Basic ECG and Arrhythmia FINAL

8/2/2019 Basic ECG and Arrhythmia FINAL

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Page 1 of16TRANSCRIBED BY: Hayzle Mallari, Abby Maralit, Ana Aurelia Santos, Carlo Benjamin Taada

INTRODUCTION

Augustus Wallerintroduced the concept that the heart haselectrical potential

The ECG provides information for:

Rhythm

Rate

Enlargement

Injury/infarction

REVIEW

Transmembrane potential (Ventricular Muscle). (What goes in, what

goes out of membrane potential)

Underlying cardiac potentials are 4 major time-dependent and

voltage-gated membrane currents:

1. The Na+current (INa) is responsible for the rapid depolarizing

phase of the action potential in atrial and ventricular muscle and

in Purkinje fibers. It is also the largest current in the heart.

2. The Ca2+

current (ICa) is responsible for the rapid depolarizing

phase of the action potential in the SA node and AV node; it also

triggers contraction in all cardiomyocytes. It passes primarily

through L-type Ca2+

channels.

3. The K+current (IK) is responsible for the repolarizing phase of

the action potential in all cardiomyocytes.

4. The "pacemaker current" (If) is responsible, in part, for

pacemaker activity in SA nodal cells, AV nodal cells, and Purkinje

fibers. It is mediated by a nonselective cation channel.

Phase 0

is the upstroke of the action potential (depolarization)

If upstroke is due only to ICa, it will be slow

If the upstroke is due to both ICa and INa, it will be fast.

Corresponds to the onset of QRS

Factors that decrease the slope of phase 0 by impairing theinflux of Na+ (e.g., hyperkalemia, or drugs such as flecainide)

tend to increase QRS duration

Phase 1

The rapid repolarization component of the action potential

(when it exists)

due to almost total inactivation of INa or ICa, and may also

depend on the activation of a minor K+

current not listed

previously, called Ito (for transient outward current).

Phase 2

plateau phase of the action potential, which is prominent in

ventricular muscle

depends on the continued entry ofCa2+

or Na+

ions through

their major channels, and on a minor membrane current due to

the Na-Ca exchangercorresponds to the isoelectric ST segment

conditions that prolong phase 2 (use of amiodarone,

hypocalcemia) increase the QT interval

shortening of this phase, as by digitalis administration or

hypercalcemia, abbreviates the ST segment

Phase 3

repolarization component of the action potential

It depends on IK

Corresponds to the inscription of the T wave

Phase 4

constitutes the electrical diastolic phase of the action potential

In SA and AV nodal cells, changes in IK, ICa, and Ifproduce

pacemaker activity during phase 4

Purkinje fibers also exhibit pacemaker activity, but use only IfAtrial and ventricular muscle have no time-dependent currents

during phase 4

Sinoatrial (SA) node / Sinus node

Located in the R atrium

Primary pacemaker

Cells fire spontaneously; i.e., they exhibit automaticity

Atrioventricular (AV) node

Located near the atrioventricular groove and the tricuspid valveSecondary pacemaker

Purkinje fibers

For rapid conduction of action potentials

Tertiary pacemaker

Any pathologies in the tricuspid, R atrium, septum, would

affect this part of the conducting system

LEGEND

Normal text : lecture ppt, 2011B trans, Guyton and ECG Made Easy

Italicized: AUDIO

BASIC ECG, CARDIAC ARRYTHMIASRanulfo Javelosa, Jr., M.D. November 09, 2010


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The bundle branches would be running along the surface

of the interventricular septum. Therefore, congenital heart

diseases like VSD, ASD, could affect this flow of electricity.

CARDIAC CYCLE

*timing of complexes to the clinical events (heart sounds)

S4 atrial contraction after p-wave

P-wave atrial depolarization

After atrial excitation, atrial contraction follows

After ventricular excitationventricular contraction

tricuspid and mitral valve closure S1

S2 and S3 comes after the p-wave

P to beginning of R-wave diastole

QRSTsystole

When AV valves (tricuspid and mitral) close, you have the S1, and

this is at the same time as QRS also. Rapid ejection phase and then

the depolarization. The T wave, you have the repeat of the cycle

during diastole.

Atrial excitation p-wave

Atrial systole at the beginning of the Q

Ventricular excitation QRS

Ventricular systole after T wave

Ventricular diastole U wave

Step I. Rapid filling of ventriclesVentricular pressure drops below atrial pressure

AV valves are open, semilunar valves are closed

Rapid ventricular filling occurs

70-90% of the ventricles fill with blood

Step II. Atrial systole

P wave occurs

Atrial contraction lateral 1/3 of diastole

Pushed 10-30% more blood into ventricle

Step III. Isovolumetric contraction

QRS just occurred

Contraction of the ventricles causes ventricular pressure to rise

above atrial pressure

AV valves close

Ventricular pressure is still less than aortic pressure

Semilunar valves are closed

Volume of blood in the ventricle is EDV

Step IV. Ejection

Contraction of the ventricles causes ventricular pressure to rise

above aortic pressure,

Semilunar valves open

Ventricular pressure is greater than atrial pressure

AV valves are still closed

Volume of blood ejected by the ventricles: stroke volume (SV)

Aortic valve opening

in ventricular pressure

Aortic valve closure


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Step V.

