*** A&p Exam 2: Ch. 21 Blood Vessels

Front 1

Describe arterial blood pressure

Back 1

Determined by 2 factors:

1. Elasticity (compliance/distensibility) of arteries to close to heart.

2. Volume of blood forced into them.

- BP near heart is pulsatile: rises and falls with each heart beat.

- systolic pressure: during ventricular systole. (120mmHg)

- diastolic pressure: during ventricular diastole.

- pulse pressure: (PP) difference between systolic and diastolic pressure. (SP-DP). 120-80 =40.

-pulse: throbbing of arteries due to difference in pulse pressures, can be felt under skin.

- mean arterial pressure: (MAP) pressure that propels blood to tissues. Heart spends more time in diastole so MAP isn't an average of SP and DP.

* Calculated by adding diastolic pressure + 1/3 pulse pressure.

Ex. 120/80, MAP= 80+(1/3)*40 =

80+(~13) = 93mmHg.

Front 2

Describe the clinical monitoring of circulatory efficiency

Back 2

- vital signs: pulse and BP, along with respiratory rate and body temp.

- taking a pulse:

- radial pulse- most routinely used.

- pressure points: areas where arteries are close to body surface.

- blood pressure: systemic arterial BP measured indirectly by auscultatory methods using a (sphygmomanometer)

Front 3

Name the body sites where the pulse is most easily palpated

Back 3

- superficial temporal artery

- facial artery

- common carotid artery

- brachial artery

- radial artery

- femoral artery

- popliteal artery

- posterior tibial artery

- dorsalis pedis artery

Front 4

What are the ranges for capillary blood pressure?

Back 4

Ranges from 35mmHg at beginning of capillary bed to ~17mmHg at the end of bed.

* low capillary pressure is desirable because: high BP would rupture fragile thin walled capillaries and most capillaries are very permeable, so low pressure forces filtrate into interstitial spaces.

Front 5

Explain venous blood pressure

Back 5

Small pressure gradient- about 15mmHg.

When veins are cut, low pressure, blood flows out due to peripheral resistance. When artery is cut, blood spurts because if higher pressure.

- low pressure of venous side requires adaptations to help with venous return.

Front 6

What factors aid in venous return?

Back 6

1. Muscular pump: contraction of skeletal muscles "milks" blood black toward heart. Valves prevent backflow.

2. Respiratory pump: pressure changes during breathing move blood toward heart by squeezing abdominal veins as thoracic veins expand.

3. Sympathetic venoconstriction: under sympathetic control, smooth muscles constrict, pushing blood back toward heart.

Front 7

What are the main factors for regulating blood pressure?

Back 7

1. CO

2. Peripheral resistance (R or PR)

3. Blood volume

- MAP = CO and PR

Recall that CO=SV×HR so if MAP=CO+PR, then MAP=SV×HR×PR.

Anything that increases SV, HR or PR will also increase MAP.

* SV is effected by venous return (EDV)

* HR is maintained by medulla oblongata

* PR is effected mostly by vessel diameter

Front 8

What can SV, HR and PR be effected by?

Back 8

- short-term regulation: NEURAL controls

- short-term regulation: HORMONAL controls

- long-term regulation: RENAL controls

Front 9

Describe short-term regulation: NEURAL controls

Back 9

Vasomotion: quick and powerful way of altering blood pressure and flow (constrict or dilate)

* 2 main neural mech.s control PR:

1. MAP is maintained by altering blood vessel diameter, which alters resistance.

2. Can alter blood distribution to organs in response to specific demands.

* neural controls operate via reflex arcs that involve:

- cardiovascular center of medulla

- baroreceptos

- chemoreceptors

- higher brain centers

Front 10

Describe whats involved in the 4 reflex arcs of neural controls

Back 10

reflex arcs involve: - cardiovascular center of medulla - baroreceptos- chemoreceptors- higher brain centers * cardiovascular center: medulla oblongata: cardioinhibitory and cardioacceleratory centers. Vasomotor center: sends steady impulses via sympathetic efferents called vasomotor fibers to blood vessels. Cause continuous moderate constriction called vasomotor tone. - receives inputs from baroreceptors, chemoreceptors, and higher brain centers.

