ECG Presenter - Dr. Srinivas

sidda. Moderator - Dr.Nagrale (prof

& Hod).

ISCHEMIC HEART DISEASE

• The Electrocardiogram is a helpful investigation in the assessment of ischemic heart disease,though limited in its scope of giving information,as it can be Deceptively normal even in presence of significant disease.

• However,because it is a safe,non-invase and inexpensive bed-side tool, it is considered essential and routine in the assessment of ischemic heart disease.

• In certain conditions,it can strongly indicate or even confirm a diagnosis as in acute myocardial infarction , severe ischemia .

Ecg manifestations of Ischemic heart disease

• Ischemia can manifest in 3 ways- ischemia, injury and infarction.

• Ischemia is always reversible .

• Infarction always irreversible.

• Injury is potentially reversible depending on the condition and type of intervention.

• There is good correlation between clinical, electrocardiographic and pathological features of these three stages of ischemia.

• Ischemia : usually manifests in the Ecg as depression of ST segment and /or inversion of the T wave.

• The ST segment can be horizontal, down -going or up-going from the J point ( the point marking the end of the

QRS complex and the beginning of the ST segment ).

• The horizontal and down-going ST segments are relatively more specific for ischemia than up-going ones.

• Injury : The next severe degree of ischemia, i.e. injury, manifests in the ECG as an elevation as ST segment ( especially coving in type with an upward convexity ).

• The patient may have unstable angina or pre-infarction angina with these changes in the ECG.

• Many times , the patient gets these ST segment changes with an impending or on-going infarction and therefore, one has to

be very careful in making a diagnosis.

• Infarction. When myocardial injury persists, MI is the result.

• During the earliest stage of MI, known as the hyperacute phase, the T waves become tall and narrow. This configuration is referred to as hyperacute or peaked T waves.

• Within a few hours, these hyperacute T waves invert.• Next, the ST segments elevate, a pattern that usually lasts from several hours

to several days. • In addition to the ST segment elevations in the leads of the ECG facing the

injured heart, the leads facing away from the injured area may show ST segment depression.

• This finding is known as reciprocal ST segment changes. • Reciprocal changes are most likely to be seen at the onset of infarction, but

their presence on the ECG does not last long.• Reciprocal ST segment depressions may simply be a mirror image of the ST

segment elevations.

• However, others have suggested that reciprocal changes may reflect ischemia due to narrowing of another coronary artery in other areas of the heart.

• The last stage in the ECG evolution of an MI is the development of Q waves, the initial downward deflection of the QRS complex.

• Q waves represent the flow of electrical forces toward the septum. Small, narrow Q waves may be seen in the normal ECG in leads I, II, III, aVR, aVL, V5, and V6.

• Q waves compatible with an MI are usually 0.04 second (one small box) or more in width or one-fourth to one-third the height of the R wave.

• Q waves indicative of infarction usually develop within several hours of the onset of the infarction, but in some patients may not appear until 24 to 48 hours after the infarction.

• Within a few days after the MI, the elevated ST segments return to baseline.

• Persistent elevation of the ST segment• may indicate the presence of a ventricular aneurysm.• The T waves may remain inverted for several weeks,

indicating areas of ischemia near the infarct region. • Eventually, the T waves should return to their upright

configuration.• The Q waves do not disappear and therefore always provide

ECG evidence of a previous MI.

• Infarction : The ECG manifestation of infarction is usually a Pathological Q wave > 0.04 seconds, i.e. 1mm wide or > 1/4 the size of followoing R wave .

• Associated with ST-T changes of injury.

• The diagnosis of MI is usually based on the diagnostic triad - history and clinical findings,ECG features and raised cardiac enzymes rather than any one parameter alone.

• Thus, one should avoid making a diagnosis of MI based only on one parameter unless it is absolutely classical.

• The Evolution of an infarct: The ECG pattern in myocardial infarction undergoes serial changes as time passes from hours to days to weeks to months.This is called evolution of infarct.

• It is therefore, obvious that serial ECGs are very important in the evaluation of the stage or the age of infarct.

• It is also clinically and prognostically important to the know the age of the infarct as the risk of the mortality and complications reduce with the passage of time.

The site of the Infarct

• It is important to diagnose the site of the infarct from the ECG.

• Most infarctions occur in the left ventricular, approximately 20% to 25% being in the atria and/or the right ventricular.

• Broadly, the sites of infarction are divided into three

• Anterior

• Inferior

• Posterior

Precordial Leads

Precordial Leads

Arrangement of Leads on the ECG

Anatomic Groups ( septum )

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

• Anterior Infarcts: The leads that reflect an anterior wall infarction are usually the precordial leads - L1 and aVL.

