MMT: pathophysiology of arrhythmias

Question 1

What are class I anti-arrhythmic drugs?

Answer 1

Sodium channel blockers

Question 2

What are class II anti-arrhythmic drugs?

Answer 2

Beta blockers

Question 3

What are class III anti-arrhythmic drugs?

Answer 3

Potassium channel blockers; they prolong the refractory period

Question 4

What are class IV anti-arrhythmic drugs?

Answer 4

Calcium channel blockers

Question 5

In an ECG, what does P represent?

Answer 5

Atrial depolarization

Question 6

In an ECG, what does QRS represent?

Answer 6

Ventricular depolarization

Question 7

In an ECG, what does T represent?

Answer 7

Ventricular repolarization

Question 8

What is the PR interval?

Answer 8

AV node conduction time

Question 9

What is the QT interval?

Question 10

Describe the action potential seen in the SA node.

Answer 10

A gradual action potential with an upstroke at phase 4 that represents a gradual depolarization due to the actions of the funny current.

Question 11

Describe the action potential seen in the atria.

Answer 11

A very fast upstroke in depolarization due to fast sodium currents. It has a short duration.

Question 12

Describe the action potential seen in the AV node.

Answer 12

Very similar to the SA node; a more gradual depolarization is seen. The conduction system is relatively slow, which allows the ventricles to fill.

Question 13

Describe the action potential of Purkinje fibers.

Answer 13

Its phase 4 is very flat, and the upstroke of depolarization is very sharp and rapid. Its repolarization is more gradual/slow.

Question 14

Compare the resting membrane potential of the SA and AV nodes with that of myocytes.

Answer 14

Myocytes have a more negative resting membrane potential of around -90, while SA and AV nodes are at around -50.

Question 15

Compare the action potential of SA and AV nodes with that of myocytes.

Answer 15

Myocytes have a very flat phase 4, a quick depolarization, and a longer lasting period of depolarization. SA and AV nodes have a less flat phase 4 and a gradual depolarization. The period of depolarization is shorter, and repolarization is more gradual.

Question 16

Which ion drives depolarization in the SA and AV nodes?

Answer 16

Calcium

Question 17

Which ion drives depolarization in myocytes?

Answer 17

Sodium

Question 18

Describe the three states of voltage-gated channels.

Answer 18

Resting: the channel is closed. Open: the channel is open and allows ions to flow through. Inactive: an inactivation gate prevents ions from entering, even though the rest of the channel is open. This is seen in an absolute refractory period.

Question 19

Which element of the heart’s electrical system has the fastest rate of automaticity?

Answer 19

The SA node

Question 20

What is considered a supra-ventricular arrhythmia?

Answer 20

Anything above the bundle of His

Question 21

If a QRS is wide, would we consider a supra-ventricular or ventricular arrhythmia? Why?

Answer 21

Ventricular; this is because a wide QRS is telling us that the conduction velocity is slow, and likely not working properly. This tells us it is going cell to cell instead of using the Purkinje system.

Question 22

Describe altered normal automaticity.

Answer 22

A change in spontaneous depolarization that can cause arrhythmia; typically seen in SA/AV nodes and His-Purkinje fibers.

Question 23

Describe triggered impulses.

Answer 23

A normal AP is interrupted or followed by abnormal depolarization, causing early and delayed afterdepolarizations. This can cause arrhythmia.

Question 24

Describe reentry.

Answer 24

An abnormal conduction pathway forms a self-perpetuating circuit, causing an arrhythmia that re-excites a region that is already depolarized. Can be caused by a critically-timed premature impulse.

Question 25

What are common properties of reentry arrhythmias?

Answer 25

1. Divided conduction pathway
2. Unidirectional block to conduction
3. Slowed conduction in the other pathway/direction

Question 26

How can we treat reentry arrhythmia in cardiomyocytes?

Answer 26

Class 1A or 1C drugs that decrease conduction velocity or class 3 drugs that prolong the refractory period.

Question 27

How can we treat reentry arrhythmia in SA and AV nodes?

Answer 27

Calcium channel blockers to decrease conduction velocity or class 3 drugs to prolong the refractory period.

Question 28

What are delayed afterdepolarizations?

Answer 28

Secondary depolarizations that occur after full repolarization has occurred.

Question 29

What is associated with delayed afterdepolarizations?

Answer 29

Increased intracellular calcium and increased SNS activity.

Question 30

What are early afterdepolarizations?

Answer 30

Secondary depolarizations that occur before repolarization is complete.

Question 31

What is associated with early afterdepolarizations?

Answer 31

Prolonged QT interval and cell damage.

Question 32

How can ischemia alter automaticity?

Answer 32

During an ischemic event, myocytes will not be able to use oxidative phosphorylation and will need to utilize anaerobic methods for ATP production. This ultimately leads to less ATP. With less ATP comes less functioning of the sodium potassium pump. This will raise the resting membrane potential, which can lead to altered automaticity and inactivation of sodium gated channels and thus slowed conduction.

Question 33

How does ischemia alter potassium?

Answer 33

Altered sodium-potassium function and lack of inhibition of potassium channels can cause more potassium outside the cell (local hyperkalemia). This raises resting membrane potential and slows conduction velocity.

Question 34

Explain how hyperkalemia impacts action potential.

Answer 34

It slows conduction velocity (less rapid spike in depolarization). There will also be a much more rapid repolarization and a very flat phase 4.

Question 35

What does hyperkalemia cause on an ECG? Why?

Answer 35

Peak T waves; it is due to the fast repolarization.

Question 36

How can hypokalemia induce arrhythmia?

Answer 36

1. Inhibition of potassium conductance which reduces repolarization 2. Suppression of sodium potassium pump activity, which causes accumulation of intracellular sodium.

Question 37

What does hypokalemia cause on an ECG?

Answer 37

Prolonged QT interval.

Question 38

Hypokalemia increases risk for which type of arrhythmia?

Answer 38

Torsade de pointes.