Chapter 19: Blood Vessels Flashcards

1
Q

Blood Vessels:

A

o Are dynamic and ever changing conduits for delivery (nutrients) and removal (wastes) to and from the body tissues that begins and ends at the heart
o Arteries: carry blood away from the heart; oxygenated except for pulmonary circulation
o Capillaries: contact tissue cells and directly serve each individual cell
o Veins: carry oxygen poor blood toward the heart

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2
Q

Structure of Blood Vessel Walls:

A

o Arteries and veins:
o Tunica intima = innermost and next to the lumen and contains the endothelium (simple squamous) that lines the inner walls of the BVs. Allows for smooth, frictionless movement of blood
o Tunica media = smooth muscle for vasoconstriction and vasodialation (affects overall blood flowà BP via sympathetic nervous system)
o Tunica externa = loose woven collagen fibers to support and anchor the BV. Vasa vasorum = small blood vessels that nourish the tunica externa (also nerves and lympathatics infiltrate).

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3
Q

Conducting (Elastic) Arteries:

A

o Large thick-walled arteries near the heart with elastin in all three tunics.
o Examples are the aorta and its major branches (vessels are 2.5 cm to 1 cm in diameter).
o Large lumens offer low-resistance and hence called Conducting Arteries.
o Elastic arteries act as pressure reservoir. Expand and recoil as blood is ejected from the heart.

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4
Q

Muscular (Distributing) Arteries:

A

o Muscular Arteries distal to elastic arteries: delivers blood to the body organs
o Have thick tunica media with more smooth muscle and less elastin (1cm to 0.3 mm in diameter).
o Since more smooth muscle is present these arteries are they are active in vasoconstriction/vasodialation.

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5
Q

Arterioles:

A

o Arterioles are the smallest arteries. Have a Thick tunic media = large amount of smooth muscle with very little elastin. Resistance vessels.
o Arterioles lead to capillary beds.
o Arterioles control flow into capillary beds via vasodilation and vasoconstriction which adjusts blood flow to capillary beds.

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6
Q

Capillaries:

A
o	Capillaries are the smallest blood vessels and microscopic in size. 
o	The walls consist of thin tunica intima = one cell thick + a basement membrane.
o	Pericytes (spider shaped smooth muscle cells) help stabilize capillary walls and help control permeability.
o	Size allows only a single RBC to pass at a time with direct contact with every body cell.
o	In all tissues except for cartilage, epithelia, cornea and lens of eye. 
o	Functions = exchange of gases, nutrients, wastes, hormones, etc. between blood and interstitial fluids.
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7
Q

The 3 Types of Capillaries:

A

o Continuous Capillaries
o Fenestrated Capillaries
o Sinusoidal Capillaries (sinusoids)

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8
Q

Continuous Capillaries:

A

o CO2 / O2 and nutrient exchange occurs in the skin and muscles (most common but the least permeable).
o Tight junctions connect endothelial cells of capillaries.
o Although tight junctions, there are intercellular clefts (small openings) between endothelial cells that allow the passage of fluids and small solutes.
o Continuous capillaries of the brain.
o Tight junctions are complete, forming the blood-brain barrier.
o Pinocytic vesicles allow nutrient exchange through endothelial cells.

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9
Q

Fenestrated Capillaries:

A

o Some of the endothelial cells contain pores (or fenestrations)
o These capillaries also have intercellular clefts and pinocytic vesicles
o More permeable than continuous capillaries to fluids and solutes
o Function in absorption or filtrate formation:
o Small intestines (absorption of nutrients).
o Endocrine glands (dumping hormones into blood).
o Kidneys (blood plasma filtration).

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10
Q

Sinusoids (Sinusoidal Capillaries):

A

o Most permeable.
o Fewer tight junctions between epithelial cells, larger intercellular clefts and very leaky, large lumens with incomplete basement membranes.
o Sinusoids are fenestrated (pores).
o Allow large molecules blood cells to pass between the blood and surrounding tissues.
o Found in the liver, bone marrow (RBC’s and leukocytes manufactured), liver, and spleen.

