Physiology E4 Circulatory

describe the brain ischemic reflex/ Cushing reflex

- concussion causes cerebral edema - extra fluid causes compression of the blood vessels= hypoxia - diameter goes down= resistance goes up - decrease of oxygen and increase of carbon dioxide (main regulator for the brain)- message sent to the pons to increase sympathetic response - increase HR- increase TPR- increase BP for blood to go back to the brain - increase BHP= more filtration= more edema= more hypoxia positive feedback loop with negative consequences

flow is the same thing as what?

CO- cardiac output

does slowing down the HR have a direct or indirect effect of contractility?

INDIRECT via negative Bowditch effect

if a patient has left ventricular failure, what type of edema occurs and why?

PULMONARY EDMEA blood is backed up BEHIND the left ventricle- increased BHP behind in the pulmonary= now pulmonary is favoring filtration instead of reabsorption= lungs are no longer dry anymore

what would happen if veins were NOT unidirectional for muscle pumps?

blood would travel in both directions- decrease venous return

how does exercise effect venous return?

both INCREASES venous return

myogenic vs. local metabolites

both are a way of local level (within the tissue) of tissue perfusion regulation 1. myogenic- smooth muscle cells via stretch ion sensitive channels - no mediators - increase pressure= increase stretch= vasoconstriction - decrease pressure= decrease stretch= vasodilation 2. local metabolites - decrease of blood flow/ accumulation of local metabolites= vasodilation (one of the metabolites will be a vasodilator- bradykinin, nitric oxide, prostaglandin or histamine) - increased blood flow/ increase oxygen= vasodilation (send blood to where there is no oxygen) - decrease oxygen= vasodilation

what is an example of a positive feedback loop with negative consequences?

brain ischemic reflex/ Cushing reflex

why is the blood flow to the capillaries described as intermittent?

can be on/ off due to precapillary sphincter based off of metabolic needs

if CENTRAL blood pressure deals with large arteries; what does PERIPHERAL blood pressure deal with?

capillaries

where does exchange of nutrients occur? what happens in other locations?

capillaries- other locations is just transportation

capillary transit time vs. pulmonary transmit time

capillary= 0.75 second pulmonary= 6 seconds

does carbon dioxide or oxygen diffuse more easily through the respiratory membrane? what happens if you increase the thickness of the respiratory membrane/ add more water?

carbon dioxide passes easier than oxygen increasing thickness/ water= slows down diffusion of oxygen even more

capillary fluid shift with counteracting hypovolemic shock

causes vasoconstriction= decrease BHP= switches from filtration to reabsorption to increase blood volume

how does sympathetic tone effect venous return? arterial vs. venous

causes venoconstriction and vasoconstriction increases VENOUS return decreases on ARTERIAL side (more blood stays inside large arteries)

what is the effect of chronic stress on diastolic pressure?

chronic stress= increase diastolic pressure - release of adrenaline= activation B1= vasoconstriction= increase TPR= increase diastolic pressure

chronotropy vs. ionotrophy

chronotropy- HR ionotropy- contractility

how does sweating affect venous return?

decrease

what does arteriosclerosis do to arterial elasticity? what is the effect on systolic pressure?

decrease arterial elasticity- will increase systolic pressure

what causes the transition point between filtration and reabsorption of capillaries? is the transition point constant or variable?

decrease of BHP as it goes from arterial to venous end VARIABLE transition point- depending on the situation

what is the first sign in change of pressures of anemic patients?

decrease of diastolic pressure

kwashiorkor

decrease of protein plasma concentration- leading to edema (decrease of BOP)

less length of a system does what to resistance and sympathetic tone?

decrease of resistance and sympathetic tone

what happens to pulmonary transit time with increased CO?

decrease of transit time- increase of flow rate

what is renin stimulated by?

decrease salt, blood volume and BP

what stimulates vasopressin secretion by posterior pituitary?

decreased atrial stretch

what stimulates renin secretion?

decreased renal BP

how does tachycardia effect on SV? (if there are no compensatory mechanisms) why? how does this effect venous return?

decreases SV cause you're decreasing filling time will DECREASE venous return

what happens to venous return with positive pressure ventilation? starling effect?

decreases venous return to both sides of the heart= further decrease in BP negative starling effect- decrease EDV and decrease SV

how does deep inspiration and deep exhalation affect venous return?

deep inspiration- increase venous return to the RIGHT side of the heart but decreases to the left side of the heart - due to increasing capacity of your lungs will stretch your capillaries= small diameter= more resistance= slow down return deep exhalation- increase venous return to the LEFT side of the heart

what must the blood cells do to pass through the narrow capillaries

deform

what can be administered for brain ischemic reflex?

