cardiovascular regulation Flashcards
what are baroreceptors
pressure receptors
what acts on baroreceptors to cause their activity to increase
a primary insult
which leads to a change in MAP
change in MAP acts
what happens when baroreceptor activity increases
- afferent pathways go into the CNS of the medulla oblongata
- out of the medulla through efferent pathways
- response coordinated at effector
what is the medulla oblongata
- coordinating centre that’s deals w afferent input
- in the brainstem of the brain
what is general result of baroreceptor activity when the MAP increases
NEGATIVE FEEDBACK LOOP
- negative feedback / output on the heart and blood vessels
- reduces heart rate and causes vasoconstriction
what do we call the reduction in heart rate and vasoconstriction contrasting the increased MAP
BRADYCARDIA
which 4 factors act to regulate increased blood pressure and increase venous return
1) increased blood volume
2) activity of skeletal muscle pump
3) respiratory pump
4) VENOconstriction
what is venoconstriction
- vein constriction
- it is weak compared to arteries (vasoconstriction)
what do the 4 factors acting to regulate increased blood pressure increase
venous return
- so as they increase, ther is an increase in venous return
how is cardiac output increased
1) decreased parasympathetic activity, increased sympathetic activity and hormones from adrenal medulla
CAUSE
2) increased heart rate
1) increased sympathetic activity and hormones from adrenal medulla and increased venous return
CAUSE
2) increased stroke volume
which increases CO
how is systemic vascular resistance increased (SVR)
1) increased number of RBCs
CAUSES
2) increased blood viscosity
1) increased body size (as in obesity)
CAUSES
2) increased total blood vessel length
2) decreased vessel radius (vasoconstriction)
2nd points increase SVR
what is the combined effect of increased cardiac output and increased systemic vascular resistance
increased mean arterial blood pressure (MABP)
what is systemic vascular resistance (SVR)
similar to total peripheral resistance
give an example of a condition where increased number of red blood cells RBCs would be observed and what does this mean
polycythemia
- increased blood viscocity if have a higher density of blood cells
how do increased sympathetic activity and hormones from adrenal medulla and increased venous return give increased stroke volume
combine via starlings mechanism
how is resistance increased
- inc in vessel length will inc it
- vasoconstriction (dec of vessel radius - incs resistance to flow)
what inputs are there to the cardiovascular centre (nerve impulses)
- from higher brain centres
- from proprioreceptors
- from baroreceptors
- from chemoreceptors
what are higher brain centres
- cerebral cortex
- limbic system
- hypothalamus
what do proprioreceptors do
monitor joint movements thus body position
what do baroreceptors do
monitor blood pressure
what do chemoreceptors do
monitor blood acidity (H+), CO2 and O2
which nerve does input into and output out of the cardiovascular centre travel in for parasympathetic + sympathetic nerves coming off of paraspinal ganglia
VAGUS (X) NERVE
what effectors does the cardiovascular centre send output to
1) vagus (CN X) nerve (parasympathetic) TO decrease heart rate
2) cardiac accelerator nerves (sympathetic) TO increase heart rate and contractility
3) vasomotor nerves (sympathetic) TO blood vessels
what is the key and primary objective of cardiovascular regulation
maintain a stable MAP
why is a stable MAP needed
- ensure adequate blood flow to vital organs to keep body as a whole going
- ESPECIALLY the brain as its extremely sensitive bc of its key role + bc it has constantly high energy demands so is most essential of the needs which the cardiovascular serves by maintaining a stable MAP
what are arterial baroreceptors
- sprays of non-encapsulated nerve endings (wall nerve endings in a sense) in the adventitial layer (outer layer) of arterial walls
- found in carotid sinus and aortic arch
what are - mechanoreceptors sensitive to
STRETCH
this is why lots of nerve endings come in at different expansive areas
what causes arterial baroreceptors to fire
- increase in arterial pressure
- increases distending pressure on arterial wall stretching it
- this excites the baroreceptors
- so they fire
- giving AFFerent input into the cardiovascular centre
where is the cardiovascular centre found
- in the central part of the medulla oblongata of the brainstem
how do baroreceptors respond when the blood pressure is high or increasing
- afferent input (baroreceptor afferents) travels along + projects into physical cranial nerves 9+10 (IX = glossopharyngeal + X = vagus) into cardiovascular centre
- respond by counteracting the increase in blood pressure
