SARAWAK GENERAL HOSPITAL

Conduction System
SA Node AV node His bundle Right bundle branch Left bundle branch
Anterior fascicle Posterior fascicle

Purkinje fibers

5 6

3
5 4

Physiology of Action Potential

An electrical impulse precedes each heartbeat (mechanical contraction). Each heart muscle cell is stimulated to contract by electrical process called action potential. (composed of five phases) The ECG records the summation of action potential of the muscle cells in the atria and ventricles. i.e records only the Echocardiogram records the mechanical contraction from the electrical event

electrical event

Muscle Cells Action Potential ECG Tracing Electrical Activity

Mechanical Activity

Cardiac Muscle

Causes
Three mechanisms: (1) Disturbances in AUTOMATICITY speeding up (tachycardia), slowing down (bradycardia), abnormal depolarization (ectopic or escape beat) May involve SA node atrium AV node ventricles

Causes
(2) Disturbances in CONDUCTION Either too rapid (WPW syndrome) or Too slow ( AV heart block)
(3) Combination of altered automaticity and conduction

Normal Pacemaker Rate

SA NODE RATE 60-100
AV JUNCTION
RATE 40-60

VENTRICLES
RATE 15-40

NORMAL SINUS RHYTHM

Pacemaker impulses are
initiated in the sinoatrial (SA) node, through atrial pathways, delayed at atrioventricular (AV) node. down the bundle branches to Purkinje fibers in the ventricles

Atrial depolarization P wave. Ventricular depolarization QRS

Sinus Rhythm & its variants Normal Sinus Rhythm Sinus Arrhythmias Sinus Tachycardia Sinus Bradycardia

NORMAL SINUS RHYTHM

CHARACTERISTICS The P wave is usually upright in leads II, III, aVF, and V1. Its morphology remains constant at all times. P-P and R-R intervals are equal and regular. Atrial and ventricular rates are identical range between 60 and 100 bpm. There is no ectopic activity.

SINUS ARRHYTHMIA (SINUS DYSRHYTHMIA)

a sinus rhythm with a rate that varies with respiration (respiratory sinus arrhythmia) characterized by alternate speeding up and slowing down of the heart rate usually benign Rarely non respiratory sinus arrhythmia

SINUS ARRHYTHMIA (SINUS DYSRHYTHMIA) In respiratory sinus arrhythmia,

the rate increases with inspiration & decreases with expiration.

In non respiratory sinus arrhythmia,

the irregularity of the rhythm, not correlated with the respiratory cycle.

SINUS ARRHYTHMIA (SINUS DYSRHYTHMIA)

ETIOLOGY Respiratory sinus arrhythmia

Normal in children and young adults.

Non respiratory sinus arrhythmia may be

with cardiac disease and MI esp with sinus bradycardia, digoxin therapy enhanced vagal tone.

Expiration

Inspiration

SINUS TACHYCARDIA
sinus rhythm at a rate 100 bpm.

ETIOLOGY 1. increased physiologic demand for oxygen

2. (stress, exercise, pain, excessive caffeine) Hyperthyroidism, heart failure, myocardial infarction, pulmonary embolism, medications (e.g., atropine, epinephrine, isoproterenol), fever, anemia, hypoxia, and shock Physiologic ST commonly observed in neonates (HR may btw 100 - 160 bpm)

3.

SINUS TACHYCARDIA
CHARACTERISTICS
same characteristics as NSR except the ventricular rate 100 bpm gradual acceleration of sinus node discharge

Sinus Bradycardia
Characteristics

same as for NSR, except the ventricular rate 60

bpm

Sinus Bradycardia
Etiology 1. physiologic causes (athletes, sleep) 2. Vagal stimulation 3. Sick sinus syndrome 4. hypothyroidism, hypothermia, electrolyte imbalances (e.g., hyperkalemia), Inferior myocardial infarction 5. medications (e.g., blk, ca2+ channel blk, digoxin)

Supraventricular Arrhythmias
Atrial Premature Complexes Atrial Tachycardia Multifoci Atrial Tachycardia Paroxymal Supraventriculat Tachycardia Atrial Flutter Atrial Fibrillation Junctional Premature Complexes

ATRIAL PREMATURE COMPLEXES (APC)

DEFINITION results from a premature supraventrictilar impulse that originates somewhere in the atria outside of sinoatrial (SA) node. also called atrial ectopic complexes

ATRIAL PREMATURE COMPLEXES

CHARACTERISTICS 1. R-R interval is irregular. The premature complex disturbs the regularity of the underlying rhythm 2. The morphology of the ectopic/premature P wave is different from the sinus P wave. 3. The premature P wave is followed by a QRS complex if the impulse conducted into the ventricles.

