physiology 1 -blood

• generated by heart
• ventricle contracts and pushes blood by force into adjacent artery

• generated by static force
• 1. stretching of elastic elements of a compartement filled w/ fluid
• 2. weight of fluid - gravity - zero at top and highest force at the bottom

• physical forces of same quality
• hydrostatic pressure can also be used for blood pressure

ARTERIES

stenosis of aortic valve would cause the heart to have a higher blood pressure than arteries

• left heart
• systemic
• 98 mm Hg

• right heart
• to lungs
• 13 mmHg

effects the absolute highest pressure is found in the larger artieris connected to the aorta

• oscillates between max systolic and min diastolic pressure
• oscillation dies out in arterioles and not found in caps and veins

• replacement of systolic/diastolic oscillations by a continuous pressure
• decreases gradually between aorta and vena cava

• max pressure in sytole
• normal 120 mm Hg

• min pressure during diastole
• 80 mm Hg

• average pressure over whole cardiac cycle (continuous pressure)
• 100 mmHg

systolic - diastolic pressure = pulse pressure

• high systolic
• low diastolic

diastolic + 1/3 pulse pressure

• difference in pressure between the inlet side and the outlet side
• (through all types of vessel)

aortic pressure - vena cava pressure

pressure at its inlet - pressure at its outlet

• aorta 98 mmHg - vena cava 5 mm Hg = 93 mmHg (perfusion pressure)
• decrease in pressure when goes away from heart

• pulmonary a. 13 mmHg - pulmonary v. 5 mmHg = 8 mmHg perfusion pressure
• decrease in pressure when goes away from heart

(8mmHg = 104 mm H20)

• when there is no pumping arterial side and venous side blood pressure equilibriates
• filling pressure slightly higher(7 mm Hg) than barometric pressure

filling pressure slightly higher(7 mm Hg) than barometric pressure

• arterial pressure to rise to 91 mmHg
• venous pressure to decrease by 4 mm Hg

arteries have lots of elastic and muscle less in veins

• proportion of increase in volume and related increase in pressure
• change volume/change in pressure = compliance
• same amount of blood in arteries and veins but veins are better distensible(increase in blood with a lower increase in pressure)

• small decrease in pressure at the venous side
• larger increase at the arterial side

• is much higher that arteries
• veins cope better

• arteries
• accept high pressure during systole and hold it durning diastole

arteries creates a continuous flow

"pressure vessels" of the circulatory system

• Volume reserviors (75%)
• receive and release large volumes with only minor changes in pressure
• reservoir for adjusting to varying demands in blood volume (exercise, hyper and hypovolaemia)
• "volume vessels"

• heart - can respond to changes in the external conditions
• Afterload - increase resistance - left ventricle affected
• Preload - increase blood flow - both sides of heart affected - increased output of heart
• Conclusion - heart can change in seconds, both venticles independently able to compensate for deviations

heart can work w/o cardiovascular center, autonomic control and humoral control

• increase resistance to blood flow by reducing diameter
• left ventricle responds by increasing the blood pressure
• blood flow return to almost initial value

• increase blood flow into right atrium heart responds by increasing output
• caused increase in filling and resistance - increased retention of blood in the left ventricle
• increased the size of the ventricle
• longer cardiac muscle fibers generate more force of contraction
• increased force causes - left side increases pressure and maintain output
• right side increases the output in order to match the increased input

• right preload - generated by returing blood to the atrium
• left preload - generated by blood returning to left atrium
• presure measured in the atrium
• increase in preload = increase in stoke volume

heart can become overstretched if preload is to large for a long time and will lose strenght instead of gaining it

• measure of workload of the heart generated by the peripheral tissues
• pressure is measured in the arteries that are directly connected to the ventricles
• aortic pressure - left afterload
• pulmonary artery - right afterload
• higher the afterload the higher the work on the heart(usually b/c of higher demand it tissues) ex. exercise

