Bsf.electrical Activity

Front 1

What are the two types of AP in the heart?

Back 1

Cardiac Myocyte AP (fast response)
Pacemaker AP (slow response)

Front 2

Describe cardiac myocyte AP

Back 2

fast response, fast Na channels, conducting and contracting AP: bundle of His, purkinje fibers, atrial and ventricular myocytes

Front 3

Describe Pacemaker AP

Back 3

slow response: slow Na response, auto-rhythmic generates the same action potential periodically over long periods of time (SA and AV nodes)

Front 4

Describe the ion conductance of the following phases of a cardiac myocyte:
0,1,2,3,4

Back 4

Phase 0: Rapid depolarization
rapid Na+ influx through the voltage-gated Na+ channels (fast Na+ channels)
Phase 1: Early partial repolarization
the efflux of K+, the transient outward K+ current (I to)
Phase 2: Plateau phase
increased Ca++ conductance
Phase 3: Final Repolarization
the efflux of K+ exceeds the influx of Ca++
Phase 4: Resting potential
is determined mainly by the K+ conductance

Front 5

What are the characteristics of a fast Na channel?

Back 5

Voltage-gated channels, phase 0 depolarization of non-pacemaker cardiac action potentials

Front 6

Characteristics of an Inward rectifier potassium channel?

Back 6

(Iir or Ik1):Maintains resting membrane potential (phase 4), permits K outflow at highly negative potential in cardiac cells

Front 7

Characteristics of a Transient Outward K channel?

Back 7

Ito: Contributes to phase 1 by transiently permitting K outflow at positive membrane potential

Front 8

Characteristics of a delayed rectifier K channel?

Back 8

Ikr: Phase 3 repolarization of cardiac action potentials, permits K outflow

Front 9

Characteristics of ATP Sensitive K channel (Ik)?

Back 9

KATP channels; inhibited by ATP; therefore, open when ATP decreases during hypoxia

Front 10

Characteristics of Achetylcholine activated and adenosine activated K channel?

Back 10

(Ik Ach Activated by acetylcholine and adenosine; G-protein coupled, hyperpolarizes membrane during phase 4 and shortens phase 2

Front 11

Characteristics of L type Ca channels?

Back 11

Voltage-gated channels, slow inward, long-lasting current; phase 2 non-pacemaker cardiac action potentials

Front 12

When is the effective refractory period and what does that mean?

Back 12

ERP; absolute refractory period. During phase 0, 1, 2, and part of 3 the cell cannot undergo a new action potential because the fast Na+ channels are not fully reactivated.

The ERP acts as a protective mechanism in the heart by preventing multiple APs
Preventing tetany. If these were to occur, the heart would be unable to adequately fill with blood and eject blood.

Front 13

When is the relative refractory period and what does that mean?

Back 13

Last part of phase 3. Early in this phase suprathreshold stimuli are required to elicit and AP.
All Na+ channels still not completely reactivated

Front 14

What channels are responsible for Pacemaker's phase 4?

Back 14

First, Na channels called funny current channels (If) open when the cell hyperpolarizes. They stay open from -60mV to -20mV.

In the later part of phase 4, T type Ca channels open. As the cell becomes more positive, L type Ca channels open until threshold is reached and many VG Ca channels open.

Front 15

What is responsible for pacemaker's phase 0?

Back 15

Upstroke: opening of VG L type channels, accompanied by low K conductance.

Front 16

Are there any fast Na channels in pacemaker cells?

Back 16

No

Front 17

What is responsible for Phase 3 in pacemaker cells?

Back 17

Voltage gated Ca2+ channels become inactivated and voltage gated delayed rectifier K+ channels open. Since K+ dominates, membrane potential moves toward – 94 mV.

Front 18

Characteristics of slow Na channels in pacemaker cells?

Back 18

"Funny" pacemaker current (If) in cardiac nodal tissue

Front 19

Characteristics of Delayed rectifier K channels?

