21–2  Cardiovascular Physiology
 
Under normal circumstances, blood flow is equal to cardiac output. The afterload of the heart is determined by the interplay between pressure and resistance in the cardiovascular network.

 

 

Diffusion and osmosis occur within the capillaries, between the blood and the surrounding interstitial fluid.


Pressure
Liquids, including blood, cannot be compressed. A force exerted against a liquid generates hydrostatic pressure (HP) , a fluid pressure that is conducted in all directions.


In the systemic circuit of the cardiovascular system, the pressure gradient is the circulatory pressure –the pressure difference between the base of the ascending aorta and the entrance to the right atrium. Circulatory pressures average about 100 mm Hg.

 

 The circulatory pressure is divided into three components:

Blood Pressure. When referring to arterial pressure, we shall use the term blood pressure (BP) to distinguish it from the total circulatory pressure. Blood pressure in the systemic arterial system ranges from an average of 100 mm Hg to roughly 35 mm Hg at the start of a capillary network.

Capillary Hydrostatic Pressure. Capillary hydrostatic pressure (CHP) is the pressure within capillary beds. Along the length of a typical capillary, pressures decline from roughly 35 mm Hg to about 18 mm Hg.

Venous pressure is the pressure within the venous system. Venous pressure is quite low: The pressure gradient from the venules to the right atrium is only about 18 mm Hg.

Resistance: any force that opposes movement. The resistance of the cardiovascular system opposes the movement of blood. For circulation to occur, the pressure gradient must be great enough to overcome the total peripheral resistance –the resistance of the entire cardiovascular system. Because the resistance of the venous system is very low attention focuses on the peripheral resistance (PR) –the resistance of the arterial system.


Vascular resistance , the resistance of the blood vessels is the largest component of peripheral resistance. The most important factor in vascular resistance is friction between blood and the vessel walls. The amount of friction depends on the length and diameter of the vessel.

Vessel Length Increasing the length of a blood vessel increases friction: The longer the vessel, the larger is the surface area in contact with blood. For example, you can easily blow the water out of a snorkel that is 2.5 cm (1 in.) in diameter and 25 cm (10 in.) long, but you cannot blow the water out of a 15–m–long garden hose, because the total friction is too great.

 

Vessel Diameter The effects of friction on blood act primarily in a narrow zone closest to the vessel wall. In a small–diameter vessel, nearly all the blood is slowed down by friction with the walls. Resistance is therefore relatively high. Blood near the center of a large–diameter vessel does not encounter resistance from friction with the walls, so the resistance is relatively low.

 
Differences in diameter have much more significant effects on resistance than do differences in length. With two vessels of equal length, one twice the diameter of the other, the narrower one will offer 16 times as much resistance to blood flow.

 

More significantly, there is no way to control vessel length, but vessel diameter can change quickly through vasoconstriction or vasodilation.

 

Viscosity- The resistance to flow caused by interactions among molecules and suspended materials in a liquid. Liquids of low viscosity, such as water (viscosity 1.0), flow at low pressures; thick, syrupy fluids, such as molasses (viscosity 300), flow only under higher pressures. Whole blood has a viscosity about 5 times that of water, owing to the presence of plasma proteins and blood cells.


Turbulence  increases resistance and slows blood flow.
Turbulence normally occurs when blood flows between the atria and the ventricles and between the ventricles and the aortic and pulmonary trunks. It also develops in large arteries, such as the aorta, when cardiac output and arterial flow rates are very high. However, turbulence seldom occurs in smaller vessels unless their walls are damaged. For example, the formation of scar tissue at an injury site or the development of an atherosclerotic plaque creates abnormal turbulence and restricts blood flow. Because of the distinctive sound, or bruit (broo–E), produced by turbulence, the presence of plaques in large blood vessels can often be detected with a stethoscope.

 

An Overview of Cardiovascular Pressures

 

As arterial branching occurs, the cross–sectional area increases and blood pressure falls rapidly. Most of the decline occurs in the small arteries and arterioles of the arterial system; venous pressures are always relatively low.

Like a fast–flowing river delivering water to a floodplain, blood flow decreases in velocity as the total cross–sectional area of the vessels increases from the aorta toward the capillaries. Blood flow then rises as the cross–sectional area drops from the capillaries toward the venae cavae.

 

 

 

Pressures are highest in the aorta, peaking at about 120 mm Hg, and reach a minimum of 2 mm Hg at the entrance to the right atrium. Pressures in the pulmonary circuit are much lower than those in the systemic circuit.

