Cardiac conduction system and the ECG

Question 1

Identify the three types of atrioventricular block

Answer 1

First degree: conduction delayed by all P-waves to the ventricles. Slow but functional

Second degree: some P waves conduct but other do not.

Third degree block: none of the P-waves conduct and a ventricular pacemaker takes over. Also called complete heart block (no more AV node :( )

Question 2

What happens when left bundle branch is blocked?

Answer 2

QRS widening and delayed conduction to the left ventricle

Question 3

What happens when the right bundle branch is blocked?

Answer 3

QRS widening with delayed conduction to the right ventricle.

Question 4

Sick sinus syndrome

Answer 4

occurs with SA node abnormalities. Slow sinus rates or takeover by other pacemaker cells which may be either slow or fast. Sick sinus syndrome often happens with age. Can cause weakness, fainting spells, etc. Need a pacemaker because SA node just not fast enough to keep up with the body’s metabolic demands!

Question 5

Explain the abnormal reentry pathway in tachyarrhythmias

Answer 5

Can be present in atria, ventricles, or junctional tissue. Occurs when there is a unidirectional block and slowed conduction through the re-entry pathway. Previously depolarized tissue has recovered, reentry occurs in the wrong direction, causes nonsynchronous muscle contraction. Most COMMON cause of serious tachycardias.

Question 6

Ectropic foci in tachyarrhythmias

Answer 6

When a part of the myocardium outside the conductin system acquired automaticity and if the rt of depolarization exceeds that of the sinus node, an abnormal rhyth occurs. Can hear isolated “ectopic beats” or sustained tachyarrhythmias

Question 7

Triggered activity in tachyarrhythmias

Answer 7

abnormal afterpolarizations may be triggered by preceding AP’s. Early afterpolarizations when AP is only partically repolarized -> usually seen as a long QT interval.

Question 8

Long QT syndrome

Answer 8

prolongation of the duration of cardiac action potentials, leading to ventricular arrythmias and sudden death. Prolongation of the plateae phase (Phase 2) of the fast reponse AP’s in ventricular myocutes initiates a polymorphic ventricular tachycardia called

TORSADES DE POINTES. (abrupt increase in sympathetic tone)

Question 9

Autosomal dominant (Romano-Ward Syndrome) of the long QT syndrome

Answer 9

Often see mutations in slow cardiac K+ channels (LQT1) and rapid cardiac K+ channels (LQT2) as well as Na+ channels (LQT3)

Question 10

Autosomal recessive form, Jervell-Lange-Neilson syndrome

Answer 10

Homozygous carriers of mutation of Iks (LQT1) also suffer from congenital deafness

Question 11

What happens in LQT1 and LQT2 mutations?

Answer 11

There seems to be a overall decrease in the number of K+ channels, reducing the size of the hyperpolarizing K+ current. Prolongation of the platue phase.

Question 12

What happens in LQT3 block?

Answer 12

Mutations in cadiac Na+ channels prevents Na+ channels from inactivating completely (gain of function mutations) thereby prolonging phase 2 response.

Question 13

Brugada syndrome

Answer 13

Ventricular fibrillation results in a survival rate of only 40% by 5 yrs. reducing peak inward Na+ current that drives action potentia