- so there is an increase in parasympathetic activity
- and reduction in sympathetic stimulation of the heart
- HR decreases so ventricular contractility must decrease to decrease BP
where do sensory, afferent neurones come from
- baroreceptors in carotid sinus
- baroreceptors in arch of aorta
where do motor efferent neurones from the medulla go to
- SA node
- AV node
where do motor efferent neurones from the spinal cord go to
- SA node
- AV node
- Ventricular myocardium
what did Hering discover in 1923
CAROTID BAROREFLEX
- shows effect of electrical stimulation of baroreceptors
what does the recording of herings work show
x axis = passage of time
y-axis = arterial pressure
- when the electrical stimulation is switched on there is a substantial drop in pressure (HYPOtension) and bradycardia
- once it is turned off the rate and pressure picks up
why does substantial drop in pressure (hypotensions) and a bradycardia occur
- heart beats occur much less frequently when baroreceptors are stimulated (ie less peaks on graph)
so electrical stimulation of carotid sinus nerves elicited a…
reflex hypotension
and
bradycardia
what is seen before and after electrical stimulation is applied
- arterial pressure at high levels and is pulsatile at this rate
what is the baroreflex
- homeostatic mechanism
- negative feedback loop
what is the set point for MAP
95mmHg
what is the speed of the response / buffering (baroreflex)
- VERY fast
- 0.5 second delay (latency) of vagal bradycardia
- changes in the sympathetic vasomotor nerve activity are complete within 1.5 seconds
what is an example of this 0.5 second delay (latency) of vagal bradycardia
on Herings graph there is about a beat after electrical stimulation is applied before slowing down of heart rate is seen
how does the baroflex in homeostasis work when blood pressure is decreased
1) stimulus causes destruction to homeostasis
2) so drop in blood pressure
3) less stretch in the baroreceptors in the arch of the aorta and carotid sinus
4) decreased rate of nerve impulses as less rapid firing from the baroreceptors
5) control centre - CV centre in medulla picks this up
6) responds by increasing sympathetic and decreasing parasympathetic stimulation
AND increased secretion of epinephrine and norepinethrine (adrenaline)
7) increased SV and HR lead to increased CO
8) constriction of blood vessels increased systemic vascular resistance
9) SO INCREASES BLOOD PRESSURE AND NEGATIVE FEEDBACK LOOP IS CLOSED
why is the negative feedback loop closed we blood pressure returns to normal
homeostasis is achieved
what do proprioreceptors do
- have input relevant to control of blood pressure
- brain is most sensitive to blood pressure because of posture
what is orthostasis and what does this prove to be
STANDING UPRIGHT
- severe challenge to cardiovascular system
- hard to keep blood flowing compared to when body is lying flat
what effects the distribution of venous blood in orthostasis
- gravity
- little muscle in walls of vessels and little pressure bc its at the far end of systemic circulations pressure gradient
so how do we maintain adequate cerebral perfusion when the head is above the level of the heart
ADDITIONAL ENERGY OUTPUT
1) inc in dependent venous vol of 500ml
2) dec in intrathoracic blood vol of 20%
3) dec in cardiac filling pressure leading to lower ventricular EDV
4) dec in stroke vol of 30-40% by frank-starling mechanism
5) causes dec in pulse pressure and MAP
6) dec in cerebral perfusion leads to SYNCOPE (fainting)
what variable is the CV centre most concerned with
- MAP
why does stimulation decrease in the carotid baroreceptors in the carotid sinus
- decreases in pulse pressure
- thus decreased carotid sinus pressure due to effects of gravity
how does the cardiovascular centre respond to preserve cerebral perfusion when we stand upright
1) decrease vagal output to heart
2) so decrease parasympathetic action
3) increased output of sympathetic signal to the heart and vasomotor nerves
4) induces vasoconstriction
what does the response of the cardiovascular centre when we stand upright mean
- HR increases by 15-20bpm
- cardiac contractility increases
- reduces fall in cardiac output to 20%
- TPR increases due to vasoconstriction
what happens when we lay a subject flat (supine) then tilt them upright then lay them supine again
1) substantial inc in HR due to tilt
2) rapidly drops down when supine again
3) decrease in SV from normal level 1 to 0.6 (60% of normal)
4) CO decreases by 20%
5) BP stays consistent (diastolic blood pressure increases slightly because of vasoconstriction)
6) TPR RATIO = increases substantially to counteract drop in SV
how do arterial baroreceptors act in the process of blood pressure control
- acutely
- in a rapid response / short term
what happens if baroreceptor afferent nerves cut?
