Coordinated CVS Responses Flashcards
Describe immediate effect of standing up (orthostasis)
- CVS changes according to effect of gravity
- gravity pulls blood
- less CVP
- less Starling’s law
- less CO
- BP falls at first (postural hypotension)
- lack of drive of flow to brain
- can cause fainting
How to recover from standing up (orthostasis)?
homeostatic mechanisms (baroreflex)
How to modulate homeostatic mechanisms (baroreflex)?
Increase in:
- HR
- Ventricular contractility (maintains SV/CO despite less blood returning to heart)
- TPR (+constriction of veins)
What happens to BP in supine position + why?
- Head, heart, feet constant as tube of blood horizontal
- Venous system p equal in head + feet
- Lower venous system p in heart where large veins due to less resistance (vital as helps blood flow back to heart)
What happens to BP when standing up + why?
-Effect of gravity
-Arterial system mean BP similar
-In head BP lower
-Feet higher BP
-Venous system p in feet high
-Low venous system p to heart
So in the feet:
Arterial p increased from 95 to 185 mmHg now standing
Venous p increased from 10 to 90 mmHg
Why does arterial blood flow down to feet + not up to
heart?
Blood higher up in arteries have higher potential energy Arterial system 95mmHg pushing blood down + potential energy caused by gravity (exerting around 90-100mHg) so small p diff between feet + heart
but large vessels to feet allow movement despite small p diff
How blood moves back up to heart?
increased potential energy at heart vs feet + increased kinetic energy of ejected blood
Why does gravity induce high BP in venous systems?
blood vessels in our leg are like tubes with
fluid in it that have diff pressures at diff depths depending on height of fluid column
What’s Bernoulli’s law?
BF = p energy + potential energy + kinetic energy
Why is fluid at bottom of tube under greater pressure than at top?
Pressure = ρhg
ρ : fluid density
h : height (of fluid column)
g : gravitational acceleration constant (gravity)
Why’s there pooling of blood in lower extremities?
veins are distensible so under pressure they stretch + increase in volume
Effect of pooling of blood in lower extremities on BP?
causes the drop in BP as less is going back to the heart
Why do veins expand with increased p?
veins are distensible so increase in p isn’t used to push
blood forward so exerted in walls expanding the veins
Describe how standing up decreases BP
- stand up
- pooling of blood (+500ml) in legs
- increases transmural p
- less BF back to heart
- decrease CVP + EDV
- less Starling’s law + SV
- less CO
- decrease in BP
How does orthostasis cause hypotension?
- causes fall in CVP
- decreased stroke volume (Starling’s)
- decreased CO
- decreased BP
- poorer perfusion of brain
- dizzy, fainting
What measures drop in BP?
Mechanoreceptors in atria + ventricles
Baroreceptors in aortic arches + carotid sinus
Reflex response to orthostasis?
- decrease in BP
- switches off afferents going back to nucleus tractus soltarius
- decrease in input to nucleus tractus soltarius.
- decrease stimulation of CVLM
- switches off its inhibitory pathway to the RVLM.
- excitatory fibres from RVLM switched on
- increases sympathetic drive to:
- SAN = ↑ pacemaker potential + HR
- Myocardium = ↑ contractility
- Resistance vessels = ↑ contraction so ↑ TPR
- Capacitance vessels (veins) = helps venous return
- decreases vagal inputs to SAN
- reduced bradycardic effects of vagus nerve on SAN
What makes postural hypotension worse?
-α-adrenergic blockers/VGCC blockers
-Varicose veins = impaires venous return –> lower CVP –> lower BP
-Lack of skeletal muscle activity from paralysis or forced inactivity = can’t use skeletal muscle pump, so
decreasing return to heart
-Reduced circulating blood volume / haemorrhage = less blood back to heart
-Heat = causes peripheral vasodilatation so blood to skin so less to heart eg standing up after a hot bath causes dizziness
Effect microgravity (space) on CVS?
- Standing or lying down same in microgravity
- Less need for ANS, RAAS, ADH, ANP systems to control BP as no gravity
Describe initial effect of mictogravity on redistribution of blood into chest region?
- Initially:
- less blood to lower extremities
- increase preload
- increase atria/ventricle volume
- increased SV sensed by cardiac mechanoreceptors
- decreased sympathetic by more stretching of the receptors
- NS, RAAS, ADH + Increased GFR, ANP
- diuresis (water loss)
- lower blood volume by 20%
Describe long-term effect of mictogravity on redistribution of blood into chest region?
- less BV
- reduced stress on heart
- heart reduces in muscle mass
- drop in BP
Describe effect after effects of mictogravity on redistribution of blood into chest region?
- severe postural hypotension
- smaller heart
- low blood volume
- baroreceptor reflex cannot compensate
- takes time for normal baroreceptors to reach former threshold
Diff between dynamic vs static exercise + eg?
