PBL 6 - control of BP Flashcards
what is the equation for BP?
blood pressure = CO x total peripheral resistance
what is cardiac output?
the volume of blood expelled by the heart per minute
varied to meet the demands of the body
what is the equation for cardiac output?
CO = SV x HR
what is stroke volume?
the volume of blood ejected per beat
what is the equation for stroke volume?
SV = end diastolic volume - end systolic volume
what 3 things is stroke volume affected by?
- preload
- contractility
- afterload
what is preload?
the tension in the cardiac myocytes before they contract
what happens if you increase the stretch in cardiac myocytes?
more forceful contraction
— the more you stretch them, the greater the tension, the more forceful the contraction
what is preload dependent on?
venous return
how does venous return affect preload?
the more blood that comes back to the heart, the more the ventricles will stretch, therefore more contraction force
what is contractility?
the contraction force of the myocardium for a given preload
what increases the contraction force for a given preload?
adrenaline
what is afterload?
the BP in the aorta and pulmonary trunk
how does afterload affect SV?
the greater the afterload/pressure, the harder is it for the LV to reach that pressure — increased afterload reduces SV
what things increase HR?
- adrenaline and noradrenaline
- increase in temperature
- thyroid hormone
- caffeine
what things decrease HR?
- acetylcholine
- decrease in temp
- intense visceral pain
what is total peripheral resistance?
the total pressure in the peripheral vessels
what 3 things affect TPR and how do they alter BP?
- viscosity of the blood — relatively stable so wouldn’t really use to alter resistance or BP
- blood vessel length — remains unchanged so wouldn’t really use to alter resistance or BP
- blood vessel radius — can easily be changed so regularly used to alter BP
what is vessel radius determined by?
the SNS
bloods vessels are maintained in what state?
a state of partial vasoconstriction
what does the maintenance of partial vasoconstriction of blood vessels provide?
sympathetic tone — a sympathetic nerve fibre is continuously partially constricting the vessel
what happens if you stop sending impulses through the sympathetic nerve fibre for a blood vessel?
vessel will dilate (this is a good way of rapidly changing the radius)
where does the control of vessel radius come from?
the vasomotor centre in the medulla oblongata
what are 4 different sensors used in the neurohormonal control of BP?
- baroreceptors
- chemoreceptors
- volume receptors
- osmoreceptors
these sensors send what kind of fibres to the CNS?
afferent nerve fibres
the areas in the brain/CNS send what type of fibres to the periphery to bring about changes?
efferent nerve fibres
where does the CNS send impulses to to bring about changes?
- heart
- blood vessels
- kidneys
what is the aim of maintaining this peripheral arterial BP?
to ensure the arterial blood pressure is adequate for oxygen perfusion
describe the neural component of BP control
- autonomic nervous system
- directly influences the heart and blood vessels
- short-term mechanism
describe the humoral component of BP control
- circulating factors/hormones
- directly influence heart and blood vessels or alter blood volume
- intermediate and long-term mechanisms
describe baroreceptors
- mechanical/stretch receptors
- at bifurcation of common carotid artery (carotid sinus) and the arch of the aorta (aortic sinus)
via what nerve do impulses travel from the carotid and aortic sinuses?
- carotid = glossopharyngeal nerve
- aortic = vagus nerve
where is the afferent information for the carotid and aortic sinuses taken to?
the nucelus solitarius in the brain stem = a collection of sensory neurons
what does the nucleus solitarius modulate the activity of?
the cardiovascular centres
describe the cardiovascular centres
3 groups of cells
1 + 2 = groups of sympathetic neurons on the medulla
3 = dorsal motor nucleus of the vagus and the nucleus ambiguus in the brain stem
- vasomotor centre — causes vasoconstriction of peripheral vessels
- cardiac accelerator centre — increases HR and force of contraction
- cardiac inhibitor centre — involved with the vagus nerve and slowing down the HR (vagus nerve has vagal tone to slow down the HR under normal circumstances)
pressor centre = upper part of medulla oblongata
depressor centre = lower part of medulla oblongata
how can the receptors be altered?
sensitivity can be altered — eg. long term hypertension - baroreceptors have been set at a higher level
how does an increase in BP affect the baroreceptors?
increased BP —> sinuses are stretched —> increase firing rate to cardiac and vasomotor centres
what is the effect of increased firing rate to the cardiac and vasomotor centres?
