Rapid 12-Lead ECG Interpretation

Dr.Ashutosh Kawade, MD[Medicine]

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INTRODUCTION

Rate Rhythm Axis Hypertrophy Infarction Other Clinical Aspects

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ECG Interpretation

• Electrocardiography (ECG or EKG) is a transthoracic interpretation of the electrical activity of the heart over time captured and externally recorded by skin electrodes. It is a noninvasive recording produced by an electrocardiographic device.

1 sm

all b

ox =

1 m

m =

0.1

mV

5 Large squares = 1 second

Time

1 Large square = 0.2 second1 Small square = 0.04 second

2 Large squares = 1 cm

6.104/11/23 21:54

Horizontal axis - 1 and 3 sec marks

1 small box = 1 mm = 0.04 sec.Every 5 lines (boxes) are bolded

Verti

cal a

xis-

vol

tageECG Graph Paper

RATE• Our main objective is to rapidly determine the heart

rate from the ECG.• First: Find a specific R wave that peaks on a heavy black

line (our "start" line).

• Next: Count off "300, 150, 100" for every thick line that follows the start line, naming each line as shown. Remember these numbers; we will use them throughout our career.

• Then: Count off the next three lines after "300, 150, 100" as "75, 60, 50."

• Now: Memorize these ‘Triplets’ & make certain that we can say the triplets without using the picture.

• Where the next R wave falls, determines the rate. It's that simple!

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Rate Determine Rate by Observation

Using the triplets:

Name the lines following the “Start” line.

Fine division/rate association: reference

300250

214

187

167

“75” “60” “50”

150136

125

115

10094

88

83

79

7571

68

65

62

60

107

May be calculated:1500

= RATEmm. between similar waves

Bradycardia (slow rates)

• Cycles/6 second strip✕ 10 = Rate

• When there are 10 large squares between similar waves, the rate is 30/minute.

Sinus Rhythm: origin is the SA Node (“Sinus Node”),normal sinus rate is 60 to 100/minute.• Rate more than 100/min. = Sinus Tachycardia

• Rate less than 60/min. = Sinus Bradycardia Determine any co-existing, independent (atrial/ventricular) rates:

• Dissociated Rhythms: A Sinus Rhythm (or atrial rhythms) may co-exist with an independent rhythmfrom an automaticity focus of a lower level. Determine rate of each.

Irregular Rhythms:• With Irregular Rhythms (such as Atrial Fibrillation) always note the general

(average) ventricular rate (QRS’s per 6-sec. strip✕ 10) or take the patient’s pulse.

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NORMAL ECG WAVES

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Rhythm ★ Identify basic rhythm…

…then scan entire tracing for pauses, premature beats,irregularity, and abnormal waves.

★ Always:• Check for: P before each QRS. QRS after each P.

• Check: PR intervals (for AV Blocks). QRS interval (for BBB).

• Has QRS vector shifted outside normal range? (to rule out Hemiblock).

Irregular RhythmsSinus Arrhythmia

Irregular rhythm that varieswith respiration.All P waves are identical.Considered normal.

Wandering Pacemaker

Irregular rhythm. P waveschange shape aspacemaker location varies.Rate under 100/minute……but if the rate exceeds100/minute, then it is called

Multifocal Atrial Tachycardia

Atrial FibrillationIrregular ventricular rhythm.Erratic atrial spikes(no P waves) frommultiple atrial automaticityfoci. Atrial dischargesmay be difficult to see.

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Rhythm continued Escape The heart’s response to a pause in pacing

pause

AtrialEscape Beat

or

Junctional

Escape Beat

Then…

the SA Nodeusally resumes

pacing.or

VentricularEscape Beat

AtrialEscape RhythmRate 60-80/min.

orJunctional

Escape RhythmRate 40-60/min.

or

+

++

+

++ + + + +

+ ++ +

++

++

+

++

+

++ + + + +

+ ++ +

++

++

+

++

+

++ + + + +

+ ++ +

++

++

(“idiojunctional rhythm”)Ventricular

Escape RhythmRate 20-40/min.