* baroreceptor reflexes (baroreflex): located in walls of large arteries of neck and thorax, signals sent to brainstem by way of:

Glossopharyngeal nerve (XII).

If MAP is low, reflex vasoconstriction is initiated that increases CO and BP.

Ex. When person stands, BP falls and triggers: carotid sinus reflex and aortic reflex.

Baroreceptors are not triggered by elevated BP levels if BP is sustained.

If MAP is high, increased BP stimulates baroreceptors to increase input to vasomotor center. Inhibits vasomotor and cardioacceleratory center. Results in decreased BP by 2 mechanisms:

1. Vasodilation: arteriolar vasodilation and vasodilation.

2. Decreased CO.

* chemoreceptor reflexes (chemoreflex): AORTIC BODIES: aortic arch and large arteries of deck detect increase in CO2 or drop ok pH or O2.

Primary role: adjust respiration to changes in blood chemistry.

Secondary role: vasomotion

* higher brain centers (medullary ischemic reflex): reflexes that regulate BP are found in medulla. Medulla monitors its own blood supply: activates corrective reflexes, when it senses ischemia (insufficient perfusion). *hypothalamus mediates redistribution of blood flow during exercise and changes in body temp.

Front 11

Describe the short-term regulation: HORMONAL controls, in regards to regulation of blood pressure.

Back 11

Hormones regulate BP in short term via changes in PR or long term via changes in BV.

* adrenal medulla hormones:

- epinephrine and NE increase CO and vasoconstriction

- most blood vessels bind to a(alpha)-adrenergic receptors = vasoconstriction

- skeletal and cardiac muscle blood vessels binds to b(beta)-adrenergic receptors = vasodilation

1. aldosterone: promotes Na+ and water retention by kidneys = increased BP and BV.

2. angiotensin II stimulates vasoconstriction = increased BP.

3. ADH (vasopressin) antidiuretic hormone, promotes water retention = increased BP.

4. atrial natriuretic peptide (ANP) increases urinary sodium excretion, reduces BV and promotes vasodilation = decreased BP by antagonizing aldosterone. Only one to decrease BP between the 4.

Front 12

Describe the long-term regulation: RENAL controls, in regards to regulation of blood pressure.

Back 12

Baroreceptors quickly adapt to chronic high or low BP so are ineffective for long term regulation. Long term mechanisms control BP by altering BV via kidneys, which regulate arterial BP by:

1. DIRECT RENAL MECHANISM (urine elimination or retention). High BP, elimination, low BP, retention. Alters BV independently of hormones.

2. INDIRECT RENAL MECHANISM (renin-angiotensin-aldosterone). Decreased arterial BP causes release of remin from kidneys, which enters blood and catalyzes conversion of angiotensinogen from liver to angiotensin I. Angiotensin-converting enzyme, especially from lungs, converts angiotensin I to angiotensin II which acts in 4 ways to stabilize arterial BP and ECF:

1. Stimulates aldosterone secretion

2. Causes ADH release from posterior pituitary

3. Triggers hypothalamic thirst center to drink more water

4. Acts as a potent vasoconstrictor, directl increasing BP.

Front 13

What is the goal of blood pressure regulation?

Back 13

To keep BP high enough to provide adequate tissue perfusion, but not so high that blood vessels are damaged.

Front 14

Name an example of what could occur if BP is too low, and too high

Back 14

- too low: loss of consciousness

- too high: stroke

Front 15

When can transient elevations in BP occur?

Back 15

Changes in posture, physical exertion, emotional upset, fever, arousal

Front 16

Define tissue perfusion and list the factors that control the rate

Back 16

Tissue perfusion: blood flow through body tissues at precisely right amount to provide function; involved in:

1. Delivery of O2 and nutrients, removal of wastes from tissue cells.

2. Gas exchange (lungs)

3. Absorption of nutrients (digestive tract)

4. Urine formation (kidneys)

Rate is controlled by:

Extrinsic control: (sympathetic nervous system and hormones) control BF through whole body.

