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Flashcards in vasculature long Deck (25):

Components of vascular system and their role

- function is distribution and exchange

o aorta – compliance dampens pulse pressure from intermittent ejection

o large arteries – distribute, can constrict and dilate but don’t regulate BP and flow normally

o small arteries – distribute and resistance (regulate bp and flow)

o aretrioles – resistance

o capillaries – exchange (of O2, CO2, water, electrolytes, proteins, hormones) between plasma and tissue interstitium
• no smooth muscle, only endothelial cells and basement membrane
• massive cross sectional area
• slow velocity of blood flow image 40
• F=VxA, flow is product of mean velocity and cross sectional area

F= change in pressure/resistance (ohm)

o Venules – exchange, collection, capacitance
• When capillaries join
• As they get larger smooth muscle reappears so can constrict and dilate – this regulates capillary pressure and venous blood volume

o Veins – capacitance (most blood volume found and regional blood volume regulated)
• Constriction decreases venous volume and increases venous pressure – affects preload


blood pressure and volume through vasculature

Blood pressure - highest in aorta and down from there 

o aorta and large arteries little resistance so less loss of pressure energy along walls, 95mmHG
o 50-70% of pressure drop happens in resistance vessels,
o capillary pressure must be low to stop edema, 25-30mmHg
o falls even more in veins
o nearly 0mmHg at SVC, (fluctuates due to respiratory activity)

Blood volume

o 60-80% in venous
o distribution depends on blood volume, intravascular pressure and compliance (depends on state of contraction – sympathetic nerves)


resistance vessels

o constrict of dilate in response to autonomic nerve activity
• sympathetic adrenergic
o have receptors that bind hormones
• catecholamines, angiotensin II
o respond to products of surrounding tissue
• adenosine, K, NO
o respond to endothelium products



- Factors that determine blood flow to organs

o Mostly SVR as arterial and venous pressure kept in a narrow range

Flow or CO = (MAP – CVP)/SVR (ohms) 




Pulse pressure and compliance

change in SV affects pulse pressure or MAP?

- pulse pressure – diff between systolic and diastolic
o increased by increase in SV or decrease in compliance

change in pressure(pulse pressure) = change in volume (stroke volume)/compliance

- compliance = change in volume/change in pressure 
o non linear – decreases with higher volumes and pressures (and age, athlerosclerosis)
o determined by components of media
• elastin – least resistance, so more compliant (aorta)
• smooth muscle
• collegen – greatest resistance

o change in compliance affects pulse pressure but not mean pressure if CO and SVR don’t change

o change in SV affects both pulse pressure and MAP if CO changes (but if CO doesn’t change, ie decreased HR, change in SV only affects pulse pressure)
• so older ppl have bigger pulse pressure cos need this to give same stroke volume as decreased compliance



o At rest MAP ~ Pdias + 1/3(Psys-Pdias)
o At high heart rate MAP ~ average of Psys and dias
o MAP = (CO x SVR) + CVP – rearrangement of ohms law 

o  MAP increases with CO, more so if increased SVR, less so if decreased. If venous pressure the same
o CO, SVR and venous pressure interdependent to try and keep MAP the same
• Change in one changes other
• Also affected by extrinsic factors
• Baroreceptors


PO 1.47 Control of BP and distribution of blood volume

total peripheral resistance and factors affecting it

o Total of veins and arteries, excludes pulmonary

SVR ~ (viscosity x length)/ radius to power of 4 
SVR = (MAP-CVP)/CO but MAP, CVP and CO do not determine SVR


  • At normal temp plasma viscosity is 1.8 x water, whole blood viscosity is 3-4 x water
  • Increased by increased haematocrit (polycythemia), decreased temp and low flow (microcirculation in shock which causes adhesive interactions)
  • Haematocrit – volume of RBC/volume blood 40%
  • Polycythemia haematocrit up

• Radius of small arteries and arterioles most important – sympathetic NS
• Relative series and parallel also important (see resistance card)
• Pressure decreases SVR because it increases diameter