(“idioventricular rhythm”)

Premature Beats From an irritable automaticity focus

Premature Atrial Beat

Premature Junctional Beat

Premature Ventricular ContractionPVC’s may be:multiple, multifocal, in runs, orcoupled with normal cycles.

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PVC’s

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Rhythm continued Tachyarrhythmias

150 250

“focus” = automaticity focus350 450

Rates: ParoxysmalTachycardia Flutter Fibrillation

multiple foci discharging

Paroxysmal (sudden) Tachycardia …rate: 150-250/min.Paroxysmal Atrial Tachycardia

An irritable atrial focus discharging at150-250/min. produces a normal wavesequence, if P' waves are visible.

• P.A.T. with blockSame as P.A.T. but only everysecond (or more) P' waveproduces a QRS.

Paroxysmal Junctional TachycardiaAV Junctional focus produces a rapidsequence of QRS-T cycles at 150-250/min.QRS may be slightly widened.

Paroxysmal Ventricular TachycardiaVentricular focus produces a rapid(150-250/min.) sequence of (PVC-like)wide ventricular complexes.

Flutter …rate: 250-350/min.Atrial Flutter

A continuous (“saw tooth”) rapid sequenceof atrial complexes from a single rapid-firingatrial focus. Many flutter waves needed toproduce a ventricular response.

Ventricular Flutter also see “Torsades de Pointes” A rapid series of smooth sine waves from asingle rapid-firing ventricular focus; usually ina short burst leading to Ventricular Fibrillation.

Fibrillation …erratic (multifocal) rapid discharges at 350 to 450/min.Atrial Fibrillation

Multiple atrial foci rapidly dischargingproduce a jagged baseline of tiny spikes.Ventricular (QRS) response is irregular.

Ventricular FibrillationMultiple ventricular foci rapidly dischargingproduce a totally erratic ventricular rhythmwithout identifiable waves. Needs immediatetreatment.

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fusion

Rhythm: (“heart”) blocks Sinus (SA) Blockthe Sinus Node usually resumes pacing, but

the pause may evoke an “escape” response from an automaticity focus.

An unhealthy Sinus (SA) Node misses one or more cycles (sinus pause)…

AV BlockBlocks that delay or prevent atrial impulses from reaching the ventricles.

1 AV Block

2 AV Block

…prolonged PR intervalPR interval is prolonged to greaterthan .2 sec (one large square).… some P waves without QRS response

cycle until the last P wave in theseries does not produce a QRS.

Wenckebach …PR gradually lengthens with each

Mobitz …some P waves don’t produce a QRSresponse. If “intermittent,” anoccasional QRS is droped.More advanced Mobitz block mayproduce a 3:1 (AV) pattern or evenhigher AV ratio

2:1 AV Block …may be Mobitz or Wenckebach.PR length and QRS width orvagal maneuvers help differentiate.3° (“complete”) AV Block …no P wave produces a QRS response

3 Block: P waves—SA Node origin.QRS’s—if narrow, and if theventricular rate is 40 to 60 per min.,then origin is a Junctional focus.P waves—SA Node origin.

QRS’s—if PVC-like, and if theventricular rate is 20 to 40 per min.,then origin is a Ventricular focus.

3 Block:

Bundle Branch BlockRight BBB

★ Always Check:• is QRS within

3 tiny squares?

R R'

…find R,R' in right or left chest leads

With Bundle BranchBlock the criteria for

ventricular hypertrophyare unreliable.

Left BBBR R' Caution:

With Left BBBinfarction is difficultto determine on EKG.QRS in V1 or V2 QRS in V5 or V6

Hemiblock★ Always Check:• has Axis shifted

outside Normalrange?

…block of Anterior or Posterior fascicle of the Left Bundle Branch.

Anterior HemiblockAxis shifts Leftward➞ L.A.D.

look for Q1S3

Posterior HemiblockAxis shifts Rightward➞ R.A.D.

look for S1Q3

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“WILLIAM MORROW”William: ‘W’ in V1 & ‘M’ in V6: LBBB

Morrow: ‘M’ in V1 & ‘W’ in V6: RBBB

Axis General Determination of Electrical Axis

Is QRS Positive ( ) or Negative ( ) in leads I and AVF?First Determine Axis Quadrant

II

Is Axis Normal?QRS in lead I …if the QRS is Positive (mainly abovebaseline), then the Vector points topositive (patient’s left) side.