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11
Q

Capillary Beds:

A

o Capillary beds are interwoven networks of capillaries form the microcirculation between arterioles and venules.
o Consist of two types of vessels:
o Vascular shunt (or metarteriole—thoroughfare channel): Directly connects the terminal arteriole and a postcapillary venule.
o True capillaries:
o Woven 10 to 100 exchange vessels per capillary bed
o True capillaries usually branch off the metarteriole (proximal end of vascular shunt that comes off a terminal arteriole) returns via the thoroughfare channel to join with a postcapillary venule).

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12
Q

Blood Flow Through Capillary Beds:

A

o Precapillary sphincters act like valves that regulate blood flow into the true capillaries at the point where they join with the metarteriole.
o Blood goes through the terminal arteriole to go either through the true capillary bed or be shunted directly to the thoroughfare channel into the postcapillary venule.
o Regulated by local chemical conditions and vasomotor nerves (whether sphincters are relaxed or contracted).

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13
Q

Venules:

A

o Formed when the capillary beds unite.
o Very porous; allow fluids and WBCs to go back and forth easily.
o Postcapillary venules consist of endothelium and a few pericytes.
o Larger venules have one or two layers of smooth muscle cells.

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14
Q

Veins:

A

o Formed when venules join together.
o Have thinner walls, larger lumens compared with corresponding arteries.
o Blood pressure is lower than in arteries.
o Thin tunica media (little smooth muscle) and a thick tunica externa (consists of collagen fibers and elastic networks).
o Veins are called capacitance vessels (blood reservoirs); and contain up to 65% of the blood supply at any time.
o Specialization of veins that ensure return of blood to the heart:
o Large-diameter lumens offer little resistance.
o Venous Valves prevent backflow of blood. Most abundant in veins of the limbs (to help counteract effects of gravity).
o Venous sinuses: flattened veins with extremely thin walls of only endothelium (e.g., coronary sinus of the heart and dural venous sinuses of the brain).

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15
Q

Vascular Anastomoses:

A

o Interconnections of branches of blood vessels where BVs come together.
o Arterial anastomoses provide alternate blood pathways (collateral channels) to a given body region = collateralization.
o Common at joints (movement of joint blocks blood flow), in abdominal organs, brain, and heart.
o Allows for adequate blood flow if another vessel is blocked (e.g.blood clot = emboli).
o Vascular shunts of capillaries are examples of arteriovenous anastomoses.
o Venous anastomoses allow multiple routes for blood.

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16
Q

Blood Flow:

A

o Volume of blood flowing through a vessel, an organ, or the entire circulation in a given period of time.
o Measured as ml/min or L/min.
o Equivalent to cardiac output (CO) for entire vascular system, except, blood to certain organs may be shunted based on needs.
o Blood Flow varies at any given time through INDIVIDUAL ORGANS depending upon their metabolic needs (blood shunting).
o Blood flow is relatively constant when at rest.
o Pressure Differences: Blood always flows form areas of high pressure to areas of lower pressure. The greater the pressure gradient, the greater the flow.
o Resistance (opposition to blood flow): the greater the resistance, the more the blood flow is impeded.

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17
Q

Resistance: Definition and Three Important Sources:

A

o Opposition to flow in systemic system.
o Measure of the amount of friction blood encounters.
o 1) Blood viscosity.
o 2) Total blood vessel length.
o 3) Blood vessel diameter.
o Small-diameter arterioles are the major determinants of PR
o Resistance varies inversely with the 4th power of the vessel radius =
o Doubling the size of a vessel =
o 1/ 2x2x2x2 = 1/16th the previous resistance larger blood vessels near the heart do not influence peripheral resistance, but vasoconstriction/dialation of the smaller arterioles pretty much determine PR.
o Abrupt changes in diameter due to fatty plaques from atherosclerosis dramatically increase PR.