Intrinsic control: autoregulation (local) control of BF: BF is adjusted locally to meet specific tissues requirements. AUTOREGULATION: local (intrinsic) conditions that regulate BF to that area. - REACTIVE HYPEREMIA: increased BF to area due to intrinsic factors.

- 2 types of intrinsic mechanisms both determine final autoregulatory response.

1. Metabolic controls: increase in tissue metabolic activites results in: declining o2, increasing level of metabolic products (H+, K+, adenosine).

Effects of change in levels of local chemicals: cause direct relaxation of aterioles and relaxation of precapillary sphincters. Cause relase of nitric oxide (NO) - powerful vasodilator by endothelial cells. Endothelins also released from endothelium l, potent vasoconstrictors. Inflammation chemicals can also cause vasodilation.

2. Myogenic controls: myogenic responses: local vascular smooth muscle responds to changes in MAP to keep perfusion constant to avoid damage to tissue.

PASSIVE STRETCH: increased MAP stretches vessel wall more than normal, smooth muscle responds by constricting, causing decreased BF to tissue.

*long-term autoregulation: when short-term autoregulation cant meet tissue nutritn requirements. Number of vessels to region increases (angiogenesis) and existing vessels enlarge. Common in heart when coronary vessel occluded, or throughout body in people in high altitude areas.

REDUCED STRETCH: decreased MAP causes less stretch than normal, smooth muscle responds by dilating, causing increased BF to tissue.

Front 17

Explain exercise in regards to redistribution of blood (intrinsic and extrinsic controls)

Back 17

* at rest, skeletal muscles recieved about 20% of total blood in body, but during exercise, skeletal muscle can receive over 70% of blood.

* intrinsic controls: skeletal muscle arterioles dilate, increasing blood flow to muscle.

* extrinsic controls: decrease BF to other organs such as kidneys and digestive organs.

* (MAP is maintained despite dilation of skeletal muscle aterioles)

Front 18

Describe the blood flow in skeletal muscles

Back 18

Blood flow varies with fiber type and activity. At rest, myogenic and neural mechanisms predominate; maintain flow at ~1L/min.

Active/exercise hyperemia: is increased BF to a muscle during activity.

Initial stimulus: Exercising skeletal muscle which leads to;

Physiological response: change in metabolic activity (O2, CO2, H+) in extracellular fluid. This then leads to

Result of: vasodilation of aterioles (overrides extrinsic sympathetic input); and muscle BF increases, up to 10x.

Front 19

Describe the blood flow in the brain

Back 19

- BF to the brain must be constant because neurons are intolerant of ischemia. Flow averages: ~750ml/min.

- control mechanisms:

METABOLIC CONTROLS: decreased pH or increased CO2 cause vasodilation. <60mmHg causes syncope (fainting).

MYOGENIC CONTROLS: decreased MAP causes cerebral vessels to dilate and increased MAP causes them to constrict. >160mmHg can result in cerebral edema.

Front 20

Describe the blood flow in skin

Back 20

Functions:

1. Supplies nutrients to cells: autoregulated in response to O2 needs.

2. Helps regulate body temp: nuerally controlled, big function. Regulated by BF through venous plexuses below skin surface, controlled by sympathetic nervous system reflexes- initiated by thermoreceptors and CNS. As temp. increases, hypothalamic signals reduce vasomotor stimulation of skin vessels, causing dilation, heat radiates from skin. As temp. decreases, blood is shunted to deeper, more vital organs. Superficial skin vessels constrict strongly, may cause rosy cheeks.

3. Provides a blood reservoir: neurally controlled.

Front 21

Describe blood flow in the lungs

Back 21

Pathway is short. Arterial resistance and pressure in pulmonary circuit is much lower than in systemic circuit. Averages: ~24/10mmHg versus 120/80.

Autoregulatory mechanisms are opposite: low O2 levels cause vasoconstriction and high levels promote vasodilation. Allows BF to O2 rich areas of the lung.

