Control of Heart Function Flashcards
What are the three main anatomical components of the heart
Muscle cells (Cardio-myocytes) - contract and relax
Specialised eletrical cells - create spontaneous currents, essential for regulating contraction
Vessels - major blood vessels responsible for transporting blood in and out
Where is the sinoatrial node located
Junction of the crista terminalis: upper wall right atrium and opening of superior vena cava
60-100bpm
Where is the atrioventricular node
Located at the triangle of koch at base of right atrium
Has pacemaker activity: slow calcium mediated action potential - normally SA node
What are the tracts of the heart
Internodal tracts
Bundle of HIS - bundle brunches - purkinje fibres - apex
Specialised conducting fibres
What is the nodal cell action potential
3 phases - 0,3,4
Phase 0 - Uptake calcium influx
Phase 3 - repolarisation due to K efflux
Phase 4 - Nodal cells don’t have a resting membrane potential - due to Na influx through a funny channel
Why do the action potential profiles have differen action potential shapes
Caused by different ion current flowing and differen ion channel expression
What is the time difference between cardiac muscle and nerve muscle
Cardiac AP is long
Why does cardiac muscle AP have a long slow contraction
Required to produce an effective pump
What is the cardiac muscle action potential
Phase 0 - upstroke
Phase 1 - early repolarisation
Phase 2 - plateau phase
Phase 3 - repolrisation
Phase 4 - membrane potential
Absolute refractory period - heart cannot start another action potential
Relative refractory period - can be elicitied if stimulus strength is high enough

What is the diagram of ventricular cell

What part fo the CNS controls the heart
Autonomic nervous system (cardio-regulatory centre & vasomotor centres in medulla)
parasymthatetic nervous system - vagus nerve
decrease slope of phase 4 - reduce activity of SAN
sympathetic nervous system
increase in heart rate (chronotropy) - increase slope of phase 4
increase force of contraction (inotropy) - increases Ca dynamics
Where is the vasomotor centre located
Bilaterally in reticular substance of medulla and lower third of pons
What are facts of the vasomotor centre
Composed of vasoconstrictor area
Composed of vasodilator area
Cardio-regulatory inhibitory area
Transmits impulses distally through spinal cord to almost all blood vessels
Higher centres of the brain can exert powerful excitatory or inhibitory effects on VMC
Lateral VMC - influencing heart rate and contractility
Medial VMC - trasmits signals via vagus nerve to heart that decreases heart rate
Parasympathetic action at the SAN
Ach act on M2 receptor of SAN
Gi protein causes inhibition fo adenylyl cyclase which converts ATP to protein kinase A
Sympathetic action at the SAN
Noradrenaline acts on B1-receptors
Stimulate increase in andenylyl cyclase
Increase in protein kinase A
Why does the heart rate dip when sympathetic nerves are cut
Already some level of sympathetic activity, occurs all the time

What do sympathetic nerves do to the kidney
Decrease glomerular filtration - decrease Na excretion - increase in blood volume
Blood bolume detected by venous volume receptors
Increase in renin secretion - increase angiotensin-11- increase in vasoconstriction and increased blood pressure
blood pressure detected by arterial baroreceptors
What happens in the glomerulus during sympathetic stimulation
Sympathetic nerve fibres innervate afferent and efferent arterioles
noradrenaline acts on a1-adrenoceptor causes vasoconstriction
decrease in glomerular filtration rate and amount of sodium filtered
b1-adrenoceptor causes renin secretion, this increases aldosterone which raises blood volume
Cardiopulmonary cicurti
Pulmonary vessels - volume sensors - send signals trhough glossopharyngeal and vagus nerves
Decrease in filling (less blood coming to the heart) - decrease in baroreceptor firing - increase in sympathetic nerve (SNS) activity
Distention (heart is full) - increase baroreceptor - decrease SNS
Arterial circuit - aortic arch, carotid sinus and afferent arterioles of kidneys
Pressure sensors: signals through glossopharyngeal and vagus nerves
Decrease in pressure - decrease in baroreceptor firing - increase SNS activity
Increase in pressure - increase baroreceptor firing - decrease SNS activity
How is venous pressure and volume affected
Venous volume distribution - peripheral venous tone, gravity, skeletal muscle pump and breathing
Central venous pressure - determines amount of blood flowing back to heart
Amount of blood flowing back to the heart determines stroke volume
Veins - constriction reduces compliance and increases venous return
Arterioles - constriction determines blood flow to downstream organs, mean arterial blood pressure, the pattern of blood flow to organs
Local mechanisms that affect blood vessels
Nitric oxide: vasodilator
Prostacylin: vasodilator - antiplatelet and anticoagulant effects
Thromboxane A2 (TXA2): vasoconstrictor that is heavily synthesised in platelets
Endotehlins: vasoconstrictors generated from nucleus of endothelial cells
Local blood flow regulation within an organ
Systemic mechanisms that affect blood vessels
Extrinsic to the smooth muscle
Autonomic nervous system and circulating hormones
Kinins: bind to receptors on endothelial cells and stimulate NO synthesis
Atrial natriuretic peptide: ANP - secreted from atria in response to stretch - vasodilator to reduce BP
Vasopressin (ADH) - binds to V1 receptors to cause vasoconstriction
Noradrenaline/adrenaline: secreted from adrenal gland - causes vasoconstriction
Angiotensin 2 - vasoconstrictor from renin-angiotensin-aldosterone axis, stimulates ADH secretion