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
Describe what happens during prolonged standing and postural hypotension
Prolonged standing leads to
- increased venous pooling
- increased fall in pulse P
- increase in HR and TPR
All lead to a fall in the mean P, cannot compensate forever
Leads to
- Sudden VD
- fall in TPR and HR
- fall in BP and cerebral flow
- Syncope
What is a vasovagal syncope
VD and vaguely mediated bradycardia
By fainting => horizontal, venous return is restored
If kept upright after syncope, BP will stay low and may lead to brain damage
What are the 3 types of muscle energy sources for exercise
How long can you use each energy source for
Immediate
- ATP and phosphocreatine
- Quickly depleted within seconds
Non oxidative
- Anaerobic glycolysis (muscle glycogen => glucose => lactate)
- For minutes
Oxidative
- Aerobic metabolism with glucose, lactate, fatty acids
- Needs more O2 delivery tp working muscle
- During prolonged exercise, FA becomes the main source
What is the relationship between muscle work and O2 consumption
Linear until max O2 consumption reached
Past this point, only a small increase of work can be down anaerobically
How would you calculate the O2 consumption
What determines the O2 consumption
O2 consumption = CO x (arterial-mixed venous O2)
O2 consumption dictated by amount of O2 delivered to tissues and extracted
What are the 3 limiting factors of max VO2
Arterial O2 content
Venous O2 content
Cardiac output
How does arterial O2 content limit the max VO2
[Hb] x arterial O2 sats x 1.34
Cannot be changed by exercise or fitness
How does venous O2 content limit the max VO2
Falls as intensity increases, limited by need to maintain capillary PO2 to drive diffusion to muscles
Falls more with training as capillary density increases and diffusion distance decreases
How does the cardiac output limit the max VO2
Increases with exercise intensity
MAX CO IS THE MAIN FACTOR DETERMINING VO2 MAX
Describe the processes that occur in the CV system during exercise
Central command
Nucleus tractus solitarius
Increased SNS and plasma catecholamines and decreased PNS
Increased HR, SV => increased CO
Increased F to muscles ATP consumption and work
Increase in metabolites (ADO) by skeletal muscle => increased VD
More blood diverted to working muscle => small increase in MABP
Baroreceptor reflex reset upwards
Increased SNS, muscle pump
Increased CVP and FS mech
Increased CO
Effects of dynamic exercise on CV function and blood O2 content
- CO?
- TPR?
- MABP?
- SV?
- HR?
- Arterial and venous O2
Increased CO, TPR so MABP increases slightly (systolic rises, diastolic can rise/fall)
SV increases initially but plateaus, balanced against increased HR and contractility => smaller diastolic timeframe
Increased HR, max dependent on fitness but age dependent
-Resting and submax lower HR with increasing fitness
Amount of arterial O2 doesnt change but volume extracted does => decreased mixed venous O2
Describe the distribution of blood in the body at rest
Renal and splanchnic get the most
Skeletal muscle gets v little
Describe the distribution of blood in the body during light exercise
Renal and splanchnic supply still high
Skeletal muscle gets more
Skin gets more for heat loss
Describe the distribution of blood in the body during heavy exercise
Renal and splanchnic supply falls
Skeletal muscle gets more
Skin gets more, venous plexuses relax => heat loss
Coronary supply increases as HR and contractlity increases
Describe the distribution of blood in the body during severe exercise
Renal and splanchnic get less
Skeletal muscle gets the most
Skin flow diverted to muscle
Coronary supply increases
How is regional blood flow affected during exercise
Active muscle
- VD and capillary recruitment due to local metabolites (ADO, H+, PCO2) and endothelium
- Metabolic VD partly opposed by SNS VC
Inactive muscle and splanchnic circulation
-SNS VC, divert blood to muscles
Skin
-Initial VC increases with SNS to lower P
Followed by VD, decrease in SNS due to increased temp
At max intensity, VC dominates to diver blood to skeletal muscle
All results in a net fall in TPR