dextran, mannitol or maltose-insoluble to favor resorption of fluid or do a spinal fluid tap

what are the special cases of hypovolemic shock that is not due to external loss of blood volume

distributive shock- anaphylactoid shock and septic shock

how do cellular elements transport across capillaries?

do not go across- they remain in the capillary

if there is high glucose in the plasma than in the cells, what way does it go?

down its concentration gradient- from plasma into cells

high- end- failure

due to not vasoconstriction to organs that are not needed under sympathetic stimulation not enough blood for circulation- not enough oxygen for some tissues- not enough pressure for circulation- heart has nothing to pump

early sign of arteriosclerosis vs. late 1. systolic pressure 2. diastolic pressure 3. pulse pressure

early 1. increase 2. decrease 3. increase late 1. increase 2. increase due to loss of compliance= arteries will empty faster

accumulation of fluid in interstitial space due to obstruction of lymphatic system

edema

extreme emotional stress vs. mild stress for sympathetic and parasympathetic tone

extreme emotional stress - decrease sympathetic - increase parasympathetic mild stress - increase sympathetic - decrease parasympathetic

syncope

fainting

pulmonary circulation speed vs. systemic circulation speed

faster for pulmonary cause same amount of blood but less distance

do capillaries typically filter more or reabsorb? what does this help create?

filter- to create instill fluid

during edema, are capillaries filtering or reabsorbing more?

filtering

does increased blood pressure tend to favor filtration or reabsorption?

filtration

with Kwashiorkor- how much of the capillary length if favoring filtration? what protein is mainly being effected?

filtration along the ENTIRE LENGTH of the capillary albumin mainly being chewed up

filtration pressure vs. reabsorption pressure at ARTERIAL end; is there filtration or absorption?

filtration- 36 mmHg reabsorption- 30 mmHg filtration

does vasodilation favor filtration or reabsorption?

filtration- increasing the size of the pores/ clefts so more can leave

graphs of pressure vs. volume/ flow for filtration vs. reabsorption

filtration- linear reabsorption- NOT linear

in hypoxic conditions, where does blood get shifted to in the lungs?

goes from base (zone 1) to apex (zone 3) low ventilation to high ventilation

the heart and the brain is controlled by what local metabolites?

heart- oxygen brain- carbon dioxide

main regulator within the brain and the heart

heart= oxygen - high oxygen induces vasoconstriction - low oxygen induces vasodilation brain= carbon dioxide - low carbon dioxide= vasoconstriction - high carbon dioxide (hypercapnia)= vasodilation

how does CAROTID SINUS SYNCOPE affect venous return and syncope?

high BP= overstimulation of carotid sinus due to compression= causing fainting increased firing of baroreceptors= causing drop in HR (vasoinhibitory), decrease CO and BP

how does a high lung volume effect pulmonary resistance and venous return back to the left side of the heart?

high lung volume= stretching capillaries= increasing pulmonary resistance= deceasing venous return back to the left side of the heart

high pressure side vs. low pressure side of systemic circulation

high= arterial low= venous

what zone/ area of the lungs has the highest amount of ventilation?

highest amount of ventilation= highest amount of air= zone 3 (apex)= lowest amount of blood

what paracrine mediator is being described? - released from mast cells in response to injury - vasoDILATOR - response for local edema in inflammation

histamine

which is worse: horizontal or vertical cuts in the gingiva?

horizontal cause blood flow is parallel to the roots

pressure imparted by water

hydrostatic pressure

what happens if you have very high cardiac output to oxygen saturation in pulmonary circulation?

hypoxemia- don't saturate the blood with oxygen cause it's so fast

what happens if you don't match ventilation and perfusion of the lungs?

hypoxic conditions

in what situation is arterial hypotension a good thing?

if you were to get into an accident and you're losing a lot of blood decrease of arterial blood pressure shifts blood from filtration to REABSORPTION- trying to reconstitute your blood volume

what happens to diastolic pressure for increase and decrease of HR?

increase HR= increase diastolic pressure decrease HR= decrease diastolic pressure

hypercapnia

increase carbon dioxide= vasodilation

an increase of compliance does what to pressure?

increase compliance= decrease of pressure

increasing blood volume 1. how does this affect blood pressure? 2. how does this affect venous return?

increase of both

what does pregnancy do to venous pressure? what can this cause?

increase of venous pressure= more filtration than reabsoprtion= edema

how does blood viscosity/ hematocrit affect peripheral resistance?

increase of viscosity (increase of RBC)= increase of peripheral resistance

hyperemia

increased blood flow= engorgement

what do most prostaglandins do?

induce VASODILATION

what is the effect of inhalation and exhalation on SV and BP?

inhalation= decrease SV to left side of the heart= decease BP exhalation= increase SV to left side of the heart= increase BP

what is the blood flow through the capillaries?

intermittent

what organ's blood flow is most influences by alpha 1 constriction?

