Electrocardiography for Anaesthesia

INTRODUCTION :

THE ELECTROCARDIOGRAM :

This is a graphic recording of the electrical potentials produced by the cardiac tissue. The heart is unique among the muscles of the body in that it possesses the properties of automatic impulse formation and rhythma contraction. Formation and conduction of these electrical impulses produce weak electrical currents that spread through the body. The ECG is recorded by applying electrodes to various locations on the body surface.

The clinical utility is its immediate availability as a non-invasive inexpensive and highly versatile test, but should not be considered as a since qua non of the diagnosis of heart disease and should always be interpreted in the light of surrounding clinical circumstances.

THE ELECTROCARDIOGRAPH :

It is a sophisticated galvanometer, a sensitive electromagnet which can detect and record changes in electromagnetic potentials. The recording are obtained on electrographic paper divided into small and large squares.

One Horizontal large square represents 0.20 seconds or 1/5th second and one small square represents 0.04 sec. Or 1/25th second. The vertical measurement reflect deflexion magnitude.

THE CONVENTIONALELECTROCARDIOGRAPHIC LEADS :

In clinical practise, there are twelve (12) conventional leads, which may be physiolgically divided into two groups depending on their orientation to the heart.

The frontal plane leads : They are oriented to the frontal or coronol plane of the body. The horizontal plane leads : They are oriented to the transuerse or horizontal plane of the body i.e. precordial leads. (Fig. 1)

THE FRONTAL PLANE LEADS : These bipolar limb leads are derived from three electrodes

Standard Lead – I : This is obtained by placement of the negative electrode on the right arm and positive electrode on the left arm.

Standard Lead – II : This is obtained by placement of the negative electrode on the right arm and positive electrode on the left leg.

Standard Lead – III : This is obtained by placement of the negative electrode on the left arm and positive electrode on the left leg.

DIAGRAM

The frontal plane leads thus form an equilateral triangle with the heart at the center. THE FINTHOVEN’S TRIANGLE :

DIAGRAM

THE UNIPOLAR LIMB LEADS :

The negative electrode is considered to be zero and the positive electrode is the exploring electrode. They are augmented instrumentally to increase the amplitude of deflexions.

AVR : This is augmented unipolar right arm lead and oriented to the cairty of the heart. Thus P-QRS-T are negotive normally in this lead.

AVL : This is augmented unipolar left arm lead and oriented to anterolateral /superior surface of left ventricle.

AVF : This is augmented unipolar left leg lead and oriented to the inferior surface of the heart.

DIAGRAM

HORIZONTAL PLANE LEADS :

The precordiol leads constitute the horizontal plane leads.

Lead V1 : This is placed over the 4th Ics immediately to the right of the sternum.

Lead V2 : This is placed over the 4th Ics immediately to the left of the sternum.

Lead V4 : This is placed over the 5th Ics in the mid-claricular line.

Lead V3 : This is placed exactly midway between V2 and V4.

Lead V5 : This is placed at the same horizontal level as lead VH on the anterior axillary line.

Lead V6 : This is placed at the same horizontal level as lead V4 and V5 on the mid-axillary line.

DIAGRAM

THE ELECTROPHYSIOLOGY OF THE HEART :

Much of the clinical ECG is based on the behaviour of transmembrane potential. Four electrophysiologic events are involved in the genesis of an ECG.

1.  
2. Impulse formation (esp. primary pacemaker of the heart, the S.A. mode)
3.  
4. Transmission of the impulse through specialized conduction fibres.
5.  
6. Depolarization.
7.  
8. Repolarization.

DIAGRAM

The resting membrane potential (RMP) is about – 80 to 90 mV (esp. SA mode) due to a gradient of Na+/K+ ions. This is maintained by active ion transport mechanism, the sodium pump.

At the onset of depolarisation, there is an abrupt change in permeability of the cell membrane to Na+ ions. This is designated as phase ‘O’. Pacemaker cells in the SA and AV node are depolarised by Ca2+ dependent slow inward current.

There is a gradual return to the RMP and this phase is divided into three phases

phase 1 : An initial rapid return to OmV largely as a result of closure of Na+ channel.

Phase 2 : This is the plateau resulting from slow entry of Ca2+ into the cells.

Phase 3 : This is due to return of intra cellular potential resulting from extrusion of K+ out of the cell.

The normal negative potential is established by the Na+/K+ pump which removed Na+ from the cell and permit influx of K+.

