Cardio Ekg

7/21/2019 Cardio Ekg

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Lead I + lead III = Lead II (Einthovens Law)

Lead I - LA RA

Lead II - LL RA

Lead III - LL LA

Kirchoffs Law The sum of the potentials of AVR + AVL + AVF = 0

NORMAL

P wave

Amplitude normally 0.5 to 2.5 mm (2.5 squares) (in limb

leads)

Duration not over 110 msec (3 squares) (in limb leads) In sinus rhythms, P wave is upright in Lead II and inverted in

aVR. If not, SA node is not pacemaker

Normal axis (frontal plane) is 0 to +90 , usually +30 to +60

Left axis 0 to -30

Right axis beyond +75

PR interval

Normal value in adults is 0.12 sec to 0.20 sec (ventricular preexcitation < 3-5 squares < 1st degree AV

block)

QRS

60-100ish ms (1.5-2.5 squares)

ST segment

Usually isoelectric, but may normally deviate between 0.5 and +1.0 mm from baseline in standard and

unipolar extremity leads

Upward displacement of 2 or 3 mm may be normal particularly in right precordial leads

T wave - 10% of amplitude of QRS is normal.

U wave

Polarity usually same as T wave

Most prominent in lead V3

Maximum amplitude should not exceed 1 mm

Alterations in automaticity of the SA node

Sinus tachycardia - sinus rhythm > 100 beats/min

Sinus bradycardia - sinus rhythm < 60 beats/min

Sinus arrhythmia - increased sinus rate with inspiration.

withdrawal of parasympathetic tone during inspiration

Sinus arrest - pause. SA node fails to fire.

can be caused by increased parasympathetics, hypersensitive carotid sinus, damage to SA node, digitalis

Irregular Rhythms

Wandering Pacemaker - pacemaker activity wanders from SA node to nearby atrial automaticity foci


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P shape varies

Atrial rate 100 then becomes multifocal atrial tachycardia) Irregular ventricular rhythm

Multifocal Atrial Tachycardia - Chaotic Atrial Rhythm

P wave shape varies (Three or more ectopic P-waves with different configurations/morphologies because P

waves come from different areas in the atrium.)

Isoelectric line between P-P intervals

Frequent occurrence of varying PR intervals

Atrial rate >100 (100-250 bpm)

Irregular ventricular rhythm

Seen in COPD

Atrial Fibrillation

Irregular rhythm and irregular ventricular rhythm

Chaotic atrial spikes

Escape beat - an automaticity focus transiently escapes overdrive suppression to emit one beat (A beat originating from a site

other than the SA node). Long pause followed by escape beat (versus premature beat where there is no pause before)

Escape Rhythm - an automaticity focus escapes overdrive suppression to pace at its inherent rate (another normal pacemaker

takes over) a sequence of similar ectopic beats (many ectopic beats). When SA node pacemaker activity is impaired

Atrial escape rhythm 60-80/min

P waves are not identical to previous P waves which are from the SA node. (The same is for the escape

beat)

Junctional escape rhythm40-60/min


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Conducts mainly to ventricles series of lone QRS complexes.

Retrograde atrial depolarization leads to an inverted P

can be immediately before the QRS

can be buried in the QRS

can be after the QRS

Ventricular escape rhythm20-40/min

large ventricular complexes can be so slow that it causes Stokes-Adams Syndrome where not enough blood reaches the brain.

Premature Beatsirritable focus spontaneously fires a single stimulus

Premature atrial beatearly P wave which can be hidden in the T wave with normal QRS following.

P can depolarize the ventricles leading to a wide QRS in the PAC beat only.

If not conducted, lone P wave with no QRS following.

Irritated by (same for premature junctional beat) - epi, increased SNS stimulation, caffeine, amphetamines,

cocaine, other beta1 stimulants, excess digitalis, toxins, etoh (sometimes), hyperthyroid, stretch

Premature junctional beatpremature irritable stimulation from AV junction which depolarizes the ventricles and

sometimes in a retrograde fashion, will depolarize the atria.


