chapters 9-11 Flashcards

1
Q

right side of the heart

A

receives blood from the peripheral organs and pumps it through the lungs

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2
Q

left side of the heart

A

receives oxygenated blood from the lungs and pumps it back to the peripheral organs

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3
Q

atria

A

primer pumps that fill the ventricles with blood

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4
Q

ventricles

A

contract and impart high blood pressure to the blood which is responsible for propelling the blood through the circulatory system.

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5
Q

Heart conduction

A

the heart has its own special conduction system that maintains its own rhythmicity and transmits action potentials throughout the heart.

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6
Q

Similarities between cardiac and skeletal muscle

A
  • both are striated
  • both have actin and myosin filaments that interdigitate and slide along each other during contraction
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7
Q

Unique characteristics of cardiac muscle

A
  • has intercalated discs between cardiac muscle cells (these discs have very low electrical resistance allowing an action potential to travel freely between cardiac muscle cells)
  • the cardiac muscle is a syncytium of many heart muscle cells in which the action potntial spreads rapidly from cell to cell
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8
Q

role of the A-V bundle

A

slowly conducts impulses from the atria to the ventricles

  • this is an exclusive pathway because the atrial synctium and ventricular synctium are normally insulated from one another by fibrous tissue.
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9
Q

resting membrane potential of cardiac muscle

A

-85 to -95 millivolts

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10
Q

Action potential of cardiac muscle

A

105 millivolts

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11
Q

for how long does the membrane remain depolarized in the atria?

A

0.2 seconds

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12
Q

for how long does the membrane remain depolarized in the ventricles?

A

0.3 seconds

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13
Q

what causes an action potential in SKELETAL muscle?

A

entry of sodium through fast sodium channels which remain open for only a few 10,00ths of a second

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14
Q

what causes an action potential in CARDIAC muscle?

A

cardiac muscle also has fast sodium channels that open at the initiation of an action potential, but

cardiac muscle also has unique slow CALCIUM channels, or calcium-sodium channels

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15
Q

how do the slow calcium-sodium channels work?

A

calcium and sodium ions flow through the slow channels into the cell after the initial spike of the action potential, and they maintain the plateau.

Calcium that enters the cell through these channels also promotes cardiac muscle contraction

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16
Q

What else contributes to the plateau of the action potential in cardiac muscle? (prevents return of the membrane potential)

A

a decrease in the permeability of cardiac muscle cells to potassium ions

when the slow calcium-sodium channels close after 0.2 - 0.3 seconds, the potassium permeability increases rapidly and thus returns the membrane potential to its resting level.

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17
Q

what promotes cardiac muscle contraction?

A

diffusion of calcium into the myofibrils

the action potential spreads into each cardiac muscle fiber along the transverse (T) tubules, causing the longitudinal sarcoplasmic tubules to release calcium ions into the sarcoplasmic reticulum.

these calcium ions catylyze the chemical reactions that promote the sliding of the actin and myosin filaments along one another to cause muscle contraction.

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18
Q

What is an additional means of entry of calcium into the sarcoplasm that is unique to cardiac muscle?

A

the T tubules of cardiac muscles have 25x as great a volume as those in skeletal muscle

these t tubules contain large amounts of calcium that are released during the action potential.

the t tubules open directly into the extracellular fluid in cardiac muscle - so their calcium content is ver dependent upon extracellular calcium concentration

at the end of the plateau of the action potential, the influx of calcuim ions into the muscle fiber abruptly stops, and calcium is pumped back into the sarcoplasmic reticulum and T tubules, ending the contraction

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19
Q

cardiac cycle

A

the events that occur at the beginning of a heartbeat and last until the beginning of the next heartbeat are called the cardiac cycle.

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20
Q

how does each heart beat begin?

A

with a spontaneous action potential that is initiated in the sinus node of the right atrium near the opening of the superior vena cava

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21
Q

what happens after the action potential is initiated in the sinus node of the right atrium?

A

the action potential travels through both atria and the A-V node and bundle into the ventricles

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22
Q

what is the delay between atrial and ventricular contraction?

A

a delay of more than 1/10 of a second occurs in the A-V node and bundle, which allows the atria to contract before the ventricles contract.

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23
Q

when do the ventricles fill with blood?

A

during diastole

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24
Q

when do the ventricles contract?

A

during systole

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25
Q

electrocardiogram

A

a recording of the voltage generated by the heart from the surface of the body during each heartbeat

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26
Q

P wave

A

caused by spread of depolarization across the atria, which causes atrial contraction

atrial pressure increases just after the P wave.

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27
Q

QRS waves

A

appear as a result of ventricular depolarization

0.16 second after the onset of the P wave

this initiates ventricular contraction

ventricular pressure increases as a result

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28
Q

T wave

A

caused by repolarization of the Ventricle

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29
Q

what occurs during diastole before contraction of the atria?

A

about 75% of ventricular filling

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30
Q

when does the other 25% of ventricular filling occur?

A

during contraction of the atria

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31
Q

Atrial pressure wave (a wave)

A

caused by atrial contraction

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32
Q

atrial pressure wave (c wave)

A

occurs during ventricular contraction because of slight backflow and bulging of the A-V valves toward the atria.

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33
Q

atrial pressure wave (v wave)

A

caused by in-filling of the atria from venous return

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34
Q

What events occur just before and during diastole?

A
  • during systole, the A-V valves are closed, and the atria fill with blood
  • begining of diastole - isovolumic relaxation caused by ventricular relaxation; when ventricular pressure decreases below that of the atria, the A-V valves open.
  • the higher pressure in the atria pushes blood into the ventricles during diastole
  • the period of rapid filling of the ventricles occurs during the first 1/3 of diastole (this provides most of the ventricular filling)
  • atrial contraction occurs during the last 1/3 of diastole and contributes about 25% of the filling of the ventricle (aka “atrial kick”)
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35
Q

What events occur during systole?

A
  • at the begining of systole, ventricular contraction occurs, the A-V valves close, and pressure begins to build up in the ventricle. NO outflow of blood occurs during the first 0.2-0.3 seconds of ventricular contraction (period of isovolumic “same volume” (in the ventricles) contraction).
  • when the left ventricular pressure exceeds the aortic pressure of about 80mm Hg and the right ventricular pressure exceeds the pulmonary artery pressure of 8mm Hg, the aortic and pulmonary valves open. Ventricular outflow occurs (“period of ejection”)
  • most ejection occurs during the 1st part of this period (period of rapid ejection)
  • this is followed by the period of slow ejection. during this period, aortic pressure may slightly exceed the ventricular pressure because the kinetic energy of the blood leaving the ventricle is converted to the pressure in the aorta, which slightly increases its pressure.
  • during the last period of systole the ventricular pressures fall below the aortic and pulmonary artery pressures. The aortic and pulmonary valves close at this time.
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36
Q

Ejection Fraction

A

the fraction of the end-diastolic volume that is ejected.

  • calculated by dividing the stroke volume by the end-diastolic volume
  • has a value of about 60%
  • the stroke volume of the heart can be doubled by increasing the end diastolic volume and decreasing the end-systolic volume.
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37
Q

end-diastolic volume

A

at the end of diastole, the volume of each ventricle is 110 - 120 mL

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38
Q

stroke volume

A

the amount of blood ejected with each beat (about 70mL)

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39
Q

end-systolic volume

A

the remaining volume in the ventricle at the end of systole (measures about 40-50 mL)

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40
Q

effect of ventricular ejection on the aorta

A

ventricular ejection increases pressure in the aorta to 120mm Hg (systolic pressure)

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41
Q

what happens when the ventricular pressure exceeds the diastolic pressure in the aorta?

A

the aortic valve opens and blood is ejected into the aorta.

Pressure in the aorta increases to about 120 mm Hg and distends the elastic aorta and other arteries.

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42
Q

what happens when the aortic valve closes at the end of ventricular ejection?

A

there is a slight backflow of blood followed by a sudden cessation of flow, which causes an incisurs, or a slight increase in aortic pressure.

During diastole, blood continues to flow into the peripheral circulation, and the arterial pressure dectreases to 80 mm Hg (diastolic pressure)

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43
Q

A-V valves (ticusped (right) and mitral (left) valves)

A

prevent backflow of blood from the ventricles to the atria during systole.

  • have papillary muscles attached to them by the chordae tendineae
  • during systole, the papillary muscles contract to help prevent the valves from bulging back too far into the atria
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44
Q

Semilunar valves (aortic and pulmonary valves)

A

prevent backflow of blood from the aorta and pulmonary artery into the ventricles during diastole

  • these valves are thicker than the A-V valves and do not have any papillary muscles attached.
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45
Q

stroke work output of the ventricles

A

the output of energy by the heart during each heart beat

(the heart performs 2 types of work)

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46
Q

volume-pressure work of the heart

A

the work done to increase the pressure of the blood;

in the left heart, it equals stroke volume multiplied by the difference between the left ventricular mean ejection pressure and the left ventricular mean input pressure

the volume pressure work of the right ventricle is onlt about 1/6 that of the left ventricle because the ejection pressure of the right ventricle is much lower.