Relation with cellular events to surface ECG :

Summation of all phase ‘O’ potentials of atrial cells result in a ‘P’ wave.

Phase 2 : PR segment.

Phase 3 : To wave of atrial repolarization.

The summation of all phase ‘O’ potentials of ventricular my ocardial cells result in QRS complex.

Phase 2 : ST segment.

Phase 3 : T wave.

THE BASIC ACTION OF THE ELECTROCARDIOGRAPH :

Sequential depolarisation of the cardiac muscle from a state of polarisation causes an activation – excitation front which results in an electrical current. This current in turn forms an electromagnetic force or vector which can be detected and recorded by the electro cardiograph.

DIAGRAM

The fundamental principle is that when an electromagnetic force is direct towards the positive pole of a lead the electrocardiograph will record an upward or positive deflection and vice-versa as shown.

THE NORMAL ELECTROCARDIOGRAM (ECG)

The ‘P’ wave represents atrial activation.

QRS : Ventricular depolarisation.

T Wave : ventricular repolarisation /recovery.

PASTE DIAGRAM

PR interval : This is the time required foratrial repolarisation plus the conduction delay in the AV node, bundle of His and Bundle branches.

Normal PR interval - 0.12 – 0.2 seconds.

QRS Interval : This is mainly from the onset of Q wave to termination of S wave and is the time for ventricular depolarisation.

Normal QRS Interval : 0.1 sec. For frontal leads and 0.11 sec. For precordial leads :

QT Interval : This is measured from onset of Q wave to the end of T wave and it represents the duration of electrical systole.

QTc is corrected for heart rate and is about 0.42 sec.

VENTRICULAR ACTIVATION TIME (VAT) : Also known as intrinsicoid deflection and is the time it takes an impulse to traverse the myocardium from endocardum to Epicardium. It is the interval from the beginning of a wave to the peak of R wave. This should not exceed 0.04 sec. In left leads and 0.02 sec. In right leads.

Genesis of ‘V’ wave is uncertain but ST segment. T wave and V wave together represent toal duration of ventricular recovery.

GENESIS OF ‘P’ WAVE :

PASTE DIAGRAM

P wave is formed by fusion of right and left activation. The first part is the contribution of right atrial activation and the second part, the contribution of left atrial activation. It is best evaluated in standard lead II. This is pyramidal in shape and somewhat rounded in lead II but normally biphasis in V1 as shown.

GENESIS OF QRS COMPLEX :

Activation of the ventricles begins in the left sub-endocardial region spreading from left to right, which dominates the activation of the right subendocardial region i.e.region i.e. from right to left (shown as vector 1).

PASTE DIAGRAM

This is followed by activation of the free walls of both the ventricles. The right to left activation vector of the left ventricle dominates the left to right activation vector of right ventride. (shown as vector 2). Hence, the above deflections are obtained.

ELECTRICAL AXIS OF THE HEART :

They are of the two types :

1.  
2. Frontal plane axis.
3.  
4. Horizontal plane axis.

FRONTAL PLANE AXIS :

This can be determined by the frontal plane hexaxial reference system which is formed by the combination of the two triaxial reference system.One is formed by the three standard leads and the other by the three unipolar limb leads.

PASTE DIAGRAM

Derivation of frontal plane QRs axis :

Examine the six frontal plane leads : I, II, III, AVR, AVL & AVF.

Determine the most equiphasic deflection : The axis of the lead perpendicular to this lead will be QRS axis.

PASTE DIAGRAM

Eg. : In the above ECG tracing,

Equiphasic deflection is seen in head I and AVF is 1 to axis of lead I.

Hence, axis of QRS is the axis of AVF which is +90 Deg. And can be confirmed visually by maximum positive deflection.

HORIZONTAL PLANE AXIS :

This is reflected in the precordial leads. The transition zone is the zone when there is a change from rs pattern in right oriented leads and qR pattern in the left oriented leads to ‘RS’ pattern. This is commonly seen in leads V3 and V4. Clockwise rotation is said to be present when the transition zone shifts to V4 – V6.

Counter clockwise rotation is said to be present when transition zone shifts to V1 – V3.

PASTE DIAGRAM

A NORMAL 12 LEADED ECG WITH THE VARIDEFLECTIONS IN DIFFERENT LEADS IS SHOWN AGAINST WHICH WE STUDY THE ABNORMAL.

Disorders which may be dianosed and significant information obtained by ECG tracing are as follows :

PASTE DIAGRAM

- Cardiac heart disease.