• pathological condition - increase in afterload
• arterioles are dominated by vasoconstriction hormones
• causes increase in total peripheral resistance (TPR), then need to increase aortic pressure in order to overcome TPR

• arterial pressure vs. hydrostatic pressure
• Zone 1, 2, and 3

determined by the height of the blood column copared to the level of the heart

• min pressure to open vessels agains opposeing barometric pressure
• systolic pressure is lower than the required pressure
• barometris pressure keeps vessles closed
• no profusion (gas exchange)
• no blood flow

• blood pressure exceeds the required hydrostatic pressure only during the systole
• not during diastole
• resting - only profused during the systole
• intermittent blood flow

• both systolic pressure as well as diastolic pressure exceed required hydrostatic pressure
• resting - is always perfused during systole and diastole
• contiuous blood flow

• Zone 1 - gets smaller
• Zone 2 - increases
• Zone 3 - increases (full lung perfusion)

• low pressure - need larger diameter for adequate blood flow
• +5 to -5 mmHg

• higher or lower than blood pressure b/c of gravity
• blood below heart - weight of blood column adds to the blood pressure and increse the total pressure
• blood above hear - decreases total pressure

• thinner muscular layer
• less elastic
• more flexible than arteries
• easily adjust to varying blood volumes by changing shape

• storage of blood
• during exercise blood shifted to the arterial side from the venous side

• when increase in demand of blood from rest muscle pumps are needed
• valves on veins open towards the heart
• muscle contractions puts pressure on the vein and blood is pushed out of the segment and towards the heart
• distal valve closes and prevents flow in wrong direction
• muscle relaxes - decrease in pressure and proximal valves close to prevent back flow, distal valve opens for filling

• muscle contracts - distal valve closes - proximal valve open - decrease in blood
• muscle relaxes - proximal valve closes - distal valve open - increase in blood

• intrathoracic pressure decreases and intraabdominal pressure increases blood sucked from abdomen to thorax
• increased blood to lungs

• venous valves prevent backflow
• increased pressure forces the blood to flow towards the heart
• blood pushed from lungs

• pressure in the right atrium
• controlled - output of the right ventricle, and blood volume returning from peripheral tissue
• normal : 0...5 mmHg
• min : -3...-5 mmHg
• max : 20...30 mmHg (b/c of pathological conditions like heart failure)

• active tissues need more blood than resting tissue
• microvessels monitor needs
• blood flow is controlled by metabolism and nerves

heart responds and adjusts to the demands of tissues

• local blood flow in tissues
• or
• control of the cardiac output

• for tansport purposes to maintain an appropriate environment
• nutrients, 02, co2, waste products, hormones, immological cells and proteins, water

• blood flow is the pressure difference between arteries and veins
• pressure is potential energy

throguh increase or decrease of cardiac output and resistance of vessels to meet varying demands

• respond to volume changes with steep pressure changes (LOW compliance)
• mainly controled by arterioles - thick muscular wall and able to change diameter
• Poiseuille's law

changes in diameter have a strong effect on the resistance and consequently on the flow of blood

• volume reservoirs
• at rest holds 2/3 of total blood volume
• most of volume in small veins and venules
• cope better
• can handle increase and decrease in blood with minor effects on venous pressure

• diameter decreases on the arterial side = velocity decreases
• increase number of vessels results in an increase in the total cross-sectional area

• capillaries
• for better exchange

very energy consuming

• less energy consumption
• circulatory system pressure and volume are stored during pumping stroke (systole)
• aorta -high pressure, increase blood volume, increase pressure
• used during refilling(diastole)
• aortic blood pressure (diastole) - stored blood leaves the aorta and the large arteries again
• Continuous flow

is more energy efficient than stop and go flow

• concentric layers of same velocity
• smooth flow
• low friction against walls b/c of low velocity of outer layers
• less energy required
• aorta, vena cava

