Supraventricular tachycardia

Tachycardic rhythm originating above the ventricular tissue. Atrial and ventricular rate = 150–250 bpm. Regular rhythm, p is

usually not discernable.

Note:

Types of SVT:

Sinoatrial node reentrant tachycardia (SANRT)

Ectopic (unifocal) atrial tachycardia (EAT)

Multifocal atrial tachycardia (MAT)

A-fib or A flutter with rapid ventricular response. Without rapid ventricular response both usually not classified as SVT

Atrioventricular (AV)-nodal reentrant tachycardia (AVNRT— commonest)

Permanent (or persistent) junctional reciprocating tachycardia (PJRT)

Atrioventricular reentrant tachycardia (AVRT)

Atrial premature beat (APB)

Arises from an irritable focus in one of the atria. APB produces different looking P wave, because depolarization vector is

abnormal. QRS complex has normal duration and same morphology.

Premature ventricular complexes (PVCs)

Occasionally irregular rhythm, broad QRS arising from ventricles

No P-wave associated with PVCs. It can be monomorphic/polymorphic.

Artificial pacemaker

Sharp, thin spike, before each complex, ventricular paced rhythm shows wide ventricular pacemaker spikes.

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Step 3: Determining the Axis

Normal QRS axis from −30° to +110°.

−30° to −90° is referred to as a left axis deviation (LAD).

+110° to +180° is referred to as a right axis deviation (RAD).

−180° to −90° is referred as north-west axis/extreme axis/axis in no man’s land as depicted in f ig.

11.5 b.

Axis LI LIII or aVF TIP (Fig. 11.5C)

Normal Positive Positive Both up

Right Negative Positive Meet-REACHING

Left Positive Negative Separate-LEAVING

Northwest Negative Negative Both down

QRS complex in leads I and aVF.

Determine if they are predominantly positive or negative.

The combination should place the axis into one of the 4 quadrants above.

Cardiac

axis

Causes

Left axis

deviation

Left anterior hemiblock, left ventricular hypertrophy, Wolff-Parkinson-White syndrome, inferior myocardial

infarction (MI), ostium primum atrial septal defect (ASD), and ventricular tachycardia

Normal variation in pregnancy, obesity; ascites

Right axis

deviation

Normal finding in children and tall thin adults, right ventricular hypertrophy (RVH), chronic lung pulmonary disease

(COPD), left posterior hemiblock, Wolff-Parkinson-White syndrome, and anterolateral MI

North

West

Dextrocardia, severe emphysema, hyperkalemia, lead transposition, artificial cardiac pacing, and ventricular

tachycardia

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Fig. 11.5B: Pictorial representation of AXIS deviation with examples.

(COPD: chronic obstructive pulmonary disease; ASD: atrial septal defects; VSD: ventricular septal

defects)

Fig. 11.5C: Axis determination based on direction of lead I and lead aVF.

Step 4: Check Individual Waves

Assess P Waves

Always positive in lead I and II

Always negative in lead aVR

<2.5 small squares in duration

<2.5 small squares in amplitude

Commonly biphasic in lead V1

Best seen in leads II

Tall (>2.5 mm), pointed P waves (P pulmonale)—suggests right atrial enlargement

Seen in chronic obstructive pulmonary disease (COPD), atrial septal defect (ASD), TS, Ebstein anomaly (Himalayan P waves)

Notched/bifid (“M” shaped) P wave (P “mitrale”) in limb leads—suggests left atrial enlargement

Seen in MS, MR, and systemic hypertension

Absent P waves—atrial fibrillation/flutter

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Inverted P waves in lead II—dextrocardia

QRS-Complex

Normal characteristics:

Duration: 0.04–0.11 seconds.

Broad/wide QRS (>0.12 s)

Ventricular hypertrophy

Intraventricular conduction disturbance

Aberrant ventricular conduction

Ventricular pre-excitation

Ventricular ectopic or escape pacemaker

Ventricular pacing by cardiac pacemaker.

Q <0.04 s, <25% of R wave

Height of QRS—Sokolow index (SV2 + RV5) <35 mm (<45 mm for young)

Increased in RV/LV hypertrophy

Decreased—low voltage QRS (<5 mV in limb leads/<10 mV in chest leads)

Obese patient

Restrictive cardiomyopathy

Pericardial effusion

Hypothyroidism

Hypothermia

Myocarditis.

Axis of ventricular depolarization −30 to +110° (abnormalities already discussed)

v entricular activation time (VAT)—time from start of q wave till top of R wave. Normal of LV <0.04 s

(V5 and V6 leads), RV <0.03 s (V1 Lead).

