Circulation 9: Special Circulations III Flashcards
Describe skin blood flow in a normothermic person. (Skin blood flow, CO, how skin blood flow can vary)
In a normothermic person, total skin blood flow is about 300-500 ml/min. or about 5-10% of the cardiac output. However, skin blood flow can vary from near 0 (in cold) to >7 liters/min (heat stress).
The oxygen and nutrient requirements of the skin are relatively small. Skin blood flow far exceeds nutritive requirements.
Which is more important in skin blood flow; neural control or local metabolic control?
neural. almost completely sympathetic
What is the primary function of cutaneous circulation? How is this achieved?
Describe its function in regards to heat loss.
The primary function of the cutaneous circulation is to maintain a constant body temperature. This function is achieved by providing convective transport of heat to the body surface for exchange with the environment. (far more blood flow than you need than to just provide nutrients. its more the regulation of temperature.)
The cutaneous vasculature is more efficient at promoting heat loss than it is in preventing heat loss. Skin blood flow may increase up to 30 times with heat but decrease by only a factor of 10 with cold. Therefore, humans acclimatize better to heat than to cold. (dep. on moisture. if you’re dehydrated you don’t lose heat effectively. if you sweat too much you can lose volume. can also lose your osmolarity bc lose more water than you do Na. )
How does blood flow contribute to skin color? When will someone be pale, cyanotic, reddish, bright pink?
Blood flow contributes to skin color by the volume and degree of oxygenation of blood in the cutaneous vessels.
Low blood flow (pale); desaturated hemoglobin (cyanotic); fully saturated hemoglobin (reddish); carbon monoxide poisoning (bright pink).
Why can skin also appear red in cold weather even though blood flow is low due to vasoconstriction?
(What does low temp do the dissociation of O from hemoglobin)?
In cold climates, the skin may also appear red (nose, ears and rosey cheeks) even though blood flow is low due to vasoconstriction.
Low temperature in the tissues decreases the dissociation (unloading) of oxygen from hemoglobin, resulting in more oxyhemoglobin, which gives arterial blood its red color.
gonna appear more red bc of the O hemoglobin dissociation which is low. have more O associated w hemoglobin in those conditions
apical skin- these are anastomoses-curled area (Slide 7). allows lots of blood flow to skin or prevents heat loss in conservation of heat-whichever way it goes. again this is why these tissues red bc holding onto O more under cold conditions. (nose toes fingertips ears)
What are the two types of resistance vessels that the skin contains?
How are they controlled? Sympathetic/Local metabolic? Basal tone?
arterioles – some basal tone; controlled by both sympathetic nerve activity and local regulatory factors.
arteriovenous (AV) anastomoses - shunts blood from the arterioles to venules and venous plexuses, bypassing the capillary beds. Exclusively under sympathetic neural control (rather than local metabolic control). No basal (non-neural) tone; no metabolic control; no reactive hyperemia or autoregulation.
In terms of blood flow there are 2 types of skin. Describe apical/non-apical.
Where present? Do they contain AV anastomoses? How innervated?
What 2 things distingush nonapical from apical?
Apical - Present on the nose, lips, ears, fingertips, hands, and feet.
High surface-to-volume ratio that favors heat loss.
Contains specialized AV anastomoses called glomus bodies that helps facilitate heat loss. (arteriovenous anastomoses-are basically shunts and they’re either vasodilated, or vasoconstricted. used for heat loss or heat conservation (dep. on if constricted)
Nonapical - Present in the rest of the body. Two features distinguish nonapical from apical skin.
Almost completely lacks AV anastomoses.
Innervated by sympathetic fibers that release acetylcholine (postganglionic) that produce active vasodilation. innervating sweat glands. cause release of bradykinin which is a vasodilator. sweating in non apical skin.
Which type of skin sweats?
nonapical
Compare the basal tone of skin to basal tone of muscle. What are the implications of this?
Graph.
Slide 5.
talking about arterioles, basal tone. basal tone of skin much lower than basal tone of muscle. can vasodilate much more than musculature of skeletal muscle system. Makes sense bc designed to get rid of heat. so can open up more.
(Basal Tone: Theoretical reference point. Amount of vascular contraction found under resting conditions without neural or hormonal (extrinsic) influences. )
Describe neural control of apical skin.