ATRIAL PREMATURE COMPLEXES

1. QRS complex is narrow if conduction in the ventricles is disturbed. 2. If the AV node conducts a premature impulse into the ventricle when they have not fully repolarized, the resulting QRS complex may appear wide and abnormally shaped. 3. This is known as an APC conducted with aberration and must be differentiated from a ventricular premature complex

Clinical tips
The best leads for assessment of atrial rhythm disturbances are II, III, aVF, and V1, P waves are usually most prominent in these leads.

WANDERING ATRIAL PACEMAKER

DEFINITION a supraventricular rhythm in which pacemaker impulses originate from 2 sites in the SA node, atria, or AV junction discharge at a rate of 60 to 100 beats per minute

WANDERING ATRIAL PACEMAKER

CHARACTERISTICS
1. P wave morphologies vary because impulses originate from different sites. 2. P-P intervals (and subsequent R-R intervals) may also vary because each impulse travels through the atria via a slightly different route. 3. One P wave for every QRS complex. 4. Overall atrial and ventrictilar rates remain between 60 and 100 bpm. 5. QRS complexes are usually unchanged. They are narrow as long as ventricular depolarization is undisturbed.

MULTIFOCAL ATRIAL TACHYCARDIA

DEFINITION Multifocal atrial tachycardia (MAT) is an ectopic supraventricular tachycardia originates from three or more atrial foci rate of 100 to 250 bpm.

MULTIFOCAL ATRIAL TACHYCARDIA

CHARACTERISTICS 1. Three or more P wave morphologies (multiple foci) 2. One P wave for every QRS complex (1: 1 conduction) 3. Irregular rhythm; varying P-P and R-R intervals 4. PR intervals varying slightly from beat to beat 5. QRS complexes possibly identical to each other or slightly widened secondary to aberrant intraventricular conduction 6. Rate than 100 bpm

ATRIAL TACHYCARDIA
DEFINITION a supraventrictilar rhythm originating outside of the SA node rate between 120 and 250 bpm. frequently a result of digitalis toxicity.

ATRIAL TACHYCARDIA
CHARACTERISTICS rhythm is regular (R-R intervals are equal) atrial rate is 120 to 250 bpm. P-P intervals are equal Conduction is commonly 1:1 (one P wave for every QRS complex). Conduction may be 2: 1 or greater especially in the presence of digitalis toxicity. (atrial tachycardia with AV block)

ATRIAL TACHYCARDIA
PR interval is short when conduction through the AV node is 1: 1. P wave morphology is often different from NSR shape of the QRS is unchanged from NSR unless conduction in the ventricles is disturbed. Atrial tachycardia may occur in paroxysms; when it terminates, there may be a long pause before NSR resumes.

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT)

DEFINITION supraventricular impulses are conducted abnormally between atria and ventricles. ventricles are depolarized 100 bpm.

ETIOLOGY
1. AV nodal reentry tachycardia (AVNRT)
Micro reentry circuit A supraventricular impulse is conducted slowly down one pathway in the AV node toward the ventricles and is then conducted rapidly back into the atria along a second pathway within the AV node. The atria and ventricles are depolarized almost simultaneously. 60-70% of PSVT

ETIOLOGY
2. Atrioventricular Reentrant Tachycardia (AVRT)
Uses a macro reentry circuit, such as bundle of Kent, that bypasses the AV node to form an accessory bridge from the atria to the ventricles Most well known Wolff-Parkinson-White (WPW) syndrome
Manifest AP Concealed AP

Less common form of PSVT The atria and ventricles are depolarized sequentially. As with AVNRT, the cycle in AVRT perpetuates itself as the impulse repeatedly travels the same route.

ATRIAL FLUTTER
DEFINITION a supraventricular dysrhythmia characterized by the appearance of saw tooth-shaped flutter waves rate between 250 and 350 bpm. associated with a reentry mechanism within the atria esp around the pulmonary veins

CHARACTERISTICS
1. P waves are absent. 2. flutter (F) waves represent depolarization of the atria.
1. 2.

abnormal

They assumed a saw tooth that is most easily seen in leads II, III, and aVF, and V1.

