant reductions in blood supply as well as the reconditioning organs.

The flow rate of blood flow through a vessel is directly proportional to the pressure gradient and inversely proportional to vascular resistance.

• F = delta P

R

• The pressure gradient is the pressure difference between the beginning and end of a vessel.

• Blood flows from an area of higher pressure to an area of lower pressure (pressure gradient).

• Resistance is the opposition to blood flow through a vessel. It depends on three factors: blood viscosity, vessel length, and vessel radius.

• The major determinant to resistance to blood flow is the radius of a vessel. A slight change in radius produces a significant change in blood flow. The blood flow arterioles is highly affected by this relationship. It is expressed by the equation:

– R is proportional to 1divided by the radius raised to the fourth power

The vascular tree consists of arteries, arterioles, capillaries, venules, and veins. • The systemic and pulmonary circulations each

consist of a closed system of vessels. • Arteries carry blood away from the heart to the

tissues. They branch into a tree of progressively smaller vessels.

• This progression forms arterioles near an organ. Regulation of the diameter of arterioles supplying an organ adjusts the volume of blood sent to that organ.

• Arterioles branch into capillaries, the smallest vessels. They are the microscopic exchange vessels with all cells, offering blood that supplies the metabolic needs of the cells.

• Capillaries merge into venules that send blood into small veins. They form progressively larger veins. Venules and veins return blood to the heart.

Arteries are the rapid-transit passageways to the tissues. They also are a pressure reservoir.

• The large radius of arteries offers little resistance to blood flow.

• The elastic recoil in the walls of arteries drives the flow of blood during cardiac relaxation (ventricular diastole).

• This elasticity is due to a thick middle layer of smooth muscle with elastic fibers in the wall of arteries.

• Arteries expand from a large volume of blood sent into them when the heart pumps blood (ventricular systole). The temporarily expand and hold this blood.

• When the heart relaxes, the stretched arteries passively recoil. This pushes the excess blood toward the tissues.

• This ensures a continuous flow of blood to the tissues.

Arterial blood pressure fluctuates in relation to ventricular systole and diastole.

• Arteries are compliant (distensible). • During ventricular systole, the stroke volume enters the arteries.

About one-third as much blood leaves the arteries at this time. • No blood enters the arteries during diastole. However, the

blood continues to leave the arteries by elastic recoil. • Systolic pressure is the maximum pressure in arteries when

blood is ejected into them during ventricular systole.• The diastolic pressure is the minimum pressure in arteries when

the blood is draining off into the remainder of the vessels during ventricular diastole.

Blood pressure can be measured indirectly.

• It is measured by a sphygmomanometer. Its cuff is wrapped around the upper arm.

• When the pressure in the cuff of this instrument is greater than the brachial artery, blood flow is blocked through the vessel. At this time no sound is heard through a stethoscope placed over the brachial artery at the inside of the elbow.

• When the pressure in the cuff is slowly released, it will fall just below systolic pressure. This creates vibrations and sound. The first sound heart indicates systolic pressure (e.g., 120 mm Hg).

• When the falling cuff pressure drops below diastolic pressure, the vibrations and sound disappears. This indicates diastolic pressure (80 mm Hg).

• The pulse pressure is the difference between the systolic and diastolic pressures (120 - 80).

A mean arterial pressure is the main driving force producing a flow of blood. It can be calculated.

• The equation is:– mean arterial pressure = diastole pressure plus 1/3 the pulse

pressure

• As one example, from the previous data : 80 plus 1/3 (40) equals 93

• This average is weighted, as about two-thirds of the cardiac cycle is spent in diastole.

Arterioles are the major resistance vessels.

• They offer high resistance to blood flow. The mean arterial blood pressure in systemic arterioles drops significantly (e.g., 93 to 37). This pressure drop drives the flow of blood.

• Their pressure is not pulsatile. • Arteriolar radii can be changed to alter the distribution of blood flow to

organs and to regulate arterial blood pressure.• Their radii change by vasoconstriction (narrowing) and vasodilation

(enlargement). To produce these changes their thick, middle layer of smooth muscle is subject to neural, hormonal, and local chemical control.

• The vascular tone of this smooth muscle establishes a baseline of vascular resistance. This ongoing tone makes changes in radius size possible. – See Figure 10-10

Local control of arteriolar resistance determines the distribution of the cardiac output.

• The driving force for blood flow is identical to all organs.

• However, differences in arteriolar resistance varies between organs. This determines the distribution of blood they receive.

• Blood flow to an organ can vary by the change in resistance in arterioles serving it.