• Anterior infarcts being quite common and covering an extensive area, are further sub divided into

• Anteroseptal

• Anterolateral

• Extensive Anterior infarcts

• Anteroseptal Myocardial infarction is diagonsed when changes are confined to leads V1 to V4.

• Anterolateral when the pattern of infarction is confined to leads V5 and V6.

• Extensive Anterior infarcts when all the chest leads show the changes.

• In all anterior infarctions these changes may manifest in leads L1 and aVL as well.

• Inferior Infarcts: The leads that reflect inferior wall or diaphragmatic infarction are L II, L III and aVF.

• Posterior Infarcts: The diagonsis of posterior wall mycardial infarction is sometimes difficult from the ECG.

• It may be associated with inferior wall myocardial infarction manifesting only as reciprocal changes i.e. ST-T changes opposite in direction to the changes seen in the area of infarction in the anterior leads - V1 to V4.

• For example:- If there are changes of inferior wall myocardial infarctions in leads L II, L III & aVF and in additional to these changes, there are opposite ST-T chnages in V1 to V4, it usually indicates posterior wall myocardial infarction.

• Posterior wall MI is uncommon and best diagonsed by esophageal ECG.

ATRIAL ENLARGEMENT

• Enlargement of the Right ,Left or both Atria can be determined from the P waves - leads II, V1 and V2.

• If the height of the tallest P wave is more than 2.5mm - it indiactes Right Atrial Enlargement.

• If the width of the broadest P wave is more than 2.5mm - it indicates Left Atrial Enlargement.

• Left Atrial Enlargement may be associated with bifid P wave where the first peak -Right atrial activity and the delayed seocnd peak-left atrial activity.

• If the P wave exceeds the stipulated values in both height and width , it indicates Biatrial Enlargement.

• In addition to the above criteria, the P wave in Leads V1-2 should be also considered while making a diagnosis of Atrial enlargement.

• P waves are biphasic in Leads V1-2.

• If the first, positive phase of P is more than 1.5mm in V1-2, indicates Right Atrial Enlargement.

• If the second, negative phase of the P wave is greater than 1.5mm in depth or more than 0.06 seconds wide, indicates Left Atrial Enlargement.

Right atrial enlargement – To diagnose RAE you can use the following criteria:

• II P > 2.5 mm, or• V1 or V2 P > 1.5 mm

Notched

Negative deflection

Notched

Negative deflection

Left atrial enlargement – To diagnose LAE you can use the following criteria:

• II > 0.04 s (1 box) between notched peaks, or

• V1 Neg. deflection > 1 box wide x 1 box deep

VENTRICULAR ENLARGEMENT

• The ECG diagnosis of ventricular enlargement is primarily based on voltage criteria which take into consideration the amplitudes of R and S waves in the chest leads.

• However, it must be emphasised here that the voltage criteria are not entirely reliable and there are the many false positive and negative results in diagnosis based soley on these grounds.

• Therefore ,various other criteria are also recommended to determine ventricular enlargement.The scoring system takes many factors into consideration and is, therefore, more time consuming and cumbersome,though more reliable and specific than voltage criteria taken in isolation.

• Estes’ scoring system for the ECG diagnosis of LVH. • R or S in limb lead = 20 mm or more or

• S in V1, V2 or V3 = 25 mm or more or 3

• R in V4, V5 or V6 = 25 mm or above

• Any ST shift ( without digitalis ) 3

• Typical “strain “ ST-T ( with digitalis ) 1

• LAD of -15 degree or more 2

• QRs interval 0.09 seconds or more 1

• Intrinsicoid deflection in V5-6 = 0.04 seconds or more 1

• P-terminal force in V1 more than 0.04 3

• Total = 13

• LVH if the score is 5 or more & probable LVH if score is 4.

LEFT VENTRICULAR HYPERTROPHY• Left Ventricular Hypertrophy - This is also determined from the voltage

of the QRS complex in V1-2 and V5-6.

• LVH criteria :

• RV 5-6 > 25mm

• SV1-2 > 20mm

• RV5-6 + SV1-2 >35mm.

• There crieteria apply only to ECG of adults and may not be entirely reliable.

• There is another conept of Pressure versus Volume overload of the ventricles , volume overload of the ventricles are depicted in the ECG by tall R waves in the respective leads.

• The tall R waves are associated with tall, positive T waves, sometimes with elevation of the ST segment.

• On the other hand, a pressure loaded ventricle is manifest in the ECG as not-so-tall R waves with deression of ST segment and inversion of the T wave.

