integrative cardiovascular responses Flashcards
key receptors (how and where) and primary CV control centre (where info to)
baroreceptors
- physical change of vessel walls telling change in MAP
- in aortic arch and carotid bodies
medulla oblongata
- send info to heart, heart arterioles and arteries
baroreceptors and MAP
- normal MAP values
- how baroreceptor firing frequency changes with BP at normal and when MAP increases and falls
- impact of increase or decrease BP
Normal MAP, systolic 120, diastolic 80 mmHg
Barorecptors firing frequency changes with changes in blood pressure.
-Pulsatile flow- shown in a curve, in diastole, lower firing frequency, at the top, in systole, there’s higher firing frequency by baroreceptors
- When MAP elevated, hypertensive stimulus received, increases firing frequency at baroreceptors, sensory info to MO, efferent- decreased sympathetic outflow to heart arterioles and veins, increased parasympathetic to heart.
- Fall in MAP cause baroreceptprs detect a hypotensive stimulus lead to decrease in afferent firing rate causing decrease parasympathetic activity and increase sympathetic outflow to heart to increase bp.
blood volume and blood pressure
- impact of high blood pressure
- blood volume and blood pressure can be the start point
- the negative feedback to both variables
-Sustained high bp, trigger kidneys lose water and sodium, reducing plasma volume, therefore BV, reduces venous return, therefore end diastolic volume and stroke volume so cardiac output falls (BP less)
-plasma volume to BV, cardiac output to BP
calculation for MAP
cardiac output x total peripheral resistance (in vessels)
regulation of MAP- CO side
- determinants of stroke volume
- determinants of heart rate
-Respiratory pump, SM pump, BV and sympathetic activity (constrict/dilate) feed into veins which determine venous return, EDV and therefore SV
-Epinephrine, Sympathetic and parasympathetic activity act on heart impacting SA node, therefore HR
regulation of MAP- TPR side
- local controls
- neural controls
- hormonal controls
- where do they inturn send info to
- what impacts blood viscosity
- what determines TPR
- vasodilators (eg. Less o2, more CO2, K+ and H+) and vasoconstrictors (internal BP and endothelin-1)
- vasoconstrictors (sympathetic nerves) and vasodilators (neurons releasing nitric oxide)
- vasoconstrictors (eg. epinephrine, vasopressin, angiotensin 2) vasodilators (eg. Epinephrine)
- arteriolar smooth muscle impacting diameter
- Haematocrit
- SM diameter and viscosity determines TPR, therefore MAP.
CV responses to standing (orthostatic stress)
- normal response
- impact if baroreceptors reset
- Drop in TPR causing venous pooling so a drop in central blood volume (blood down, less to brain), Transient drop in map and brain blood flow, reduced baroreceptors firing rate lead to increased ventilation, vagal withdraw and increased sympathetic stimulation, to increase HR and TPR which restores MAP (within 10-15 secs) maintaining blood flow to brain.
- Baroreceptors can reset (due to short or long term higher MAP) so they don’t fire as much and regulate bp, more blood stays pooled in LL, lower TPR and larger fall in central blood volume, we hyperventilate reducing co2 to too low constricting vessels to brain, is no sympathetic activation so HR doesn’t increase and TPR drops meaning MAP drops, leading to reduced brain blood flow potentially a faint
Cardiovascular response to haemorrhage
- what is a haemorrhage
- what does it cause
- how reflexes respond
-Haemorrhage is a loss of lots of blood from vessels in short time.
-Causes a drop in SV which reduces Q if bleeding cannot be stopped and therefore MAP falls.
-Reflex compensations are to increase Q (SV and HR) and TPR to increase MAP to as close to normal as possible
Mechanisms for control of ventilation
- cause of initial rise and the supplementation
- what impacts the more gradual rise
- why does it plateau
- due to motor cortex signalling the rcc to increase ventilation and mechanoreceptors in muscles and limbs detect movements further supplementing.
- fine tuning due to central command ensuring right levels of ventilation being done for the demands
- plateua found at steady state where O2 demand is met
Mechanism for control of q
- 3 causes of the initial rise due to increase SV
- what causes the fine tuning gradual rise
- firstly by central command, secondly by starling effect (increased venous return, actin and mysosin further stretched to more optimal overlap and contraction is stronger increasing SV) and by Input from mechanoreceptors in muscles
- Chemoreceptors in muscles responsible
Metaboreflex
- what happens with metabolism when exercise begins
- what receptor detects change
- what it leads to
- muscle metabolism increases and metabolites accumulate in working muscles (metabaroreceptors detect chemical composition in limbs- eg. la, k+, adenosine).
- metabaroreceptors in muscle detect accumulation and afferent info sent to MO
- Lead to increased sympathetic nerve activity to remove metabolites.
- what happens do MAP during exercise
- how does this change occur
- Resetting of baroreceptors so operate at higher point. Around 85 at rest, 93mmHg during exercise (depends on intensity)
-sympathetic stimulation increase, parasympathetic decreases- cardiac- increased contractility (SV) and HR, all affecting CO. increase diameter of muscle arterioles reducing PR. CO and TPR determine MAP.
redistribution of q during exercise
- where increased blood flow
- where decreased blood flow
- how to increase and decrease flow to an area
- net effect of these mechanisms to distribute flow
- Increases Q in heart (needs oxygen for faster contraction, cardiac muscle can take out almost all o2 from blood), skin (dissipation of heat by vasodilation) and sm (majority of blood- supply of po2 and removal of metabolic waste), brain slightly but not large as causes damage to capillaries
- Decreased Q to organs as not required there (why should not eat too much close to or during events)
- vasodilation to decrease PR
- vasoconstriction to increase PR
-Net effect on body in exercise is reduction in total peripheral resistance.
diastolic pressure and volumes
- what happens to diastolic arterial pressure in rest and exercise
- how does EDV and SV increase
- its regulated within a very narrow range
- due to increased venous return due to- muscle pump, respiratory pump, sympathetic stimulation
control of cv responses to exercise
- what receptors are important
- what stimulation causes vasoconstriction
- what causes vasodilation
- baroreceptors, mechano and chemoreceptors (last 2 in muscles)
- sympathetic increases, parasympathetic decreases
- local controls, eg. o2, temp, etc.
