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Physio > Regional Circulations > Flashcards

Regional Circulations Flashcards

1
Q

Coronary circulation

A

Heart has high resting blood flow (70-80 ml/min/100g)
. Max cardiac work: 300-400ml O2/min/100g
. Heart has high capillary density (1 capillary per myocyte) resulting in large SA for exchange and short diffusion distances
. Myocardial blood flow has almost complete O2 extraction (70-75%) from blood across coronary capillaries
. Blood flow must inc. to inc. O2 delivery to heart (flow-limited)
. Aortic pressure provides driving force for coronary blood flow

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2
Q

What type of control is very strong in coronary circulation?

A

. Metabolic control

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3
Q

Functional or active hyperemia in coronary blood flow

A

. Primary determinant of flow is myocardial O2 consumption (MVO2) dependent on metabolic activity
. Myocardial O2 consumption influenced by cardiac pressure development, wall tension, HR, CO, inotropic state, pre and afterload
. Adenosine important metabolic vasodilator
. Opening of kATP channels when ATP levels dec. causes hyperpolarization and NO release causing vasodilation
. Exhibits reactive hyperemia and adenosine is important mediator of this

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4
Q

Autoregulation of coronary blood flow

A

. Flow constant at perfusion pressures from 60-150 mmHg
. Curve of blood flow vs perfusion pressure elevates at elevates MVO2 like during exercise to allow coronary blood flow to stay elevated during exercise
. Autoregulatory capacity important in maintaining flow when vessels are partially obstructed

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5
Q

Neural control of coronary circulation

A

. Minor compared w/ local control
. Coronary sympathetic vasoconstrictor fibers have tonic activity via alpha1 adrenoreceptors
. Net effect of sustained sympathetic stimulation of heart is to inc. coronary blood flow due to inc. in production of metabolic vasodilators w/ inc. O2 consumption (SNS also inc. HR and contractility)
. Parasympathetic cholinergic fibers trigger dilation of coronary resistance vessels via endothelial release of NO
. Net effect parasympthaertic stimulation may be reduced coronary blood flow from dec. HR and O2 consumption

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6
Q

What vessels in coronary blood flow are mostly responsible for autoregulation?

A

Pre-arterioles

. Extramyocardial and are not exposed to myocardial metabolites

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7
Q

What blood vessels are responsible for metabolic regulation in coronary circulation?

A

. Arterioles

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8
Q

Extravascular compression effect on coronary blood flow

A

. Coronary vessels subject to compressive forces w.in wall of myocardium (intramyocaridal pressure)
. Greater in systole, esp. for endocardium in LV
. Effect bigger in endocardium bc it is subject to higher pressures than epicardium
. In endocardium blood flow occurs mostly in diastole
. Epicardium received more blood in systole than endocardium
. Compressive forces less marked in RV due to smaller muscle mass and lower pressure development

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9
Q

Response to obstruction of coronary blood flow

A

. Sudden obstruction (clot) causes severe ischemia and acidosis
. Result is angina and impaired contractility and death of affected cardiac m. Cells if flow not restored
. Slowing developing partial obstruction due to progressive atherosclerotic disease in larger coronary aa. Results in metabolic vasodilation (autoregulation) of resistance vessels distal to obstruction to maintain flow near normal at rest
. During stress, further dilation is not enough to meet metabolic needs resulting in ischemia and angina

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10
Q

Under normal conditions, coronary blood flow is primarily regulated by ___

A

. vagal innervation of coronary vasculature
. Sympathetic innervation of coronary vasculature
. Metabolites released from cardiac cells
. Accentuated antagonism

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11
Q

Skeletal muscle circulation

A

. Large mass of tissue (40-45% body weight)
. At rest gets 20% CO, during exercise gets 80-85% CO
. Resistance vessels have high resting tone
. TPR is greatly influenced by resistance in skeletal m. Circulation

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12
Q

Neural control of skeletal m. Vasculature

A

. Done by sympathetics
. Dominates at rest via alpha 1 and 2 adrenergic receptors
. Inc. in SNS can drastically. Dec. blood flow (particular at rest in absence of metabolic vasodilation)
. Vasodilation at rest will occur upon withdrawal of SNS activity

