Blood Pressure Flashcards
Which 2 factors is MABP dependant on
Cardiac output (volume per min)
And total peripheral resistance
What is total peripheral resistance
Sum of resistance to flow in all vessels
How do you work out MABP
CO x TOtal peripheral resistance
What would happen to blood pressure if CO or TPR increased
It would also increase
What 3 things affects TPR
1- blood viscosity
2- vessel length
3- vessel diameter
SV x HR = CO
Which factors affect HR
Control of HR by the autonomic NS (efferent)
How does the PNS have effect on heart rate
PNS sends signal down the vagus X nerve
This causes release of acH which then later binds to the muscarinic receptors
This binding causes decrease in HR
What 2 things does muscarinic binding via Ach do to decrease HR in SAN
Slows depolarisation in the pacemaker potential
Makes more negative RMP so that threshold is reached slower
What effect on channels does ach have which reduces HR at san
Increases K permeability which allows repolarisation instead
What is lowered HR called
Bradycardia
The SNS allows release of Nadr and adr from adrenal medulla, what does this allow
Increase HR
By binding at the B1 receptor which causes increased HR
As well as increased HR, what does SNS adr/nadr binding to B1 do
Increases contraction at heart muscles
What stimulation effects on the SAN does the SNS adr/nadr release have
Increases rapid depolarisation in pacemaker potential
Also causes a less negative RMP
Threshold reached quicker
What is increased HR called
Tachycardia
What is a change in HR called
Chronotopic effects
To control stroke volume (factor of CO) what 2 mechanisms are there
Intrinsic and extrinsic mechanisms
What is the intrinsic control of stroke volume about
Suggests stroke volume is dependant on muscle fibre length when in diastole
How can an increased VR cause an increase in SV/force
Increased VR will mean cardiac muscle stretches more in late diastole (when filling)
This increased stretch/EDV will increase the force so increases volume out of the heart(SV)
Why is less ca2+ needed to cause tension in stretched muscle fibres
Increased sensitivity of proteins to calcium when muscle fibre is stretched due to increased VR which causes increased EDV
Why is the intrinsic law to regulating SV important
It allows CO to be equal to VR
If VR increases so does SV which increases CO
What would happen if VR and CO weren’t equal eg if Right ventricle was higher output
More blood would be going to the lungs(VR) than to the body(CO)
This causes oedema (flooding of the lungs)
What 5 things maintain VR which allows to maintain CO by affecting SV intrinsically
Venous- atria pressure gradient
Venous valves - stop back flow
Respiratory pump
Skeletal muscle pump
Venomotor tone
What is the venomotor tone which maintains VR
It’s the fact that veins smooth muscle is supplied with SNS which allows contraction
What is the extrinsic mechanism to controlling SV
Contractility of muscle dependant in the SNS (B1 adr/nadr binding)
Which system is activated when adr/nadr binds to B1 to increase contraction
Adenylate cyclase
Causes production of camp
Which 2 proteins does cAMP phosphorylate
Ca2+ channels
Phospholamban
What happens when ca2+ channels are phosphorylated by pka system (SNS)
Increases opening of Ca2+ channels which increases trigger calcium
Increased trigger calcium causes increased release of calcium via ryanodine channels on SR
This increases amount which binds to troponin = contraction
How does phospholamban increase contraction
It increases Ca2+ ATPase activity to increase calcium in SR so more is released
Why does phospholamban cause shorter contractions of heart muscle
Increased Ca2 ATPase activity causes more ca to be removed from the troponin site, which means contraction occurs shorter
What is change in muscle relaxation called
Lusitropic effects
What is increased contractility via SNS called
Positive ionotropic effects
