Blood pressure: role of cardiac output & peripheral resistance L8 Flashcards

1
Q

what is needed for blood to flow

A

need a pressure gradient

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2
Q

what is the more precise version of blood pressure

A

mean arteriole blood pressure
- needs to be maintained in order to get blood to flow

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3
Q

what is mean arteriole blood pressure the product of

A
  1. Product of the input to the arterial system
    Cardiac output
  2. total peripheral resistance
    - Sum of individual vessels resistance to flow
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4
Q

what is the equation for mean arteriole blood pressure

A

cardiac output X total peripheral resistance

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5
Q

what is the typical values of SV, HR and CO at rest

A

SV: 70mL
HR: 70 beats per min
CO: 4.9l/min

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6
Q

during exercise, CO can increase
why is this

A

due to the autonomic neural control of the heart

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7
Q

describe the systems that decrease heart rate
- what do the nerves release and what do they act on
- what type of receptor does the neurotransmitter bind to

A

parasympathetic nerves (vagus)
- realease ACH on to the SA and AV node
- ACh binds to muscarinic receptors which decreases heart rate

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8
Q

describe the systems that increase heart rate and contractility
- what do the nerves release and what do they act on
- what type of receptor does the neurotransmitter bind to

A

sympathetic nerves
- releases noradrenaline on to SA, AV node and cardiac muscle
- binds to beta 1 adrenergic receptors
- increases heart rate and contractility

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9
Q

if an antagonist is added to parasympathetic nerves

A

heart rate would increase
- small amount of ACh is being released which dampens down heart rate
therefore, if this is blocked, heart rate would increase
- increases dynamic range

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10
Q

on a graph that shows the sympathetic stimulation with SA node pacemaker activity,
what does the curve look like compared to the curve of membrane potential at rest

A

there is more pacemaker potentials when sympathetically stimulated
- there is a steeper slope of pacemaker potentials and the resting membrane potential is less negative so threshold value is reached quicker
- increases heart rate

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11
Q

what is increased heart rate called

A

tachycardia

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12
Q

how does the sympathetic supply increase heart rate

A

noradrenaline causes sodium channels activity to increase so more Na+ entering allowing depolarisation

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13
Q

on a graph that shows the parasympathetic stimulation with SA node pacemaker activity,
what does the curve look like compared to the curve of membrane potential at rest

A

there is less pacemaker potentials when parasympathetically stimulated
- there is a shallow slope and the resting membrane potential is more negative to being with making it harder to reach threshold
- decrease heart rate

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14
Q

what is decrease in heart rate called

A

bradycardia

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15
Q

why does parasympathetic supply decrease heart rate

A

ACH binds to K+ channels activating them
- increasing K permeability, more K leave then Na in
- MORE neg so harder to depolarise

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16
Q

what are the two mechanisms of controlling stoke volume

A
  1. intrinsic
    - Frank-Starling Mechanism or Starling’s Law of the heart
  2. extrinsic
    - Increase in sympathetic activity
17
Q

describe Starling’s Law of the heart

A

the force of contraction is proportional to the initial muscle fibre length in diastole
(Initial means just before contraction commences)

18
Q

explain how Starling’s Law of the heart increases stroke volume

A
  1. an increase in blood returning to the heart (venous return) will increase the end diastolic volume which stretches the cardiac muscle
  2. this stretching increases the force of the subsequent contraction causing stoke volume to increase
    - The heart will pump whatever volume of blood it receives
    - the more you will a ventricle, the harder it will contract
19
Q

describe the resting stroke volume and stoke volume after stretching on a Left ventricular function curve

A

If you increase venous return to left side of the heart, the stroke volume will be higher than when at rest due to the stretching and increased filling

20
Q

why does stretching increase stroke volume and force of contraction

A

when muscle fibres stretch, they become more sensitive to calcium
therefore, when given fibre at rest and one that has been stretched the same amount of calcium, stretched fibre will produce the bigger contraction
- intracellular [Ca2+] required to generate 50% maximum tension is lower when the muscle fibre is first stretched

21
Q

what is the importance of starling effects

A
  1. helps to match output of right and left sides of the heart
  2. enables heart to adapt its pumping capacity when either venous return or arterial blood pressure changes
22
Q

why is matching output important

A

if the right output is higher than left (even by as little as 1%),
more blood would be going to lungs than the rest of the body at every heart contraction
Pulmonary blood volume would go from 0.6 to 2.1 litres in 30 mins
This would cause severe oedema in the lungs and you would literally ‘drown’!!
This is prevented from happening because if RV output goes up then LV filling increases during diastole, producing more stretch, and thus SV, and therefore CO, goes up to match this increase in VR.

23
Q

explain how extrinsic mechanisms control stroke volume

A

there is an increase in sympathetic activity
- this doesnt change muscle fibre length but instead enhances contractility of cardiac muscle

24
Q

how does sympathetic activity enhances the contractility of cardiac muscle

A

increases adrenaline or noradrenaline binding to B1 adrenergic receptors
- Results in enhanced stroke volume
- Smaller ESV at the end of contraction
Known as a positive inotropic effect

25
Q

what type of hormones are adrenaline and noradrenaline

A

catecholamines

26
Q

How do catecholamines increase contractility

A
  1. bind to B1 on myocardial contractile cell activating the cAMP pathway
  2. causes the phosphorylation of Voltage gated calcium channels and phospholamban
  3. when voltage gated sodium channels are phosphorylated, channels stay open for longer, so more trigger calcium allowed in, so more calcium released from SR causing more forceful contraction
  4. the phosphorylation of phospholamban causes increase activity of Ca ATPase
    - this increase Ca in SR which can be released and
    - means Ca is removed from cytosol quicker so shorter time it is bound to troponin so shorter contraction duration
27
Q

what are Changes in the rate of muscle relaxation known as

A

lusitropic effects

28
Q

what needs to be maintained when cardiac output changes

A

venous return

29
Q

how is venous return maintained

A
  1. Venous to atrial pressure difference
  2. Venous valves
    prevent ‘back-flow’ of blood
  3. skeletal muscle contraction (‘skeletal muscle pump’)
  4. Venomotor tone
    some veins have smooth muscle and receive sympathetic supply
  5. Respiration (‘respiratory pump’)
    inspiration aids venous return