Lead I

AVF L. AVF

Normal: { QRS upright in I and AVF“two thumbs-up” sign

I

Ex.R.A.D

QRS in lead AVF

Lead AVF

…if the QRS is mainly Positive, thenthe Vector must point downward topositive half of the sphere.

R.A.D. NormalI

AVFAVF

Axis in Degrees (Frontal Plane)After locating Axis Quadrant, find limb lead where QRS is most isoelectric:Extreme Right Axis Deviation

lead AxisI –90 -150

AVL –120III –150

AVF –180 -180 o

-90o-120o

-90o-60o

o

. L.A.

D.0o

0o

-30o

Left Axis Deviationlead Axis

I –90AVR –60

II –30AVF 0

Normal Rangelead Axis

AVF 0III +30

AVL +60I +90

Right Axis Deviationlead Axis

AVF +180II +150

AVR +120I +90

+180o

+150o A.

D.+120o

+90o +90o

+30o

+60o

R.

Axis Rotation (left/right) in the Horizontal PlaneFind transitional (isoelectric) QRS in a chest lead.

transitional QRS is “isoelectric”

Patient’sRight

V1

Rotation

n

Rightwards Leftwards

Normal Range

Patient’sLeft

V2 V3 V4 V5V6

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Normal

Ex.R.A.D

Axis Axis refers to the Mean Frontal Plane QRS axis (or vector) during ventricular depolarization. As we recall when

the ventricles depolarize (in a normal heart) the direction of current flows leftward and downward because most of the ventricular mass is in the left ventricle. We like to know the QRS axis because an abnormal axis can suggest disease such as pulmonary hypertension from a pulmonary embolism.

Abnormalities of axis can hint at: Ventricular enlargement Conduction blocks (i.e. hemiblocks) Determining the Axis:• The Quadrant Approach• The Equiphasic Approach

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Predominantly Positive

Predominantly Negative

Equiphasic

Leads I and aVF

LEFT Axis Deviation

LVHLBBBWPWHigh diaphram, pregnancyWNL – obese, elderly

RIGHT Axis Deviation

RVHRBBBLV PVCsPulmonary- emphysema, PEWNL – thin, young

Determine which lead contains the Determine which lead contains the most equiphasic QRS complex. most equiphasic QRS complex. The fact that the QRS complex The fact that the QRS complex in this lead is equally positive in this lead is equally positive and negative indicates that the and negative indicates that the net electrical vector (i.e. overall net electrical vector (i.e. overall QRS axis) is perpendicular to QRS axis) is perpendicular to the axis of this particular lead.the axis of this particular lead.

Examine the QRS complex in Examine the QRS complex in whichever lead lies 90° away whichever lead lies 90° away from the lead identified in step from the lead identified in step 1. If the QRS complex in this 1. If the QRS complex in this second lead is predominantly second lead is predominantly positive, than the axis of this positive, than the axis of this lead is approximately the same lead is approximately the same as the net QRS axis. If the as the net QRS axis. If the QRS complex is predominantly QRS complex is predominantly negative, than the net QRS axis negative, than the net QRS axis lies 180° from the axis of this lies 180° from the axis of this lead.lead.

Hypertrophy Atrial HypertrophyRight Atrial Hypertrophy

• large, diphasic P wave with tall initial componentInitial component

Left Atrial Hypertrophy• large, diphasic P wave with wide terminal component

terminal component

Ventricular HypertrophyRight Ventricular Hypertrophy

• R wave greater than S in V1, but R wave getsprogressively smaller from V1 - V6.

• S wave persists in V5 and V6.• R.A.D. with slightly widened QRS.• Rightward rotation in the horizontal plane.

Left Ventricular HypertrophyS wave in V1 (in mm.)

+ R wave in V5 (in mm.)Sum in mm. is more than 35 mm. with L.V.H.