- stimulates cardioinhibitory centre — increases PNS activity to SA node — decreases HR
- inhibits cardioaccelerator and vasomotor centres — decreases SNS activity — decreases HR and vasodilation
how does haemorrhage affect BP?
causes fall in BP
what does haemorrhage result in?
- vasoconstriction (look pale)
- increased force of contraction
- increased HR
what happens if blood volume is not replaced after haemorrhage?
- venous return continues to fall
- decreased EDV
- HR increases — systole cannot shorten therefore diastole shortens — fill heart during diastole — decreased filling time — EDV decreases even more — decreased force of contraction (starling’s law of the heart) — decreased SV/CO/BP
describe the valsalva manoeuvre
= forced expiration against a closed glottis
- increases in intrathoracic pressure increases compression of the vena cava
- slow down VR — decrease EDV — decrease CO — decrease BP
- baroreceptors decrease output
increase force of contraction/HR/total peripheral resistance
what do chemoreceptors detect?
chemical changes in the blood
what are catecholamines?
adrenaline and noradrenaline — released by the SNS
what factors are part of the humoral control of BP?
- catecholamines
- RAAS
- Atrial Natriuretic Peptide (ANP)
- Antidiuretic Hormone (ADH) / Arginine Vasopressin (AVP)
what releases catecholamines and when are they released?
- release by the adrenal medulla
- produced by chromaffin cells
- released during stress, exercise, blood loss, emotion, excitement, pain
- 80% adrenaline and 20% noradrenaline
what is the effect of catecholamines on a1 vascular smooth muscle?
vasoconstriction
what is the effect of catecholamines on a2 presynaptic membrane?
negative feedback
what is the effect of catecholamines on B1 SA node and cardiac muscle?
increase HR and contraction force
what is the effect of catecholamines on b2 vascular smooth muscle in heart and skeletal muscles?
vasodilator (to increase blood supply to the heart to increase HR)
what is the effect of catecholamines on b2 airway smooth muscle?
bronchodilator
what is the effect of catecholamines on B3 adipocytes?
lipolysis
what is RAAS stimulated by?
- a decrease in renal perfusion pressure:
less blood flowing through the kidneys causes a drop in pressure in the kidneys — triggers the system
- also stimulated by sympathetic stimulation
- also stimulated by decrease in sodium delivery to the distal tubule
briefly describe the RAAS
- renin released from juxtaglomerular cells
- renin acts on angiotensinogen and inverts it to angiotensin 1
- ACE (angiotensin converting enzyme) converts angiotensin 1 to angiotensin 2
describe some of the effects of angiotensin 2
- acts on adrenal cortex to bring about aldosterone secretion — reabsorbed Na and water (increases blood volume)
- acts on release of ADH to bring about water reabsorption
- makes you thirsty — drink more
all of these increase blood volume and at high doses is also a vasoconstrictor (increase total peripheral resistance) —> increase BP
describe atrial natriuretic peptide (ANP)
- released by cells in the atria
- responds to atrial stretch, sympathetic stimulation, angiotensin 2 (high levels)
- acts on kidneys to increase glomerular filtration rate, natriuresis, diuresis — increase urinary output
- decrease renin and aldosterone release
- these all decrease blood volume, CO and BP
= COUNTER-REGULATORY SYSTEM FOR THE RAAS
describe ADH
- made by hypothalamus, stored and secreted by posterior pituitary
- stimulated by increase in plasma osmolarity, angiotensin 2, sympathetic stimulation, stretch receptors (atria and veins)
- leads to water reabsorption in the collecting duct (not sodium)
- increases blood volume and BP
- also causes vasoconstriction when the levels are very high
concentrated blood = increase levels of ADH - increase fluid
