CFB L3 Flashcards
Define blood pressure
The force exerted by blood on walls of blood vessels.
Definition of blood pressure reflects large arteries
In patients, measured in brachial artery
- aorta
-brachial arteries
State the units of BP
mm Hg (millimitres mercury)
What does a BP of 120 mm Hg tell us?
This is the force the blood exerts on wall of vessel. Also, this force can cause a column mercury to rise by 120 mm
What is systolic pressure?
Highest pressure in arteries when the heart contracts, heart beats + blood flows into it
Normal: 120 mm Hg
What is diastolic pressure?
Lowest pressure in arteries
When heart is relaxing between heart beats / contractions
Normal: 80 mm Hg
Define pulse pressure
Also known as arterial pulse
Difference beteween systolic pressure + diastolic pressure.
Felt as pulsation by palpating eleastic arteries
Occurs during systole, ventricles contract, blood ejeceted into arteries, they then expand.
Pulse pressure directly proportion to stroke volume,
High pulse pressure = high stroke volume
Why is Mean Arterial Pressure taken ?
Alternative value to pulse pressure (arterial pulse)
MAP
Blood ressure in aorta / arteries fluctuates with each heart beat
Pulse pressure fluctuates
What is MAP?
Avg of systolic and diastolic pressure
Avg BP in arteries during 1 cardiac cycle ( 1 heart beat)
How do you calculate MAP?
(2x diastolic) + (1 x systolic) / 3
What is a healthy MAP ?
70 - 110 mm Hg
<60 mm Hg - organ hypoxia, organ ischemia
What happens if MAP is too low?
<60 mm Hg - organ hypoxia, organ ischemia, NO FILTRATION IN KIDNEYS
How is blood pressure regulated?
- Neural control
- Hormonal control
- Local factors
These factors control heart rate, blood volume, stroke volume
This allows consistent control of blood pressure
NHL
(NHS took an L)
Where is neural control of blood pressure regulated?
Cadiovascular centre
(bundle of neurones in medulla oblongata)
State the location of the cardiovascular centre
Medulla oblongata
State the function of the cardiovascular centre
Control heart rate
Control ventricular contractility
Control blood vessel diamater
State the four centres in the cardiovascular centre
There are 4 groups of neurones the CV centre:
Cardiostimulatory centre - stimulates heart function
Cardioinhibitory centre - inhibits heart function
Vasodilator centre - reduces diameter of blood vessels
Vasocontrictor centre - expands diameter of blood vessels
What are the inputs of the CV centre?
Inputs = impulses towards CV centre
INputs from higher brain centres:
-Cerebral cortex
-Limbic system
-Hypothalamis
Input from sensory receptors:
-Barroreceptors
-Chemoreceptors
-Proprioreceptors
- Barroreceptors - detect changes in BP
- Chemorecepors - detect changes in O2 + CO2 levels of blood (blood acidity)
- Proprioceptors - detect changes in muscle + joint movement
State sympathetic efferents from the CV centre
- Electrical signals sent via cardiac accelearotr nerves to heart to increase heart rate and increase ventricular contractility
- Electrical signals sent via vasomotor nerves to blood vessels, vasoconstriction of blood vessels
State parasympathetic efferents from CV centre
Electrical signals sent via vagus nerve to heart to decrease heart rate
Describe sympathetic stimulation of the heart
- Sympathetic stimulation occurs via the spinal nerves (cervical to upper thoracic T1-T4)
- Fibres reach pacemaker + most of myocardium
- Activation leads to release of stimulatory neurotransimitter - noradrenaline
- Noradrenaline binds to beta adrenergic receptors
- Increase in Ca 2+ influx
- Increases heart rate + contraction force
Describe what happens during parasympathetic activation
By Vagus nerve
Fibres reach the pacemaker + some of myocardium
Activation leads to release of ACh
ACh binds to cholinergic muscarinic receptros
Acivating them
Closes Ca2+ channels
Decreases heart rate + force of contraction
Why is MAP more clinically relevant than SBP?
