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Physiology > short term control of blood pressure > Flashcards

short term control of blood pressure Flashcards

1
Q

Mechanisms For Controlling Blood Pressure: Aldosterone

A

hormonal. activation time:hours activation strength: medium

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2
Q

Mechanisms For Controlling Blood Pressure: Baroreceptors

A

nervous activation time: seconds activation strength: large 7)

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3
Q

Mechanisms For Controlling Blood Pressure: Capillary fluid shift

A

physiological minutes medium

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4
Q

Mechanisms For Controlling Blood Pressure: Chemoreceptors

A

nervous seconds medium

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5
Q

Mechanisms For Controlling Blood Pressure: CNS ischemic response

A

nervous seconds large 11

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6
Q

Mechanisms For Controlling Blood Pressure: renal blood volume pressure control

A

kidneys hours infinite

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7
Q

Mechanisms For Controlling Blood Pressure: renin angiotensin-vasoconstriction

A

hormonal minutes medium

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8
Q

Mechanisms For Controlling Blood Pressure:stress relaxation of vasculature

A

physiologic second medium

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9
Q

cns ischemic response range

A

0-75

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10
Q

chemreceptors response range

A

25-115

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11
Q

barreceptors response range

A

50-225 decrease prssures

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12
Q

renin angiotensin vasocontriction range

A

30-120

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13
Q

renal blood volume and capillary fluid shift range

A

work over all pressures.

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14
Q

Parasympathetic

A

 Regulation of heart rate
Small affect on contractility
 Minimal regulation of
circulation

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15
Q

sympathetic

A

 Regulation of circulation

 Regulation of contractility

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16
Q

vasomotor center

A 
Parasympathetic impulses via
vagus nerve (heart)
 Sympathetic impulses via
spinal cord & peripheral
sympathetic nerves to all
arteries, arterioles, veins
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17
Q

Sympathetic Innervation of Blood Vessels

A

Arteries, arterioles, venules, veins of most tissues receive
sympathetic innervation
 Some metarterioles & precapillary sphincters of mesenteric blood
vessels innervated

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18
Q

 Most sympathetic nerve fibers are

A

vasoconstrictor (few
vasodilator)
 Vasoconstriction potent in kidneys, intestines, spleen, and skin
 Vasoconstriction weaker in skeletal muscle and brai

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19
Q

When sympathetic impulses sent to blood vessels

A

impulses
also go to adrenal medulla resulting in secretion of epinephrine
& norepinephrine

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20
Q

 Small arteries / arterioles are able

A

o change resistance / change flow through each tissue

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21
Q

Veins are Able to change

A

volume held in vessels thus changing venous return

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22
Q

Vasomotor Center - Location

A

bilateral.

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23
Q

Reticular substance

A

 Medulla

 Lower third of pons

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24
Q

Sympathetic impulses via spinal cord and periphereal

A

go to arteries arterioles and veins.Regulates amount of vascular
constriction AND cardiac
activity (i.e. heart rate &
contractility)

25
Q

Vasoconstrictor area

A

Bilateral -Anterolateral part of upper medulla
 Sends fibers to all areas of spinal cord
 Fibers excite vasoconstrictor neurons of
sympathetic system

26
Q

Vasodilator area

A

 Bilateral -Anterolateral part of lower medulla
 Sends fibers to vasoconstrictor area
 Fibers inhibit activity of vasoconstrictor area

27
Q

Sensory area

A

Bilateral in tractus solitarus in posterolateral
part of medulla & lower pons
 Receives sensory signals from circulatory
system via vagus & glossopharynegeal nerves
 Sends output to vasoconstrictor and
vasodilator areas
 Allows control of vasoconstrictor / vasodilator areas
based on input from circulatory system

28
Q

Lateral portions of vasomotor center

A

Sends excitatory impulses via sympathetic nerves to heart

[increase heart rate & contractility]

