LECTURES:
1. Basic Components of Cardiac Cycle
2. PR Interval Basics
3. PR Interval Basics
4. Short PR Interval
5. Full ECG Course
6. The EKG Guy Lectures

Overview

• PR interval: measured from P wave onset to QRS complex onset
• PR interval = [P wave] + [PR segment]
• Note: includes both atrial depolarization (P wave) & atrial repolarization (Tp wave)
• “PQ” interval used interchangeably if Q wave is initial wave of QRS; thus, representing actual measured period
• Represents time for impulse to travel from atria (adjacent to SA node) through AV node, bundle of His, bundle branches, & Purkinje fibers until ventricular depolarization begins
• Does not include duration of SA conduction (ie, conduction from SA node to RA)
• Cardiac events: (1) atrial depolarization & repolarization; (2) stimulation of AV node, His bundle, bundle branches, & Purkinje system
• Most of PR interval reflects slow conduction through AV node (ie, proximal to His bundle)
• AH interval: 0.050-0.13 s (50-130 ms) [1,2,3]
• AH interval = time b/t lower part of RA & His bundle spike
• HV interval: 0.035-0.055 s (35-55 ms)
• HV interval = time b/t His bundle spike & onset of ventricular deflections
• Controlled by autonomic nervous system – sympathetic & parasympathetic balance
• Hence, PR interval varies with heart rate (HR)
• Sympathetic predominates => faster HR => shorter PR interval
• Parasympathetic predominates => slower HR => longer PR interval

PR Interval Duration

• Measure in lead with largest, widest P wave & longest QRS interval
• Avoids inaccuracies in which early portion of P wave or QRS is isoelectric
• Normal adults: 0.12–0.20 s (120–200 ms) [4]
• Tends to increase with age [5]
• Childhood: 0.10–0.12 s (110–120 ms)
• Adolescence: 0.12–0.16 s (120–160 ms)
• Adulthood: 0.14–0.21 s (140–210 ms)
• In general:
• Short PR interval: <0.12 s (120 ms) => preexcitation (ie, accessory pathway b/t atria & ventricles) or junctional rhythm
• Prolonged PR interval: >0.20 s (200 ms) => 1st-degree AV block

Short PR Interval

• Duration: <0.12 s (120 ms)
• Differential diagnosis: normal variant; junctional or low atrial rhythms; preexcitation syndromes (eg, Lown-Ganong-Levine syndrome, Wolff-Parkinson-White syndrome); glycogen storage disease; hypertension; Fabry’s disease; pheochromocytoma

Junctional rhythm

• Regular rhythm arising from AV node
• ECG features:
• Absent or inverted retrograde P wave
• Short PR interval (<120 ms)
• Narrow QRS complex (without delta waves)

Preexcitation syndromes

• Accessory pathway: bypasses normal physiologic block  conducts impulses faster than normal => short PR interval
• Acts as anatomical reentry circuit, making patients vulnerable to reentry tachyarrhythmias
• Presentation: episodic paroxysmal SVT (esp. AVRT) with characteristic resting ECG features

1. Lown-Ganong-Levine (LGL) syndrome

• Often benign; possible association with tachycardias
• Bypass tract: James fiber (connection b/t atria & below normal physiologic block)
• Short PR interval due to accessory pathway (James fiber), which bypasses normal physiologic block at AV node
• Normal QRS because conduction through His bundle & bundle branches proceeds normally
• ECG features:
• Normal P wave to QRS ratio (1:1)
• Short PR interval (<120 ms)
• Narrow QRS complex (without delta wave)

2. Wolff-Parkinson-White (WPW) syndrome

• Can be life-threatening
• Bypass tract: Kent bundle (connection b/t atria & ventricles)
• Short PR interval due to accessory pathway (Kent bundle), which bypasses normal physiologic block at AV node
• Impulses travels through atria & reaches AV node & Kent bundle nearly simultaneously; impulse traveling down:
• Pathway 1: Kent bundle => no physiologic block => spreads slowly through ventricles
• Slow Kent bundle impulse superimposed or fused on normal impulse => forms fusion beat with delta wave
• Delta wave = initial QRS slurring; represents ventricular tissue stimulated by Kent bundle impulse
• Pathway 2: AV node => physiologic block => depolarizes rest of ventricles
• Impulses from pathways eventually meet & cancel each other out
• Note: conduction through ventricles outside normal conduction system progresses slowly via cell-to-cell spread => wide QRS (eg, PVC)
• Conduction to ventricles through Kent bundle occurs before normal conduction pathway due to lack of physiologic block => cell-to-cell ventricular depolarization
• ECG features:
• Normal P wave
• Short PR interval (<120 ms)
• 12% with normal PR interval
• Wide QRS (≥ 120 ms) + delta wave
• ± ST-T wave changes or abnormalities
• Associated with paroxysmal tachycardias (wide, regular/irregular, & very fast)
• If all above present without tachycardia = WPW pattern
• Distinction b/t SVT & VT is difficult; treat wide-complex tachycardia as VT until proven otherwise
• 3 types of WPW: A, B, & C
• All may be mistaken for infarct (pseudoinfarct) when:
• Negative delta wave in inferior leads (resembles Q wave mimicking inferior MI)
• Tall R wave in V1 with WPW type A (mimics posterior MI)
• Differential diagnosis of tall R wave in V1: WPW type A, posterior MI, RBBB, RVH, normal in adolescents
• 1. WPW Type A
• Kent bundle: often left-sided
• ECG features:
• QRS positive in V1-V6 (note: tall R wave in V1 mimics posterior MI)
• May resemble RBBB with RSR’ pattern
• ST-T wave repolarization abnormalities in right-precordial leads (often STD & TWI)
• To recall: look at V1; drawing a line across QRS resembles “A” for WPW type “A”
• 2. WPW Type B
• Kent bundle: often right-sided
• ECG features:
• QRS negative in V1-V2 & positive in V4-V6
• May resemble LBBB
• ST-T wave repolarization abnormalities in left-precordial leads (often STD & TWI)
• To recall: think of the “B” in WPW type “B” as similar to an “R” for “Right”-sided
• 3. WPW Type C
• Very rare
• QRS positive in V1-V4 & negative in V5-V6
• Accessory pathway can result in impulse traveling in a reentry circuit, resulting in AVRT:
• 1. Antidromic (fast-slow) AVRT
• Anterograde conduction down Kent bundle => retrograde conduction up AV node
• ECG features: wide-QRS tachycardia (difficult to distinguish from VT)
• Can be very fast with atrial flutter or atrial fibrillation where transmission can be 1:1
• 2. Orthodromic (slow-fast) AVRT
• Anterograde conduction down AV node => retrograde conduction up Kent bundle
• ECG features: narrow-QRS tachycardia
• Less dangerous because physiologic block of AV node => slower & more controlled