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47
Q

work to be done to supply kinetic energy to the blood

A

= MV 2/2

M = the mass of blood ejected

V = Velocity

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48
Q

what % of the work of the heart creates kinetic energy?

A

usualy only about 1%

upto 50% if there is severe aortic stenosis

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49
Q

Phases of the Cardiac Cycle (Phase I)

A

period of filling during which the left ventricular volume increases from the end-systolic volume to the end-diastolic volume, or from 45 mL to 115 mL (a 70 mL increase)

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50
Q

Phases of the Cardiac Cycle (Phase II)

A

Period of isovolumic contraction during which the volume of the ventricle remains at the end-diastolic volume but the intraventricular pressure increases to the level of the aortic diastolic pressure, or 80mm Hg

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51
Q

Phases of the Cardiac Cycle (Phase III)

A

Period of ejection during which the systolic pressure increases further because of additional ventricular contraction, and the ventricular volume decreases by 70 mL (which is the stroke volume)

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52
Q

Phases of the Cardiac Cycle (Phase IV)

A

period of isovolumic relaxation during which the ventricular volume remains at 45 mL, but the intraventricular pressure decreases to its diastolic pressure level

Preload - end-diastolic pressure

Afterload - the pressure in the artery exiting the ventricle (aorta or pulmonary artery)

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53
Q

what determines oxygen consumption by the heart?

A

cardiac work

mainly the volume-pressure type of work

this oxygen consumption has also been found to be proportional to the tension of the heart multiplied by the time the tension is maintained

wall tension in the heart is proportional to the pressure times the diameter of the ventricle. Ventricular wall tension increases at high systolic pressures or when the heart is dilated

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54
Q

what intrinsically regulates cardiac pumping ability?

A

the Frank-Starling Mechanism

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55
Q

Frank-Starling Mechanism of the heart

A

within physiological limits, the heart pumps all the blood that comes to it without allowing excess accumulation of blood in the veins.

  • alternate wording- when venous return of blood increases, the heart muscle stretches more, which makes it pump with a greater force of contraction.

the extra stretch of the cardiac muscle during increased venous return, within limits, causes the actin and myosin filaments to interdigitate at a more optimal length for force generation

more stretch of the right atrial wall causes a reflex increase in the heart rate of 10% - 20% which helps the heart pump more blood

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56
Q

what happens to the heart when there is strong sympathetic stimulation?

A

the heart rate of an adult increases from a resting value of 72 beats per minute up to 180 - 200 beats per minute, and the force of the contractions of the heart increase dramatically

sympathetic stimulation therefore can increase cardiac output 2-3 fold

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57
Q

what happens to the heart when the sympathetic system is inhibited?

A

heart rate decreases and the force of contraction of the heart and cardiac output decreases

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58
Q

how does parasympathetic stimulation affect the heart?

A

it mainly affects the atria and can decrease the heart rate dramatically and the force of contraction of the ventricles slightly. The combined effect decreases cardiac output by 50% or more

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59
Q

what factors affect cardiac contractility?

A
  • extracellular electrolyte concentrations - excess potassium in extracellular fluid causes the heart to become flaccid and reduces the heart rate, causing a large decrease in contractillity; excess calcium in the extracellular fluid causes the heart to go into spastic contraction; a decrease in calcium ions causes the heart to become flaccid
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60
Q

Heart and its rhythmical impulses

A

the heart has a special system for self-excitation of rhythmical impulses to cause repetitive contraction of the heart

this system conducts impulses through the heart and causes the atria to contract 1/6 of a second before the ventricles (allows extra filling of the ventricles before contraction)

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61
Q

Sinoatrial Node (Sinus Node)

A

initiates the cardiac impulse and controls the rate of beat of the entire heart

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62
Q

internodal pathway

A

conducts impulses from the sinus node to the atrioventricular node

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63
Q

A-V Node

A

delays impulses from the atria to the ventricles

  • this allows the atria to empty their contents into the ventricles before ventricular contraction occurs
  • a delay of .09 second occurs between the A-V node and the A-V bundle (slow velocity 1/12 that of normal cardiac muscle
  • b/c 1) membrane potential is much less negative in the A-V node and bundle than in normal cardiac muscle and 2) few gap junctions exist between the cells in the A-V node and bundle, so the resistance to ion flow is great
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64
Q

A-V Bundle (bundle)

A

delays impulses and conducts impulses from the A-V node to the ventricles

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65
Q

Bundles of Purkinje Fibers (right and left)

A

conduct impulses to all parts of the ventricles

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66
Q

Sinus Node membrane potential

A

the membrane potential of a sinus node fiver is -55 to -60 millivolts compared with -85 to -90 millivolts in a ventricular muscle fiber

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67
Q

Action Potential in the Sinus Node

A
  • fast sodium channels are inactivated at the normal resting membrane potential, but there is slow leakage of sodium into the fiber
  • between action potentials the resting potential gradually increases because of this slow leakage of sodium until the potential reaches -40 milivolts
  • then the calcium-sodium channels become activated, allowing rapid entry of calcium and sodium, but especially calcium (causes an action potential)
  • greatly increased #s of potassium channels open within about 100-150 milliseconds after the calcium-sodium channels open, allowing potassium to escape from the cells. This returns the membrane potential to its resting potential, and the self-excitation cycle starts again (with sodium leaking slowly into the sinus nodal fibers)
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68
Q

what transmits pathways in the atrium?

A

internodal and interatrial pathways

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69
Q

Parts of the internodal pathway

A
  • anterior internodal pathway
  • middle internodal pathway,
  • and posterior internodal pathway
  • all carry impulses from the sinoatrial node to the A-V node.
  • Small bundles of atrial muscle fibers transmit impulses more rapidly than the normal atrial muscle
  • anterior interatrial band - conducts impulses from the right atrium to the anterior part of the left atrium
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70
Q

Rapid transmission of impulses throught the Purkinje System and Cardiac Muscle

A

the purkinje fibers lead from the A-V node, through the A-V bundle, and into the ventricles

  • the A-V bundle lies just under the endocardium and receives the cardiac impulse first.

the A-V bundle then divides into the left and right bundles

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71
Q

Charachteristics of the purkinje system

A
  • action potentials at 6 times the velocity found in cardiac muscle
  • high permeability of gap junctions at the intercalated discs between the purkinje fiber cells likely causes the high velocity of transmission
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72
Q

Atrial and Ventricular Syncytia (separate and insulated from one another)

A

the atria and ventricles are separated by a fibrous barrier that acts as an insulator, forcing the atrial impulses to enter the ventricles through the A-V bundle.

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73
Q

spread of action potential to ventricular muscle

A

purkinje fiber lie just under the endocardiun, so the action potential spreads into the rest of the ventricular muscle from this area.

thente cardiac impulses travel up the spirals of the cardiac muscle and finally reach the epicardial surface

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74
Q

why is the sinus node the pacemaker?

A

it discharges faster than the other tissues in the cardiac conduction system

when the sinus node discharges, it sends impulses to the A-V node and Purkinje fibers and thereby discharges them before they can discharge intrinsically

the tissues and sinus node thenrepolarize at the same time, but the sinus node looses its hyperpolarization faster and discharges again before the A-V node and Purkinje fibers can indergo self-excitation

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75
Q

ectopic pacemaker

A

when some cardiac tissue develops a rhythmical rate faster than that of the sinus node

most common location of the new pace maker is the A-V node or penetrating portion of the A-V bundle

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76
Q

A-V Block (stokes-adams syndrome)

A

during A-V block, the atria beat normally, but the ventricular pacemaker lies in the purkinje system, which normally discharges at a rate of 15 to 40 beats per minute. After a sudden block, the Purkinje system doesn’t emit its rhythmical impulses for 5-30 seconds because it has been overdriven by the sinus rhythem.

during this time, the ventricles fail to contract, and the person may faint due to lack of cerebral blood flow

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77
Q

Stimulation of the parasympathetic (vagal) nerves to the heart releases what neurotransmitter?

A

acetylcholine

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78
Q

What are the effects of Acetylcholine?

A
  • the rate of sinus node discharge decreases
  • the excitability of the fibers between the atrial muscle and the A-V node decreases
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79
Q

Vagal Stimulation and Heart Rate

A

the heart rate decreases to 1/2 normal under mild or moderate vagal stimulation, but

  • strong stimulation can temporarily stop the heart beat, resulting in a lack of impulses traversing the ventricles.
  • under these conditions, the Purkinje fibers develop their own rhythem at 15-40 beats per minute (ventricular escape)
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80
Q

what are the mechanisms of vagal effects on the heart?