29
Q

Medial portion of vasomotor cente

A

Sends impulses to dorsal motor nuclei of vagus nerves which
sends parasympathetic impulses to heart [decrease heart
rate & some decrease in contractility]

30
Q

Vasomotor Center – Cardiac Control normally

A

increased cardiac activity is stimulated when
vasoconstriction center is stimulated
 decreased cardiac activity is stimulated when
vasoconstriction center is inhibited

31
Q

Sympathetic Vasoconstrictor Tone

A

Amount of vascular constriction is proportional to
number of impulses sent out by vasoconstrictor area
 Increase number of impulses per second – Increased
constriction
 Decrease number of impulses per second – Decreased
constriction

32
Q

Sympathetic Vasoconstrictor Tone under normal conditions

A

 Vasoconstrictor center sending 1.5 to 2.0 impulses per
second
 Results in partial constriction – normal vasomotor tone

33
Q

spinal anesthesia can block

A

blocks transmission of
sympathetic impulses
from spine to periphery

34
Q

Vasomotor Center – Control by CNS
 Reticular substance of pons, mesencephalon,
diencephalon controls

A

 Lateral / superior portions excite vasomotor center

 Medial / inferior portions inhibit vasomotor center

35
Q

Vasomotor Center – Control by CNS hypothalamus

A

 Posterolateral portions excite vasomotor center
 Anterior portion produced mild excitation or inhibition
 Depends on which part of anterior portion is stimulated

36
Q

Vasomotor Center – Control by CNS cerebral cortex

A

 Motor cortex excites vasomotor center
 Multiple areas can excite or inhibit depending on specific
area stimulated

37
Q

General Effect of Nervous Control Able to produce rapid increase in ___ which stimulates and inhibits______

A

vasoconstrictor area (sympathetic) increases cardiac activity (sympathetic) and inhibits parasympathetic vagal signals to heart

38
Q

General Effect of Nervous Control physiologic response

A

Constriction of most arterioles of systemic circulation
 Increased SVR  Increased MAP
 Strong constriction of veins / some constriction of larger
arteries
 Transfer volume from veins to arteries  Increased venous return 
Increased preload  Increased stroke volume  Increased MAP
 Increased cardiac performance
 Increased HR (major effect)  Increased CO  Increased MAP
 Increased contractility  Increased stroke volume  Increased MAP

39
Q

Baroreceptors are located

A 
in walls
of most large arteries of the
thorax and neck regions. Many located in wall of the
internal carotid arteries above the
bifurcation (carotid bodies in
carotid sinus) and in wall of aortic
arch
40
Q

Carotid baroreceptors send

impulses

A 
via Hering’s nerves to
glossopharyngeal nerves which
carry impulses to sensory area of
vasomotor center
 Aortic baroreceptors send
impulses to vasomotor center via
vagus nerves
41
Q

Baroreceptors Response to Pressure

A 
Carotid receptors not
stimulated until
pressure 50 to 60
mmHg
 Aortic receptors not
stimulated until
pressure 80 to 90
mmHg Receptors produce
greater response when
pressure changing
(could be twice the
response)
 Stimulates changes in
vascular resistance and
cardiac performance
42
Q

Baroreceptors and Long Term Control

A

Some controversy in terms of their importance
 If pressure changes and remains at new level,
baroreceptors will RESET to new level
 Takes 1 to 2 days
 Will produce normal rate of impulse generate at the
“new” pressure
 Happens no matter which way the pressure changes
 Long term, may mediate changes in sympathetic
tone to the kidneys
 Increased pressure  mediate decreased sympathetic
tone to kidneys  promotes increases sodium and
water excretion

43
Q

chemoreceptors sensitive to and located in

A

lack of oxygen and excess carbon dioxide and
hydrogen ions
 Location
 Carotid bodies (2) in bifurcation of each common carotid artery
 Aortic bodies (1 to 3) adjacent to aorta