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18
Q

Blood Viscosity:

A

o The thickness or viscosity of the blood due to formed elements (RBCs) and plasma proteins.
o The greater the viscosity, the greater the PR and the greater the BP (usually a constant except for e.g. polycythemaia, anemias).

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19
Q

Blood Vessel Length:

A

o The longer the vessel, the greater the PR encountered and the greater the BP (obese people have many more miles of blood vessels) but usually a constant.

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20
Q

Blood Vessel Diameter:

A

o This is the variable that constantly changes PR!!

21
Q

Arterial Blood Pressure:

A

o Force per unit area exerted on the wall of a blood vessel by the blood (= a hydrostatic pressure)
o Expressed in mm Hg and taken at the brachial artery.
o Contraction of the ventricles generates the BP.
o Highest in the aorta, decreases progressively, lowest at the right atrium, biggest drop of BP occurs at the arterioles.
o The pressure gradient provides the driving force that keeps blood moving from higher to lower pressure areas and back to the heart.
o Systolic blood pressure: the highest pressure exerted during ventricular systole (contraction) = the high number of a blood pressure reading
o Diastolic pressure: lowest level of arterial pressure during ventricular diastole = the lower number of the blood pressure reading)
o Pulse pressure = difference between systolic and diastolic pressure and amount of pressure to feel a pulse
o BP is measured by using a sphygmomanometer or via a catheter within a blood vessel
o Normal BP = 120/80 mmHg (systolic BP/diastolic BP)
o Hypertension = HTN = >140/90 mmHg
o Hypotension = low blood pressure (from blood loss, dehydration, anemia, etc…)
o Mean arterial blood pressure (MABP): defined as an approximation of an “average” blood pressure in the arteries between systole and diastole. Because diastole lasts longer than systole, MEAN pressure is not simply the value halfway between systole and diastole: MABP = diastolic pressure + (pulse pressure divided by 3).

22
Q

Equation for BP Regulation:

A

o MABP is proportional to CO (cardiac output) X PR (peripheral resistance)
remember, CO = SV X HR
o When CO goes up, so does BP.
o When Peripheral Resistance goes up, so does MABP.
o Increased stroke volume or heart rate will increase MABP.
o When anything about peripheral resistance (PR) goes up (i.e., increased viscosity, vasoconstriction) MABP will go up.
o When anything about CO or PR goes down, MABP goes down.

23
Q

Capillary Blood Pressure:

A

o MABP ranges from 15 to 35 mm Hg in capillaries.
o Low capillary pressure is a must.
o High BP would rupture fragile, thin-walled capillaries.
o Most capillaries are very permeable, so low pressure still pushes filtrate into interstitial spaces.

24
Q

Venous Blood Pressure:

A

o MABP of the venous vessels changes little during the cardiac cycle.
o Venous Blood pressure represents a small pressure gradient = about 15 mm Hg (as compared to 35 mm Hg at arterioles).
o Due to low venous pressure, adequate blood return to the right atrium is compromised.

25
Q

Factors Aiding Venous Return:

A

o To accomplish venous return to the heart: Respiratory “pump”: pushes blood toward heart by pressure changes created during breathing moving blood by squeezing abdominal veins.
o Muscular “pump”: contraction of skeletal muscles “milk” blood toward the heart and valves prevent backflow.
o Vasoconstriction of veins under sympathetic control….veins do have some tunica media.

26
Q

Control of Blood Pressure:

A

o Short-term = local, neural and hormonal controls.
o Both counteract fluctuations in blood pressure by altering peripheral resistance.
o Long-term = regulation by kidney.
o Kidney counters changes in blood pressure by altering blood volume.