• CO and SVR are independent but MAP changes with both


PO 1.47 Control of BP and distribution of blood volume

total peripheral resistance and factors affecting it

Poiseuille's equation

Flow ~ (change in pressure x radius to power 4)/ viscosity x length

combo of following 2 equations:

F=change in P/R

R ~ visocity x length/radius to power of 4

• Incorrectly assumes
• vessels are long, straight, rigid
• blood behaves as a Newtonian fluid (viscosity constant and independent of flow)
• blood flowing is laminar

• important as describes dom influence of radius on resistance and flow
• change in diameter really affects flow (or perfusion pressure if flow held constant)
• F ~ r to the power of 4
• assumes driving pressure, viscosity an vessel length constant


PO 1.47 Control of BP and distribution of blood volume

total peripheral resistance and factors affecting it

how to calculate resistance


• organ circulation is in parallel which decreases total vascular resistance
• poiseuille’s equation only applies to single vessel, if 1 or a small number of vessel to kidney contricts by 50% only those vessels have 16 fold increase in resistance but change to overall kidney resistance is immeasurable
• reciprocal of total resistance =  sum of reciprocal of all resistances in parrelel
o so total resistance is less than the single lowest resistance

• but within an organ it’s a combo of series and parallel
• Total resistance = sum of all segments of resistance in series
o Change in large artery resistance has little effect on total resistance unless decreased by more than 60-70% (critical stenosis) because it may only contribute to 1% of total resistance so even a 16 fold increase (if constrict by 50%) in resistance doesn’t do much
o But change in small artery and arteriol has a great effect on total resistance


PO 1.47 Control of BP and distribution of blood volume
total peripheral resistance and factors affecting it

factors affecting vascular tone

• Resistance vessels usually sit partially constricted from smooth muscle contraction

• Extrinsic
o Sympathetic nerves
o Circulating hormones – angiotensin II
• Intrinsic
o Endothelial derived factors – endothelin-1, NO
o Myogenic tone of smooth muscle
o Locally produced hormones
o Local produced metabolites –adenosine and H+ both relax

• Vasocontrict – for BP and SVR
• Vasodilate – for blood flow



- CVP is specifically the BP in the thoracic vena cava
o Determines filling pressure, which contributes to preload, which affects stroke volume which affects CO

change in pressure = change in venous volume/venous compliance

o Factors that increase venous pressure:

• Decreased Venous compliance

  • Sympathetic adrenergic vasoconstrictor tone occurs basally, decreases volume too
  • (Nitrodilators increase compliance, decrease pressure and increase volume
  • Circulating vasoconstrictors - Catecholamines, angiotensin II
  • Valsalva (forced expiration) - Compresses thoracic vena cava as intrapleural pressure rises
  • Limb and abdo muscle contraction - Compresses veins

• Increased Venous volume:

  • Total blood volume increase - Renal failure, Activation of renin-angiotensin-aldosterone system
  • Decreased CO - From low HR (av block) or SV (vent failure), As blood backs up
  • Resp activity – mechanical, Inspiration, decreases RAP so increased VR
  • Contraction of skeletal muscle pump- mechanical- Espec leg and abdo, Forces blood into thoracic compartment, Venous valves
  • Gravititational forces – standing to supine - mechanical - Shifts blood volume into thoracic venous compartment
  • arterial dilation- withdrawal of sympathetic or use of vasodilator drugs increases flow of arterial to venous, decreases resistance to venous return, increases VR

Diagram below 

• At lower pressure and volume more compliance as vein collapses

  • Until stretched small pressure change can cause large volume change

• At high pressure/volume compliance is low

  • Once stretched can’t increase volume much due to collagen, smooth muscle and elastin


Factors that influence VR

Anaesthetic factors too


• those that change mean systemic filling pressure see image 50

  • blood volume – kidney, can increased Mean circ filling so increased VR fasting decreased VR
  • venous compliance – sympathetic can cause decreased venous compliance which increases mean circ filling so increased VR (or think about like decrease compliance increases pressure, preload and CO which increases VR) GA /spinal venodilation decreased VR, vasodilate decrease RVR but overall decrease VR