• no layers, same velocity
• chaotic movements in and along the vessels
• high friction against the wall
• more energy required
• valves

• RBC become bell shaped to squeeze through vessels that have a smaller diameter than theirs
• aggregate
• move in single file(bolus flow) reducing viscosity of blood
• flow resistance is reduced
• turbulent flow of plasma facilitates metabloic exchanges w/ tissues

• heart never empties completely
• volume of blood ejected per min by one ventricle
• stroke volume times the number of strokes per minute = heart rate
• stroke volume x heart rate = cardiac output

• 75 - 150 beats/min man
• 1000 beats/min humming bird

• volume ejected by on ventricle during a systole
• end-diastolic volume - end-systolic volume = stroke volume

• preload, after load, and contractility
• 70 - 140 mL in man

Cardiac output max / Cardiac output rest = cardiac reserve

man (25L/min) / (5L/min) = 5

• man 5 L/min
• cow 30 L/min

man 25 L/min

• driving force of flow
• independent on diameter of vessels
• inlet pressure - outlet pressure = perfusion pressure (change in pressure)

• is determined by perfusion pressure and the resistance of a vessel
• resistance depends on the diameter

• FLow = (change in pressure) / (resistance)
• small tube, low flow = high resistance
• large tube, high flow = low resistance

• resistance of a vessle is determined by
• diameter
• length
• fluid viscosity
• Radius- determines mainly the resistance of flow, only variable that changes
• (8 x velocity x 1) / (pi x r^4) basically 1/r^4

• radius resistance
• 1 1/1
• 2 1/16
• 4 1/256

• arterioles control the blood flow in tissues by adjusting their diameter
• highest resistance

• total resistance to blood flow of all vessels of the systemic circulation
• (mean aortic pressure - vena cava pressure) / cardiac output = TPR

(systemic perfusion pressure) / cardiac output = TPR

mmHg / L min - units of TPR

• radius of vessels (power of 4)
• number of vessels
• length (minor influence)
• blood velocity

• Flow=change pressure / resistance
• same as
• cardiac output = perfusion pressure / TPR
• (perfusion pressure = arterial pressure - venouse pressure) neglect vena cava too low
• Cardiac output = blood pressure / TPR
• Blood Pressure = Cardiac output x TPR

determined by only the cardiac output and the TPR

per cent of blood that is cells

• higher the friction between cells, plasma and wall
• normal - 45%
• anemia - <45% about 14
• polycythemia - >45% about 65

• Determines the viscosity of blood
• anemia - less friction
• normal - 3
• polycythermia - higher friction

• decrease in resistance
• faciciltates perfusion of tissure
• low hermatocrit
• Low viscosity

• high hermatocrit
• living in high altitude
• dehydatration
• impeding
• hihg viscosity
• might lead to cessation of flow in capillaries and cause blood clotting

• is lower than in larger vessels
• RBC in single file and not touching walls = less friction

• increases when velocity decreases
• formation of larger aggregates
• increase viscosity
• can lead to blood clotting

• exchange between capillaries and ECF
• CO2 diffuses 20 times better that O2 - b/c higher diffusion coeficient
• rate of diffusion = (diffusion coeficient x area x change in ICF & ECF) / (change in Distance)
• hypoxia and hypercapnia
• lower molecular weight = higher permeability

• deficiency in O2
• more likely
• less diffusion

• excess in CO2
• less likely b/c high diffusion

• depends on molecular size
• larger less permeability
• impermeable - albumin and myoglobin
• permeable - water and salt

• high permeability
• intersitial protein con almost same as in cap blood
• fast diffusion can cause edema quickly with heart failure

• high permeability
• high rate of synthesis and decomposition of proteins

• LOW
• protection of brain from toxic substances

blood pressure filters fluid and solutes into intersititium

• Oncotic pressure
• generated by blood proteins
• resorption of fluid and solutes from the intersititium back to blood