• For example, during exercise more blood flow is shifted to the skeletal muscles. Less flows to the digestive tract. In this case the arterioles to the skeletal muscles dilate, offering less resistance. The arterioles serving the digestive tract constrict.

• Local chemical influences on the resistance of arterioles include local metabolic changes and histamine release. Local physical influences include local heat and cold and myogenic responses to stretch.

Local chemical changes on the smooth muscle of arterioles are important. These changes meet the metabolic needs of cells.• During increased metabolic activity (e.g. skeletal muscle activity during exercise)

the local concentration of oxygen decreases. This and other local chemical changes relax the smooth muscle wall in arterioles. They dilate by this response, called active hyperemia.

• Less metabolic activity causes the opposite condition and response of the arterioles.

• Other local chemical changes that relax the smooth muscle in arterioles, causing vasodilation, are:

– increased carbon dioxide

– increased acidity

– increased K+ ion concentration

– increased osmolarity

– adenosine release

– prostaglandin release

• Local vasoactive mediators also have an effect– See Figure 10-12

Local histamine release pathologically dilates

arterioles.– It is synthesized and stored in special connective tissue cells.

• Local physical changes influence arteriolar radius.– Local heat produces vasodilation. Local cold produces

vasoconstriction.

– Arteriolar smooth muscle that is passively stretched increases its tone.

– By reactive hyperemia, arterioles in a region dilate when other local blood vessels are blocked.

– By pressure autoregulation local mechanisms in the arterioles keep blood flow constant when there are wide variations in the mean arterial blood pressure driving the blood.

Extrinsic sympathetic signaling controls arteriolar radii.

• This regulates blood pressure. Sympathetic neurons supply the smooth muscle in the walls of most arterioles.

• Increased sympathetic signaling produces generalized arteriolar vasoconstriction. This increases the total peripheral resistance (TPR, the total resistance of all peipheral vessels).

• Mean arterial pressure (MAP) equals:– cardiac output x TPR

• As the TPR increases, the mean arterial pressure increases by direct proportion.

• The increase in TPR is a generalized increase. Many arterioles constrict to produce this effect, increasing the MAP. Organs supplied by these constricting vessels receive less blood flow. However, some arterioles serving organs (e.g., skeletal muscles during exercise) dilate during this increase in TPR. These organs receive more blood as the MAP increases.

Norepinephrine released from sympathetic nerve endings when combining with alpha-1 receptors. This binding produces vasoconstriction.

• Cerebral vessels lack these kind of receptors. They are subject to local controls.

• Skeletal and cardiac muscle tissue have local control mechanisms that overide generalized sympathetic control mechanisms.

• Parasympathetic innervation is absent at arterioles.

A cardiovascular control center in the medulla regulates blood pressure along with several hormones.• The medulla is the integrating center for

sending signals through sympathetic motor pathways to the arterioles.

• Epinephrine and norepinephrine reinforce sympathetic activity. They are secreted by the adrenal medulla.

• Vasopressin and angiotensin are vasoconstrictors. Vasopressin controls water balance. Angiotensin controls salt balance.

Capillaries are the sites of exchange between the blood and body cells.• This exchange is accomplished mainly by diffusion. This

process is enhanced the thin walls and narrow openings of capillaries, plus their branching.

• Their thin walls is one, flat layer of epithelial cells. This is called the endothelium.

• Capillaries are very abundant, offering a large surface area to serve cells.

• The blood through capillaries is slow due to the tremendous cross-sectional area of all capillaries in an area. This enhances the opportunity for diffusion.

• Compared to arterioles, the resistance offered by capillaries is low due to the large cross-sectional areas of these microscopic vessels.

Capillaries have pores, water-filled clefts in their walls.

• The pores allow the passage of small, water-soluble substances such as ions and glucose.

• Lipid-soluble substances dissolve through the lipid bilayer in the endothelial cells in the capillary wall.

• Tight junctions connecting the walls of capillary cells in the brain form a blood-brain-barrier. This blocks transport.

• Histamine increases capillary permeability.

Under resting conditions many capillaries do not open.

• Precapillary sphincters surround capillaries. A sphincter is a ring of smooth muscle around the entrance to a capillary.

• The contraction of these sphincters reduces the blood flowing into the capillaries in an organ.

• The relaxation of these sphincters (e.g., an exercising skeletal muscle) has the opposite effect.

• A metarteriole is a throughfare channel from an arteriole to a capillary. Some capillaries are served by them.

The interstitial fluid is a passive intermediary between the blood and tissue cells.• 20 percent of the ECF is blood plasma. 80 percent of the ECF is

interstitial fluid. This fluid bathes the tissue cells and is where these cells exchange materials with the ECF.

