Physiology Flashcards
What is autorhythmicity
When the heart is capable of generating electrical signals for rhythmic beating without an external stimuli
Where does the excitation originate normally
In pacemaker cells in the Sino-atrial node in the upper right atrium close to the SVC entrance
The SAN drives the heart in __________
Sinus rhythm
How is a normal cardiac excitation formed (3)
SAN cells generate spontaneous pacemaker potentials instead of having a stable resting membrane potential
This takes the membrane potential to a threshold where an action potential is created
This results in regular spontaneous action potentials forming
Causes of the spontaneous pacemaker potential (3)
Decrease in K+ efflux
Na+ influx - Funny current
Transient Ca2+ influx via T-type Ca2+ channels
What type of polarization is involved in the spontaneous pacemaker potential
Slow depolarization
Cause of rising phase of action potential
Activation of long lasting L-type Ca2+ channels causing Ca2+influx
What type of polarization is involved in the rising phase of pacemaker action potential
Depolarization
Causes of falling phase of action potential
Inactivation of L-type Ca2+ channels
Activation of K+ channels causing K+ efflux
What type of polarization is involved in the falling phase of pacemaker action potential
Repolarization
How does the cardiac excitation normally spread across the heart
Sino-atrial Node => Atrioventricular Node => Bundle of His => Left and Right branches => Purkinje fibres
Which parts of the heart have cell-to-cell spread of excitation (3)
From SAN through both atria
From SAN to AVN
Within ventricles
How does cell-to-cell current flow
Via gap junctions containing low resistance protein channels
AVN characteristics (4)
Located at base of right atrium above the junction of atria and ventricles
Only point of electrical contact between atria and ventricles
Small diameter
Slow conduction velocity
Importance of conduction delay in AVN
To ensure atrial systole precedes ventricular systole
How is the action potential on atrial and ventricular myocytes different from pacemaker cells (2)
The resting membrane potential remains at -90mV
There are 5 phases (phase 0 to 4) for myocytes but only phase 0,3 and 4 for pacemaker cells
Phase 0 (5)
Ventricular action potential is triggered via SAN impulses
Involves rapid activation of voltage-activated Na+ channels at a threshold potential (-65 mV) generating a Na+ conductance and an inward, depolarizing, Na+ current
This drives Vm towards the Na+ equilibrium potential (74mV)
Voltage-activated Na+ channels rapidly inactivate during depolarization and only recover upon repolarization
Overall influx of Na+ is dominant
Phase 1 (2)
Caused by rapid inactivation of Na current and activation of transient outward K+ current mediated via voltage-activated potassium channels
Overall efflux of K+ is dominant
Phase 2 (3)
A plateau occurs due to a balance of conductances between an inward depolarizing Ca2+ flow via voltage-activated L-type channels and an outward repolarizing K+ flow
During the plateau outward K+ current in phases 4 and 1 decreases
Voltage activated delayed rectifier K+ channels slowly open, generating the repolarizing current that increases with time
Phase 3 (3)
Occurs when outward K+ currents exceed inward Ca2+ current
This is due to Ca2+ L-type channels closing
Overall efflux of K+ is dominant
Phase 4 (4)
Membrane potential is steady at -90mV
It is close to equilibrium potential for K+ (-94 mV) due to K+ conductance via inward rectifier K+ channels - This forms an outward hyperpolarizing current
Membrane potential is not at Ek due to inward depolarizing leak Na+ conductance
Overall efflux of K+ is dominant
Sympathetic stimulation increases/decreases heart rate
Increases
Parasympathetic stimulation increases/decreases heart rate
Decreases
What is the continuous parasympathetic supply to the SAN and AVN
Vagus nerve