Front 22

Describe the blood flow in the heart

Back 22

Influenced by aortic pressures and ventricular pumping.

- During ventricular systole, coronary vessels are compressed, causing myocardial BF to cease and stored myoglobin supplies sufficient O2.

- During diastole, high aortic pressure forces blood through coronary circulation.

- at rest, coronary BF is ~250ml/min.

- increasing coronary BF is only way to provide more O2 and is important because cardiac cells use 65% of O2 delivered.

Front 23

How do capillary beds work?

Back 23

Diffusion principles: absorption and filtration.

Velocity of BF: changes as blood travels through systemic circulation. Fastest in aorta, slowest in capillaries, then increases again in veins. Speed is inversely related to total cross-sectional area. Capillaries have largest area so slowest flow which allows adequate time for exchange between blood and tissues (exchange of respiratory gases and nutrients):

Vasomotion: intermittent flow of blood through capillaries, due to opening/closing of precapillary sphincters.

- many molecules pass by diffusion between blood and interstitial fluid down their concentration gradients: O2 and nutrients from blood tissues and CO2 and metabolic waters from tissues to blood.

- molecules use 4 different routes to cross capillary:

1. Diffuse directly through endothelial membranes. Ex. Lipid-soluble molecules such as respiratory gases.

2. Pass through clefts. Ex. Water-soluble solutes.

3. Pass through fenestrations. Ex. Water-soluble solutes.

4. Active transport via pinocytotic vesicles or caveolae. Ex. Larger molecules, such as proteins.

Front 24

Capillary transport mechanisms

Back 24

Front 25

Describe the bulk flow of fluid movements

Back 25

Fluid is forced out clefts of capillaries at arterial end and most returns to blood at venous end. Extremely important in determining relative fluid volumes in blood and interstitial space. Bulk fluid flows across capillary walls causing continuous mixing of fluid between plasma and interstitial fluid: maintains interstitial environment.

Direction and amount of fluid flow depends on 2 OPPOSING FORCES:

1. hydrostatic pressures (HP): force exerted by fluid pressing against wall; 2 types.

1a. capillary hydrostatic pressure (HPC): capillary blood pressure that tends to force fluids through capillary walls. Greater at arterial end (35mmHg) of bed than at venule end (17mmHg).

1b. Interstitial fluid hydrostatic pressure (HPIF): pressure pushing fluid back into vessel; usually assumed to be zero because lymphatic vessels drain interstitial fluid.

2. colloid osmotic pressures:

- capillary colloid osmotic pressure (oncotic pressure- OPC): "sucking" pressure ceated by nondifuusible plasma proteins pulling water back into capillary, draw water toward themselves. OPC~26mmHg.

- interstitial fluid colloid osmotic pressure (OPIF): pressure is inconsequential because interstitial fluid has very low protein content. OPIF around only 1mmHg.

Front 26

Describe the hydrostatic-osmotic pressure interactions

Back 26

Net filtration pressure (NFP): comprises all forces acting on capillary bed. Determines the direction of fluid movement.

NFP = (HPC + OPIF) - (HPIF + OPC)

NFP = (HPC - HPIF) + (OPIF - OPC)

- net fluid out of arterial end (filtration)

- net fluid in at venous end (reabsorption)

- more fluid leaves at arterial end than is returned at venous end. Excess interstitial fluid is returned to blood via lymphatic system.

Front 27

Net filtration pressure (NFP) determines the direction of fluid movement. What 2 kinds of pressure drive fluid flow?

Back 27

Hydrostatic pressure (HP): due to fluid pressing against a boundary (capillary wall). HP "pushes" fluid across the boundary. In blood vessels, is due to BP.

Osmotic pressure (OP): due to nondiffusible solutes that cannot cross the boundary. OP "pulls" fluid across the boundary. In blood vessels, is due to plasma proteins.

Front 28

How do the pressures drive fluid flow across a capillary?

Back 28

Net filtration occurs at the arteriolar end of a capillary.