• Exchange between the interstitial fluid and plasma membranes of tissue cells can be active (e.g., active carrier-mediated transport) or passive (e.g., diffusion).

• Exchange across the capillary wall, between the plasma and interstitial fluid, is largely passive.

• Diffusion across the capillary walls is important in solute exchange (e.g., gases). Only the passage of plasma proteins is limited.

• Some substances cross the capillary wall by bulk flow. Constituents in a fluid move through in bulk. For example, fluid moving inside a capillary can be pushed through the wall to the outside of the capillary (from higher fluid pressure to lower fluid pressure)

By ultrafiltration, the capillary wall acts as a sieve when fluid moves from its inside (site of higher pressure) to the interstitial fluid outside the capillary.

– Plasma proteins remain in the capillary by this process, unable to pass through the pores in the capillary wall.

• By reabsorption there is a net inward movement of fluid from the interstitial fluid into the capillary. – This occurs when inward-driving pressure exceeds

an outward opposing pressure across the capillary wall.

Bulk flow occurs by the differences in hydrostatic (fluid) and colloidal osmotic pressures between the plasma and interstitial pressures. • Capillaries have pores allowing fluid passage.

• Capillary blood pressure is the hydrostatic pressure exerted on the inside of capillary walls by the blood. This forces fluid out of the capillaries (the outward pressure).

• The plasma-colloid pressure encourages fluid movement into the capillaries (the inward pressure). The plasma has a higher protein concentration compared to the interstitial fluid. This produces a water concentration difference. Water enters the plasma from the interstitial fluid by osmosis.

• The interstitial fluid hydrostatic pressure is the pressure exerted on the outside of the capillary wall by the interstitial fluid. It has a small value.

• The interstitial fluid-colloid osmotic pressure is also insignificant in most cases, as plasma proteins normally remain in the blood plasma.

A net exchange of fluid occurs across the capillary wall.

• At the arteriolar end of the capillary the outward pressure is greater than the inward pressure. Fluid leaves the capillary by this difference. Ultrafiltration occurs.

• At the venular end of the capillary the inward pressure is greater than the outward pressure. The outward pressure has dropped due to a drop of blood pressure at this end compared to the arteriolar end. Reabsorption occurs.

• Both ultrafiltration and reabsorption occur by bulk flow. Fluid moves by a passive process. This is not important in the exchange of individual solutes between the blood and tissue cells, as very few solutes move across capillary walls by bulk flow.

• Bulk flow does regulate the distribution of fluid between the two regions of the ECF, the blood plasma and interstitial fluid. Fluid shifts between these two regions compensate for changes to this distribution (.e.g, excessive fluid intake can expand the plasma volume).

The lymphatic system is an accessory route for the return of interstitial fluid to the blood. • Normally this return is not 100 percent. • The lymphatic system is an extensive system of one-way vessels that begins

with initial lymphatics. • Lymph is interstitial fluid that enters a lymphatic vessel. This fluid contains

escaped plasma proteins and bacteria that are not reclaimed by the blood plasma.

• Smooth muscle beyond the initial lymphatics propels lymph into larger lymphatic vessels. The lymph is eventually combined with venous blood near the heart.

• The functions of the lymphatic system are:– return excess filtered fluid– return filtered fluid– defense against disease by the lymph nodes– transport of absorbed fat from the digestive tract– See Figures 10-25 and 26

An accumulation of too much interstitial fluid can produce edema, an accumulation of fluid in the interstitial fluid. Several conditions can produce this.

• A reduced concentration of plasma proteins allows a drop in the main inward pressure. More fluid enters the interstitial fluid.

• An increased permeability of the capillary wall allows more plasma proteins to pass from the blood fluid into the interstitial fluid.

• An increased venous blood pressure increases the capillary blood pressure. This elevates the outward pressure along the capillary wall.

• Blockage of lymph vessels retains fluid in the interstitial fluid rather than returning the fluid to the capillaries.

Blood flows from the capillaries to the veins. Veins return blood to the heart.

• The have large radii and offer low resistance to the flow of blood.

• From the capillaries the velocity of blood flow increases in the veins, as they have a smaller total cross-sectional area.

• Compared to arteries, veins are thinner-walled and less elastic.

• Veins are capacitance vessels, serving as a large blood reservoir. They are highly distensible, able to accommodate large volumes of blood. They hold 60% of the blood volume of the body at rest.

• Extrinsic factors can drive this blood to the heart for pumping.

Extrinsic factors enhance venous return.• Venous return is the volume of blood entering each atrium per minute. By

their high venous capacity, veins have a large volume of blood for this return.

