Regulation/Mediation Of Cardiac Conduction Flashcards
The predominant tone is created by the ?
Vagus nerve
Releasing Ach spontaneously
Slows down your heart rate
The sympathetic tone is supplied by?
Maintained by NE…
Will stimulate ventricular myocytes to contract harder/faster
Sympathetic activation = increased heart rate and stroke volume
Mechanism of sympathetic innervation on the heart
- NE binds to the beta-1 adrenergic receptor on the heart (they are GPCR stimulatory)
- Alpha subunit binds adenylyl cyclase (AC) —> causing elevation in cAMP and subsequent activation of PKA
- PKA phosphorylates proteins like the L-type Ca2+ channel
- Ca2+ channel opens
- Ca2+ influx
- Huge I-Ca created
Mechanism for parasympathetic innervation on heart
- Ach binds muscarinic receptors (inhibitory GPCRs)
- Reduces cAMP and PKA activation
- Opens K+ channels
- Efflux of K+
- Increased I-K,Ach
Modulation of AVN conduction (high yield)
Predominantly dependent on I-Ca
Which is much smaller than I-Na…which makes it good for slow conduction through the AVN
Sympathetic stimulation:
—> increase I-Ca —> shorter PR segment on EKG
(Higher upstroke velocity, higher AP amplitude, shorter AVN ERP
Vagal stimulation:
—> decreases I-Ca —> longer PR segment
(lower upstroke velocity, lower AP amplitude, longer AVN ERP)
In the AVN,
The AP upstroke is mediated by what channels?
L-type Ca2+ channels
Effect of NE on the % of L-type Ca Channels available
Fight-or-flight response —> NE secreted
Number of functional Ca channels increases
Therefore…fewer Ca channels will be needed to recover from inactivation to produce the next stimulation/AP
This helps offset the influence of the K+ channels…allowing predominantly sympathetic tone
In general, how does the AVN act as a ‘electrical filter’
AVN regulates electrical impulse by making sure that the ventricles are paced enough so that…
They fill in with blood before contracting
How the AVN ‘electrical filter’ role comes into play during atrial tachyarrhythmia
= heart rhythm problem where the heart’s atrial electrical impulse comes from an ectopic pacemaker (not SAN)
the AVN works to make sure that the ventricles stay paced…
By increasing the VAGAL TONE…thus increasing the effective refractory period (ERP)
AVN = “backup for the SAN”
Definition of automaticity in regards to the heart
Ability to spontaneously produce an AP
In the heart, the ranking of best pacemakers
- SAN
- AVN
- Purkinje fibers
Purkinje fibers role in automaticity
I-f (or I-h) = hyperpolarization-activated current in the purkinje fibers
Comes into play when the SAN and AVN are both compromised
This current is only activated when the cells are hyperpolarized (past -50mV during phase 4)…this is slow acting
I-f = a Na+ current
Effect of vagal stimulation on automaticity
Leads to increased P-k
—> causes efflux of K+ … while there is still a normal influx of Na+
—> AP threshold is never reached (currents cancel each other out)
Overall: decreased automaticity
Sympathetic effect on automaticity
Leads to increase P-Na
Leads to spike in Na+ influx
Rapid depolarization and firing of the AP as threshold is reached quiker
Overall: increase in automaticity
Effect of Hypokalemia on heart
These patients usually have congestive heart failure as well
Will increase cases of ectopic pacemakers!!
Cells are more hyperpolarized with hypokalemia…and purkinje fiber conduction is mediated by hyperpolarization
Therefore, this will cause them to fire!
Aka. Hypokalemia increase purkinje fiber automaticity
**hyperkalemia will do the opposite
Mechanism of the effects of hypokalemia on automaticity
- Causes E-k to be more negative —> cell is now in a hyperpolarized state
- Maximum diastolic potential hyperpolarizes…at the state of phase 4, P-k is high
- I-f becomes more fully activated
- P-k during late phase 4 (I-k1) is reduced (channels need extracellular K+ to complete against mild channel blocking effect of extracellular Na+)
- 3&4 cause phase 4 slope to become steeper - increased AP firing