44
Q

chemoreceptors excite

A

nerve fibers that pass through Hering’s nerves and vagus

nerves to vasomotor center

45
Q

CHEMORECEPTORS :Nutrient artery to each body

A

ensures good supply of blood to
sample
 Decreased flow through artery causes decrease in oxygen and an
increase in carbon dioxide and hydrogen ions.
Impulse generation increases with decreased flow through
nutrient artery which results in excitation of vasomotor center
 Increased impulses from chemoreceptors EXCITE the
vasomotor center
 Kick in when pressure falls below 80 mmHg

46
Q

CNS ISCHEMIC REPSONSE

A

DIRECT RESPONSE OF VASOMOTOR CENTER DUE TO ISCHEMIA. VERY POWERFUL!!!!! INCREASE BP TO 250. CUTS OFF FLOW TO LESS IMPORTANT TISSUE LIKE KIDNEYS. INITIATED AT 60 RREACHES GREATEST STIMULATION AT 15-20

47
Q

Atrial / Pulmonary Stretch Receptors

 Located

A

in walls of atria and pulmonary arteries
 Low-pressure receptors – similar to baroreceptors of
large systemic arteries

48
Q

Atrial / Pulmonary Stretch Receptors MINIMIZE

A

changes in arterial pressure due to sudden

changes in blood volume

49
Q

Atrial Reflexes and the Kidney (A) PATHWAY

A

Increased atrial stretch  Reflex dilation afferent
arterioles of kidney
 Reflex dilation afferent arterioles  Increased glomerular
capillary pressure
 Increased glomerular capillary pressure  Increased
glomerular filtration
 Increased glomerular filtration  Increased urine output
 Increased urine output  Decreased circulating blood
volume
 Decreased circulating blood volume  Decreased venous
return and decreased cardiac output

50
Q

Atrial Reflexes and the Kidney (B PATHWAY

A

Increased atrial stretch  Signals hypothalamus to
produce less antidiuretic hormone (ADH)
 Decreased concentration of ADH  Decreased
reabsorption of water from renal tubules
 Decreased reabsorption of water  Increased urine
output
 Increased urine output  Decreased circulating blood
volume
 Decreased circulating blood volume  Decreased
venous return and decreased cardiac output

51
Q

Bainbridge Reflex

A

Increase in atrial pressure causes an increase in heart
rate
 Part of the response due to direct stretch of the sinus
node (can increase heart rate up to 15%)
 An additional 40 to 60% increase caused by
Bainbridge reflex

52
Q

BAINBRIDGE REFLEX

A

Increased atrial stretch  Increased impulses via vagus
nerves to medulla
 Increased impulses to medulla  Increased sympathetic
impulses to heart increasing heart rate and contractility

53
Q

Respiratory Waves

 Change in arterial pressure

A

of 4 to 6 mmHg during each

inspiration/expiration cycle

54
Q

Change in arterial pressure INSPIRATION

A

Pressure in thoracic cavity becomes more negative
 Blood vessels in chest expand
 Expansion of blood vessels decreases venous return which decreases
cardiac output and arterial pressure

55
Q

CHANGE IN ARTERIAL PRESSURE EXPIRATION

A

 Pressure in thoracic cavity becomes positive
 Blood vessels in chest constrict
 Constriction of blood vessels increases venous return which increases
cardiac output and arterial pressure

56
Q

 Signals from respiratory center spill over

A

into vasomotor center

57
Q

Pressure changes in thoracic vessels due to inspiration/expiration can

A

stimulate the vascular and atrial stretch receptors

58
Q

Vasomotor Waves

A

Possible to see slow oscillation in arterial pressure
waveform of 10 to 40 mmHg
 Cycle duration is approximately 7 to 10 seconds

59
Q

Oscillation Baroreceptor / Chemoreceptor reflexes:

A

Increased pressure produces increased baroreceptor
response which produces vasodilation (etc.) which
causes the pressure to fall. The decreased pressure
causes a decrease in baroreceptor response which
produced vasoconstriction (etc.) which causes the
pressure to rise. Creates a cycle of pressure oscillations

Physiology (27 decks)

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