- Disorder of impulse condution.

- Drug and electrolytes : effects on ECG.

CARDIC ENLARGEMENT /HYPERTROPHY :

RIGHT ATRIAL HYPERTROPHY :

- The right atrial component of the P wave is increased both in amplitude and duration (amplitude > 2.5 mm). This is best seen in lead II where it is peaked.

- The initial deflection of the P wave in V1 becomes taller, more pointed and is usually

- Cardiac enlargement /hypertrophy

- Ischaemic heart disease.

- Disorder of impulse formation.

- Disorder of impulse conduction.

- Drug and electrolytes - effects on ECG.

CARDIAC ENLARGEMENT /HYPERTROPHY :

Dominantly positive with a relatively small negative component.

• •  
  • In atrial enlargement due to acquired heart disease, there will be tall ‘P waves with right axis deviation of the ‘P’ wave known as ‘P’ PULMONALE.

• •  
  • In right atrial enlargement usually due to congenital heart disease, tall and peaked ‘P’ wave with left axis deviation of the ‘P’ wave is present known as ‘P’ CONGENITALE.

PASTE DIAGRAM

The above ECG shows tall ‘P’ in II, III, AVF and indicating right atrial abnormality.

LEFT ATRIAL HYPERTROPHY :

• •  
  • The left atrial component is prolonged due to delay of the terminal part of ‘P’ wave as shown, results in double peaked notched and broad ‘P’ wave > 0.125 sec.

PASTE DIAGRAM

• • Since, the left atrial component is prolonged and increased in magnitude and directed more posteriorly, in lead V1, negative terminal is relatively deep, delayed and widened.

-Left axis deviation usually present and the ‘P’ wave is directed to +45 Deg. To –30 Deg. On the frontal plane.

PASTE DIAGRAM

• • Broad, notced ‘P’ waves best seen in leads 11, AVF and V2 – V5.

• • Terminal negative deflection prominent in V1.

This patient had mitral stenosis.

COMBINED RIGHT AND LEFT ATRIAL HYPERTROPHY :

This may manifest as :

- Frontal plane leads may reflect a ‘P’ wave shich is wide and notched and in addition increased in amplitude.

- Lead V1 may reflect ‘P’ wave whose initial component is taller and peaked and further associated with terminal deep, wide and delayed component.

1.  
2. Eg. This is (as shown) a case of mitral stenosis with tricuspid regurgitation having left and right atrial enlargement and right ventricular hypertrophy.

PASTE DIAGRAM

• • Wide, notched tall ‘P’ wave in I, II, AVL.

• • Bizarre, biphasic ‘P’ in V1.

RIGHT VENTRICULAR HYPERTROPHY :

This may result from

1.  
2. COAD

1.  
2. Pulmonary : Hypertrophy (pulmonary embolism, primary pillmonary hypertension, mitral stenosis, mitral stenosis, mitral regurgitation).
3.  
4. Tricuspid regurgitation.
5.  
6. ASD

• •  
  • Right axis deviation : The mean frontal axis QRS deviates to the right. It is usually an expression of right free wall hypertrophy.

• •  
  • Clockwise rotation of the heart : There is a shift of transition zone to V5 – V6.

• •  
  • Dominance of R wave : This becomes increasingly more deminant in the right oriented leads and there is progressively diminution of the S wave.

• •  
  • There may be a small initial slur of QRS complex and may take form of relatively thick and slow inscribed deflection resulting in v"R" deflection.

• •  
  • There is increase in VAT (i.e. > 0.02 sec).

• •  
  • Left oriented leads (V5/V6/AVL) there is an expression of a diminishing R wave and increase of S wave reflecting the increasing dominance of the right oriented leads.

• •  
  • T wave will be directed away from the right and T wave inversion will be seen in right oriented leads V1 – V4.

• •  
  • U wave may become diminished in amplitude or even inverted in right precordic leads and in II, III, AVF.

ECG CRITERIA FOR RVH :

1.  
2. R Wave > S wave in V1 (R:S > 1.0)
3.  
4. qR pattern in V1.
5.  
6. VAT > 0.03 sec. In V1.
7.  
8. Persistant S in V5/V6.
9.  
10. ST segment depression and T wave inversion.

Eg :

PASTE DIAGRAM

LEFT VENTRICULAR HYPERTROPHY :

This occurs as a result of two basic haemodynamic abnormalities, systolic overload or pressure overload occurs as a result of aortic stenosis, systemic hypertension, hyper trophic cardiomyopathy, co-arctation of aorta, stenosis. Diastolic overload or volume overload occur in aortic regurgitation, mitral regurgitation, PDA.

