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