kidney- can stop urine production completely

- accumulation of abdominal fluid - decreased BOP - body is chewing up ALBUMIN due to malnutrition - favoring filtration along entire length of capillary

kwashiorkor

pressure difference between arterioles and the arterial side of the capillary bed

large drop arterioles- 90 mmHg arterial side of capillary bed- 35 mmHg

failure of what ventricle leads to pulmonary edema

left ventricle

which ventricle is more susceptible to ischemia and why?

left ventricle - more blood supply to the left ventricle - during ventricular systole you will have a compression of the blood vessel= increased flow during diastole - sometimes cannot bring blood supply cause vessels are compressed

what ventricle has a larger supply of blood and why? what are the arteries that provide the blood?

left ventricle cause it's larger left coronary artery (off of ascending aorta) into: 1. circumflex branch 2. anterior inter ventricular branch

what substances go through the endothelial cells?

lipid soluble substances (oxygen, carbon dioxide)

what kind of drugs can pass through BBB?

lipophilic

how much epinephrine needs to be released to stimulate alpha 1 vs. beta 2?

little- beta 2 (greater affinity) more- alpha 1 (less affinity)

which organ received more blood supply than needed for survival? what does it mean about its correlated vein?

liver- hepatic vein has higher oxygen levels than other veins of other organs

since pores/ clefts can be varying diameters... where is there the largest diameter in the body?

liver/ kidneys where there is a lot of filtration/ exchange

if sympathetic tone doesn't control constriction/ dilation of blood vessels in the lungs, then what does?

local anoxia

bradykinin, prostaglandins, histamine and nitric oxide control what level of the arterial and venous tone?

local level- for perfusion WITHIN each tissue

what is a muscle pump? how does this effect venous return?

muscles compressing the veins to INCREASE venous return veins are UNIDIRECTIONAL- blood is forced back to the heart

does pressure in the venous side ever become zero? why or why not?

no cause you still need pressure to bring blood back to the vena cava

where does blood flow when precapillary sphincters are constricted?

no more blood through capillary bed= flows through met arterioles

why is there little/ no autonomic regulation to the brain?

no- done by baroreceptors already

under normal conditions, do plasma proteins leave capillaries? what about abnormal conditions?

no- too big to leave but under allergic conditions they will leave

what does the lymphatic system do?

picks up extra fluid filtered by the capillaries (capillaries typically filter more than reabsorb)

how do medium proteins transport across capillary wall?

pinocytosis- endocytosis on one side and exocytosis on the other

how does things enter or leave the capillaries?

pores/ clefts BETWEEN the cells in different diameters

prehypertension BP vs. hypertension BP

prehypertension: 120/80- 140/90 hypertension: over 140/90

what do valves in the vein do?

prevents backflow- allows for UNIDIRECTIONAL flow

NPY co-neurotransmitter helps stimulate what?

prolonged sympathetic action- prolonged VASOCONSTRICTION

what affects vasoconstriction/ dilation in pulmonary vs. systemic?

pulmomnary= local anoxia systemic- reflex control/ baroreceptors

is pulmonary or circulatory more compliant?

pulmonary

what is the difference in resistance between pulmonary and systemic systems and why?

pulmonary= 0.1 PRU systemic= 1 PRU pulmonary is lower based off of Poiseuille's law- less length

blood volume/ velocity in pulmonary vs. systemic

pulmonary= 10% blood vL= faster velocity cause it's the same amount of blood flow systemic= 90% blood vL= blood circulates slowly

local anoxia in pulmonary vs. systemic

pulmonary= constriction (trying to send blood to where there actually is oxygen) systemic= dilation

mean capillary hydrostatic pressure for pulmonary vs. systemic

pulmonary= lower systemic= higher

tendency to filer in pulmonary vs. systemic

pulmonary= zero (do not want to filter, want to reabsorb to keep lungs try) systemic- slight

does the nephron reabsorb or secrete more?

reabsorb

is reabsorption or filtration happening at venous end?

reabsorption

in pulmonary circulation, is there filtration or reabsorption and why? is there vasodilation or vasoconstriction?

reabsorption along the entire length- trying to keep lungs try reabsorption= vasoCONSTRICTION

main clinical sign of shock

reduction of blood pressure

what happens to the baroreceptor reflex with age

reflex becomes slower

what is used for LONG TERM regulation of blood pressure?

renin-angiotension- aldosterone system via regulating water volume inside your body

what 2 arteries come off of the ASCENDING aorta

right and left coronary arteries

describe the rate of change of flow with the right and left ventricle

right ventricle- constant left ventricle- not constant cause it is more susceptible to ischemia

failure of what ventricle leads to systemic edema

right ventricleo

how does pulmonary artery flow compare to systemic circulation artery flow? what about the autonomic regulation?

