STRUCTURE AND FUNCTION OF BLOOD VESSELS
Identify the different types of blood vessels in the body.
Describe the functional properties of arteries.
Explain how the sympathetic nervous system affects blood vessel diameter
Explain how blood bypasses capillary beds.
Distinguish among the different types of capillaries and where they are found.
List the three ways substances enter and leave capillaries.
Describe the substances that use diffusion as a capillary exchange method.
Describe transcytosis and the types of substances to be transported.
Discuss the importance of bulk flow, the pressures involved in bulk flow, and the pressure changes that occur for bulk flow to happen.
HEMODYNAMICS: PHYSIOLOGY OF CIRCULATION
Explain the factors that regulate the velocity of blood flow.
Describe the three factors that contribute to the return of venous blood to the heart.
Explain how blood pressure changes throughout the cardiovascular system.
Explain the factors that determine the systemic vascular resistance.
CONTROL OF BLOOD PRESSURE AND BLOOD FLOW
Describe the structure and function of the cardiovascular center.
Identify the sources of input to the cardiovascular center.
Identify the outcome of sympathetic and parasympathetic output from the cardiovascular center.
Describe the role of baroreceptors in the aortic and carotid sinus reflexes and the purpose of these reflexes.
Examine the effects of renin-angiotensin-aldosterone, epinephrine, norepinephrine, ADH and ANP on blood pressure.
SHOCK AND HOMEOSTASIS
Define shock and its general consequences.
Discuss the four causes of shock.
Describe the characteristic signs and symptoms of shock.
Chapter Lecture Notes
Blood vessels form a closed system of tubes that carry blood away from the heart, transport it to the tissues of the body, and then return it to the heart (Table 21.1 & Fig 21.6)
Types of blood vessels
Functions of Blood Vessels
Carry blood to the tissues
The functional properties of arteries are
elasticity - allows arteries to accept blood under great pressure from the contraction of the ventricles and to send it on through the system
contractility - allows arteries to increase or decrease lumen size and to limit bleeding from wounds
due to the smooth muscle in the tunica media
Smooth muscle in blood vessels is innervated by the sympathetic nervous system
increase in stimulation causes muscle contraction or vasoconstriction
injury to artery or arteriole causes muscle contraction reducing blood loss (vasospasm)
decrease in stimulation or presence of certain chemicals causes vasodilation
nitric oxide, K+, H+ and lactic acid cause vasodilation
Connect arteries to capillaries
Arteriole walls have fewer layers of smooth muscle than arteries
Metarterioles form branches into capillary beds (Fig 21.3)
to bypass a capillary bed, a precapillary sphincter, a band of smooth muscle around the metarteriole, contracts, vasoconstricting the metarteriole & blood flows out of the bed and into a thoroughfare channel
vasomotion - intermittent contraction & relaxation of precapillary sphincters that allow filling of capillary beds 5-10 times/minute
Site of substance exchange between the blood and body tissues
connect capillaries to larger veins
very porous endothelium allows for escape of many phagocytic white blood cells
convey blood from the venules back to the heart
contain valves to prevent the backflow of blood
Found near every cell in the body but more extensive in highly active tissue (muscles, liver, kidneys & brain) (Fig 21.1)
entire capillary bed fills with blood when tissue is active
not found in epithelia, cornea and lens of eye & cartilage
Capillary walls are composed of only a single layer of cells (endothelium) and a basement membrane
Types of capillaries (Fig 21.4)
nearly complete basement membrane
intercellular clefts - gaps between neighboring cells
Locations: skeletal & smooth muscle, connective tissue and lungs
basement membrane mostly intact
endothelial cells have fenestrations – holes or pores through the plasma membrane
Locations: kidneys, small intestine, choroid plexuses, ciliary process & endocrine glands
very large fenestrations
large intercellular clefts
allow large structures like proteins or blood cells to enter or exit the bloodstream
Locations: liver, bone marrow, spleen, anterior pituitary, & parathyroid gland
Movement of materials in & out of a capillary (Fig 21.7)
Diffusion (most important method)
Substances such as O2, CO2, glucose, amino acids, hormones, and others diffuse down their concentration gradients
all plasma solutes except large proteins pass freely across
through lipid bilayer, fenestrations or intercellular clefts
blood brain barrier does not allow diffusion of water-soluble materials (nonfenestrated epithelium with tight junctions)