- as they carry baroreceptor sensory input into cardiovascular centre
- BP becomes much less stable BUT MAP stays the same overall over a period of hours to days
what does the graph for arterial baroreceptors show on its axis
- arterial pressures (mmHg) on x axis
- how freq they occur on y axis (%)
FOR SHORT TERM ACTIVITY
what does the graph for arterial baroreceptors show
1) normal subject = vast majority of arterial pressures at any given point in time are in narrow range of 100mmHg (v little below 90 or above 110)
2) if baroreceptors cut (denervated) = control is much poorer as subject spends less time in central optimal pressure band of 100 with a lot more higher + lower either side
BUT if average out all of values for each person the result wouldn’t be substantially different
what is long term regulation primarily due to
1) cardiopulmonary pressure receptors
2) hormonal influences regulating blood vol for instance
where are cardiopulmonary stretch receptors found
- left + right pulmonary arteries
- superior + inferior vena cava
- on pulmonary vein
what do cardiopulmonary stretch receptors do
- respond to much lower pressures than the arterial baroreceptors (pressure levels of veins in systemic side + pulmonary circulation BP is on average lower so never subjected to pressures as high as aorta / great vessels)
what is the primary role of cardiopulmonary stretch receptors
regulate blood volume
BUT
this is a primary determinant of CO (bc it increases SV)
SO
along with TPR is determines arterial pressure
what do cardiopulmonary stretch receptors if venous blood pressure drops
- reduction in atrial pressure
- reduced stimulation of cardiopulmonaryn stretch receptors
- reflex release of anti-diuretic hormone (ADH) from hypothalamus
- ADH acts in the kidney to increase fluid reabsorption from the renal tubules (incs permesbility of tubules to H2O)
- SO PRODUCTION OF concentrated urine with less water (actions of ADH retains water)
- A NEURAL REFLEX tightens the afferent renal arterioles SO rate of glomerular filtration of blood decs
- blood volume and BP increase
what does anti-diuretic mean
it is acting in opposition to dilute resource which is an inc in urine
what are afferent renal arterioles
arterioles feeding glomerular line / the kidney)
what do actions of ADH and the neural reflex have in common
- kidney = active site
- reduces fluid loss into the urine / from blood out into urine
- both act to increase blood volume because more fluid retention in the blood
what type of effect does ADH have
vasocontrictor effect
explain the vasocontrictor effect of ADH
1) esp in splanchnic circulation
2) incs TPR bc even though it’s diff part of blood system its where part of blood vol is contained (so if it incs TPR will too)
3) fall in arterial pressure due to dec in blood vol causes series of compensatory measures to be taken in response which are all aimed to restore MAP either directly or by restoring / inc’ing blood vol
what is splanchnic circulation
- circulation of blood of the gut and spleen
- abdonimal anatomy… blood supply goes to spleen, gut etc
- then portal veins go from these organs to the liver
- supplying 70% of livers blood (other 30% comes from hepatic arteries)
what does the vasocontrictor effect of ADH underline
that MAP is a primary regulated variable
effect of denervating both the arterial baroreceptors AND the cardiopulmonary stretch receptors
1) marked increase in MAP
2) in addition to short term minute to minute instability variation when arterial baroreceptors alone are denervated
what does it mean if a receptor is denervated
their input is cut off
what does the graph for denervating both the arterial baroreceptors AND the cardiopulmonary stretch receptors show on its axis
- x-axis = arterial pressure mmHg
- y-axis = relative occurance %
what does the graph for denervating both the arterial baroreceptors AND the cardiopulmonary stretch receptors show
1) control in a tight margin
2) broader spread of arterial pressures experienced
3) shift of where centre of denervated curve is = significantly higher at 140mmHg (only 100 when ONLY arterial baroreceptors are denervated)
- so significant upward shift in BP in addition to increased spread because of poor control
what do chemoreceptors do
monitor the chemical composition of arterial blood
where are chemoreceptors found
close to arterial baroreceptors in carotid and aortic bodies
