Coordinated Cardiovascular Responses - Effect of Gravity and Exercise - Flashcards
Changing posture - Orthostasis
what happens to cvs when we stand up at first?
what three changes happen?
On standing up (orthostasis), the cardiovascular system changes according to the effect of gravity
Blood pressure falls at first
Postural hypotension, lack of blood flow to brain – faint
Quickly recovers
Due to homeostatic mechanisms
Integration of three smaller changes
Higher Heart rate
More Heart contractility
More Total peripheral resistance
Effects of gravity on blood pressures during orthostasis
what affect does gravity have in supine position?
how does this change when we stand up?
how does blood flow from heart to feet?
state equation and why blood flows
what is the issue at venous end?
supine position - gravity has a standard effect on all of body
standing - bp rises in legs for both arterial and venous system
So, how to get blood flow from heart to feet to heart??? Arterial pressure gradient is 95-185 mmHg - How will Darcy’s law work??
But we have Bernoulli’s law
Blood flow = pressure energy + potential energy + kinetic energy
Increased potential energy at heart level vs. feet
+ increased kinetic energy of ejected blood
Total energies mean blood flow from heart to feet
issue is at venioud end as its gravity vs pressure so relies on the momentum of blood as we go from venous system to heart
Why does gravity induce high blood pressures
in venous system
what type of vessels are veins? what does this mean?
where is pressure greatest and what can this lead to?
veins are very complaint vessesl so under pressure they will increase in volume
pressure will be greatest at the bottom due to gravity hence in veins the greater pressure will cause volume expansion because the walls of the veins are compliant which means veins hokd more blood when we stand up and it can lead to hypotension
How does orthostasis cause hypotension
what does standing cause?
what affect does this have on circulation and effect of this?
venous pooling means we can have +500ml pooling in the legs
this means Decreased CVP = Decreased EDP = Decreased SV (Starling’s law) = Decreased CO = Decreased BP hence Poorer perfusion of brain = Dizzy, Fainting (less drive to get blood from heart to brain)
Reflex response to orthostasis - Pressor response -
what will be stimulated less? what does this reduce activity towards? what fibres are switched off and what are switched on?
effect of this? (4)
net effect?
Less stimulation (unloading) of baroreceptors which reduces afferent fibre activity to NTS where it switches off inhibitory nerves in CVLM which switches on excitatory nerves in RVLM
Increased Sympathetic drive SA node = Higher HR Myocardium = More Contractility Vasoconstriction (arterioles, veins) = More TPR, More Venous return \+ Less Vagal activity to SA node
Together = Increase BP
What makes postural hypotension worse?
5 things
2 are linked to standing on a sunny day
medication - how?
physical issue?
what can cause severe drop in bp?
Drugs that reduce sympathetic activity/block vascular tone
e.g. Side effect with VGCC blockers used to treat hypertension, angina
Varicose veins - impairs venous return
Lack of skeletal muscle activity due to paralysis or forced inactivity
e.g. Long term bed rest, Soldiers on guard
Reduced circulating blood volume
e.g. Haemorrhage
Increased core temperature
Peripheral vasodilatation, less blood volume available
e.g. standing up after hot bath
Postural hypotension is an serious issue in the elderly - falls
Effect of Microgravity (space) on cardiovascular system
what will there be a less need for?
why?
Standing/lying down is the same in microgravity
There is less need for ANS, RAAS, ADH, ANP systems
to control blood pressure (systems needed to adapt under gravity)
All those systems we have involved to maintain CVS when we function under gravity so usually will go to lower extermities but during microgravity, more will return back to the heart
hence redistribution cause decrease in blood volume as you don’t need it due to microgravity as you don’t need BP to drive blood flow against gravity
initial effects of Microgravity (space) on cardiovascular system
what will increase and what is this detected by?
effect of this?
Initially: Increase preload/EDP, increase atria/ventricle volume
Sensed by baroreceptors/cardiac receptors (Reflex lecture)
Decreased Sym NS, RAAS, ADH + Increased GFR, ANP
Diuresis - Reduction in blood volume (BV) by 20%
Long term effects of microgravity (space) on cardiovascular system
what reduces and why?
Less BV, reduced stress on heart, heart reduces in muscle mass, general drop in BP – less BP is needed to drive circulation in space
On return to gravity - effects of Microgravity (space) on cardiovascular system
initially?
what happens over time? (2)
Severe postural hypotension, due to much smaller heart, Baroreceptor reflex can not compensate
BUT over time, this can be corrected with more fluids hence more blood volume therfore the kidneys won’t discrete it and heart will adapt and get bigger due to the demands
Cardiovascular responses to exercise
4 main things?
what three systems cause this?
Increase lung O2 uptake
Increase O2 transport around body
Increased O2 supply to selective tissues, e.g. exercising muscle
Control BP in face of huge increase in CO – prevent excessive afterload on heart
Due to Brain Central Command (early phase, more sym NS), Muscle mechanoceptors (less vagal, more sym), muscle metaboreceptors (more sym)
O2 uptake by pulmonary circulation can increase
13 times during strenuous exercise
How is this very big change brought about?
3 different mechanisms?
by the integration of three smaller changes
higher Heart rate 3 x
More Stroke volume 1.5 x
Both increase cardiac output/blood flow to lungs
More Arteriovenous O2 difference, (A-V)O2 3 x
We use up more O2 – greater concentration gradient in lungs
3 x 1.5 x 3 = 13.5 times
How is O2 uptake from the lungs increased?
