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.