Lecture 8 - Cardiac Pacemaker Mechanisms Flashcards

1
Q

What is the primary pacemaker with the fastest inherent beating rate?

A

SA node!

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2
Q

What are the latent/ectopic (subsidiary) pacemakers? When do they come into play?

A

Atrial and Ventricular

  • come into play when SA Node malfunctions
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3
Q

How are pacemakers arranged in the heart?

A

ANATOMICALLY

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4
Q

What is the hierarchy of anatomical pacemakers and what is it based on?

A

Based on INHERENT BEATING RATE (fastest is first)

  1. Sa Node
  2. Latent Atrial Pacemakers
  3. AV Node/ Bundle of His
  4. Bundle Branches
  5. Purkinje FIbers
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5
Q

The SA node pacemaker is primarily based on what?

A

DIASTOLIC DEPOLARIZATION (Phase 4 of Slow Calcium channels)

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6
Q

What are the 4 mechanisms that underlie SA node pacemaker activity?

A
  1. T- type Calcium current
  2. Hyperpolarization activated inward current (If channel of Na into cell)
  3. Deactivation of K+ current (IK)
  4. Inward Na/Ca exchange current activated by intracellular Calcium release
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7
Q

Diastolic depolarization occurs primarily in what two areas?

A
  1. SA Node

2. Purkinje fibers

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8
Q

What is the most vital to Purkinje fibers in order to achieve diastolic depolarization?

A
  1. If current (funny)
  2. Deactivation of K+ current (decrease in outward K current means membrane potential becomes more positive & can achieve depolarization)
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9
Q

Diastolic depolarization corresponds to which phase of the slow response Ca release?

A

Phase 4

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10
Q

What activates the If current?

A

HYPER POLARIZATION of the cell

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11
Q

What is the function of If channels?

A

inward Na current, hyper polarization

  • controls the SA rate –> thus the CARDIAC RATE
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12
Q

Pacemaker cells upstroke is reliant on what? This is different from non-pacemaker cells how?

A
  • dépendant on CALCIUM

- non-pacemaker cells are only dependent on Na

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13
Q

How does parasympathetic (vagal) and sympathetic stimulation change the diastolic depolarization graph?

A
  1. Vagal = decrease slope, - slow HR

2. Sympathetic = increase slope - increase HR

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14
Q

A decrease in K permeability is necessary to achieve Diastolic Depolarization. Why?

A

decrease in potassium conductance means less( + ) charge leaving the cell

  • more positive charge in cell and hyperpolarization activated inward Na channels (If) both contribute to diastolic depolarization
  • deactivating K makes Na influx more affective in depolarizing diastolic voltage by decreasing outward positive current

= cell DEPOLARIZES when at threshold

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15
Q

What are the 4 mechanisms responsible for changes in heart rate? (pacemaker cell changes)

A
  1. Change in the slope of DIASTOLIC depolarization
  2. Change in MAX diastolic potential
  3. CHange in threshold
  4. Pacemaker shifts - changes in pacemaker site can cause abrupt changes in HR buck of the HIERARCHY of pacemaker activities
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16
Q

How would decreasing and increasing max diastolic potential affect the Heart Rate?

A
  1. Decrease max diastolic potential = increase firing = increase HR
  2. Increase max diastolic potential = decrease firing = decrease HR
17
Q

How would decreasing and increasing Diastolic threshold potential affect the firing frequency (heart rate)?

A
  1. Decreasing = increase firing rate

2. Increase Diastolic threshold = decrease firing rate

18
Q

Define the following:

When Pacemaker is stimulated (driven) at a frequency HIGHER than its intrinsic frequency,

STOPPING the stimulation results in a temporary SUPPRESSION OF PACEMAKER activity

A

OVERDRIVE SUPPRESSION

  • SA node normally “overdrives” all subsidiary (ectopic0 pacemakers in the heart
  • thus suppresses ectopic pacemaker activity
19
Q

What are the 3 mentioned clinical applications of OVERDRIVE SUPPRESSION?

A
  1. SA nodal or AV nodal Block (2nd or 3rd degree block)
2nd = not all P followed by QRS (2:1)
3rd = complete AV nodal block = no consistent P-R interval
  1. Stopping artificial pacemakers
  2. Sick sinus syndrome
20
Q

How do sympathetics & parasympathetics affect AV nodal conduction?

