Crr Week 1: Cardiac Electrophysiology

Front 1

Why is the SA node said to be the pacemaker for the heart?

Back 1

Although other cells in the heart undergo spontaneous depolarization, the SA node cells have the fastest intrinsic rate.

Front 2

How do the cells in the SA node compare to other cardiac cells?

Back 2

They have a reduced quantity of contractile proteins and are smaller than contractile cells or Purkinje cells

Front 3

What is the conduction velocity in the atria?

Back 3

1 meter/sec

Front 4

Which specialized conduction pathways in the atrium directly connect the SA node with the AV node and contribute to the action potential through Bachmann's bundle?

Back 4

Atrial muscle fibers
Atrial internodal tracts

Front 5

How are action potentials rapidly conducted from the right atrium to the left atrium?

Back 5

Via Bachmann's bundle

Front 6

Why is the conduction velocity in the AV node much slower than that in the SA node?

Back 6

The cells are small and have fewer gap junctions connecting the cells

Front 7

What is the conduction speed in the AV node?

Back 7

0.01 - 0.05 meters/sec

Front 8

What are the 2 functions of the AV node?

Back 8

1. Serves as the only electrical connection between the atrial and ventricle muscle fibers

2. Delays the spread of excitation from the atria to the ventricles

Front 9

List the order of propagation of action potentials in the heart.

Back 9

1. SA node
2. AV node
3. Bundle of his
4. R and L bundle branches
5. Purkinje fibers

Front 10

As in nerve and skeletal muscle, the resting membrane is very permeable to ____ions and relatively impermeable to _____ions.

Back 10

Permeable to K+ ions
Impermeable to Na+ ions

Front 11

What type of channels open during Phase 0 of an action potential in cardiac muscle cells?

Back 11

Fast Na+ voltage-gated channels
(rapid depolarization)

Front 12

During phase 0 of the cardiac action potential, inactivation of fast Na+ channels close in response to a peak depolarization value of about ________mV.

Back 12

+20 mV

Front 13

What type of ionic flow is responsible for phase 1 of the cardiac action potential?

Back 13

(fast Na+ channels have closed)

K+ channels open and K+ flows out of cell (initial repolarization)

Front 14

Which phase of the cardiac action potential represents a membrane potential near 0 mV?

Back 14

Phase 2 (plateau).

Front 15

Describe the flow of ions responsible for phase 2 of the cardiac action potential.

Back 15

Influx of Ca++ through L-type Ca++ channels

Efflux of K+ ions

Front 16

Nifedipine, dilitiazem, and verapamil can block which type of channels?

Back 16

L-type Ca++ channels.

Front 17

When do L-type Ca++ channels open during the cardiac action potential?

Back 17

At the end of the initial repolarization

Front 18

Describe the flow of ions during phase 3 of the cardiac action potential.

Back 18

The efflux of K+ begins to overcome the influx of Ca++, so repolarization begins to occur. The Ca++ current continues to diminish until it reaches zero, so repolarization rate increases.

Front 19

What is the resting membrane potential of a cardiac contractile cell?

Back 19

About -85 mV.

Front 20

Describe the conductance and driving forces of K+, Na+, and Ca++ relative to each other during Phase 4 of the cardiac action potential

Back 20

(current = conductance x driving force)

K+ --> Conductance is high, driving force is low

Na+, Ca++ --> Conductance is low, driving force is high

Front 21

How are the excess Na+ ions that entered the cell during phase 0 eliminated during phase 4 of the cardiac action potential?

Back 21

Na+/K+-ATPase

(3 Na+ ions exit, 2 K+ ions enter)

Front 22

How are the excess Ca++ that entered the cell during the plateau phase of the cardiac action potential eliminated?

Back 22

1. Na+-Ca++ exchanger (3 Na+ for 1 Ca2+)
2. True Ca2+ pumps in the cell membrane
3. Ca2+ion ATPase (SERCA_ pump (2 H+ ions for 2 Ca2+ ions for each ATP hydrolyzed)

Front 23

How do action potentials in the SA node differ from action potentials in cardiac contractile cells?

Back 23

1. Exhibits automaticity-- action potentials are generated spontaneously
2. Does not have a stable resting membrane potential
3. Does not exhibit a plateau fase

Front 24

Describe the flow of ions during phase 0 of a pacemaker action potential.

Back 24

Influx of Ca2+ through T-type Ca2+ channels

Front 25

What is the difference between the Ca2+ channels in the cardiac contractile cells and those in the SA node?

Back 25

Contractile cells = L-type Ca2+ channels (blocked by nifedipine, diltiazem, and verapamil).

Conduction cells = T-type Ca2+ channels (not blocked by drugs)

Front 26

Describe the flow of ions during phase 3 of the pacemaker potential.

Back 26

Efflux of K+ ions

Front 27

Compare the speeds of depolarization in contractile and pacemaker potentials.

Back 27

Contractile cells = rapid depolarization

Pacemaker cells = slow depolarization

Front 28

Describe phase 4 of the pacemaker potential.

Back 28

Spontaneous depolarization produced by the opening of Na+ channels ("If current).

Front 29

The "If" current describes the flow of which ions in which type of action potential?

How is "If" turned on?

Back 29

Flow of Na+ ions during the slow, spontaneous depolarization of the pacemaker potential.

Turned on by the repolarization of the previous action potential

Front 30

Of the latent pacemakers, which are the slowest?

Back 30

Purkinje fibers

Front 31

What is the conduction velocity in the Purkinje fibers?

Back 31

2 - 4 meters/sec.

Front 32

Which cardiac fibers have the highest conduction velocity?

Back 32

Purkinje fibers
(2 - 4 m/sec)

Front 33

The conduction velocity of an action potential depends on what 3 factors?