3. The flutter waves appear contiguously with no isoelectric baseline visible. Some flutter waves may be obscured by the QRS complex. 1. atrial rate (flutter rate) ranges btw 250 - 350 bpm (average is 300bpm). 2. The ventricular rate is usually slower than the atrial rate

CLINICAL TIP
Flutter waves may be difficult to identify if 2:1 conduction Vent rate of 150 bpm Vagal maneuvers like carotid sinus massage or drugs to increase block at the AV node slowing the ventricular resp enough to unmask hidden flutter waves. Atril flutter must be differentiated from atrial tachycardia by closely examine the P wave.
In atrial flutter, F waves is contiguous In atrial tachycardia, ectopic P waves are separated by an isoelectric baseline.

ATRIAL FIBRILLATION
DEFINITION A supraventricular dysrhythmia characterized bv multiple ectopic atrial foci, uncoordinated atrial contractions, and a classically irregular ventricular rate. May occur intermittently, (paroxysmal atrial fibrillation), but it frequently becomes a chronic condition.

CHARACTERISTICS
1. 2. There are no P waves. fibrillatory (f) waves arise within the atria. small, poorly defined, and distort the baseline, may be fine or coarse in appearance. R-R intervals are irregular because conduction through the AV node is highly variable. QRS complexes are usually narrow unless conduction in the ventricles is abnormal. As impulses are conducted irregularly through the AV node with some of these impulses aberrantly conducted thru the ventricular Ashman's phenomenon (characterized by wide QRS complexes that can easily be mistaken for (VPCs).

3.

4.

5.

JUNCTIONAL PREMATURE COMPLEXES

DEFINITION a premature (ectopic) supraventricular impulse that originates from the area in and around the AV junction. is also known as a premature junctional complex (PJC).

AV NODAL EXTRASYSYTOLES
Conduction
Antegrade conduction To ventricle only (retrograde conduction is blocked)

1. Retrogadely to the Atria and 2. Antegradely to the ventricle

CHARACTERISTICS
R-R interval is irregular. The premature complex disturbs the regularity of the underlying rhythm. A visible P wave may or may not be associated with a premature QRS complex If the P wave is visible, commonly occurs either just before or just after the QRS complex usually inverted in II, III, aVF

JUNCTIONAL PREMATURE COMPLEXES

An inverted P wave implies that the ectopic impulse from the AV junction was conducted retrogradely (backward) into the atria. If the P wave appears before the QRS complex, the atria were depolarized before the ventricles. If the P wave occurs immediately after the QRS complex, the atria were depolarized after the ventricles. If the P wave is buried in the QRS complex, it is assumed that the atria and ventricles were depolarized simultaneously)

JUNCTIONAL EXCAPE RHYTHM

DEFINITION A passive escape rhythm that originates in the AV junction and usually appears secondary to depression of the higher sinus pacemaker.

CHARACTERISTICS
1. The ventricular rate is between 40 and 60 bpm 2. The R-R interval is regular. 3. There is one P wave for every QRS complex (1: 1 conduction). The P wave may appear before the QRS or after the QRS, or it may be buried within the QRS complex. 4. The P wave is usually inverted in the inferior leads (II, III, aVF). 5. If the ectopic P wave precedes the QRS complex, the resultant PR interval is abnormally short-often less than 0. 1 2 second. 6. The QRS complex is narrow as long as intraventricular conduction is undisturbed.

ACCELERATED JUNCTIONAL RHYTHM AND JUNCTIONAL TACHYCARDIA

DEFINITION Represent supraventricular dysrhythmias arising from the AV junction at rates exceeding the inherent junctional escape rate of 40 to 60 bpm.

CHARACTERISTICS
All the characteristics described for junctional escape rhythm apply, except for ventricular rate. In accelerated junctional rhythm the ventricular rate is between 60 and 100 bpm. In junctional tachycardia the ventricular rate is 100 bpm or faster.

Is there a normal looking QRS complex ?