- In early stages, it is normally directed, but in long standing cases, particularly in systemic hypertension, QRS frontal axis may deviate to the left between 0 Deg. To – 30 Deg. Or more may be due to LAHB.

- Counter clockwise rotation of the heart : This usually occurs in horizontal plane so that the transition zone may occur in V2 – V3.

- Increased magnitude of QRS complex : There is a deep ‘S’ wave in right oriented leads and a tall ‘R’ wave produced due to systolic overload.

- Normally R in V5 is taller than V6. If R wave in lead V6 > V5 is taller than V6. If R wave in lead V6 > V5, it constitutes a corroborative sign of left ventricular hyper trophy.

- Increase in VAT : This exceeds 0.04 sec. In left oriented leads (normal – 0.04 Sec.) and it is the time taken for the impulse to traverse the thickness of the ventricular was it is increased.

- Y wave is usually directed away from the compromised region and with left ventricular pressure overload. It is generally under strain Y wave will be consequently inverted in left oriented leads in V5, V6.

- Compromised left ventricle may result in inverted V Wave and this is a sensitive sign of impaired left ventricle.

ECG Criteria for LVH :

1.  
2. R wave in V5 / V6 > 27mm.
3. S in V1 + R in V5/V6 > 35 mm.
4. VAT > 0.05 sec.in V5/V6.
5.  
6. QRS interval may be prolonged > 0.15 sec.
7.  
8. ST segment depression and T wave inversion in V5/V6.
9.  
10. R wave in AVL > 11 mm. (Horizontal heart)

> 20 mm. (Vertical heart)

PASTE DIAGRAM

BIVENTRICULAR HYPERTROPHY :

This should be suspected when there is

1. ECG presentation of LVH with right axis deviation.
2. ECG presentation of LVH with clockwise electrical rotation and shift of transition zone to the left.
3. ECG will tall ‘R’ in V1. Manifested as

- Tall R wave in right precordial leads.

- Equiphasic QRS in mid precordial leads.

- Mean QRS frontal plane axis is +105 Deg. (to the right)

- SV1 + RV5 is 39mm. (combination of right axis deviation + LVH)

- Biventricular hypertrophy.

ISCHAEMIC HEART DISEASE :

MYOCARDIAL ISCHAEMIA :

Myocardial ischaemia occurs when coronary artery blood flow is insufficient to meet myocardial metablic requirements. Since the underlying process is transient, so are the ECG features.

CELLULAR BASIS

A. Injury current at rest : An electrode overlying the injured muscle will record a depression relative to the baseline as the injured tissue is electrically negative than normal muscle tissue. Any electrode over the Injured area is relatively positive as there is a constant flow of current from uninjured to injured area.

PASTE DIAGRAM

1. On stimulating overlying electrode records a positive deflection and the opposite electrode a negative deflection.

C. When there ceases to be a potential difference, the deflections return to the baseline.

D. When the muscle returns to the resting state, the deflection recorded return to their original position.

This is a practical rule, an ECG tracing recorded directly over injured muscle records ST segment elevation. If a normal muscle is present between electrode and injured muscle, ST depression results.

ECG PATTTERNS RESULTING FROM MYOCARDIAL ISCHAMIC :

1. Abnormalities of ST segment :

1. 1. Depression of ST segment : This may take one of the forms which in order of severity are :-

• • Horizontality of ST segment :

• •  
  • Upward slopping ST depression :

• •  
  • Plane ST segment depression :

• •  
  • Downslopping ST segment depression.

1. 1.  
   2. ELEVATION OF ST SEGMENT : This is usually the expression of transmural myocardial injury dominantly epicardial region and also seen in reciprocal leads with areas of sub-endocardial injury.

1. 1.  
   2. Reciprocal lead which shows depression.
   3.  
   4. Additional area sub-endocardial ischaemia

2. Abnormalities of T wave : The T wave vector points away from an area of ischaemia and towards an area of normal myocardium. The cause is not known but may be due to leakage of intracellular K+ from cells and producing local hyperkalaemia.

The normal T wave is asymmetrical. T wave associated with coronary insufficiency are symmetrical with sharp-pointed,arrow head vertex or Nadir. T wave inversion and low T waves are also signs of coronary insufficiency.

If following exercise T in V4 is > 5 mm. Than normal resting values, coronary insufficiency should be suspected.