• L.A.D. with slightly widened QRS.• Leftward rotation in the horizontal plane.

Inverted T wave:slants downwardgradually,

but up rapidly.

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‘P’ PULMONALE

‘P’ MITRALE

LVH

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Several Criteria for determining LVH

Sokolow-Lyon indices — There are two criteria with these widely used indices:1) Sum of S wave in V1 and R wave in V5 or V6 3.5 mV (35 mm)and/or 2) R wave in aVL 1.1 mV (11 mm)

• LAD

• V1,2 deep S andV5,6 tall R >35mm

• aVL “R” > 12mm

• Secondary ST depress

• Most frequently seen with hypertension

• RAD

• V1 R + V6 S >10mm

• V1 rSr’ (incomplete RBBB)

• Secondary ST depress

• Usually will be seen with pulmonary pathology

HYPERTROPHY

LVH RVH

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Q wave = Necrosis• Significant Q wave is one millimeter (one small square)

wide, which is .04 sec. in duration…… or is a Q wave 1/3 the amplitude (or more)of the QRS complex.

• Note those leads (omit AVR) where significant Q’s are present… see next page to determine infarct location, and to identifythe coronary vessel involved.

• Old infarcts: significant Q waves (like infarct damage) remainfor a lifetime. To determine if an infarct is acute, see below.

Q

ST (segment) elevation = (acute) Injury (also Depression)• Signifies an acute process, ST segment returns to

baseline with time.• ST elevation associated with significant Q waves

indicates an acute (or recent) infarct.• A tiny “non-Q wave infarction” appears as significant

ST segment elevation without associated Q’s. Locate byidentifying leads in which ST elevation occurs (next page).

elevation• ST depression (persistent) may represent “subendocardial

infarction,” which involves a small, shallow area just beneaththe endocardium lining the left ventricle. This is also a varietyof “non-Q wave infarction.” Locate in the same manner as for

infarction location (next page).T wave inversion = Ischemia

• Inverted T wave (of ischemia) is symmetrical (left half

and right half are mirror images). Normally T wave is

upright when QRS is upright, and vice versa.T

• Usually in the same leads that demonstrate signs ofacute infarction (Q waves and ST elevation).

note those leads where T wave inversion occurs, thenidentify which coronary vessel is narrowed (next page).

inversion • Isolated (non-infarction) ischemia may also be located;

NOTE: Always obtain patient’s previous ECG’s for comparison!04/11/23 21:54

Infarction

Infarction Location & Coronary Vessel Involvement

Coronary Artery Anatomy Right Coronary

ArteryLeft Coronary

Artery

circumflex

Anteriordescending

Infarction Location/Coronary Vessel Involvement Posterior

• large R with

ST depression in V1 & V2

• mirror test or reversedtransillumination test

(Right Coronary Artery)

LateralQ’s in lateral leads I and AVL

(Circumflex Coronary Artery)

Inferior(diaphragmatic)Q’s in inferior leads

II, III, and AVF(R. or L. Coronary Artery)

AnteriorQ’s in V1, V2, V3, and V4

(Anterior Descending

Coronary Artery)

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Right Ventricular Infarction

Infarct Location• On ECG the QRS complex represents ventricular contraction. The Q

wave is the first downward wave of the QRS complex, and it is followed by an upward R wave, however the Q wave is often absent on ECG. Necrosis (death) of an area of the heart muscle produces a Q wave on ECG.

• The Q wave makes the diagnosis of infarction.• If there are Q waves in lead I and lead AVL, there is a lateral infarction.• Inferior ("diaphragmatic") infarction is diagnosed by the presence of Q

waves in II, III, and AVF. • Q waves in chest leads V1, V2, V3, or V4 signify an anterior infarction. • It is common practice to determine the general location of an

infarction, but with a little anatomical knowledge of the heart's coronary blood supply*, we can make a far more sophisticated diagnosis.

• A lateral infarction is caused by an occlusion of the Circumflex branch of the Left Coronary Artery. An anterior infarction is due to an occlusion of the Anterior Descending branch of the Left Coronary Artery.

