Blood pressure: role of cardiac output & peripheral resistance L8 Flashcards
what is needed for blood to flow
need a pressure gradient
what is the more precise version of blood pressure
mean arteriole blood pressure
- needs to be maintained in order to get blood to flow
what is mean arteriole blood pressure the product of
- Product of the input to the arterial system
Cardiac output - total peripheral resistance
- Sum of individual vessels resistance to flow
what is the equation for mean arteriole blood pressure
cardiac output X total peripheral resistance
what is the typical values of SV, HR and CO at rest
SV: 70mL
HR: 70 beats per min
CO: 4.9l/min
during exercise, CO can increase
why is this
due to the autonomic neural control of the heart
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
parasympathetic nerves (vagus)
- realease ACH on to the SA and AV node
- ACh binds to muscarinic receptors which decreases heart rate
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
sympathetic nerves
- releases noradrenaline on to SA, AV node and cardiac muscle
- binds to beta 1 adrenergic receptors
- increases heart rate and contractility
if an antagonist is added to parasympathetic nerves
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
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
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
what is increased heart rate called
tachycardia
how does the sympathetic supply increase heart rate
noradrenaline causes sodium channels activity to increase so more Na+ entering allowing depolarisation
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
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
what is decrease in heart rate called
bradycardia
why does parasympathetic supply decrease heart rate
ACH binds to K+ channels activating them
- increasing K permeability, more K leave then Na in
- MORE neg so harder to depolarise
what are the two mechanisms of controlling stoke volume
- intrinsic
- Frank-Starling Mechanism or Starling’s Law of the heart - extrinsic
- Increase in sympathetic activity
describe Starling’s Law of the heart
the force of contraction is proportional to the initial muscle fibre length in diastole
(Initial means just before contraction commences)
explain how Starling’s Law of the heart increases stroke volume
- an increase in blood returning to the heart (venous return) will increase the end diastolic volume which stretches the cardiac muscle
- 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
describe the resting stroke volume and stoke volume after stretching on a Left ventricular function curve
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
why does stretching increase stroke volume and force of contraction
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
what is the importance of starling effects
- helps to match output of right and left sides of the heart
- enables heart to adapt its pumping capacity when either venous return or arterial blood pressure changes
why is matching output important
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.
explain how extrinsic mechanisms control stroke volume
there is an increase in sympathetic activity
- this doesnt change muscle fibre length but instead enhances contractility of cardiac muscle
how does sympathetic activity enhances the contractility of cardiac muscle
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
what type of hormones are adrenaline and noradrenaline
catecholamines
How do catecholamines increase contractility
- bind to B1 on myocardial contractile cell activating the cAMP pathway
- causes the phosphorylation of Voltage gated calcium channels and phospholamban
- 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
- 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
what are Changes in the rate of muscle relaxation known as
lusitropic effects
what needs to be maintained when cardiac output changes
venous return
how is venous return maintained
- Venous to atrial pressure difference
- Venous valves
prevent ‘back-flow’ of blood - skeletal muscle contraction (‘skeletal muscle pump’)
- Venomotor tone
some veins have smooth muscle and receive sympathetic supply - Respiration (‘respiratory pump’)
inspiration aids venous return