To determine the pressure driving the fluid out of the capillary at any given point, we calculate the NFP- outward pressures (HPC and OPIF) minus the inward pressures (HPIF and OPC).

So...

NFP = (HPC + OPIF) - (HPIF + OPC) =

(35+1) - (0+26) = 10mmHg (net outward pressure)

- as a result, fluid moves from the capillary into the interstitial fluid.

Front 29

How do the pressures drive fluid flow back in venules at the venous end?

Back 29

Net absorption occurs at the venous end of capillary.

Again, we calculate the NFP:

NFP = (HPC + OPIF) - (HPIF + OPC) =

(17+1) - (0+26) = -8mmHg (net inward pressure)

- notice that the NFP at the venous end is a negative number. This means that reabsorption, not filtration, is occurring and so fluid moves from the interstitial space into the capillary.

Front 30

What is edema?

Back 30

Accumulation of excess fluid in a tissue (abnormal increase in amount of interstitial fluid). Occurs when fluid filters into as tissue faster than it is absorbed. 3 primary causes:

Caused by either an increase in outward pressure (driving fluid out of capillaries) or a decrease in inward pressure.

1. Increased capillary filtration. Kidney failure, histamine release, old age, poor venous return.

2. Reduced capillary absorption. Hypoproteinemia, liver disease, dietary protein deficiency.

3. Obstructed lympathic drainage. Surgical removal of lymph nodes.

Consequences:

- tissue necrosis (O2 delivery and waste removal impaired).

- pulmonary edema (suffocation threat).

- cerebral edema (headaches, nausea, seizures and coma).

- severe edema or circulatory shock (excess fluid in tissue spaces causes low BV and low BP).

- an INCREASE IN CAPILLARY HYDROSTATIC PRESSURE accelerates fluid loss from blood (increased capillary filtration). incompetent valves, localized blood vessel blockage, CHF or high BV.

- an INCREASE IN INTERSTITIAL FLUID OSMOTIC PRESSURE can result from an inflammatory response. Increases capillary permeability and allows proteins to leak into interstitial fluid. Causes large amounts of fluid to be pulled into interstitial fluid.

- a DECREASE IN CAPILLARY COLLOID OSMOTIC PRESSURE hinders fluid return to blood (reduced capillary absorption). Can be caused by hypoproteinemia, low levels of plasma proteins caused by malnutrition, liver disease, or glomerulonephritis (loss of plasma proteins from kidneys).

- EXCESS OF INTERSTITIAL FLUID in subcutaneous tissues generally causes pitting edema.

Front 31

What is hypertension?

Back 31

Sustained elevated arterial pressure of 140/90mmHg or higher.

Prehypertension is values are elevated but not yet in hypertension range.

Prolonged hypertension major cause of heart failure, vascular disease, renal failure and stroke.

Primary hypertension: 90% of hypertensive conditions. No underlying cause identified.

Secondary hypertension: less common, due to identifiable disorders including obstructed renal arteries, kidney disease, and endocrine disorders such as hyperthyroidism and Cushing's syndrome.

Front 32

What is hypotension?

Back 32

Low BP below 90/60mmHg.

Orthostatic hypotension: temporary low BP and dizziness when suddenly rising from sitting or reclining position.

Chronic hypotension: hint of poor nutrition and warning sign for addison's disease or hypothyroidism.

Acute hypotension: important sign of circulatory shock.

Circulatory shock: (abnormal perfusion) blood vessels inadequately fill and cannot circulate blood normally, cant neet tissue needs.

- hypovolemic shock: results from large scale blood loss.

- vascular shock: results from extreme vasodilation and decreased peripheral resistance.

- cardiogenic shock: results when an inefficient heart cannot sustain adequate circulation.

- neurogenic shock: loss of vasomotor tome, vasodilation. Causes from emotional shock or brainstem injury.

- septic shock: bacterial toxins trigger vasodilation and increased capillary permeability.

- anaphylactic shock: severe immune reaction to antigen, histamine release, generalized vasodilation, increased capillary permeability.