• those that change RAP

  • respiration – inspiration drops RAP so increased VR PPV decreased VR, lithotomy and pneumoperitoneum increases intrabdopresure so decreased VR 
  • increased intrapericardial pressure increases RAP so less VR

• those that affect RVR

  • valsalva, increases RVR so decreased VR

• muscle pump and valves GA decreased VR
• gravity – when stand decrease RAP and CO and flow so decreased VR even though increased lower limb pressure should make blood flow to low flow RAP trendelenburg increased VR,
• atrial contribution to ventricular filling

? also decreased SVR increases VR


PO 1.45 factors that determine and control cardiac output and implications for practise

cardiac output and vascular function curves

vascular function curve

Mean circ filling pressure/means systemic pressure

• pressure at zero systemic flow, if CO stops, RAP rises and aortic pressure falls until they equal. 7mmHg. 
• RAP increases cos blood not going through, less arterial blood volume and more venous blood volume
• If heart stops intravascular pressure in whole system is a function of total blood volume and vascular compliance
• Magnitude of relative change between RAP and aortic p determined by venous to arterial compliance, change in arterial volume equals change in venous volume so cancel each other out, image 46
• If ratio is 15mmHg, get 1mmHg increase in RAP for every 15mmHg drop in aortic pressure


PO 1.45 factors that determine and control cardiac output and implications for practise

cardiac output and vascular function curves

vascular function curve

VR or CO or flow = (MAP - CVP)/SVR

- venous return depends on pressure diff between aorta and RA divided by resistance – short segment only
- factors determining venous return from capillaries

  • diff between mean capillary and right atrial pressure divided by resistance of all post capillary vessels
  • or to determine venous return of entire systemic flow its diff between aortic pressure and RA pressure over SVR


• cardiac output is the independent and its effect on RAP
• CO max value is limited cos onces RAP negative veins collapse
• OR RAP is the independent and its effect on Venous return (then call it venous return curve)

  • curve A -blood volume and compliance shifts the curve
  • curve B – decreased SVR increases RAP cos vessels dilate so arterial pressure and volume decrease so more venous volume so more RAP(how does graft B reflect this? What is the slope reflecting? The reciprocal of SVR? – compliance?)
  • note – change in SVR (arterial constriction and hence BP) does not affect mean circulatory filling pressure because only 2% of blood volume in arterioles. Vasoconstriction increases BP and afterload so decreases VR and CO ? arterial compliance has little effect on overall vascular compliance, it is determined by venous compliance. Small change in arterial diameter casues large change in arterial resistance

• Sumary of factors that affect curve (same as factors that influence VR)

  • Volume, venous compliance, muscle pump, respiration, posture


PO 1.45 factors that determine and control cardiac output and implications for practise

cardiac output and vascular function curves

cardiac output curve

o Like frank starling, CO vs RAP, as RAP (independent) increases so does CO (dependant), depends on inotropy and afterload, HR also shifts image 51
• If RAP = 0mmHg, CO = 5L/min
• Shifts up and to left with increased cardiac performance

  • Increased HR - symp
  • Increased inotropy - symp
  • Decreased afterload

• Shifts down and to right with decreased cardiac performance

  • Myocardial damage, ischaemia, infection, neoplasm, parasympathetic, rate/rythem disturbance, expiration or open thoracic cage as increased ITP

• Magnitude of change is determined by the systemic vascular function 


PO 1.45 factors that determine and control cardiac output and implications for practise
cardiac output and vascular function curves

equilibrium point

- venous return should equal cardiac output over time as it’s a closed system, right and left pump in series

  • except not really cos fluid lost by kidney, skin, GI

- blood flow (cardiac output/venous return) depends on cardiac and systemic vascular function and where they intercept

  • o these are interdependent
  • o where the lines of each graft intercept is the equilibrium point where the heart functions, usually 5L/min and 0mmHg

• systemic vascular function curve moved by

  • venous compliance from sympathetic activation
  • systemic vasacurlar resistance