Back 19

Found in pacemaker cells, Phase 3 repolarization of cardiac action potentials

Front 20

Characteristics of ATP sensitive K channels?

Back 20

KATP channels; inhibited by ATP; therefore, open when ATP decreases during hypoxia

Front 21

Characteristics of L type Ca channels?

Back 21

Slow inward, long-lasting current; phase 2 non-pacemaker cardiac action potentials and phases 4 and 0 of SA and AV nodal cells; important in vascular smooth muscle contraction

Front 22

Characteristics of T type Ca channels?

Back 22

Transient current that contributes to phase 4 pacemaker currents in SA and AV nodal cells

Front 23

What are the normal bpm for :

SA node?
AV node?
Purkinje fibers?

Back 23

60-100
40-55
25-40

Front 24

What is the conduction pathway of the heart?

Back 24

SA node, Internodal pathway, AV node, AV bundle (bundle of His), Bundle branches, Purkinje fibers

Front 25

Pacemaker cells are primarily innervated by ____ nerve fibers, and Cardiac muscle cells are predominately innervated by _____ nerve fibers

Back 25

Parasympathetic nerve fibers (from Vagus)

Sympathetic nerve fibers (from sympathetic chain)

Front 26

What are consequences of Sympathetic stimulation of the heart?

Back 26

NE triggers Beta 1 receptors, thus causing positive chronotropic (↑HR) , dromotropic (↑ conduction velocity of electrical impulses) and ionotropic (↑ contractile forces) effects.

It increases Na funny channel current in SA node (increasing the steepness of phase 4), and increases the Ca current in all myocardial cells increasing steepness of phase 4 and moving threshold more negative.

Front 27

What are the consequences of Parasympathetic stimulation of the heart?

Back 27

Parasympathetic (Ach) neurons act on M2 receptors and they will inhibit the heart causing negative chronotropic, dromotropic , and ionotropic. It effects Na funny channels, T type Ca channels, and K conductance.
Ach decreases Na funny current channels, therefore reducing the steepness of phase 4 (increasing the ERP).
Ach also reduces Ca current through T type Ca channels moving threshold more positive.
Ach opens G protein coupled K channels, increasing K conductance, therefore hyperpolarizing the membrane.

Front 28

What are two ways to decrease the firing frequency of the pacemaker cells?

Back 28

Firing frequency can be reduced by increasing the length of the effective (absolute) refractory period (↑ERP):
Increasing the duration of AP
Increasing the maximal negative potential (hyperpolarization during the phase 4)

Front 29

How do Ca channel blockers decrease the firing frequency of pacemaker cells?

Back 29

Ca channel blockers: reducing the slope of phase 4 thereby decreasing the rate of spontaneous depolarization; decreasing the slope of phase 0 which slows conduction velocity within the AV node; and increasing the threshold potential level

Front 30

How do blockers of the delayed rectifier K channel decrease firing frequency of pacemaker cells?

Back 30

By increasing the length of phase 3 repolarization

Front 31

What does activation of G protein coupled K channels do in regards to pacemaker cells?

Back 31

Activation increases the maximal negative potential, and therefore decreases firing frequency of the pacemaker cells

Front 32

What are common causes of abnormal electrical activity in the heart? (4)

Back 32

Inadequate myocardial blood flow (myocardial hypoxia)

Changes in ion concentrations in the ECF ([K+]o, [Ca+ +]o, [Na+]o,)

Changes in membrane ionic conductances (ion channels, exchangers)

Changes in the ATPase (Na,K-ATPase, Ca-ATPase)

Front 33

What are common consequenes of abnormal electrical activity in the conducting and contracting myocytes?

Back 33

Transformation of non-pacemaker into pacemaker cell action potential
(Ectopic beats)

Alteration of duration of the refractory period
(Abnormal myocardial contractility and rate of contraction)

Front 34

What is the primary cause of abnormal electrical activity in cardiac pts?