2 things
Increase blood flow + Greater O2 gradient
Increased lung O2 uptake
How is cardiac output increased during exercise?
equation
which one is the limiting factor for increase
Increase in SV reaches max value
Plateau phase on Starling’s curve + maximum contractility
Rate increase is main factor increasing cardiac output
at high work loads hence increase in HR is relied upon during strenous exercise
Exercise-induced Tachycardia
what happens to hr before exercise?
what causes this?
what happens on initiation of exercise?
so what is decreased and what is increased?
Heart rate increases before exercise begins (ready for exercise)
Brain central command – higher centres -> says you’re gonna do exercise and trigger sympathetic system which increase HR
On initiation of exercise, muscle mechanoreceptors provide fast feedback to brain to increase heart rate
Maximum HR = 220 – age, 30 year old = increase 65 to 195 (3x)
decreased Vagal tone (to SA & AV nodes)
increased Sympathetic activity (to SA & AV nodes)
Exercise induced Stroke Volume
what happens to SV and why?
how does it increase?
what happens to ejection and how?
what happens to edv? how and what does this mean?
Stroke volume changes - increased sym activity (due to more contractility)
70 ml to 105 ml for 30 year old male = 1.5x
Increased end-diastolic volume
Increased Venous return/CVP through venoconstriction
Increased Sym NS + calf muscle pump - activates Starling law as more blood is returned to the heart
Faster ejection
More Contractility by Sym NS activation of B1 receptors
Decreased end-systolic volume (increased ejection fraction) hence more ejection
Accounts for increased stroke volume
Increased Contractility by sympathetic activation of B1 receptors + Starling’s law
What happens to increase in cardiac output – flow changes
how does blood flow increase to certain areas?
what 3 mechanims cause increased blood flow?
Vasodilatation of arterioles in active muscle (more O2/energy supply) myocardium and skin (cool down) during moderate exercise (heart, muscles and skin get supply of blood)
Fall in local arteriole resistance + Metabolic Hyperaemia
Metabolic vasodilatation -increased K+/H+
β2-mediated vasodilatation via circulating adrenaline
so more vessels are opened up and more blood flow to the area
What happens to blood pressure when CO up by x4.5?
BP = CO x TPR
what happens to co?
systolic pressure? diastolic?
what happens to BP? why? importance of this?
Large increase in CO
systolic pressure goes up slightly due to ejection at high pressure
diastolic pressure will have little to no increase
Relatively small increase in mean BP due to dilated
skeletal muscle arterioles (40%) therefore decreased TPR which has large drop
Prevents excessive afterload on heart
Compensatory vasoconstriction of non-essential circulations prevents hypotension due to exercise-induced low TPR
what does this prevent?
what controls this?
Compensatory vasoconstrictions in inactive or unrequired tissues
e.g. Kidney, GI tract, inactive muscle
Prevents BP from falling
RVLM controls specific pre-ganglionic sympathetic nerves in spinal cord which send out post-ganglionic nerves to specific vascular beds
Different exercise has varying action on BP
static - effect on hr and pressure
dynamic - effect on hr and bp
resistive - effect on hr and bp
Static
Constant contraction of small number of muscles, high load e.g. Handgrip (hr slightly up and pressure up a lot)
Dynamic
Shorten/length of many muscles, low load
e.g. Running (increase in HR but bp doesnt change much due to skeletal dilation)
Resistive
Dynamic + static with high load e.g. Weightlifting
V. High BP! and HR
Why does static raise BP more than dynamic exercise
Role of muscle metaboreceptors
what happens to muscles contracted in static form for long time? what does this stimulate? what are they sensitive to?
what is the reflec effect?
when is this very important?
why is the raised bP important?
muscle contracted in static form for long time builds up metabolites in it which will stimulate sensory nerves that go to brainstem + set up reflex effects
Small diameter sensory fibres in skeletal muscle
Chemosensitive - Stimulated by K+, H+, lactate, which increase in exercising muscle
Reflex effects
Increased sympathetic activity
Increased blood pressure – due to significant increased TPR, not such a large increase in HR (increase in tpr due to working 1 skeletal muscle hence don’t have to spread metabolic vasodilation with lots of muscle)
‘Pressor response’ to exercise
Especially important during isometric exercise (increased muscle load)
Raised BP creates more blood flow drive to contracted muscle So - more drive and greater local vasodilatation (metabolic hyperaemia) keeps blood flowing to contracted muscle
(can drive blood flow because you have lots of metabolic vasodilation occuring in muscle therfore in contracted muscle the blood vessels are dilated which means as long as you can force blood flow into contracted muscle, you will get blood flow in the tissue becuase vessels will be dilated hence static pressure where 1 or 2 muscles are contracted for a long time causes an increase in BP to drive blood into contracted muscle)
Summary of cardiovascular responses in exercise
what happens to o2 during exercise? how?
Direct the increased O2 supply to the exercising muscle via? (4)
Stabilization of BP - how?
Increase lung O2 uptake and Increase O2 transport around body via increased HR and SV
Direct the increased O2 supply to the exercising muscle via:
More extraction of O2 from blood - More O2 use
More capillary recruitment – greater capillary density
Metabolic hyperaemia
β2-mediated vasodilatation
Stabilization of BP
Vasoconstriction in non-exercising/non-required tissue
balances metabolic vasodilatation and β2-mediated vasodilatation