3. Abnormalities of ‘V’wave :

Normally it is in the direction of the T wave. Inverted "V’ wave is diagnostic of cardiac disease especially coronary artery and of hypertensive origin. If it developed after exercise it indicates ischaemina.

Eg :

PASTE DIAGRAM

MYOCARDIAL INFARCTION :

This occurs when insufficient coronary artery blood flow occurs over a critical length of time. This may result from atherosclerotic after exercise it indicates ischaemia.

Eg :

PASTE DIAGRAM

• • ST elevation most prominent in V2-5 indicating transmural myocardial ischaemia observation or thrombotic /embolic occlusion of the crornary artery.

Serial ECG and clinical correlation are mandatory in making the correct diagnosis. Additionally ECG distinction between transmural and non-transmural infarct based on ECG is misleading. This occurs in three phases.

1. The hyperacute phases.
2. The fully evolved phases.
3. The chronic stabilised phase.

The fully evolved phase.

TRANSMURAL MYOCARDIAL INFARCTION :

The following figure represents an idealised presentation of the fully evolved phase of acute myocardial infarction.

The myocardial nerosis is represented by a "QS" complex.

PASTE DIAGRAM

Myocardial injury by elevated ST segment and myocardial ischaemia by inverted, symmetrical pointed T wave.

The QS complex : This is a totally negative QRS complex with no positively. Necrotic tissue is electrically inert and cannot be activated or depolarised. Thus an electrode oriented towards this necrotic muscle will reflect the resultant rector of the septal wall and then the free wall of the other ventride and hence will result in a negative deflection a ‘QS’ complex.

This also applies to any inert region of myocardial tissue eg. Large compact region of fibrosis, an end result of myocardial infarction or a ventricular aneurysm.

PASTE DIAGRAM

The most diagnostic ECG finding is therefore an abnormally wide (0.04 sec) and deep Q wave (25%) of the height of ‘R’ wave.

Small non-pathogenic ‘q’ wave :

Commonly recorded in leads, I AVF and V4=V6 and represents left right depolarisation of the interventricular septum. This should non exceed 0.03 sec. Or 25% of the height of ‘R’ wave.

PASTE DIAGRAM

‘QS’ complexes evident V2-V4.

DEVIATION OF ST SEGMENT : Myocardial injury is reflected by deviation of ST segment. If the injury is dominantly epicardial ST segment will be raised as seen in lead oriented towards this surface and leads placed in approximately 180 Deg. And oriented to the uninjured surface will reflect ST depression.

PASTE DIAGRAM

In dominant sub-endocardial injury the opposite will occur.

‘T’ WAVE INVERSION : This reflects myocardial ischaemia. Leads oriented to the ischaemic region will have inverted. Symmetrical and pointed T waves because it always points away from ischaemic area.

NON-TRANSMURAL MYOCARDIAL INFARCTION :

This is depicted in an ECG as :

1.  
2. The loss of ‘R’ wave amplitude: This occurs generally in leads which are oriented towards the periphery of the infarction.
3. PASTE DIAGRAM

   The QRS vector are dimenished in magnitude by a sub endocardial or subepicardialrinds of necrosis, but are still of sufficient magnitude to counter-modify or balance the QRS vector directed away from the rector.

4. ‘Qr’ complex : Deep wide pathological Q wave followed by a relatively small ‘r’ wave. This also occurs in endocardial or epicardial rinds of necrosis away from the periphery of infarction and may result from a significant loss of unilateral QRS forces as reflected by ‘Q’ wave.

THE HYPERACUTE PHASE :

Thie occurs before the fully evolved phase. This is frequently ignored or not recognised.

1.  
2. Increase in V.A.T.
3. This is the time from the beginning of QRS complex to R wave and this delayed beyond 0.45 sec. and may reach values of 0.6 seconds.
4. Increased amplitude of ‘R’ wave :
5. The acutely injured tissue is not yet necrosed and therefore is still able to conduct the electrical activation but slowly.
6. Tall and widened T wave :

This stage is particularly critical and vulnerable for it is during this phase that the complication of primary ventricular fibrillation is must likely to occur.

THE CHRONIC STABILISED PHASE :

There is gradual resolution of the abnormalties and hence the acuteness of myocardial ischaemic is not present which is diagnosed primarily by the behaviour of the ST segment and T wave.

LOCALISATION OF MYOCARDIAL INFARCTION :

The ECG features of myocardial infarction may be localised to the following principle region of the left ventricular cone.