A
  • Acetylcholine increases the permeability of the sinus node and A-V junctional fibers to potassium, which causes hyperpolarization of these tissues and makes them less excitable
  • the membrane potential of the sinus nodal fibers decreases from -55 to -60 millivolts to -65 to -75 millivolts

the normal upward drift in membrane potential that is caused by sodium leakage in these tissues requires a much longer time to reach the threshold for self-excitation.

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81
Q

what are the effects of stimulation of the sympathetic nerves to the heart ?

A
  • rate of sinus node discharge increases
  • cardiac impulse conduction rate increases in all parts of the heart
  • force of contraction increaeses in both atrial and ventricular muscle
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82
Q

what is released during sympathetic stimulation?

A

norepinephrine

83
Q

where is norepinephrine released?

A

at the sympathetic nerve endings

84
Q

effects of norepinephrine on the heart (we think)

A
  • increases the permeability of cardiac muscle fibers to sodium and calcium, which increases the resting membrane potential and makes the heart more excitable, increasing heart rate
  • the greater calcium permeability increases the force of contraction of cardiac muscle
85
Q

electrocardiogram

A

rocording of the small part of the depolarization wave that reaches the surface of the body after passing through the heart ad the surrounding tissue.

86
Q

P wave

A

caused by electrical potential generated from depolarization of the atria before contraction

87
Q

QRS complex

A

electrical potential generated from the ventricles before their contraction

88
Q

T wave

A

potential generated from repolarization of the ventricles

89
Q

relationship between ekg and atrial and ventricular contractions

A
  • P wave immediately preceeds atrial contraction
  • QRS complex immediately precedes ventricular contraction
  • ventricles remain contracted until a few milliseconds after the end of the T repolarization wave
  • Atria remain contrated until they are repolarized, but an atrial repolarization wave cannot be seen on the ekg because it is obscured by the QRS wave
  • the P-Q or P-R interval on the EKG has a normal value of 0.16 second and is the duration of time between the 1st deflectionof the P wave and the begining of the QRS wave; this represents the time between the begining of atrial contraction and the beginning of ventricular contraction.
  • the Q-T interval has a normal value of 0.35 second, which is the duration of time from the begining of the Q wave to the end of the T wave. This approximates the time of ventricular contraction
  • HR can be determined with the reciprocal of the time interval between each heartbeat
90
Q

What is the direction of flow of the electrical current during the depolarization process

A

the average electrical current flows from the base of the heart toward the apex

the heart is suspended in a highly conductive medium, so when one area of the heart depolarizes current flows from this area toward a polarized area

91
Q

what is the order of depolarization?

A
  • the 1st area that depolarizes is the ventricular septum, and current flows quickly from this area to the other endocardial surfaces of the ventricle
  • then current flows from the electronegative inner surfaces of the heart to the electropositive outer surfaces, with the average current flowing from the vase of the heart to the apex in an elliptical pattern. An electrode placed near the base of the heart is electronegative, and one placed near the apex is electropositive.
92
Q

Bipolar limb leads

A
  • involve anelectrocardiogram recorded from electrodes on 2 different limbs
  • there are 3 bipolar limb leads
93
Q

Lead I

A
  • the negative terminal of the ekg is connected to the right arm, and the positive terminal is connected to the left arm.
  • during the depolarization cycle, the point at which the right arm connects to the chest is electronegative compared with the point at which the left arm connects, so the ekg records positively when this lead is used
94
Q

Lead II

A
  • the negative terminal of the ekg is connected to the right arm, and the positive terminal is connected to the left leg.
  • during most of the polarization cycle, the left leg is electropositive compared with the right arm, so the ekg records positively when this lead is used.
95
Q

Lead III

A
  • the negative terminal is connected to the left arm, and the positive terminal is connected to the left leg.
  • during most of the depolarization cycle, the left leg is electropositive compared with the left arm, so the ekg records positively when this lead is used.
96
Q

Einthoven’s Law

A

the electrical potential of any limb lead equals the sum of the potentials of the other two limb leads

  • the + and - signs of the various leads must be observed whenusing this law

Known:

  • right arm: -0.2mv
  • left arm: +0.3mv
  • left leg: +1.0mv

Therefore:

  • lead I potential: 0.5mv
  • lead II potential: 1.2mv
  • lead III potential: 0.7mv
97
Q

Chest (precordial) Leads

A
  • can be used to detect minor electrical abnormalities in the ventricles
  • V1, V2, V3, V4, V5, V6
  • connected to the positive terminal of the electrocardiograph, and the indifferent electrode, or the negative electrode, is simultaneously connected to the left arm, left leg, and right arm.
  • the QRS recordings from the V1 and V2 lead, which are placed over the heart near the base, usually read negatively, and the QRS recording from leads V4, V5, and V6 which are closer to the apex, usually read positively.
  • Because these leads can record the electrical potential immediately underneath the electrode, small changes in electrical potential of the cardiac musculature can be detected, such as that generated by a small myocardial infarction
98
Q

Augmented Unipolar leads

A
  • 2 of the limbs are connected through electrical resistances to the negative terminal of the ekg, and the 3rd limb is connected to the positive terminal.
  • when the positive terminal is on the right arm, the lead is known as the aVR lead
  • when it is on the left leg (or foot) , it is known as the aVF lead.
99
Q

pulmonary circulation

A

supplies the lungs

100
Q

systemic circulation

A

supplies all tissue other than the lungs

101
Q

arteries

A
  • transport blood under high pressure to the tissues
  • have strong vascular walls and rapid blood flow
102
Q

arterioles

A
  • the last small branches of the arterial system
  • act as control valves through which blood is released into the capillaries
  • have strong muscular wallsthat can be constricted or dilated, giving them the capability of markedly altering blood flow to the capillaries in response to changing tissue needs
103
Q

capillaries

A
  • exchange fluids, nutrients, and other substances between the blood and the interstitial fluid
  • they have thin walls and are highly permeable to small molecules
104
Q

venules

A
  • collect blood from the capillaries and gradually coalesce into progressively larger veins
105
Q

veins

A

function as conduits to transport blood from the tissues back to the heart

  • serve as reservoirs for blood
  • have thin walls, low pressure, and rapid blood flow
106
Q

circulation as a complete circuit

A

contraction of the left heart propels blood into the systemic circulation through the aorta –> empties into smaller arteries, arterioles, and eventually capillaries (because blood vessels are distensible, each contraction distends the vessels; during relaxation of the heart, the vessels recoil, continuing flow to the tissues, even between heartbeats.) –> Blood leaving the tissues enters the venules and then flow into increasingly larger veins, which carry the blood to the right heart –> the right heart then pumps the blood through the pulmonary artery, small arteries, arterioles, and capillaries, blood flos into venules and large veins and empties into the left atrium and left ventricle before it is again pumped into the systemic circulation.

-

107
Q

How does the change of flow in one part of the circuit affect the flow in other parts?

A

because blood flows around the same vessels, any change in flow in a single part of the circuit transiently alters flow in other parts

ex. - strong constriction of the arteries in the systemic circulation can transiently reduce the total cardiac output, in which case blood flow to the lungs decreases equally as much as flow through the systemic circulation.

108
Q

what happens when a blood vessel suddenly constricts?

A

there must be opposite dilationof another part of the circulation because blood volume cannot change rapidly and blood itself is not compressible

  • ex. - strong constriction of the veins in the systemic circulation displaces blood into the heart, dilating the heart and causing it to pump with increased force.
109
Q

Where is most of the blood volume distributed?

A
  • in the veins of the systemic circulation
  • about 84% of the total blood volume is in the systmic circulation (64% in the veins, 13% in the arteries, 7% in the systemic arterioles and capillaries)
  • Heart contains 7%
  • pulmonary vessels contain 9%
110
Q

relationship between velocity of blood flow and the vascular cross-sectional area

A

velocity of blood flow is inversely proportional to the vascular cross-sectional area

  • because approximately the same volume of blood flows throgh each segment of the circulation, vessels with a large cross-sectional area, such as the capillaries, have slower blood flow velocity
111
Q

approximate total cross-sectional areas of the systemic vessels:

A
  • aorta: 2.5 cm^2
  • small arteries 20 cm^2
  • arterioles 40 cm^2
  • capillaries 2500 cm^2
  • venules 250 cm^2
  • small veins 80 cm^2
  • venae cavae 8 cm^2
  • so, velocity of blood flow in the capillaries is onlt about 1/1000 the velocity of flow in the aorta
112
Q

varrying pressures in different parts of the circulation

A

Aortic Arterial Pressure

  • rises to its highest point (systolic pressure) during systole (120 mmHg)
  • falls to its lowest point (diastolic pressure) at the end of diastole (80 mmHg)
113
Q

Pulse pressure

A
  • difference between systolic and diastolic pressure (40 mmHg)
114
Q

what happens to pressure as blood flows through the systmic circulation?