• hydrostatic pressure
• push back into the blood
• opposes blood pressure

• Oncotic pressure
• pulls from blood
• opposes blood oncotic pressure

• resorption into side it is on
• only proteins of blood

• sum of all 4 pressures
• direction is determined by polarity ( + filtration, - resorption)
• rate of transport is determined by its value

(Pblood - Poncotic) - (Phydrostat - P oncotic) = net P

• filtration into interstitium b/c blood pressure is higher than oncotic
• net pressure : 10 mmHg
• net 1 to venous side to more filtration

• resorption b/c oncotic pressure is higher than blood pressure
• Net pressure : - 9 mmHg

• ~7,000 liters a day
• 5 Liters per min
• 20 Liters to intersititium

net pressure = hydrostatic pressure - oncotic pressure

• net pressure favors filtration into interstitium
• net flow from caps into interstitium
• net 1 mmHg on arterial side

• net pressure = hydrostatic pressure = oncotic pressure
• net pressure 10 times higher then other tissuses
• 10 mmHg
• higher permeability to plasma proteins
• protein concentration in ECF almost as high as in capillary blood

causes a contiunuous flow of water, solutes and proteins from capillaries into the interstitium

in interstitium (water, solutes, and proteins) would be lethal w/in 24 hr

maintains homeostasis by removing excess water, solutes and proteins from the interstitium

• through lymphatic vessels to the right ventricle
• catchment areas(lymph nodes)
• flows back to right atrium via ductus thoracicus or ductus lymphaticus dexter and joins venous blood

• lymphocentrum lumbale
• iliosacrale
• inguinale profundum

• cells are not connected, they overlap
• causing valves between intersititium and lymph duct
• fluid from interstitium is called lymph
• valves direct the lymph toward the heart

• passage of high molecular weight substances possible
• valves prevent reverse flow and limit hydrostatic pressure

• stretch of lymph vessels by fluid
• contraction of smooth muscles
• pressure up to 50 mmHg

• contraction of muscles
• movement of body parts
• arterial pulsations
• compression of tissues from outside

• movement of surrounding tissue enlarge and fill capillaries
• capillary valves prevent reverse flow and dircet lymph

• increases cap blood pressure
• decreases cap oncotic pressure (less into blood)
• increased cap permeability
• increased interstitial fluid protein

• accumulations of fluid in interstitium
• to much fluid would increase the distance between cap and cells = less exchange
• edema

• limited
• values above 1 mmHg flow cant increase and is at max value
• increase from -6 to 0 = 12 fold increase
• increase from 0 to 1 = 7 fold increase

• has bility to control its own local blood flow in proportion to its needs
• autoregulation can be superseded by central control

• perfusion is controlled by diameter of vessels
• diameter of vessels controlled by - local effects, neural activity, and hormonal signals

increase release of vasodilators (high O2 consumption)- increase concentration of vasodilators (decrease in concentration of O2) - arteriol constriction and resistance - increase in blood flow and number of open caps - increase in blood flow and surface area of caps w/ decrease in diffusion distance - concentration of vasodilators decreases - negative feed back

• Potassium
• CO2
• Adenosine

• decrease in oxygen and nutrients
• increase in metabloic wastes

• increases blood flow through dilation of arterioles
• potassium
• CO2
• Adenosine

• limits the increase in blood flow
• increase in O2
• decrease in concentration of vasodilators
• to much blood arterioles close

• from inside = tissue itself
• critical tissue
• brain, heart, working skeletal muscle

• from outside
• non-critical tissues
• kidney, stomach, intestines, liver, resting skeletal muscle

excessive blood volume in a tissue

• episodic color changes of fingers and toes in response to cold and stress
• vasospasm - white fingers
• compensatory vasodilation - red areas

• metabolism in tissue increases (exercise) cells produce more vasodilators (K, CO2, adenosine)
• increased vasodilators - aterioles dilate, increase blood flow
• vasodilation continues - removal of vasodilators by blood meets production of tissue cells, production and removal match, arterioles remain in opening stage, tissue has increased volume of blood