Prolonged PR Interval

• Duration: >0.20 s (200 ms)
• Delayed conduction through AV node
• Delay often in AV node; possible intraatrial or His Purkinje disease
• May occur in isolation or coexist with other blocks (eg, 2nd-degree AV block, trifascicular block)
• Differential diagnosis: normal variant; AV block 2/2 coronary artery disease or rheumatic heart disease; hyperthyroidism
• Other causes:
• Increasing HR while on digoxin or with conduction system disease
• Increased paced rate in artificially paced atria
• Healthy middle-aged male + prolonged PR interval + normal QRS => normal prognosis & not related to ischemic heart disease
• Questions to consider:
• 1. Are all PR intervals & P waves the same?
• If yes => likely 1st-degree AV block
• If no => consider premature atrial contraction, wandering atrial pacemaker (WAP), multifocal atrial tachycardia (MAT), or another type of block
• 2. Do PR intervals vary consistently?
• Are all P waves the same?; if yes => type of block; if no => WAP, MAT
• Are PR intervals progressively lengthening?
• Are grouped beats present?
• Are P wave & QRS dissociated?
• AV Blocks (AVB) = conduction disturbances in AV node or His bundle
• Not same as bundle branch blocks (blocks in left- or right-bundle branches or their fascicles)
• 1st-degree AVB:
• Prolongation of normal physiologic block
• PR interval >0.20 s (200 ms)
• Defect often at level of AV node
• Causes: organic heart disease, drug toxicity (eg, digoxin, calcium-channel blocker, tricyclic antidepressant, β-blocker), hypercalcemia, hypothermia, increased vagal stimulation (eg, inferior MI)
• 2nd-degree Mobitz type I (Wenckebach) AVB:
• Defective AV node with long refractory period
• Grouped beats with progressive PR interval prolongation until P wave not conducted => dropped beat
• RR interval shortens until dropped beat
• Distance b/t QRSs with dropped beats: <2x shorted RR interval in group
• 2nd-degree Mobitz type II (non-Wenckebach) AVB
• More dangerous than Mobitz type I; can lead to 3rd-degree AVB
• Constant PR interval with intermittent dropped beats
• Note: if 2:1 complex, cannot tell if Mobitz type I or II; get long rhythm strip to help differentiate as block is often continuous (eg, if grouping seen, think Mobitz type I)
• 3rd-degree (complete) AVB:
• Complete impulse block at AV node
• Dissociation of P wave & QRS
• Atrial beat: often normal sinus rhythm or sinus tachycardia
• Ventricular beat: junctional (narrow QRS) or ventricular (wide QRS) origin
• Rate: atrial (P wave) > ventricular (QRS)
• If ventricular (QRS) ≥ atrial (P wave) => AV dissociation

Abbreviations: b/t, between; AV, atrioventricular; SVT, supraventricular tachycardia; VT, ventricular tachycardia; AVRT, AV reentrant tachycardia; WAP, wandering atrial pacemaker; MAT, multifocal atrial tachycardia

REFERENCES

1. Castellanos A Jr, Castillo C, Agha A. Contribution of His bundle recording to the understanding of clinical arrhythmias. Am J Cardiol 28:499, 1971.

2. Dhingra RC, Rosen KM, Rahimtoola SH. Normal conduction intervals and responses in 61 patients using His bundle recording and atrial pacing. Chest 64:55, 1973.

3. Narula OS, Scherlag RJ, Samet P, et al. Atrioventricular block: localization and classification by His bundle recordings. Am J Med 50:146, 1971.

4. Lepeschkin E. Duration of electrocardiographic deflections and intervals: man. In: Altman PE, Dittmer DS (eds): Respiration and Circulation. Bethseda, MD, Federation of American Societies for Experimental Biology, 1971, p 277.

5. Beckwith JR. Grant’s Clinical Electrocardiography. New York, NY, McGraw-Hill, 1970, p 50.