Lecure 6 - Cardiac ElectroPhysiology Flashcards

1
Q

What are specialized regions of intercellular connections between cardiac cells called?

A

Intercalated disks

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2
Q

What are the 3 types of junctions within an intercalated disk?

A
  1. Fascia Adherens
  2. Macula Adherens
  3. Gap Junctions
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3
Q

What are the anchoring sites for actin that connect to the closest sarcomere?

A

Fascia Adherens

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4
Q

What adhering junctions have low resistance connections that allow current (Action potentials) to conduct between cardiac cells?

A

GAP JUNCTIONS

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5
Q

What holds cells together during contraction by binding intermediate filaments, joining cells together like a SPOT WELD?

A

Macula Adherens

  • DESMOSOMES
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6
Q

What is HEALING OVER?

A

an increase in INTERNAL RESISTANCE that results from a decrease in the # of open gap junctions

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7
Q

What are 2 causes of healing over?

A
  1. Increase in intracellular (cytosolic) Ca2+
  2. increase in intracellular H+ ions (decrease ph)
    - Ca is usually LOW in the cell
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8
Q

What is a clinical application of HEALING OVER?

A

Electrical isolation of damaged tissue that results from Myocardial Infarction

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9
Q

Describe the following for SA & AV Nodes:

  1. Function
  2. Conduction ( slow/fast)
  3. Contraction (weak/strong)
  4. DIAMETER
  5. # of Gap Junction connections
  6. Myofibrils
A
  1. Pacemaker activity
  2. SLOW CONDUCTION
  3. WEAK CONTRACTION
  4. small diameter (large internal resistance, small space constant)
  5. few gap junctions
  6. few Myofibrils
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10
Q

Describe the following for Atrium and Ventricles:

  1. Function
  2. Conduction ( slow/fast)
  3. Contraction (weak/strong)
  4. DIAMETER
  5. # of Gap Junction connections
  6. Myofibrils
A
  1. Conduction/ Contraction
  2. Fast conduction
  3. STRONG contraction
  4. medium diameter
  5. Abundant gap junctions
  6. Abundant MYOFIBRILS
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11
Q

Describe the following for His Bundle, Bundle Branches, and Purkinje Fibers:

  1. Function
  2. Conduction ( slow/fast)
  3. Contraction (weak/strong)
  4. DIAMETER
  5. # of Gap Junction connections
  6. Myofibrils
A
  1. VERY RAPID CONDUCTION!!!!!!!!!!!!
  2. VERY RAPID conduction
  3. weak contraction!
  4. LARGE DIAMETER
  5. abundant gap junctions
  6. FEW MYOFIBRILS
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12
Q

What factors determine cardiac conduction?

A
  1. Space Constant

2. Rate of Rise AND Amplitude of Action Potential

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13
Q

How is Rm (membrane resistance) related to K+ permeability?

A

INVERSLEY related

-as membrane resistance decreases, K+ permeability increases

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14
Q

How is Ri (internal resistance) related to gap junctions and cell diameter?

A
  • Inversely related to both

- internal resistance decreases with GREATER number of GAP JUNCTIONS and a GREATER CELL DIAMETER

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15
Q

How is the space constant defined by Rm and Ri?

A

space constant = (Rm/Ri) 1/2

square root

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16
Q

What 3 factors determine the rate of rise AND amplitude of AP?

A
  1. Level of Resting Membrane Potential (fast -response only)
  2. Slow vs. fast response AP’s
  3. Premature Responses initiated during RELATIVE REFRACTORY period
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17
Q

At what mV is the number of NA+ channels maximum? When is it ZERO?

A
  1. Max at about -80, -90
  2. Zero at -50

(at -60 = 50% of Na channels open OR conductance)

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18
Q

What defines conductance?

A

The number of channels open or closed

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19
Q

What are 3 conditions that influence the AP upstroke (depolarization phase- Na influx) as a result of changes in the RMP?

A
  1. Hyperkalemia (more positive RMP)
  2. Premature Excitation during relative refractory period
  3. Ischemia or Myocardial Injury
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20
Q

An abnormal increase in EXTRACELLULAR K+ will cause a more positive or negative RMP?

  • What CHannels are inactivated as a result?
A

More POSITIVE

  • fast Na channels are inactivated
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21
Q

If Na channels are inactivated due to increase in extracellular K+, what happens to the rate of rise & amplitude size?
What is the MAJOR result of this?

A
  1. SLOWER rate of rise,
  2. Decrease Amplitude AP
  3. SLOWER CONDUCTANCE!!!! of the AP
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22
Q

During ischemia/infarct, what can leak out of damaged cells?

A

K+ ions

  • accumulate in interstitial (extracellular) fluid bathing the cells
  • LOCAL concentration of K+ can increase to 20 mEq/L ( normal is 4)
23
Q

An increase in interstitial (extracellular) K+, causes what change to the voltage?

A

MORE POSITIVE VOLTAGE (positive RMP)

  • since K+ moving from high to low, thus moving IN to the cell instead of out
  • inactivates Na channels
24
Q

What is a major cause of arrhythmia? How is this defendant on K+ concentration and Na+ channel?