Arterioles, AV anastomoses and venules receive innervation by sympathetic adrenergic nerves.
At rest, reflex stimulation produces vasoconstriction of cutaneous vessels. Withdrawal of sympathetic nerve activity produces passive vasodilation.
neural control of apical skin is actively vasoconstrict or passively vasodilate. by far its pre-capillary arterioles and AV anastomoses.
Describe neural control of nonapical skin.
In addition to sympathetic vasoconstriction (norepinephrine), this tissue exhibits active vasodilation elicited by sympathetic cholinergic fibers through a sweat-dependent release of bradykinin.
nonapical skin. symp. chol. release Ach on post-ganglionic fibers. activates rel. of bradykinin from sweat glands. causes vasodilation.
When someone is completely white during hypovolumic shock, what has happened?
hypovolumic shock..go into baroreceptor vasoconstriction. closes off blood flow to skin. skin is white.. completely vasoconstricted, no blood flow to skin.
not just matter of temp. regulation. skin also responds along w other symp. responses in body
Describe the reflex control as it pertains to temperature regulation.
What controls temperature regulation?
What will increases and decreases in internal temperature lead to?
When does maximum vasodilation occur?
Temperature Regulation – is primarily controlled by major sensory sites in hypothalamus and less by receptors located in the spinal cord. (core body talking about. not temp. on skin that regulates blood flow. its really core body temp. sensed by hypothalamus.)
Increases in internal temperature cause withdrawal of sympathetic nerve activity and vasodilation (increase in blood flow). Maximum vasodilation results from block of sympathetic nerve activity.
Decreases in internal temperature cause activation of sympathetic nerve activity and vasoconstriction (decrease in blood flow).
Why is it that when you exercise, sympathetic activity can be cranked up but also can sweat (vasodilate)?
core body talking about. not temp. on skin that regulates blood flow. its really core body temp. sensed by hypothalamus.
-can be exercising and symp. NS can be cranked up but bc core body temp rising, withdraw of symp. to skin are occurring at same time as rest of symp. being activated. seperate system for controlling symp. to skin.
exercising, increasing symp. nerve activity. temp goes up and want to vasodilate so hypothalamus withdraws symp. nerve activity to vascular system skin causing massive vasodilation.
Describe the effect of moderate changes in local skin temperature.
ambient temperature on skin doesn’t have much of effect.
warmer get a little bit more vasodilation but main regulator is core temp/hypothalamus.
In addition to reflex controls, moderate changes in local skin temperature are accompanied by directionally similar responses in local skin blood flow.
In a normothermic person, how do changes in cutaneous vascular resistance effect total peripheral resistance and blood pressure?
(What induces changes in cutaneous vascular resistance?)
In a normothermic person, total skin blood flow is only 5-10% of cardiac output and therefore changes in cutaneous vascular resistance induced by changes in blood pressure (baroreceptor reflex) exert only a small effect on overall total peripheral resistance and blood pressure.
In heat stress, how can total skin blood flow change?
If someone was in desert, experiencing heat stress and then shot, how will bp be affected?
However, in heat stress, total skin blood flow can approach 8 liters/min. (total cardiac output increases to 13 liters/min) or about 60% of cardiac output. Under these conditions, a decrease in blood pressure (hemorrhage) results in a significant baroreceptor-mediated vasoconstriction of cutaneous vessels (increase in peripheral resistance) that helps maintain blood pressure. However, the competing vasodilation (due to reflex temperature regulation) limits the vasoconstrictor response and blood pressure is not as well maintained compared with normothermic conditions.
if 120 outside max. vasodilated. lots of blood flow to skin, if you get shot and start bleeding have have baroreceptor response to hemorrhage, its more difficult for symp. NS to fight vasodilation that’s occurring bc of temperature to maintain bp. amount of blood to skin in heat stress does have impact to prevent baroreceptors from raising bp.
if losing blood, baroreceptors trying to maintain arterial pressure.
baroreceptors have much harder time if under heat stress.. to maintain bp bc of all blood going to skin
(rel. between diff mechanisms going on. have temp. causing vasodilation. at same time could have baroreceptors trying to cause vasoconstriction. opposing e/o.)
How will an increase in bp affect sympathetic nerve activity and skin blood flow in warm conditions?