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13
Q

Functions hyperemia in skeletal m. Circulation

A

. At rest SNS controls vascular tone (constriction), blood flow is low, and metabolic regulation is relatively small
. During exercise there is inc. O2 demand, SNS activity still present BUT flow inc. greatly duper to metabolic vasodilation
. SNS tone necessary to avoid excessive reduction in TPR

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14
Q

Potential mediators of vasodilation in skeletal m. Circulation

A

. Endothelial flow-mediated vasodilation-NO, prostaglandins
. Interstitial acidosis/hypoxia and high levels of CO2
. High interstitial K
. Adenosine
. Elevated temperature

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15
Q

Hormonal effect on skeletal m. Circulation

A

. Circulating E dilates circulation at low conc. Via beta2-adrenergic receptors
. Constricts at high conc. Via alpha1/2 adrenergic receptors

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16
Q

Muscle pump

A

. Cyclical contraction and relaxation of active skeletal mm. Vessels
. Vessels compressed during contractions nd venous blood is pushed to heart
. Pumping action lower venous pressure which inc. pressure gradient driving flow so when mm. Relax the high pressure gradient inc. flow into active mm.
. Adds kinetic energy to venous blood that aids in returning blood to heart (aids venous return)

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17
Q

Splanchnic circulation

A

. Intestinal/pancreas/spleen/liver
. Gets 25% CO at rest and can inc. by 30-100% after a meal
. Livers contains 15% blood volume at rest and half can be rapidly expelled into systemic circulation via SNS stimulation of venous vessels
. Venous drainage from capillary bed of GI tract, spleen and pancreas flows into portal vein that provides most of blood flow to hepatic circulation
. Hepatic a. Provides remainder flow to liver
. Contains high compliance venous system that acts as reservoir for venous blood (esp. in liver)

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18
Q

Sympathetic control of splanchnic of blood flow

A

. Innervates arterioles and venous capacitance vessels
. Little to no basal SNS tone
. Inc. in SNS activity results in strong vaso and venocontriction
. Strong venoconstriction mobilizes venous volume (during exercise, in response to low bp)
. Vasoconstriction redistributes arterial flow away from intestinal organs (exercise, response to low bp)

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19
Q

Parasympathetic effect of splanchnic blood flow

A

. No direct innervation of blood vessels
. Does innervate enteric nervous system that affects GI motility
. Inc. PNS activity -> inc. motility -> inc. metabolism
. Results in functional hyperemia due to inc. production of local vasodilator metabolites

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20
Q

Autoregulation of splanchnic circulation

A

. Poorly developed

. Metabolic mechanisms dominate

21
Q

Functional hyperemia in splanchnic circulation

A

. Local metabolic control
. Very important
. Good in GI tract inc. intestinal activity followed by inc. in blood flow
. Absorption of food also inc. blood flow

22
Q

Hormonal control of splanchnic circulation

A

. GI hormones cause hyperemia

23
Q

Cutaneous circulation

A

. Regulates internal temp and bp control
. Receives 6% CO at rest, can dec. by 50% to retain heat or inc. 7-fold to lose heat
. Up to 25% of elevated CO can be sent to skin circulation during heavy exercise in heat
. Control both locally in response to temperature ad via reflex (neural) mechanisms

24
Q

Apical skin

A

. Non-hairy/glabrous skin
. In areas of high SA to volume ratio where rate of heat loss/gain is rapid
. Nail bed, palmar surface of hands, soles of feet, ear, lips, nose
. Presence of arteriovenous anastomoses (AVAs)

25
Q

Non-apical skin

A

. Hairy
. Non-glabrous skin
. Covers most of body surface

26
Q

Arteriovenous anastomoses

A

. In apical skin
. Provide direct connections btw dermal arterioles and venous plexus (skips capillaries)
. Provide low resistance shunt pathways when open
. Little intrinsic basal tone
. Little metabolic control (no autoregulation or reactive hyperemia)
. SNS vasoconstrictor innervation has exclusive control, has strong tonic activity
. Vasodilation occurs due to withdrawal of resting SNS activity as initiated by hypothalamus (for thermoregulation/heat loss)
. Cooling further inc. SNS activity and dec. blood flow

27
Q

Apical skin control of blood flow

A

. Arterioles, veins, AVA innervated by alpha-adrenergic receptors causing vasocontriction
. SNS active in thermoneutral conditions to keep blood flow low in this area at rest
. Body cooling: SNS activity inc. and vasocontriction occurs via NE (alpha-adrenergic) and cotransmitter neuropeptide Y and its receptor
. Body heating: SNS activity dec., partially constricted vessels dilate and flow inc. (passive vasodilation)