Continuous contraction + relaxation (running) Just contracting (lifting weight)
Purpose of CVS during exercise?
- ↑ pul circulatory O2 uptake
- ↑ O2 transport
- Direct increased O2 supply to exercising muscle
- Maintain BP despite increase in CO by changing TPR (prevent afterload + reduced output of heart)
Reflex of muscle mechanoreceptors?
- Respond to movement in muscle
- Decreases vagal activity
- Prevents heart being slowed down
- Respond to increased metabolites in response to exercise
- Increases sympathetic
eg of integration?
O2 uptake by pul circulation which increases 13x during strenuous exercise
Small integrations response to exercise?
- ↑ HR
- ↑ SV
- ↑ CO
- ↑ arterio-venous O2 diff due to more O2 being removed from blood by muscle so helps gradient to get oxygen into pul circulation + get O2 out into tissues
How is O2 uptake from lungs increased?
- pulmonary BF = CO
- increases with exercise
- O2 consumption increases
- same saturation of blood
- more blood going to lungs picking up more O2
- tissues extract more O2
- greater arterio-venous O2 diff
Describe how greater arterio-venous O2 diff is done
- increasing BF to skeletal muscle
- increases capillary recruitment
- more area for O2 uptake + shorter distance
- quicker passive diffusion
- more extraction of O2 into tissue
Describe how increased cardiac output is done
- HR increases gradually for strenuous exercise
- provides extra CO needed
- SV increases rapidly for light exercise
- harder exercise HR starts to take over
- SV plateaus
- starts to decrease as BP increases
- greater afterload
What’s the potential increase of HR?
3x
220 – Age
eg 30yr has max HR change of 65 - 190bpm
How HR increased?
due to central command getting body for
exercise + muscle metaboreceptors/mechanoreceptors
-increases HR by decreasing vagal para:
removes vagal tone setting
resting HR at SAN
effecting conduction speed of AVN
-increase in sympathetic:
drive increase in HR (acting at SAN + AVN)
-release of adrenaline (catecholamines) acting at β1 on heart
Why’s driving increase in HR vital in transplant patients?
lost innervation of heart from sympathetics so rely fully on adrenaline/NA to increase HR
How much does SV increase?
- increase in sympathetic
- increase in SV
- 30yr SV 70ml to 105ml (1.5x increase)
Describe how increased SV is done?
-increase in sympathetic causes venoconstriction
-increase venous return (CVP) to heart
-if using calf muscle pump drives venous return.
-Starling’s law:
small increase in end-diastolic volume so greater contractility so greater SV
-sympathetics also cause increase in contractility via activating β1
-Ca2+ influx
-cardiac myocytes = increase contractility (inotropic effect)
-faster contraction
-decrease in end-systolic volume (increase in ejection fraction)
-ejecting more from a full chamber so increase in SV
Remember the equation: CO = HR x SV
Why’s CO increased?
-increase in CO (increase of 4.5x, 5 to 22l/min) can be accounted for by increase in HR (3x) + increase in SV (1.5x)
Describe how increased CO targets muscle during exercise?
- increase CO
- more blood oxygenated
- target flow/CO to right tissue
- A binds to β2 –> vasodilation
- fall in local resistance in vascular skeletal muscle arterioles
- also metabolic vasodilatation.
- vasodilatation of active muscle, myocardium, skin during exercise increases BF
Describe what happens to BP when CO increases by X4.5?
-BP = CO x TPR so expect to increase HOWEVER
-increases slightly when exercising heavy.
-diastolic pressure unchanged
-systolic increases due to increased power of
contraction
-increase in CO so large drop in TPR due to vasodilatation in muscle
-so can exercise hard +long but keep BP same so heart can pump against a reasonable BP
Role of RVLM?
controls specific pre-ganglionic symp nerves in spinal cord which send out post-ganglionic nerve to specific tissues
What prevents hypotension due to exercise-induced drop in TPR?
-compensatory vasoconstriction in inactive tissues prevents BP falling
-BF decrease in splanchnic vessels,
kidneys, other inactive muscles occurs via α1
-huge increase in flow to lungs
Why do static exercises raise BP more than dynamic exercises?
- Dynamic big increase in HR due to contract+relax continuously
- Static HR increases slightly, but BP increase a lot due to muscle contracted constantly, so BF to muscle prevented + low, build up in metabolites, so increase drive of blood to tissue increasing BP
Describe metaboreceptors
-static exercise = mechanoreceptors (small diameter sensory fibres) activated in muscle, metaboreceptors (chemosensitive) recognise rise in metabolites(K+, H+, lactate) –> stimulate symp to increase BP (pressor response to exercise) + slight tachycardia to maintain perfusion to contracted muscle
Especially occurs in isometric exercises (increased muscle load)