27
Q

Short-Term Mechanisms:

Neural Controls

A

o Neural controls of peripheral resistance:
o Maintain MABP by altering blood vessel diameter.
o Can Alter or shunt blood distribution in response to specific demands by different organs.
o Neural controls operate via REFLEX ARCS that involve:
o Baroreceptors, Chemoreceptors (afferent sensory information is carried by Cranial Nerves IX and X).
o to
o The control vasomotor centers = medulla oblongata (nuclei called the cardiovascular center = cardiac output and vasomotor).
o to
o Vascular smooth muscle constriction caused by sympathetic efferent fibers.

28
Q

Short-Term Mechanisms:

Baroreceptor-Initiated Reflexes

A

o Baroreceptors (stretch receptors) are located in:
o Carotid sinuses = dialated areas in the internal carotid arteries (blood to head) at point where it bifurcates from the common carotid artery.
o Aortic arch:
o Walls of large arteries of the neck and thorax.
o Increased blood pressure stimulates baroreceptors which are mechanical stretch receptors (increased stretch) and sends this information to the vasomotor and cardio centers of the medulla oblongata.
o Acts on the vasomotor center causing arteriole dilation and venodilation = decreased sympathetic innervation to the blood vessels.
o Decreases the cardioacceleratory center = decreased sympathetic innervation to heart.
o Increases the cardioinhibitory center of the medulla through increased parasympathetic innervation to the heart.

29
Q

Baroreceptor Reflexes for Decreased BP:

A

o Decreased BP: causes a decreased stretch in the arterial walls that is also sensed by the baroreceptors = sensory information travels by afferent sensory from Cranial Nerves IX, X.
o Increases the cardioacceleratory center in the medulla oblongata= increased sympathetic innervation to the heart = increased heart rate = increased BP.
o Decreases cardioinhibitory center in the medulla oblongata which decreases parasympathetic to the heart.
o Increases vasomotor center in the medulla oblongata = increased sympathetic to the blood vessel walls = vasoconstriction = increased PR = increased BP.

30
Q

Short-Term Mechanisms:

Chemoreceptor-Initiated Reflexes

A

o Chemoreceptors respond to rise in CO2 (hypercapnia) drop in pH (acidosis) or drop in O2 (hypoxia)…..information from receptors travel through afferent nerves via Cr. Nerve IX, X.
o To:
o Medulla oblongata: chemoreceptors increase blood pressure and blood flow via the vasomotor center and the cardioacceleratory center in the medulla oblongata.
o Pons: Respiratory centers in the brainstem (pons) stimulate an increase rate and depth of breathing.
o Chemoreceptors are located in the:
o Carotid sinus (bifurcation of external/internal common carotid artery).
o Aortic arch.
o Large arteries of the neck.
o Medulla oblongata (watch dog for brain).

31
Q

Short-Term Mechanisms:

Hormonal Controls

A

o Adrenal medulla (kidney): releases norepinephrine (NE) and epinephrine cause generalized vasoconstriction and increased heart rate
o Activation of the baroreceptors due to decreased MABP in the kidney cause the kidney to release renin (an enzyme) which ultimately causes the generation of Angiotensin II (comes from liver and lung tissue and then released into blood)
o Angiotensin II = a potent vasoconstrictor which acts immediately on smooth muscle of blood vessel
o Atrial natriuretic peptide released due to increased BP and blood volume = causes blood volume and blood pressure to decline, causes generalized vasodilation. This hormone is produced by the cardiac muscle cells of the right atrium when stretched.
o Antidiuretic hormone (ADH) (or vasopressin) released from the pituitary gland causes intense vasoconstriction in cases of extremely low BP.