• The base of the left ventricle receives its blood supply from branches of either the Right or the Left Coronary Artery, depending on which artery is "dominant.“

“Septal / Anterior Infarct.“

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Other Clinically Significant AspectsPulmonary Embolism • S1Q3T3 – wide S in I, large Q and inverted T in III

• Acute Right BBB (transient, often incomplete)• R.A.D. and rightward rotation (horizontal plane)• Inverted T waves V1 V4 and ST depression in II➞Artificial Pacemakers

Modern artificial pacemakers have sensing capabilities and also provide aregular pacing stimulus. This electrical stimulus records on ECG as a tinyvertical spike that appears just before the “captured” cardiac response.

• are “triggered” (activated) whenthe patient’s own rhythm ceasesor slows markedly.

sinus rhythm ceases

pacemaker spikes

• are “inhibited” (cease pacing)if the patient’s own rhythmresumes at a reasonable rate.

PVC stops pacemaker, but…• will “reset” pacing(at same rate) tosynchronize with apremature beat.

▼ ▼ ▼ ✕

Pacemaker Impulse ▲

(delivery modes)pacemaker resumes in step

with premature beat.

▲ ▲

Ventricular Pacemaker (electrode in Right Ventricle)

(Asynchronous) Epicardial PacemakerVentricular impulse not linked to atrial activity.

Atrial pacemaker

Atrial Synchronous Pacemaker P wave sensed, then after a brief delay,

ventricular impulse is delivered.

Dual Chamber (AV sequential) PacemakerExternal Non-invasive Pacemaker

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ElectrolytesPotassium wide,

flat Ppeaked T

no P

Increased K+ (hyperkalemia)wide QRS QRS widens

moderate extreme

prominentU wave

Decreased K+ (hypokalemia)flat T

moderate extreme++Calcium Hyper Ca ++ Hypo Ca

short QT prolonged QT

DigitalisECG appearance with digitalis (“digitalis effect”)

•Remember Salvador Dali.• T waves depressed or inverted.

• QT interval shortened.Digitalis Excess(blocks)• SA Block• P.A.T. with Block• AV Blocks• AV Dissociation

Digitalis Toxicity(irritable foci firing rapidly)• Atrial Fibrillation

• Junctional or Ventricular Tachycardia• multiple P.V.C.’s

• Ventricular FibrillationQuinidine Effects

Quinidinewide,

notchedP

wide QRS

U

• ECG appearance with quinidine ST

long QT interval• Excess quinidine or other medications

that block potassium channels (or evenlow serum potassium) may initiate Torsades de Pointes

Other Clinically Significant Aspects

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Digitalis causes a gradual down-sloping of the ST segment, to give it the appearance of Salvador Dali's moustache.

Type of VT known as “twisting of the points.”Usually seen in those with prolonged QT intervals

Other Clinically Significant Aspects

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Say “300, 150, 100” …“75, 60, 50”

• but for bradycardia:

1. RATE

rate = cycles/6 sec. strip✕ 10

2. RHYTHMIdentify the basic rhythm, then scan tracing for prematurity,

pauses, irregularity, and abnormal waves.

• Check for: P before each QRS. QRS after each P.

• Check: PR intervals (for AV Blocks).QRS interval (for BBB).

• If Axis Deviation, rule out Hemiblock.

3. AXIS • QRS above or below baseline for Axis Quadrant (for Normal vs. R. or L. Axis Deviation).

For Axis in degrees, find isoelectric QRS in a limb lead

of Axis Quadrant using the “Axis in Degrees” chart.

• Axis rotation in the horizontal plane: (chest leads)

find “transitional” (isoelectric) QRS.

4. HYPERTROPHY

Check V1 {P wave for atrial hypertrophy.

R wave for Right Ventricular Hypertrophy.

S wave depth in V1…+ R wave height in V5 for Left Ventricular Hypertrophy.

5. INFARCTION

Scan all leads for:

• Q waves

• Inverted T waves

• ST segment elevation or depression

Find the location of the pathology (in the Left ventricle),

and then identify the occluded coronary artery.