Prolonged in ischemia, bundle branch block

Precordial R wave progression, i.e. R wave amplitude progressively increases from V1 to V6.

Absent R wave progression sign of anterior wall MI.

Q Waves

The normal Q wave in lead I is due to septal depolarization

It is small in amplitude—less than 25% of the succeeding R wave, or less than 3 mm

Its duration is <0.04 sec or one small box

It is seen in L1 and sometimes in V5 and V6

The pathological Q wave of infarction in the respective leads is due to dead muscle

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It is deep in amplitude—more than 25% of the succeeding R wave, or more than 4 mm. Its duration is

>0.04 sec or >1 small box

Pathological Q waves may be seen in cardiomyopathies—hypertrophic obstructive cardiomyopathy

(HOCM), infiltrative myocardial disease

Absent Q waves in V5–V6 is most commonly due to left bundle branch block (LBBB).

T Wave

Normally repolarization directs from epicardium to endocardium = T wave is concordant with QRS

complex

Ischemic area: A repolarization is delayed, an action potential is extended

Vector of repolarization is directed from ischemic area:

Subendocardial ischemia—to epicardium—T wave elevation

Subepicardial ischemia—to endocardium—T wave inversion.

Asymmetrical T wave inversion— the first half having more gradual slope than the second half

Symmetrical→T wave inversiobn seen in ischemia

Amplitude rarely exceeds 10 mm.

Causes of T wave inversions Tall T waves (more than two-thirds of neighboring QRS)

CAD/ischemia

Cardiomyopathies—hypertrophic

Myocarditis and pericarditis Wellens syndrome

Pulmonary embolism

Raised ICT—CNS bleed

Ventricular hypertrophy

Bundle branch block

Pacing

Persistent juvenile T wave pattern

Hyperkalemia—Steeple T waves

Hyperacute MI

Benign early repolarization (BER)

U Waves

The U wave is a wave on an electrocardiogram that is not always seen. It is typically small, and, by

definition, follows the T wave. U waves are thought to represent repolarization of the papillary muscles

or Purkinje fibers

Normal U waves are small, round and symmetrical and positive in lead II. It is the same direction as T

wave in that lead.

Prominent U waves are most often seen in hypokalemia, but may be present in hypercalcemia,

thyrotoxicosis, or exposure to digitalis, epinephrine, and class 1A and 3 antiarrhythmics, as well as in

congenital long QT syndrome, and in the setting of intracranial hemorrhage.

An inverted U wave may represent myocardial ischemia or left ventricular volume overload.

The Osborn wave (J wave) is a positive deflection at the J point (negative in aVR and V1), characteristically seen in hypothermia

(typically temperature <30°C), but also can be seen in raised ICT, hypercalcemia

Epsilon wave is a small positive deflection buried in the end of the QRS complex. It is the characteristic of arrhythmogenic right

ventricular dysplasia (ARVD).

Step 5: Calculate Intervals

PR Interval (Figs. 11.6A to C)

Normal: 0.12–0.20 seconds.

Long PR interval may indicate heart block.

First degree heart block

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P wave precedes QRS complex but PR intervals prolong (>5 small squares) and remains constant from beat to beat

Second degree heart block

Mobitz Type I or Wenckebach

Runs in cycle, first PR interval is often normal. With successive beat, PR interval lengthens until there will be a P wave with no

following QRS complex.

The block is at AV node, often transient, may be asymptomatic.

Mobitz Type 2

PR interval is constant, duration is normal/prolonged. Periodically, no conduction between atria and ventricles—producing a p

wave with no associated QRS complex (blocked P wave).

The block is most often below AV node, at bundle of His or BB,

May progress to third degree heart block.

Third degree heart block (complete heart block)

No relationship between P waves and QRS complexes.

An accessory pacemaker in the lower chambers will typically activate the ventricles—escape rhythm. Atrial rate = 60–100 bpm.

Ventricular rate based on site of escape pacemaker. Atrial and ventricular rhythm, both are regular.

Causes of Conduction Block

CAD, acute MI, remote MI, pulmonary embolism

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Drugs

Aortic stenosis, SABE + abscesses in conduction

Cardiac trauma and hyperkalemia

Lenegre’s disease (idiopathic fibrosis of conduction)

Lev’s disease (calcification of the cardiac skeleton)

Cardiomyopathy—dilated and hypertrophic

Infiltrative—Chagas disease

Myxedema, amyloidosis, and ventricular hypertrophy

Idiopathic.