32
Q

Long-Term Mechanisms:

Renal Regulation:

A

o Long-term mechanisms regulate BP by altering BLOOD VOLUME through the kidneys
o Direct renal mechanism: Alters blood volume independently of hormones
o Increased BP or blood volume causes the kidneys to eliminate more urine (more pee), thus reducing BP.
o Decreased BP or blood volume causes the kidneys to conserve water, and BP rises (less pee).
o Indirect renal mechanism: (renin-angiotensin system).
o Angiotensin II stimulates the release of Aldosterone from adrenal cortex of the adrenal glands = increases water reabsorption causes the increase in blood volume which causes an increase in BP.
o Angiotensin II stimulates the pituitary gland to release Antidiuretic Hormone (ADH) which increases blood volume (retention of water).

33
Q

Blood Pressure Regulation:

A

o 1. Local control = autoregulation
o a) Metabolic activity: If a tissue isn’t getting enough blood perfusion (e.g., because it is suddenly more metabolically active), it will eventually become hypoxic with a build up of wastes (CO2, H+, K+, lactic acid, adenosine, etc.) and release chemicals as a result. These chemicals tend to stimulate VASODILATION which increases perfusion. Once the wastes are carried away, the blood vessels constrict.
o b) Special cellular secretions under specific conditions: Endothelial cells (cells lining all blood vessels), blood platelets (thromboxane, serotonin), and some types of cells that are present close to blood vessels (e.g., mast cells) can secrete chemicals that can cause either vasodilation (as with the inflammatory process) or vasoconstriction (as with the need for vascular spasm with a blood vessel break):
o = VASODILATOR CHEMICALS: histamine, bradykinin, some prostaglandins, prostacyclin (also prevents clumping of platelets), nitric oxide
o = VASOCONSTRICTOR CHEMICALS: endothelins (secreted by endothelial cells), serotonin, thromboxane A-2 (platelets)
o Special note: Remember that HISTAMINE also increases the LEAKINESS of capillaries!
o c. Reactive hyperemia: If a tissue’s blood supply is reduced for a while, then restored, it will often exhibit an increased blood flow (above normal) temporarily. Your text uses the example of how a person’s face flushes after they come inside from the very cold.
o d. Angiogenesis: Over longer periods of time, tissues that chronically do not get enough oxygen will grow new blood vessels! This is controlled by local growth factors.

34
Q

Medullary Ischemic Response:

A

o MEDULLARY ISCHEMIC REFLEX: This is a reflex designed to ensure proper blood perfusion to the brain. If the medulla oblongata becomes ischemic, it sends autonomic sympathetic nervous system output to:
o 1) Heart: increase heart rate and force of contraction
o 2) Smooth muscle of blood vessels: widespread vasoconstriction
o The resulting increase in BP should provide better brain perfusion.

35
Q

Systemic Shock:

A

Failure of the cardiovascular system to deliver enough O2 and nutrients to meet tissue needs… many types, but all are characterized by inadequate blood flow to body tissues leads to cell death = necrosis.

36
Q

Signs of Shock:

A

o Systolic BP

37
Q

Types of Shock:

A

o 1. CARDIOGENIC SHOCK from heart failing to pump adequately.
o Most common causes = MI and arrhythmias (fibrillation).
o Also electrocution, heart ischemia, valve problems, or anything that impairs contractility of myocardium.
o 2. HYPOVOLEMIC SHOCK from inadequate blood volume
o Common cause: acute hemorrhage (aka hemorrhagic shock)
o Also excessive loss of body fluids from : Excessive sweating, severe burns, excessive diarrhea or vomiting, excessive urination (as in uncontrolled DM).
o Volume of blood falls leads to decreased venous return to heart leads to decreased stroke volume leads to the body trying to keep CO going by increasing heart rate (can only increase HR so far) and by vasoconstriction.
o VASCULAR SHOCK from inappropriate vasodilation
o Anaphylactic shock (release of inflammatory substances that increase vasodilation and capillary permeability) = Histamine
o Neurogenic shock (trauma to head that causes disorders of the Cardiac Vasomotor center in the medulla) (or occasional anesthesia reactions that depress the activity of the vasomotor centers in the medulla) = massive vasodilation
o Septic shock = bacterial toxins cause vasodilation and increased capillary permeability. Over 100,000 deaths/year!
o Emotional shock = vasovagal syncope (emotions cause strong parasympathetic stimulation of heart… also results in vasodilation of blood vessels in skeletal muscles and in the viscera) = BP down
o MISCELLANEOUS LOW VENOUS RETURN SHOCK
o A) OBSTRUCTED VENOUS RETURN SHOCK:
o When a tumor or an aneurysm compresses a vein and impedes the return of blood to the heart
o Most common cause = pulmonary embolism
o Also common = intestinal obstruction can cause large amounts of plasma to go from the blood into the interstitial spaces (or the intestine).
o B) VENOUS POOLING SHOCK:
o When blood volume is normal, but it has pooled in the limbs (from long periods of standing/sitting without adequate movement).