A

As blood flows through the systemic circulation, its pressure falls progressively to approximately 0 mmHg by the time it reaches the termination of the venae cavae in the right atrium of the heart

115
Q

pressure in the systemic capillaries

A

varies from as high as 35 mmHg near the arteriolar ends to as low as 10 mmHg near the venous ends

  • average functional capillary pressure is about 17 mmHg
116
Q

pressure in pulmonary circulation vs. pressure in systemic circulation

A
  • pressures in the pulmonary circulation are much lower than those in the systemic circulation
  • systolic pressure is about 25 mmHg
  • diastolic pressure is about 8 mmHg
  • mean pulmonary artery pressure is 16 mmHg
  • average Pulmonary capillary pressure - 8 mmHg
  • yet total blood flow through the lungs is the same as that in the systemic circulation because the lower vascular resistance of the pulmonary blood vessels
117
Q

3 basic principles that underlie the major functions of the circulatory system

A
  1. Blood flow to each tissue of the body controlled according to the tissue’s needs (tissues need more blood flow when they are active than when they are at rest - occasionally as much as 20 times more. The microvessels of each tissue continuously monitor the tissue needs and control the blood flow at the level required for the tissue activity. Nervous and hormonal mechanisms provide additional control of tissue and blood flow
  2. the cardiac output is the sum of all the local tissue blood flows. - after blood flows through a tissue, it immediately returns by way of the veins to the heart. The heart responds automatically to the inflow of blood by pumping it almost immediately back into the arteries. in this sense, the heart responds t the demands of the tissues, although it often needs help in the form of nervous stimulation to make it pump the required amounts of blood flow
  3. the arterial pressure is usually controlled independently of local blood flow or cardiac output control. - the circulatory system is provided with an extensive system for controlling arterial pressure. If an arterial pressure falls below normal, a barrage of nervous reflexes elicits a series of circulatory changes that elevate the pressure back toward normal, including increased forct of heart pumping, contraction of large venous reservoirs to provide more blood to the heart, and constriction of most of the srterioles throughout the body. Over more prolonged periods of time, the kidneys play additional roles by secreting pressure-controlling hormones and by regulating blood volume
118
Q

Formula for flow of blood through a vessel

A

F = (Delta P)/R

F= blood flow (ml/minute)

(delta P) = pressure difference between the 2 ends of the vessel (mmHg)

R = vascular resistance (mmHg/m per minutel)

  • it is the difference in pressure between the 2 ends of the vessel that provides the driving force for flow, not the absolute pressure of the vessel
119
Q

pressure gradient and blood flow in pulmonary circulation

A
  • the pressure gradient is much lower than in systemic circulation
  • blood flow is the same as in systemic circulation
  • therefore: the total pulmonary vascular resistance is much lower than the systemic vascular resistance
120
Q

Poiseuille’s Law

A
  • vessel diameter has a marked effect on resistance to blood flow
  • vascular resistance is directly proportional to the viscosity of the blood and the length of the blood vessel and inversely proportional to the radius of the vessel to the 4th power

Resistance alpha (Constant x Viscosity X Length) / radius^4

121
Q

effect of a decreased radius of a blood vessel

A
  • the decreased radius of a blood vessel markedly increases vascular resistance
  • because vascular resistance is inversely related to the 4th power of the radius, even small changes in radius can cause very large changes in resistance.
  • for example, if the radius of a blood vessel increases from one to two (2x normal), resistance decreases to 1/16 of normal (1/24) and flow increases to 16 times normal if the pressure gradient remains unchanged.
  • small vessels in the circulation have the greatest amount of resistance, whereas large vessels have little resistance to blood flow
  • for a parallel arrangement of blood vessels, as occurs in systemic circulation in which organs are each supplied by an artery that branches into multiple vessels, the total resistance can be expressed as:

1/Rtotal = 1/R1 + 1/R2 …

Rtotal = resistance of total systemic circulation

R1, R2 … - the resistances of each of the vascular beds in the circulation

  • the total resistance is less than the resistance of any of the individual vascular beds
  • for a series arrangement of blood vessels, as occurs within a tissue in whichblood flows through arteries, arterioles, capillaries, and veins, the total resistance is the sum of the individual resistances:

Rtotal = R1 + R2 …

R1, R2 - the resistances of the various blood vessels in series within the tissues

122
Q

Conductance

A

a measure of the ease of which blood can flow through a vessel and is the reciprocal of resistance

conductance = 1/resistance

123
Q

effect of increased hematocrit and increased viscosity on vascular resistance and blood flow

A
  • increased blood hematocrit and increased viscosity raise vascular resistance and decrease blood flow
  • the greater the viscosity, the less is the flow of blood in a vessel if all other factors remain constant.
  • the normal viscosity of blood is about 3x the viscosity of water
  • blood is so viscous due to its large numbers of red blood cells (each exerts frictional drag on adjacent cells and on the wall of the vessel)
124
Q

Hematocrit

A
  • the percentage of blood that is comprised of cells
  • normally 40% (remainder is plasma)
  • the greater the percentage of cells in the blood (the greater the hematocrit) –> the greater the viscosity of blood –> the greater the resistance to blood flow
125
Q

how does autoregulation affect arterial pressure and blood flow?

A
  • the effect of arterial pressure on blood flow in manytissues is usually far less than expected because an increase in arterial pressure usually initiates compensatory increases in vascular resistance withn a few seconds through activation of the local control mechanisms discussed in ch 17
  • conversely, wiht reductions in arterial pressure, vascular resistance is promptlyreduced in most tissues and blood flow is maintained relatively constant
126
Q

blood flow autoregulation

A

the ability of each tissue to adjust its vascular resistance and to maintain normal blood flow during changes in arterial pressure between approximately 70 and 175 mmHg

127
Q

how long do changes in tissue blood flow last?

A
  • changes in tissue blood flow rarely last more than a few hours even when increases in arterial pressure or increased levels of vasoconstrictors or vasodilators are sustained
  • the reason for the relative constancy of blood flow is that each tissue’s local autoegulatory mechanisms eventually override most of the effects of vasoconstrictors to provide a blood flow that is appropriate for the needs of the tissue
128
Q

Vascular distensibility

A
  • the distensibility of the arteries allows them to accomodate the pulsatile putput of the heart and average out the pressure pulsations
  • this provides smooth, continuous flow of blood through the small blood vessels
  • veins are more distensible than arteries, allowing them to store large quantities of blood that can be called into use when needed
  • veins are 8x more distensible than arteries in the systemic circulation
  • the distensibility of veins in the pulmonary circulation is similar t othat of the systemic circulation

arteries in the lungs are more didtensible than those of the systemiccirculation

Vascular distensibility = increase in volume / (increase in pressure x original volume)

129
Q

Vascular compliance (capitance)

A
  • the total quantity of blood that can be stored in a given part of the circulation for each millimeter of mercury of pressure
  • how to calculate:

the greater the compliance of the vessel, the more easily it can be distended by pressure

Vascular Compliance = Increase in Volume / Increase in Pressure

  • Compliance is related to distensibility as follows:

Compliance = Distensibility x Volume

  • the compliance of a vein in the systemic circulation is about 24 times as great as its corresponding artery because it’s about 8x as distensible and has a volume that is 3x as great
130
Q

what effect does sympathetic stimulation have on vascular capacitance?

A
  • sympathetic stimulation decreases vascular capacitance
  • sympathetic stimulation increases smooth muscle tone inveins and arteries, causing a shift of blood to the heart, which is an important method the body uses for heart pumping
  • ex. durring hemorrhage, enhanced sympathetic tone of the vessels, especially the veins, reducesblood vessel size so the circulation can continue to operate almost normally even when as much as 25% of the total blood volume has been lost.
131
Q

what happens to vessels exposed to increased volume?