same flow but less autonomic regulation of flow to pulmonary cause just going gas exchange

how many layers of endothelial cells of capillaries?

single layer

scalloping effect

small changes in blood pressure due to respiratory activity inhalation= decrease SV= decrease BP exhalation= increase SV= increase BP

what substances can leave between pores?

small water- soluble substances and water

what type of autonomic responses for somatic pain vs. visceral pain?

somatic= sympathetic visceral= parasympathetic

what does stroke volume mainly effect? diastolic pressure?

stroke volume mainly effects pulse pressure diastolic pressure mainly affects TPR- total peripheral resistance cardiac output and TPR both affect MAP (arterial)

blood flow to superficial face vs. deep face

superficial- facial artery deep face- maxillary artery

1. pallor 2. diaphoresis- sweating 3. glazed appearance 4. reduced awareness

syncope symptoms

systemic edema vs. pulmonary edema

systemic edema- right ventricular failure pulmonary edema- left ventricular failure

an increase in blood volume and decreased arterial compliance means what?

systolic hypertension

what happens to systolic pressure and diastolic pressure during exercise? PP? SV? MAP?

systolic- slightly elevate - increase SV and increase ejection rate diastolic pressure- doesn't change much cause depends on body composition increase PP= increase SV= increase MAP

internal carotid arteries and vertebral arteries supply blood to what?

the brain

Why must RBCs be flexible?

they're larger than capillary size

how does oxygen and carbon dioxide transport across capillary cells?

through endothelial cell (through lipid bilayer)

what are the 2 locations where there are no pores/ clefts between cells for no exchange? what is there instead?

tight junctions in BBB and placenta

why is increase of contractility needed with an increase of HR?

to compensate for increase HR if you increase HR without any compensatory mechanisms- decrease of SV overtime

if you are sitting for a long period of time on an airplane, why is it a good idea to squeeze your calves once in a while?

trying to increase venous return back to the heart to reduce swelling (capillary BHP is higher than the venous side of capillaries to increase filtration)

clefts in liver and kidneys

typically larger than other organs

what is the counter- current flow of vasa recta and what is its purpose?

urine going left to right while blood supply is going from right to left used for concentrating urine

exhale against a closed glottis

valsalva maneavur

what could cause decreased effective cardiac output?

valve incompetency

what is valve incompetency? what valves are these typically seen with? how does this effect effective CO? what is the effect on venous return?

valve regurgitation- with semilunar valves will decrease CO- less blood return to the other side of the heart DECREASE of venous return

what is the effect of vasoconstriction vs. venoconstriction?

vasoconstriction- increase peripheral resistance= increase BP venoconstriction- increase venous return= increase SV= increase CO= increase BP

when is blood pulsatile? when does it become continuous? intermittent?

when it is first leaving the heart and becomes more continuous as it gets further away from the heart and becomes intermittent when it reaches the capillaries

common value of TOP and THP at arterial end?

TOP- 1 mmHg THP- 5 mmHg

active hyperemia vs. reactive hyperemia

active- due to local metabolic changes/ local metabolites diffusing through tissue - increase blood flow (more than what you need) - can turn red - boner reactive- post occlusion increase in blood flow - local metabolites are being built up= keeps blood vessel dilated for a long period of time trying to drain the local metabolites away

what is secreted from the adrenal cortex vs. the adrenal medulla?

adrenal cortex- aldolesterone (long term effect for blood pressure) adrenal medulla- epinephrine and norepinephrine (short term effect for blood pressure)

describe the affinity for epinephrine for alpha 1 vs. beta 2?

alpha 1= less affinity beta 2= greater affinity

what is the effect of epinephrine to alpha vs beta 2

alpha- vasoconstriction beta 2- vasodilation

where is the only location in the body where hypoxic conditions will induce VASOCONSTRICTION? why?

alveolar hypoxia- trying to shift blood to areas in the body/ lung where oxygen is more available

what glia cell creates the BBB?

astrocytes

according to starling's hypothesis, how does bulk flow move throughout the body?

balance of hydrostatic and oncotic pressures across capillary endothelium

what receptors are located on the cells towards the lumen on a blood vessel?

beta 2

how does urea, glucose, lactate, ADH/ vasopressin and insular transport across capillaries?

between endothelial cells

elephantiasis

blockage of lymph- example of edema in low extremities and genitalia

what is the bulk flow a day through capillaries? how much FILTERED out of capillaries? how much REABSORBED by capillaries? how much collected by lymphatic system?

7200 L/day 20 L/day FILTERED out 17 L/day REABSORBED 3 L/day collected by lymphatic system

how much % of the blood is stored in the veins?