 

The difference between the systolic and diastolic pressures is the pulse pressure. For a systolic pressure of 120 mm Hg and a diastolic pressure of 90 mm Hg, the MAP is 100 mm Hg:

Elastic Rebound
As systolic pressure climbs, the arterial walls stretch. This expansion allows the arterial system to accommodate some of the blood provided by ventricular systole. When diastole begins and blood pressures fall, the arteries recoil to their original dimensions. Most of the push generated by arterial recoil forces blood toward the capillaries. This phenomenon, called elastic rebound , helps to maintain blood flow along the arterial network while the left ventricle is in diastole.

The pulse pressure fades as a result of the cumulative effects of elastic rebound. The effect is like that of a loud shout creating a series of ever–softer echoes.. Eventually, the echo disappears. By the time blood reaches a precapillary sphincter, no pressure oscillations remain, and the blood pressure remains steady at approximately 35 mm Hg.


When pressures shift outside of the normal range, clinical problems develop. Abnormally high blood pressure is termed hypertension , abnormally low blood pressure, hypotension .

 

Hypertension is much more common, and in fact many cases of hypotension result from overly aggressive drug treatment for hypertension.

 

The usual criterion for hypertension in adults is a blood pressure greater than 150/90. One study estimated that 20 percent of the white U.S. population has blood pressures greater than 160/95 and that another 25 percent is on the borderline, with pressures above 140/90.

 

Hypertension significantly increases the workload on the heart, and the left ventricle gradually enlarges. More muscle mass means a greater oxygen demand. When the coronary circulation cannot keep pace, symptoms of coronary ischemia appear. Increased arterial pressures also place a physical stress on the walls of blood vessels throughout the body. This stress promotes or accelerates the development of arteriosclerosis and increases the risk of aneurysms, heart attacks, and strokes.

Checking the Pulse and Blood Pressure
 The inside of the wrist is commonly used to feel your pulse, because the radial artery can easily be pressed against the distal portion of the radius.

 

The instrument used to measure blood pressure is called a sphygmomanometer.

 

 

The distinctive sounds heard during this test, called sounds of Korotkoff are produced by turbulence as blood flows past the constricted portion of the artery.

 

Capillary Exchange
As blood flows through peripheral tissues, blood pressure forces water and solutes out of the plasma, across capillary walls. Most of this material is reabsorbed by the capillaries, but about 3.6 liters of water and solutes flows through peripheral tissues each day and enters the lymphatic system , which then returns the fluid to the bloodstream.

 

(This is one of he most important physiological functions you learn this semester.)

It ensures that plasma and interstitial fluid, two major components of extracellular fluid, are in constant communication.

It accelerates the distribution of nutrients, hormones, and dissolved gases throughout tissues.

It assists in the transport of insoluble lipids and tissue proteins that cannot enter the bloodstream by crossing the capillary walls.

It has a flushing action that carries bacterial toxins and other chemical stimuli to lymphoid tissues and organs responsible for providing immunity from disease.

The most important processes that move materials across typical capillary walls are diffusion , filtration , and reabsorption .

Diffusion is the net movement of ions or molecules from an area where their concentration is higher to an area where their concentration is lower. The difference between the high and low concentrations represents a concentration gradient , and diffusion tends to eliminate that gradient. Diffusion occurs most rapidly when (1) the distances involved are small, (2) the concentration gradient is large, and (3) the ions or molecules involved are small.
Diffusion across capillary walls can occur by five routes:

Ions and small organic molecules, such as glucose, amino acids, and urea, can usually enter or leave the bloodstream by diffusion between adjacent endothelial cells or through the pores of fenestrated capillaries. The same routes are involved in the osmotic flow of water.

Many ions, including sodium, potassium, calcium, and chloride, can diffuse across endothelial cells by passing through channels in cell membranes.

Large water–soluble compounds are unable to enter or leave the bloodstream except at fenestrated capillaries, such as those of the hypothalamus, the kidneys, many endocrine organs, and the intestinal tract.

Lipids, such as fatty acids and steroids, and lipid–soluble materials, including soluble gases such as oxygen and carbon dioxide, can cross capillary walls by diffusion through the endothelial cell membranes (remember the phospholipid bilayer).

Plasma proteins are normally unable to cross the endothelial lining anywhere except in sinusoids, such as those of the liver, where plasma proteins enter the bloodstream.

Filtration is driven by hydrostatic pressure, which, pushes water from an area of higher pressure to an area of lower pressure.

 

From capillary hydrostatic pressure (CHP) and capillary filtration , water is forced across a capillary wall, and small solute molecules travel with the water.