Summary

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Important Precautions Must be Performed & Interpreted by the treating physician Correct Lead placement and good contact

Proper earth connection, avoid other gadgets

Deep inspiration record of III,aVF

Compare serial ECGs if available

Relate the changes to Age, Sex, Clinical history

Consider the co-morbidities that may effect ECG

Make a xerox copy of the record for future use

Interpret systematically to avoid errors

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Be’ware of Normal ECG Normal Resting ECG – cannot exclude disease

Ischemia may be covert – supply / demand equation

Changes of MI take some time to develop in ECG

Mild Ventricular hypertrophy - not detectable in ECG

Some of the ECG abnormalities are non specific

Single ECG cannot give progress – Need serial ECGs

ECG changes may not co-relate with Angio results

Paroxysmal event may be missed in single ECG

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Life Preserving Syndromes• Regardless of our expertise and level of education, we

should look for the following - easily identified - electrocardiographic signs of impending (life-threatening!) problems, even in apparently healthy persons.

• The atria contract, pumping blood into the ventricles just before ventricular contraction. The electrical current ("depolarization") that causes atrial contraction is conducted very slowly to the ventricles to allow time for blood to fill the ventricles.

• The AV Node, the only electrical connection between the atria and the ventricles, conducts the depolarization impulse (from the contracting atria to the ventricles) very slowly. This provides a brief pause for ventricular filling after atrial contraction. On ECG, the P wave (representing atrial contraction) is normally followed by a short span of level baseline (pause) before the QRS complex (ventricular contraction).

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Wolff-Parkinson-White Syndrome [WPW]• In some people, an anomalous conduction pathway, the "Kent

bundle," connects the atria and the ventricles, short-circuiting the AV Node. The anomalous conduction pathway allows rapid conduction to the ventricles without the normal delay. This produces Wolff Parkinson White (WPW) syndrome, which is characterized by conduction of the atrial depolarization current to the ventricles immediately after atrial contraction

• On the ECG of patients with WPW syndrome, the usual short span of baseline following the P wave is replaced by a curving "delta wave," representing too-early stimulation ("pre-excitation") of a portion of the ventricles. This is easy to detect in most leads as a gentle upward curve that connects the P wave and the QRS complex.

• Pre-excitation of the ventricles, per se, is not serious, but it may lead to rapid ventricular rhythms that are dangerous, particularly in elderly persons or those with heart conditions. WPW is easily treatable; the Kent bundle can be ablated (destroyed) using a radio frequency intra-cardiac catheter. Therefore, early detection of delta waves on ECG can allow these patients to enjoy a normal life span.

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Brugada Syndrome• Brugada syndrome is a recognized cause of sudden death in

apparently healthy individuals. It is responsible for about one-half of sudden deaths in young persons without structural heart disease, therefore early detection is critical. This familial condition is due to malfunctioning sodium (Na+) channels in the heart cells.

• Although the deadly arrhythmias (abnormal rhythms) that victims experience cannot be prevented, they can be successfully treated with an Implantable Cardioverter-Defibrillator (ICD), which corrects the arrhythmia immediately upon its occurrence. But persons with this syndrome must be identified in order to provide this life-saving treatment.

• In Brugada syndrome, the QRS is widened and has two upward peaks in (chest) leads V1 and V2, and the ST segment is elevated. The ST segment begins at the second peak of the widened QRS then slopes gradually downward. In Brugada syndrome, lead V3 also has a wide QRS and ST elevation that is stereotypical for this condition. All medical personnel who frequently observe cardiac monitors or ECG strips should make a mental note of this ECG pattern.

• If we keep a mental reference of the ECG morphology of Brugada syndrome in leads V1, V2, and V3, perhaps we can prevent an untimely death, since lead MCL1, which is a variation of leads V1 and V2, is the most common lead used for cardiac monitoring.

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On the standard ECG, there is usually a short segment of level baseline ("ST segment") immediately following the (normally narrow) QRS complex. The ST segment is normally level with the baseline in all ECG leads.