60%- blood reservoir

2 types of distributive shock and does it cause vasodilation or vasoconstriction

1. anaphylactoid shock 2. septic shock both causing vasodilation

Valsalva maneuver - what is the effect on venous return - what is the effect on HR

- forcible exhalation against a closed glottis, resulting in increased intrathoracic pressure - REDUCE venous return - REDUCE heart rate cause increase thoracic pressure= increase baroreceptor

describe the hearts oxygen extraction rate? why is this a good and a bad thing? what type of metabolism does the heart need in order to survive?

- high oxygen extraction rate (good thing) - it can also be a bad thing cause it cannot extract anymore oxygen if needed (on the verge of aerobic and anaerobic metabolism) - heart needs AEROBIC metabolism to survive

Bowditch effect

- homeometric autoregulation - increasing HR traps more calcium inside= increase of contractility with an increase of HR

vasovagal syncope (what happens to the autonomic regulation) (what is the effect on the heart)

- increase parasympathetic (goes to nodal tissue to slow down HR) - decrease sympathetic

what do blisters and hives do to capillary permeability? what does this cause?

- increases membrane permeability= more proteins leaving= higher TOP= favoring more filtration - vasodilation= pores/ clefts are larger= more leaving - also more blood is rushing through cause of inflammation= higher BHP= more filtration

how does viagra work?

- inhibits the breakdown of cGMP - nitric oxide causes the formation of cGMP which causes the removal of calcium in smooth muscles- causes VASODILATION - thus, viagra keeps vasodilation

what is the effect of alcohol and caffeine on renin- angiotensin- aldosterone system?

- prevents breakdown of cAMP - reduces release of ADH/ vasopressin - no fluid uptake= more urine excretion

polycythemia

- too many RBC - increase viscosity - decrease flow - more resistance - more time for large arteries to empty - increase of DP

ACE inhibitors

- used to treat high blood pressure - prevents ACE within the lungs to work - prevents conversion of angiotensin I to angiotensin II so there is no fluid uptake/ increase of blood pressure

what is the change in oncotic pressure? 1. 0.9% saline 2. lactate ringer 3. 5% albumin in saline 4. 6% heastarch in saline 5. dextran 70 in saline

1. 0 2. 0 3. 20 mmHg 4. 30 mmHg 5. 60 mmHg

2 locations of absent clefts

1. BBB 2. placenta

filtration pressures

1. BHP- blood hydrostatic pressure 1. TOP- tissue oncotic pressure

what 2 pressures increase during blisters, hives, allergic reactions? what does this cause?

1. BHP- due to inflammatory cells migrating causing increased pressure= more filtration 2. TOP- increased membrane permeability and vasodilation allows proteins to leave and increasing TOP= favoring filtration causing edema

absorption pressures

1. BOP- blood oncotic pressures 2. THP- tissue hydrostatic pressures

2 ways to induce vasodilation of sweat glands and blood vessels to skeletal muscle

1. beta 2 via epinephrine 2. M3 muscarinic for special case sympathetics

what 2 factors affect peripheral resistance? which plays a bigger role and why?

1. blood viscosity- not going to affect that much cause blood viscosity/ hematocrit should stay pretty constant 2. arteriole diameter- can vary= thus plays a larger role in peripheral resistance

what happens to cardiac output and arterial pressure if: (hypovolemic shock) 1. 10% of blood is loss 2. 20% of blood is loss 3. 45% of blood is loss

1. both are maintained 2. CO decreased; arterial pressure maintained due to increase of peripheral resistance 3. PHP- both cannot be maintained any longer

central vs. local levels for arteriole and venous tone

1. central level: regulated by AUTONOMIC control to each regional area (arm, GI, kidneys) 2. local level: regulated by LOCAL FACTORS to within each tissue (bradykinin, prostaglandins, histamine and nitric oxide)

where do these capillaries reabsorb filtrate from? 1. peritubular capillaries 2. vasa recta capillaries

1. cortical tubules 2. renal pyramid tubules

what is the effect of DP for: 1. anemia 2. polycythemia 3. aging 4. arteriosclerosis

1. decrease 2. increase 3. increase 4. early stage- decrease but later will rise

anemic patients 1. DP 2. SV 3. CO

1. decrease 2. increase- via increase venous return 3. increase low # RBC= less viscosity= increase flow

4 causes of edema

1. decrease of BOP (e.g. kwashiorkor) 2. increased permeability of capillary walls (e.g. blister/ hives) 3. increased venous pressure (e.g. pregnancy) 4. blockage of lymph (e.g. elephantiasis)

how does ORTHOSTATIC HYPOTENSION affect venous return and syncope?

1. decrease venous return (due to gravity pulling down the blood) 2. most people will not faint from just standing

NO- nitric oxide 1. produced by what cells? 2. what is the stimulator? 3. what is the action? 4. mode of action

1. endothelial cells 2. acetylcholine produced relaxation of vascular smooth muscle 3. vasodilation 4. paracrine

what hormones does the adrenal medulla release? what receptors do they go to?

