S2: Coordinated Cardiovascular Responses: Effect of Gravity and Exercise Flashcards
List some changes that may elicit responses by principle of adaptation by integration
- Excersize
- Flight and Fight
- Diving
- Microgravity
- Sleeping
Explain CVS changes during orthostasis (standing up)
CVS changes according to the effect of gravity
Blood pressure falls first due to pooling of blood in our extremities carried by our veins due to gravity (less CVP, less starlings law and less CO). Postural hypotension due to less BP (caused by decreased CO) causes lack of blood flow to brain causing people to feel faint.
However we quickly recover due to homeostatic mechanisms
What are the three homeostatic changes that occur to increase BP and BF to our brain?
- Increase heart rate
- Increase heart contractility
- Increase total peripheral resistance
Effect of gravity on blood pressure during orthostasis (feet to heart and heart to feet in arteries, feet to heart in veins)
- Feet to Heart in arteries - Blood flow gets from heart to feet to heart by arterial pressure gradient.
- Heart to feet in arteries - There is Bernoulli’s Law (blood flow = pressure energy + potential energy + kinetic energy. Increased potential energy at heart level vs feet (gravity) and increased kinetic energy of ejected blood. Total energies means blood flow from heart to feet.
- Feet to heart in veins - Blood from venules pool into larger veins which increase in velocity and kinetic energy of blood overcoming the effect of gravity so blood can flow from feet back to the heart
What is Bernoulli’s Law?
blood flow = pressure energy + potential energy + kinetic energy.
Why does gravity induce high blood pressures in venous system?
Gravitational (hydrostatic) pressure of a fluid in a solid tube:
Pressure (P) is higher at bottom of tube and this depends on height of column, density of fluid and gravity.
Gravitational (hydrostatic) pressure of a fluid in veins:
Veins are tubes with compliant walls. They expand and increase in volume so less blood is at the top of the tube and it pools at the bottom. The veins therefore have to constrict at the bottom to push blood back up (to the heart).
Equation for pressure in a tube
Pressure = phg
p= fluid density g= gravity h= height
How does orthostasis cause hypotension?
Blood not evenly distributed in veins and their is venous pooling in the legs.
Decreased CVP = Decreased EDP/EDV = Decreased SV (starling’s law) = Decreased CO = Decreased BP
Poor perfusion of brain causes dizziness and fainting
Describe the reflex response to orthostasis
Pressor Response
A drop in BP is sensed by baro and carotid receptors.
A decrease in BP will switch off the afferents going back to NTS, in other words there will be decrease in input to NTS. This decrease in input will decrease stimulation of CVLM, the decrease in stimulation of CVLM will switch off its inhibitory pathway to the RVLM.
Because the inhibition of RVLM is now turned off, the excitatory fibres from RVLM get switched on.
Which increases sympathetic drive, veno/vasoconstriction, incease HR, SV and therefore BP and BF) to:
· SAN -> increases pacemaker potential -> Increases HR
· Myocardium -> Increases contractility
· Resistance vessels -> increase contraction to increase TPR
· Capacitance vessels (veins) -> Helps venous return
This pathway also switches off vagal nerves which also increases sympathetic response
These reflexes is why we don’t faint when we stand up
What makes postural hypotension worse?
- Drugs that reduce sympathetic activity e.g. side effect with VGCC blockers used to treat hypertension and angina
- Varicose veins (increase in compliance of vein increases pooling of blood and makes vasoconstriction harder)- impairs venous return
- Lack of skeletal muscle due to paralysis or forced inactivity
- Reduced circulating blood volume
- Increased core temperature - Peripheral vasodilatation, less blood volume available (when baroreceptors try to work, not as much blood in heart) - uneven distribution of blood
Effect of microgravity (space) on CVS
Standing/ lying down is the same in microgravity (no gravity e.g. In space). No pooling on blood under microgravity, CVP greatly increases and blood returns to heart very easily.
There is less need for ANS, RAAS, ADH, ANP systems to control blood pressure (All those systems we have involved to maintain CVS when we functions under gravity)
What are the long term and short term effects of redistribution of blood into chest region in microgravity?
Initially: Increase preload/EDP, increase atria/ventricle volume. Sensed by baroreceptors/cardiac receptors
Decreased sympathetic nervous system (depressor response), RAAS, ADH and increased GFR, ANP diuresis - Reduction in blood volume (BV) by 20%
Long term: Less BV, reduced stress on heart, heart reduces in muscle mass, general drop in BP - less BP is needed to drive circulation in space. Body has adapted to microgravity enviroment.
On return to gravity - Severe postural hypotension, due to much smaller heart (lower BV, pooling of blood in extremities, less SV, CO, BP cannot be maintained). Baroreceptor reflex can not compensate.
Explain the cardiovascular response to excersize
CVS in excersize must acheive:
- Increase lung O2 uptake
- Increase O2 transport around the body
- Increase O2 supply to selective tissues e.g. excersing muscles not GI
- Control BP in face of huge increase in Co - prevent excessive afterload on heart
Control mechanism:
- Due to brain central command (early phase, increase sympathetic NS)
- Reflexes (feedback mechanisms): Muscle mechanoreceptors (decrease vagal, increase sym) , muscle metaboreceptors (increase sympathetic)
How is O2 uptake from the lungs increased during excersize?
Increase Heart Contractility and Increase SV both increase CO/BF to lungs.
There is a larger atriovenous difference as more O2 is used during excersize so a greater concentration gradient in lungs.
O2 uptake by pulmonary circulation can increase 13 times during strenuous exercise.
How is cardiac output increased during excersize?
Explain metabolic hyperaemia
Main factor during excersize: HR increases to increase CO for level of excersize though it is quite linear (increases up to a point)
SV reaches maximum contractility and plateaus.
CO = SV x HR
Vasodilatation of arterioles in active muscle (more O2/energy supply) myocardium and skin (cool down) during moderate exercise
Leg muscles –> work hard –> Metabolites (K+/H+) –> metabolic vasodilation –> metabolic hyperaemia
Sympathetic release NA primarily act at B2 receptors in skeletal muscle arterioles causing local vasodilation in the specific areas. B2 is also found in the coronary circulation so BF is also increased to the heart.