Short PR interval

Tachycardia

Pre-excitation syndromes

Lown–Ganong–Levine syndrome

Wolff-Parkinson-White (WPW) syndrome

Mahaim pathway.

The diagnostic triad of WPW consists of a wide QRS complex associated with a relatively short PR

interval and slurring of the initial part of the QRS (delta wave), with the latter effect being due to aberrant

activation of ventricular myocardium. The presence of a bypass tract predisposes to re-entrant

supraventricular tachyarrhythmias.

QT Interval

It represents the time taken for ventricular depolarization and repolarization.

The duration of the QT interval is proportionate to the heart rate. The faster the heart beats, the faster

the ventricles repolarize so the shorter the QT interval. Therefore what is a “normal” QT varies with

the heart rate.

QT interval should be 0.35–0.45 s.

For each heart rate you need to calculate an adjusted QT interval, called the “corrected QT” (QTc):

QTc = QT/square root of RR interval—Bazett’s formula.

Figs. 11.6A to C: (A) Normal atrioventricular impulse transmissions; (B) First-degree AV block; (C) Preexcitation.

Prolonged QTc (>440 ms)—a prolonged QT can be very dangerous. It can predispose an individual to a type of ventricular

tachycardia—Torsades de pointes.

Hypokalemia

Hypomagnesemia

Hypocalcemia

Hypothermia

Myocardial ischemia

Raised intracranial pressure

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Congenital long QT syndrome—Example: Jervell and Lange–Nielsen syndrome or Romano-Ward syndrome

Drugs—chlorpromazine, haloperidol, quetiapine, quinidine, procainamide, disopyramide, flecainide, sotalol, amiodarone,

amitriptyline, diphenhydramine, astemizole, loratadine, terfenadine, chloroquine, quinine, and macrolides.

Short QTc (<350 ms)

Hypercalcemia

Digoxin effect.

Bundle branch blocks:

Left bundle branch block (LBBB)—indirect activation causes left

ventricle contracts later than the right ventricle.

Right bundle branch block (RBBB)—indirect activation causes

right ventricle contracts later than the left ventricle

QS or rS complex in V1—W-shaped

RsR’ wave in V6—M-shaped

Terminal R wave (rSR’) in V1—M-shaped

Slurred S wave in V6—W-shaped

Mnemonic: WILLIAM Mnemonic: MARROW

Step 6: Assess for Hypertrophy

Right Ventricular Hypertrophy (RVH)

Criteria of RVH

Tall R in V1 with R >S, or R/S ratio >1

Deep S waves in V4, V5, and V6

Associated right axis deviation, right atrial enlargement (RAE)

Deep T inversion in V1, V2, and V3.

Cause of RVH

Long-standing mitral stenosis

Pulmonary hypertension of any cause

Ventricular septal defect (VSD) or atrial septal defect (ASD) with initial L to R shunt

Congenital heart with RV over load

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Tricuspid regurgitation, pulmonary stenosis.

Left Ventricular Hypertrophy (LVH)

Causes of LVH

Pressure overload—systemic hypertension and aortic stenosis

Volume overload—AR or MR-dilated cardiomyopathy

Ventricular septal defect—cause both right and left ventricular volume overload

Hypertrophic cardiomyopathy.

Criteria of LVH

High QRS voltages in limb leads:

Sokolow and Lyon criteria: S (V1) + R (V5 or V6) >35 mm

Cornell criteria: S (V3) + R (aVL) >28 mm (men) or >20 mm (women)

Others: R (aVL) >13 mm.

Deep symmetric T inversion in V4, V5, and V6

QRS duration >0.09 sec, associated left axis deviation, left atrial enlargement (LAE).

Fig. 11.7: ECG showing voltage criteria for LVH.

Romhilt–Estes Score: Score >5—definite LVH, <3 LVH unlikely

ECG criteria Points

Voltage criteria (any of) (Fig. 11.7):

R or S in limb leads ≥20 mm

S in V1 or V2 ≥30 mm

R in V5 or V6 ≥30 mm

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ST-T abnormalities:

ST-T vector opposite to QRS without digitalis

ST-T vector opposite to QRS with digitalis

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Negative terminal P mode in V1, 1 mm in depth and 0.04 sec in duration (indicates left atrial enlargement) 3

Left axis deviation (QRS of –30° or more) 2

QRS duration ≥0.09 sec 1

Delayed intrinsicoid deflection in V5 or V6 (>0.05 sec) 1

TYPES OF LVH

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