 

 

 

 

The solute molecules must be small enough to pass between adjacent endothelial cells or through the pores in a fenestrated capillary; larger solutes and suspended proteins are filtered out and remain in the bloodstream. Filtration occurs primarily at the arterial end of a capillary, where CHP is highest.

Reabsorption occurs as the result of osmosis. Water molecules tend to diffuse across a membrane toward the solution containing the higher solute concentration.

 

The osmotic pressure (OP) of a solution is an indication of the force of osmotic water movement–in other words, the pressure that must be applied to prevent osmotic movement across a membrane. The higher the solute concentration of a solution, the greater the solution's osmotic pressure. The osmotic pressure of the blood is also called blood colloid osmotic pressure (BCOP) , because only the suspended proteins are unable to cross the capillary walls. Osmotic water movement will continue until either the solute concentrations are equalized or the movement is prevented by an opposing hydrostatic pressure.

Remember that hydrostatic pressure forces water out of a solution, whereas osmotic pressure draws water into a solution.

 
The net hydrostatic pressure tends to push water and solutes out of capillaries and into the interstitial fluid. The net hydrostatic pressure is the difference between the capillary hydrostatic pressure (CHP), which ranges from 35 mm Hg at the arterial end of a capillary to 18 mm Hg at the venous end, and the hydrostatic pressure of the interstitial fluid (IHP).


The net colloid osmotic pressure tends to pull water and solutes into a capillary from the interstitial fluid. The net colloid osmotic pressure is the difference between the blood colloid osmotic pressure (BCOP) , which is roughly 25 mm Hg, and  the interstitial fluid colloid osmotic pressure (ICOP).

 

The net filtration pressure (NFP) is the difference between the net hydrostatic pressure and the net osmotic pressure.

 

Fluid will tend to move out of the capillary and into the interstitial fluid. At the venous end fluid fluid tends to move into the capillary. Both due to NFP differences.


The transition between filtration and reabsorption occurs where the CHP is 25 mm Hg, because at that point the hydrostatic and osmotic forces are equal–that is, the NFP is 0 mm Hg.

 

Of the roughly 24 liters of fluid that moves out of the plasma and into the interstitial fluid each day, 85 percent is reabsorbed. The remainder (3.6 liters) flows through the tissues and into lymphatic vessels, for eventual return to the venous system.

 
Any condition that affects hydrostatic or osmotic pressures in the blood or tissues will shift the balance between hydrostatic and osmotic forces.

 

If hemorrhaging occurs, both blood volume and blood pressure decline. This reduction in CHP lowers the NFP and increases the amount of reabsorption. The result is a reduction in the volume of interstitial fluid and an increase in the circulating plasma volume. This process is known as a recall of fluids .

If dehydration occurs, the plasma volume decreases owing to water loss, and the concentration of plasma proteins increases. The increase in BCOP accelerates reabsorption and a recall of fluids that delays the onset and severity of clinical symptoms.

If the CHP rises or the BCOP declines, fluid moves out of the blood and builds up in peripheral tissues, a condition called edema.


Edema is an abnormal accumulation of interstitial fluid. The underlying problem in all types of edema is a disturbance in the normal balance between hydrostatic and osmotic forces at the capillary level. For instance,  

In the U.S. population, most serious cases of edema result from an increase in arterial blood pressure, in venous pressure, or in total circulatory pressure. The increase may result from heart problems, such as heart failure, venous blood clots that elevate venous pressures, or other circulatory abnormalities.

Edema can also result from problems with other systems, such as a blockage of lymphatic vessels or impaired urine formation: If the lymphatic vessels in a region become blocked, the volume of interstitial fluid will continue to rise, and the IHP will gradually increase until capillary filtration ceases. In filariasis, parasites can block lymphatic vessels and cause a massive regional edema known as elephantiasis, a disease still common in equatorial regions.

 

 

 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


With renal failure, if the kidneys are unable to produce urine but the individual continues to drink liquids, the blood volume will rise. This situation ultimately leads to elevated CHP and enhances fluid movement into the peripheral tissues.

Venous Pressure and Venous Return determines the amount of blood arriving at the right atrium each minute.

 

Pressures at the entrance to the right atrium fluctuate, but they average about 2 mm Hg. Although venous pressures are low, veins offer comparatively little resistance so pressure declines very slowly as blood moves through the venous system. As blood continues toward the heart, the veins become larger, resistance drops, and the velocity of blood flow increases.