T-wave occurs

Ventricular pressure drops below aortic pressure

Back pressure causes semilunar valves to close

Step VI. Isovolumetric relaxation

AV valves are still closed

Semilunar valves are still closed

Volume of blood in ventricles: ESV

Ventricular pressure drops

ECG

ECG Leads

Configured so that a positive (upright) deflection is recorded in a

lead if a wave of depolarization spreads toward the positive pole

of that lead, and a negative deflection if the wave spreads toward

the negative pole.

If the mean orientation of the depolarization vector is at right

angels to a given lead axis, a biphasic (equally positive & negative)

deflection will be recorded

Limb Leads

Record potentials transmitted onto the frontal plane

3 standard bipolar leads (I, II, III) and 3 augmented unipolar

leads (aVR, aVL, aVF)

P Q R S T U


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Step 1: RATE

Identify an R wave that falls on the marker of a big block

Each large square (5mm) represents 0.2 seconds, so there are

five large squares per second, and 300 per minute.

Count the number of the big blocks to the next R wave

300 # of big squares

1500 # of small squares

Relationship Between the Number of Large Squares Covered by the

R-R Interval and the Heart Rate

R-R Interval (Large Squares) Heart Rate (beats/minute)1 300

2 150

3 100

4 75

5 60

6 50

What is the Rate?

3 big squares: 300/3 = ~100bpm

4 big squares: 300/4 = ~75bpm

19 small squares: 1500/19 = 79bpm

Step 2: RHYTHM

Sinus?

Junctional (AV node)?Ventricular?

Pacemaker?

Atrial fibrillation?

Ventricular Fibrillation?

The normal pacemaker is the SA node; the signal thenpropagates through the AV node, and activates the ventricles.

When the heart follows this pathway at a normal rate and in

this sequence, the rhythm is called a "normal sinus rhythm."

SA Node: 60-100bpm

AV Node: 40-60bpm

Ventricular: no p-wave,


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7 big squares: 300/7 = 42bpm

Nodal Escape: if region around the AV node takes over as the focus

of depolarization

Rate is 100/minute

No P waves in junctional beats (indicates either no atrial

contraction or P wave lost in QRS complex)

Normal QRS complexes

Ventricular Rhythm

originate from purkinje fibers

Wide QRS

Impulse originates from one side of the ventriclecausing prolonged/delayed activation of the ventricles

No P-wave

HR is slower (40-60bpm)

Ventricular Escape

most commonly seen when conduction between the atria and

ventricles is interrupted by a complete heart block

After three sinus beats, the SA node fails to discharge. No atrial

or nodal escape occurs. After a pause, there is a single wide and

abnormal QRS complex with an abnormal T wave

8.5 big squares: 300/8.5 = 35bpm

HR: 150bpm (for figure below)

MI, metamphetamine, drugs

Patient can collapse

Can be tolerated in younger individuals

If with pulse and normal BP, give anti-arrhytmics

If no pulse is detected, start CPR and defibrillate

Ventricular Tachycardia

No P waves

Regular QRS complexes, rate 200/minute

Broad QRS complexes, duration 240 milliseconds with a veryabnormal shape

No identifiable T waves

8 small squares: 1500/8= 188bpm

Pacemaker Rhythm

Impulses originate at transvenous pacemaker

Wide QRS

Pacemaker spikes

Ventricular rhythm with faster HR

No p-wave

Atrial Fibrillation (AF)

ECG has many but not identical P waves

RR interval is not constant

8.5 big

squares

Spike R S T


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Usually 5-10 P: 1 QRS

Irregularly irregular rhythm

HR variable

Causes: drugs, alcohol, ischemia, metabolic disturbances, heart

failure, dilatation, HTN

Aka Holiday Heart Syndrome

Course vs. Fine Fibrillation

Baseline coarsely or finely irregular; P waves are absent. Ventricular

(QRS) irregular, slow or rapid

Atrial Flutter

4P : 1 QRS

Saw-toothed configuration of the p-waves

Regular RR intervals

Step 3: QRS AXIS

The subtotal of the direction of the electrical activity of the

heart; normally, downward and to the left

Frontal QRS Axis


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Using leads I and aVF, the axis can be calculated to within one of the

four quadrants at a glance.

Shortcut:

1. You normally look at leads I and aVF.

2. Hold the results of lead I of the ECG with your left hand and

that of the aVF with your right.3. With the index finger and middle finger of each hand, follow

the deflection of the waves (upward = +, downward = -) found

in the corresponding leads.

