Cell Mechs Of Cards Dysrhythmias I, Ii

Front 1

Normal sinus rhythm: defn

Back 1

1) Originates in SA node
2) HR is 60-100 bpm and regular
3) Excitation occurs in normal sequence and with normal timing

Front 2

Normal sequence of cardiac activation

Back 2

1) SA Node
2) Atria (R then L)
3) AV Node (with AV delay)
4) His-Purkinje system
5) Ventricles

Front 3

The endocardium is depolarized (before, after) the epicardium

Back 3

Before

Front 4

The endocardium is repolarized (before, after) the epicardium

Back 4

After

Front 5

An increase in HR causes an (increase, decrease) in APD.

Back 5

Decrease. (also vice versa)

Front 6

Why does prolongation of AP duration favor dysrhythmias?

Back 6

Due to early afterdepolarizations

Front 7

Where are Ca2+ channels responsible for the upstroke (phase 0)?

Back 7

SA node, AV node.

Note that I_Ca in these areas is much smaller in amplitude than I_Na in atria, ventricles, or Purkinje system.

Front 8

How does increase K+ or Ca2+ affect AP duration and Effective refractory period?

Back 8

Shortens AP duration and ERP

Front 9

Why does increase K+ or Ca2+ Shorten AP duration and ERP?

Back 9

Causes increased K+ conductance and therefore increased K+ efflux during phase 2 and 3, which acts to decrease APD

Front 10

What does increased serum/extracellular K+ due to the membrane potential?

Back 10

Depolarizes Em

Front 11

Why does elevated interstitial K+ during ischemia slow conduction?

Back 11

It causes Na+ channels to inactivate, reducing dV/dt

Front 12

Why do small increases in serum K+ increase conduction velocity?

Back 12

Bring the cell closer to threshold potential.

Front 13

Automaticity: defn

Back 13

Intrinsic ability of specialized cells to spontaneously depolarize and initiate action potential.

Front 14

What is termed a "membrane stabilizer"?

Back 14

Ca2+

Front 15

Why is Ca2+ termed a "membrane stabilizer"?

Back 15

Hypercalcemia makes it more difficult for membrane depolarization to open Na+ channels.

If this is the case, the myocyte must further depolarize to open a sufficient number of Na+ channels to generate an AP. This means threshold potential shifts positive.

Front 16

Increased serum Ca2+ (reduces, increases) excitability. Why?

Back 16

Reduces. Threshold potential is shifted positively.

Vice versa is also true.

Front 17

How does K+ affect threshold potential and excitability?

Back 17

it alters Em. Depolarization causes inactivates of Na+ channels, and with fewer Na+ channels, the cell must further depolarize to open a sufficient number, threshold potential shifts positively. Excitability is reduced.

Front 18

T/F Ectopic, latent, and subsidiary pacemakers include the AVN and His-Purkinje system.

Back 18

T

Front 19

What is the affect of increasing the rate of diastolic (Phase 4) depolarization?

Back 19

Increasing phase 4 depolarization brings the cell to threshold potential faster, and thus increases the HR.

Front 20

what is the affect of shifting threshold potential closer to maximum diastolic potential?

Back 20

Shifting threshold potential closer to maximum diastolic potential makes it easier to generate an AP (requires less positive charge), thus increasing the spontaneous rate of firing.

Front 21

what is the affect of shifting maximum diastolic potential lower?

Back 21

Makes it harder for the cell to reach threshold potential and fire an AP, slows HR.

Front 22

Catecholamines (Increase, Decrease) Normal Automaticity

Back 22

Increase

Front 23

β1 receptor activation (Increases, Decreases) Normal Automaticity

Back 23

increases

Front 24

Hyperkalemia and hypercalcemia (Increases, Decreases) Normal Automaticity

Back 24

decreases

Front 25

Anti-dysrhythmic drugs (Increases, Decreases) Normal Automaticity

Back 25

decreases

Front 26

What are early afterdepolarizations?

Back 26

Oscillations of membrane potential that arise during the plateau phase (2) or in phase 3.

Front 27

What are delayed afterdepolarizations?

Back 27

Oscillations of membrane potential that arise during diastole (Phase 4)

Front 28

What initiates early afterdepolarizations? (EADs)

Back 28

Enhancing I_Na or I_Ca, depressing I_K. In some cases, the depolarization reaches threshold potential and fires an AP.