• Venous return is enhanced by:• increased sympathetic stimulation of the veins; Contraction of the smooth

muscle in the wall of the veins leads to their constriction. This squeezes blood back to the heart.

• increased skeletal muscle activity; This compresses veins and increases venous pressure. This drives blood toward the heart.

• Various mechanisms counteract the effect of gravity on venous return.• The closure of valves inside veins ensures that blood does not flow

backward.• The respiratory pump creates a pressure gradient in the chest cavity,

drawing fluid toward the heart.– See Figures 10-30 and 31

Blood pressure is regulated.

• It is regulated by cardiac output and total peripheral resistance. Consider the equation:

• mean arterial pressure = cardiac output x total peripheral • resistance• Cardiac output depends on heart rate x stroke volume.

Heart rate depends on autonomic control plus some hormone signaling. Stroke volume depends on sympathetic stimulation.

• Stroke volume also increases by venous return. Venous return depends on several factors such as venous vasoconstriction and the skeletal muscle pump.

Total peripheral resistance depends on the radius of arterioles plus blood viscosity.

– This radius size depends on sympathetic stimulation to the arterioles and local metabolic/chemical controls. It is also controlled by several hormones.

• Effective circulating blood volume influences the blood volume returning to the heart.– This blood volume depends on capillary exchange

which in the long term means controlling salt and water balance.

• Mean arterial pressure is controlled by long-term and short-term measures.

The baroreceptor reflex is a short-term mechanism for regulating blood pressure.

• Baroreceptors are found in the carotid sinus and aortic arch. These receptors are sensitive to fluctuations in pulse pressure.

• Baroreceptors generate action potentials through afferent pathways to a cardiovascular (integrating center) in the medulla.

• The efferent pathway is the autonomic nervous system. The center in the medulla alters the ratio of sympathetic and parasympathetic activity to the heart and blood vessels.

• The heart and blood vessels are the effector organs that respond to control blood pressure.

Here is one example of the baroreceptor reflex.• Arterial blood pressure becomes elevated for some reason.• Baroreceptors detect this change and increase the rate of action

potentials firing along afferent pathways from the receptors to the medulla.

• The cardiovascular center interprets this input. • Sympathetic output decreases. Parasympathetic output increases. • There is a decrease in the following responses: heart rate, stroke

volume, arteriolar resistance, and venous resistance. The veins dilate.

• Therefore, cardiac output and total peripheral resistance decrease. • The elevated blood pressure returns to normal.• A drop in blood pressure produces an opposite series of trends and

responses.

Other reflexes and responses influence blood pressure.

• Left atrial receptors and hypothalmic osmoreceptors regulate salt and water balance. They control plasma volume for long-term blood pressure regulation.

• Chemoreceptors in the carotid and aortic arteries are sensitive to low oxygen and high acid levels in the blood. They increase respiratory activity to reverse these trends.

• Behaviors and emotions from the cerebral cortex/hypothalamus influence cardiovascular responses.

• Exercise modifies cardiovascular responses.• The hypothalamus controls skin arterioles for temperature

regulation.• Vasoactive substances have an effect.

Hypertension is a serious national problem.

• Its causes are largely unknown.• Secondary hypertension occurs secondary to other primary problems. Its

categories are renal (from the renin-angiotensin mechanism), cardiovascular, endocrine, and neurogenic.

• 90 percent of hypertension cases are primary. Potential causes include: • defects in salt management by the kidneys• excessive salt intake• diets low in fruits, vegetables, and dairy products• plasma protein abnormalities• variation in the gene that encodes for angiotensinogen• endogenous digitalis-like substances• excess vasopressin• Baroreceptors adapt to hypertension. They regulate blood pressure,

maintaining it at a higher level.

Complications of hypertension include:

– congestive heart failure– stroke – heart attack– Without complications, hypertension is without

symptoms.– It can be treated with therapy.

• Orthostatic hypotension results from transient inadequate sympathetic activity.– This is a fall in blood pressure.

Circulatory shock occurs when blood pressure drops to a point where blood flow is inadequate to serve the tissues.• There are four main types:• hypovolemic - caused by a fall in blood volume• cardiogenic - due to a weakened heart• vasogenic - from widespread vasodilation due to a release of

vasodilator substances• neurogenic - from widespread vasodilation, but not from the

release of vasodilator substances• Compensatory measure for circulatory shock include:• response by the baroreceptor reflex with increased sympathetic

activity and increase parasympathetic activity• fluid shifts in the capillaries and interstitial fluid (autotransfusion)• responses by the liver, urinary system, and thirst sensation

Reversible shock can be corrected by compensatory mechanisms and effective therapy.• Sometimes shock is irreversible.