1.  
2. Anterior wall : This is oriented towards the precordial leads and the anterolateral surface towards AVL and std lead I and hence THE typical patten are reflected in these leads.

Anterior wall infarctions are further divided into :-

1.  
2. Extensive anterial wall MI :
3. Std. I, AVL and all precordial leads.
4. Anteroseptal wall MI: : Lead V1-V4.
5.  
6. Apical wall MI : Typically appear in V5-6.

PASTE DIAGRAM

‘QS’ waves 1, AVL, V5-V6 (-)

QS Complexes V3 & V4

‘T’ wave inversion ST – 1, AVL, V3-V6.

Inferior wall MI : This wall of left ventricular mass is reflected in II, III, AVF.

The reciprocal changes are reflected in the negative pole I & AVL.

The initial superior and leftwardly directed QRS obliterate the normal, small initial ‘q’ wave in this lead. This is a corroborative sign of inferior wall infarction.

PASTE DIAGRAM

• • Q wves III, II, AVF.
  • Reciprocal changes I, AVL.

3. Posterior wall MI : No conventional electrode is oriented directly be diagnosed by the inverse or mirror image changes reflected by the electrode oriented to the uninjured anterior myocardial wall. This can be depicted as follows :

The right precordial leads V1-V3 esp. V2 oriented to the anterior wall reflect the inverse changes.

PASTE DIAGRAM

- Mirror image of QS complex – reflected by tall and widened ‘R’ wave.

- Elevated ST segment reflected as concave upward ST segment.

- Upright tall and widened T waves is essentially the diagnosis of posterior wall infarction.

PASTE DIAGRAM

• • Tall ‘T’ waves in V1-3 esp V2.
  • Tall widendd ‘R’ in V2.

PASTE DIAGRAM

‘Q’ waves - II, III, AVF

LVH – Deep ‘s’ in V1-4.

DISORDERS OF CARDIAC RHYTHM :

Rate and rhythm of the heart is controlled by the SA node. The heart has many other potential pacemakers. AV node, Bundle of His, atria and ventride. This is the property of automaticity in which spontaneous depolarisation occurs. The SA node has the fastest inherent discharge rate, usually ranging from 79-80 min whereas the AV node 60/min, Bundle of His – 50/Min. The inherent rate of purkinje cells of ventricular mass is about 30-40 /min. Normally the SA node serves as the pacemaker for the heart. If this should fail, the slower subsidiary pacemaker cells will take over the function of pacemaker.

The sinus impulse leaves the SA node and spreads through the atrial muscle and represented graphically by the steep slope. This eventually reaches the AV node where it is slightly delayed reflected by a gradual slope. Impulse is finally conducted relatively quickly down the bundle of this, Bundle branches and purkinje network system reflected by a steep slope.

Disorders of cardiac rhythm may be categorised.

1.  
2. Disorders of impulse formation.
3.  
4. Disorders of impulse condition.

DISORDERS OF IMPULSE FORMATION :

Sinus Rhythm :

* Normal sinus rhythm : This is reflected by normal ‘P’ wave followed by sequential inscriptionof QRS-T at a rate which ranges between 60-100 min. as shown.

• •  
  • Sinus arrhythmia : This is caused by alternating period of slow and fast rate, is normally associated with respiration with faster rates towards end of inspiration and slower rate at end of expiration. This is a normal physiological phenomenon and most marked in young persons.

• •  
  • Sinus tachycardia : This occurs when the SA node discharges faster than 100/min in an adult. This is characterised by normal P-QRS-T complex recorded in rapid succession. It is a normal physiological phenomenon to exercise and emoition and physiological status like toxaemia, thyrotoxicosis and cardiac failure.

• • Sinus bradycardia : This results when the SA node discharges at a rate slower than 60/min. and again characterised by normal P-QRS-T complexes. This is a normal phenomenon in athletes and physiological response to sleep. It is also associated with myxoedema, obstructive jaundice, uraemia, glaucoma, B-blocking agents.

Atrial extrasystole : This is due to a premature discharge of the atrial ectopic focus. The discharge occurs from a point other than the SA node and since they pass through atria by unusual pathways, this results in an abnormal bizarre P wave different from sinus P wave. This may be pointed, notched, biphasic or inverted.

This ectopic ‘P’ wave raches SA node discharging it prematurely i.e.before, next, anticipated ‘P’ wave. This premature impulse may or may not be conducted through the AV node depending on the recovery state of the AV node. Thus, the abnormal ‘P’ wave may or may not be followed by QRS complex.