If there is a abnormal looking QRS complex consider Ventricular arrhythmias. If there is no QRS complexes at all, consider Asystole

Ventricular Arrhythmias
VENTRICULAR PREMATURE BEAT (VPB) VENTRICULAR ESCAPE COMPLEXES VENTRICULAR TACHYCARDIA (VT) TORSADE DE POINTES ACCELERATED IDIOVENTRICULAR RHYTHM VENTRICULAR FIBRILLATION (VF)

VENTRICULAR PREMATURE BEATS

early occurring widened QRS complexes microreentry at the level of the Purkinje fiber bizarre morphology
QRS complex of a VPB is widened, bizarre, and often notched, with a QRS duration >0.16 seconds It may have a morphology which resembles a right or left bundle branch block depending upon the location of origin.

VENTRICULAR PREMATURE BEATS

Unifocal VPBs
all have a single morphology; the interval between the VPB and the preceding sinus beat is usually identical (fixed coupling cycle).

Multifocal VPBs
multiple different QRS morphologies caused by various different reentrant circuits varying coupling cycles between the sinus beat and the VPB.

In general there is no P wave identified before a premature QRS complex.

VENTRICULAR PREMATURE BEATS

A full compensatory pause usually follows the VPB; interval between the QRS complexes before and after the premature beat is 2X the interval btw two successive sinus beats. On occasion, the VPB may be interpolated, ie, it occurs between two normal sinus QRS complexes and does not alter the underlying sinus or ventricular rate. Other findings on the ECG include marked repolarization abnormalities, manifested as ST segment and T wave abnormalities.

VENTRICULAR PREMATURE BEATS

Ventricular bigeminy
ventricular premature beat follows each sinus beat often becomes self perpetuating, a situation known as the rule of bigeminy. This occurs because the long cycle length tends to precipitate a VPB.

VENTRICULAR PREMATURE BEATS

Ventricular trigeminy
two sinus beats are followed by the ventricular premature beat. Thus, every third beat is a ventricular premature beat (show ECG 3).

VENTRICULAR PREMATURE BEATS

Ventricular couplets
two VPBs in a row (show ECG 4) there is often a compensatory pause after the second premature beat the two premature beats may have an identical morphology (unifocal couplet), or their morphology may differ (multifocal couplet) the RR interval between the two successive VPBs varies widely.

VENTRICULAR PREMATURE BEATS

Interpolated VPBs
VPB may be interpolated between two successive sinus beats without altering the underlying sinus RR interval (show ECG 5).

VENTRICULAR ESCAPE COMPLEXES OR RHYTHM

when there is failure of the sinus and AV node to generate an impulse absence of P wave activity associated with a widened QRS complex that resembles a VPB and occurs after a pause of variable duration (but always greater than the normal sinus RR interval) persistence of this activity leads to multiple successive ventricular complexes representing an escape ventricular rhythm with a rate that is slower than the normal sinus rhythm

VENTRICULAR TACHYCARDIA
is defined as three or more successive ventricular complexes. non sustained VT is a series of repetitive ventricular beats which have a duration of less than 30 seconds; sustained VT lasts for more than 30 seconds. the rate of VT is generally greater than 100 beats per minute, but may vary widely the rhythm is usually regular, although there may be slight irregularity of the RR intervals.

VENTRICULAR TACHYCARDIA
features of ventricular tachycardia include:
abnormal morphology of the QRS complex, the QRS axis is typically shifted (often to the left), the width of the QRS complex is generally >0.16 sec. positive or negative concordance of the QRS complex across the precordial leads (eg, R waves or S waves only) a monophasic Rr' pattern in lead 1 (termed rabbit ears) with a taller left ear. an indeterminate axis (between -90 and -180)

VENTRICULAR TACHYCARDIA
Monomorphic VT
all QRS complexes of an episode are identical often displays subtle changes of the QRS complexes with regard to morphology and width

VENTRICULAR TACHYCARDIA
Polymorphic VT
QRS complexes within each episode display markedly different morphologies the RR intervals may be grossly irregular (show ECG 9). The differences in QRS morphology result from changes in the direction (vector) of myocardial activation due to marked heterogeneity of the electrophysiologic characteristics of the ventricular myocardium.