1. epinephrine (90%)- alpha 1 and 2 (less affinity) vasoconstriction and beta 2 vasodilation (greater affinity) 2. NE (10%)- alpha 1 vasoconstriction

what is happening at these nephron locations? 1. glomerular 2. peritubular capillaries 3. vasa recta

1. filtration 2. secretion and reabsorption 3. concentration of urine

how can ADH be stimulated for release?

1. hypothalamus can sense change in osmolarity 2. angiotensin II

what are the 3 locations in the brain without BBB? what is the purpose of this?

1. hypothalamus- used to detect different substances for regulation 2. pituitary gland- releasing substances into circulation 3. respiratory control area- detecting pH levels and carbon dioxide levels

what happens to these factors during exercise? 1. MAP 2. TPR 3. CO 4. HR 5. skeletal muscle blood flow 6. muscle arteries via what receptor 7. visceral arteries via what receptor 8. systolic pressure 9. diastolic pressure

1. increase 2. decrease- via beta 2 or special case sympathetic M3 so you can send blood throughout your body faster 3. increase 4. increase 5. increase 6. vasodilation via beta2 7. vasoconstriction via alpha1 (do not want to send blood to organs where it is not needed during sympathetics) 8. slightly elevated 9. normal to low

determine whether an increase or decrease of these LOCAL METABOLITES will cause vasodilation or vasoconstriction? 1. myogenic activity 2. oxygen 3. carbon dioxide/ other metabolites 4. metabolites from renin- angiotensin- aldosterone system 5. sympathetic activity 6. histamine 7. heat 8. cold

1. increase= vasoconstriction; decrease= vasodilation 2. increase= vasoconstriction; decrease= vasodilation 3. increase= vasodilation; decrease= vasoconstriction 4. increase= vasoconstriction; decrease= vasodilation 5. increase= vasoconstriction; decrease= vasodilation 6. increase= vasodilation; decrease= vasoconstriction 7. increase= vasodilation 8. increase= vasoconstriction

what happens to blood flow to a tissue with increased metabolic needs? what happens if all the tissues in the body have an increased metabolic demand?

1. increased blood flow 2. increased CO and heart work= goes from 5L/min to 25L/min so the blood is circulating faster

what organ produces these hormones and what are their functions: 1. renin 2. angiotensinogen 3. aldolesterone 4. ADH/ vasopressin

1. kidney- converts angiotensinogen to angiotensin I 2. liver 3. adrenal CORTEX- goes to the KIDNEY to cause reabsorption of sodium and water and VASOCONSTRICTION 4. made by hypothalamus but secreted by posterior pituitary gland- increase water reabsorption from kidney tubules

autoregulation 1. what are the 2 types? 2. does this fall under central or local level for REGULATION OF TISSUE PERFUSION?

1. myogenic and local metabolites 2. local level

Bradykinin is released from what types of stimulation? what is its target and what is the effect?

1. parasympathetic stimulation to salivary glands 2. sympathetic cholinergic stimulation to sweat glands causes vasodilation and increase of filtration

3 vasodilator agents- what does this mean about filtration or reabsorption?

1. prostaglandins 2. histamine- injured tissue and mast cells (arterioles, met arterioles and capillaries) 3. bradykinin- glands favors FILTRATION

ANP (atrial natriuretic peptide) 1. where is it secreted from? 2. what are the 3 stimulators? 3. what are its 4 actions? 4. what is its overall goal?

1. secreted from atria 2. in response to stretch of the atria from increase sodium, increase ECF, or increased atrial BP 3. all INHIBITION of: - Na reabsorption by kidneys= increase of sodium excretion (followed by water) - renin- angiotension- aldosterone system= increase of sodium excretion (followed by water) - afferent arteriole vasoconstriction= causing vasodilation= increase GFR= increase water and sodium excretion - sympathetic nervous system= decrease CO and TPR= decrease atrial BP 4. overall goal= increase urine production and decrease of atrial BP

what is orthostatic hypotension? what is the greatest factor that causes this? what happens to venous return, SV and BP? what is the difference between the capillary blood pressure vs. venous pressure? what does this do to feet and ankles?

1. standing position and not moving 2. gravity 3. decrease venous return= decrease SV= decrease BP (hypotension) 4. capillary blood pressure is GREATER than venous end of capillaries (15 mmHg) due to gravity 5. causes greater BHP= greater filtration= swollen feet and ankles

what happens to the blood supply to these areas during exercise? why? 1. heart 2. skeletal muscle 3. GI 4. kidneys

1. still receiving 4% 2. more 3. less 4. less trying to send blood elsewhere where it is needed during exercise

in a fight or flight response- what 2 things work together for vasoconstriction?

