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FHB Exam 1 - Cardiovascular Physiology > Lecture 5 - Cardiac Electrophysiology > Flashcards

Lecture 5 - Cardiac Electrophysiology Flashcards

1
Q

What are the 5 components of the SPECIALIZED conduction system of the heart?

A
  1. SA Node
  2. AV Node
  3. Bundle of His
  4. Bundle Branches
  5. Purkinje Fibers
  • pumps from ENDO to EPICARDIUM (end = inside)
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2
Q

What do the following components of the heart mirror in the Electrocardiogram (EKG):

  1. Atrial Activation
  2. Ventricular Activation
  3. Ventricular Recovery
A
  1. P-R
  2. QRS
  3. T
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3
Q

What equations represent the Theoretical and ACTUAL membrane potentials?

A
  1. Nernst is theoretical

2. Goldman-Katz is ACTUAL

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4
Q

Define the following for the Na/K Pump:

  1. net current (inward or outward)
  2. Metabolic energy?
  3. inhibited by?
  4. MAIN FUNCTION
A
  1. net OUTWARD (3 Na+ out, for every 2 K+ in)
  2. ATP!
  3. Digitalis (in a flower)
  4. Maintain Na/K gradient across membrane (used later for depolarization - AP!)
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5
Q

Define the following for the Ca2+ Pump:

  1. net current (inward or outward)
  2. low or high intracellular Ca?
  3. driven by what gradient?
A
  1. 3 Na+ in, for 1 Ca2+ out = net INWARD
  2. LOW intracellular calcium (high outside) –> pumps CA out
  3. driven by Na (sodium) gradient
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6
Q

What kind of relationship between Ek (equilibrium K) & extracellular K does the nernst equation predict? How does Vm relate to this? At which values ESPECIALLY?

A

Linear relationship!

  • Vm deviates from that predicted by Nernst Equation
  • especially at LOW extracellular K+ (low K+ means that the cell hyper polarizes of Vm plateaus)
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7
Q

What are 2 reasons for the deviation of Vm from that predicted by the Nernst Equation?

A
  1. Small Na+ influx
  2. Decrease in K+ permeability
    = Anamolous Rectification
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8
Q

Why is the Left Ventricle 3x thicker than Right ventricle?

A

resistance is higher in systemic regulation (aorta) than in pulmonary system

  • more resistance = increased pressure = difficult t push blood from ventricle into Aorta
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9
Q

What is the primary pacemaker of the heart? Conduction?

A

SA Node + AV node = pacemaker (small diameter = poor conduction)

Bundle of his/purkinje = CONDUCTION (large cells,)

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10
Q

What is the term for a decrease in K+ permeability (IK1) when either the electrical or chemical driving force on K+ is increased?

What are two ways this can occur?

A

Anamolous Rectification!

  1. decrease in extracellular K+ (K high inside usually - moves OUT)
    - if too little on outside cell could hyper polarize
    - increase threshold for AP to be reached
  2. Depolarization of membrane
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11
Q

At negative voltages to Ek, where does K+ flow? At voltages positive to Ek where does K+ flow?

A
  1. negative to Ek –> K+ flows out
  2. at more positive voltages, K+ outflow is REDUCED (flows out & then anomalous rectification occurs)
    = flows out during phase 4, and anomalous rectification occurs during phase 2
  • K+ permeability decreases and depolarization is decreased
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12
Q

Define 3 important criteria for HYPERKALEMIA(high extracellular K+):

  1. K+ permeability(increase/decrease)
  2. K+ gradient (increase/decrease)
  3. more +/- RMP? (Resting Membrane Potential)
A
  1. increases K+ permeability
  2. decreases K+ concentration gradient across membrane
  3. more POSITIVE RMP
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13
Q

Define 3 important criteria for HYPOKALEMIA (low extracellular K+):

  1. K+ permeability(increase/decrease)
  2. K+ gradient (increase/decrease)
  3. more +/- RMP? (Resting Membrane Potential)
A
  1. Decreases K+ permeability
    (less moving in)
  2. Increases K+ gradient on membrane
  3. Little to NO CHANGE on RMP due to INWARD RECTIFICATION
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14
Q

What order are the components of the heart activated?

A
  1. Atrium activated by SA node
  2. Atrial Muscle
  3. AV node activated
  4. Bundle of His activated next
  5. Ventricular Muscle
  6. Ventricular Muscle recovery
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15
Q

What does the x axis and y axis of the EKG represent?

A

x = Time

y = VOLTAGE

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16
Q

Which EKG interval represents the AV Nodal Conduction time, which carries impulses from the Atria to the Ventricle?

A

P-R interval

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17
Q

The RMP of the heart is the same as a nerve and is dependent on which ion?

A

dependent on K+ (potassium)

  • diffuses out, leaves negative charges (inside of cell negative) Na/K pump restores this
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18
Q

Calcium is low or high within the cell?

A

LOW in the cell

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19
Q

How does Hyperkalemia & Hypokalemia usually occur? What is the normal range of K?

