what is the siphon principle
blood will continue to flow at a constant rate (standing or lying) if pump pressure is more than outflow presure
aka pressure in LV > RV
on what basis will flow rate not chnge
if tubes are rigid and in a closed system
mean capillary pressure at supine
30mmHg
mean arterial and venous pressures in supine position:
outflow from heart
flow into heart
pressures at feet (artery and vein)
outflow = 100mmHg
inflow = 4mmHg
feet arterial = 96
feet veous = 10
mean arterial and venous pressures immediately after standing:
outflow from heart
flow into heart
pressure at feet (artery and vein)
outflow = 11 mmHg
inflow = 1 mmHg
feet arterial = 186
feet venous = 100
what’s happens in the feet after standing
- capillary pressure (hydrostatic) increases due to pressure by column of blood
- more filtration = swell
- pressure gradient is the same: all pressures increase by same amoung
main events that occur during orthostasis
- decrease CO
- loss of plasma volume
why does CO decrease during orthostasis
- venous valves in lower limb shut transiently so blood flow out of heart > going in
- excess CO in veins for 45secs (300-500ml more)
- increase pressure in veins = open valves
- CVP reduced by 3mmHg so Frank starling = CO falls
why does plasma volume fall during orthostasis
- no change in oncotic pressure
- hydrostatic > oncotic so more outflow
describe the mechanism limiting effects of orthostasis by symp system and veno-arteriolar reflex
- blood pools at feet - lower CO, stoke vol, flow to brain and MABP in the upper body
- activate baro and volume (in heart) receptors
- sympathetic: vasooconstriction, raise HR and TPR
- local axon reflex: baro in veins sense distention = signals to arteriolar muscle to constrict
- reduce capillary pressure
describe the mechanism limiting effects of orthostasis physically
skeletal muscle pump
- aids venous return
- lower venous pressure to 20-30mmHg so therefore reduce capillary pressure behind
consequence of valve failure
more oedema
- fail in veins next to muscle exposes them to high pressure = not empty =
- varicose veins: remain distended
what happens to the vein above heart on standing
- veins outside craium collapse due to low pressure (flow through side margins to prevent sub-zero pressure)
- arteriovenous pressure gradient falls (drives cerebral perfusion)
- cerebral blood flow decreases by 20% on standing = faint
what happened to veins in the cranium on standing
- stay open
- gravity causes downwards displacement of CSF in subarachnoid space so -ve intracranial pressure
- expands bran and keeps veins open
- negative pressure WITHIN vein = air embolism opened during surgery
how does the following change from supine to upright: central blood vol CVP stroke vol HR CO cerebral flow
CBV: -400ml CVP: -3 mmHg stroke: -40% HR: +25% CO: -25% (net) cerebral: -20%
what progressively happens with prolonged standing
progressive. ..
- venous poling
- fall in pulse presure
- rise in HR and TPR
- fall in mean pressure
what suddenly happens in prolonged standing
- fall in TPR (vasodilate)
- fall in HR
- steep fall in BP and cerebral blood flow results in syncope (faint)
what is vasovagal syncope
vasodilation
vagally mediated bradycardia
describe response of CV to exercise: describe the muscle energy sources
- immediate: muscle ATP and phosphocreatine
- non-oxidtive: anaerobic glycolysis , glycoen–> lactate
- oxidative: aerobic metabolism. uses glc, lacate and FA. Increase O2 to muscle, prolonged
what is VO2 max
measure of ones ability to do exercise
reach max = small increase can e done anaerobically
eqn for O2 consumption
CO x (arterial - mixed venous O2 content)
= CO x (mls blood delivered to tissue) - (mls O2 rmoved from each ml blood)
what is O2 consumption determined by
- O2 delivered to tissues
- what the o2 extract (used up)
eqn for arterial O2 conc and what can affect this
[Hb] x arterial O2 saturation x 1.34
unaffected by exercise or fitness
what happens to venous o2 content during exercise
- falls as intensity increases
- can’t fall below certain level to maintain capillary pO2 to drive diffusion from blood to muscle (slow enough0
