control of heart function Flashcards
what cells can contract and relax in response to electrical stimuli
muscle cells (cardiac myocytes) essential for pumping blood around the body
what do specialised electrical cells do
they are cells that create spontaneous currents and those that transmit currents exist within the heart - essential for regulation contraction of cardiac myocytes
what are the vessels responsible for
the major blood vessels are responsible for transporting the blood in and out of the heart
while the coronary blood vessels are responsible for supplying blood to the heart
what cells are the most prominent in controlling heart function
electrical cells
although cardiac myocytes and vessels of the heart are able to modulate function
what are the 2 nodes of the heart
SAN
AVN
what is the SAN and where is it found
pacemaker of the heart - 60-100 bpm
at the junction of crista terminalis - upper wall of right atrium and opening of superior vena cava
what is the AVN and where is it found
has pacemaker activity : slow calcium mediated action potential
traingle of Koch at the base of right atrium
what is the bundle of His and bundle branches
internodal tracts - specialised myocytes
connect the SAN to AVN
bundle of His that goes from the atria down through interventricular septum
what are purkinje fibres
specialised conducting fibres along ventricles of the heart
how many phases does nodal action potential have
3 phases (0, 3 and 4)
in the order 4 0 3
(pre potential, upstroke and then repolarisation)
what is upstroke and what is it due to
depolarisation due to Ca2+ influx
what is repolarisation due to (in terms of ions)
K+ efflux
do nodal cells have a resting membrane potential
no
only a pre potential due to Na+ influx through a “funny” channel
why do different parts of the heart have different action potential shapes
caused by different ion currents flowing and different ion channel expression in cell membrane
which AP is longer - cardiac or nerve
cardiac AP
what does the duration of AP control the duration of
contraction of the heart
what kind of contraction is required to produce an effective pump
long slow contraction
how many phases does AP have
5 phases labelled 0-4
describe phase 0
upstroke
start off with resting membrane potential around -80/90 mV then upstroke takes it up to 20/30 mV
describe phase 1
early repolarisation
brings the membrane potential back down to a slightly more negative value
describe phase 2
plateau
maintains the cell at a level of depolarisation
describe phase 3
repolarisation
repolarisation at around 270 ms
describe phase 4
resting membrane potential
what is the absolute refractory period (ARP)
time during which no AP can be initiated regardless of stimulus intensity
(phases 0, 1 and 2)
what is the relative refractory period (RRP)
period after ARP where an AP can be elicited but only with larger stimulus strength
(phases 3 and 4)
what are 3 major organ systems that have the ability to modulate the activity of the heart
the brain/CNS
the kidneys
the blood vessels
how can the brain/CNS modulate heart activity
can effect immediate changes through nerve activity or slower changes through hormonal activity
the CNS also impacts other systems > subsequently affecting the heart
how can the kidneys modulate heart activity
the heart and kidneys share a bidirectional regulatory relationship usually through indirect mechanisms
how can the blood vessels modulate heart activity
by regulating the amount of blood that goes to and from the heart, the blood vessels are able to influence cardiac activity
how is the autonomic nervous system involved in CNS control of the heart
cairo-regulatory centre and vasomotor centres in medulla
how is the parasympathetic nervous system involved in CNS control of the heart
rest and digest
PS nerves leave from medulla and goes via vagus nerve to heart
PS nerve is activated > causes a decrease in HR
decreases slope of phase 4 reducing HR by affecting SAN
affects pre-potential of AP within nodal cell
how is the sympathetic nervous system involved in CNS control of the heart
fight or flight
increase in HR (positive chronotrophy) - increases the slope of phase 4 (sympathetic nerves decreases time taken to get back to depolarisation phase)
increase force of contraction (inotropy) - increases Ca2+ dynamics
what does an increase in volume and pressure activate
baroreceptors
reduce SNS activity and HR
design of the ANS
split into PNS and SNS
describe the parasympathetic nervous system
parasympathetic nerves arising from cranial part of spinal cord and sacral part of spinal cord
rest and digest
preganglionic fibres (long) use ACh as NT
PNS post ganglionic NT = ACh
PNS is important for controlling the HR
describe the sympathetic nervous system
arises from thoracic vertebrae and lumbar vertebrae
fight or flight
preganglionic fibres (short) use ACh as their NT
SNS post ganglionic NT = NA (noradrenaline)
SNS is important for controlling the circulation
where is the vasomotor complex located
located bilaterally in reticular substance of medulla and lower third of pons
what is the vasomotor cortex composed of
vasoconstrictor (pressor) area
vasodilator (depressor) area
cardioregulatory inhibitory area
where are impulses transmitted through
distally through spinal cord to almost all blood vessels
what can exert powerful excitatory or inhibitory effects on the vasomotor complex/centre
many higher centres of the brain such as the hypothalamus
what do lateral portions of Vasomotor complex/centre control
heart activity by influencing heart rate and contractility
what do medial portions of the vasomotor complex/centre transmit
signals via the vagus nerve to the heart that tend to decrease heart rate
what does the PS release to inhibit the SAN
releases ACh
acts on M2 muscarinic receptors on cell membrane of SAN cell and by a G protein known as Gi protein > inhibition of adenylyl cyclase > prevents conversion of ATP to protein kinases
what does the sympathetic system release to activate/stimulate the SAN
releases noradrenaline > acts on beta 1 receptors > stimulates adenylyl cyclase and cause increase in level of protein kinase A
what is shown if you cut sympathetic nerves
the heart rate goes down suggesting that there was already some level of S activity occurring all the time
describe how sympathetic nerves in the renal system regulate blood volume and can therefore affect BP
sympathetic nerves innervate the kidneys
they reduce glomerular filtration (less filtered) > decreases Na+ excretion > increasing blood volume (aldosterone)
what is blood volume detected by
venous volume receptors
sympathetic nerves can also increase activity
how do the kidneys regulate blood volume and pressure with increased renin secretion?