When you stand, the venous blood returning from your body inferior to the heart must overcome gravity as it ascends within the inferior vena cava. Two factors assist the low venous pressures in propelling blood toward your heart: (1) muscular compression of peripheral veins and (2) the respiratory pump .

Muscular Compression
The contractions of skeletal muscles near a vein compress it, helping push blood toward the heart. The valves in small and medium–sized veins ensure that blood flows in one direction only.

 

The Respiratory Pump
As you inhale, your thoracic cavity expands and pressure within the pleural cavities declines. This drop in pressure pulls air into your lungs. At the same time, blood is pulled into the inferior vena cava and right atrium from the smaller veins of your abdominal cavity and lower body. The effect on venous return from the superior vena cava is less pronounced, as blood in that vessel is normally assisted by gravity.


As you exhale, your thoracic cavity decreases in size. Internal pressure then rises, forcing air out of your lungs and pushing venous blood into the right atrium. This mechanism is called the respiratory pump , or thoracoabdominal pump . The importance of such pumping action increases during heavy exercise, when respirations are deep and frequent.

 

Cardiovascular Regulation
 
Homeostatic mechanisms regulate cardiovascular activity to ensure that
tissue perfusion , or blood flow through tissues, meets the demand for oxygen and nutrients. The three variable factors are (1) cardiac output, (2) peripheral resistance, and (3) blood pressure. When a group of cells becomes active, the circulation to that region must increase to deliver the necessary oxygen and nutrients and to carry away the waste products and carbon dioxide they generate. The goal of cardiovascular regulation is to ensure that these blood flow changes occur (1) at an appropriate time, (2) in the right area, and (3) without drastically changing blood pressure and blood flow to vital organs.


Factors involved in the regulation of cardiovascular function include autoregulation, neural mechanisms, and endocrine mechanisms

Homeostatic Adjustments That Compensate for a Reduction in Blood Pressure and Blood Flow

 

Autoregulation occurs when local factors change the pattern of blood flow within capillary beds in response to chemical changes in interstitial fluids. Autoregulation causes immediate, localized homeostatic adjustments. If autoregulation fails to normalize conditions at the tissue level, neural mechanisms and endocrine factors are activated.

Neural Mechanisms respond to changes in arterial pressure or blood gas levels at specific sites. When those changes occur, the cardiovascular centers of the autonomic nervous system adjust cardiac output and peripheral resistance to maintain blood pressure and ensure adequate blood flow.

Endocrine Mechanisms release hormones that enhance short–term adjustments and that direct long–term changes in cardiovascular performance.

Autoregulation of Blood Flow Within Tissues

 Factors that promote the dilation of precapillary sphincters are called vasodilators . Local vasodilators act at the tissue level and accelerate blood flow through the tissue of origin. Examples of local vasodilators include:

Decreased tissue oxygen levels or increased levels.

The generation of lactic acid or other acids by tissue cells.

The release of nitric oxide (NO) from endothelial cells.

Rising concentrations of potassium ions or hydrogen ions in the interstitial fluid.

Chemicals released during local inflammation, including histamine and NO.

Elevated local temperatures

These factors work by relaxing the smooth muscle cells of the precapillary sphincters. All of them indicate that conditions in the tissue are abnormal in one way or another. An improvement in blood flow, which will bring oxygen, nutrients, and buffers, may be sufficient to restore homeostasis.

 

 

 
Aggregating platelets and damaged tissues produce compounds that stimulate the constriction of precapillary sphincters. These compounds are local vasoconstrictors . Examples include prostaglandins and thromboxanes released by activated platelets and white blood cells and the endothelins released by damaged endothelial cells.

 
Neural Mechanisms
The nervous system is responsible for adjusting cardiac output and peripheral resistance in order to maintain adequate blood flow to vital tissues and organs. Centers responsible for these regulatory activities include the cardiac centers and the vasomotor centers of the medulla oblongata. they are often considered to form complex cardiovascular (CV) centers.

 

Each cardiac center consists of a cardioacceleratory center , which increases cardiac output through sympathetic innervation, and a cardioinhibitory center , which reduces cardiac output through parasympathetic innervation.

Vasomotor Tone
 The sympathetic vasoconstrictor nerves are chronically active, producing a significant vasomotor tone . Vasoconstrictor activity is normally sufficient to keep the arterioles partially constricted. Under maximal stimulation, arterioles constrict to about half their resting diameter, whereas a fully dilated arteriole increases its resting diameter by roughly 1.5 times. Constriction has a significant effect on resistance, because the resistance increases sharply as the diameter of the vessel decreases. The resistance of a maximally constricted arteriole is roughly 80 times that of a fully dilated arteriole. Because blood pressure varies directly with peripheral resistance, the vasomotor centers can control arterial blood pressure very effectively by making modest adjustments in vessel diameters. Extreme stimulation of the vasomotor centers will also produce venoconstriction and a mobilization of the venous reserve.

