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CVS II > Coordinated CVS Responses > Flashcards

Coordinated CVS Responses Flashcards

1
Q

Describe immediate effect of standing up (orthostasis)

A
  • 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
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2
Q

How to recover from standing up (orthostasis)?

A

homeostatic mechanisms (baroreflex)

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3
Q

How to modulate homeostatic mechanisms (baroreflex)?

A

Increase in:

  • HR
  • Ventricular contractility (maintains SV/CO despite less blood returning to heart)
  • TPR (+constriction of veins)
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4
Q

What happens to BP in supine position + why?

A
  • 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)
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5
Q

What happens to BP when standing up + why?

A

-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

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6
Q

Why does arterial blood flow down to feet + not up to

heart?

A

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

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7
Q

How blood moves back up to heart?

A

increased potential energy at heart vs feet + increased kinetic energy of ejected blood

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8
Q

Why does gravity induce high BP in venous systems?

A

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

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9
Q

What’s Bernoulli’s law?

A

BF = p energy + potential energy + kinetic energy

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10
Q

Why is fluid at bottom of tube under greater pressure than at top?

A

Pressure = ρhg
ρ : fluid density
h : height (of fluid column)
g : gravitational acceleration constant (gravity)

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11
Q

Why’s there pooling of blood in lower extremities?

A

veins are distensible so under pressure they stretch + increase in volume

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12
Q

Effect of pooling of blood in lower extremities on BP?

A

causes the drop in BP as less is going back to the heart

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13
Q

Why do veins expand with increased p?

A

veins are distensible so increase in p isn’t used to push

blood forward so exerted in walls expanding the veins

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14
Q

Describe how standing up decreases BP

A
  • 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
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15
Q

How does orthostasis cause hypotension?

A
  • causes fall in CVP
  • decreased stroke volume (Starling’s)
  • decreased CO
  • decreased BP
  • poorer perfusion of brain
  • dizzy, fainting
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16
Q

What measures drop in BP?

A

Mechanoreceptors in atria + ventricles

Baroreceptors in aortic arches + carotid sinus

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17
Q

Reflex response to orthostasis?

A
  • 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
18
Q

What makes postural hypotension worse?

A

-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

19
Q

Effect microgravity (space) on CVS?

A
  • Standing or lying down same in microgravity

- Less need for ANS, RAAS, ADH, ANP systems to control BP as no gravity

20
Q

Describe initial effect of mictogravity on redistribution of blood into chest region?

A
  • 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%
21
Q

Describe long-term effect of mictogravity on redistribution of blood into chest region?

A
  • less BV
  • reduced stress on heart
  • heart reduces in muscle mass
  • drop in BP
22
Q

Describe effect after effects of mictogravity on redistribution of blood into chest region?

A
  • severe postural hypotension
  • smaller heart
  • low blood volume
  • baroreceptor reflex cannot compensate
  • takes time for normal baroreceptors to reach former threshold
23
Q

Diff between dynamic vs static exercise + eg?

A 
Continuous contraction + relaxation (running)
Just contracting (lifting weight)
24
Q

Purpose of CVS during exercise?

A
  • ↑ 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)
25
Q

Reflex of muscle mechanoreceptors?

A
  • Respond to movement in muscle
  • Decreases vagal activity
  • Prevents heart being slowed down
  • Respond to increased metabolites in response to exercise
  • Increases sympathetic
26
Q

eg of integration?

A

O2 uptake by pul circulation which increases 13x during strenuous exercise

27
Q

Small integrations response to exercise?

A
  • ↑ 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
28
Q

How is O2 uptake from lungs increased?

A
  • 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
29
Q

Describe how greater arterio-venous O2 diff is done

A
  • increasing BF to skeletal muscle
  • increases capillary recruitment
  • more area for O2 uptake + shorter distance
  • quicker passive diffusion
  • more extraction of O2 into tissue
30
Q

Describe how increased cardiac output is done

A
  • 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
31
Q

What’s the potential increase of HR?

A

3x
220 – Age
eg 30yr has max HR change of 65 - 190bpm

32
Q

How HR increased?

A

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

33
Q

Why’s driving increase in HR vital in transplant patients?

A

lost innervation of heart from sympathetics so rely fully on adrenaline/NA to increase HR

34
Q

How much does SV increase?

A
  • increase in sympathetic
  • increase in SV
  • 30yr SV 70ml to 105ml (1.5x increase)
35
Q

Describe how increased SV is done?

A

-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

36
Q

Why’s CO increased?

A

-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)

37
Q

Describe how increased CO targets muscle during exercise?

A
  • 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
38
Q

Describe what happens to BP when CO increases by X4.5?

A

-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

39
Q

Role of RVLM?

A

controls specific pre-ganglionic symp nerves in spinal cord which send out post-ganglionic nerve to specific tissues

40
Q

What prevents hypotension due to exercise-induced drop in TPR?

A

-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

41
Q

Why do static exercises raise BP more than dynamic exercises?

A
  • 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
42
Q

Describe metaboreceptors

A

-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)

CVS II (19 decks)

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