increased renin secretion > releases angiotensin 2 (causes release of aldosterone - impacts blood volume/increased production of aldosterone leads to vasoconstriction and increases blood pressure)
what cells is blood pressure detected by
arterial baroreceptors
decreases SNS activity and decreases HR
what nerve fibres innervate afferent and efferent arterioles of the glomerulus and nephron tubule cells
sympathetic nerve fibres
where is the primary site of sympathetic activity
afferent arterioles
STEPS for what happens at afferent arterioles upon release of NA
release of NA
1) activation of alpha 1 adrenoreceptor
2) reduced chronotropy and increased intropy for heart
3) activation of receptors causes vasoconstriction (reduces GFR and increases blood volume)
4) reduction in GFR = reduction in Na+ filtered
5) sympathetic nerves act on juxtaglomerular cells (site of synthesis, storage and release of renin)
6) stimulation of beta 1 adrenoreceptor leads to renin secretion
7) renin increases blood volume by sympathetic nerves at the kidney
what do volume sensors do
also atria and right ventricle
send signals through glossopharyngeal and vagus nerves
what does a decrease in filling (less blood returning to the heart) lead to
reduction in baroreceptor firing > increased SNS activity
increased HR
what does distension (heart is full - more blood returning to the heart) lead to
increased baroreceptor firing
decreased SNS activity
what regulates how much blood coming back to the heart
kidneys and blood vessels
what is involved in the arterial circuit
aortic arch
carotid sinus
afferent arterioles of the kidneys
what do pressure receptors do
send signals through glossopharyngeal and vagus nerves
what does a decrease in pressure lead to
reduction in baroreceptor firing
increases SNS activity
what does an increase in pressure lead to
increased baroreceptor firing
decreased SNS activity
what is the relationship between baroreceptor firing and SNS activity
they are reciprocals
how many circulations are there and what are their names
2 circulations
pulmonary and systemic
right heart > lungs > left heart > body
what is venous volume and what is venous volume distribution affected by
venous volume = amount of volume in veins
affected by peripheral venous tone, gravity, skeletal muscle pump and breathing
what is central venous pressure and what does it determine
mean pressure in right atrium
determines the amount of blood flowing back to the heart
determines filling pressure and distension of the heart
what determines stroke volume
the amount of blood flowing back to the heart (Starling’s Law of the heart)
in veins, what does constriction do
constriction reduces compliance and increases venous return - greater pressure (bigger effect than decreased volume due to constriction)
in arterioles (less blood but higher pressure) constriction determines? (3)
blood flow to downstream organs
mean arterial blood pressure
the pattern of blood flow to organs
what are local mechanisms for regulating blood flow (characteristics not actual things)
intrinsic to smooth muscle (or closely associated)
important for reflex local blood flow regulation within an organ
what are some endothelium derived vasodilators
Nitric oxide
prostacyclin
what are some endothelium derived vasoconstrictors
thromboxane A2
endothelins
what does NO do
potent vasodilator
diffuses into vascular smooth muscle cells
what does prostacyclin do
vasodilator
has antiplatelet and anticoagulant effects
what does thromboxane A2 do
aka TXA2
vasoconstrictor that is also heavily synthesised in platelets
what do endothelins do
ET
vasoconstrictors generated from nucleus of endothelial cells
what are characteristics of systemic mechanisms
extrinsic to smooth muscle
these include the autonomic nervous system and circulating hormones
what are some non endothelium derived vasodilators
kinins
atrial natriuretic peptide (ANP)
what are some non endothelium derived vasoconstrictors
vasopressin
noradrenaline/adrenaline
angiotensin 2
what do kinins do
vasodilator
binds to receptors on endothelial cells and stimulates NO synthesis
what does atrial natriuretic peptide (ANP)
vasodilator
secreted from the atria in response to stretch to reduce BP
what does vasopressin do (ADH)
vasoconstriction
secreted from the pituitary gland
binds to V1 receptors on smooth muscles to cause vasoconstriction
what does noradrenaline/adrenaline do
vasoconstriction
secreted from the adrenal glands (and SNS) causing vasoconstriction
what does angiotensin 2 do
potent vasoconstrictor from the renin-angiotensin-aldosterone axis
also stimulates ADH secretion