Back 33

1. Size of the inward current during the initial upstroke
2. Rate of rise of the upstroke (dV/dT0
3. Cable properties of the cardiac muscle (internal resistance)

Front 34

Why can no action potential be initiated during the absolute refractory period, no matter how large a stimulus is applied?

Back 34

Because the Na+ channels are closed

Front 35

During a cardiac action potential, Na+ channels begin to recover during which period?

Back 35

Effective refractory period

Front 36

Which period lasts from the end of the absolute refractory period until the membrane potential reaches approximately -70 mV?

Back 36

Relative refractory period (RRP)

Front 37

During which period have the Na+ channels recovered, making it possible to generate another action potential with a greater than normal stimulus?

Back 37

Relative refractory period (RRP).

Front 38

Describe the parameters of the supranormal period (SNP).

Back 38

From the end of the RRP until the membrane is fully repolarized at about -85 mV.

Front 39

What is the clinical importance of the supranormal period of the cardiac action potential?

Back 39

A lethal arrhythmia can be initiated at if another action potential from some other site is generated during this time.

Front 40

What are the 3 possible mechanisms by which the rate of firing of pacemaker potentials could be altered?

Back 40

1. Steepness of phase 4 depolarization
2. Maximum diastolic potential to which the cell repolarizes.
3. Threshold potential

Front 41

What would happen to the firing rate if the maximum diastolic potential to which the cell repolarizes become more negative?

Back 41

The cell would take longer to reach threshold and the rate of firing would DECREASE

Front 42

In the SA node, norepinephrine activates which receptors?

How is the flow of ions affected?

Back 42

B1 adrenergic receptors

Increaed influx of Na+ ("If") results in a steeper phase 4 depolarization.

Front 43

What are the two effects of NE on the heart?

Back 43

1. Increases inward Na+ current (If), increasing steepness of depolarization.
2. Increases conduction velocity of action potentials through the AV node

*Positive chronotropid AND dromotropic effect

Front 44

ACh binds to which muscle receptors in the heart?

Back 44

Muscarinic cholinergic (M2) receptors.

Front 45

List the 3 effects that ACh has on cardiac tissue.

Back 45

1. Decreases inward Na+ current (If), slowing rate of spontaneous depolarization
2. Increases K+ conductance, hyperpolarizing the cell.
3. Decrease the influx of Ca2+, increasing the threshold potential.

Front 46

What causes triggered activity?

Back 46

Afterdepolarizations

Front 47

When do early and delayed afterdepolarizations occur?

Back 47

Early --> late phase 2 to middle phase 3

Delayed --> late phase 3 to early phase 4

Front 48

Which interval of the ECG correlates with the conduction time through the AV node?

Back 48

PR interval
(time from the onset of atrial activation to the onset of ventricular activation)

Front 49

How long is the normal PR interval?

Back 49

0.16 sec

Front 50

The P wave and QRS complex have similar durations -- what is the normal time span?

Back 50

0.06 - 0.10 sec

Front 51

Which portion of the ECG represents the isoelectric time period?

Back 51

ST segment.

Front 52

Describe the duration of the ST segment in terms of depolarization and repolarization.

Back 52

Lasts from the end of the ventricular depolarization to the beginning of ventricular repolarization.

Front 53

Shifts downward or a downward sloping ST segment are indicative of what type of injury?

Back 53

Myocardial infarction

Front 54

Elevations above the baseline of the ST segment in an ECG are usually indicative of what type of injury?

Back 54

Acute myocardial injury

Front 55

What is the normal value of the QT interval (in seconds)?

Back 55

0.4 seconds

Front 56

How can heart rate be determined from an ECG?

Back 56

By measuring the R-R interval, one cardiac cycle can be determined.

heart rate = 1/ cycle length

Front 57

Fast-response action potentials are recorded from what type of fibers?

Back 57

Atrial and ventricular myocardial fibers and from ventricular specialized conducting (Purkinje) fibers.

Front 58

Slow-response action potentials are recorded from what type of cells?

Back 58

SA and AV nodal cells and from abnormal myocardial cells that have been partially depolarized

Front 59

Which type of afterdepolarizations are more likely to occur when the basic cycle length of the initiating beats is very long and when the cardiac action potentials are abnormally prolonged?

Back 59

Early afterdepolarizations
(during phase 3)

Front 60

Which type of afterdepolarization is more likely to occur when the basic cycle length of initiating beats is short and when the cardiac cells are overloaded with Ca2+?

Back 60

Delayed afterdepolarizations
(late in phase 3 or in phase 4)

Front 61

What is the effect of tetrodotoxin on cardiac action potentials?

Back 61

Blocks the fast Na+ channels in the action potentials recorded in a purkinje fiber

Front 62

What is the effect of Isoproterenol on T-type and L-type Ca2+ channels?

Back 62

Isoproterenol (beta adrenergic agonist)

*Significantly increases the L-type Ca2+ current, but has little affect the T-type channel

Front 63

What is the threshold for the pacemaker potential?

Back 63

-55 mV

Front 64

What is the effect of Ca2+ channel antagonists on cardiac afterload?

Back 64

Decrease cardiac afterload
(heart contracts at lower pressure)

Front 65

What type of pathology is characterized by an inverted P wave and normal QRS complexes and T waves?

Back 65

Premature atrial depolarization

Front 66

What type of pathology is characterized by bizarre QRS complexes and T waves and is followed by an compensatory pause?

Back 66

Premature ventricular depolarization

Front 67

What type of pathology is characterized by a long P-R interval (> 0.2 sec)?

Back 67

First-degree AV block

Front 68

What type of pathology is characterized by a 2:1 ratio of P waves to QRS complexes?

Back 68

Second-degree AV block