Again, if the impulse reaches when only one BB has recovered will result in bundle branch block.

Wandering atrial pacemaker : Here some atrial impulse originate in the sinus node and others in varius portions of the atria which is seen as multiple ‘p’ waves contours. There is variability in atrial rate and PR interval.

• •  
  • Paroxysmal atrial tachy-cardia : This is due to rapid discharge of an ectopic atrial focus which results in an abnormally shaped ‘P’ wave. AV conduction may be normal leading to normal PR or shorter leading to short PR.

•  
• Depending on the recovery of the AV node, there may be a 1 Deg. Or a 2 2 Deg. AV block or a fluctuating ratio in the degree of AV block known as PAT with block.

•  
• Intraventricular conduction may or may not be normal depending on the recovery of the system.

•  
• ‘P’ – bizarr
•  
• Atrial rate – 250.
•  
• AV Block 3:1 and 2:1.

•  
• MULTIFOCAL ATRIAL TACHY-CARDIA : This is atrial arrhythmias characterized by varying ‘P’ wave coatours reflecting different foci of origin and variable PP and PR interval. This is same as wandering pacemaker but its rate are usually fast i.e. > 100/min. and generally 150-180/min.

•  
• ‘P’ wave contours differ.

•  
• PP and PR are different giving rise to irregular ventricular rhythm.

ATRIAL FLUTTER : This is the expression of rapid and regular atrial excitation. This may result from.

1.  
2. Circus movement : self prepetuating circular path of excitation.
3.  
4. Rapid discharge from ectopic foci.

The ventricular response depends on the efficacy of the AV conduction.

The atrial waves of atrial flutter are classically saw-toothed in appearance.

Type I flutter waves : The rate are between 250-300/min.

Type II flutter waves : The occurs at a faster atrial rate i.e. between 350-430/min. It is more regular than fibrillation and the baselines does not undulate.

Atrial fibrillation : The excitaiton and recovery of the atria are disorganised and chaotic and may range from 400-600/min. The ‘f’ waves are irregular, chaotic, resulting in a ragged baseline. The ventricular response depends on the integrity of AV conduction.

This is generally found in :

1.  
2. Coronary artery disease.
3.  
4. Mitral and tricuspid valvular disease leading to atrial enlargement.
5.  
6. Hyperthyriodism.
7.  
8. Constrictive pericarditis.

ATRIOVENTRICULAR NODAL RHYTHM or JUNCTIONAL RHYTHM :

When the focus arises in the AV node, the impulse is conducted to atria and ventricle concommitantly. Atrial depolarisation is reversed and hence results in an inverted ‘P’ wave best seen in II, III and AVF. It also proceeds along the normal A-V conduction pathway and results in a near normal QRS-T complex.

AV nodal extrasjstole :

1. If retrograde conduction of the atria is faster than anterograde conduction, P will preceds QRS but PT interval will be short.
2. If antegrade conduction is faster than retrograde conduction then P follows QRS :
3. If antegrade conduction and retrograde conduction occurs at the same time, P wave will be hidden in the QRS complex.
4. Retrograde conduction may be blocked by a concommitant sinus impulse.

That retrograde impulse blocked since

Paroxysmal AV nodal tachycardia : This is succession of thru or more AV node extrasystole. Sometimes a sinus impulse canfind the AV node in a momentarily non refractory phase and the sinus impulse is conducted to the ventricle and help revert back to normal and identical in both tachycard and sinus rhythm as seen in the ECG.

Idionodal tachycardia : This is accelerated inherent idionodal rhythm.

VENTRICULAR RHYTHMS :

Ventricular extrasystole : This is due to premat discharge of an ectopic focus in the ventric. The beat arises in the diastolic period of the preceding sinus beat and hence receive earlier than the next anticipated sinus beat since the impulse does not travel through the normal pathway, the QRS complex is bizarreividened, slurred, nothed. ST segment is depressed if the QRS is dominantly upwards and T wave.

Ventricular extrasystole can manifest at the same time as the ‘P’ wave and hence ‘P’ wave will be hiddened by bizarre QRS.

Ventricular extrasystole may manifest just before the following sinus discharge and hence ‘P’ wave will be recorded later.

The discharge of the SA node is not interfered with and hence protected from the ectopic impulse. The next sinus impulse occurs as schedule and the pause following is thus complete.