passage of material across endothelium in tiny vesicles by endocytosis and exocytosis
large, lipid-insoluble molecules such as insulin or maternal antibodies passing through placental circulation to fetus
Movement of large amount of dissolved or suspended material in same direction
Movement is in response to pressure
from area of high pressure to area of low
Faster rate of movement than diffusion or osmosis
Most important for regulation of relative volumes of blood & interstitial fluid
Filtration - movement of material into interstitial fluid
promoted by blood hydrostatic pressure & interstitial fluid osmotic pressure
Blood hydrostatic pressure (BHP) – Amount of force exerted on the walls of a blood vessel due to contraction of the heart and the amount of blood within the vessel
At arteriole end is 35 mmHg and at venule end is 26 mmHg
Interstitial fluid osmotic pressure (IFOP) – Amount of “pull” exerted by solutes in the interstitial fluid
assume value is 1 mmHg
Reabsorption - movement from interstitial fluid into capillaries
promoted by blood colloid osmotic pressure and interstitial fluid hydrostatic pressure
Blood colloid osmotic pressure (BCOP) – Amount of “pull” exerted by solutes, mostly large proteins that are not able to leave the capillaries, within the capillaries
BCOP = 26 mmHg
Interstitial fluid hydrostatic pressure (IFHP) – the amount of back pressure “pushing” fluid back into the capillaries
because fluid is drained away from the capillaries almost as soon as it leaves, the IFHP is close to zero, so assume a value of zero
The balance between filtration and reabsorption determines whether fluids leave or enter capillaries, it depends on a balance of the pressures
Net Filtration Pressure (NFP)
NFP = (BHP + IFOP) – (BCOP + IFHP)
At the arterial end of a capillary bed, the BHP is high and the NFP is 10 mm Hg of outward pressure (net filtration)
At the venule end of a capillary bed, the BHP has dropped and the NFP is 8-9 mm Hg of inward pressure (net reabsorption)
About 85% of the filtered fluid is returned to the capillary
Starling’s law of the capillaries states that the volume of fluid & solutes reabsorbed is almost as large as the volume filtered
escaping fluid and plasma proteins are collected by lymphatic capillaries (3 liters/day)
Hemodynamics – Blood Flow
Blood flow - The volume that flows through any tissue in a given period of time
The velocity of blood flow is inversely related to the total cross-sectional area of all blood vessels
blood flows most slowly where total cross-sectional area is greatest
Blood flow velocity decreases from the aorta to arteries to capillaries and increases as it returns to the heart (Fig 21.11)
flow in aorta is 40 cm/sec while flow in capillaries is 0.1 cm/sec
slow rate in capillaries allows for exchange
Circulation time is time it takes a drop of blood to travel from right atrium back to right atrium
Volume of blood flowing back to the heart from the systemic veins depends on
pressure difference from venules (16 mm Hg) to right atrium (0 mm Hg) – siphon effect
decreased thoracic pressure and increased abdominal pressure during inhalation, moves blood into thoracic veins and the right atrium
Skeletal muscle pump (Fig 21.9)
contraction of muscles & presence of valves
Blood pressure – force exerted by blood on walls of a vessel
caused by contraction of the ventricles
highest in aorta
120 mm Hg during systole & 80 during diastole
Pressure falls steadily in systemic circulation with distance from left ventricle (Fig 21.8)
35 mm Hg entering the capillaries
0 mm Hg entering the right atrium
Factors that affect blood pressure (Fig 21.10)
Cardiac output – heart rate and force of contraction
If decrease in blood volume is over 10%, BP drops
Water retention increases blood pressure
Vascular resistance - opposition to blood flow as a result of friction between blood and the walls of the blood vessels
average blood vessel radius
smaller vessels offer more resistance to blood flow
can cause moment to moment fluctuations in pressure by changing the size of blood vessels
blood viscosity (thickness)
ratio of red blood cells to plasma volume
increases in viscosity increase resistance
dehydration or polycythemia
total blood vessel length
the longer the vessel, the greater the resistance to flow
obesity causes high blood pressure
Systemic vascular resistance (also known as total peripheral resistance) refers to all of the vascular resistances offered by systemic blood vessels;
most resistance is in arterioles, capillaries, and venules due to their small diameters
arterioles control BP by changing diameter
Control of Blood Pressure & Flow