SO similar location but looking at different component of arterial blood
what do chemoreceptors contain
- cells sensitive to changes in CO2, O2, H+ levels in arterial blood
what is the primary role of chemoreceptors
- respiratory regulation
BUT - also give input to the cardiovascular centre
which conditions stimulate the chemoreceptors
- HYPOXIA (low O2)
- HYPERCAPNIA (elevated CO2)
- ACIDOSIS (elevated H+)
- input at afferent level and through the efferent level
- all stimulate chemoreceptors
- all initiate sympathetically-mediated vasoconstriction (sympathetic output to cause vasoconstriction)
what do chemoreceptors have and indirect effect on and how
- heart rate
- bc chemoreceptor stimulation (primary role concerned w pulmonary regulation) causes the respiratory centre to inc the rate + depth of breathing
what would be the response in hypoxia
- breathe more
- breather deeper
to expel CO2 and take in more O2 - this increases lung tidal volume initiating a ‘lung inflation reflex’
what is a ‘lung inflation reflex’
- marked increase in heart rate
- small degree of vasodilation
explain the overall effect of chemoreceptor stimulation by both direct and indirect means
1) increased CO
2) increased TPR
3) thus increasing MAP
why is the significance of chemoreceptor stimulation limited
- doesnt usually play a great degree of role in physiology
- BUT it is imp in preserving cerebral perfusion
where is chemoreceptor stimulation the most acutely critical and what are these
in the case of asphyxia or major haemorrhage
- MAJOR crises where effect is to preserve blood flow to brain
- most severe + irreparable damage will be done + done quickest due to a drop in MAP
what is the cushing reaction (aka cushing reflex, cushings triad) of Harvey Cushing
another chemoreceptor driven reflex designed to preserve cerebral perfusion
what is the cushing reactionq
- response to elevations of intracranial pressure / hypertension
- changes body experiences to compensate for rising intracranial pressure (ICP)
why might the Cushing reaction occur in cases of cerebral ischemia (insufficient blood flow to brain)
- when intracranial pressure (ICP) becomes greater than MAP, the brain cannot receive enough oxygen
- because ICP results in decreased blood flow and lack of O2
- SO sympathetic nervous system activated to increase arterial BP and HR
- increased BP signals carotid and aortic baroreceptors to activate parasympathetic nervous system which decs HR
what happens in cerebral ischemia (insufficient blood flow to brain)
1) blood vessels supplying brain compressed
2) reduced blood flow to brain (ischemia)
3) ischemia causes arteries leading to brain to dilate so capillary and intracranial pressure increase
4) O2 delivery to brain decreases
5) capillaries become permeable and leak
what is the cushing reaction described as
results in cushings triad = hypertension, bradycardia and irregular respirations (slow deep breaths then periods of apnea)
all associated with increased intracranial pressure
what does the cushings response indicate
severe lack of O2 in brain tissue
- it is the final attempts to oxygenate the brain and prevent infarction
- medical emergency requiring urgent medical attention
- can eventually lead to cardiac arrest too
what evokes bradycardia in cushings reaction
the baroreflex
what drives moment to moment changes in MAP
neural reflexes
allow rapid responses + quick reaction in the cardiovascular system to return the MAP back to normal asap
what is the most important determinant of arterial pressure caused by the blood in the long term regulation of blood volume
the blood volume
what achieves long term regulation of blood volume
THE KIDNEYS
- greater the renal arterial perfusion pressure
- greater the rate of glomerular filtration
- therefore greater rate of urine production
what amplifies the relationship between the kidney and long term arterial blood pressure level
- renin-angiotensin-aldosterone system
series of 3 hormones
how do changes in cardiac output (increased HR + contractility) bring about hormonal regulation of blood pressure
- incd heart rate + contractility
- norepinephrine + epinethrine increase arterial BP
what are norepinephrine + epinethrine
noradrenaline + adrenaline
- NO difference
- epinethrine is common name in north america
- as netherin and renal both refer to kidneys
what does ‘epi’ mean in epinethrine
at the location of the glands from which to a large extent they are produced relative to the kidney