Reflex Control of Cardiovascular Function
The cardiovascular centers detect changes in tissue demand by monitoring arterial blood, with particular attention to blood pressure, pH, and the concentrations of dissolved gases. The baroreceptor reflexes respond to changes in blood pressure, and the chemoreceptor reflexes monitor changes in the chemical composition of arterial blood. These reflexes are regulated through a negative feedback loop: The stimulation of a receptor by an abnormal condition leads to a response that counteracts the stimulus and restores normal conditions.

Baroreceptors monitor the degree of stretch in the walls of expandable organs. The baroreceptors involved with cardiovascular regulation are located in the walls of (1) the carotid sinuses , expanded chambers near the bases of the internal carotid arteries of the neck  (2) the aortic sinuses , pockets in the walls of the ascending aorta adjacent to the heart, and (3) the wall of the right atrium. These receptors are components of the baroreceptor reflexes , which adjust cardiac output and peripheral resistance to maintain normal arterial pressures.

 

When blood pressure climbs, the increased output from the baroreceptors alters activity in the CV centers and produces two major effects

A decrease in cardiac output , due to parasympathetic stimulation and the inhibition of sympathetic activity.

Widespread peripheral vasodilation , due to the inhibition of excitatory neurons in the vasomotor centers.

The decrease in cardiac output reflects primarily a reduction in heart rate due to the release of acetylcholines at the sinoatrial (SA) node. The widespread vasodilation lowers peripheral resistance, and this effect, combined with a reduction in cardiac output, leads to a decline in blood pressure to normal levels.
When blood pressure falls below normal, baroreceptor output is reduced accordingly. This change has two major effects:

An increase in cardiac output , through the stimulation of sympathetic innervation to the heart. This results from the stimulation of the cardioacceleratory centers and is accompanied by an inhibition of the cardioinhibitory centers.

Widespread peripheral vasoconstriction , caused by the stimulation of sympathetic vasoconstrictor neurons by the vasomotor centers.

The effects on the heart result from the release of NE by sympathetic neurons innervating the SA node, the atrioventricular (AV) node, and the general myocardium. In a crisis, sympathetic activation occurs, and its effects will be enhanced by the release of both NE and epinephrine (E) from the adrenal medullae. The net effect is an immediate increase in heart rate and stroke volume and a corresponding rise in cardiac output.

 

The vasoconstriction, which also results from the release of NE by sympathetic neurons, increases peripheral resistance. These adjustments– increased cardiac output and increased peripheral resistance–work together to elevate blood pressure.

The atrial reflex responds to a stretching of the wall of the right atrium.
Under normal circumstances, the heart pumps blood into the aorta at the same rate at which blood arrives at the right atrium. When blood pressure rises at the right atrium, blood is arriving at the heart faster than it is being pumped out. The atrial baroreceptors solve the problem by stimulating the CV centers and increasing cardiac output until the backlog of venous blood is removed. Atrial pressure then returns to normal.

Chemoreceptor Reflexes respond to changes in carbon dioxide, oxygen, or pH levels in blood and cerebrospinal fluid (CSF)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

The chemoreceptors involved are sensory neurons located in the carotid bodies , situated in the neck near the carotid sinus, and the aortic bodies , near the arch of the aorta. These receptors monitor the composition of the arterial blood. Additional chemoreceptors located on the ventrolateral surfaces of the medulla oblongata monitor the composition of CSF.

When chemoreceptors in the carotid bodies or aortic bodies detect either a rise in the carbon dioxide content or a fall in the pH of the arterial blood, the cardioacceleratory and vasomotor centers are stimulated and the cardioinhibitory centers are inhibited. This dual effect causes an increase in cardiac output, peripheral vasoconstriction, and an elevation in arterial blood pressure. A drop in the oxygen level at the aortic bodies will have the same effects.

 

The chemoreceptors of the medulla oblongata are involved primarily with the control of respiratory function and secondarily with regulating blood flow to the brain. For example, a steep rise in CSF carbon dioxide levels will trigger the vasodilation of cerebral vessels, but will produce vasoconstriction in most other organs. The result is increased blood flow–and hence increased oxygen delivery to the brain.