A

sympathetics INCREASE AV NODAL conduction

  • parasympathetics DECREASE conduction
21
Q

Why does stopping artificial pacemakers bring Cardiac Output to ZERO?

A

latent pacemakers not at the same speed as SA Node (SA node suppresses electrical activity of other pacemakers)

  • thus need to bring pacemaker to rate of latent pacemakers (which are slower than SA node)
22
Q

How does VAGAL stimulation affect the pacemakers? Norepinephrine? (sympathetic)

A
  • INHIBITS PACEMAKERS within the SA node, atria, and AV nodal regions
  • STIMULATE all cardiac pacemakers
23
Q

How does Vagal stimulation (ACETYLCHOLINE) affect the following:

  1. K+ permeability
  2. Adenylate Cyclase activity (cAMP synthesis)
  3. Slope of diastolic depolarization and maximum diastolic potential?
A
  1. INCREASES
  2. AC activity decreases (less cAMP –> less CA released )
  3. slope DECREASES and maximum diastolic potential HYPERPOLARIZED (more negative)–> need greater stimulus to reach threshold
    - If (Na+) channels only activated at certain (-) value BUT this value has become even MORE negative than threshold
24
Q

What is Sinus Arrhythmia?

A

Normal variability in pacemaker cycle length (heart rate) caused primarily by respiratory changes in PARASYMPATHETIC (vagal) nerve activity to SA NODE!!

25
Q

How does ACETYLCHOLINE affect L-Type Ca2+ current and If current?

A

INHIBITS L-type Calcium current and If current by inhibiting cAMP synthesis

26
Q

How is Sinus Arrhythmia in aerobically trained individuals compared to more sedentary individuals?

A

Sinus Arrhythmia is more pronounced (have lower resting heart rate)

27
Q

How does Inspiration and Expiration change the cycle length (heart rate)? How is it affected by the parasympathetic activity?

A
  1. Inspiration = decreased cycle length (increased HR)
    - inhibit parasympathetic nerve activity
  2. Expiration = increased cycle length (decrease HR)
    - stimulate parasympathetic nerve activity
28
Q

How does NE (sympathetic stimulation) affect slow inward L-Type Calcium current? Does it increase or decrease cAMP synthesis?

A

INCREASE slow inward L-type Ca2+ current and If

  • by increasing cAMP synthesis
29
Q

Does NE increase or decrease the slope of diastolic depolarization?

A

Increases the slope of Diastolic Depolarization

30
Q

How does SA node decrease the cycle length upon inspiration and expiration?

A

VAGAL MODULATION

  • inspire = inhibit vagal stimulation
  • expire = stimulate vagus
31
Q

What does SINUS TACHYCARDIA resemble?

A

looks like SUPRAVENTRICULAR TACHYCARDIA

  • appears this way when we exercise
32
Q

In sinus Bradycardia, what increases on an EKG

A
  • long Q-T interval

= long diastole

33
Q

What does inotropic mean??

A

Affecting the contractility of muscular tissue

34
Q

Is there an RMP in pacemaker cells?

A

NO!!

- pacemaker cell are never at rest so they do not have a resting membrane potential

35
Q

What is Sick Sinus Syndrome?

A

Sick sinus syndrome (SSS), also called sinus node dysfunction (SND),

is an umbrella term for a group of abnormal heart rhythms (arrhythmias) presumably caused by a malfunction of the SINUS node, the heart’s primary pacemaker

36
Q

How does hypokalemia affect HR? It exerts this affect by changing the slope of what? (does it also increase or decrease the slope)

A
  1. Latent pacemakers HAVE anomalous rectification: thus during low K extracellularly, this decreases the permeability of K across the membrane and prevents K from leaving the cell
    - this allows for the action potential to reach threshold sooner (since it has a more positive threshold) & depolarize QUICKLY

resulting in a quicker AP and an increased SLOPE of diastolic depolarization

LATENT PACEMAKERS overcome the overdrive suppression of the SA node, thus causing a quicker HR due to faster conduction times

(always a transient increase in K+)

37
Q

What are 3 reasons a slurred QRS can occur?

A
  1. Hyperkalemia
  2. Ischemia
  3. ventricular Tachycardia
38
Q

What is a reason for a notched QRS?

A

Right or Left Bundle Branch block