CV1 Flashcards
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
what happens to CO with exercise
progressively increases as intensity increases
-max CO is the main factor for VO2 max
what is the main control centre for CV adjustments to exercise
nucleus tract solitarii
eqn for max HR
is relatively independent of fitness but dependent on age
= approx. 220-age
eqn for BP
CO x TPR
what happens to systolic and diastolic p with dynamic exericse
sys increases
dias changes less
describe main ways to control regional flow in active muscle
- vasodilationa and more capillaries open
- due to local metabolites effects on vasular muscle (CO2, less O2, inc H, inc ADENOSINE - via endothlium)
- opposed by symp vasocosntrit
describe main ways to control regional flow in inactive muscle and splanchnic circulation
sympathetic vasoconstrict
describe main ways to control regional flow in skin
- initial vasoconstrict (symp) followed by vasodilation due to inc in temp
- maximim exercise: vasoconstrict
- net effect: fall in TPR
why is increase in CO also needed during exercise
redistribution by vasoconstruction is not enough - increase muscle blood flow
what is the increase in stroke vol due to exercise caused by
inc CVP, inc skeletal muslce pump – frank straling
-enhanced emptying (sympathetic - increases contractiliy) so greater ejection fraction
describe changes to BP and HR with isometric exercise. when wil these changesbe seen
> 20% maximalvoluntary contraction (MVC)
- progressive rise in BP and HR
- systolid and dias both increase
- BP rise is greater than in dynamic exercise and does not plateau
net effect of dynamic exercise
-little diastolic change
inc in systolic
mean BP moderately increases