Torsade de pointes
is an atypical, rapid, and bizarre form of ventricular tachycardia it means "twisting of points" a name that refers to the continuously changing axis of polymorphic QRS morphologies that are observed during each episode the polymorphic VT is associated with a congenital or acquired prolongation of the QT interval, suggesting a prolonged refractory period and repolarization time

Torsade de pointes
there often is heterogeneity of repolarization or dispersion of refractoriness. Torsade is usually initiated by a long RR interval (often a post VPB compensatory pause) followed by a short RR cycle, generally due to another VPB

ACCELERATED IDIOVENTRICULAR RHYTHM

a repetitive ventricular rhythm occurring at a rate between 60 and 100 beats per minute it may be the result of an accelerated ventricular focus which generates an impulse faster than the sinus node and therefore assumes control if the idioventricular rhythm represents an escape rhythm (generally the result of third degree AV nodal block), the P waves are dissociated from the QRS impulses and the atrial rate is faster than the ventricular rate.

VENTRICULAR FIBRILLATION
complete absence of properly formed QRS complexes and no obvious P waves no uniform activation of the ventricular myocardium and therefore no distinct ventricular complexes coarse fibrillatory waves when the fibrillation is recent in onset (eg, only a few minutes) high amplitude oscillations occurring at rate greater than 320 beats per minute which manifest random changes in morphology, width, and height, leading to the appearance of a completely chaotic rhythm. fibrillatory waves become fine when VF continues for a longer time and may not be obvious; they may resemble asystole in these cases.

Anti Arrhythmic
Class IA Quinidines, Procaninamide, Disopyramide Class IB Mexilitine, Lignocaine Class IC Flecanide, Propafenone Class II Blocker Class III Sotalol, amiodarone Class IV Diltiazam, Verapamil

Heart Block
SA Block AV Block
First degree Second degree Third degree

Bundle Branch Block

LBBB RBBB

Fascicular Block
Anterior Posterior

Atrioventricular block
FIRST DEGREE ATRIOVENTRICULAR BLOCK SECOND DEGREE ATRIOVENTRICULAR BLOCK
Mobitz type I (Wenckebach) Mobitz type II

THIRD DEGREE ATRIOVENTRICULAR BLOCK

FIRST DEGREE ATRIOVENTRICULAR BLOCK

defined as a prolonged PR interval (>0.20 seconds) most often occurs when there is a prolongation or delay in impulse conduction through the AV node (show ECG 1). The PR interval generally varies with the heart rate;
in the presence of sinus bradycardia (usually the result of enhanced vagal tone), the PR interval lengthens. the PR interval becomes shorter during sinus tachycardia.

SECOND DEGREE ATRIOVENTRICULAR BLOCK

Mobitz type I (Wenckebach) or Mobitz type II. Mobitz type I
Wenckebach second degree AV block result of an intermittent block of the impulse within the AV node, with subsequent failure to conduct an atrial impulse from the atria to the ventricles.

SECOND DEGREE ATRIOVENTRICULAR BLOCK

The ECG correlates of these electrical events include the following (show ECG 2):
There is a progressive lengthening of the PR interval until a normally occurring P wave is not followed by a QRS complex because of failure of the node to conduct the impulse to the ventricle. The completely blocked P wave is on time; the surrounding RR interval is prolonged. The impulse that arrives at the node following the completely blocked beat is conducted normally again because the node has had time to become totally repolarized.

SECOND DEGREE ATRIOVENTRICULAR BLOCK

Mobitz type II
usually indicative of underlying structural disease involving the AV node that is characterized by episodic and unpredictable failure of the node to conduct the impulse from the atria to the ventricles. The block occurs below the AV node in some cases, within the bundle of His, or within both bundle branches.

SECOND DEGREE ATRIOVENTRICULAR BLOCK

In contrast to Mobitz type I, there is no change in the PR interval prior to or after the nonconducted P wave (show ECG 3). There may be more than one successive nonconducted P wave, resulting in several P waves in a row without QRS complexes. An escape ventricular focus may generate a QRS complex in some cases after a variable duration

THIRD DEGREE ATRIOVENTRICULAR BLOCK

occurs when there is complete failure of the AV node to conduct any impulses from the atria to the ventricles. Causes:
intrinsic AV nodal disease. Drugs that depress and block nodal conduction such as digoxin, beta blockers, or calcium channel blockers Enhanced vagal tone, such as that occurring during sleep Infrequently it is congenital. result of infranodal block occurring within the bundle of His or in both bundle

THIRD DEGREE ATRIOVENTRICULAR BLOCK

The P waves are completely dissociated from the QRS complexes on the ECG (show ECG 4). Thus, the PR intervals are irregularly variable. The atrial and ventricular rates are both stable; the former is faster than the latter.