1. sympathetic response 2. adrenaline (aka norepinephrine)

when are people in TEMPORARY horizontal position? and why? what happens to blood pressure? venous return? CO?

1. syncope- fainting 2. due to not enough blood flow to the brain 3. decrease of blood pressure 4. increasing venous return- increase CO- bring back normal circulation to the brain

stimulation of these Endothelin receptors cause what? 1. EdnrA 2. EndrB

1. vasoconstriction 2. vasodilation

what is being favored here? be specific on the changes in filtration/ absorption pressures 1. vasoconstriction 2. arterial hypotension 3. venous hypotension 4. dehydration 5. hemorrhage

1. vasoconstriction- decreased BHP 2. arterial hypotension- decreased BHP (reabsorption forces are now more powerful) 3. venous hypotension- decreased BHP (reabsorption forces are being reinforced) 4. dehydration- decrease of blood vL= decrease BHP 5. hemorrhage- decrease blood vL= decrease BHP REABSOPRTION

what is being favored here? be specific on the changes in the filtration/ absorption pressures 1. vasodilation 2. arterial hypertension 3. venous hypertension 4. increased plasma leakage 5. plasma protein deficiency

1. vasodilation- increased BHP 2. arterial hypertension- increased BHP 3. venous hypertension- increased BHP (overpowering the normal reabsorption forces) 4. increased plasma leakage- decreased BOP and increased TOP 5. plasma protein deficiency- decreased BOP (Kwashiorkor) FILTRATION/ edema

what is the venous end of capillary pressure on avg?

15 mmHg

at REST, what percentage of the capillary beds are open?

20-25%

if a specific capillary bed were to be vasoconstricted/ precapillary sphincter is shut off- describe the flow of blood for the capillary beds ABOVE/OPEN and BELOW/CLOSED this constricted capillary bed what is happening at that specific capillary bed once the precapillary sphincter is open?

ABOVE/OPEN= filtration (increase of BHP) due to backup blood flow BELOW/ CLOSED= reabsorption (decrease of BHP) no blood flow coming in specific capillary bed- increased of filtration cause inflow of more blood due to backpack behind the precapillary sphincter

chest pain indicates what?

ANAEROBIC metabolism in your heart

what are the 2 places where there are no pores/ clefts between cells? tight junctions only

BBB and placenta

what limits the fluid movement in the brain?

BBB- due to astrocytes

common value of BHP at arterial end? BOP? does this mean that there is more filtration or reabsorption at the arterial end?

BHP- 35 mmHg BOP- 25 mmHg more FILTRATION at arterial end

what is the ONLY pressure (out of the 4 of starling's hypothesis) that changes? how does it change?

BHP- blood hydrostatic pressure higher at ARTERIAL end and decreases as it reaches towards VENOUS end- reason why there is more filtration at arterial than venous

blood pressure inside capillary, what happens if you increase this?

BHP- blood hydrostatic pressure increase will cause filtration

what paracrine mediator is being described? - parasympathetic stimulated aids in its release from salivary glands - cholinergic sympathetic fibers aids in release from sweat glands - causes vasodilation- increase BHP- more filtration- more secretion

Bradykinin

what is the flow from the heart vs. the capillaries?

FLOW IS THE SAME

nitric oxide is derived from what AA? what enzyme?

L- arginine with nitric oxide synthetase

what is typically dominate in the heart, M2 or B1?

M2- parasympathetic is more dominate than sympathetic

(CO)(TPR)=?

MAP

does epinephrine or NE have a better effect for increasing venous return?

NE cause it has a higher affinity for alpha receptors (vasoconstriction) than epinephrine

is the adrenal medulla hormones for long term or short term regulation of blood pressure?

SHORT TERM

what type of autonomic control is to blood vessels? via what receptors?

SYMPATHETIC only alpha 1- vasoconstriction beta 2- vasodilation

at rest, are blood vessels under sympathetic constrictor tone or parasympathetic constrictor tone?

SYMPATHETIC- no parasympathetic to blood vessels

if a patient has right ventricular failure, what type of edema occurs and why?

SYSTEMIC EDEMA- swollen joints, fingers, everywhere blood is backed up BEHIND the right ventricle- increased of BHP behind

is more resistance on the arterial side or venous side? why?

arterial side arterioles= resistance vessels

low volume/ high pressure network vs. high volume/ low pressure network

arterial system vs. venous system

pressure at arterial end of capillaries vs. venous end of capillaries

arterial- 35 mmHg venous- 15 mmHg

what happens to BP if you increase volume inside arterial blood vessels vs. venous side?