• cardiac function curve moved by

  • increased HR from sympathetic
  • increased inotropy from sympathetic

• means that for cardiac output to increase signif more than just the cardiac function curve needs to change, also need to move the systemic vascular function curve to augment venous return and maintain RAP
• SO cardiac output limited by factors that determine vascular function


PO 1.45 factors that determine and control cardiac output and implications for practise
cardiac output and vascular function curves

equilibrium point

heart failure

o Heart failure effect on combined cardiac and systemic function curve
• Cardiac function limits venous return cos decreased inotropy and increased afterload
• This increases RAP and vent pressure and preload so frank starling compensates for loss of inotropy
• Also increased blood volume, decreased venous compliance and ? increased SVR (should it be decreased) moves vascular function curve up so increased CO
• Both of these at expence of increased RAP


effect of HR on CO

see image 55

• This alone doesn’t really increase CO from HR 50 - 170 unless there is a change in demand for flow from tissues
• Eg exercise – muscle arterioles dilate, drop SVR, veins less compliant increasing VR
• Eg anaesthesia – brady cardia may drop CO if spinal anaesthetic and hypovoleamic (increased venous compliance and decreased volume
• HR <40 and >170 drop CO as too slow and increased RAP and not enough time for ventricular filling


PO 1.48 Discuss cardiovascular response to change in posture

lying to standing

what happens pre compensation


  • Supine aortic BP 95mmHg, feet 20mmHg, CVP 0mmHg
  • level of heart and feet same so no appreciable hydrostatic pressure difference
  • Diff between MAP and CVP is systemic perfusion pressure
  • Mean capillary hydrostatic pressure is between MAP and CVP ~ 25mmHg


  • Circulation is subject to effects of gravity, acts as hydrostatic column of fluid
  • If heart to feet is 120cm, get 120cmH2O exercted on capillaries = 88mmHg on top of 20mmHg (mercury is 13.6 times denser than water so 120 x 10/13.6, times cmH20 by .77 to get mmHg)
  • Or brain 30cm = decrease of 22mmHg from 90mmHg
  • This drop happens immediately
  • Hydrostatic force increases transmural pressure (intravascular – extravascular pressure, ie distending pressure)
  • blood from thoracic compartment accumulates in lower extremeties in veins as vasculature is compliant.
  • This causes oedema in feet and loss of intravascular volume
  • CVP falls, reduces preload and stroke volume (frank starling), reduces CO and MAP (its like CVP and MAP resviour are in the legs)
  • Fall in MAP is 10-20 times greater than fall in CVP
  • Systolic BP drop >20mmHg – orthostatic/postural hypotension
  • Decreases cerebral perfusion, syncope


PO 1.48 Discuss cardiovascular response to change in posture

lying to standing

compensatory mechanisms to maintian MAP and blood flow

 • Normally only get 10-20mmHg increase in capillary/venous pressure and drop in CVP and MAP reversed after few seconds:

o baroreceptor reflex:

  • decreased BP in carotid and aortic receptors detected by high pressure baroreceptors so decreased firing and removal of inhibition of vasomotor centre in medulla
  • Sympathetic causes:
  • Vasoconstriction (more so)– increased SVR and so MAP
  • Venoconstriction (less so)– increased VR and CO and so MAP
  • Increased HR
  • Increased ionotropy, SV and CO

o Mygenic reflex
o Venous valve functioning – one way, breaks up column of blood,
o Muscle pump keeps pressure <30mmHg, espec if move quickly after standing
o Abdominothoracic pump
o Thoracic pump with respiration


PO 1.48 Discuss cardiovascular response to change in posture
lying to standing

compensatory mechanisms to maintian cerebral blood flow

limits drop to 20% so don’t get ischeamia
• CBF = Cerebral perfusion pressure (CPP)/cerebro vascular resistance = MAP-CVP(ICP)/CVR

• CVR affected by

  • Metabolic autoreguation – blood redistributed to part of brain needed to maintain consciousness via local release of vasoactive substances
  • Pressure autoregulation (myogenic mechanism) – low MAP = low CPP = decreased stretch on arterioles so get reflex decreased resting tone and increased diameter so less CVR over seconds to minutes
  • Decreased flow decreases pCO2, increases pH and decreases pO2 which vasodilate so decreased CVR

