PR INTERVAL

Question 1

What does the PR interval represent and what is it on the EKG?

Answer 1

PR interval represents time from atrial depolarization to the beginning of ventricular depolarization

On the EKG the PR interval is the time from the beginning of the p-wave to the QRS complex

Question 2

Sequence of events during the PR interval?

Answer 2

First the sinus node fires and this causes the impulse to travel in the atria via the fast Bachmann bundles which activates the surrounding atrial myocytes. However, the impulse reaches the AV node faster than all the atrial myocytes depolarize but the depolarization of the AV node is masked by the stronger atrial depolarization.

In the AV node conduction slows down and this physiologic slowing is needed to allow the blood to empty into the ventricles from the atria. The His bundle is the next to be activated after which the bundle branches get activated and finally the purkinjie fibers. The purkinjie fibers activate the ventricular myocytes and this leads to QRS on the EKG

Question 3

Baseline of the EKG is measured from ?

Answer 3

One TP segment to another TP segment

Question 4

If the PR segment falls below the baseline then it is?

Answer 4

Depressed

Question 5

If the PR segment falls above the baseline then it is?

Answer 5

Elevated

Question 6

Differential diagnosis of PR depression?

Answer 6

1. Normal variant : PR segment can be depressed because of atrial repolarization which is the Tp wave and usually burried in the QRS and can pull the PR segment down. However, to be normal it cannot be depressed more than 0.8 mm below the baseline
2. Pericarditis: This can present with PR depression greater than 0.8 mm
3. Atrial infarction : This is very rare due to thin non-muscular walls of the atria and also because circulation is via thebsian veins that bypass the coronary system

Question 7

EKG features of pericarditis?

Answer 7

Tachycardia

PR depression

ST-elevation (concave, scooped out elevations) usually diffuse

Notching of the terminal portion of the QRS especially in the lateral precordial leads

Question 8

Tp wave?

Answer 8

This is atrial repolarization and usually is burried in the QRS segment. It can sometimes depress the PR but usually less than 0.8 mm and is a normal variant. In very fast sinus and SVTs it can be seen as ST segment depressions as it causes ST depressions

Question 9

Features in this EKG?

Answer 9

Here we should pick some complexes and use a ruler to measure the baseline TP-TP segment. Then we should see if there is PR segment changes. Here we see PR depression. We also see diffuse ST elevations with concave scooped out appearence. There can also be notching of the terminal portion or S wave of the QRS complex

Question 10

The normal PR interval is from?

Answer 10

The normal PR interval is from 0.12 s to 0.20 s

Question 11

PR interval is considered short when it is?

Answer 11

Less than or equal to 0.11 s

Question 12

PR interval is considered prolonged when it is?

Answer 12

Greater than 0.2 sec or 200 msec

Question 13

Where should we measure the PR interval?

Answer 13

In the lead with the widest P wave and widest QRS complex

Question 14

What is a short PR interval and what are the main causes?

Answer 14

Short PR interval occurs when it is less than or equal to 0.11 seconds /110 msec

The main causes are:

(1) . Retrograde P-waves : These can be seen as inverted P-waves in II, III and aVF
(2) . Lown Ganong Levine syndrome: This is a benign condition with James fibers which connect the top of the AV node to the His system and this leads to a short PR interval but normal QRS conduction. The normal delay is bypassed giving a short PR interval. In some patients it is associated with tachycardias but is over all a benign condition
(3) . Wold Parkinson White syndrome

Question 15

Featrues of WPW pattern and syndrome?

Answer 15

In WPW pattern we have:

(1) . Shortened PR interval <0.12 seconds
(2) . Wide QRS > .11 seconds
(3) . Presence of a delta wave
(4) . ST-T wave changes or abnormalities

Note: If these findings are also associated with tachycardias then we have WPW syndrome. These tachycardias can be regular, irreuglar, narrow or wide complex

Question 16

Physiology of WPW?

Answer 16

In WPW we have a bypass tract called the bundle of Kent. Impulse coming down the atria reaches the AV node and the bypass tract at the same time. Both AV node and Kent Bundle have their own refractory periods. As the impulse reaches the Kent bundle it doesn’t have to go through a delay like the AV node and goes to the ventricular mycocardium but it progesses slowly. This gives an intial depolarization of the ventricles which is early therefore giving a delta wave, shortened PR and wide QRS. However, the impulse through the AV node travels faster and when it meets the other impulse they extinguish eachother. In a way the Kent bundle is causing a superimposed PVC on the normal conduction beat.

Question 17

Delta waves, ST-T segments in WPW?

Answer 17

Note that not all leads will have delta waves. Some leads are isoelectric to the delta wave component. Also in leads III and aVF (inferior leads) we can have negative delta waves which resemble Q waves but these are not true Q waves and therefore represent a pseudoinfarct pattern.

We can also have ST elevations, inverted T waves. This is because just as depolarization is abnormal so is repolarization. Therefore, a patient with WPW can have all sorts of ST-T wave changes.

Question 18

What are the different types of WPW patterns?

Answer 18

Type A: In this pattern QRS complexes are positive in all precordial leads. ST-T wave changes such as ST depressions and T wave inversions are usually seen in the right precordial leads but can occur anywhere. It can be mistaken for a RBBB pattern. In type A the tall R wave in V1 can be mistaken for an acute MI

Type B: In this type QRS complexes are negative in V1 and V2 and uprgiht in left precordial leads. It can be mistaken for a LBBB. Repolarization abnormalities are usually seen in the left precordial leads.