An increase in blood pressure causes withdrawal of cutaneous sympathetic nerve activity. This has little effect on skin blood flow in warm conditions, where apical vessels are already dilated.
Describe what happens with frostbite.
Which system freezes first, venous or arterial? Why?
What are some mechanisms of frostbite injury?
Below O degrees C (32 degrees F) negligible cutaneous blood flow allows the skin to freeze.
Without circulation, skin temperature drops at a rate exceeding 0.5o C per min.
Smaller blood vessels (microvasculature) freeze before larger blood vessels.
The venous system freezes before the arterial system because of lower flow rates.
Mechanisms of frostbite injury:
Direct thermal damage to cells.
Direct cell damage from ice crystals.
Microvascular stasis, thrombus and ischemia
Reperfusion inflammatory injury
cutaneous circulation when jump into lake, squeezing really hard to try to prevent blood from going to skin to prevent heat loss.
damage membranes.. low blood flow when blood flow gets cold. get clots forming and become ischemic. thats why it hurts to get frost bite. can get re-perfusion injury. don’t just warm vessels right up … have to warm it up slowly. open up too quickly, increase in blood flow could cause metabolic damage to tissues.
Describe the competing demands for blood flow in exercise.
What happens with continued exercise in regards to initial cutaneous vasoconstriction?
Competing demands for blood flow.
Sympathetic stimulation vasoconstricts to shunt blood from skin to exercising muscle. However, internal metabolic heat production stimulates cutaneous vasodilation for heat loss. (when start to exercise before muscles metabolically active, global sympathetic activity does cut off some blood flow to skin can see that in diagram where discussed blood flow in exercise, gets smaller at first. as muscles warm up and core temp warms up you start to vasodilate.)
With continued exercise, initial cutaneous vasoconstriction converts to net vasodilation.
During exercise, skin blood flow increases with internal temperature but only to a limit, beyond which there are only small increases in skin blood flow despite further significant increases in internal temperature.
What are the things that can happen if you over-exercise? (Run a marathon and didn’t drink enough water..)
if you over-exercise, continue to exercise and can’t dissipate additional heat, then your core body temp can rise and you become hyper-thermic … go into shock. happens more quickly if not hydrated. bc ability to get rid of temp. is convective so need water to reduce body temp. if dehydrated running marathon and not drinking enough fluid can become overheated and get permanent brain damage.
What happens if you drink too much water?
if drink too much water can get neural seizure or cardiac arrhythmia and die from it. over hydrated… getting ready for marathon. over hydrate… dilute the amount of Na in blood stream, hypo-neutemic. Na in blood causes upstroke of AP, conduction blocks in heart. blood is hypo-osmotic. less solute per volume of water. as a result neural tissue starts to swell, cells take up that water…neural seizure.
Describe splanchnic circulation.
What is supplied?
How much CO supplied in resting individual?
Describe arterial and venous components.
The splanchnic circulation consists of the blood supply to the abdominal organs of digestion, including the gastrointestinal tract, liver, pancreas, and spleen.
Splanchnic organs receive ~25% of the cardiac output in a resting, fasting individual.
Arterial blood delivers O2 and metabolic substrates to the splanchnic organs.
Venous blood carries away CO2 and other metabolic by-products and nutrients that have been absorbed from the intestinal lumen.
If you go hunting in winter and sit and drink whiskey what could happen. Why?
High altidues, or
sit in woods and drink in cold weather. vasodilates you, lose body heat more quickly, hyperthermia. can die from it. foods and beverages that vasodilate, you.
lose body heat quicker at high altitudes, lower atmospheric pressure means evaporate heat. in airplane, pressurized at 8000 feet. losing more moisture due to sweat loss. have to stay hydrated… in terms of blood clots in legs. in climbing mountains, at high altitudes, do lose more moisture, do dehydrate more quickly… water boils at a lower temp. at high altitudes.
What happens if venous pressure backs up into the splanchnic region?
if venous pressure backs up into splanchnic region you have edema formation which is ascites
Describe the major vessels of the splanchnic circulation.
Celiac artery – supplies blood to stomach, spleen and pancreas.
Superior mesenteric artery (SMA) and inferior mesenteric artery (IMA) supplies small and large intestines with branches to stomach and pancreas.
The superior and inferior mesenteric arteries form anastomoses that limit ischemia.
Describe the microcirculation of splanchnic region.