• normal blood flow - supply in and demand match
• metabolism increases - decrease in supply of O2 and relief of wastes
• feedback on arterioles - causes dilation, increase blood flow, now supplied at higher level
• increased profusion based on increase in metabolism
• longer blood flow adjustment to meet metabolic tissue demands

• blockage of blood flow - no supply and relief of cells stops
• increase in waste and vasodilators increases
• vasodilators have no effect b/c of the block
• when block is removed blood perfuses the tissue through dilated arteries
• vasodilators are washed away w. increased blood flow, arterioles constict
• balance

• interruption of blood flow - cessation of O2 supply and relief of wastes
• increase in vasodilators, blockage removed more blood flow through dilated arterioles, vasodilator level in interstitial fluid returns to normal and supply and relief levels are normal
• increased perfusion caused by a decrease in blood flow
• temporary increase of blood flow to cover the metabolic dept b/c of vasuclar occlusion

• blood flow usually returns to normal within minutes
• shorter time w/ blood loss = resupply w/ less blood flow for a shorter length of time
• longer time w/ blood loss = resupply w/ higher blood flow for a longer period

• perfusion pressure decreases sharply
• blood flow initially decreases too then returns to inital value in a short period of time
• steep decrease in perfusion pressure causes steep decrease in blood flow
• returns it almost to initial value

• perfusion pressure increases steeply
• blood flow initially increases too, returns almost the initial value within a chort period of time
• steep increase in perfusion causes initially an increase blood flow, deviation is compensated in seconds

• wide range of perfusion pressue 60 - 190 mmHg
• corresponding blood changes are very small
• if perfusion pressure drops below 60 mmHg = critical level, bad

• blood pressure increases (no change in metabolic rate)
• blood flow increases
• number of open capillaries increases
• increase in O2
• decrease in vasodilator concentration
• increase in arteriolar vasoconstriction
• increase in vascular resistance
• negative feedback

• metabolic control mechanism also accounts for autoregulation
• increase or decrease of the cencentration of vasodilators in the EFC changes the vascular resistance and thus the blood flow

• metabolism of tissue controls its perfusion
• slow but continuous

• increase of blood pressure streches the muscle fibers in the vascular wall
• muscle fibers respond with contraction
• responds faster
• protects the capillaries from excessively high blood pressures

• diastole - cardiac muscle is best supplied w/ nutrients (mostly from left ventricle), longer that systole
• shorten diastole - increased heart rate, less supply, limits max achievable heart rate

• compensated w/in a few seconds
• some deviations remain

• over a period of hours to weeks
• more precise

• Low pressure - increase in size and number of vessels
• increase in metabloism has same effect as low pressure
• high pressure - decrease in siz and number of vessels

• fast in young animals (days)
• fast in cancerous tissue
• slow in older tissure (months to years)

development of blood vessels

• angiogenic factors
• released from ischemic tissue
• rapidly growing tissues
• tissue with a high metabolic rate
• 3 factors
• Endothelia growth factor
• Fibroblast growth factor
• angiogenin

• Nor and Epi
• Angiotensin
• Antiduretic

• vasoconstrictor
• norepi more powerful
• (epi can also dilate)

• vasoconstrictor
• one of the most powerfull
• 1 microgram increase blood pressure more than 50 mmHg
• Renin - from kidney, angiotensinogen (liver), angiotensin (lung), aldosteron (hypothalamus)

• vasoconstrictor
• most powerful
• small quanitites released
• pressure regulation, important to kidneys which then reabsorb water
• stops urin production

• Bradykinin
• Histamine
• Prostaglandin

• vasodilator
• arteriolar dilation and increase permability of capillaries
• formed in tissue fluid
• (kallikrein converts kallidin to bradykinin)
• (constricts smooth muscle)

