Regulation of BP Flashcards
Heart and BVs integrated and controlled - required to maintain tissue perfusion across whole of the body - this is to…
- To keep a relatively constant arterial BP
Too low -> blood flow to organs would fail
Too high -> damage to vessels and organs - To control distribution of total CO
5L/min not sufficient to perfuse entire body
Needs to respond to tissue demands
Satisfied by local control mechanisms
To what extent can nervous control influence arterial pressure?
Can increase to 2x normal within 5-10sec
Can decrease to 50% normal within 10-40s
Reflex control of BP - describe fundamental components of a reflex control system
Fundamental components of a reflex control system:
- Internal variable to be maintained
- Receptors sensitive to change in variable
- Afferent pathways form receptors
- An integrating centre for afferent inputs
- Efferent pathways from integrated centre
- Target effectors that alter their activities
mean art BP = CO x TPR
What are baroreceptors and their function?
Found in carotid artery (afferent fibres follow glossopharyngeal nerve) and the aortic arch (afferent fibres follow vagus nerve)
They are stretch receptors and respond to changes in arterial BP by sensing change in tension of arterial wall - fast response
Firing rate increases when BP inc and decreases when BP dec
Sensitive around a set point
Primary purpose is to reduce the minute to minute variations or arterial pulse
What are cardiopulmonary baroreceptors?
Low pressure receptors that sense central blood volume - atria, ventricles, veins and pulmonary vessels
If rate of baroreceptor firing decreases (signalling decreased blood volume) then symp nerve activity to heart and BVs increase and parasymp activity to heart decreases
What is medullary cardiovascular control (MCVC) ‘vasomotor’ area?
- Sensory area - input from baroreceptors
- Lateral portion - efferent symp nerves
- Medial portion - efferent parasymp (vagal) nerves
Describe symp and parasymp effects on heart and BVs
Symp and parasymp effect the heart - both control HR and normally function simultaneously - at rest parasymp is predominate tone and symp can significantly effect SV and rate
Symp effects on BVs - continuous low level tone affects TPR - sympathetic vasoconstrictor tone exerts vasomotor tone on vessels, therefore kept partially constricted
Veins also innervated by symp - decreases capacitance -> increased venous return -> increased SV -> inc CO
What is CNS ischaemic response?
Emergency pressure control system - last ditch stand
When blood flow to CVCC is decreased - increased peripheral vasoconstriction (almost completely occludes some peripheral vessels), increased symp stimulation of heart, increased systemic arterial pressure
Fine control of blood flow
Local control superimposed on organ distribution of CO - tissues auto-regulate blood flow - build up of local factors (i.e. adenosine) and independent of innervation/hormonal control
Intrinsic ability to maintain blood flow safely across capillaries if Bp increases - myogenic theory (acute auto-regulation) - stretch induced vascular depolarisation of SM due to increased arterial pressure
Remember not all capillaries in an organ perfuse simultaneously
Summarise TPR - influencing factors
Influenced by:
- Arteriolar radius - neural controls, hormonal controls, local controls
- Blood viscosity - hematocrit
How is BP regulated long-term?
Control of body fluid volume by kidneys - when arterial pressure increases, urine production increases and vice versa
The two primary determinants are:
- Renal output curve for salt and water
- The level of salt and water intake
What is ADH released in response to?
Released by the pituitary gland in response to:
- Increased osmotic pressure - hypothalamic osmoreceptors
- Hypovolemia - atrial baroreceptors normally inhibit ADH release, decreased volume leads to decreased firing rate and increased ADH release
- Hypotension - decreased areyrial baroreceptor firing, increased symp activity and increased ADH release
- Angiotensin II
How does ADH work?
Increases blood volume by increasing water permeability in renal collecting ducts - decreased urine production
In severe hypovolemic shock ADH release is high, causes vasoconstriction, increases TPR
What is renin and what is it released in response to?
Enzyme released from kidneys in response to:
- Symp nerve activation - mediated by baroreceptor feedback
- Renal artery hypotension - independent of baroreceptor feedback
- Decreased sodium in kidney distal tubules
What are the effects of Angiotensin II (product of renin)?
- Acts on resistance vessels - increases TPR
- Acts directly on kidneys - constricts renal arteries and therefore decreases blood flow via kidneys
- Causes release of aldosterone from adrenal glands - increased sodium and water reabsorption
- Stimulates release of ADH from pituitary