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P wave can be before, during or after the QRS.

Upper AV Junctional Rhythm

AV node not pacemaker. Retrograde/inverted P waves precede the QRS complexes by short P-R intervals (start pacemake

near AV node travels faster because shorter distance) in leads II, III, and aVF

Middle AV Junctional Rhythm

P waves cannot be identified since they are buried in the QRS complexes. Atrial fibrillation is ruled

out since the base line shows no oscillations.

Lower AV Junctional Rhythm

Retrograde P waves follow QRS complexes. They are best seen in leads II, III, and aVF

Atria depolarized AFTER the ventricles depolarize.

Premature ventricular beatirritate the ventricles

Wide and tall QRS with opposite polarity of the normal QRS Only depolarizes the ventricles, not the SA node.

Irritated by - airway obstruction, hypoxia, reduced CO, low potassium, mitral valve prolapse, stretch,

myocarditis

Ventricular Parastolefrom an entrance block but not irritable PVCs coupled to long series of normal cycles

Multifocal PVCseach focus is own unique identifiable PVC

R on TPVC falls on a T wave/falls on a vulnerable period and starts shit

from hypoxia and low serum potassium.

Tachyarrhythmiasrapid ventricular rhythms originating in a very irritable automaticity foci

Paroxysmal (sudden) tachycardia150-250 (sinus tachycardia is not sudden like paroxysmal)

Paroxysmal Atrial Tachycardia (PAT)

rapid rate, spike P waves

2:1 ratio P:QRS

(suspect digitalis excess or toxicity - digitalis can inhibit the AV node)


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PAT with AV block more than one P wave for every QRS response

Paroxysmal Junctional Tachycardia (PJT)- sudden rapid pacing of a very irritable automaticity foci in the

AV junction

inverted P before, during, or after the QRS - can depolarize the atria in a retrograde fashion from

below

Wide QRS from depolarizing left before right

Junctional Tachycardia AV nodal reentry tachycardia


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continuous reentry circuit rapidly paces the atria and ventricles. Each pacing stimulus records in

an origin near the coronary sinus.

Supraventricular tachycardia irritable automaticity foci that produce both paroxysmal atrial and

junctional tachycardia (above the ventricles)

Paroxysmal Ventricular Tachycardia resembles a series of PVCs

SA node still paces atria independent pacing of the atria and ventricles (AV dissociation)

Indicates coronary insufficiency leading to poor O2 to the heart.

Distinguishing wide QRS insufficiency complex SVT from VTach.

SVT VTach

Pt with coronary disease or infarction uncommon very common

QRS width (duration) 0.14s

AV dissociation showing captures orfusions

rare yes

Axis - extreme RAD rare yes

Torsades de Pointes (250-350)

caused by low potassium, meds that block the K+ channels, congenital abnormalities,

long/lengthened QT segment.

Possibly from two irritable foci in different ventricular areas.

Flutter250-350

Atrial flutter- saw-tooth shape


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Originates in the atrial automaticity focus

Ventricular Flutter

single ventricular automaticity focus

Sine waves of similar amplitude

Tends to go to VFib.

Fibrillation350-450 (multiple foci discharge rapidly)

atrial fibrillation

many irritable parasystolic atrial foci

causes many irregular spokes on the EKG

No identifiable P or P waves with irregular QRS response.

Ventricular Fibrillation

Many irritable parasystolic ventricular automaticity foci pacing rapidly (entrance block)

Wolff-Parkinson-White Syndrome


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Delta wave = area of preexcitation

Can have paroxysmal tachycardia

rapid conduction - SVT (atrial flutter and afib) can be rapidly conducted through the

accessory pathway

some bundles have automaticity foci that can initial paroxysmal tachycardia

Re-entry - ventricular depolarization may immediately re-stimulate the atria in a

retrograde fashion via the accessory pathway causing a theoretical circus reentry loop

Lown-Ganong-Levine Syndrome (LGL)

AV node is bypassed by an extension of the anterior internodal tract (James Bundle) which

conducts atrial depolarizations directly to the Bundle of His without delay

No significant PR interval delay

P waves are adjacent to the QRSs on EKG.