38
Q

Capillary Exchange:

A

o 1) Goal: gases/solutes/fluid in blood can exchange with gases solutes/fluid in interstitial spaces surrounding living & working cells.
o 2) Not everything can leave the blood to exchange with cells. Most cells (e.g., RBCs) and most proteins are too large to leave the blood.
o 3) Capillaries are basically just simple squamous epithelial cells (i.e., endothelial cells) with a basement membrane… with slight spaces between the cells (intercellular clefts)… some capillaries have fenestrations (pores which are large enough to allow some proteins to go in/out)… whereas sinusoidal capillaries are very very leaky and can even let cells/proteins in and out.

39
Q

Mechanisms of Capillary Exchange:

Diffusion

A

o a) Diffusion: Passive movement of substances down a concentration gradient (osmolarity) = WATER FOLLOWS SOLUTE
o How: pass thru intercellular clefts (spaces between the endothelial cells of the capillary wall) or thru fenestrations. Lipid soluble substances can diffuse directly through the phospholipid bilayer of the endothelial cells membrane (just a simple squamous epithelial cell!).
o What: O2, CO2, most nutrients (glucose, amino acids, fatty acids, vitamins), some hormones, metabolic wastes.
o Significance: ESSENTIAL FOR SOLUTE EXCHANGE between blood and interstitial fluid.

40
Q

Mechanisms of Capillary Exchange:

Carrier Mediated Transport

A

o b) Carrier mediated transport: Specialized protein transporters (or “taxi’s”), through specialized ion channels, can be involved in the transport of polar substances (such as ions) and across the capillary membrane. This can be along a concentration gradient (FACILIATATED DIFFUSION–no ATP required), or against a concentration gradient (ACTIVE TRANSPORT, requiring ATP). Not as significant for capillary exchange as diffusion.

41
Q

Mechanisms of Capillary Exchange:

Transcytosis

A

o c) Transcytosis: (Pinocytic vesicles)
o How: active process of enclosing substances in vesicles that enter the endothelial cells of the capillary, move across to the other side of the cell, exit into the IF (interstitial fluid) by exocytosis.
o What: Only small quantities of material cross the capillary walls in this manner…primarily for large lipid- insoluble molecules that can’t cross the capillary walls in any other way, e.g. INSULIN (a large protein hormone) and some antibodies (also proteins).
o Significance: Important for solute exchange of very large molecules between blood and interstitial fluid.

42
Q

Mechanisms of Capillary Exchange:

Bulk Flow of Fluids

A

o d) BULK FLOW OF FLUIDS: While plasma solutes, nutrients, and gas exchanges are occurring via diffusion/transcytosis, BULK FLUID FLOWS are also occurring via a balance between FILTRATION & REABSORPTION.
o Definition of BULK FLOW OF FLUIDS: flow of large numbers of ions, molecules, or particles in fluid that move together in the same direction at rates far greater than could be predicted by diffusion alone.
o How: FILTRATION = pressure driven movement of fluids and solutes from an area of high pressure to an area of low pressure… fluid is forced through the capillary thru the intercellular clefts at the arterial end of the capillary from the blood into the interstitial spaces.