Where do small arteries penetrate?
Describe the countercurrent flow system.
Small arteries penetrate through the muscularis layer of the intestinal wall and branch extensively in the submucosal layer.
The arrangement of microvessels within an intestinal villus forms a countercurrent flow system. The incoming arteriole courses up the center and branches into many capillaries towards the tip of the villus. Capillaries converge into venules that carry blood back to the base of the villus. Arterioles and venules run parallel to one another.
Therefore, solutes (e.g. Na+) absorbed in the capillaries pass into the venules and can then diffuse into the interstitium and then into the arterioles. The higher arteriolar osmolarity increases blood flow.
eating something and absorbing more Na, gets into venule, over to arteriole, increases osmolarity of arteriole blood, increases water absorption and get more blood flow through capillaries in villi and this helps absorb more nutrients.
Draw a diagram of portal circulation.
Where does portal vein collect blood from? Where does it enter next?
What do hepatic veins collect blood from and empty into?
What is unique about splanchnic circulation?
How does blood get to liver, explain percentages and source.
Slide 16.
The portal vein collects blood from the capillary beds of the intestine, stomach, pancreas and spleen. Portal venous blood then enters the liver capillaries.
Hepatic veins collect blood from the liver and empty into the vena cava.
Therefore, the splanchnic circulation encounters two capillary beds in series, i.e. portal system.
The pressure in the portal vein is normally 10 mm Hg, only a few mm Hg above the pressure in the vena cava.
percentages imp. CO of 6L/min. 1500 ml blood into liver. 30 percent coming in through artery. 70 percent of that coming in through portal vein.
Describe how pulmonary hypertension can affect the liver.
vena cava- going back to heart. if problem w heart, (pulmonary hypertension) high after load on RV. fails over time…pressure backs up in RA into vena cava and will back up into liver. once liver fibrotic will back up into portal system and have portal hypertension. all this is venous. start filtering fluid bc of high capillary hydrostatic pressure and you have ascites. that is why R sided heart failure causes ascites bc increase in vena cava pressure, hepatic vein pressure, and portal pressure
How does R sided heart failure cause ascites?
vena cava- going back to heart. if problem w heart, (pulmonary hypertension) high after load on RV. fails over time…pressure backs up in RA into vena cava and will back up into liver. once liver fibrotic will back up into portal system and have portal hypertension. all this is venous. start filtering fluid bc of high capillary hydrostatic pressure and you have ascites. that is why R sided heart failure causes ascites bc increase in vena cava pressure, hepatic vein pressure, and portal pressure
portal hypertension-from damage to liver. cirrhosis of liver causes increase of pressure in portal vein and that backs up and have ascites (classic sign of cirrhosis of liver)
Is venous or arterial pressure more important in terms of capillary hydrostatic pressure?
Why?
venous pressure..
pressure in portal vein.. coming into liver normally about 10mmHg. in vena cava normally 5 mmHg. low pressures. diff between pressure in vena cava or portal vein isn’t much and doesn’t take much to wind up w portal hypertension. low pressures so a small change causes a large effect in venous system.
Describe portal hypertension. What things can cause portal hypertension?
What can it lead to?
Portal Hypertension can result from increases in either the vena cava pressure (congestive heart failure) or the hepatic vascular resistance (cirrhosis, hepatitis B or C).
Portal hypertension (>25 mm Hg) can lead to abdominal edema formation or ascites (fluid in the peritoneal cavity, liver ripped apart by high pressures inside. fibrotic and damages it over time). As pressure increases further, portal blood flows through and dilates portal anastomoses with systemic veins in the lower esophagus, stomach and rectum. Rupture of swollen esophageal veins (esophageal varices) can lead to life-threatening hemorrhage.
Describe esophageal varices and hemorrhoids. When might a patient bleed to death from hemorrhoids?
Rupture of swollen esophageal veins (esophageal varices) can lead to life-threatening hemorrhage.
see esophageal varices- veins in esophagus start to bulge in the esophagus and they start to bleed and pt. vomit volumes of blood
in stomach around umbilicus. anastomoses. veins around umbilicus bulging.
hemorrhoids…can bleed to death from hemorrhoids. (but not always from hemorrhoids. so why in some cases?) bc liver which prod. clotting factors damaged so now when have hemorrhoid rupture nothing to clot blood and can bleed to death.