• vasodilator
• released in all tissues
• (damage, inflammation, allergic reaction)
• causes arteriolar dilation and increased capillary permeability
• fluid leaks out = edema

• vasodilation
• almost each tissue
• some cause constriction, most dilation
• importance in circulatory regulation not completely clear

• Calcium
• increase cause constriction
• stimulation of smooth muscles (contraction)
• stimulation = contraction of smooth muscle

• Potassium
• Magnesium
• Sodium
• Hydrogen ions
• Carbon dioxide
• Dilation = inhibit smooth muscle contraction

• increase causes vasodilation
• results from ability to inhibit smooth m. contraction

• increase causes powerful vasodilation
• inhibits smooth muscle generally

• increase causes mild vasodilation
• results from ability to inhibit smooth m. contraction
• (vasomotor in brain)

• vasodilation
• CO2 can cause constriction effect on vasomotor center

• normally little to do with adjustment of blood flow in individual tissue
• blood flow is usually controlled locally
• Controls global functions- redistributes blood flow, adjustment of cardiac output, reapid control of arterial blood pressure

cardiovascular centers in the medulla oblongata and formation reticularis

• norepi
• alpha 1 and 2 - all organs, arterioles, abdomenal organs and veins - vasoconstriction (inside cells)
• Beta 1 - heart and cardiac muscle cells - increase activity

• Epi and norepi
• beta 2 - heart coronary arterioles and skeletal muscle arterioles - vasodilation

• acetylcholine
• M 2 - heart, SA, AV, atrial cells - decrease heart rate
• M 3 - heart coronary arterioles - vasodilation

decrease heart activity b/c of high blood pressure

b/c dont want them to constrict which would decrease blood to cardiac muscle

causes - vasodilation in coronary circulation and skeletal muscles

• circulating epi and norepi
• beta 2 receptors
• vasodilation

• norepi from sympathetic nerve
• alpha 1 receptor
• vasoconstriction

• arterial baroreceptor reflex
• atrial volume receptor reflex

• responds to pressure changes (by sensing stretch or distortion of wall of vessels)
• location - carotid and aortic arch
• nerves - carotid sinus (glossopharyng), aortic arch (vagus)

• decrease in mean aortic blood pressure
• decrease in baroreceptor activity
• cardiovascular center in medualla oblongata
• increase sympathetic output - more Norepi
• Arterioles (alpha receptors)....... Ventricles(beta1 receptors)................SA node (Beta 1)
• increase vasoconstriction.......... increase force of contraction............... increase Ht rate
• increase peripheral resistance.... increase CO.......................................increase CO
• increase blood pressure

• decrease in mean aortic blood pressure
• decrease in baroreceptor activity
• cardiovascular center in medualla oblongata
• Parasymp output - Acetyle
• mescarinic receptor
• SA node
• increase heart rate
• increase cardiac output
• increase in blood pressure

• responds to volume changes (senses stretch of distortion of wall of an atrium)
• location - walls of the left and right atria
• nerve - vagus
• (cant measure pressure)

• inhibiting reflex causes wide variations in arterial blood pressure
• there is no long term adjustment
• standing up quickly from a lying position causes a drop in the pressure b/c of a change in the distribution of blood
• barorecptor responds immediately to change and returns blood pressure to its normal level

• afferent fibers of para
• receptors located in carotid arteries and aortic arch
• responds to stretch of arterial wall (baro = pressure)
• high speed of response
• requency of AP is proportional to arterial blood pressure - low pressure = low frequency
• slow adaptation to long term changes in blood pressure

• decrease in blood volume
• decrease in atrial stretch
• decrease volume receptor activity
• cardiovascular center in medulla oblongata
• increase sym & decrease para
• increase renin, increase in ADH, increase in thirst
• increase Na resporption, increase water resportion, increase water intake
• increase in blood volume

• immediate - use reserve venous volume in vessels = decrease in systemic volume (vasoconstriction, increase in cardiac activity) can use the 20L of fluid in ECF to supplement blood volume
• Long term - secure resources and replace losses (thirst, reduced Na excretion, stop urin production)

