Regulation/Mediation Of Cardiac Conduction Flashcards

1
Q

The predominant tone is created by the ?

A

Vagus nerve

Releasing Ach spontaneously

Slows down your heart rate

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2
Q

The sympathetic tone is supplied by?

A

Maintained by NE…

Will stimulate ventricular myocytes to contract harder/faster

Sympathetic activation = increased heart rate and stroke volume

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3
Q

Mechanism of sympathetic innervation on the heart

A
  1. NE binds to the beta-1 adrenergic receptor on the heart (they are GPCR stimulatory)
  2. Alpha subunit binds adenylyl cyclase (AC) —> causing elevation in cAMP and subsequent activation of PKA
  3. PKA phosphorylates proteins like the L-type Ca2+ channel
  4. Ca2+ channel opens
  5. Ca2+ influx
  6. Huge I-Ca created
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4
Q

Mechanism for parasympathetic innervation on heart

A
  1. Ach binds muscarinic receptors (inhibitory GPCRs)
  2. Reduces cAMP and PKA activation
  3. Opens K+ channels
  4. Efflux of K+
  5. Increased I-K,Ach
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5
Q

Modulation of AVN conduction (high yield)

A

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)

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6
Q

In the AVN,

The AP upstroke is mediated by what channels?

A

L-type Ca2+ channels

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7
Q

Effect of NE on the % of L-type Ca Channels available

A

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

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8
Q

In general, how does the AVN act as a ‘electrical filter’

A

AVN regulates electrical impulse by making sure that the ventricles are paced enough so that…

They fill in with blood before contracting

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9
Q

How the AVN ‘electrical filter’ role comes into play during atrial tachyarrhythmia

A

= 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”

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10
Q

Definition of automaticity in regards to the heart

A

Ability to spontaneously produce an AP

In the heart, the ranking of best pacemakers

  1. SAN
  2. AVN
  3. Purkinje fibers
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11
Q

Purkinje fibers role in automaticity

A

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

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12
Q

Effect of vagal stimulation on automaticity

A

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

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13
Q

Sympathetic effect on automaticity

A

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

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14
Q

Effect of Hypokalemia on heart

A

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

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15
Q

Mechanism of the effects of hypokalemia on automaticity

A
  1. Causes E-k to be more negative —> cell is now in a hyperpolarized state
  2. Maximum diastolic potential hyperpolarizes…at the state of phase 4, P-k is high
  3. I-f becomes more fully activated
  4. P-k during late phase 4 (I-k1) is reduced (channels need extracellular K+ to complete against mild channel blocking effect of extracellular Na+)
  5. 3&4 cause phase 4 slope to become steeper - increased AP firing
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16
Q

Effect on intracellular Na and Ca concentration on contractility

A

Increase [Na]i or [Ca]i or [Ca]o

Will increase contractility

17
Q

How [Na] concentration regulates contractility (2 mechanisms)

A
  1. Na/K pump —> if [K]o is large, pump turns on —> maintains ion concentration gradient
  2. Na/Ca exchanger —> uses Na conc. Gradient to eject Ca so that you don’t have a build up of Ca inside the cell over time