A
  1. SLOWER CONDUCTANCE
  2. If K+ higher outside cell, RMP is positive, thus cell depolarizes and Na channels inactivated
  3. If fast Na channels inactivated in a damaged region = SLOWER CONDUCTION

(reliant on slow Ca2+ channels)

25
What interval on an EG is responsible for the conduction time of Atria to Ventricular Muscle? For Intra- Ventricular Conduction time?
1. P-R interval | 2. QRS interval
26
Does Atrio-Ventricular delay or increase conduction?
DELAY to increase optimal ventricular filling
27
The AP of Atrio-Ventricular conduction is slow or fast?
SLOW conduction= slow response AP due to slow inward Calcium current
28
Atrio-Ventricular conduction (AV Node) has a long or short refractory period? What is the function of this?
LONG refractory period - long because if protects the ventricles from abnormally HIGH ATRIAL rates = Atrial Flutter/Fibrillation - AV conduction time determined by P-R interval
29
Describe the following blocks in AV Nodal Abnormalities: 1st Degree Heart Block 2nd Degree Heart Block 3rd Degree
1. abnormally prolonged P-R interval (more than 200 milliseconds or 0.2 seconds) 2. Atrial Impulses fail to activate ventricles, not all P waves followed by QRS complex 3. complete AV nodal bloc, no consistent P-R interval
30
The following describes 1st, 2nd, or 2rd degree block: complete AV nodal bloc, no consistent P-R interval
3rd
31
The following describes 1st, 2nd, or 2rd degree block: abnormally prolonged P-R interval (more than 200 milliseconds or 0.2 seconds)
1st
32
The following describes 1st, 2nd, or 2rd degree block: Atrial Impulses fail to activate ventricles, not all P waves followed by QRS complex
2nd
33
Is Ventricular conduction rapid or slow?
RAPID - conduction through His-Purkinje System
34
Where does Ventricular Conduction bring the electrical impulse?
- to the endocardial surface - from there it goes from ENDO to EPICARDIUM Result = end to epicardial activation of the ventricles
35
Because the Ventricular Conduction is so rapid, how does the QRS interval look as a result?
very NARROW - less than 100 msec
36
What determines intra-ventricular conduction time? What is the function of Ventricular Conduction?
Duration of the QRS complex (interval) - to synchronize ventricular activation (contraction)
37
Hyperkalemia, Ischemia, and Ventricular tachycardia show what kind of EKG recording?
SLURRED QRS complex - slowed intra-ventricular conduction = abnormal wall motion
38
Asynchronous electrical activation of left and right ventricles is often caused by what? How does this look on EKG?
1. Left and/or right bundle branch BLOCKS | 2. Notched QRS complex
39
What occurs during Supraventricular Tachycardia?
1. conduction is normal in ventricles - impulse comes from Atria and travels thru AV node into His-Purkinje system 2. QRS is normal 3. Ventricular wall motion is normal = stroke volume not significantly affected
40
What occurs during Ventricular Tachycardia?
1. Conduction in Ventricles is not normal = SLOW 2. impulse originates in ventricular muscle & does not travel through His -Purkinje 3. QRS is abnormally prolonged (SLURRED)
41
What happens to the ventricular wall motion & stroke volume in Supraventricular & Ventricular Tachycardia?
1. Normal 2. Ventricular wall motion is abnormal - Stroke volume compromised
42
The shape of the P wave of EKG determined what conduction?
ATRIAL
43
During Atrial & Ventricular Fibrillation, what occurs? Which is life threatening?
- atria & ventricles NOT IN SYNCHRONY = pumping action ceases - Ventricular Fibrillation is FATAL, but Atrial is not
44
Where is acetylcholine released from? (Parasympathetic or sympathetic?)
Vagus nerve --> PARASYMPATHETIC
45
Which receptors does acetylcholine use? Norepinephrine?
1. MUSCARINIC | 2. beta-1 adrenergic receptors
46
What does ACh do to the permeability of the membrane?
- increases K+ permeability via G-protein | - HYPERPOLARIZES away from threshold
47
What inhibits adenylyl cyclase acitvity & cAMP synthesis? What is the result of this inhibition?
- ACETYLCHOLINE! | - decreases slow inward Ca current indirectly via inhibition of cAMP synthesis
48
``` What NT (ACh or Norepinephrine) : 1. Inhibits ATRIAL muscle contraction (negative ionotropic effect) ``` 2. Inhibits SA node pacemaker activity = SLOWER HEART RATE 3. INHIBITS AV NODE CONDUCTION What does inhibiting AV node conduction result in?
1. ACh!! | - inhibiting AV node conduction results in LONGER P-R interval
49
Does ACh have an effect onbasal ventricular muscle function?
NO EFFECT on basal ventricular muscle function
50
Where is NE released?
SYMPATHETIC NERVES
51
NE acts via what receptors? What areas of the heart does it act on?
1. ALL AREAS OF HEART | 2. Beta-1 adrenergic receptors to INCREASE cAMP
52
How does NE affect the Calcium current? What does this do to atrial and ventricular contraction? Is this a positive or negative inotropic effect?
- INCREASES slow inward Calcium current (calcium low inside) - INCREASES contraction - positive inotropic effect
53
Which NT (NE or ACh) inhibits and which increases SA node and AV node conduction?
1. Ach inhibits both SA node = sow heart rate, lengthen R-R AV Node = lengthens P-R interval 2. NE: INCREASES both - increases atrial & VENTRICULAR contraction - increases SA NODE RATE = increase heart rate = decrease R-R interval -icrease AV NODE CONDUCTION = decrease P-R interval
54
What is the effect of increases AV node conduction on the EKG? What about increasing SA node conduction?
1. increase AV node = DECREASE P-R interval | 2. increase SA node = DECREASE R-R interval (from one QRS to next)