Integrated cardiovascular responses I, orthostasis and exercise Flashcards
Definition of vasovagal syncope
Vasodilation and vaguely mediated bradycardia leads to fainting
Mechanism to be supine and restore the venous return as fast as possible
Definition of orthostasis
Normal physiological response of SNS to counteract a fall in BP when a person is supine and then stands upright
Describe how blood flows in the body
What is the arterial pressure and the venous pressure out and into the heart
At any given level above or below the heart, arterial pressure will always be higher than the venous pressure so flow continues
Arterial pressure = 95mmHg
Venous pressure = 4mmHg
What are the blood pressures at the heart and at the feet (arterial and venous) when supine
What is the mean capillary pressure
What is the pressure gradient at the feet
Arterial pressure leaving heart = 100mmHg
Arterial pressure at feet = 96mmHg
Venous pressure at feet = 10mmHg
Venous pressure entering heart = 4mmHg
Mean capillary pressure = 30mmHg
Pressure gradient at the feet = 86mmHg
What are the blood pressures at the heart and the feet (arterial and venous) when upright
Explain why this occurs
Arterial pressure leaving heart = 100mmHg
Arterial pressure at feet = 186mmHg
Venous pressure at feet = 100mmHg
Venous pressure entering heart = 1mmHg
Pressure gradient at the feet = still 86mmHg
Foot capillary P increases => increased filtration => oedema
Effects of orthostasis on cardiac output
Veins are distensible, increased P => increased D
When you stand
-Venous valves close transiently
-CO transiently exceeds F => heart
Excess CO pools in veins that distend
-Increased P in veins => opens valves => blood flows into heart
-However, CVP falls, FS mechanism => decreased CO
Effects of orthostasis on plasma volume
Net hydrostatic P increases due to increased pooling
Net fluid filtration into interstitium => oedema
Describe the pathway that limits the effects of orthostasis in terms of cardiac output
What are the results of this mechanism
Orthostasis Blood pools in extremities Decreased SV, CO, F to brain and MABP in upper body Baro, volume receptors activated Increased HR, VC, TPR Restored CVP Change reversed/minimised
Results in increased HR, CO, SV, systolic and diastolic (but gradually fall)
Describe the mechanisms that limit the effects of orthostasis in terms of plasma volume
What are the results of this mechanism
Arteriolar constriction reduces flow on standing
- Reflex sympathetic VC via baroreceptors of arterioles
- Axons sense VD, local axon sympathetic reflex => VC of terminal arteries
Results in
- decreased F in microcirculation
- decreased filtration
- decreased capillary P
Describe the mechanism that limits the effects of orthostasis in terms of the valves
Skeletal muscle pumping aids venous return
Valves open when muscle contracts, closes to stop back flow
Can lower foot venous P by 20-30mmHg from around 100mmHg
What happens in valve failure
What can happen as a result
Venous P doesn’t fall as far
Failure in tributary superficial veins exposes them to chronic high P => varicose veins
How does the venous pressures above the head change when you stand for a long time
P in veins above heart are low
Veins outside the cranium collapse a few cm above the heart
This prevents internal P from falling below 0 so F continues
Atriovenous pressure gradient driving cerebral perfusion falls
Veins in cranium don’t collapse => int P falls to -10mmHg => cerebral F falls by 20% => syncope
Describe how the venous pressure in the cranium is different to other veins
CSF is displaced downwards by gravity in subarachnoid space
Results in -ve intracranial P, prevents collapse
Summaries the typical CVS changes in orthostasis in terms of the heart and the overall effect
Direct effects of venous pooling
Central BV falls
CVP falls
SV falls
Due to reflex response
HR rises
Contractility rises
Net effect = decreased CO
Summaries the typical CVS changes in orthostasis in terms of the peripheral blood flow and the overall effect
Due to reflex response
Limb and splanchnic flow falls
TPR rises
Net effect = transient fall in BP (decreased CO x increased TPR)
Cerebral flow falls due to fall in P grad
Venous P falls less than arterial P