control of heart rate Flashcards
how is heart rate determined
primarily by autonomic influence on the SA node
set by the depolarisation rate of the sinoatrial note
how is the heart innervated
by both divisions of the autonomic nervous system even though nervous stimulation is not required to initiate contraction
affect heart rate by changing the slope of the pacemaker potential
what is tachycardia
increased activity in the sympathetic nerves to the heart which increases HR
what is bradycardia
increased activity in the parasympathetic nerves to the heart which decreases HR
what is the chronotropic effect
changes in rate
effect of parasympathetic nervous system on the heart
the vagus nerve releases acetylcholine to muscarinic receptors
alter the activity of the cAMP second messenger pathway in innervated cardiac cells
Ach is coupled to an inhibitory G-protein that reduces activity of the cAMP pathway
decreases heart rate through 2 effects on pacemaker tissue - hyperpolarisation of the SA node membrane so it takes longer to reach threshold - decreases the rate of spontaneous depolarisation (Ach increases K+ permeability by G-protein-coupled inwardly-rectifying potassium channels)
decreases the AV nodes excitability which prolongs transmission of impulses to the ventricles
shortens the plateau phase of the action potential in atrial cotractile cells, weakening atrial contraction
has little effect on ventricular contraction
summary of the effect of the parasympathetic nervous system on the heart
decrease in HR
the time between atrial and ventricular contraction is increased
atrial contraction is weaker
effect of sympathetic nervous system on the heart
releases noradrenaline to beta1 adrenergic receptors
alter the activity of the cAMP second messenger pathway in innervated cardiac cells
NorAd is coupled to a stimulatory G-protein that accelerates activity of the cAMP pathway
speedsup heart rate through its effect on pacemaker tissue (tachcardia) - speeds up depolarisation, so threshold is reached more rapidly (NorAd augments funny channels, If, and transient-type Ca2+ channels, T)
reduces AV nodal delay by increasing conduction velocity
speeds up spread of action potential throughout the specialised conduction pathway
increased contractile strength of the atrial and ventricular contractile cells - heart beats more forcefully and squeezes out more blood - increase Ca2+ permeability through prolonged opening of L-typed Ca2+ channels
speeds up relaxation
summary of the effect of the sympathetic nervous system on the heart
increases heart rate
decreases the delay between atrial and ventricular contraction
decreases conduction time through the heart
increases the force of contraction
speed up the relaxation process so that more time is available for filling
what are cardiac centres
cardiac centres in the brain stem (medulla oblongata) mediate sympathetic and parasympathetic control of the SA and AV node depolarisation
what is the CIC
parasympathetic activity arises in the cardioinhibitory centre of the medulla
neurotransduction through the vagus nerve mediates inhibitory input
Ach increases SA node permeability to K+ (slow closure of K+ channels) and so increased leakage of +’ve charge. SA node hyperpolarises between contraction cycles resulting in fewer action potentials at the SA node, does not alter AV node function
heart rate decreases
what is the CAC
sympathetic activity arises in the cardioacceleratory centre of the medulla
motor neurons linking to T1-T5 level of the spinal cord synapse with ganglionic neurons located in cervical and upper thoracic symoathetic chain ganglia. postganglionic fibres innervate the SA and AV node to raise HR and CO
NorAd accelerates closure of K+ channels so reducing K+ permeability. SA and AV node membrane potential moves closer to threshold due to accumulation of +’ve charge in the cell between depolarisation cycles. increase in Na+ and T-type Ca2+ channel activity further accelerates depolarisation and raises action potential frequency
heart rate increases
what is vagal tone
parasympathetic and sympathetic effects on heart rate are antagonistic
heart rate is determined by the balance between inhibition of the SA node (vagus nerve) and stimulation (sympathetic nerves)
under resting conditions parasympathetic discharge dominates (vagal tone ≅ 70bpm to 100bpm)
heart rate can be altered by shiftim the balance of autonomic nervous stimulation
increase heart rate = increase symp, decrease para
decrease heart rate = decrease symp, increase para
autonomic innervation of the SA node
para = decreased heart rate
symp = increased heart rate
autonomic innervation of the AV node
para = increased nodal delay
symp = decreased nodal delay
autonomic innervation of ventricular conduction
para = no effect
symp = sped up
autonomic innervation of the atrial muscle
para = decreased contractility and strength
symp = increased contractility and strength
autonomic innervation of the ventricular muscle
para = no effect
symp = increased contractility and strength
autonomic innervation of veins
para = no effect
symp = reduces capacitance and increases venous return
autonomic innervation of the adrenal medulla
para = no effect
symp = increased adrenaline release
