Basic ECG Part III-P Wave & PR Interval

Basic ECG Part III

P Wave & PR Interval

Credit To Dr Rayney Azmi Bin Ali

++Characteristics Of The Normal Sinus P Wave++

Morphology

Smooth contour

Monophasic in lead II

Biphasic in V1

Axis

Normal P wave axis is between 0° and +75°

P waves should be upright in leads I and II, inverted in aVR

Duration

*< 120 ms

Amplitude

*< 2.5 mm in the limb leads,

*< 1.5 mm in the precordial leads

Atrial abnormalities are most easily seen in the inferior leads (II, III and aVF) and lead V1, as the P waves are most prominent in these leads.

The Atrial Waveform-Relationship To The P Wave

*Atrial depolarisation proceeds sequentially from right to left, with the right atrium activated before the left atrium.

*The right and left atrial waveforms summate to form the P wave.

*The first 1/3 of the P wave corresponds to right atrial activation, the final 1/3 corresponds to left atrial activation; the middle 1/3 is a combination of the two.

*In most leads (e.g. lead II), the right and left atrial waveforms move in the same direction, forming a monophasic P wave.

*However, in lead V1 the right and left atrial waveforms move in opposite directions. This produces a biphasic P wave with the initial positive deflection corresponding to right atrial activation and the subsequent negative deflection denoting left atrial activation.

*This separation of right and left atrial electrical forces in lead V1 means that abnormalities affecting each individual atrial waveform can be discerned in this lead. Elsewhere, the overall shape of the P wave is used to infer the atrial abnormality.

First Degree AV Block Vs Second Degree Mobitz Type I (Wenckebach)

++First Degree AV Block++

*PR interval > 200ms (five small squares)
*‘Marked’ first degree block if PR interval > 300ms

Causes of First Degree AV Block

*Increased vagal tone

*Athletic training

*Inferior MI

*Mitral valve surgery

*Myocarditis (e.g. Lyme disease)

*Electrolyte disturbances (e.g. Hyperkalaemia)

*AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone)

*May be a normal variant

++Second Degree Mobitz Type I (Wenckebach)++

Definition Of Wenckebach Phenomenon:

*Progressive prolongation of the PR interval culminating in a non-conducted P wave.

*The PR interval is longest immediately before the dropped beat.

*The PR interval is shortest immediately after the dropped beat.

Other Features Of Second Degree Mobitz Type I

*The P-P interval remains relatively constant.

*The greatest increase in PR interval duration is typically between the first and second beats of the cycle.

*The R-R interval progressively shortens with each beat of the cycle.

*The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4.

Mechanism 

*Mobitz I is usually due to reversible conduction lock at the level of the AV node.

*Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct an impulse.

*This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly (i.e. producing a Mobitz II block).

Causes of Wenckebach Phenomenon

*Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone

*Increased vagal tone (e.g. athletes)

*Inferior MI

*Myocarditis

*Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)

Clinical Significance of AV Block: Second Degree, Mobitz I

*Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance and with low risk of progression to third degree heart block.

*Asymptomatic patients do not require treatment.

*Symptomatic patients usually respond to atropine.

*Permanent pacing is rarely required.

++Second Degree Mobitz Type II++

AV Block: 2nd degree, Mobitz II Overview

*Intermittent non-conducted P waves without progressive prolongation of the PR interval (compare this to Mobitz I).

*The PR interval in the conducted beats remains constant.

*The P waves ‘march through’ at a constant rate.

*The RR interval surrounding the dropped beats is an exact multiple of the preceding RR interval (e.g. double the preceding RR interval for a single dropped beat, treble for two dropped beats, etc)

Mechanism

*Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node).

*While Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs, reversible ischaemia), Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis).

*Patients typically have a pre-existing LBBB or bifascicular block, and the 2nd degree AV block is produced by intermittent failure of the remaining fascicle (“bilateral bundle-branch block”).

*In around 75% of cases, the conduction block is located distal to the Bundle of His, producing broad QRS complexes.

*In the remaining 25% of cases, the conduction block is located within the His Bundle itself, producing narrow QRS complexes.

*Unlike Mobitz I, which is produced by progressive fatigue of the AV nodal cells, Mobitz II is an “all or nothing” phenomenon whereby the His-Purkinje cells suddenly and unexpectedly fail to conduct a supraventricular impulse.

*There may be no pattern to the conduction blockade, or alternatively there may be a fixed relationship between the P waves and QRS complexes, e.g. 2:1 block, 3:1 block.

Causes of Mobitz II

*Anterior MI (due to septal infarction with necrosis of the bundle branches).

*Idiopathic fibrosis of the conducting system (Lenegre’s or Lev’s disease).

*Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair)

*Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease).

*Autoimmune (SLE, systemic sclerosis).

*Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis).

*Hyperkalaemia.

*Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.

Clinical Significance

*Mobitz II is much more likely than Mobitz I to be associated with haemodynamic compromise, severe bradycardia and progression to 3rd degree heart block.

*Onset of haemodynamic instability may be sudden and unexpected, causing syncope (Stokes-Adams attacks) or sudden cardiac death.

*The risk of asystole is around 35% per year.

*Mobitz II mandates immediate admission for cardiac monitoring, backup temporary pacing and ultimately insertion of a permanent pacemaker.

Second Degree AV Block Vs SVT

++AV Block:Second Degree, “Fixed Ratio” Blocks++

Fixed Ratio AV blocks

*Second degree heart block with a fixed ratio of P waves: QRS complexes (e.g. 2:1, 3:1, 4:1).

*Fixed ratio blocks can be the result of either Mobitz I or Mobitz II conduction.

Mobitz I or II?

*It is not always possible to determine the type of conduction disturbance producing a fixed ratio block, although clues may be present.

*Mobitz I conduction is more likely to produce narrow QRS complexes, as the block is located at the level of the AV node. This type of fixed ratio block tends to improve with atropine and has an overall more benign prognosis.

*Mobitz II conduction typically produces broad QRS complexes, as it usually occurs in the context of pre-existing LBBB or bifascicular block. This type of fixed ratio block tends to worsen with atropine and is more likely to progress to 3rd degree heart block or asystole.

*However, this distinction is not infallible. In approximately 25% of cases of Mobitz II, the block is located in the Bundle of His, producing a narrow QRS complex. Furthermore, Mobitz I may occur in the presence of a pre-existing bundle branch block or interventricular conduction delay, producing a broad QRS complex.

*The only way to be certain is to observe the patient for a period of time (e.g. watch the cardiac monitor, print a long rhythm strip, take serial ECGs) and observe what happens to the PR intervals. Often, periods of 2:1 or 3:1 block will be interspersed with more characteristic Wenckebach sequences or runs of Mobitz II.

++High Grade AV Block++

High Grade AV Block Definition

*Second degree heart block with a P:QRS ratio of 3:1 or higher, producing an extremely slow ventricular rate.

*Unlike 3rd degree heart block there is still some relationship between the P waves and the QRS complexes.

*High-grade AV block may result from either Mobitz I or Mobitz II AV block.

++AV Block: Third Degree (Complete Heart Block)++

Complete Heart Block (CHB) Overview

*In complete heart block, there is complete absence of AV conduction – none of the supraventricular impulses are conducted to the ventricles.

*Perfusing rhythm is maintained by a junctional or ventricular escape rhythm. Alternatively, the patient may suffer ventricular standstill leading to syncope (if self-terminating) or sudden cardiac death (if prolonged).

*Typically the patient will have severe bradycardia with independent atrial and ventricular rates.

Mechanism

*Complete heart block is essentially the end point of either Mobitz I or Mobitz II AV block.

*It may be due to progressive fatigue of AV nodal cells as per Mobitz I (e.g. secondary to increased vagal tone in the acute phase of an inferior MI).

*Alternatively, it may be due to sudden onset of complete conduction failure throughout the His-Purkinje system, as per Mobitz II (e.g. secondary to septal infarction in acute anterior MI).

*The former is more likely to respond to atropine and has a better overall prognosis.

Causes Of Complete Heart Block

The causes are the same as for Mobitz I and Mobitz II second degree heart block. The most important aetiologies are:

*Inferior myocardial infarction

*AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-blockers, digoxin)

*Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s disease)

Clinical Significance

*Patients with third degree heart block are at high risk of ventricular standstill and sudden cardiac death.

*They require urgent admission for cardiac monitoring, backup temporary pacing and usually insertion of a permanent pacemaker.

Complete Heart Block Should Not Be Confused With

*High grade AV block: A type of severe second degree heart block with a very slow ventricular rate but still some evidence of occasional AV conduction.

*AV dissociation: This term indicates only the occurrence of independent atrial and ventricular contractions and may be caused by entities other than complete heart block (e.g. “interference-dissociation” due to the presence of a ventricular rhythm such as AIVR or VT).

PAC Vs Junctional Rhythm

Inverted P Wave

*P-wave inversion in the inferior leads indicates a non-sinus origin of the P waves.

*When the PR interval is < 120 ms, the origin is in the AV junction (e.g. accelerated junctional rhythm).

*When the PR interval is ≥ 120 ms, the origin is within the atria (e.g. ectopic atrial rhythm).

Multiple P Wave Morphologies

*The presence of multiple P wave morphologies indicates multiple ectopic pacemakers within the atria and/or AV junction.