• CPP affected by

  • Decreased CVP from upright posture
  • Monroe-kelly doctrine – cos cranium vault CPP and ICP must balance
  • So decreased CVP get decreased ICP, allowing increased CPP and CBF
  • Hydrostatic pressure with standing makes CSF pool in spinal cord so further decreased ICP

o This happens in seconds


PO 1.48 Discuss cardiovascular response to change in posture

soliders collapse standing still

o No muscle pump, blood pools, decresed VR and CO, decreased CPP
o If hot get venodilation, valve may even become incompetent
o Carotid sinus reflex isn’t good at venoconstrction


abdomino thoracic respiratory pump


• Pressure diff between abdo vena cava and RA divided by resistance determines venous return
• Increased RAP = decreased venous return = decreased stroke volume
• Intrapleural pressure (normally negative) determines pressures in vena cava, heart chambers and pulm vasc

• Right heart

  • More negative with inspiration due to chest wall expansion and diaphragm down
  • This expands lungs, vena cava, atria and ventricles which decreases pressure in them
  • Increased pressure gradient for venous return
  • Also, increased transmural pressure means atria more expanded, increased sarcomere length and filling/preload 
  • opposite in expiration

• Left heart

  • Same happens to pressures of left ventricle and atria but filling not enhanced cos pulm vaculature acts as a capacitance and its blood volume increases, in expiration blood forced into left heart so increased filling and therefore stroke volume

NET effect of increased rate and depth of respiration is increased venous return and cardiac output


skeletal muscle pump

• Veins have one way valves towards heart
• When muscles around veins contract they compress veins
• Closes upstream (where blood came from )valves and opens downstream valves facilitating venous return, lowers venous and capillary pressure
• Counteracts gravity
• Varicose veins – veins enlarge, valve incompetent, increased venous and capillary pressure, oedema


PO 1.48

cardiovascular response to valsalver maneouvre

• Exhale forcefully against closed glottis (or sealed mouth/nostrils)
• Increases intra thoracic pressure – increased intrapleural pressure, collapses thoracic vena cava, decreases venous retun
• Decreased transmural pressure, chamber volume decreases (despite large increase in pressure in chamber)
• Decreased preload and stroke volume and CO and MAP. 4 phases: see image 54

  • 1. Raised ITP squeezes pulm vasc so initial increased VR to left heart, so increased SV and BP for few seconds, raised ITP also compresses aorta so increased BP. HR steady
  • 2. Get decreased CO and BP, picked up by baroreceptor, sympathetic increase HR and vasoconstrict to maintain BP (goes above usual) but CO low so organ blood flow low. Can’t do this if under anaesthesia or adrenergic failure. Pulse pressure drops cos less CO (drops systolic) but vasoconstric (keeps diastolic up)
  • 3. When release get opposite, less squeeze of pulm vessels, less VR to left heart, BP drops. HR steady
  • 4. Continued relief of straining, increased VR to left heart, CO restored, BP overshoots cos peripheral vessels still constricted from phase 2. Sensed by baroreceptor, vagal slow of heart and vasodilation, BP normal

• valsalver ratio  - fastest HR in phase 2:slowest HR in phase 4 (>1.5)

• CCF – square wave response

  • BP high all through phase 2 no increased in HR. because increased resevior of blood in pulm vasc (like phase 1 is longer)
  • BP low in phase 4 and no decrease in heart rate


  •  Won’t get increased HR in phase 2 so when phase 4 starts HR lower and less overshoot in BP

If alpha blocked

  • Lower BP in phase 2 cos cant constrict, ? increased overshoot in phase 4

Clinical use

  • Revert SVT due to vagal response in phase 4
  • Test autoommic function
  • Hear murmers of HOCM and mitral valve prolapse better

• Same with straining to use bowels or lifting heavy weight while breath holding

absent overshoot in phase 4 with autonomic dysfunction