28
Q

Non-apical skin control of blood flow

A

. Major difference is addition of sympathetic cholinergic control of blood flow
. SNS cholinergic is prominent to sweat glands via activation of muscarinic receptors
. Activation of cholinergic nn. Results in active vasodilation
. SNS adrenergic nn. Also innervate arterioles and vv. In non-apical skin but are less active in thermoneutral conditions compared w/ apical skin (depends more on active vasodilation than passive), activation causes vasoconstriction

29
Q

How active vasodilation occurs via cholinergic nn. In non-apical skin

A

. ACh actis via muscarinic receptors on endothelial cells to produce NO to vasodilator
. Vasoactive intestinal peptide (VIP) is co-released and causes vasodilation
. Histamine, substance P, and prostaglandins are mediators that result in active vasodilation to allow blood flow to inc. and heat transfer to occur

30
Q

Body cooling in non-apical skin

A

. Activate SNS adrenergic nn. To cause vasocontriction
. Reduces blood flow and blood volume in skin
. Reduced heat loss to environment

31
Q

Body heating in non-apical skin

A

. Hypothalamus initiates Activation cholinergic nn. To cause active vasodilation
. Inc. blood flow and volume in skin to facilitate sweating and loss of body heat to environment
. Sympathetic cholinergic nn. Stimulate sweating which triggers evaporative loss to environment

32
Q

Skin response Cold local temperature

A

. Causes direct vasoconstriction through NO inhibition AND reflex vasoconstriction
. Begins when skin temp is under 35 C and max when skin temp is 31 C
. Reflex vasoconstriction: activation of cold thermal receptors in skin and temp. Of cooled blood are sensed by hypothalamus, initiated inc. in SNS adrenergic activity to skin
. Local cooling inc. number of alpha2-adrenergic receptors on cutaneous smooth mm.
. Shivering inc. metabolic heat production

33
Q

Skin response to warm local temperature

A

. Local warming causes vasodilation via direct effect on cutaneous vessels (NO important mediator)
. Also activates warm thermal sensory receptors (appears as axon reflex) causing local release of neural mediators like substance P or calcitonin gene related peptide (CGRP) to get vasodilator response
. Reflex withdrawal of SNS adrenergic and activation of SNS cholinergic vasodilator nn.
. Sensory info from warm receptors is transmitted to hypothalamus and initiates vasodilator response

34
Q

Central hypothalamic control and skin blood flow

A

. Hypothalamus senses core body temp. And skin temp.
. If too high, hypothalamus withdraws SNS adrenergic activity, activates SNS cholinergic activity to skin to inc. flow and heat loss
. If core temp. Is too low, SNS adrenergic to skin inc.

35
Q

Hypotension in cutaneous circulation

A

. Low by sensed by internal baroreceptors
. Reflex cutaneous vasoconstriction occurs w/ a dec. in bp due to activation of SNS
. Supports TPR and venous return
. Plays role in compensating for acute dec. in bp during heat stress when flow to skin is elevated due to thermoregulatory factors

36
Q

Heat effect of CO to cutaneous circulation

A

. Progressive inc. of CO sent to skin for thermo purposes can affect cardiovascular homeostasis during exercise
. Cutaneous venous circulation is high compliance and can hold up to 30% of CO at the expense of central venous blood volume (cardiovascular drift/strain)

37
Q

Heat and exercise effect on cutaneous circulation

A

. High skin blood flow, compliant skin vessels, loss of BV through sweating results in dec. central venous volume, filling of heart, and dec. exercise SV
. HR inc. in attempt to maintain CO
. Further SNS vasoconstriction will divert more blood away from visceral organs as compensatory mechanism
. In severe heat stress and intense exercise, the CO may be below levels seen during exercise at temperate places compromising skin and muscle blood flow so exercise performance dec.
. Arterial bp can dec. leading to syncope
. Reduced skin blood flow and resultant reduced heat dissipation can result in heat disorder

38
Q

Cerebral circulation

A

. Least tolerant to ischemia: dec. flow for 5s causes loss of consciousness, dec. flow for a few min. Causes irreversible damage
. Gets 15% CO at rest (750 ml/min)
. During moderate exercise global cerebral flow inc. and returns to baseline during vigorous exercise
. Extracts 35% O2 at rest, accounts for 20% of resting total body O2 consumption despite being 2% of body weight
. Excellent at autoregulation
. Blood flow to regions of brain can vary based on neural activity