Describe the regulation of intestinal blood flow very broadly:
local factors (metabolic and mechanical)
hormonal
neural
mostly metabolic and mechanical factors. squeezing of intestinal mucosa can change blood flow.
mucosa-what you eat, can also det. blood flow.
hormonal- GI tract..
neural input ..parasym. nerve stimulations increases motility in gut.
symp. NS -decrease motility. and para. stimulates motility. diff than heart. opposite. cAMP inhibits contraction in some vascular beds.
During an increase/decrease in metabolism how do O2 and metabolites change?
During an increase in metabolism, O2 decreases and metabolites (CO2, H+ and adenosine) increase. Both factors cause vasodilation and increases in intestinal blood flow.
When metabolism decreases, opposite changes cause vasoconstriction and decreases in blood flow.
What is the primary determinant of intestinal blood flow?
Intestinal blood flow is determined primarily by the rate of active transport of solutes across the mucosal epithelium (independent of intestinal content).
How is mucosal blood flow increased?
Mucosal blood flow is specifically increased in response to increased metabolism and increases in O2 demand.
need more O if increase metabolism
How will increases in intestinal motility increase metabolic activity?
How is muscularis metabolism and blood flow affected?
Increases in intestinal motility increase metabolic activity in the intestinal smooth muscle.
However, increases in motility cause only modest increases in muscularis metabolism and blood flow. Total intestinal blood flow often decreases during intestinal contractions due to compression of blood vessels (like in the heart).
can cut off dep. on arrhythmic contractions in intestinal system… vascular smooth muscle not letting go, can cause ischemia and feel that as a cramp.
Is intestinal blood flow auto-regulated? To what extent?
Intestinal blood flow exhibits moderate autoregulation due to vasodilation resulting from metabolites (primarily adenosine as well as CO2, H+, K+, or osmolarity). The opposite changes cause vasoconstriction. Not as well developed as in brain or kidney.
Describe hormonal regulation of intestinal blood flow.
Of the many gastrointestinal hormones important in digestion, only cholecystokinin and neurotensin exert physiological important effect on intestinal circulation.
These hormones increase blood flow by inducing vasodilation.
released on diff. conditions dep. on when you eat.
Describe the major neural influence on intestinal blood flow?
Which vessels receive this innervation?
What receptors/neurotransmitter?
postganglionic sympathetic vasoconstriction.
Except for the capillaries, all splanchnic blood vessels receive sympathetic innervation.
The sympathetic neurotransmitter is norepinephrine.
Vasoconstriction results from activation of alpha-adrenergic receptors on vascular smooth muscle.
Beta-adrenergic receptors also exist and their activation causes vasodilation.
symp. activity can reduce muscular activity on vascular smooth muscle..the coat that causes peristalsis. symp. on smooth muscle that controls contractions of intestines is inhibitory. and para. sym. system is excitatory.
What happens during stress or exercise to intestinal circulation?
What about during hemorrhage?
During stress or exercise sympathetic vasoconstriction (and venoconstriction) shifts blood flow from intestinal circulation to skeletal muscles, heart and brain (brain autoregulated-mostly goes to skel. muscles and heart).
During hemorrhage, significant volumes of blood are shifted from splanchnic to central circulation.
During hemorrhage, prolonged, intense sympathetic vasocontriction can result in ischemic bowel.
Describe parasympathetic activity in regards to intestinal blood flow.
Parasympathetic preganglionic fibers contact postganglionic neurons in the intestinal wall.
Parasympathetic activity INDIRECTLY stimulates intestinal blood flow by stimulating intestinal motility and glandular secretions, which in turn, increases metabolism.
Describe postprandial hyperemia.
Food ingestion increases intestinal blood flow through a complex interplay of metabolic, mechanical, hormonal, and neural influences.
The nature of the luminal content also determines the magnitude of the increased blood flow. Partially digested fats and carbohydrates are especially effective inducing hyperemia.
after you eat… postpranial=after eating. after eat feel tired bc insulin secreted in response to food that’s being absorbed, glucose taken into system causes shift of glucose into cells, reduces glucose concentration in blood and feel tired after you eat
postprandial hyperemia- after eat, additional increase in blood flow to intestines to absorb all these nutrients. nature of luminal content det. to some extent blood flow.