ECG analysis
Rate Rhythm Axis Interval & Morphology
P, PR, QRS duration & Amplitude, Q, ST, T, QT,

Ischaemia, infarction

ECG analysis
Three simple questions: (1) Is there a normal looking QRS complex ? (2) Is there a P wave ? (3) What is the relationship between the P wave and QRS complexes ?

Is there a P wave ?
If the QRS complexes are normal proceed to examine P wave If P wave is normal, consider sinus rhythm and its variants If P wave is absent or abnormal, consider supraventricular tachycardia.

Pulseless Electrical Activity

Electrical Mechanical Dissociation Any rhythm or electrical activity that fails to generate a palpable pulse The one major action is to search for reversible cause while non-specific interventions is administered

Defibrillation
Therapeutic use of electric current delivered in large amounts over very brief periods of time The defibrillation shock temporarily STUNS an irregularly beating heart and thus allows normal electrical activity to occur (more coordinated contractile activity to resume)

Rationale for early defibrillation

The most frequent initial rhythm in sudden cardiac arrest is VF The only effective treatment for VF is electrical defibrillation The probability of successful defibrillation diminishes rapidly over time VF tends to convert to asystole within a few minutes

Cardioversion
Cardioversion is the delivery of energy that is synchronized to the QRS complex, while defibrillation is nonsynchronized delivery of energy, ie, the shock is delivered randomly during the cardiac cycle.

Cardioversion
terminates arrhythmia by the delivery of a synchronized shock that depolarizes the tissue involved in a reentrant circuit and make the tissue refractory (the circuit is no longer able to propagate or sustain reentry). terminates those arrhythmias resulting from a single reentrant circuit (as atrial flutter, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia or monomorphic ventricular tachycardia.)

FACTORS AFFECTING DEFIBRILLATION AND CARDIOVERSION SUCCESS

Electrodes The placement of defibrillation electrodes on the thorax, while determining the transthoracic current pathway for external defibrillation, may have only a minimal effect on the myocardial distribution of the 4 to 5 percent of energy that actually reaches the heart There are two conventional positions:
Anterolateral orientation Anteroposterior orientation

Several studies have suggested that less energy is required and the success rate is higher with the anteroposterior electrode position in patients cardioverted for atrial fibrillation In some patients one, but not the other position, may be effective; thus, it has been suggested that if initial shocks are unsuccessful in terminating the arrhythmia, the electrodes should be relocated and cardioversion repeated

 Electrode pad size is an important determinant of transthoracic current flow during external countershock A larger pad or paddle surface is associated with a decrease in resistance and increase in current However, there appears to be an optimal electrode size (approximately 12.8 cm); an increase in electrode area beyond this size causes a decline in current density

FACTORS AFFECTING DEFIBRILLATION AND CARDIOVERSION SUCCESS

Transthoracic impedance
During transthoracic defibrillation, a considerably larger current must be delivered to the thorax to compensate for transthoracic impedance. Impedance results in the dissipation of energy due to shunting to the lungs, the thoracic cage, and other elements of the chest.

Transthoracic impedance
Transthoracic impedance is determined by multiple factors including:
Energy level Electrode size Electrode-to-skin interface Interelectrode distance Electrode pressure Phase of ventilation Thoracic impedance Myocardial tissue and blood conductive properties

Transthoracic impedance
To reduce impedance, the operator should always apply electrode gel or specifically made paste/ gelled pad

Asystole
No evidence to support the use of defibrillation in asystole Empiric shocks of asystole can inhibit the recovery of natural pacemakers in the heart and completely eliminate any chance of recovery

Ventricular Asystole (Cardiac Standstill)

Total absence of ventricular electrical activity and subsequently no ventricular contraction. May occur as primary event or follow VF or pulseless electrical activity Can occur also in patients with compete heart block without escape pacemaker Must always differentiate it from fine VF (different management)

What is the relationship between the P wave and QRS complexes ?

In the normal ECG every QRS complexes is preceded by a P wave The interval between P and QRS is less than 0.21 second Consider heart block when the above relationship is disturbed.