• volume and pressure overloads of ventricle are also termed diastolic and systolic overloads or alternatively, eccentric and concentric hyertrophy respectively .

• This concept, orignally developed by Cabera and Monroy,is not reliable in all cases

There is left axis deviation (positive in I, negative in II) and there are tall R waves in V5, V6 and deep S waves in V1, V2.

The deep S waves seen in the leads over the right ventricle are created because the heart is depolarizing left, superior and posterior (away from leads V1, V2).

Left ventricular hypertrophy– To diagnose LVH you can use the following criteria*:

• R in V5 (or V6) + S in V1 (or V2) > 35 mm, or• avL R > 13 mm

A common cause of LVH is hypertension.

RIGHT VENTRICULAR HYPERTROPHY• Right Ventricular Hypertrophy - This condition is diagnosed from tall R waves in V1-2

implying dominant right ventricular activity.

• The corresponding S waves in V5-6 are deeper than 5mm.

• It should be remembered here that from each pair of leads the taller or deeper wave is taken into consideration.

• For example, if the R in V2 is 20mm tall and is taller than the R in V1, then RV2 has to be considered,

• similarly,if the S in V6 is 7mm deep and is deeper than the S in V5, then SV6 should be taken into consideration.Hence ,Voltage criteria for the diagnosis of right ventricular hypertrophy are;

• RV 1-2 > SV1-2

• SV5-6 > 5mm.

• A common cause of RVH is left heart failure.

Right ventricular hypertrophy – To diagnose RVH you can use the following criteria:

• Right axis deviation, and• V1 R wave > 7mm tall

Right ventricular hypertrophyCompare the R waves in V1, V2 from a normal ECG and one from a person with

RVH.Notice the R wave is normally small in V1, V2 because the right ventricle does not

have a lot of muscle mass.But in the hypertrophied right ventricle the R wave is tall in V1, V2.

•

• Summary -1. Atrial Enlargement can be diagnosed from the magnitude of P

wave in leads II, V1 and V2.

2. Right atrial enlargement shows tall P waves > 2.5mm and left atrial enlargement broad P waves >0.10 sec, while bilateral enlargement is diagnosed when the P waves are both tall and broad.

3. Right Ventricular hypertrophy is diagnosed if R/S > 1 in V1, V2 or SV5-6 is deeper than 5mm.

4. Left Ventricular hypertrophy is diagnosed if SV1-2 is deeper than 20mm or RV5-6 taller than 25mm or RV5+6 + SV1-2 > 35mm.

5. Depending on the height of the R wvaes and the presence or absence of associated ST-T changes in the respective chest leads, a diagnosis of pressure ( systolic )or Volume ( diagnostic ) overload of the ventricles can be made.

Atrial septal defect

1. RBBB in 90% of cases.

2. P-congenitale in a few cases.

3. Right Atrial and Right Ventricular Hypertrophy.

4. In Ostium secondum defect there may be Right Axis Deviation , rSR’ pattern in right precordial leads and occassionaly First degree AV block.

5. In Ostium primum defect there may be Left Axis Deviation.

Ventricular septal defect

• The ECG pattern in VSD depends to a great extent on the size of the defect and the presence & degree of pulmonary hypertension.

• While small VSD may not show any ECG abnormality at all, moderate VSDs show evidence of Left Ventricular volume overload,with tall R and T waves in precordial Leads V5-6. There may also be Wide ‘P’ waves indicating Left Atrial Enlargement.

• Large VSDs show the characteristic ECG pattern of Biventricular hypertrophy, the Katz-Wachtel phenomenon, with equiphasic tall R and deep S waves in three or more consecutive precordial leads V1-3 , V2-5.

• The characteristic ECG patterns of these shunt lesions often disappear with the onset of Pulmonary Hypertension, which manifests as tall P waves, tall R waves in V 1-2, deep S waves in V 5-6 and a Rightward shift of axis , due to right atrial enlargement and right ventricular hypertrophy.

• Prominent Q waves in Leads II,III,aVF.

• High voltage equiphasic QRS complexes in Leads V3 and V4.

• Evidence of LVH , combined Ventricular hypertrophy or RVH.

• RBBB pattern in 20-30 % cases.

Ventricular septal defect

–Johnny Appleseed

“Type a quote here.”

Tetralogy of Fallot

• This is the most common cyanotic heart disease above the age of 4 years.

• Right Axis Deviation.

• Peaked P waves and a tall R in V1 suggestive of Right ventricular hypertrophy and inverted T wave in lead V1.

• P- congenitale.

