Regulation of blood pressure Flashcards
Definition of systolic
BP in aorta and large arteries that increases rapidly during L ventricular contraction
Definition of diastolic
BP when cardiac ejection stops due to the aortic valve closure
Minimum pressure reached before next systole
Definition of total peripheral resistance
Made up of resistance arteries and arterioles in the system
Definition of mean arterial blood pressure
Pressure in aorta
Definition of central venous pressure
Pressure in vena cava, normally near 0
Definition of afterload
Heart pumps against blood already in the blood vessels
Definition of capacitance
Ability to accommodate a greater blood volume
Definition of mechanoreceptors
Stretch sensitive, found in baroreceptors
Definition of pressure natriuresis
Mechanism within the kidneys by which increased renal perfusion due to increased BP leads to increased Na excretion
What does BP consist of
Where is it measured
How does BP vary in the body
Refers to the pressure in large arteries and oscillates with cardiac cycle
Systolic and diastolic, normally 120/80, mean = 93mmHg
Measured in the brachial artery at the height of the heart
BP is lower in the head and higher in the lower limbs
How does pressure change in there arteries
Blood ejected => P and F rapidly propagated
P wave increases down arterial tree due to greater stiffness
Enters arterioles and capillaries, P falls due to increased elasticity
How does pressure change in low resistance vascular beds
Low resistance vascular beds = kidney, brain, heart
P wave smoothed out less, high pulsatility can damage structures
How does flow in the aorta change
Pulsatile but smoothed out as blood => arterioles and capillaries
Elastic vessels take up energy from pressure and pulsatility
What happens to arterial BP and flow in systole
75% of SV transiently stored in aorta and large arteries as vessels are compliant
25% SV pushed into smaller arteries
Pressure energy stored in elastic walls
What happens to arterial BP and flow in diastole
Still distended but rebound
Arterial recoil pushes blood into smaller arteries
Stored energy keeps flow in diastole
How does the speed of the pressure waves compare to the rate of blood flow
Pressure wave propagates faster than blood flow
What is mean arterial blood pressure
95mmHg
What is the central venous pressure
0-5mmHg, v little resistance
Which arteries have the most R resistance and why?
How does this affect P
Resistance arteries, arterioles due to friction
P falls steeply
What is the relationship between Pressure difference, MABP and CVP
P difference = MABP - CVP
What is the relationship between ABP, F and R
ABP = F x R
What is the relationship between ABP, CO, TPR
ABP = CO x TPR
What are the short term factors that affect BP
Sleep
Posture
Exercise
Stress
How does pressure change over a day
Oscillates in small range
Average does not change much
Why is the baroreceptor reflex important
In carotid sinus and aortic arch
Maintains BP in upper body, preserving flow to brain
Allows body to change F to some organs without affecting F to others
-Due to parallel circulation
Can alter BP set point, allow body to cope with stress/exercise
What does arterial tone affect
Total peripheral resistance
What does the total peripheral resistance affect
Afterload
What can affect CVP preload/Starling forces
Venous capacitance
BV
What can affect stroke volume
Afterload can decrease SV
Cardiac contractility
CVP preload/Starling forces
What can affect venous capacitance
Venous tone
What can affect BV
Na excretion/retention
What does the ANS affect as a result of the baroreceptor reflex
Arterial and venous tone
Cardiac contractility
HR and SV
All of these stabilize MABP
Can also modulate RAAS
What determines MABP in the long term
What does it act on
RAAS system
Receives input from BP
Acts on Na+ excretion/retention
Arterial and venous tone
What are the effects of increased Na retention
Increased Na
Increased H2O
Increased BP
Increased MABP
And vice versa
Describe how afferents of the baroreceptor loop reach the brain
Aortic nerve from aortic arch => 4th cranial nerve/vagus
Carotid sinus nerve from external carotid => 9th cranial nerve/glossopharyngeal nerve
Both reach nucleus solitairius tractus and are compared to the set point
What happens in the efferents of the baroreceptor loop when the BP is too low
Increased sympathetic drive => b1 => HR and force increase
Increased sympathetic drive => a1 => increased veno and arterial constriction, CVP, TPR
Decreased parasympathetic drive => M2 => HR increase
All of these contribute to an increased CO
How do the baroreceptors function
Mechanoreceptors sensitive to stretch
Thin carotid sinus wall => small P changes detected
Increased P => increased firing => NST which mediates response
When are the baroreceptors most sensitive
When mean BP = 80-150mmHg but sensitivity increased by large pulse pressure
What happens in the baroreceptor reflex when there is a new sustained pressure
Can adapt to new sustained pressure but not for long terms
When is adrenaline secreted and what adrenergic receptors does it stimulate?
Adrenal secretions during
- Exercise
- Hypotension
- Hypoglycaemia
a1, VC most vascular beds
b1, +ve chronotrope, inotrope
b2, VD in skeletal muscle
When is noradrenaline secreted and what adrenergic receptors does it stimulate?
Sympathetic secretion
-Mediates SNS efferents
More often used, more important
a1, VC most vascular beds
b1, +ve chronotrope, inotrope
b2, has a low affinity
Describe mechanisms for the long term regulation of MABP
Due to maintenance of constant ECF via [Na] in ECF/plasma
What happens if the amount of Na consumed is too low
Less Na consumed Decreased plasma [Na] Decreased Posm Decreased ADH secreted Decreased water consumption/Increased water excretion
Decreased BV and preload
Decreased BP
Decreased diuresis and natriuresis
Overall, mean BV and BP lowered and then stabilised
How is the RAAS system activated when BV, plasma [Na] and BP are too low
Decreased CVP => decreased atrial stretch => decreased ANP released
Decreased atrial stretch => decreased activation of cardiopulmonary receptors => increased SNS outflow to kidney => Renin released from juxtaglomerular cells
How does the RAAS system function in the kidney
Renin release => Angiotensinogen converted to Ang1
Ang1 =ACE=> Ang2
Ang => Increased VC, ADH, renal Na reabsoprtion, aldosterone secretions
How does increased VC, ADH, renal Na reabsorption and aldosterone secretion increase BV, BP and plasma [Na]?
Increased VC => increased R so P increases to maintain flow
Increased ADH secretion => more water retained => increases BV and BP
Increased renal Na reabsorption and aldosterone => increased plasma [Na] => increased water reabsorbed => increased BV and BP
How does ANP affect the RAAS system
If less ANP released => increase in renal Na reabsorption
Describe the process of renal regulation of Na excretion by pressure natriuresis
Increased renal perfusion due to increased BP => increased Na excretion
Only small changes in MABP needed to cause large response
Increased renal perfusion P
Increased in BF in vasa recta
Increased in intrarenal release of NO => VD
Greater outward P from VR, favours secretion => Decrease in renal Na reabsorption
Describe other mechanisms to maintain BP in the long term other than RAAS
SNS activation => increased BP when kidneys denervated, can contribute to long term control
Changes in BP don’t always affect Na excretion
Na excretion can occur without BP changes
Baroreceptor reflex does not turn off completely after a short time