• afferent fibers of para
• receptors located in right and left atrium
• responds to stretch of atrial wall (more volume = more stretch)
• high speed response
• frequency of AP is proportional to the filling of the atria (low volume = low pressure = low frequency)
• immediate adaptation via sym and para activity
• long- term adjustment (kidneys)

• shift from venous to arterial to maintain pressure
• decrease in atrial pressure causes response from atrial volume receptor response
• sever blood loss - systemic pressure cant be maintained arterial baroreceptors respond too

• activates sym
• increase cardiac activity - increase in blood pressure, vasoconstriction, pale skin, dry mouth, mydriasis
• hormones - ADH, angiotensin, corticotropin
• central control - overpowers non-central control, baroreceptor reflex set to an elevated leve

• decrease in supply and relief cells by blood
• dilation of arterioles in skeletal muscles
• decrease in TPR
• decrease in systemic blood pressure
• decrease in baroreceptor activity
• increase sym, decrease para
• increase cardiac output (increase in CO, increase respiration and muscle pump)

• contraction increases blood pressure in veins
• proximal values open - blood pushed to heart
• relation - closes proximal valves, distal open and fill

• inspiration - decrease in pressure, pull veins from abdomen, lungs expand and fill w/ blood
• expiration - incease pressure and blood goes to heart

• heavy exercise - CO can increase 4-5 times resting level (RESERVE CAPACITY)
• CO limits exercise
• no limitation of respiratory system, or metabloism of skeletal muscles
• heart failure - exercise intolerance

• long term increase in blood pressure for a give output
• increase constriction of arterioles - increase in vascular resistance
• heart is forced to generate higher pressure
• occurs in pulmonary or sytemic circulation or both

• occurs w/o underlying reasons
• frequent in humans (~95%)
• rare in animals

• b/c of another primary disease
• Dog - renal failure and hyperadrenocorticism, angiotensin causes vasoconstriction and aldosterone via NaCl retention an increase in blood volume, causing increase in blood pressure
• Cat - renal failure and hyperthyroidism, thyroxine enhaces the effects of epinephrine and nore, increases blood pressure

impressions remain after crushig the edema

• from clostridium novyi infection
• anaerobic bacteria - produces toxins and gas, toxins cause edema (increase profusion of fluid)

• bilateral edema - after long time in bed in horizontal position
• insect bite

• clinically noticilble excess of intersitial fluid
• imbalance between filtration and resorption + lymph
• increase cap hydrostatic pressure (out of caps)
• decrease in plasma oncotic pressure (into caps)
• lesion of capillary cell membrane
• decrease of lymph flow

• arterial - hydrostatic pressure > oncotic pressure
• out of cap into interstitium, filtration

• venous - oncotic pressure > hydrostatice pressure
• into cap from interstitium, resorption

• 20 L per day are filtered from plasma into EFC
• 18 L return to plasma
• 2 L (10%) return to the circulation by lymphatic system

• increase in venous side
• decrease plasma oncotic pressure (hypoproteinemia)
• filtration exceeds resorption plus lymph flow = Edema

• 1. filtration limited- increase interstitial hydrostatic pressure
• 2. filtration reduced - decrease of interstitial oncotic pressure
• 3. lymph flow promoted - increase of interstitial hydrostatic pressure

• cardiac failure - left: lung(fluid filtered into alveoli and air spaces, cough of frothey fluid) right: abdomen
• increase venous pressure
• increase cap hydrosatice pressure
• increase filtration
• increase interstitial fluid volume (edema)
• increase intersitial fluid pressure
• increase lymph flow
• decrease concentration on interstitial protein