Wellen’s Syndrome• Rarely are we warned of an impending myocardial infarction long

before it occurs. However, in patients with Wellens syndrome, stenosis (narrowing) of the Anterior Descending (the most important) branch of the Left Coronary Artery is revealed on ECG in patients with negligible or even absent symptoms. Therefore it is important that all medical personnel be ever-vigilant for the tell-a-tale signs of this important syndrome.

• On normal ECG's the T wave (which follows the ST segment) is usually upright or somewhat flattened in leads V2 and V3. However, in the ECG of some patients with stenosis of the Anterior Descending coronary artery, the T waves are markedly inverted (upside down) long before symptoms are present. For those patients with Wellens syndrome , this easily detected ECG sign is life-saving only if the person observing the ECG are savvy enough to recognize this important problem. Be that person!

• Stenosis of the Anterior Descending coronary artery is very treatable, and it is important that treatment be initiated before the artery is totally occluded causing myocardial infarction... even death. Using a special expandable catheter placed in the stenosed artery, the narrowed area can be dilated by a cardiologist using a procedure known as "angioplasty.“

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Currently, most angioplasty procedures employ the implantation of a metal mesh tube known a "stent" inside the artery, to keep it open and prevent re-stenosis of this vital artery. Intervention using angioplasty with stenting can indeed be life saving, but our recognition of Wellens syndrome is the critical link.

Long-QT Syndromes• There is a group of familial syndromes collectively known as Long QT

syndrome . There are at least six different forms of Long QT syndrome thought to be caused by dysfunctional ion channels; they all can produce dangerous or deadly ventricular arrhythmias. Early treatment with proper medications should be instituted as soon as this syndrome is detected, ideally during childhood. There are, however, perhaps many thousands of people with undetected Long QT syndrome who require treatment.

• Although the heart rate varies somewhat (in response to physiological needs), the QT interval (measured on ECG from the beginning of the QRS to the end of the T wave) always remains less than one-half of the cardiac cycle.

• With Long QT syndrome the QT interval is longer than one-half the length of the cardiac cycle (usually measured from R wave to R wave). A quick glance at any lead will reveal the lengthened QT interval.

• Lengthening of the QT interval can be caused by a variety of medications that block ion channels (usually K+ channels). Certain types of cardiac pathology or metabolic conditions can also lengthen the QT, but in general, lengthening of the QT interval, regardless of the etiology, predisposes the patient to Torsades de Pointes, and other dangerous arrhythmias. Don't overlook it!

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THANKS !

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Q-T Interval & QTcDefinition: Time interval between beginning of QRS complex to the end of T wave.

– measurement of the refractory period or the time during which the myocardium would not respond to a second impulse; measured from the beginning of the QRS complex to the end of the T wave

– Best leads to measure the QT are V2 or V3– Q-T interval should be roughly less than half the preceding R-R intervalTip: Instead of calculating the QTc, a quick way to estimate if the QT interval long is to use the following rule:A QT > half of the RR interval is probably long.– It is longer with slower rates and shorter with faster rates

Normally: At normal HR: QT ≤ 11mm (0.44 sec) • QT interval varies based on heart rate

Abnormalities:1. Prolonged QT interval: hypocalcemia and congenital long QT syndrome.2. Short QT interval: hypercalcemia.3. 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. For each heart rate you need to calculate an adjusted QT interval, called the “corrected QT” (QTc):

The Q-T interval can be corrected for heart rate using Basset's formula: Normal QTc interval = 0.39 ± 0.04 sec A prolonged QT can be very dangerous. It may predispose an individual to a type of

ventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyte abnormalities, CNS disease, post-MI, and congenital heart disease.04/11/23 21:54

Sick Sinus Syndrome • SSS: The function of sinus node was degenerated. SSS encompasses both disordered SA node

automaticity and SA conduction.• Causes: CAD, SAN degeneration, myopathy, connective tissue disease, metabolic disease, tumor,

trauma and congenital disease.• With marked sinus bradycardia, sinus arrest, sinus exit block or junctional escape rhythms• Bradycardia-tachycardia syndrome

ECG Recognition:1. Sinus bradycardia, ≤40 bpm; 2. Sinus arrest > 3s3. Type II SAB4. Non-sinus tachyarrhythmia ( SVT, AF or Af).5. SNRT > 1530ms, SNRTc > 525ms6. Instinct heart rate < 80bmp

Therapy:1. Treat the etiology2. Treat with drugs: anti-bradycardia agents, the effect of drug therapy is not good.3. Artificial cardiac pacing.