Sinus Block

SA node may temporarily fail to pace for at least one cycle then resumes pacing

The pause can induce an escape beat from an automaticity foci

Sick Sinus Syndrome

seen in the elderly with heart disease

Marked sinus bradycardia without normal escape mechanisms or atrial and junctional foci

can develop bradycardia-tachycardia syndromeintermittent episodes of SVT (a flutter or afib)

AV Block

First Degree AV block


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lengthened PR interval > 0.2 s (1 large square) No wide QRS

Second degree AV block

Wenckebach lengthening of PR interval until QRS is dropped.

Mobitz 2 1 normal cycle preceded by a series of paced P waves that fail to conduct through the

AV node

Third degree AV block

block of the conduction of atrial stimuli to ventricles. Atria and ventricles pace at different rates.

Bundle Branch Block/Intraventricular Conduction Delay

block of one bundle branch which produces a delay of depolarization of the ventricle it supplies.

Wide QRS with rabbit ears (>0.12s) (3 squares or more in any lead) -- RSR

RBBB- rabbit ears in V1, V2


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Deep and round S-waves in I, aVL and V4-6

Secondary S-T, T-wave change in V1-3

abnormal depolarization and repolarization

Complete RBBB with RVH > 15 mm. Can Dx only with RBBB.

LBBB - rabbit ears in V5, V6

Absence of septal q-waves in V4-6 (small q from septal activation not seen)

RSR or M pattern of QRS in I, aVL and V4-6

Secondary S-T, T-wave change in I, aVL and V4-6

Septal activation in opposite direction (R L)

If RSR of normal QRS duration incomplete BBB

Intermittent mobitz - occasional dropped QRS due to permanent BBB with intermittent BBB of other side.

Hemiblock


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Anterior Hemiblock

LADusually associated with an MI (or other heart dz)

Normal or slightly widened QRS (0.10-0.12s)

Q1S3Q in I or wise/deep S in III)

Left Anterior block

Mean and terminal QRS vectors are directed to the left of -30 in frontal plane

Initial 0.02-second QRS vector

Directed right and inferiorly and produces a small 0.02-second Q-wave in Lead I and

AVL Small 0.02-second R-wave in Leads II, III and AVF

Other causes of abnormal left axis deviation are ruled out i.e., inferior wall myocardial infarction

Anterior hemiblock with RBBB

RBBB - mean QRS vector is within normal range or shows minimal RAD

RBBB + LAD = anterior hemiblock

Posterior hemiblock

RAD (usually associated with an MI)

normal or slightly widened QRS

S1Q3 - Wide S in I and Q in III

Posterior block

This condition is very difficult to diagnose - right ventricular enlargement and lateral infarctions

Mean and terminal QRS vectors in frontal plane show right axis deviation

Initial 0.02-second QRS vector

Directed slightly leftward and superiorly and produces a small 0.02-second R-wave in

Lead I and AVL (r/o anterolateral infarction)

Small 0.02-second Q-wave in Leads II, III and AVF

Bifascicular block

RBBB + anterior hemiblock

RBBB + posterior hemiblock

Intermittent block

continuous EKG pattern with intermittent wide QRS characteristic of intermittent BBB or with intermittent

changes of QRS axis.