A
  • Vessels exposed to increased volume at 1st exhibit a large increase in pressure, but delayed stretch of the vessel walls allows the pressure to return toward normal

(aka “delayed compliance” or “stress relaxation”)

132
Q

Delayed compliance

A
  • A VALUABLE MECHANISM BY WHICH THE CIRCULATION CAN ACCOMODATE EXTRA AMOUNTS OF BLOOD WHEN NECESSARY, SUCH AS AFTER A TRASFUSION THAT WAS TOO LARGE
  • DELAYED COMPLIANCE IN THE REVERSE DIRECTION PERMITS THE CIRCULATION TO READJUST ITSELF OVER A PERIOD OF MINUTES OR HOURS TO A DIMINISHED BLOOD VOLUME AFTER SERIOUS HEMORRHAGE
133
Q

effect of distensibility of the arterial system

A
  • without the distensibility of the arterial system, blood flow through the tissues would occur only during cardiac systole, with no blood flow durring diastole
  • the combination of distensibility of the arteries and their resistance to flow reduces the pressure pulsations to almost none by the time the blood reaches the capillaries, allowing continuous rather than pulsatile flow through the tissues
134
Q

Pulse pressure

A
  • difference between systolic and diastolic pressure (usually 40 mmHg)
135
Q

2 most important factors that can increase pulse pressure

A
  1. increased stroke volume (the amount of blood pumped into the aorta with each heartbeat)
  2. decreased arterial compliance - results when the arteries harden with aging (arteriosclerosis)
136
Q

Pressure pulses in Smaller Vessels

A

pressure pulsations in the aorta are progressively diminished (damped) by

  1. the resistance to blood movement in the vessels, and
  2. the compliance of the vessels
    - the resistance damps the pulsations because a small amount of blood must flow forward to distend the next segment of the vessel, the greater the resistance, the more difficlt it is for this to occur
    - the compliance damps the pulsation because the more compliant a vessel, the greater is the quantity of blood required to cause a rise in pressure
    - the degree of damping of arterial pulsations is directly proportional to the product of the resistance and compliance
137
Q

Mean Arterial Pressure

A

MAP = 2/3 diastolic pressure + 1/3 systolc pressure

  • 93.3 mmHg for the avg. young adult
138
Q

Veins

A
  • can constrict/enlarge to store small or large quantities of blood
  • can propel blood forwardby means of a “venous pump”
  • helps regulate cardiac output
139
Q

how right atrial pressure affects pessure elsewhere

A
  • because blood flow from systemic veins flows into the right atrium, anything that affects the right atrial pressure usually affects venous pressure everywhere in the body
  • right atrial pressure is regulated by a balance between the ability of the heart to pump blood out of the right atrium and a tendency of blood to flow from the peripheral vessels back to the right atrium
  • normal right atrial pressure is about 0mmHg, but it can rise to as high as 20-30 mmHg under abnormal conditions, such as with serious heart failure or after a massive transfusion
140
Q

effect of increased venous resistance on the peripheral venous pressure

A
  • increased venous resistance can increase the peripheral venous pressure
  • when large veins are distended, they offer little resistance to blood flow
  • many of the large veins entering the thorax are compressed by the surrounding tissues, however, so they are at least partially collapsed, or collapsed to an ovoid state
  • so, large veins usually offer significant resistance to blood flow, and the pressure in the peripheral veins is usually 4-7 mmHg higher than the right atrial pressure
  • partial obstruction of a large vein markedly increases the peripheral venous pressure distal to the obstruction
141
Q

effect of increased right atrial pressure on peripheral venous pressure

A
  • increased right atrial pressure increases peripheral venous pressure
  • when the right atrial pressure rises above its normal state of 0mmHg, blood begins to back up in large veins and open them up.
  • pressures in the peripheral veins don’t rise until the collapsed points between the peripheral veins and the large central veins have opened, which usually occurs at a right atrial pressure of 4-6mmHg
  • when the right atrial pressure rises stll further, as occurs during severe heart failure, it causes a corresponding rise in peripheral venous pressure
142
Q

how does gravitational pressure affect venous pressure?

A
  • the pressure at the surface of a body of water exposed to air is equal to the atmospheric pressure, but the pressure rises 1mmHg for each 13.6mmHg distance below the surface
  • this pressure results from the weight of the water (gravitational hydrostatic pressure) - also occurs in the vascular system because of the weight of the blood in the vessels
  • in an adult who is standing still, pressure in the veins of the feet is approximately +90mmHg because of the hydrostatic weight of the blood in the veins between the heart and the feet
143
Q

effect of the venous valves and the “venous pump” on venous pressure

A
  • without the valves of the veins, the gravitational pressure effect would cause venous pressure in the feet to always be about +90 mmHg in a standing adult
  • each time one tightens the muscle and moves the leg, however, it compresses the veins either in the muscles or adjacent to them and squeezes the blood out of the veins
144
Q

arrangement of the valves in the veins

A
  • the valves in the veins are arranged so the direction o blood flow can only be toward the heart
  • so, each time a person moves the legs or tenses the muscles, a certain amount of blood is propelled toward the heart, and the pressure in the veins is lowered (“venous pump” - keeps the pressure in the feet of a walking adult near 25 mmHg (d/n work if a person d/n move))
  • if the valves of the venous system become incompetent or are destroyed, the effectveness, of the venous pump is also decreased
  • when valve incompetance develops, greater pressure in the veins of the legs may further increase the size of the veins and finally destroy the function of the valves entirely (results in varicose veins), and the capillary pressures increase to high levels causing leakage of fluid from the capillaries and edema in the legs while standing
145
Q

Veins as blood reservoirs

A
  • more than 60% of the blood in the circulatory system is usually contained in the veins
  • for this reason and because veins are so compliant, the venous system can serve as a blood reservior for the circulation
  • ex - when blood is lost from the body, activation of the sympathetic nervous system causes the veins to constrict, which takes up much of the “slack” of the circulatory system caused by the lost blood
146
Q

Special blood reservoirs in the circulatory system (very compliant)

A
  • spleen - can decrease in size to release as much as 100mL of blood into the reservoir of the circulation
  • liver - sinuses of which can release several hundred millimeters of blood into the rest of the circulation
  • large abdominal veins - contribute as much as 300mL
  • venous plexus underneath the skin - contributes several hundred ML
147
Q

what happens in the capillaries?

A

transportation of nutrients to the tissues, and removal of waste products

148
Q

capillary structure

A
  • capillaries only have a single layer of highly permeable endothelial cells
  • this permits rapid exchange of nutriants and cellular waste products between the tissues and the circulating blood
  • 10 billion capillaries
  • total surface area of 500-700 square meters (1/8 the size of a footfball field)
  • capillaries are very porous with several million slits, or pores, between the cells that makeup their walls to each square centimeter of capillary surface
  • because of the high permeability of the capillaries for most solutes and the high surface area, as blood flows through the capillaries large amounts of dissolved substances diffuse in both directions through the pores
  • in this way, almost all disolved substances in the plasma, except the plasma proteins, continually mix with the interstitial fluid
149
Q

structure of microcirculation

A
  • blood enters the capillaries through an arteriole and leaves through a venule
  • blood from the arteriole passes into a series of metaarterioles, which have structures midway between those of arterioles and capillaries
  • arterioles - highly muscular, play a major role in controlling blood flow to the tissues
  • metaarterioles - d/n have a continuous smooth muscle coat, but smooth muscle fibers encircle the vessel at intermittent points called precapillary sphincters. Contraction of the muscle in these sphincters can open and close the entrance to the capillary
  • metaarterioles and arterioles are in close contact with the tissues thay serve, and local conditions, such as changes in the concentration of nutrients or waste products of metabolism, can have direct effects on these vessels in controlling the local blood flow
150
Q

vasomotion

A
  • blood flows intermittently through the capillaries
  • in many tissues the blood flow through capillaries isn’t continuous but, turns on and off every few seconds
  • the cause is contraction of the metaarterioles and precapillary sohincters, which are influenced by oxygen and waste products of tissue metabolism
  • when oxygen concentrations of the tissue are reduced, the periods of blood flow occur more often and last longer, thereby allowing the blood to carry increased quantities of oxygen and other nutrients to the tissue
151
Q

Diffusion

A
  • the most important means for transfering substances between plasma and interstitial fluid
  • as blood traverses the capillary, large #s of water molecules and dissolved substances diffuse back and forth through the capillary wall, providing a continual mixture of the interstitial fluid and plasma
  • lipid soluble substances such as oxygen and carbon dioxide can diffuse directly through the cel membranes without having to go through the pores
  • water soluble substances, such as glucose and electrolytes, diffuse only through intercellular pores in the capillary membrane. The rate of diffusion for most solutes is so great that cells as far as 50 micro meters away from the capillaries can receive adequate quantities of nutrients
152
Q

Factors that affect the rate of diffusion across the capillary walls

A
  • pore size in the capillaries 6-7 nanometers - the pores of some capillary membranes such as the liver capillary sinusoids are much larger and are therefore more permeable to substances disolved in plasma
  • molecular size of the diffusing substance - water, and most electrolytes, such as sodium and chloride, have a molecular size that is smaller than the pore size, allowing rapid diffusion across the capillary wall. Plasma proteins, however, have a molecular size that is slightly greater than the width of the pores, restricting their diffusion
  • concentration difference of the substance between the 2 sides of the membrane - the greater the difference between the concentrations of a substance on the 2 sides of the capillary membrane, the greater is the rate of diffusion in one direction through the membrane. the concentration of oxygen in the blood is normally higher than in the interstitial fluid, allowing large quantities of oxygen to move from the blood toward the tissues
  • conversely, the concentrations of the waste products of metabolism are greater in tissues than in blood, allowing them to move into the blood and to be carried away from the tissues
153
Q

Interstitium, and interstitial fluid

A

1/6 of the body consists of spaces between cells, which are collectively called the interstitium

2 types of solid structures:

  1. collagen fiber bundles
  2. proteoglycan filaments
    - the collagen provides most of the tensional strength of the tissues
    - proteoglycan filaments - composed mainly of hyaluronic acid - very thin and form a filler of fine reticular filaments, often described as “brush pile”
    - gel in the interstitium consists of proteoglycan filaments and entrapped fluid
154
Q

how is fluid in the interstitium derived?