• malnutrition - Kwashiorkor, humand ascites, fluid in abdomen dont get enough protein, protien holds water, no absorption, use own body protein
• loss of proteins - nephrotic syndrome (glomerula permeable to proteins), sever burns (loss of through damaged capillaries) decrease in protein concentration of blood
• decrease protein concentration
• decrease blood oncotic pressure
• increase filtration Net
• increase interstitial fluid volume = edema
• increase interstitial fluid pressure
• increaser lymph flow
• decrease intersitital protein concentration

• mountain sickness - limited O2 transport capacity, 8-24 hr after first arrival(>3,000m)
• decrease O2
• increase areriolar dilation in brain
• increase cap blood pressure
• increase filtration
• increase intersitial fluid volume = edema
• increase fluid pressure
• increase lymph
• decrease intersitial protein concentration

• lymphedema - tumor, location depends on tumor
• parasites, disease - microfilaria(obstruct lymph vessels), elephantiasis, tuberculosis, pneumonia
• lymphatic obstruction
• decrease lymph flow
• increase interstitial protein concetration
• increase filtration
• increase intersitial fluid volume = edema
• increse interstitial fluid pressure

decrease - blood volume, central venous pressure, cardiac output, arterial pressure, haematocrit, nutrients, O2

• goal - return arterial blood pressure Survival
• Sym and para
• baroreceptors
• volume receptors
• CNS ischemic mechanism
• Chemoreceptors for O2

• Conservation
• vasoconstriction - decrease in renal flow, renin, decrease in loss of NaCl, antiburetic released
• vasodilation - stress relaxation mechanism, protect against too high blood pressure,
• (caonstiction maybe to stong and cut off circulation to an area so that is why dilation is needed so that tissues done die from full constiction)
• Capillary fluid shift - low cap hydrostatic pressure, fluid shift from interstitium to blood

• restoration
• renal body fluid controls
• decrease in renal blood flow
• renin release
• thirse - baroreceptor reflex, atrial volume reflex, hypothalumus (1-2days) thirst
• replacement of blood components - plasma proteins (liver, several days), blood cells (bone marrow, erythorpoetin) weeks

• ex - blood pressure at 50 mmHg
• pressure compensation in min
• w/o angiotensin and renin - 60mmHg
• w/ 83 mmHg

generalized inadquacy of blood flow throughout the body to the extent that the tissues are damaged b/c of too little flow

• vasoconstriction - cold limbs (exception : septic shock), pale skin
• Hypoxia - cyanosis, (blue tonguem blue conjunctivae)
• Low blood pressure - pulse thread like, oliguria (reduced urin formation)
• Sypathetic activity - mydriasis (dilation of the pupil)

external or internal bleeding

burn, sever bruises - loss of plasma

• loss of body fluid
• diarrhea, peritonitis

allergic reaction - loss of plasma

• vasomotor paralysis - smooth m. of vessels
• produced from bacteria

• depending on severity - full recovery w/o treatment
• vasoconstriction by ANS, Catecholamines (nor and epi), hormones reduces blood supply to non-vital organs
• heart - barorecptor reflex (lower AP b/c of lower aortic pressure)
• kidney - renin...angiotensin
• hypothalamus - ADH (vasopressin)
• suprarenal gland - cateholamines
• Increase in carbonic acid - decrease in pH = death of tissues
• dogs - 40 % of blood loss

• depending on severity - will fully recover possible with treatment
• nerval depression - O2 deficiency affects CNS : clouding of consciousness
• Cardiac depression - decrease arterial pressure, decreases coronary cirulation
• Vasomotor failure - O2 deficiency, nutrient deficiency, increase of metabolic wates in tissues : damage to cap membranes(arteriole smooth m. cant constrict), plasma shift to interstitium, decrease in blood volume, increase in viscosity, danger of thrombus

• No return possible - regardless of treatment = eventual death
• cardiac failure and failure of cardiovascular centers
• too much tissue damage
• too many destructive enzymes released into body fluids
• too much acidosis has developed
• even restoration of blood pressure in an irreverisble shock can't prevent death