Electrical Events of the Cardiac Cycle Flashcards
Sino-Atrial Node
Spontaneously firing cells of the heart; located at the right atrial wall near the opening of the SVC
Natural Pacemaker
Atrio-ventricular cells
Sponteneously firing cells located at the base of the right atrium near the septum, just above the AV junction
How does an Action Potential travel along the heart
An impulse begins in the Sinoatrial Node; this sends a wave of excitation across both atria simultaneously
That impulse then travels to the Atrioventricular Node
This action potential then travels through the bundle of His and separates along the septum; traveling down where it reaches the purkinje fibres then the myocardial cells that make up the ventricles
Spontaneous Discharge Rates of the heart nodes
SA Nodes: 70-80 Action Potentials/min
AV Nodes: 40-60 Action Potentials/min
Purkinje Fibres: 20-40 Action Potentials/min
What happens to the cells of the pacemaker when action potential reaches membrane resting potential (-60mv)
The voltage changes properties of ion channels in cells
Na+ channels open
Ca2+ channels open
K+ channels close
This causes charge to increase as Na+ and Ca2+ are at higher concentrations outside than inside the cell, leading to depolarisation
What happens when the voltage of pacemaker cells reach threshold potential
More Ca2+ channels open and the voltage increases even more to about 0mv as a result of the concentration gradient
What happens to the cells of the pacemaker when action potential reaches 0mv
Some Na+ and Ca2+ channels begin to close, but more importantly, K+ channels open, causing an efflux that decreases the voltage leading to repolarisation
Roughly how long does an impulse take to go through the SA node
Approximately one impulse per second
look at x-axis
Describe the rates of impulses that travel during a cardiac impulse
Impulse travels rapidly from the SA node through the atria, then significantly slows down at the AV node by a factor of 20 to cause a delay
After this it rapidly goes through the bundle of his and purkinje fibres where it spreads rapidly through ventricular muscle cells
Properties that allow waves of excitation to travel rapidly between myocardial cells
Gap junctions (nexi) that provide low resistance pathways, allowing cardiac muscles to function as a syncitium (single unit)
What is the role of the AV delay during cardiac contraction
This allows atrial excitation and contraction to be complete before ventricular contraction, enabling efficient emptying of blood from atria to ventricles
How is ventricular excitation kept synchronous
The rapid spread of impulse down the septum and through purkinje fibres
What is the resting potential of a pacemaker cell versus a ventricular cell
Pacemaker: -60mV
Ventricular: -90mV
How does an action potential of a ventricular contractile cell begin
Unlike pacemaker cells, they are not spontaneous at resting potential (-90mV) until extrinsic factors come into play
When a wave of excitation arrives at the cell, Na+ channels open, causing significant Na+ influx
What happens to a ventricular cell’s action potential after becoming positive
K+ channels open and some K+ ions leave the cell
What creates the plateau phase of ventricular cells during contraction
Ca2+ ion channels open and create a plateau as Ca2+ influx counteracts the K+ efflux
What causes the ending of the plateau phase of ventricular contraction
K+ efflux eventually increases as more channels open, leading to rapid depolarisation back to resting potential
Excitation-contraction coupling (Systole)
Influx of Ca2+ moves into myocardial contractile cells during action potential; triggering release of further Ca2+ from sarcoplasmic reticulum
Free Ca2+ activates contraction of myocardial fibres (SYSTOLE)
Amount of Ca2+ determines force of contraction
Excitation-contraction coupling (Diastole)
Once Ca2+ reaches a certain level
there is an uptake of Ca2+ by the sarcoplasmic reticulum
AND
An extrusion of Ca2+ by Na+/Ca2+ exchange
AND
Outward Ca2+ pump
This lowers free Ca2+ allowing relaxation
(Diastole)
Role of plateau phase of ventricular contractile cells
Cardiac contractile cells have a long refractory period unlike skeletal muscle; this allows the cell to beat then relax as opposed to simply staying contracted as additional stimuli in SkM can cause fused contraction
Plateau phase is what provides that long refractory period, preventing tetanus
Describe the direction at which cardiac impulse travels
From endocardium to epicardium; from apex to base
Sympathetic Neuronal Modulation of Heart Rate
Noradrenaline activates the β1 adrenoceptors in SA node which open ion channels, leading to an increase in the funny current and Ca2+ induced impulse
Increases heart rate (Yellow is sympathetic)
Funny Current
Mixed sodium–potassium current that causes depolarisation of the heart alongside the calcium induced impulse
Parasympathetic Neuronal Modulation of Heart Rate
Parasympathetic nerves release acetyl choline which activate M2 muscarinic receptors in SA node
ACh causes hyperpolarisation of cardiac cells by increasing K+ permeability, making them further away from threshold potential
Additionally, ACh decreases the amount of sodium in the funny current, as well as decreasing Ca2+ moving into the pacemaker cells
Decreases heart rate (green is parasympathetic)