• The tall R in V1 abruptly changes to a rS pattern in V2 — a feature unique to this condition.

Ebstein’s Anamoly

• In this defect , the ECG features P waves which are tall and wide.

• The PR interval is prolonged ( 1st degree AV block ), but may be apparently normal in the presence of WPW syndrome.

• The QRS complex is typically very wide and “ splintered “ with a pattern suggestive of bizarre right bundle block.

Tricuspid Atresia

• This condition can be reliably diagnosed from ECG in a caynotic child from the following features :

1. Left Axis Deviation.

2. Tall, Peaked P waves signifying Right Atrial Enlargement.

3. Signs of LVH with deep S waves in V1- V2 and tall R waves in V5-V6.

Anomalous origin of the left coronary artery from the pulmonary artery

• An ECG depicting an infarct pattern in a sick infant clinches the diagnosis of this condition.

• Pathological Q waves with characteristic ST-T changes are more pronounced in the lateral leads (I, aVL, V5-V6).

Single Ventricle

• The ECG is a reliable tool though not specifically diagnostic of this condition.

• The QRS axis may have a leftward deviation or be inderminate (The S1 S2 S3 syndrome).

• The charateristic feature is the presence of similar, monotonous, often large QRS complexes in all the precordial leads.

Inverted transposition of the great vessels.

• Left axis deviation, prolonged PR interval and a distinctive Q wave abnormality form the ECG picture in this disorder.

• The Q wave, though normal in amplitude and duration is characteristically absent in the left precordial leads (V5-V6), and is found in the right precordial leads (V1-V2) instead.

• Almost 85% of the patients have some degree of AV block, often of a high degree.

Dextrocardia• True dextrocardia is characterised by a positive aVR, a

negative aVL and absence of R wave progression in the precordial leads, which however can be seen if right precordial leads are placed.

• The ‘P’ wave is negative in lead I and positive in aVR.

• In some instances, dominntly negative QRS complexes in aVL and positive ones in aVR are present with no abnormality in the precordial leads.

• This “Technical Dextrocardia” occurs when the upper limb leads are interchanged, an artefact that should be identified and corrected.

Effect of Drugs and Electrolytes

• Digoxin (DIGITALS)

• Digoxin (Digitals) Effect: A patient receiving digoxin may have changes in his ECG as adequate digitalisation is reached. They do not indicate the need to reduce the dose of digoxin. These changes are:

• ST segment depression (reverse tick)

• QT interval shortening

• T wave size reduction

Effect of Drugs and Electrolytes

• The ST segment is depressed, rounded and concave (scooped). The T wave is dragged downwards giving an appearance of T wave inversion.

• These ST-T changes occuring in leads with a prominent R wave suggest a threapeutic effect. However, if these changes occur in leads with mainly a negative QRS complex, it indicates that the drug is causing relative subendocardial coronay insufficiency and therefore the drug must be stopped.

• The QT interval is shortened due to the shortening of the ventricular systole.

Effect of Drugs and Electrolytes • Digoxin Toxicity: The toxic effects of digitals may be as follows:

• Sinus bradycardia

• Premature beats: Unifocal, multifocal or bigeminy

• Supraventricular arrhythmias: Paroxysmal atrial tachycardia, atrial flutter or atrial fibrillation.

• Ventricular arrhythmias: Ventricular tachycardia, ventricular flutter or ventricular fibrillation.

• SA block, first, second or third degree AV block or bundle branch block.

• Symptoms of digoxin (anorexia, vomiting, abdominal pain, visual disturbances), digoxin levels and hypokalemia should be checked.

Quinidine Toxicity

• SA block

• First, second and third degree AV block

• Bundle branch block

• Ventricular arrhythmias- idioventricular rythm, ventricular premature beats, ventricular tachycardia, ventricular fibrillation and cardiac assytole.

• AV junctional rythm

QUINIDINE

• Quinidine Effect: Quinidine produces ST depression and flattening of the T wave like digitalis, but unlike digitalis there is increased QT interval and the T wave may be notched and widened.

POTASSIUM• Hyperkalemia: ECG changes with gradual rise in potassium are

as follows:

• Peaked, tall and tented T waves (This also occurs in posterior wall myocardial infarction)

• The amplitude of the P wave decreases and finally disappears completely because though the sinoatrial node fires an impulse, the artial myocardium is not activated.

• The amplitude of the R wave decreases and the QRS complex gradually widens and blends with the T waves giving a wide, bizarre, biphasic deflection (sine wave pattern) followed by asystole.

• Severe hyperkalemia can cause cardiac arrest and needs immediate treatment.