Incomplete Trifascicular Block

First-degree A-V block plus a right bundle branch block plus either a left anterior hemiblock or posterior

hemiblock

Axis- direction of depolarization as it passes through the heart origin of mean QRS vector is the AV node = tail of the

vector. 0-90 is normal

Mean QRS vector will point toward hypertrophy and away

from infarct

V1, V2 = rightward rotation

V5, V6 = leftward rotation

Hypertrophy

Diphasic wave = atrial enlargement

Right atrial enlargement - initial large deflection in V1. Tall

P wave


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if height > 2.5mm in II and >0.12s, suspect right atrial enlargement

pointed P wave greater than 2.5 mm, which is best seen in leads perpendicular to the heart bottom wall (II,

III, aVF) and chest leads V1 and V2

Left atrial enlargement- large terminal deflection in V1. Long P wave

P wave is a prolonged and biphasic (bifid). It is best seen in leads I, II and aVL and sometimes possibly in

leads V5 and V6. (http://www.health-tutor.com/p-mitrale-ecg.html)

Right ventricular hypertrophy
http://www.google.com/url?q=http%3A%2F%2Fwww.health-tutor.com%2Fp-mitrale-ecg.html&sa=D&sntz=1&usg=AFQjCNE-yV6j2gKLbnTH6EbcBDGK-onpXQ


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Large R wave in V1, S wave is much smaller

The large R wave in V1 progressively becomes smaller in V2, V3, V4

RVH causes RAD + rightward shift.

Left ventricular hypertrophy

QRS complexes are exaggerated in amplitude eps. in chest leads.

Very tall R waves in V5

Height/depth of S in V1 + height of R in V5 > 35 mmLVH.


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Can see an asymmetrical inverted T wave (ideal leads V5/V6)

ventricular strain

V1 provides the most information regarding hypertrophy -- diphasic waves, R wave in V1, S wave in V1, R

wave in V5

Accompanied by

left atrial abnormality

>0.11s

Left axis deviation 0-30

ST segment T wave changes left ventricular strain pattern (systolic overload)

Extremity leads

Amplitude of R-wave in Lead I and/or AVL > 15 mm Amplitude of R-wave in AVF > 21 mm

Sum of R-wave in Lead I plus S-wave in

Lead III > 25 mm

Precordial leads

SV1 + RV5 or SV1 + RV6 > 35 mm

R-wave in V5 or V6 > 26 mm

R-wave in V6 taller than R-wave in Lead V5

Infarction

Ischemia - reduced blood supply

characterized by symmetric inverted T waves

Leads V2-V6 is pathological

Marked T wave inversion in leads V2, V3 is Wellens SyndromeStenosis of anterior descending

artery.

Injury - acute or recent

if no Q waves, can be non-Q wave infarction

ST elevation is infarct. Depression in reciprocal changes.

Pericarditis


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ST segment is elevated (diffuse) and usually flat or concave (middle sags down).

Entire T wave may be elevated off baseline

Subendocardial infarction


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Necrosis - dead tissue

Q wave indicates necrosis can Dx infarction

Insignificant Q waves < 0.04s (1mm)

Significant Q waves > 0.04s (or QRS amplitude - old criterion)

Anterior Infarct


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elevated ST segments and Q waves in V1, V2, V3, V4anterior descending of left coronary

artery

Posterior Infarct

Mirror image of anterior infarct

ST depression in V1, V2

Large R waves, maybe Q in V6

Lateral infarct


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I, AVL Q waves

Circumflex left coronary artery

Inferior Infarct

II, III, AVF Q waves

right/left coronary artery Cannot Dx infarction with LBBB


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hyperkalemia

wide, flat P

peaked T

wide QRS

Hypokalemia

T/U wave fusion. Flat T wave

Prominent U wave

Hypercalcemia

short QT interval


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Hypocalcemia

prolonged QT interval

Digitalis

positive inotrope - Improve contractility of the failing heart (mechanical effect)

Prolong the refractory period of the AV node in patients with supraventricular arrhythmias (electrical effect)

inhibits the cell membrane sodium-potassium ATPase pump

Therapeutic use for treating Atrial fibrillation

Salvador Dalis mustache

Toxicity - Sinus bradycardia, AV block, VTach secondary to ectopic beats

Quinidine

Class IA antiarrhythmic (blocks Na and K channels)

retards and repolarizes

Long QT interval can lead to Torsades

Wide, notched P

Wide QRS

depression ST

U wave

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Cardio Ekg

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