43
Q

Mechanisms of Capillary Exchange:

A

o Fluid is then REABSORBED = pressure driven movement of fluids from the Interstitial Fluid (IF)back INTO THE CAPILLARY at the venous end of the capillary
o What: primarily fluid (and ions/small particles dissolved in fluid)
o Significance: regulation of VOLUME of blood vs. VOLUME of IF (interstitial fluid = around cells)
o Frank Starling’s Law of Capillaries: Filtration is almost equal to reabsorption… what is filtered out from the blood at the arterial end of the capillary is mostly reabsorbed at the venous end of the capillary.
o Only 5% of the blood is in the systemic capillaries at any one time.
o Capillary beds dramatically increase the cross-sectional area of space for a given amount of blood to “spread out”… thus, velocity of blood decreases… this increases the EXCHANGE TIME
o Hydrostatic pressure = force exerted by a fluid pressing against a wall. In the capillaries, hydrostatic pressure is the same as capillary BP = the pressure of blood against the capillary wall.
o Overall BP in the capillaries is low… capillaries are fragile, and high pressure would rupture them. Also most capillaries are fairly permeable, and even low-capillary pressure forces filtrate out of the blood into the interstitial space.

44
Q

Hydrostatic Pressures:

A
o	BHP (blood hydrostatic pressure): 
o	When blood reaches the FIRST PART (beginning or arteriole end) of the capillary, BP has dropped from 100 mm to 35 mm Hg = BHP (blood hydrostatic pressure).  (The Marieb & Hoehn text refers to this as HPc (hydrostatic pressure of the capillary)  By the time blood reaches the venous end of the capillary, the BHP has dropped even further to 16-17 mm Hg.  
o	IFHP:  (interstitial fluid hydrostatic pressure)
o	The BLOOD HYDROSTATIC PRESSURE is OPPOSED by a hydrostatic pressure that may be present in the interstitial space = IFHP (interstitial fluid hydrostatic pressure).  The Marieb & Hoehn text refers to this as HPif.  There is usually very little fluid in the interstitial spaces because it is constantly being withdrawn by lymphatic vessels.  
o	IN A HEALTHY PERSON, THIS PRESSURE IS ZERO, although it might vary slightly.
45
Q

Colloid Osmotic Pressure:

A
o	COLLOID OSMOTIC PRESSURE is another pressure existing at the capillary level… sometimes called ONCOTIC PRESSURE.  (The Marieb & Hoehn text refers to this as OP.)  This is the pressure created by the presence of large non-diffusing molecules/particles (i.e., that cannot cross the capillary membrane) that draw water toward them… that is, these molecules/particles encourage osmosis (diffusion of water across a semipermeable membrane down its concentration gradient from an area high in water concentration to an area lower in water concentration).
o	BCOP  (BLOOD COLLOID OSMOTIC PRESSURE): The osmotic pressure exerted by the plasma proteins in the blood.  (The Marieb & Hoehn text refers to this as OPc.)  The plasma proteins cannot leave the capillary, so they sit in the capillary and attract water.  Because the plasma proteins don’t leave the capillaries, this osmotic pressure is constant down the entire capillary bed… we will assume that this BCOP is approximately 25 mm Hg.
o	IFOP (INTERSTITIAL FLUID OSMOTIC PRESSURE): the osmotic pressure exerted by proteins (or high concentrations of other solutes) in the interstitial spaces.  (The Marieb & Hoehn text refers to this as Opif).  This is usually quite low… again, because the lymph vessels remove any stray proteins or solutes and eventually return them to the blood.  This pressure has been estimated to be about 0.1 to 5 mm Hg = very, very small, and in a healthy person, fairly insignificant.  In this class, we will just for the sake of calculations pretend that it is 1 mm Hg.
46
Q

Mechanisms of Capillary Exchange:

Filtration

A

o TWO PRESSURES THAT PROMOTE FILTRATION (i.e., stuff LEAVING the capillary):
o 1. BHP (blood hydrostatic pressure) àPUSHING fluid OUT (typically 35 mm Hg at arteriole end)
o 2. IFOP (interstitial fluid osmotic pressure) àPULLING fluid OUT (typically 1 mm Hg)
o TWO PRESSURES that promote REABSORPTION (i.e., stuff coming back into the capillary):
o 1. BCOP (blood colloid osmotic pressure) à PULLING fluid back IN (about 25 mm Hg)
o 2. IFHP (interstitial fluid hydrostatic pressure) à PUSHING fluid back IN (typically zero)

47
Q

Net Filtration Pressure:

A

o NET FILTRATION PRESSURE (NFP): The balance between all these pressures mentioned at a given point along the capillary bed.
o NFP (net filtration pressure) = [BHP + IFOP ] (forces promoting fluids into interstitial fluids) minus [BCOP + IFHP ] (forces promoting fluid into capillaries)
o (Marieb & Hoehn abbreviations): NFP = (HPc + OPif) minus (OPc + HPif)
o ARTERIAL END OF CAPILLARY:
o NFP = [BHP + IFOP] minus [BCOP + IFHP]
o BHP = 35 mm IFOP = 1 mm BCOP = 25 mm IFHP = zero
o So… [35 + 1] minus [25 + 0 ] = 36 minus 25 = +11 mm Hg = NFP
o 11 mm Hg is a positive number, which means there is net FILTRATION into the interstitial spaces AT THE ARTERIAL END OF THE CAPILLARY!!!
o VENOUS END OF THE CAPILLARY:
o BHP = 17 mm; IFOP = 1 mm; BCOP = 25 mm; IFHP = zero
o NFP = [BHP + IFOP] minus [BCOP + IFHP]
o So… [17 + 1] minus [25 + 0] = 18 minus 25 = negative 7 mm Hg
o Negative 7 mm Hg means that more fluid RETURNS to the capillary than is pushed out… REABSORPTION is favored at the VENOUS END OF THE CAPILLARY!!!
o So at the arterial end of a bed, hydrostatic forces dominate. At the venous end, osmotic forces (from blood) dominate.

48
Q

Starling’s Law of Capillaries:

A

o Starling’s Law of the Capillaries: The volume of fluids and solutes reabsorbed is ALMOST as large as the volume that is filtered.
o On average, 85% of the fluid filtered out of capillaries IS reabsorbed…
o About 20 L of fluid/day leave the capillaries
o About 17 L of fluid/day return to the capillaries
o On average, 15% of the fluid is not immediately reabsorbed, but is eventually returned to the blood via lymphatic vessels… about 3 L of fluid/day is “captured” by the lymphatic vessels and eventually returned to the venous system

49
Q

Edema:

A

o EDEMA = abnormal build up of fluid in the interstitial spacesàtissue swelling
o Not usually detectable in tissues until interstitial volume is 30% above normal… can be seen as swelling in the ankles, fingers, abdomen, etc.
o Because excess fluid in the interstitial space increases the DISTANCE nutrients and oxygen must diffuse, edema CAN impair tissue function… but bigger effect on the cardiovascular system…Edema can cause blood volume and BP can drop… efficiency of circulation can be impaired. Edema can also impinge upon local nerves and cause pain.
o Causes of Edema:
o 1) Excess capillary filtration = abnormally increased flow of fluid OUT of the blood:
o a) increased capillary BP if systolic BP is > 175 mm Hg
o 2) inadequate capillary reabsorption = anything that hinders the return of fluid BACK TO the blood, hypoproteinemia = plasma proteins too low in the blood which means decreased BCOP (decrease in blood osmolarity) and results in decreased reabsorption.
o 3) obstructed lymphatic drainage (which means there will be an increased IFOP = increased solutes in the IF (interstitial fluid) which means fluid is pulled out of capillaries.