• Sreumpotassium > 5.5 mEq/L is associated with repolarization abnormalities:• Peaked T waves (usually the earliest sign of hyperkalaemia)

Serum potassium > 6.5 mEq/L is associated with progressive paralysis of the atria:

• P wave widens and flattens• PR segment lengthens• P waves eventually disappear

Serum potassium > 7.0  mEq/L is associated with conduction abnormalities and bradycardia:

• Prolonged QRS interval with bizarre QRS morphology• High-grade AV block with slow junctional and ventricular escape rhythms• Any kind of conduction block (bundle branch blocks, fascicular blocks)• Sinus bradycardia or slow AF• Development of a sine wave appearance (a pre-terminal rhythm)

Serum potassium level of > 9.0 mEq/L causes cardiac arrest due to:• Asystole• Ventricular fibrillation• PEA with bizarre, wide complex rhythm

( Caution- In individual patients, the serum potassium level may not correlate closely with the ECG changes. Patients with relatively normal ECGs may still experience sudden hyperkalaemic cardiac arrest.)

Serum potassium levels and ECG findings

POTASSIUM• Hypokalemia: ECG changes with gradual fall in potassium are

follows:

1. Flattened or inverted T waves

2. Depressed ST segment

3. Prominent U waves

4. Prolonged QT interval and PR interval

5. SA block rarely

6. Decreased QRS voltage

• Changes appear when K+ falls below about 2.7 mmol/l

• Increased amplitude and width of the P wave

• Prolongation of the PR interval

• T wave flattening and inversion

• ST depression

• Prominent U waves (best seen in the precordial leads)

• Apparent long QT interval due to fusion of the T and U waves (= long QU interval)

• With worsening hypokalaemia• Frequent supraventricular and ventricular ectopics

• Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia

• Potential to develop life-threatening ventricular arrhythmias, e.g. VT, VF and Torsades de Pointes

Effects of hypokalaemia on the ECG

• Hypokalaemia is often associated with hypomagnesaemia, which increases the risk of malignant ventricular arrhythmias• Check potassium and magnesium in any patient with an arrhythmia• Top up the potassium to 4.0-4.5 mmol/l and the magnesium to > 1.0 mmol/l to  stabilise the myocardium and protect against arrhythmias – this is standard practice in most CCUs and ICUs

CALCIUM

• Hypercalcemia:

• Normal serum corrected calcium = 2.1 – 2.6 mmol/L

• Mild hypercalcaemia =  2.7 – 2.9 mmol/L

• Moderate hypercalcaemia = 3.0 – 3.4 mmol/L

• Severe hypercalcaemia =  greater than 3.4 mmol/L

CALCIUM

• Hypercalcemia:This causes shortening of the QT interval due to shortening of the ST segment.

• This gives an abrupt slope to the proximal limb of the T wave

• In severe hypercalcaemia, Osborn waves (J waves) may be seen

• Ventricular irritability and VF arrest has been reported with extreme hypercalcaemia

Hypercalcaemia causing marked shortening of the QT interval (260ms)

Osborn waves caused by severe hypercalcaemia (4.1 mmol/L)

CALCIUM

• Hypocalcemia:

• Normal serum corrected calcium = 2.2 – 2.6 mmol/L.

• Mild-moderate hypocalcaemia =  1.9 – 2.2 mmol/L.

• Severe hypocalcaemia = < 1.9 mmol/L

CALCIUM

• Hypocalcemia:

• This causes a prolonged QT interval due to lengthening of theST segment. In some patients, there is, in addition, terminal T wave changes in some leads.

• These changes may also occur in hypomagnesemia.• Dysrhythmias are uncommon, although atrial fibrillation has been reported.

• Torsades de pointes may occur, but is much less common than with hypokalaemia or hypomagnesaemia

QT prolongation in a patient with DiGeorge’s syndrome and serum calcium of 1.32 mmol/L 

SUMMARY

Digoxin Effect QT interval shorteningST depression

Digoxin Toxicity T wave inversionArrhythmias

Qunidine Effect ST depressionQT interval increased

Hyperkalemia Peaked, tented, tall T wavesSevere: ‘Sine wave’ pattern

Hypokalemia Flat/inverted T wavesST depression

Hypercalcemia QT interval (ST segment) shortening

Hypocalcemia QT interval (ST segment) lengthening

REFERENCES

– Understanding ECG ,6th edition, P.J.Mehta’s.

– A Primer of ECG , K.P.Misra.

– The ECG in Practice, 6th edition, Jhon R.Hampton.

– Harrison’s Principles of Internal medicine, 19th edition

– Internet.