A

fluid in the interstitium is derived by filtration and diffusion from the capillaries and has almost the same constituency as plasma except with lower concentrations of protein

  • the interstitial fluid is mainly entrapped in the minute spaces among the proteoglycan filaments and has te characteristics of a gel
  • because of the large #s of proteoglycan filaments, fluid and solutes don’t flow easily through the tissue gel. Instead, solutes mainly diffuse through the gel. This diffusion occurs about 95%-99% as rapidly as it does through free liquid
155
Q

how much “free” fluid is in the interstitium?

A
  • the amount of “free” fluid in the interstitium in most tissue is less than 1%
  • although almost all the fluid in the interstitium is entraped in the tissue gel, small amounts of “free” fluid are also present
  • when the tissue develops edema, these small pockets of free fluid can expand tremendously
156
Q

what determines capillary fluid filtration?

A
  • capillary fluid filtration is determined by hydrostatic and colloid osmotic pressures, and capillary filtration coefficient
  • although the exchange of nutrients, oxygen, and metabolic waste products across the capillaries occurs almost entirely by diffusion, the distribution of fluid across the capillaries is determined by another process - the bulk flow of ultrafiltration of protein-free plasma
  • capillary walls are highly permeable to water and most plasma solutes, except plasma proteins, therefore, hydrostatic pressure differences across the capillary wall push protein-free plasma (ultrafiltrate) through the capillary wall into the interstitium
  • in contrast, osmotic pressure caused by the plasma proteins (called colloid osmotic pressure) tends to produce fluid movement by osmosis from the interstitial spaces into the blood.
  • interstitial fluid hydrostatic andcolloid osmotic pressures also influence fluid filtration across the capillary wall
157
Q

what determiones the rate at which ultrafiltration occurs across the capillary?

A

the rate at which ultrafiltration occurs across the capillary depends on the difference in hydrostatic and colloid osmotic pressures of the capillary and interstitial fluid. These forces are often called starling forces.

158
Q

4 forces determine fluid filtration through the capillary membrane

A
  1. Capillary Hydrostatic Pressure (Pc) - forces fluid outward through the capillary membrane
  2. Interstitial Fluid Hydrostatic Pressure (Pif) - forces fluid inward through the capillary membrane when the Pif is positive, but outward into the interstitium when the Pif is negative
  3. Plasma Colloid Osmotic Pressure - tends to cause osmosis of the fluid inward through the capillary membrane
  4. Interstitial Fluid Colloid Osmotic Pressure - tends to cause osmosis of fluid outward through the capillary membrane
159
Q

what determines the net rate of filtration out of the capillary?

A
  • determined by the balance of these forces as well as by the capillary filtration coefficient
160
Q

Functional Capillary Hydrostatic Pressure

A
  • averages 17 mmHg in many tissues
  • when blood is flowing through many capillaries, the pressure averages 30-40mmHg on the arterial ends, and 10-15 mmHg on the venous ends, and about 25 mmHg in the middle
  • when the capillaries are closed, the pressure in the capillaries beyond the closure is about equal to the pressure at the venous ends of the capillaries (10 mmHg)
  • when averaged over a period of time, including the periods of opening and closure of the capillaries, the functional mean capillary pressure is closer to the pressure in the venous end of the capillaries than to the pressure in the arteriole ends (averages 17mmHg in many tissues; in some tissues such as the kidneys, capillary hydrostatic pressure may be as high as 60-65 mmHg)
161
Q

Interstitial fluid hydrostatic pressure in different kinds of tissue

A
  • interstitial fluid hydrostatic pressure is subatmospheric (negative pressure) in Loose SubQ tissue, and positive in tightly encased tissues
  • measurements of interstitial fluid hydrostatic pressure have yeilded and average value of about -3 mmHg in loose subQ tissue
  • one basic reason for this negative pressure is the pymphatic pumping system. When fluid enters the lymphatic capillaries, any movement of the tissue propels the fluid forward through the lymphatic system and eventually back into the circulation. In this way, free fluid that accumulates in the tissue is pumped away as a consequence of tissue movement
  • this pumping action of the lymphatic capillaries appears to account for the slight intermittent negative pressure in the tissues at rest.
  • in tissues surrounded by tight encasements (brain, kidneys, skeletal muscle), interstitial fluid hydrostatic pressures are usually positive (ex, the brain interstitial fluid hydrostatic pressure averages +4-+16 mmHg; kidneys - about +6mmHg)
162
Q

Plasma Colloid Osmotic Pressure

A
  • averages about 28mmHg
163
Q

Proteins and the Capillary Membrane

A
  • the proteins are the only disolved substances in the plasma that don’t readily pass through the capillary membrane.
  • these proteins, exert an osmotic pressure referred to as the colloid osmotic pressure
  • the normal concentration of plasma protein averages about 7.3 g/dL.
  • about 19 mmHg of the colloid osmotic pressure is due to the positively charged cations, mainly sodium ions, that bind to the negatively charged plasma proteins (Donnan Equilibrium Effect) causes the colloid osmotic pressure in the plasma to be about 50% greater than that produced by the proteins alone
164
Q

Plasma Proteins

A
  • mainly a mix of albumin, globulin, and fibrinogen
  • about 80% of the total colloid osmotic pressure of the plasma results from the albumin fraction, 20% from the globulin, and only a tiny amount from the fibrinogen
165
Q

Interstitial Fluid Colloid Osmotic Pressure

A
  • averages 8mmHg
  • although the size of the usual capillary pore is smaller than the molecular size of the plasma protein, this is not true of all pores; therefore, small amounts of plasma protein leak through the pores into the interstitial spaces
  • the average protein concrentration of the interstitial fluid is around 40% of that in the plasma, or about 3g/dL, giving a colloid osmotic pressure of about 8mmHg
  • in some tissues, such as the liver, the interstitial fluid colloid osmotic pressure is much greater because the capillaries are much more permeable to plasma proteins
166
Q

Summary of Fluid Volume Exchange through theCapillary Membrane

A
  • the average capillary pressure at the arteriolar ends of the capillaries is 15 - 25 mmHg greater than at the venular ends
  • because of this difference, fluid filters out of the capillaries at the arteriolar ends, and fluid is reabsorbed back into the capillaries at their venular ends
  • a small amount of fluid flows through the tissues from the arteriolar ends of the capillaries to the venular ends
  • under normal conditions, a state of near-equilibrium exists between the amount of fluid filtering outward at the arteriolar ends of the capillaries and the amount of fuiid returned to the circulation by absorption at the venular ends of the capillaries
  • there is a slight disequalibrium that occurs, and a small amount of fluid is filtered in excess of that reabsorbed.
  • this fluid is eventually returned to the circulation by way of the lymphatics
  • mean capillary hydrostatic pressure - 17.3 mmHg
  • Negative interstitial free fluid pressure - 3.0 mmHg
  • Interstitial fluid Colloid osmotic pressure - 8.0 mmHg
  • TOTAL outward force - +28.3
  • plasma colloid osmotic pressure - 28
  • TOTAL inward force - 28
  • NET OUTWARD FORCE - +0.3
  • the small imbalanceof forces causes slightly more filtration than reabsorption of fluid into the interstitial spaces
167
Q

Capillary Filtration Coefficient

A
  • the rate of filtration in the capillarties is also determined by the capillary filtration coefficient
  • the filtration coefficient in an average tissue is about .01 mL of fluid per minute per millimeter of mercury per 100g of tissue.
  • for the entire body, the capillary filtration coefficient is about 6.67 mL of fluid per minute per mL of mercury
  • the net rate of capillary filtration for the entire body is expressed as follows: net filtration = Kf x Net Filtration Pressure = 6.67 x 0.3 = 2mL/min
  • because of the extreme differences in the permeabilities and surface areas of the capillary systems in different tissues, the capillary filtration coefficient may vary more than 100-fold among tissues
  • ex - capillary filtration coefficient in the kidneys is about 4.2 mL/min per milimeter of mercury per 100g of kidney weight, a value almost 400 times as great as the Kf of many other tissues. This causes a much greater rate of filtration in the glomerular capillaries of the kidney
168
Q

Lymphatic System

A
  • carries fluid from tissue spaces into the blood
  • also carry away proteins and large particulate mater from the tssue spaces, neither of which can be removed through absorption directly into the blood capillary
169
Q

where are the lymph channels?

