Control of Blood Pressure Flashcards
why is blood pressure so tightly controlled
BP - driving force of tissue perfusion
too low bp - tissue will not perfuse properly
too high bp - pathological damage occurs in tissues
poor renal perfusions lead to
drop in filtration and acute kidney injury
poor brain defusion leads to
unconsciousness and death
too high blood pressure in the eye
retinopathy (damage to the capillaries in the eye)
too high blood pressure in the nephrons
– nephropathy (damage to the nephrons in the kidney)
too high blood pressure in the CVS
remodelling of the cardiovascular system (both heart and vasculature)
pressure gradient /_\
flow (Q) x Resistance (R)
flow is equal to
pressure gradient / resistance
how does flow vary in relation to pressure gradient
• Flow varies proportionally with the pressure gradient and inversely with resistance
mean arterial pressure
product of the volume of blood in the
circulation and the resistance to flow
– mean arterial pressure = cardiac output x total peripheral resistance
mean arterial pressure
product of the volume of blood in the
circulation and the resistance to flow
– mean arterial pressure = cardiac output x total peripheral resistance
systemic arterial pressure
120/80 mmHg
pulmonary arterial pressure
25/10 mmHg
Systemic Pulse Pressure
40 mmHg
Pulmonary Pulse Pressure
15mmHg
Systemic Mean Arterial Pressure
93 mmHg
Pulmonary Mean arterial pressure
15
Systemic capillary pressure
17
pulmonary capillary pressure
6-10
systemic venous pressure
0-4
pulmonary venous pressure
2-6
how is blood pressure monitored and mediated
baroreceptor reflex Sensory afferents (baroreceptors) -> Central relays -> CVS centres of brain stem (medulla oblongata) -> effector efferents (innervating heart and blood vessels)
what do baroreceptors sense
rate of rise in pressure and the magnitude of pressure
– rate = dynamic sensitivity
– magnitude = static sensitivity
as the arterial pressure increases what happens to the baroreceptors
baroreceptor firing rate increases too
A fibres of baroreceptors
fewer - fast conducting (small diameter unmyelinated)
high threshold 70-140mmHg
no. activated increases as pressure rises
where is the primary site for regulating SNS and PNS outflow
medulla oblongata
what part of the medulla oblongata receives input from baroreceptors and chemoreceptors
nucleus tractus solitarius
what modifies the activity of the medullary centres
hypothalamus and higher centres
how does the venous return change when in the supine position
When supine, venous return is increased
– effect of gravity is reduced and so preload is ample (Starling’s Law)
how does venous return change when standing and why
On standing, gravity causes venous pooling and venous return falls
– with falling preload, so cardiac output drops (Starling’s Law again)
– as so does cardiac output (since VR = CO
how does a fall in cardiac output change the blood pressure
A falling cardiac output leads to a decrease in blood pressure
– MAP = CO x TRP, so if CO falls so does MAP
baroreceptor reflex
drop in blood pressure
firing of baroreceptors
central control - medulla and hypoth
drop in PNS - increase heart rate
Increase in SNS - increase force of contraction, venoconstriction and vasoconstriction
Thus increasing peripheral resistance and cardiac output
cardiac effects of baroreceptor reflec
– increased heart rate (due to increased SNS/decreased PNS)
– increased contractility (due to increased SNS)
– increased preload (due to SNS venoconstriction)
– overall increase in cardiac output
vascula r effect of baroreceptor reflex
increased vasoconstriction (due to increased SNS) – overall increased in total peripheral resistance
how can chemoreceptor in carotid body induce change in blood pressure
pH/PaO2
sensors in carotid bodies, primarily involved in ventilation control
cardiopulmonary reflexes
contribute to overall circulatory regulation
– diverse group of receptors located mainly on low pressure side of circulation
how long will baroreceptor reflex last
1-2 days
long term regulation example
fluid regulation
examples of fluid regulation
renin-angiotensin system (RAS)
– anti-diuretic hormone (vasopressin)
– natriuretic peptides
Renin-Angiotensin System
Angiotensinogen (453 aa) - from liver SNS drops = increase in blood pressure Angiotension I - inactive precursor Angiotensin II - > vasocontriction Aldosterone - promotes water expansion by increasing Na+ retention Salt and water retention
Renin-Angiotensin System is regulated
by production of renin
when is renin relesaed
in response to SNS activity particularly due
to low blood pressure and/or volume
how is renin released
SNS activation via the baroreceptor reflex (β1
-AR)
– intrarenal stretch receptor (juxtaglomerular cells)
hypertension
Consistent readings with a systolic over 140 mmHg or a diastolic over 90 mmHg (Grade I)
grade II hypertension
150/100mm
grade II hypertension
150/100mm hG
HOW DOES SYSTOLIC Pressure change with age
~120 mmHg at 20 to an average of
160 mmHg by 70 years of age
– mainly due to arterial stiffening