A

HYPERKALEMIC = result of kidney failure

HYPOKALEMIC = diuretics, cause loss of potassium

  • normal is between 3-5millimolar
20
Q 
Describe what occurs during the following phases:
0
1
2
3
4
A

0 - Na+ channels open, Membrane approach Ena

1 - Na+ channels inactivate, K+ channels(Ito) open

2 - Ca channels open, and K+ conductance (Ik1) decreases = INWARD RECTIFICATION

3 - delayed activation of K+ channels (Ik) and background Ik1 conductance increases again

4 - background K conductance (Ik1) is high, delayed Ik channels closed (deactivated)

  • Ca channels closed and Na channels recover from inactivation but remain closed
21
Q

Which phase represents inward rectification?

A

Phase 2 on the graph,

Ca open, and K (Ik1) channels decrease in conductance

22
Q

What is the effect of TTX on Purkinje fiber action potential?

1) Fast Na channels
2) slow Ca channels
3) plateau
4) repolarization

A
  1. Fast Na channel (phase 0 ) blocked by TTX
  2. slow Ca channels unaffected, responsible for phase 0 upstroke!!
  3. plateau (phase 2 ) unchanged
  4. repolarization (phase 3 ) unchanged
23
Q

What channels are blocked by Tetrodotoxin? Which channels replace the function of the blocked channels?

A
  1. Fast Na channels!!
  2. Calcium channels responsible for upstroke! (phase 0)
    - Ca influx (ca low inside) can depolarize the membrane = SLOW RESPONSE ACTION POTENTIAL
    - no affect on other channels
24
Q

What do all fast responses contain?

A

SLOW responses

(Na and Ca activated)

  • fast responses can become slow responses
25
Q

What changes to the conductance result from TTX?

A
  • slow action potential since Na channels blocked
  • CA slow channels are unaffected THUS

CONDUCTANCE IS SLOWED DRAMATICALLY

26
Q

If all fast responses were changed to slow response AP’s, what would result in the heart?

A

Could not conduct or contract normally, resulting in CARDIAC ARREST

27
Q

If only a small portion of the heart changed from fast to slow response because of local damage (infarct), what is the result?

A
  1. Conduction is SLOWED in the DAMAGED REGION ONLY

2. slow conduction = ARRHYTHMIA

28
Q

What are slow response tissues? Fast response?

A
  1. SA, AV node

2. ATRIAL, Bundle of His-Purkinje, VENTRICULAR

29
Q

How long is the duration of a fast response vs a slow response?

A

Fast response has a LONG duration - 200 - 400 millisecond

  • slow response = 100-200 milliseconds
30
Q

Do SA & AV node have slow or fast conduction?

A

SLOW conduction

31
Q

What determines the configuration of the QRS complex?

A

HIS PURKINJE SYSTEM activating the VENTRICLES

  • ventricle depolarization
  • if not conducting through HIS PURKINJE then would lead to arrhythmia
32
Q

During a premature beat, is the Action potential normal? What happens to the QRS complex?

A

YEs, ap is normal since heart is at normal RMP

  • BUT QRS is different = different route of conduction (not end to epic = SOWER)
  • QRS is SLURRED = not normal conduction time
33
Q

What changes the amplitude from higher to lower in an EKG?

A
  • route of conduction is more parallel to the lead

= LARGER AMPLITUDE

34
Q

When the permeability of the cell is closer to ENa of sodium, what does the graph look like? If more similar to Ek?

A
  1. UPSTROKE of AP when membrane more permeable to Na

2. At rest more permeable to Ek and during REPOLARIZATION (negative values)

35
Q

If more current is able to flow down a cell rather than OUT, does the space constant increase or decrease?

A

INCREASES Space COnstant

  • reaches node and causes AP and another AP
36
Q

In cardiac tissue, space constant depends on what 2 things?

A
  1. Nexal Connections (gap junctions)
  2. SIZE of cell

(Parking cells larger than AV nodal cells)

  • less nexal = increased resistance = SLOWER CONDUCTION and a SMALLER space constant
37
Q

When do gap junctions change?

A

HEALING OVER

  • increase in internal resistance due to a decrease in number of open gap junctions caused by:
    1. INCREASE in Ca (cytosolic/intracellular)
    2. increase in H+ ions
  • during MI
38
Q

In hyperkalemia , how does the QRS complex change? Conduction?

A
  • it depolarizes all cells (lose Na channels), RMP more POSITIVE
  1. SLURRED QRS
  2. SLOW CONDUCTION (lose Na channels)
39
Q

In ISCHEMIA , how does the QRS complex change? Conduction?

A
  • lack of blood flow causes a shift in RMP to more + values
    1. SLURRED QRS
    2. SLOWED CONDUCTION
40
Q

When RMP becomes more + in an area and conduction slows dramatically, what can occur?

A
  • conduction can block and go in an aberrant direction
    = ABNORMALLY SLOW AP
    1. VF or
    2. Re-Entry of Excitation can occur
41
Q

A longer AP can lead to what? (slower conduction)

A
  1. Torsades de Pointes

2. EAD

42
Q

What does the AV node refractory period depend on?

A

TIME (calcium channels are time dependent)

43
Q

If a person is in AFIB, what drug can be given?

A

CALCIUM CHANNEL BLOCKER

- slow down ventricular rate through AV NODE (which filters SA node)

44
Q

What is valsalva maneuver? How can it be used to stop an arrhythmia?

A
  1. Forced expiration on a closed GLOTTIS

2. activates VAGAL STIMULATION - stop an arrhythmia

45
Q

If conduction slows enough, what can it cause?

A

a BLOCK

FHB Exam 1 - Cardiovascular Physiology (26 decks)

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