Arrhythmias Pathophysiology Flashcards

1
Q

Bradycardia can arise from what two basic mechanisms?

A

First, reduced automaticity of the sinus node can result in slow heart rates or pauses.

Second, slow heart rates can occur if the cardiac impulse is prevented from activating the ventricles normally because of blocked conduction

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2
Q

What happens if sinus node pacemaker activity ceases?

A

The heart will usually be activated at a slower rate by other cardiac tissues with pacemaker activity.

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3
Q

When does reduced sinus node automaticity occur physiologically?

A

During periods of increased vagal tone (sleep, carotid sinus massage, “common faint”), with increasing age and secondary to drugs (beta blockers, calcium channel blockers).

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4
Q

Does bradycardia occur in a bundle branch block?

A

Although block can be observed in either the left or right bundle branches, bradycardia does not necessarily occur, because the ventricles can still be activated by the contralateral bundle.

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5
Q

What is 1st degree AV block defined as?

A

Atrioventricular block has been classified as first degree when there is an abnormally long atrioventricular conduction time (PR interval >0.22 s) but activation of the atria and ventricles still demonstrates 1:1 association

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6
Q

What is 2nd degree AV block defined as?

A

In second-degree atrioventricular block, some but not all atrial impulses are conducted to the ventricles.

Finally, in third-degree block, there is no association between atrial and ventricular activity.

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7
Q

How can AV block occur?

A

occur with increasing age, with increased vagal input, and as a side effect of certain drugs

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8
Q

What congenital diseases cause AV block ?

A

muscular dystrophy, tuberous sclerosis, and maternal systemic lupus erythematosus

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9
Q

What acquired diseases cause AV block ?

A

sarcoidosis, gout, Lyme disease, systemic lupus erythematosus, ankylosing spondylitis, and coronary artery disease

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10
Q

Tachycardias can arise from three basic cellular mechanisms. What are they?

A

First, increased automaticity resulting from more rapid phase 3 depolarization can cause rapid heart rate. (EAD)

Second, if repolarization is delayed (longer plateau period), spontaneous depolarizations (caused by reactivation of sodium or calcium channels) can sometimes occur in phase 3 or phase 4 of the action potential. (DAD)

Third, and most commonly, tachycardias can arise from a reentrant circuit.

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11
Q

EADs and DADs are called what?

A

triggered activity because they are dependent on the existence of a preceding action potential. If these depolarizations reach threshold, tachycardia can occur in certain pathologic conditions.

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12
Q

What is a re-entrant circuit?

A

In reentry, two parallel pathways with different conduction properties exist (perhaps at the border zone of a myocardial infarction or a region of myocardial ischemia). The electrical impulse normally travels down the fast pathway and the slow pathway, but at the point where the two pathways converge the impulse traveling down the slow pathway is blocked since the tissue is refractory from the recent depolarization via the fast pathway (a)

However, when a premature beat reaches the circuit, block can occur in the fast pathway, and the impulse will travel down the slow pathway (shaded region) (b).

After traveling through the slow pathway the impulse can then enter the fast pathway in retrograde fashion (which because of the delay has recovered excitability), and then reenter the slow pathway to start a continuous loop of activation, or reentrant circuit (c).

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13
Q

What causes Torsades de pointes?

A

spontaneous depolarizations during phase 3 (early afterdepolarizations; EAD) or phase 4 (late after-depolarizations; DAD) can repetitively reach threshold and cause tachycardia.

observed in some patients taking procainamide or quinidine and the arrhythmias associated with digoxin toxicity.

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14
Q

What is the best example of re-entrant tachyarrhyhtmias?

A

Wolff-Parkinson-White syndrome

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15
Q

What happens in WPW syndrome?

A

As mentioned, the AV node normally forms the only electrical connection between the atria and the ventricles. Perhaps because of incomplete formation of the annulus, an accessory atrioventricular connection is found in approximately 1 in 1000 persons.

This accessory pathway is usually composed of normal atrial or ventricular tissue.

Because part of the ventricle is “pre-excited” over the accessory pathway rather than via the AV node, the surface ECG shows a short PR interval and a relatively wide QRS with a slurred upstroke, termed a delta wave. Because the atria and ventricles are linked by two parallel connections, reentrant tachycardias are readily initiated. For example, a premature atrial contraction could be blocked in the accessory pathway but still conduct to the ventricles via the AV node. If enough time has elapsed so that the accessory pathway has recovered excitability, the cardiac impulse can travel in retrograde fashion to the atria over the accessory pathway and initiate a reentrant tachycardia.

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16
Q

The best example of tachycardias from triggered activity is what?

A

the long QT syndrome

17
Q

Long QT intervals can be due to what?

A

several specific ion channel defects. For example, reduced function of potassium channels leads to a prolonged plateau period. The prolonged plateau phase in ventricular tissue leads to a prolonged QT interval. These patients are prone to triggered activity because of reactivation of sodium and calcium channels (early after depolarizations).

Triggered activity in the ventricles can lead to life-threatening ventricular arrhythmias.

18
Q

Regardless of the mechanism, the approach to immediate clinical management of tachycardias depends on what?

A

whether the QRS complex is narrow or wide.

If the QRS complex is narrow, depolarization of the ventricles must be occurring normally over the specialized conduction tissues of the heart, and the arrhythmia must be originating at or above the AV node (supraventricular)

19
Q

What are some supraventricular arrhythmias?

A
  • a fib
  • a flutter
  • AV nodal reentrant tachycardia
  • atrioventricular tachycardia
  • atrial tachycardia
20
Q

What causes a fib?

A

multiple microreentrant circuits can lead to chaotic activation of the atrium

Because impulses are reaching the AV node at irregular intervals, ventricular depolarization is irregular.

21
Q

What causes a flutter?

A

a macroreentrant circuit, traveling up the interatrial septum and down the lateral walls, can activate the atria in a regular fashion at approximately 300 bpm. The AV node can conduct only every other or every third beat, so that the ventricles are depolarized at 150 or 100 bpm.

22
Q

What happens in AV nodal reentrant tachycardia?

A

In AV nodal reentrant tachycardia, slow and fast pathways exist in the region of the AV node and a microreentrant circuit can be formed

23
Q

What happens in atrioventricular reentry?

A

In atrioventricular reentry, an abnormal connection between the atrium and ventricle exists so that a macroreentrant circuit can be formed with the AV node forming the slow pathway, and the abnormal atrioventricular connection, the fast pathway.

24
Q

What happens in atrial tachycardia?

A

In atrial tachycardia an abnormal focus of atrial activity as a result of either reentry, triggered activity, or abnormal automaticity can activate the atria in a regular fashion.

25
Q

A wide QRS suggests what?

A

The tachycardia either is arising from ventricular tissue or is a supraventricular tachycardia with aberrant conduction over the His-Purkinje system or an accessory pathway. Criteria have been developed for distinguishing between ventricular and supraventricular tachycardia with aberrance.