B4-004 Cardiovascular Control Mechanisms Flashcards by Felicia Jones

3 reasons for changing blood vessel diameter

to change local blood flow
to change TPR
to change CO

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changes in local blood flow allow for discrete arterial dilation such as

GI vasodilation during a meal
erection

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local arterial dilation [….] resistance, so local flow is […]

decreases; increased

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results in no significant change in TPR or MAP

change to local blood flow

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TPR is determined by

arterial blood vessel diameters in vascular beds

mainly renal, GI, and skeletal muscle

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changing TPR can compensate for

changes in aterial pressure due to standing or blood loss

causes reduced blood to brain

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MAP=

CO x TPR

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if TPR is increased by arterial vasoconstriction and CO stays the same, MAP will

increase

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do increases in TPR normally decrease CO?

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veins and venules store about […] of total blood volume

2/3

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because the heart is a Starling pump, increased venous return increases

cardiac output

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venous smooth muscle contractions return

blood to the heart

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increased venous return and cardiac output will increase…

MAP

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innervate arterial and venous smooth muscle

vasomotor nerves

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only relevant constrictor nerves

sympathetic nerves

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sympathetic noradrenergic nerves only

constrict

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excite vascular smooth muscle by NE acting on a1 receptors

sympathetic nerves

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increase MAP by increasing TPR

sympathetic nerves

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increase MAP by increasing venous return

sympathetic nerves

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induce discrete dilation via NO

parasympathetic nerves

won’t affect TPR under normal conditions

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level of activity of nerves and targets

tone

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determined by the balance between vasoconstrictor influences and vasodilation influences

vascular tone

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determined by concurrent dischange of excitatory sympathetic and inhibitory parasympathetic nerves

cardiac tone

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heart rate is increased by […] sympathetic discharge and/or […] parasympathetic discharge

increasing; decreasing

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to change blood pressure/output, change

cardiovascular tone

when horizontal, the body is [...] hydrostatic column

20cm

in upright position, hydrostatic column is

180 cm

as a result of increased hydrostatic pressure, veins in lower body | standing

distend leading to venous pooling

[...] mL of blood is lost from venous return in the first few minutes after standing

700

decreased venous return leads to

decreased cardiac output, which leads to decreased MAP

arterial pressure below [...] is insufficent to maintain neural activity

90/60 mmHg

result of lost somatic motor control due to diminshed cardiac output

syncope

when cardiac output is diminshed, arterial blood pressure can be maintained by

arterial vasoconstriction venoconstriction increased cardiac tone

sympathetic contraction of venous smooth muscle reduces

compliance and capacitance, forces blood back to heart

arterial vasoconstriction increases TPR, leading to

increased MAP

venoconstriction causes increased CO, leading to

increased MAP

by increasing cardiac sympathetic tone and decreasing vagal parasympathetic tone, heart rate and force of contraction

increase, making the heart a more effective pump

increased cardiac tone leads to increased

stretch receptors located on vessel walls that tell the brain to modulate autonomic CV tone

baroreceptors

measure venous return

cardiopulmonary baroreceptors

located in right atria, vena cava, and pulmonary vessels

cardiopulmonary baroreceptors

"low pressure" receptors

cardiopulmonary baroreceptors

located in aortic arch and carotid sinus

arterial baroreceptors

assess blood flow to entire body and brain

arterial baroreceptors

"high pressure" receptors

arterial baroreceptors

decreased MAP leads to [...] baroreceptor stretch

decreased

decreased baroreceptor stretch leads to

decreased vagal/glossopharyngeal afferent nerve firing

decreased afferent axon firing leads to

decreased firing in nucleus of tractus solitarius

decreased firing in nucleus of tractus solitarius leads to

decreased stimulation of preganglionic cardiac parasympathetic axons in DMV and NA

decreased stimulation of preganglionic cardiac parasympathetic axons in DMV and NA leads to

decreased cholinergic inhibition of the heart

decreased firing in NTS leads to

decreased inhibition of C1

decreased inhibition of C1 leads to

firing of sympathetic nerves to the heart and vasculature

baroreflex activates the SNS **without**

large effects on adrenomedullary secretion

baroreflex selectively increases resistance in which arteriolar beds?

* renal * splanchnic * cutaneous * skeletal muscle

primary mechanism maintaining MAP under normal conditions

baroreflex

nerves are "buffer nerves" | if cut, more variablity in BP, but no significant change in set point

baroreflex

the baroreflex can be overridden by what?

pain and emotions

* mainly involved in respiration * active when MAP falls below 60 mmHg * detects low O2 in carotid and aortic body

chemoreflex

* reduced perfusion of the medulla * results in discharge of C1 * final line of defense to restore MAP and CO

central ischemic response

when ICP is abnormally high, cerebral vessels collapse, brain perfusion stops and CIR is initiated, this is called?

cushing reaction

inability to compensate for reduced CO associated with upright posture

orthostatic hypotension

orthostatic hypertension can be caused by:

* CNS diseases * postganglionic axon degeneration * degeneration of postganglionic sympathetic neurons

* variant of orthostatic hypotension * characterized by rapid heart rate, dizziness and fatigue

POTS

abnormal sensitivity of the carotid sinus baroreceptors to touch or stretch

carotid sinus syndrome

slight pressure to the neck is perceived as high blood pressure, leading to vagal slowing of heart and fainting

carotid sinus syndrome

abnormally robust response to emotional stimuli leading to withdrawal of vasomotor tone and vagal parasympathetic activation

vasovagal syncope

may be a vestige of an adaptive response for dealing with danger | playing dead

vasovagal syncope

represent short term regulator mechanism

nerves

represent intermediate-term effects

circulating hormones

represent long term regulatory effects

factors effecting volume

* released into circulation * augments sympathetic nervous system during "fight or flight"

epinephrine

* activates all adrenoreceptors, including b2 receptors * elicitis skeletal muscle vasodilation

epinephrine

adrenomedullary catechloamine release is not strongly affected by

baroreceptors

exerts intermediate CV control via baroreceptor mediated release

ADH

potent vasocontrictor for both arterioles and veins

ADH

increases plasma volume by reducing urine output

ADH

increased by diminished renal blood flow and sympathetic activation

plasma renin (Ang II)

intermediate effects on CV control via direct action on arteriolar smooth muscle

Ang II

mediates long term volume increases by directly suppressing urine formation and indirectly by causing aldosterone release from adrenal cortex

Ang II

augments NE release from sympathetic varicosities

Ang II

stored in atrial myocardial cells

ANP

elicited by increased plasma volume causing atrial stretching

ANP

acts on kidney to induce sodium excretion into the urine to reduce plasma volume and blood pressure

ANP

if sympathetic neurons are compromised what key function is lost?

vasoconstriction --> decreased TPR

# after taking the drug: * cardiac output is increased * total peripheral resistance is unchanged * central venous pressure is increased * heart rate is unchanged | what kind of drug?

mineralcorticoid like volume expander

an Alpha 1 adrenoreceptor agonist would increase

TPR

a beta 2 adrenoreceptor agonist would decrease

TPR

# what kind of drug? will decrease * cardiac output * TPR * central venous pressure.

ganglionic blocker

* lost sensation in hands/feet * does not sweat * becomes light headed standing rapidly

elevated ADH

sympathetic innervation to the kidney is the major means for

increasing TPR

expansion of plasma volume will result in what hormone changes?

* decreased Ang II * increased ANP * decreased epi * decreased ADH