39
Q

Notable anatomic characteristics of brain

A

. Cerebral circulation enclosed by skull of constant volume
. Brain floats in CSF
. High capillary density causing larger SA and short diffusion distances
. BBB: tight junctions btw endothelial cells that prevent many circulating factors from leaving vascular space and entering interstitial space
. Easily diffuses gases and water
. Facilitated diffusion of glucose
. Poorly diffuses everything else

40
Q

Driving pressure for cerebral blood flow

A

. Pressure gradient of cerebral perfusion pressure = MAP - intracranial pressure (ICP under 15 mmHg usually)
. ICP represents cerebral venous pressure and CSF pressure
. If ICP inc. too much perfusion of brain will dec.

41
Q

. Sympathetic control of cerebral blood flow

A

. SNS innervation, but little tonic influence on cerebral vascular resistance
. Metabolic control, response to CO2, and autoregulation dampen effect of SNS activity
. Max. SNS activity causes only small vasoconstrictor response
. Inc. in SNS activity may prevent hyperperfusion during acute inc. in MAP

42
Q

Arterial PCO2 effect on cerebral blood flow

A

. Hypercapnia (inc. PCO2) -> dilation and inc. blood flow
. Hypocapnia (dec. PCO2) -> constriction and dec. blood flow potentially causing dizziness/lightheadedness
. CO2 also released into CSF from active neurons
. CO2 diffuses from blood into brain ECF/CSF and results in extracellular acidosis
. Inc. in interstitial H+ causes vasodilation
. Dec. arterial pH w/o high CO2 (metabolic acidosis) has little effect bc H+ does not cross BBB

43
Q

Arterial PO2 effect on cerebral circulation

A

. Normal 80-100 mmHg
. O2 diffuses easily from blood to cerebral ECF
. Hypoxia (under 40-50 mmHg) -> dilation due to adenosine release form hypoxia brain
. Hyperoxia (over 100 mmHg) -> little effect on vascular status

44
Q

Potassium effect on cerebral circulation

A

. Inc. K from seizure or hypoxia -> vasodilation
. Transient effect and is not responsible for prolonged vasodilation
. Small inc. in extracellular K activates membrane K-activated K channels and hyperpolarizes vascular smooth muscle relaxing them

45
Q

Adenosine effect on cerebral circulation

A

. Inc. interstitial adenosine conc. Occurs w/ hypoxia, ischemia, dec. perfusion pressure, inc. metabolic activity, and dec. O2 supply/demand ratio
. Vasodilation parallels inc. in adenosine conc.

46
Q

NO effect on cerebral circulation

A

. synthesis occurs in vascular smooth muscle under basal conditions
. Has tonic vasodilator effect

47
Q

Autoregulation of cerebral circulation

A

. Autoregulatory capacity from 50-170 mmHg
. Has myogenic and metabolic components
. High CO2 or other metabolic vasodilator will modulate degree of autoregulation
. Cerebral perfusion pressure is too low, syncope results
. Cerebral perfusion pressure too high resulting in cerebral edema

48
Q

CNS ischemic response

A

. Is cerebral perfusion pressure dec. below autoregulatory range (MAP-ICP less than 50 mmHg) then medullary vasomotor center becomes ischemic
. Result is inc. in SNS vasoconstrictor activity to systemic resistance vessels inc. TPR which Inc. MAP and inc. pressure gradient and cerebral blood flow
. HR response can be variable
. Rapid onset cerebral ischemia assoc w/ tachycardia which overtime progresses to persistent bradycardia

49
Q

Cushing’s reflex

A

. Tumor/lesion inc. ICP, may involve direct brainstem compression
. Cerebral perfusion dec. and brainstem becomes ischemic
. Results in inc. SNS vasomotor drive to systemic resistance vessels
. Inc. TPR, MAP, causing inc. pressure gradient and inc. cerebral blood flow
. Rapid rise in ICP and rapid dec. inn cerebral perfusion is more likely assoc. w/ tachycardia
. Cushing’s triad: systemic hypertension, bradycardia, and respiratory depression: ominous sign from sudden ICP inc., normalizes after ICP is lower

Physio (62 decks)

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