Interpolated ventricular Extrasystole : This is ventriculated extrasystole sanditched between two conducted sinus beat. Ventricular extra systole occurs early when AV are in a refractory period and normal sinus beat occurs on time but owing to ectopic impulse. AV node is still partially refractory and hence sinus beat conducted with some delay resulting in an increased PR interval.

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• Does not disturb sinus rate

Extrasystolic ventricular bigeminy : This is alternate ventricular extrasystole i.e. which occurs after every other sinus beat.

Ventricular trigeminy : When every 2 sinus beat is followed by a ventricular extrasystole.

Ventricular quadrigeminy : When every 3 sinus beats is followed by a ventricular extrasystole.

Multifocal multiform ventricular extrasystole : This occurs from different foci and consequently give rise to different QRS forms.

Extrasystoles in pairs : When a ventricular ectopic focus discharges prematurely and turce in succession, a pair of extrasystole follows a normal sinus beat.

This may occur occasionally but should be viewed with suspicion. Ventricular extrasystole is always associated with myocardial infarction. Therefore, frequent ventricular extrasystole especially these occurring in pairs often herala ventricular tachycardia or ventricular fibrillation.

Ventricular extrasystole with very short coupling interval – R on T phenomenon.

Ventricular extrasystole may occur with a short coupling interval and will consequently coincide with and be superimposed upon, or near the apex or distal limb of the preceding T wave. They are thus likely to occur during the vulnerable phase of the recovering myocarduim and will consequently precipitate ventricular flutter and ventricular fibrillation.

Ventricular tachycardia : This is due to rapid discharge of ventricular pacemaking focus or due to re-entry phenomenon.

Paroxysmal ventricular tachycardia : This a series of three or more consecutive ventricular extrasystoles. The QRS complexes are bizarre, prenature and occur in rapid succession.

The ectopic ventricular rhythm and sinus rhythm may be disociated and they meet at AV node and impede each others mutive progress. Therefore, P waves have no relationship to QRS complex. The ectopic impulse may progress retrogradely then QRS may followed by retrograde P waves.

Ventricular and atrial systole may together with sufficient time for ventricular filling will lead to stroke volume falling rapidly and hence cerebral hupoperfusion.

Idioventricular tachycardia : An inherent idio ventricular rhythm may be accelerated resulting in idioventricular tachycardia.

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• Bizarre QRS show ventricular origin with a relatively rapid rate i.e. about 70-80/min.

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• Capture beats both complete and incomplete may be present.

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• There is absence of pacemaker protection i.e. ectopic rhythm is abolished if sinus rhythm regains its dominance.

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• This is generally associated with fever and acute corditis and this rhythm rarely requires treatment as it rarely causes haemodynamic embarrassment.

Ventricular flutter : A very rapid and regular ectopic ventricular discharge and grossly abnormal intraventricular conduction.

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• QRS-T is very wide and difficult to define or separate.

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• Paroxysmal ventricular tachycardia and ventricular flutter are expression of the same mechanism and change of paroxysmal ventricular tachycardia to flutter is associated with fall in blood pressure and cardiac output.

Torsades-de-pointes : When ventricular flutter present as multiform bizarre QRS complexed which appear to undulate around an isoelectric baseline is known as torsades-de-pointes.

Ventricular fibrillation : This is the expression of chaotic un-coordinated ventricular depolarization. The haemodynamic pumping action of the heart therefore ceases and death ensures within minutes if defibrillation is not instituted.

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• This is frequently associated with myocardial infarction and may accompany quinidine and digitalis toxicity (secondary to hypokalaemia)

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• The source may be ventricular extrasystoles esp. which coincides with T wave i.e. R-on-T phenomenon.

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• Very rapid ventricular rate may also predispose to ventricular fibrillation.

PARASYSTOLE : It is an abnormal rhythm in which two or more pacemakers discharge independently. Normally, the dominant or fastest pacemaker determines the heart rate i.e. S.A. node. The parasystole pacemaker may be situated in the atria, AV node or ventride (most commonly). The impulses from the faster S.A. node pacemaker cannot penetrate this focus which as a result may discharge at its own inherent rate, unusually slower rate, unhindered i.e. 20-100/min. Thus, it abnormal intraventricular conduction dischargers activating the myocardium when it finds it in a responsive state.

ESCAPE RHYTHMS :

When the SA node with highest automaticity fails to discharge, spontaneous discharge from slower subsidiary pacemaker occurs which is an escape beat. If the pacemaker is able to discharge tw