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval)

Sinus arrest with pause of 4.4 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

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Bifascicular/ Trifascicular Blocks

• RBBB with either left anterior or left posterior fascicular block• Diagnostic criteria• 1.Prolongation of the QRS duration to 0.12 second or longer• 2.RSR’ pattern in lead V1,with the R’ being broad and slurred• 3.Wide,slurred S wave in leads I,V5 and V6• 4.Left axis or right axis deviation Trifascicular

• The combination of RBBB, LAFB and long PR interval • Implies that conduction is delayed in the third fascicle

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Bifascicular

Cardiac Pacemakers

• Indications For Implantation of Permanent Pacing in Acquired AV Blocks

• 1.Third-degree AV block, Bradycardia with symptoms

• Asystole

• e.Neuromuscular diseases with AV block (Myotonic muscular dystrophy)

• 2.Second-degree AV block with symptomatic bradycardia

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Cardiac Pacemakers• Definition

– Delivers artificial stimulus to heart– Causes depolarization and contraction

• Uses– Bradyarrhythmias– Asystole– Tachyarrhythmias (overdrive pacing)

• Types

– Fixed• Fires at constant rate• Can discharge on T-wave• Very rare

– Demand• Senses patient’s rhythm• Fires only if no activity sensed after preset

interval (escape interval)– Transcutaneous vs Transvenous vs Implanted

• Demand Pacemaker Types– Ventricular

• Fires ventricles– Atrial

• Fires atria• Atria fire ventricles• Requires intact AV conduction

• Demand Pacemaker Types– Atrial Synchronous

• Senses atria• Fires ventricles

– AV Sequential• Two electrodes• Fires atria/ventricles in sequence

• Problems– Failure to capture

• No response to pacemaker artifact• Bradycardia may result• Cause: high “threshold”• Management

– Increase amps on temporary pacemaker– Treat as symptomatic bradycardia

– Failure to sense• Spike follows QRS within escape interval• May cause R-on-T phenomenon• Management

– Increase sensitivity– Attempt to override permanent pacer with

temporary– Be prepared to manage VF

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Implanted Defibrillators• AICD

– Automated Implanted Cardio-Defibrillator• Uses

– Tachyarrhythmias– Malignant arrhythmias

• VT• VF

• Programmed at insertion to deliver predetermined therapies with a set order and number of therapies including:

– pacing– overdrive pacing– cardioversion with increasing energies– defibrillation with increasing energies– standby mode

• Effect of standby mode on Paramedic treatments

• Potential Complications– Fails to deliver therapies as intended

• worst complication• requires Paramedic intervention

– Delivers therapies when NOT appropriate• broken or malfunctioning lead• parameters for delivery are not specific enough

– Continues to deliver shocks• parameters for delivery are not specific enough and device

senses a reset• may be shut off (not standby mode) with donut-magnet

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ECG Monitoring• Einthoven’s Triangle• The positioning for leads I, II,

and III were first given by Einthoven. Form the basis of Einthoven’s triangle.– Each lead “looks” from a

different perspective– Can determine the direction

of electrical impulses– Upright electrical recording

indicates electricity flowing towards the + electrode

• positive deflection

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1901 - Dr. William Einthoven invented the ECG machine

• Unipolar Leads

– 1 positive electrode– 1 negative “reference point”

• calculated by using summation of 2 negative leads

– Augmented Limb Leads• aVR, aVF, aVL• vertical plane

– Precordial or Chest Leads • V1-V6• horizontal plane

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• Bipolar Leads

– 1 positive and 1 negative electrode

• RA always negative• LL always positive

– Traditional limb leads are examples of these

• Lead I• Lead II• Lead III

– Provide a view from a vertical plane

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