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Physiology > Cardiovascular Regulation > Flashcards

Cardiovascular Regulation Flashcards

1
Q

Regulatory mechanisms

A

Pressurecontrol
Local
Nervous
Humoral

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2
Q

Acute control

A

Local
Fast blood flow changes
S-min
Vasodilation or vasoconstriction

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3
Q

Long term control

A

Local
Slow blood flow changes
Days-months
Change in size and numbers of vessels

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4
Q

Vasodilator theory

A

Increase in metabolism/O2 consumption leads to release of vasodilators that increase blood flow
Increase8 in metabolism=4 increase in acute blood flow

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5
Q

O2-lack theory

A

Low O2 in tissues leads to vasodilation and increase in local blood flow
Means that O2 keeps smooth muscles contracted, when O2 is low they dilate
25% O2 saturation=3* acute blood flow

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6
Q

Myogenic regulation

A

Not related to metabolism
Pressure stretches walls=constriction
Low stretch of walls=dilation
High AP=sudden big stretches of small vessels=vasodilation=decrease of blood flow
Low AP=little stretch of small vessels=vasodilation=increase of blood flow

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7
Q

Endothelial Regulation

A

Increased velocity leads to release of NO (inhibitory)= vasodilation=decreased velocity in blood flow

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8
Q

Nervous control

A 
ANS
SNS main regulator for circulation
Redistribution of blood flow
Regulation of heart activity
Rapid control of atrial pressure
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9
Q

When SNS senses high AP

A

Arteriol and vein constriction
Increase heart rate and contractility
Vasomotortone regulated by norepinephrine

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10
Q

Where is cardioregulatory and vasomotorcenters located

A

Medulla oblongada

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11
Q

Excitatory effect

A

Alpha-adrenogenic receptors (noradrenaline+adrenaline)

Vasomotortone/vasoconstriction

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12
Q

Inhibitory effect

A

Beta-adrenergic receptors in skeletal muscle

Stimulates vasodilation by adrenaline

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13
Q

Parasympathetic NS

A

Only important in heart beat frequency

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14
Q

Humoral control

A

By sybstances set reread/absorbed in body fluids

Pressurecontrol-vasoconstriction/vasodilation

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15
Q

Humoral effects on vasoconstriction

A

Norepinephrine/epinephrine
Angiotensin II
vasopressin/ADH
Endothelin A

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16
Q

Humoral effects on vasodilation

A

Bradykinin
Histamine
Prostaglandins

17
Q

Ions effecting vasodilation/constriction

A 
Ca++- constriction
K+- dilation
Mg++- dilation (often inhibiting Ca++)
H+- when increase=dilation, when decrease=constriction
Anions- dilation
CO2- dilation
18
Q

Short term AP-regulation

A

Recovers pressure quickly
Limited time of action
ANS via baroreceptors, chemoreceptors
CNS ischemic response

19
Q

Medium term AP-regulation

A

When AP is not recovered by short term
Endocrine/humoral mechanisms
Effective for hours

20
Q

Long term AP-regulation

A 
Can act for hours-months
Renal activity (RAAS)
21
Q

Baroreflex

A

Baroreceptors in aortic arch+carotid sinuses
Senses increase in AP-sympathetic and parasympathetic fibers-vasodilation and decreases HR
Signals also sent by SNS to adrenal medulla- releases of epinephrine+norepinephrine

22
Q

Chemoreceptors reflex

A

Receptors in carotid body+aortic body
Senses levels of chemicals-signals to medulla oblongada
Sympathetic and parasympathetic response

23
Q

CNS ischemic response/Cushing reflex

A

Decreased blood flow to vasomotorcenter and high CO2
Very strong sympathetic stimulation=increase in vasoconstriction and HR
emergency system

24
Q

Bainbridge reflex/atrial reflex

A

Stretch receptors in atrial wall
Activated when preload or AP is increased
Increases HR
Opposite effect of baroreflex

25
Q

Long term regulation of AP by kidneys

A 
Control level of H2O, NaCl
Controlling volume of EF and blood
Control of AP
When AP is high- pressure diuresis or pressure naturesis keeps AP constant 
Hormone based-RAAS
26
Q

2 systems of kidney control

A

RAAS- when high blood pressure, most important hormonal cascade in control of AP, tissue perfusion, EC volume

Atrial natiuretic peptide ANP- when blood pressure decrease ANP secreted by atria=decreasing BP by stimulation Na+H2O excretion by kidneys

Physiology (13 decks)

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