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FHB Exam 1 - Cardiovascular Physiology > Lecure 6 - Cardiac ElectroPhysiology > Flashcards

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
Q

What interval on an EG is responsible for the conduction time of Atria to Ventricular Muscle? For Intra- Ventricular Conduction time?

A
  1. P-R interval

2. QRS interval

26
Q

Does Atrio-Ventricular delay or increase conduction?

A

DELAY to increase optimal ventricular filling

27
Q

The AP of Atrio-Ventricular conduction is slow or fast?

A

SLOW conduction= slow response AP due to slow inward Calcium current

28
Q

Atrio-Ventricular conduction (AV Node) has a long or short refractory period? What is the function of this?

A

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
Q

Describe the following blocks in AV Nodal Abnormalities:

1st Degree Heart Block
2nd Degree Heart Block
3rd Degree

A
  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
Q

The following describes 1st, 2nd, or 2rd degree block:

complete AV nodal bloc, no consistent P-R interval

A

3rd

31
Q

The following describes 1st, 2nd, or 2rd degree block:

abnormally prolonged P-R interval (more than 200 milliseconds or 0.2 seconds)

A

1st

32
Q

The following describes 1st, 2nd, or 2rd degree block:

Atrial Impulses fail to activate ventricles, not all P waves followed by QRS complex

A

2nd

33
Q

Is Ventricular conduction rapid or slow?

A

RAPID

  • conduction through His-Purkinje System
34
Q

Where does Ventricular Conduction bring the electrical impulse?

A
  • to the endocardial surface
  • from there it goes from ENDO to EPICARDIUM

Result = end to epicardial activation of the ventricles

35
Q

Because the Ventricular Conduction is so rapid, how does the QRS interval look as a result?

A

very NARROW

  • less than 100 msec
36
Q

What determines intra-ventricular conduction time? What is the function of Ventricular Conduction?

A

Duration of the QRS complex (interval)

  • to synchronize ventricular activation (contraction)
37
Q

Hyperkalemia, Ischemia, and Ventricular tachycardia show what kind of EKG recording?

A

SLURRED QRS complex

  • slowed intra-ventricular conduction
    = abnormal wall motion
38
Q

Asynchronous electrical activation of left and right ventricles is often caused by what? How does this look on EKG?

A
  1. Left and/or right bundle branch BLOCKS

2. Notched QRS complex

39
Q

What occurs during Supraventricular Tachycardia?

A
  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
Q

What occurs during Ventricular Tachycardia?

A
  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
Q

What happens to the ventricular wall motion & stroke volume in Supraventricular & Ventricular Tachycardia?

A
  1. Normal
  2. Ventricular wall motion is abnormal
    - Stroke volume compromised
42
Q

The shape of the P wave of EKG determined what conduction?

A

ATRIAL

43
Q

During Atrial & Ventricular Fibrillation, what occurs? Which is life threatening?

A
  • atria & ventricles NOT IN SYNCHRONY = pumping action ceases
  • Ventricular Fibrillation is FATAL, but Atrial is not
44
Q

Where is acetylcholine released from? (Parasympathetic or sympathetic?)

A

Vagus nerve –> PARASYMPATHETIC

45
Q

Which receptors does acetylcholine use? Norepinephrine?

A
  1. MUSCARINIC

2. beta-1 adrenergic receptors

46
Q

What does ACh do to the permeability of the membrane?

A
  • increases K+ permeability via G-protein

- HYPERPOLARIZES away from threshold

47
Q

What inhibits adenylyl cyclase acitvity & cAMP synthesis? What is the result of this inhibition?

A
  • ACETYLCHOLINE!

- decreases slow inward Ca current indirectly via inhibition of cAMP synthesis

48
Q 
What NT (ACh or Norepinephrine) :
1. Inhibits ATRIAL muscle contraction (negative ionotropic effect)
  1. Inhibits SA node pacemaker activity = SLOWER HEART RATE
  2. INHIBITS AV NODE CONDUCTION

What does inhibiting AV node conduction result in?

A
  1. ACh!!

- inhibiting AV node conduction results in LONGER P-R interval

49
Q

Does ACh have an effect onbasal ventricular muscle function?

A

NO EFFECT on basal ventricular muscle function

50
Q

Where is NE released?

A

SYMPATHETIC NERVES

51
Q

NE acts via what receptors? What areas of the heart does it act on?

A
  1. ALL AREAS OF HEART

2. Beta-1 adrenergic receptors to INCREASE cAMP

52
Q

How does NE affect the Calcium current? What does this do to atrial and ventricular contraction? Is this a positive or negative inotropic effect?

A
  • INCREASES slow inward Calcium current (calcium low inside)
  • INCREASES contraction
  • positive inotropic effect
53
Q

Which NT (NE or ACh) inhibits and which increases SA node and AV node conduction?

A
  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
Q

What is the effect of increases AV node conduction on the EKG? What about increasing SA node conduction?

A
  1. increase AV node = DECREASE P-R interval

2. increase SA node = DECREASE R-R interval (from one QRS to next)

FHB Exam 1 - Cardiovascular Physiology (26 decks)

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