*If ≥ 3 different P wave morphologies are seen, then multifocal atrial rhythm is diagnosed.

*If ≥ 3 different P wave morphologies are seen and the rate is ≥ 100, then multifocal atrial tachycardia (MAT) is diagnosed.

P Pulmonale

Right Atrial Enlargement-Lead II

*In right atrial enlargement, right atrial depolarisation lasts longer than normal and its waveform extends to the end of left atrial depolarisation.

*Although the amplitude of the right atrial depolarisation current remains unchanged, its peak now falls on top of that of the left atrial depolarisation wave.

*The combination of these two waveforms produces a P waves that is taller than normal (> 2.5 mm), although the width remains unchanged (< 120 ms).

Right Atrial Enlargement-Lead V1

*Right atrial enlargement causes increased height (> 1.5mm) in V1 of the initial positive deflection of the P wave.

P Mitrale

Left Atrial Enlargement-Lead II

*In left atrial enlargement, left atrial depolarisation lasts longer than normal but its amplitude remains unchanged.

*Therefore, the height of the resultant P wave remains within normal limits but its duration is longer than 120 ms.

*A notch (broken line) near its peak may or may not be present (“P mitrale”).

Left Atrial Enlargement-Lead V1

Left atrial enlargement causes widening (> 40ms wide) and deepening (> 1mm deep) in V1 of the terminal negative portion of the P wave.

Biatrial Enlargement

*Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.

*The spectrum of P-wave changes in leads II and V1 with right, left and bi-atrial enlargement is summarised in the following diagram.

*Common P Wave Abnormalities.

Common P Wave Abnormalities

*P mitrale (bifid P waves), seen with left atrial enlargement.

*P pulmonale (peaked P waves), seen with right atrial enlargement.

*P wave inversion, seen with ectopic atrial and junctional rhythms.

*Variable P wave morphology, seen in multifocal atrial rhythms.

Wolff-Parkinson-White Syndrome Pre Excitation Atrial Fibrillation

Wolff-Parkinson-White Syndrome With Delta Wave

++PR Interval++

*The PR interval is the time from the onset of the P wave to the start of the QRS complex.

*It reflects conduction through the AV node.

*The normal PR interval is between 120 – 200 ms duration (three to five small squares).

*If the PR interval is > 200 ms, first degree heart block is said to be present.

*PR interval < 120 ms suggests pre-excitation (the presence of an accessory pathway between the atria and ventricles) or AV nodal (junctional) rhythm.

*Type Of AV Block has been describe above.

Short PR interval (<120ms)

A short PR interval is seen with:

*Preexcitation syndromes.

*AV nodal (junctional) rhythm.

Wolff-Parkinson-White (WPW) And Lown-Ganong-Levine (LGL) Syndromes.

*These involve the presence of an accessory pathway connecting the atria and ventricles.

*The accessory pathway conducts impulses faster than normal, producing a short PR interval.

*The accessory pathway also acts as an anatomical re-entry circuit, making patients susceptible to re-entry tachyarrhythmias.

*Patients present with episodes of paroxsymal supraventricular tachycardia (SVT), specifically atrioventricular re-entry tachycardia (AVRT), and characteristic features on the resting 12-lead ECG.

Wolff-Parkinson-White Syndrome

*The characteristic features of Wolff-Parkinson-White syndrome are a short PR interval, broad QRS and a slurred upstroke to the QRS complex, the delta wave.

*Short PR (<120ms), broad QRS and delta waves in WPW syndrome

Wolff -Parkinson- White Syndrome Cases Usually

*ECG pattern depends on where the accessory pathway inserts.

Classically:

*Short PR interval <120 msecs.

*QRS > 100msecs.

*Delta wave-slurred upstroke at beginning of QRS.

Different insertions:

*Normal QRS if pathway inserts into infranodal conduction tissue just below AV node

*Grossly wide and abnormal QRS if pathway inserts into non-conduction tissue.

Key Management Points For WPW

*A heart rate ≥ 200 should make you think of a pre-excitation syndrome.

*Narrow complex SVT is treated identically to non-WPW SVT.

*Don’t try and be clever with drugs in broad complex tachycardias and WPW.

*Using AV nodal blockers in WPW and AF can result in 1:1 conduction to the ventricles.

*This is also know as Ventricular Fibrillation.

*Just shut-up + DC cardiovert them.

Lown-Ganong-Levine Syndrome

*The features of LGL syndrome are a very short PR interval with normal P waves and QRS complexes and absent delta waves.

*Short PR interval with normal QRS complexes in LGL syndrome

AV Nodal (Junctional) Rhythm

*Junctional rhythms are narrow complex, regular rhythms arising from the AV node.

*P waves are either absent or abnormal (e.g. inverted) with a short PR interval (retrograde P waves).