A
  • almost all tissues of the body have lymphatic channels
  • most of the lymph from the lower part of the body flows up the thoracic duct and empties into the venous system at the juncture of the left interior jugular vein and subclavian vein
  • lymph from the left side of the head, left arm, and parts of the chest region also enter the thoracic duct before emptying into the veins.
  • lymph from the right side of the neck and head, right arm, and parts of the thorax, enter the right lymph duct, which then empties into the venous system at the juncture of the right subclavian vein and internal jugular vein
170
Q

where does lymph come from?

A
  • lymph is derived from interstitial fluid
  • as lymph first flows from the tissue, it has almost the same composition as the interstitial fluid.
  • in many tissues, the protein concentration averages about 2g/dL, but in other tissues such as the liver the protein concentration may beas high as 6 g/dL
  • in addition to carrying fluid and protein from the interstitial spaces to the circulation, the lymphatic system is one of the mahor routes for absorption of nutrients from the GI tract. After a fatty meal, thoracic duct lymph sometime contains as much as 1-2% fat.
171
Q

what is the rate of lymph flow?

A
  • the total rate of lymph flow is approximately 120 mL/hr, or 2-3 L per day
  • this rate of formation can change dramatically, however, in certain pathological conditions associated with excessive fluid filtration from the capillaries into the interstitium
172
Q

what effect does increased interstitial fluid hydroststic pressure have on lymph flow rate?

A
  • increased interstitial fluid hydrostatic pressure increases the lymph flow rate
  • at normal interstitial hydrostatic pressures in the subatmospheric range, lymph flow is very low
  • as the pressure rises to values slightly higher than 0mmHg, the lymph flow increases by more than 20-fold
  • when interstitial pressure reaches 1-2 mmHg, lymph flow fails to rise further, this results form the fact that rising tissue pressure not only increases the entry of fluid into the lymphatic capillaries but also compresses the larger lymphatics, thereby impeding lymph flow
173
Q

lymphatic pump

A
  • increases lymph flow
  • valves exist in all lymph channels
  • each segment of the lymph vessel functions as a separate automatic pump; that is, filling of a segment causes it to contract, and the fluid is pumped through the valve into the next lymph segment
  • this fills the lymph segment, and within a few seconds it too contracts, with the process continuing along the lymph vessel until the fluid is finally emptied
  • this pumping action propels the lymph forward toward the circulation
  • in addition to pumping caused by intrinsic contraction of the vessels, external factors also compress the vessels (contraction of muscles surrounding lymph vessels or movement of body parts may increase lymph pumping
  • under some conditions, such as during exercise, the lymph pump may increase lymph flow by 10-30 fold
174
Q

the lymph system as an overflow mechanism

A
  • the lymph system is an important “overflow mechanism” that returns to the circulation excess proteins and fluid volume that enters the tissue spaces
  • when the lymph system fails, proteins and fluid accumulates in the interstitium causing edema
  • the accumulation of protein in the interstitium is especially important in causing edema because the lymphatics provide the only mechanism for proteins that leak out of the capillaries to re-enter the circulation in significant quantities
  • when protein accumulates in the interstitial spaces owing to lymph failure, there is an increase in colloid osmotic pressure of the interstitial fluid that tends to alow more fluid filtration into the interstitium
175
Q

Lymph nodes

A
  • bacteria and debris from the tissues are removed by the lymph system at the lymph nodes
  • because of the very high permeabiltiy of the lymph capillaries, bacteria and other small particulate matter in the tissues can pass into the lymph
  • the lymph passes through a series of nodes on its way out to the blood
  • in these nodes, bacteria and other debris are filtered out, pagocytized by macrophages in the nodes, and finally digested and converted to amino acids, glucose, fatty acids, and other lw-molecular-weight substances before being released into the blood
176
Q

Local Tissue and the autoregulation of blood flow

A
  • local tissues autoregulate blood flow in response ot their individual needs
  • in most tissues, bloodflow is autoregulated meaning the tissue regulates its own blood flow, this is beneficial to the tissue because it allows the delivery of oxygen and nutrients and removal of waste products to parallel the rate of tissue activity to be regulated independently of flow to another tissue
  • in certain organs, blood flow serves purposes other than supplying nutrients and removing waste products. ex - blood flow to the skin influences heat loss from the body and in this way helps control body temp. Delivery of adequate quantities of blood to the kidneys allows them to excrete repidly the waste products of the body
  • the ability of the tissues to regulate their own flow permits them to maintain adequate nutrition and perform necessary functions to maintain homeostasis
  • in general, the greater the rate of metabolism in an organ, the greater its blood flow. ex - high blood flow in glandular organs such as the thyroid and adrenal glands which have high metabolic rates. blood flow in resting skeletal muscles is low because the metabolic activity of the muscle is also low in the resting state (during heavy exercise, skeletal muscle metabolic activity can increase by more than 60x and the blood flow can increase 20x
177
Q

Mechanisms of local blood flow control

A
  • local tissue blood flow control can be divided into 2 phases
    1. Acute control
    2. long-term-control
  • acute control occurs within seconds to minutes via constriction or dilation of arterioles, metaarterioles, and precapillary sphincters. Long-term control occurs over a period of days, weeks, months, and in general, provides even better control of flow in proportion to the neds of the tissues.
  • long-term control occurs mainly as a result of increases or decreases in the physical size and number of blood vessels supplying the tissues
178
Q

effect of increased tssue metabolic rate on local blood flow

A
  • increased tissue metabolic rate usually increases local blood flow
  • in many tissues, such as skeletal muscle, increases in metabolism, up to 8x normal acutely increase the blood flow about 4x
  • initially, the rise in flow is less than that of the metabolism, but once the metabolism increases sufficiently to remove most of the nutrients from the blood a further rise in metabolism can occur only with a concomitant increase in blood flow to supply the required nutrients
179
Q

effect of decreased oxygen availability on tissue blood flow

A
  • decreased oxygen availability increases tisue blood flow
  • one of the required nutrients for tissue metabolism is oxygen
  • whenever the availability of oxygen in the tissues decreases, such as at high altitude, in the presence of pneumonia, or with carbonmonoxide poisoning (which inhibits the ability of hemoglobin to transport oxygen), the tissue blood flow increases markedly.
  • cyanide poisoning, which reduces the ability of the tissues to utilize oxygen, can increase tissue blood flow 7x
180
Q

effect of increased demand for oxygen and nutrients on blood flow

A
  • increased demand for oxygen and nutrients increases tissue blood flow
  • in the absence of an adequate supply of oxygen and nutrients as a result of either increased tissue metabolism, the arterioles, metaarterioles, and precapillary sphincters relax, thereby decreasing vascular resistance and allowing more flow to the tissues.
  • the relaxation of prcapillary sphincters allows flow to occur more often in capillaries that are closed because of periodic contraction of precapillary sphincters (vasomotion)
181
Q

Effect of accumulation of vasodilator metabolites on tissue blood flow

A
  • accumulation of vasodilator metabolites increases tissue blood flow
  • the greater the rate of metabolism in the tissue, the greater is the rate of production of tissue metabolites, such as adenosine, adenosine phosphate compounds, carbon dioxide, lactic acid, potassium ions, and hydrogen ions.
  • each of these substances has been suggested to act as a vasodilator that contributes to increased blood flow associated with stimulation of tissu metabolism
182
Q

effect of lack of other nutrients

A
  • lack of other nutrientsmay cause vaso dilation
  • a deficiency of glucose, amino acids, or fatty acids, may contribute to local vaso dilation, although not proven
  • vasodilation occurs with beriberi where the patient has a dificiency of the B vitamin substances thiamine, niacine, and riboflavin. because these vitamins are all invloved in the oxidative phosphorylation mechanism for generating ATP, a deficiency of these vitamins may lead to diminished ability of the smooth muscle to contract, causing vasodilation
183
Q

reactive hyperemia

A
  • occurs when the blood supply to a tissue is blocked for a short time
  • if blood flow is blocked for a few seconds to several hours and then unblocked, flow to the tissue usually increases to 4-7x normal
  • the increased flow continues for a few seconds or much longer if the flow has been stoped for 1 hour or longer.
  • this appears to be a manifestation of local “metabolic” blood flow regulation mechanisms. After vascular occlusion, there is an accumulation of tissue vasodilator metabolites and the development of oxygen deficiency in the tissues.
  • the extra blood flow durring reactive hyperemia lasts long enough to almost exactly repay the tissue oxygen deficiency and to wach out te accumulated vasodilator metabolites
184
Q

active hyperemia

A
  • occurs when the tissue metabolic rate increases
  • when a tissue becomes highly active, such as muscle during exercise or even the brain during increased mental activity, blood flow to the tissue increases
  • appears related to increases in local tissue metabolism that cause accumulation of vasodilator substances and possibly a slight oxygen deficit
  • the dilation of local blood vessels helps the tissue receive the additional nutrients required to sustain its new level of function
185
Q

what happens to tissue blood flow during changes in arterial pressure?