Better representation of perfusion pressure faced by organs
Why is neural function only required for altercations to heart rate and ventricular contractility
Heart beats independent of neural regulation and the CV centre, therefore, neural regulation is only needed to alter
-heart rate
-ventricular contractility
-diameter of blood vessels
State the function of barroreceptors
- Stretch receptors found in wall of blood vessels
-Mechanoreceptor sensory neurones that are excited when stretched
-When stretched / distended (by changes in BP), send electrical impulses to CV centre
-Found in carotid sinus and arotic arch
Detect changes in blood pressure (in major arteries)
State the function and location of chemoreceptors
Detect change in blood chemistry - Detect changes of CO2 and O2 levels in the blood (blood acidity)
Found near carotid and aortic barroreceptors - in aortic and carotid bodies
State the function of proprioceptors
Detetct changes in joint + muscle movements
State the parasympathetic efferents from the CV centre
Electrical impulses sent via vagus nerve to heart, decreases ventricular contractility and thereofore, heart rate
Explain how the CV centre controls blood vessel diameter
Narrowing diameter: (When Low BP + generally, arterials have “vasomotor” muscle tone”)
CV centre innervates smooth muscle of blood vessels (mainly arterioles)
It does this by sympathetic nerves from the vasoconstrictor centre - vasomotor nerves
Upon activation, vasomotor nerves release a neurotransmitter, noradrenaline
Noradrenaline binds to alpha-adrenergic receptors,
leading to constriction of vessels (Ca2+ and cAMP mediated)
Vasomotor nerves constantly innervate smooth muscle of arterioles, allowing them to maintain muscle tone and regulate BP
Describe the location of vasomotor nerves
Branch from spinal cord, go through all thoracic and first 2 lumbar nerves
Explain how the CV centre controls blood vessel diameter
Widening diamater (when high BP)
Vasomotor nerves constantly innervate smooth muscle of arterioles, allowing them to maintain muscle tone - therefore, in constant state of moderate contriction - “vasomotor tone”
When high BP, detected by barrorecptors in aortic arch + carotid sinus
Impulse sent to vasodilator centre in CV centre, stimulates vasodilator centre which inhibits vasoconstrictor centre
Leads to widening of vessels as activity of vasocontrictor centre is surpressed (activity of vasomotor nerves therefore surpressed)
Describe the distrobution and power of the sympathetic vasodilator nerves
All segments of circulation
More powerful
-spleen
-gut
-kidney
-skin
Less powerful
-skeletal muscle
-cardiac muscle
-brain
State the hormones involved in control of BP
Renin-Angiotensin aldosterone system (RAAS)
ADH
Adrenaline, Noradrenaline
ANP - atrial natiuretic peptide
Describe how the RAAS system leads to an increase in BP
Angiotensinogens is released into blood. Produced in liver
Upon low blood pressure, low renal perfusion, reduced Na+ delivery, kidney secretes renin which cleaves angiotensinogens to produce angiotensin 1
Angiotensin I is converted to angiotensin II by ACE (angiotensin converting enzyme) in lungs
Angiotensin II
-Potent vasoconstrictor, increases BP
-Stimulates adrenal cortex to release aldosterone, which increases water + sodium reabsorption, increasing blood volume, increasing blood pressure
-Stimulates release of ADH, increases permeability of kidney tubules (collecting ducts), increases reabsorption of water, increasing blood pressure
Angiotensin II stimulates thirst sensation
Which cells in the kidney produce ACE?
Juxtaglomerular cells
State the function of adrenaline and noradrenaline in BP regulation
- Both secreted by the adrenal medulla and sympathetic nerve fibres
- Both hormones and neurotransmitters
- Both increase ventricular contractility, heart rate, cardiac output + BP
- Both increase vasoconstriction in arterioles + veins, increasing TPR and BP
State where ADH is produced
Posterior pituirary gland
What stimulates the release of ADH?
Hypervolemia (reduced blood vol)
High blood plasma osmolarity
Angiotensin II
Explain how ADH regulates blood pressure
Osmoreceptors in hypothalamus detect
-hypovolemia
-high blood plasma osmolarity - less water in blood
This causes less water to diffuse into osmoreceptors, they then contract, increasing afferant neural firing, stimulating posterior pituitary gland to secrete ADH
ADH increases the permeability of the kidney tubules (collecting ducts) to water, therefore, increasing the amount of water reabsorbed from urine to the blood
By planting “water channels” called aquaporins 2 channels in the membrane of collecting duct, dct
Transport water through tubular cells back into blood
This leads to decrease in plasma osmolarity, increase in blood vol, therefore, increase in BP
ADH = vasoconstrictor, increases BP
COMBINED EFFECT, increased blood volume + vasocnstriction - high BP
HIGH URINE OSMOLARITY - LESS WATER IN URINE, URINE CONCENTRATED
State the two principle sites of action during ADH regulation of BP
Kidneys
Blood vessels
State factors stimulating ADH release
Ang II
Thirst
Decreased atrial receptor firing
Sympathetic stimulation of barroreceptors
Hypovolemia / high plasma osmolarity
Describe the role of ANP in reg of BP
Produced + stored in atrial myocytes
Secreted in response to atrial stretch secondary to hypervolemia and thus hypertension
Increases renal excretion of water, reduces blood vol, reduces BP
VASODILATOR
Describe the physiological effects of ANP
- Constricts efferent glomerular arteriole, incrrease glomerular capillary pressure, increase GFT, increase Na+ + H2O excretion
- Decrease sodium reabsorption in DCT, more Na+ H2O excretion
- Decrease renin secretion, inhibits RAAS
- Reduces responsiveness in alpha-adrenergic receptors in blood vessels to adrenaline, vasodilation
- Inhibits sympathetic output from CV, reduced CO
- Acts on hypothalamus to reduce ADH release
Define auto-regulation
Body tissues automatically regulate their blood flow + according to metabolic demand for oxygen, nutrients, disposal of waste materials
Describe how local factors play a role in reg of BP
Physical factors
TEMP: warming = vasodilation
cool = vasoconstriction
Chemical mediators
WBC, metabolically active, vasodilators - bradykinin, hisyamine, H+, NO
platelets -less metabolically active, vasoconstrictors, serotonion, prostaglan F2 alpbha, thromboxane A2
True or false
“NO is a vasodilator released by vascular endothelial cells”
True