arterial- will raise blood pressure MORE venous- will raise blood pressure LESS due to the idea that veins have more compliance/ distensibility than arteries

resistance vessels to bring blood towards/ away from capillary bed

arterioles

low BP vs. high BP for reflex control

low BP 1. decrease stimulation of cardio inhibitory (trying to activate sympathetic) 2. decrease inhibition of cardioacceleatory and vasomotor (trying to activate sympathetic) high BP 1. increase stimulation on cardio inhibitory (trying to lower HR) 2. increase inhibition of cardioacceletory and vasomotor (causing dilation and trying to activate parasympathetic)

what is the difference between pulmonary and systemic for mean pressure, SP and DP and pulse pressure?

lower for pulmonary than systemic

where does extra water from interstitial fluid go?

lymphatic system- 3L/day

main function of baroreceptors

maintaining blood flow to heart and brain

bypass channel and regulate flow into capillary beds

metaarterioles

what determines if the precapillary sphincter is open or closed? what are the factors?

metabolic needs- oxygen and CO2

sympathetic tone for pulmonary vs. systemic

minimal for pulmonary and marked for systemic

what is the effect on cardiac output and heart work by controlling tissue percussion so each tissue recieves just enough blood?

minimizing CO and heart work

capillaries inside the liver vs other locations

more leaky- need to uptake a lot of substances from the blood

does epinephrine or norepinephrine cause a greater increase in central blood pressure and why?

norepinephrine cause norepinephrine only does vasoconstriction (and has a higher affinity for alpha- vasoconstriction) while epinephrine does vasodilation and vasoconstriction (and has a higher affinity for vasodilation with a higher affinity with beta 2 receptor)

what do these 3 have in common? 1. hypothalamus 2. pituitary gland 3. respiratory control area

not a lot of BBB for detection and secretion

vasal motion

on/ off circulation in the capillary beds via precapillary dilation or constriction

pressure provided by proteins to hold onto water

oncotic pressure

where is there parasympathetic innervation to the heart? what is the receptor? how does this effect the Bowditch effect?

only to nodal tissue M2 receptor- inhibits adenyl cyclase activity; activated phosphodiesterase increases K+ conductance= hyperpolarization= takes longer to reach T-tubules= slows down HR has a negative Bowditch effect- decreases HR so SLIGHTLY decreases contractility

aldolesterone is secreted from what? where is its target?

origin- adrenal cortex target- peripheral arterioles for vasoconstriction and kidney for uptake of salt and water

How does the Valsalva maneuver affect blood pressure?

originally increases your BP= large baroreceptor activation to reduce BP

opening and closing of precapillary sphincter is determined by what needs?

oxygen and carbon dioxide

even though the heart has dual autonomic innervation, what is normally dominate? how will the normality be overcome?

parasympathetic (M2) typically dominates but an increase in epinephrine to beta1 will cause an increase in heart rate

does epinephrine typically want to vasodilate or vasoconstrict? how does it have the other effect? how does t effect peripheral resistance?

vasodilate cause epinephrine has a higher affinity for beta than it does for alpha small dose= beta 2= vasodilation= decrease peripheral resistance large dose= alpha 1= vasoconstriction= increase peripheral resistance

does cGMP do vasoconstriction or vasodilation?

vasodilation

what will happen under these conditions? - high adenosine (from broken down ATP) - high co2 - low oxygen - high H+ - high K+

vasodilation

in reference to SPECIFIC capillaries- what happens under vasodilation? vasoconstriction? and why?

vasodilation- filtration along the entire length (more blood coming in= higher BHP) vasoconstriction- reabsorption along the entire length (less blood coming in= higher BHP)

how does VASOVAGAL SYNCOPE affect venous return and syncope? what is the overall effect on BP?

vasovagal syncope- amplified PARASYMPATHETIC response via inhibiting sympathetic responses 1. increase parasympathetic- HR decreasing- CO decreases- BP decreases 2. decrease sympathetic- dilation of vessels- dropping BP increases venous return cause they will FAINT/ syncope

what is lowest pressure in your body blood vessels?

vena cava- end of venous circuit

is alpha 2 receptor mostly for vasoconstriction or venoconstriction?

venoconstriction- but alpha1 is still more dominant than alpha2

what is the most useful method to counteract hypovolemic shock?

venoconstriction- increases venous return cause veins are a blood reservoir

what happens if you have an increased venous pressure?

venous end typically favors REABSORPTION but with increased venous pressure you will favor FILTRATION= edema

does arterial or venous side have more distensibility/compliance? why?

venous side- veins are the blood reservoir

reflex control for pulmonary vs. systemic and why?

via BARORECEPTORS pulmonary- minimal cause no reason to regulate blood flow cause all it is doing is gas exchange= thus minimal sympathetic tone systemic- marked effect on the veins

describe the 3 pulmonary vascular zones - how much air - how much blood - how much resistance

zone 1= base - least amount of air - most amount of blood - least amount of resistance zone 2= right above the heart - middle of each - intermittent blood flow zone 3= apex - least amount of blood - most amount of air - most resistance