Front 29

How does prolongation of AP duration (eg, in Long QT syndrome) favor early afterdepolarizations? (EADs)

Back 29

Allows more time for recovery of both the Calcium current and the Sodium current.

Front 30

What initiates delayed afterdepolarizations? (DADs)

Back 30

Spontaneous release of Ca from overloaded sarcoplasmic reticulum. This increase in [Ca] causes both an after-contraction and a transient depolarization that sometimes reaches threshold and fires an AP.

Front 31

What is triggered activity and why is it called this?

Back 31

Abnormal automaticity (the DADs and EADs) because the oscillation is triggered by the preceding AP.

Front 32

What type of afterdepolarization does increased heart rate favor?

Back 32

DADs - enhances Ca2+ influx and the SR to become overloaded with Ca2+.

Front 33

What are boundary currents?

Back 33

normal cells depolarized by surrounding disease cells that aren't repolarizing normally.

Front 34

____ are commonly caused by drug-induced
block of K currents or enhancement of Ca or Na current

Back 34

EADs

Front 35

The sodium current is much (less than, greater than) the calcium current.

Back 35

Greater than.

Front 36

What are the 2 main determinants of conduction velocity?

Back 36

1) Size of the inward current (either Na or Ca, depending on the site).

2) Passive properties: membrane resistance, capacitance, cell to cell resistance.

Front 37

Why does ischemia slow conduction velocity?

Back 37

Cell-to-cell resistance is increased by elevated [Ca2+] and intracellular acidosis during ischemia.

In the extreme case, cells become electrically uncoupled and can't communicate with the rest of the heart.

Front 38

Reflects the amount of current required to initiate an AP

Back 38

Excitability.

Front 39

If recovery of excitability is delayed, what happens to the effective refractory period and relative refractory period?

Back 39

They're prolonged.

Front 40

Why is a recovery period at a more negative potential required following depolarization?

Back 40

To reprime G_Na and enable channels to again open on depolarization. Channels move from inactivated to closed state.

Front 41

dV/dt: defn

Back 41

rate of rise of the upstroke of the action potential

Front 42

dV/dt is roughly proportional to what?

Back 42

I_Na

Front 43

As membrane potential gets more negative, max dV/dt (increases, decreases).

Back 43

Increases

Front 44

How do Disease & Antidysrhythmic Agents affect the responsiveness relationship between max dV/dt and membrane potential?

Back 44

They lower it, making it so that max dV/dt is less than normal at the same membrane potential.

Front 45

Time when Action potential cannot be elicited

Back 45

Absolute refractory period

Front 46

Can elicit AP.
Increased current required.
Conduction slow or fails.

Back 46

relative refractory period.

Front 47

Time when Cannot elicit conducted AP.

Back 47

effective refractory period

Front 48

How does effective refractory period (ERP) change with increasing HR?

Back 48

Shortens

Front 49

Where are the longest AP duration and ERP?

Back 49

Terminal purkinje fibers

Front 50

conduction defect that results in impulse formation

Back 50

reentry, reentrant excitation or circus movement

Front 51

What happens in Reentry?

Back 51

The impulse is initially blocked at some location, travels slowly over an alternate route, excites tissue distal to the block, and then can re-excite the same tissue one or more times.

Front 52

What are the requirements for a reentrant circuit?

Back 52

1) Unidirectional block

2) Functional loop in the conduction pathway

3) Total conduction time around the loop must exceed ERP of tissue proximal to the region of block.

Front 53

Therapeutic Approaches to Terminate Reentry: Depression of conduction. What happens?

Back 53

Convert unidirectional block to bidirectional block

Front 54

Therapeutic Approaches to Terminate Reentry: Improve conduction. What happens?

Back 54

Convert unidirectional block to a region of slow conduction.

The APs collide and terminate excitation.

Front 55

Therapeutic Approaches to Terminate Reentry: Slow conduction. What happens?

Back 55

Next sinus beat interrupts the reentry process.

Front 56

What is the "slow response?"

Back 56

When depolarized atria, ventricles, and Purkinje fibers generate an AP based on Ca2+ channels.

Front 57

Characteristics of the slow response

Back 57

Slow maximum upstroke velocity

Conducts very slowly

responds to Ca channel blockers instead of Na channel blockers (because it's based on a calcium current).