Integrated cardiovascular responses I, orthostasis and exercise Flashcards

1
Q

Definition of vasovagal syncope

A

Vasodilation and vaguely mediated bradycardia leads to fainting
Mechanism to be supine and restore the venous return as fast as possible

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2
Q

Definition of orthostasis

A

Normal physiological response of SNS to counteract a fall in BP when a person is supine and then stands upright

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3
Q

Describe how blood flows in the body

What is the arterial pressure and the venous pressure out and into the heart

A

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

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4
Q

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

A

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

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5
Q

What are the blood pressures at the heart and the feet (arterial and venous) when upright
Explain why this occurs

A

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

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6
Q

Effects of orthostasis on cardiac output

A

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

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7
Q

Effects of orthostasis on plasma volume

A

Net hydrostatic P increases due to increased pooling

Net fluid filtration into interstitium => oedema

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8
Q

Describe the pathway that limits the effects of orthostasis in terms of cardiac output

What are the results of this mechanism

A
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)

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9
Q

Describe the mechanisms that limit the effects of orthostasis in terms of plasma volume

What are the results of this mechanism

A

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
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10
Q

Describe the mechanism that limits the effects of orthostasis in terms of the valves

A

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

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11
Q

What happens in valve failure

What can happen as a result

A

Venous P doesn’t fall as far

Failure in tributary superficial veins exposes them to chronic high P => varicose veins

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12
Q

How does the venous pressures above the head change when you stand for a long time

A

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

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13
Q

Describe how the venous pressure in the cranium is different to other veins

A

CSF is displaced downwards by gravity in subarachnoid space

Results in -ve intracranial P, prevents collapse

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14
Q

Summaries the typical CVS changes in orthostasis in terms of the heart and the overall effect

A

Direct effects of venous pooling
Central BV falls
CVP falls
SV falls

Due to reflex response
HR rises
Contractility rises

Net effect = decreased CO

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15
Q

Summaries the typical CVS changes in orthostasis in terms of the peripheral blood flow and the overall effect

A

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

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16
Q

Describe what happens during prolonged standing and postural hypotension

A

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
17
Q

What is a vasovagal syncope

A

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

18
Q

What are the 3 types of muscle energy sources for exercise

How long can you use each energy source for

A

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
19
Q

What is the relationship between muscle work and O2 consumption

A

Linear until max O2 consumption reached

Past this point, only a small increase of work can be down anaerobically

20
Q

How would you calculate the O2 consumption

What determines the O2 consumption

A

O2 consumption = CO x (arterial-mixed venous O2)

O2 consumption dictated by amount of O2 delivered to tissues and extracted

21
Q

What are the 3 limiting factors of max VO2

A

Arterial O2 content
Venous O2 content
Cardiac output

22
Q

How does arterial O2 content limit the max VO2

A

[Hb] x arterial O2 sats x 1.34

Cannot be changed by exercise or fitness

23
Q

How does venous O2 content limit the max VO2

A

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

24
Q

How does the cardiac output limit the max VO2

A

Increases with exercise intensity

MAX CO IS THE MAIN FACTOR DETERMINING VO2 MAX

25
Q

Describe the processes that occur in the CV system during exercise

A

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

26
Q

Effects of dynamic exercise on CV function and blood O2 content

  • CO?
  • TPR?
  • MABP?
  • SV?
  • HR?
  • Arterial and venous O2
A

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

27
Q

Describe the distribution of blood in the body at rest

A

Renal and splanchnic get the most

Skeletal muscle gets v little

28
Q

Describe the distribution of blood in the body during light exercise

A

Renal and splanchnic supply still high
Skeletal muscle gets more
Skin gets more for heat loss

29
Q

Describe the distribution of blood in the body during heavy exercise

A

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

30
Q

Describe the distribution of blood in the body during severe exercise

A

Renal and splanchnic get less
Skeletal muscle gets the most
Skin flow diverted to muscle
Coronary supply increases

31
Q

How is regional blood flow affected during exercise

A

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