how does vasoconstriction bring about hormonal regulation of blood pressure
- adrenaline + noreadrenalin drive vasoconstriction via their action on vascular smooth muscle cells in addition to their impact on heart rate by nodal cells in the heart + ventricular cardiomyocytes stimulate them to inc contractility
- angiotensin II
- ADH
- ALL increase BP
how does vasodilation bring about hormonal regulation of blood pressure
- ALL decrease BP
- atrial natriuretic pepride
- adrenaline
- nitric oxide
which hormone is one of the main ways the heart has endocrine functions
atrial natriuretic pepride
how does blood volume increase bring about hormonal regulation of blood pressure
- INCREASES blood pressure
- aldosterone
- ADH
how does blood volume decrease bring about hormonal regulation of blood pressure
- DECREASE BP
- atrial natriuretic pepride
what is adrenaline mainly
- vasocontrictive
but can be vasodilative (depends on vessels + where they’re serving) as blood flow is needed in flight or fight
what is the RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
- stimulated by fall in blood vol or renal blood flow
- detected by juxtaglomerular cells
- they release renin enzyme and trigger the system’s chain of events
what are juxtaglomerular cells
small clusters of endocrine cells in the kidney
describe the chain of events for the RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
1) dec arterial BP
2) dec renal perfusion pressure
3) renal juxtaglomerular complex (kidneys)
4) increase in renin (cuts into angiotensinogen protein (inactive plasma protein) + generates angiotensin I)
5) angiotensinogen converting enzyme expressed in lungs converts angiotensin I to angiotensin II (active form) as it passes through lung capillaries (angiotensin II causes vasoconstriction)
7) angiotensin II acts at zona glomerulosa to increase aldosterone secretion
8) aldosterone acts in renal tubular cells to increase sodium reabsorption from distal convoluted tubule into peritubular capillaries / bloodstream and consequently inc water retention
water that moves into blood increases blood volume to prevent further fall of arterial blood pressure and inc BP
what does angiotensin converting enzyme being generated in lungs underline
- fact that all blood passes through the lungs at some point
- ## so any hormone in blood stream can be acted on by enzymes + released by the cells there
what is angiotensin converting enzyme the target of
important class of anti-hypertensive drugs ace inhibitors (though these have been overtaken recently by angiotensin II inhibitors)
so what are the end results of the RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
1) angiotensin II causes vasoconstriction = raises TPR
2) osmotic pressures of inc’d reabsorption of Na+ from renal tubules results in inc in water reabsorption down osmotic gradient = raises blood vol so CO incs + TPR incs
3) INC IN CO + TPR TOGETHER CAUSES INC IN MAP
where and what is the adrenal medulla
- centre part of the 2 adrenal glands (one above each kidney)
- extension of the sympathetic nervous system releasing same / similar hormones /neurotransmitters
what do the adrenal medulla release in response to stimulation of sympathetic preganglionic fibres
catecholamines into circulation + bloodstream rather than by one neurone to the next
what is the major effect of adrenaline
- inc CO (via increasing HR + SV)
- beta adrenoreceptors mediate these effects (beta 1 in ventricular cardiomyocytes)
what is the major effect of noradrenaline
- vasoconstriction via alpha adrenoreceptors which INCS TPR
whar is the combined effect of adrenaline + noradrenaline
increase in MAP
due to ad inc’ing CO and norad inc’ing TPR
how does ANTIDIURETIC HORMONE affect MAP
- increase it
- bc of effects on blood vol and direct vasoconstrictor effect (esp in the splanchnic circulation)
how does ATRIAL NATRIURETIC PEPTIDE (ANP) affect MAP (opposite of aldosterone)
- REDUCE MAP
endocrine function in the heart
released by cells in heart atria in response to higher cardiac filling pressure (incd blood volumes thus higher filling pressures w/in heart)
ANP is released as a response to above
reduced MAP by causing vasodilation + promoting Na+ excretion (hence water lost by osmotic pressure in kidneys)
how does NITRIC OXIDE affect MAP
- LITTLE EFFECT ON MAP
causes vasodilation
acts primarily down at a local level in microvasculature