Nervous control of blood pressure and flow is regulated by the cardiovascular center (CV) - a group of neurons in the medulla that regulates heart rate, contractility, and blood vessel diameter (Fig 21.12 & 21.13)
higher brain regions such as cerebral cortex, limbic system & hypothalamus
increase in body temperature
input during physical activity
changes in pressure within blood vessels
monitor concentration of chemicals in the blood
output from the CV flows along sympathetic and parasympathetic fibers
Parasympathetic impulses along vagus nerves decrease heart rate
Sympathetic impulses along cardioaccelerator nerves increase heart rate and contractility
The sympathetic division also continually sends impulses to smooth muscle in blood vessel walls via vasomotor nerves. The result is a moderate state of tonic contraction or vasoconstriction, called vasomotor tone
Baroreceptor reflexes controlled by the CV (Fig 21.14)
carotid sinus reflex
swellings in internal carotid artery wall
glossopharyngeal nerve to cardiovascular center in medulla
maintains normal BP in the brain
receptors in wall of ascending aorta
vagus nerve to cardiovascular center
maintains general systemic BP
Hormonal Control of Blood Pressure (Table 21.2)
Renin-angiotensin-aldosterone system (Fig 18.16)
release of renin by kidneys results in conversion of a protein made by the liver, angiotensinogen, into angiotensin II by the lungs
Angiotensin II stimulates systemic vasoconstriction
Angiotensin II stimulates the adrenal gland to release aldosterone
Aldosterone influences kidney function during urine production, decreasing the amount of urine production and increasing the amount of H2O & Na+ retained by the blood
Net effect of the Renin-Angiotensin-Aldosterone System is to increase blood volume and blood pressure
Epinephrine & norepinephrine
increases heart rate & force of contraction
causes vasoconstriction in skin & abdominal organs
vasodilation in cardiac & skeletal muscle
increases blood pressure
ADH (anti diuretic hormone)
promotes retention of water by the blood during urine production
increases blood volume and pressure
ANP (atrial natriuretic peptide) lowers BP
loss of salt and water in the urine
decreases blood volume and pressure
Shock is the condition in which cardiac output (CO) cannot deliver enough oxygen and nutrients to meet the needs of body cells.
There are three stages of shock.
Nonprogressive or compensated
If the cause is removed the body's negative feedback mechanisms alone can usually restore homeostasis.
Progressive or Decompensated
Shock becomes steadily worse. Recovery from progressive shock is possible but there will be some damage to tissues.
In this condition body cells have been too long without adequate oxygen and nutrients. All forms of known therapy are unable to save a person's life at this point even though cardiac output and arterial pressure may appear to be restored to normal.
There are four main types of shock
Hypovolumic - decreased blood volume (Fig 21.16)
may be caused by acute hemorrhage (internal or external bleeding) or excessive fluid loss (as occurs in excessive vomiting, diarrhea, sweating, urine production, dehydration and burns)
Cardiogenic (cardiac shock, power failure syndrome) - decreased cardiac output
may be caused by cardiac abnormalities that decrease the ability of the heart to pump blood (for example, myocardial infarction, severe valve dysfunction, heart arrhythmias)
85% of people who develop cardiogenic shock do not survive
Neurogenic - occurs without any loss of blood
vascular capacity increases so much than even the normal amount of blood cannot adequate fill the circulatory system
may be caused by sudden loss of vasomotor tone throughout the body causing especially massive dilation of veins (venous pooling) causing reduction of venous return to the heart (may occur in deep general anesthesia, spinal anesthesia, and brain damage)
Anaphylactic (an allergic reaction)
allergic reaction of anaphylactic shock causes massive release of histamine from basophils and mast cells dilates arteries and veins reducing venous return
Septic (blood poisoning, toxic shock syndrome)
widely disseminated, blood borne bacterial infection causing extensive tissue damage
important in hospital setting because this type of shock, more often than any other type of shock besides cardiogenic, causes patient death in the hospital
may be caused by blockage of blood flow through part of the circulation
blockage causes backup of blood and increases pressure behind the blockage leading to leaking of plasma and proteins out of capillaries (loss of blood volume) into surrounding tissues (for example, pulmonary emboli)
Signs and symptoms of shock
rapid resting heart rate (tachycardia)
clammy, cool pale skin
altered mental state
decreased urine formation