Type C: In this type the QRS complex is upright in V1 to V4 and negative in V5 to V6. It is very rare.

All type of WPW patterns can be mistaken for infarcts when the delta wave is negative. This is especially true when the deflections are negative in the inferior leads giving a pseudoinfarct pattern.

Question 19

Conduction in WPW?

Answer 19

Antidromic: This occurs when the impulse travels down the Kent Bundle and up the AV node. This gives a wide complex tachycardia which can be very fast especially in cases an atriak flutter or fibrillation is present.

Orthodromic: This occurs when the impulse travels down the AV node and back up the Kent bundle. This usually presents as a narrow complex tachycardia and is less dangerous as the AV node is still able to exert its physiological block.

Question 20

Can patients with WPW have a normal or prolonged PR interval?

Answer 20

About 12% of patients with WPW can have a normal PR interval. This is because the delta wave just hides the underlying PR interval. So if the patient has an underlying prolonged PR interval then they will have a normal or prolonged PR interval when the delta wave is superimposed.

Question 21

Type A and Type B WPW anatomical locations?

Answer 21

Type A is usually on the left side

Type B is usually on the right side

However, many patients can have multiple tracts and this rule isnt always true

Question 22

Features in this EKG?

Answer 22

Here we have a PAC which is the sixth beat. We know this is a PAC because the delta wave is shorter so most of the conduction went down the AV node.

We also have different P wave morphologies and PR intervals making this a wandering pacemaker.

This is Type B WPW with a pseduoinfarct pattern in lead III and aVF and V1.

Question 23

Features in this EKG?

Answer 23

We can see delta waves

PR is normal but we know this can occur in 12% of patients with WPW

Here we have positive QRS complexes in V1 and V2 which then become negative in left sided precordial leads. This is Type C WPW pattern.

We also see Q waves in II, III and aVF.

Note: In a patient with WPW delta waves in inferior leads can be negative and are not true infarct Q waves. These can mimic Q waves of an inferior MI

Question 24

Differential diagnosis of a tall R wave in V1?

Answer 24

WPW Type A

Posterior MI

RBBB

RVH

Question 25

Posterior MI blood supply?

Answer 25

An isolated posterior MI is less common than the posterior extension of an inferior or lateral MI. Blood supply to the posterior wall in 80-85% of people comes from the right coronary artery (RCA) giving rise to the posterior descending artery (PDA). The remaining 15-20% of hearts are roughly divided between left dominant and codominant. In left dominant hearts, the PDA is supplied by the left circumflex (LCx) or less commonly by the left anterior descending (LAD) coursing around the apex of the heart. In a codominant heart, a single or duplicated PDA is supplied by branches of both the RCA and LAD or LCx. Posterior MI can therefore occur with occlusion of any one of these arteries depending on the patients anatomy. Posterior extension of inferior or lateral infarct indicates a larger area of ischemic myocardium, and these patients are at increased risk of complications related to MI

Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction.

Isolated posterior MI is less common (3-11% of infarcts).

Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death.

Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed.

Posterior extension of an inferior MI : ST elevations in II, III and aVF & reciprocal ST depression in aVL + deep ST depressions in V1-V3 and large R waves in these leads (usually V2-V3)

Question 26

Features of a posterior MI?

Answer 26

As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3.

Posterior MI is suggested by the following changes in V1-3:

Horizontal ST depression

Tall, broad R waves (>30ms)

Upright T waves

Dominant R wave (R/S ratio > 1) in V2

In patients presenting with ischaemic symptoms, horizontal ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI.

The anteroseptal leads are directed from the anterior precordium towards the internal surface of the posterior myocardium. Because posterior electrical activity is recorded from the anterior side of the heart, the typical injury pattern of ST elevation and Q waves becomes inverted:

ST elevation becomes ST depression

Q waves become R waves

Terminal T-wave inversion becomes an upright T wave

Question 27

How to confirm a posterior MI?

Answer 27

Leads V7-9 are placed on the posterior chest wall in the following positions:

V7 – Left posterior axillary line, in the same horizontal plane as V6.

V8 – Tip of the left scapula, in the same horizontal plane as V6.

V9 – Left paraspinal region, in the same horizontal plane as V6.

The degree of ST elevation seen in V7-9 is typically modest – note that only 0.5 mm of ST elevation is required to make the diagnosis of posterior MI!

Question 28

Features of RVH?

Answer 28

Diagnostic criteria

Right axis deviation of +110° or more.

Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).

Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).

QRS duration < 120ms (i.e. changes not due to RBBB).

Supporting criteria

Right atrial enlargement (P pulmonale).

Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads.

S1 S2 S3 pattern = far right axis deviation with dominant S waves in leads I, II and III.

Deep S waves in the lateral leads (I, aVL, V5-V6).

Other abnormalities caused by RVH

Right bundle branch block (complete or incomplete).

There are no universally accepted criteria for diagnosing RVH in the presence of RBBB; the standard voltage criteria do not apply.

However, the presence of incomplete / complete RBBB with a tall R wave in V1, right axis deviation of +110° or more and supporting criteria (such as RV strain pattern or P pulmonale) would be considered suggestive of RVH.