Back 34

Myocardial hypoxia

Front 35

What are the consequences when Outside [K] is increased?

Back 35

An increased [K+]o contributes to transformation of non-pacemaker into pacemaker cell action potential

The resting membrane potential becomes less negative (K doesn't flow out as much as it used to, because concentration gradient is not as intense, therefore electrostatic gradient overpowers chemical pressure more so than normal keeping more K inside). The amplitude, duration of AP and steepness of upstroke all diminish and so does the conduction velocity.

Front 36

How does myocardial hypoxia transform non pacemaker cells in pacemaker cells?

Back 36

In response to hypoxia the membrane depolarizes and closes fast Na+ channels.
AP can still be elicted by the inward Ca current (similar to those found in pacemaker cells), this can sometimes occur spontaneously and be the reason for ectopic beats or irregular heart beats.

Front 37

What effect does Tetrodotoxin have on the heart?

Back 37

It blocks the VG Na channels, and can trigger transformation of non-pacemaker cells into pacemaker cells by preventing fast response AP from occuring

Front 38

How do K and Na channel blockers increase the ERP?

Back 38

K+ channel blockers delays phase 3 repolarization and increase the action potential duration

Na+ channel blockers decrease slope of the phase 0, depress the peak of the AP, and increase the inactivation state of fast-Na channels (voltage-gated Na-channels)

Front 39

Define conduction block

Back 39

failure of propagation in a cardiac fiber

Front 40

Define Reentry

Back 40

A cardiac impulse may reenter previously excited tissue when the impulse is conducted slowly around the loop and the impulse is blocked unidirectionally in some sections of the loop

Front 41

Early afterdepolarization occurs at the end of phase ___ or about midway through phase __.

Back 41

2, 3

Front 42

Later afterdepolarization occurs at the end or just after full ______. It is associated with elevated ____ .

Back 42

repolarization,

Intracellular [ca]

Front 43

What are reasons for tachycardia?

Back 43

Increased automaticity: anything that increases rate of the pacemaker. Drugs, sympathetic stimulation

Spontaneous depolarizations: can occur during phase 3 or 4 of AP and referred to as triggered tachycardias. This can be caused by mutation in ion channels

An ectopic pacemaker (ectopic focus): a single beat or series of beats that occurs outside the normal pacemaker region (premature systole).

Front 44

What are reasons for bradycardia?

Back 44

Depressed impulse formation: pacemaker problem in the SA node.
Abnormal autonomic influences (due to excessive parasymapthetic tone)

Impaired impulse conduction: A block in the conduction pathway slows the electrical signal
Tissue damage, change in anatomy
Drugs

Front 45

ECG is a measure of ___ and ___

Back 45

voltage and time

Front 46

ECG and Ventricular AP correlation:

Phase 0 (upstroke) of ventricular AP corresponds to the____ in the ECG
Phase 2 (plateau) of ventricular AP corresponds to the______ of the ECG
Phase 3 (repolarization) of the ventricular AP corresponds to the _____(ventricular repolarization) in the ECG

Back 46

R wave
ST segment
T wave

Front 47

The ECG cannot show the electrical activity of what 5 structures?

Back 47

SA node, AV node, Bundle of His, Bundle braches, purkinje network

Front 48

What is the normal range of, and what events occur during PR interval?

Back 48

0.12–0.20
Atrial depolarization and conduction thru AV node

Front 49

What is the normal range of, and what events occur during QRS interval?

Back 49

0.08 - 0.10
Ventricular depolarization
Atrial repolarization

Front 50

What is the normal range of, and what events occur during QT interval?

Back 50

0.4 - 0.43
Ventricular depolarization
Ventricular repolarization

Front 51

What is the normal length of, and what occurs during the ST interval?

Back 51

0.32
Ventricular repolarization
(QT-QRS)

Front 52

What is sinus arrhythmia?

Back 52

subtle change in HR with respiratory cycle. Inspiration accelerates, expiration slows