A
  • in any tissue of the body, acute increases in arterial pressure cause an immediate increase in blood flow
  • in less than 1 minute, the blood flow in many tissues returns toward the normal level even though the arterial pressure remains elevated

(“autoregulation of bloodflow”)

186
Q

metabolic theory of autoregulation

A
  • when arterial pressure rises and blood flow becomes too great, the excess provides too much oxygen and too many nutrients to the tissues, causing the blood vessels to constrict and the flow to return toward normal despite the increased arterial pressure
187
Q

myogenic theory of autoregulation

A
  • sudden stretch of small blood vessels causes the smooth muscles in the vessel walls to contract automatically. This is an intrinsic property of smooth muscles that allows them to resist excessive stretching
  • conversely, at lower pressures the degree of stretch of the vessel is less, and the smooth muscle relaxes, decreasing vascular resistance and allowing flow to be maintained relatively constant despite the lower blood pressure
188
Q

Additional Mechanisms for blood flow control in the kidneys

A
  • blood flow control is vested, in part, in a mechanism called tubuloglomerular feedback, in which the composition of fluid in the early distal tubule is detected by the macula densa, which is located where the tubule abuts the afferent and efferent arterioles at the juxtaglomerular apparatus
  • when too much fluid filters from the blood through the glomerulus into the tubular system, feedback signals from the macula densa cause constriction of the afferent arterioles, therby reducing renal blood flow and returning the glomerular filtration rate toward normal
189
Q

additional mechanism for blood flow control in the brain

A
  • the concentrations of carbon dioxide and hydrogen play prominent roles in local blood flow control.
  • an increase in either dilates the cerbral blood vessels, which allows rapid washout of the excess carbon dioxide and hydrogen ions
190
Q

additional mechanism for blood flow control in the skin

A
  • blood flow control is closely linked to body temperatre and is controlled largely by the central nervous system through the sympathetic nerves
  • when we overheat, skin blood flow may increasemanyfold to as high as 7-8L/min for the entire body
  • when body temp is reduced, skin blood flow decreases, falling to barely above 0 at very low temps
191
Q

where do the local mechanisms for controlling tissue blood flow act?

A
  • the local mechanisms for controlling tissue blood flow act mainly on the very small microvessels of the tissues because local feedback by vasodilator substances or oxygen deficiency can reach only these vessels, not the larger arteries upstream.
  • when blood flow through the microvascular portion of the circulation increases, the endothelial cells lining the larger vessels release a vasodilator substance called endothelium derived relaxing factor which appears to be mainly nitric oxide
  • this release of nitric oxide is caused in part by increased shear stress on the endothelial walls, which occur as blood flows more rapidly through the larger vessels
  • the release of nitric acid then relaxes the larger vessels, cauding them to diltate
  • without the dilation of larger vessels, te effectiveness of local blood flow would be compromised because a signifficant part of the resistance in blood flow is in the upstream arterioles and small arteries
192
Q

endothelial cells also release vasoconstrictor substances

A
  • the most important of these is endothelin, a peptide that is released when blood vessels are injured
  • the usual stimulus for release is damage to the endothelium, such as that caused by crushing the tissues or injecting a traumatizing chemical into the blood vessel
  • after severe blood vessel damage, release of local endothelin and subsequent vasoconstriction helps to prevent extensive bleeding from arteries
193
Q

long term blood flow regulation

A
  • most of the mechanisms that have been discussed thus far act within a few seconds to a few minutes after the local tissue conditions have changed
  • even with full function of these acute mechanisms, blood flow usually is adjusted only about 3/4 of the way backto the exact requirements of the tissues
  • over a period of hours, days and weeks, ;ong-term local blood flow regulation develops that helps adjust the blood flow so it matches precisely the metabolic needs of the tissues
194
Q

Changes in tissue vascularity contribute to long-term regulation of blood flow

A
  • if metabolism of a tissue is increased for prolonged periods of time, the physical size of the vessels in a tissue increases
  • under some conditions, the # of blood vessels also increases
  • one of the major factors that stimulate this increased vascularity is low oxygen concentration in the tissues
  • animals that live at high altitudes, have increased vascularity; fetal chicks hatched at low oxygen levels have up to 2x as much vascular conductivity as in normal fetal chicks
195
Q

angiogenesis

A
  • growth of new vessels
  • occurs mainly in response to the presence of angiogenic factors released from
    1. ischemic tissues
    2. tissues that are growing rapidly
    3. tissues that have excessively high metabolic rates
196
Q

Many angiogenic factors are small peptides

A
  • 3 of the best characterized angiogenic factors:
    1. vascular endothelial growth factor (VEGF)
    2. fibroblast growth factor (FGF)
    3. angiogenin
  • each has been isolated from tumors or other tissues that are rapidly growing or have inadequate blood supply
  • all angiogenic factors promote new vessel growth by causing the vessels to sprout from small venules or, occassionally capillaries
  • the basement membrane of the endothelial cells is dissolved, followed by the rapid production of new endothelial cells that stream out of the vessel in extended cords directed toward the source of the angiogenic factor
  • the cells continue to divide and eventually fold over into a tube.
  • the tube then connects with another tube budding from another donor vessel and forms a capillary loop through which blood begins to flow
  • if the flow is sufficient, smooth muscle cells eventually invade the wall so that some of these vessels grow to be small arterioles and/or even larger vessels
197
Q

collateral blood vessels develop when an artery or a vein is blocked

A
  • new vascular channels usually develop around a blocked artery or vein and allow the affected tissue to be at least partially resupplied with blood
  • an important example is the development of collateral blood vessels after thrombosis of one of the coronary arteries.
  • in many people over 60, there is a blockage of at least one of the smaller coronary vessels, yet most people dont know that it happened because collateral blood vessels have gradually developed as the vessels have begun to close, thereby providing blood flow to the tissue sufficient to prevent an mycardial dammage. if a thrombus develops too rapidly for the development of collaterals, a serious heart attack could occur
198
Q

norepinephrine and epinephrine

A
  • released by the adrenal medulla
  • act as vasoconstrictors in many tissues by stimulating alpha - adrenergic receptors
  • epinephrine is much less potent as a vasoconstrictor and may even cause mild vasodilation throughstimulation of Beta-adrenergic receptors in some tissues, such as skeletal muscle
199
Q

Angiotensin II

A
  • is a powerful vasoconstrictor that is usually formed in response to volume depletion or decreased BP
200
Q

Vasopressin (ADH)

A
    • aka ADH
  • one of the most powerful vasoconstrictors in the body
  • formed in the hypothalamus and transported to the posterior pituitary where it’s releasedin response to decreased blood volume as occurs with hemorrhage or increased plasma osmolarity, as occurs with dehydration
201
Q

prostaglandins

A
  • formed in almost every tissue in the body
  • have important intracellular effects, but some of them are released in the circulation, especially prostacyclin and prostaglandins of the E series, which are vaso dilators
  • some prostaglandins, such as thromboxane A2 and prostaglandins of the F series, are vasoconstrictors
202
Q

Bradykinin

A
  • formed in the blood and in tissue fluids
  • powerful vasodilator that also increases capillary permeability
  • increased levels may cause marked edema as well as increased blood flow in some tissues
203
Q

Histamine

A
  • a powerful vasodilator, is released into the tissues when they become damaged or inflammed
  • most of the histamine is released from mast cells in damaged tissues or from basiphils in the blood
  • histamine, like bradykinin increases capillary permeability and causes edema as well as greater blood flow
204
Q

ions and other chemical factors canalso alter local blood flow

A
  • increased calcium ion concentration causes vasoconstriction
  • increased potassium ion concentration causes vasodilation
  • increased magnesium ion concentration causes vasodilation
  • increased sodium ion concentration causes vasodilation
  • increased osmolarity of the blood , caused by increased quantities of glucose or other nonvasoactive substances, cause vasodilation
  • increased hydrogen ion concentration (decreased pH) causes vasodilation
  • increased carbon dioxide concentration causes vasodilation in most tissues and marked vaso dilation in the brain