control 2 Flashcards
calculations
SV = EDV - ESV CO = SV*heart rate MAP = Q*TPR
design of the CVS
2 circulations - pulmonary and systemic central venous pressure determines the amount of blood that flows back to the heart - starling’s law, this determines the SV
in veins constriction reduces compliance and venous returns
arterioles -constriction affects MAP and flow
flpw changed by vessel radius
R heart - lungs - L heart - body
peripheral venous tone, gravity, skeletal muscle pump and breathing affect venous volume return `
Describe the control of flow
in veins - constriction restrict compliance and venous return
in arterioles - constriction determines: flow to downstream organs, MAP, pattern of blood flow to organs
flow many changed by changing vessel radius: viscosity and length of vessel only changes very slowly - Poiseuille’s equation
ways to regulate blood flow: - local
- intrinsic to the smooth muscle of the vessel itself, for local reflex blood flow
autoregulation (without it a pressure drop would = an increase in flow)
myogenic theory - increase in tension cause the vessles to constrict - stretch sensitive channels are involves, mechanically gated and allow Ca into the cell
metabolic theory - as flow decreases metabolites build up - vessels dilate to allow metabolites to be washed away
injury - -serotonin from platelets = constriction
ways to regulate flow - systemic
hormonal or neuronal (autonomic nervous system), extrinsic to SM. hormones from the adrenal gland affect vasodilation/constriction
- endothelium derived hormones
NO - vasodilator
prostacyclin - cardioprotective vasodilator
thromboxane A2 - vasoconstrictor
endothelin - vasoconstrictor (minor vasodilation effects)
circulating hormones
kinins - stimulate NO - vasodilator
atrial natriuretic peptide - vasodilator
ADH - vasoconstrictor
noradrenaline/adrenaline - vasoconstriction
Angiotenisin II - vasoconstriction
organisation of the sympathetic nervous system
preganglionic neuron is short, post ganglionic neuron is long
SNS comes from the thoracic vertebrae and lumbar vertebrae
the SNS is under reciprocal innervation - increase the signal from the vasomotor centre down afferent nerve to autonomic system
inhibit SNS impulse - decrease heart rate and the vessels dilate
venous return is increased with an increase in SNS because reduces capacitance of vein by causing vasoconstriction - increases venous pressure and so venous return; this increases arterial pressure as well
role of sympathetic nervous system
fight/flight
controls circuolation and the radius of vessels
innovates heart and vessels (except capillaries, precapillary sphinsters and metarterioles)
strong innervation to kidney, gut, spleen and skin
weak innervation to sskeletal muscle and brain
BV get innervation from SNS by NA
SNS always has some tonic activity so the bv are slightly contracted, increase activity - increase vasoconstriction
SNS stimulated - increase in heart rate because the threshold is reached faster
increased SNS efferents to heart, increases force of contraction - increase sv
the vasomotor sensor
bilaterally
in pons and reticular substance of medulla
made of vasoconstrictor presser area, vasodilator depressor area and cardioregulatory inhibitory area
transmit impulses through spinal cord to almost all vessels
hypothalamus has excitatory/inhibit effects on VMC
lateral sections increase heart rate and contractility
medial section - impulses via vagus nerve to decrease heart rate
takes into account nervous action about thinking about a reflex
parasympathetic
rest and digest
pregabglionin - ACh, postganglionic ACh
comes form cranial and sacral part of the spinal cord
preganglionic is long, post ganglionic is short
when stimulated there is a decrease in heart rate - due to a decrease in depolarisation
always some degree of PNS stimulation cutting down the heart rate
control of bv diameter
sympathetic vasoconstrictor nerves, local controls and circulating hormones
if you increase heart rate and SV ….
increase CO
to increases SV you:
increase, SNS efferents to the heart, plasma adrenaline, venous return, arterial pressure abd so EDV
also increase respiratory movements and decrease intrathoracic pressure
Reciprocal innervation
increased pressure detected by the baroreceptor
increased signal down the afferent nerve
increase in PNS nerve proportionally to the increase down the afferent
SNS signal goes through an inhibitory neuron so the signal is inhibited, so a decreased signal arrives at the vessel
this causes vasodilation
PNS innervation
increased pressure = increased baroreceptor stretch
in carotid - signal to heart by glossopharyngeal nerve
from aortic baroreceptors signal down the vagus nerve
this decreases the heart rate
where are the cardioregulatory and vasomotor centres
in medulla oblongata
proportion of blood in each part of the cardiac system
veins and venules 61% heart 9% pulmonary circulation 17% arteries 11% arterioles and capillaries 7%
action of baroreceptors
they are mechanoreceptors and respond to changes in stretch. more stretch =fire more
carotid sinus baroreceptor respond to pressures between 60-180mmHg
most sensitive range is 90-100mmHg
if stretched more, there is a higher bp so they inhibit the SNS - causing vasodilation and reducing venous blood pressure
they sense the new Bp - send signals to the cardiovascular control centre which acts to increase or decrease blood pressure (increase by increasing SNS,Ang II, and ADH and decreasing PNS and decrease by decreasing SNS, Ang II and ADH and increasing PNS
location of baroreceptors
They are in the aortic arch and carotid sinus
MECHANISM of baroreceptors
send signals down glossopharyngeal nerve from carotid sinus and down vagus nerve from aortal arch to vasomotor sensor
change firing rate with response to arterial pressure
increase in basoreceptor firing down afferent vagus nerve (PNS) to cardiovascular centre and vasomotor centre then back along efferent Vagus nerve - slows the heart beat
signal from baroreceptors through sympathetic nerves to vasomotor centre and cardiovascular centre - through reciprocal innovation SNS signal is reduced - causes a reduction in heart rate and causes vasodilation
Reflexes caused by increased pressure in the carotid sinus nerve
pressure higher - detected by baroreceptors
increase nerve activity in the carotid sinus nerve
vagus nerve mirrors this traffic
sympathetic cardiac nerves have reciprocal innovation - so there is a reduction in activity
sympathetic vasoconstrictor nerves - very little nerve activity = vasodilation = lower Bp because lower heart rate and resistance - these nerves act on the resistance and capacitance vessels
describe the role of the baroreceptor in a haemorrhage
decrease in: blood volume venous pressure venous return atrial pressure EDV SV cardiac output Bp detected by the baroreceptor - stretches less increases activity of SNS vasoconstriction venous pressure
describe the vagus nerve
vagus nerve has both afferent and efferent communication
afferent to VMC
efferent to SAN
response to standing
stimulate skeletal muscle pump - more blood return to heart
valves - unidirectional flow
respiratory pump - easy blood back to heart as quickly as possible - diaphragm drops = -ve intrathoracic pressure
effect of a haemorrhage:
low volume venous pressure venous return atrial pressure EDV SV CO (Q) Bp
maintaining arterial pressure after a haemorrhage
haemorrhage causes: low sv low baroreceptor firing induces reflexes: reflexes: less PNS discharge to the heart and increased SNS discharge to the heart increase contractility increase SV increase CO increase MAP increase SNS discharge to the veins increase venous tone increase venous pressure increase EDV Increase Q Increase MAP increase SNS to arterioles increased arteriolar constriction increased TPR increased MAP
MAP
mean pressure exists in system when blood redistribute to all tissues