4. If both point upward, then it is normal. If both point downward,then it is NW axis deviated.

5. If one is positive and the other is negative, then the opposite ofthe hand holding the negative is the side where the deviation is

(in short, the one holding the upward deflection is the side of

the deviation)

Another way (for the mathematically gifted):

1. Plot the heights of the deflection of waves-

- +

+

2. Get the vector-

- +

+

3. Report in degrees of deviationThe QRS Axis

Normal Axis both I and aVF (+)

Right axis deviation lead I (-) and aVF (+)

Causes:

Normal finding in children and tall thin adults

Right ventricular hypertrophy

Chronic lung disease even without pulmonary HTN

Anterolateral myocardial infarction

Left posterior hemiblock

Pulmonary embolism

Wolff-Parkinson-White syndrome left-sided accessory

pathway

Atrial septal defect

Ventricular septal defect

Left axis deviation lead I (+) and aVF (-)Causes:

Left ventricular hypertrophy

Inferior myocardial infarction

Artificial cardiac pacing

Emphysema

Hyperkalemia

Wolff-Parkinson-White syndrome right-sided accessory

pathway

Tricuspid atresia

Ostium primum - OSD

Northwest territory both lead I and aVF (-)

Causes:

Emphysema

Hyperkalemia

Lead transposition

Artificial cardiac pacing

Ventricular tacchycardia

Normal

Right Axis Deviation

Left Axis Deviation


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Step 4: P-R INTERVALS FOR AV BLOCK

A-V Block First-Degree

AV conduction lengthened

May be seen in normal individuals

Usually caused by drugs such as -blockers (metoprolol,

atenolol, propanolol), Ca2+

channel blockers (verapamil,

diltiazem) that can prolong the AV conduction

Associated with the ff:

coronary artery disease acute rheumatic carditis Beta blockers digitalis cardiomyopathy normal sinus rhythm prolonged PR interval (>1 big square or 0.2s)

o delay from SA node firing and spread of impulsesto AV node

A-V Block Second Degree

sudden dropped QRS

absence of QRS after 1 P-wave

Mobitz type I (Wenckebach)

P-R intervals become progressively longer until one P wave is

totally blocked and produces no QRS. After a pause, during

which the AV node recovers, this cycle is repeated.

Rate: depends on rate of underlying rhythm

Rhythm: irregular

P waves: normal (upright and uniform)

PR interval: progressively longer until one P wave is blocked

and a QRS is droppedQRS: normal (0.06-0.10 sec)

Mobitz type II

no gradual prolongation (PR-PR-PR-dropped QRS)

more dangerous and indicates excessive damage to AV node

AV Block Third Degree

When there is complete dissociation between P wave and QRS

(Atrioventricular dissociation)

QRS occurs independently whenever it wants to

Atrial rate and ventricular rate are not the same

Indication for pacemaker


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Causes of AV blocks

Autonomic

Carotid sinus hypersensitivity

Metabolic/endocrine

Hyperkalemia

Hypothyroidism

Hypermagnesemia

Adrenal insufficiency

Drug-related

Beta blockers

Adenosine

Ca channel blockers

Anti-arrythmics (class I & III)

Digitalis

LithiumInfectious

Endocarditis

Tuberculosis

Lyme disease

Diphtheria

Chagas disease

Toxoplasmosis

Syphilis

Dengue fever

Heritable/congenital

Congenital heart disease

Maternal SLE

Kearns-Sayre syndrome

Emery-Dreiffus MDMyotonic dystrophy

Progressive familial heart block

Inflammatory

SLE

MCTD

Rheumatoid arthritis

Scleroderma

Infiltrative

Amyloidosis

Hemochromatosis

Sarcoidosis

Coronary artery disease

Acute MI (esp. inferior wall MI or R Coronary a.

involvement)Neoplastic/traumatic

Lymphoma

Radiation

Mesothelioma

Catheter ablation

Melanoma

Degenerative

Lev disease

Lenegre disease

Step 5: ECTOPIC BEATS

Atrial vs. Ventricular Ectopy


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Premature Atrial Contraction (PAC

)

Originates from the atria; an independent focus decided to fire

a few msec ahead of the expected beat and override or insert

into the sequence of the P-wave firing

Not coming from the SA node

The following QRS is narrow

With P-wave

Premature Ventricular Contraction (PVC)

No P wave

Wide QRS

With gap

Step 6: CHAMBER ENLARGEMENT

Left Atrial Enlargement

P wave duration equal or more than 0.12 sec.

Notched, slurred P wave in lead I and II (P mitrale).

Biphasic P wave in lead V1 with a wide, deep and negative

terminal component.

Right Atrial Enlargement

P wave duration equal or less than 0.11 sec.

Tall, peaked, narrow T wave equal or more than 2.5 mm inamplitude in lead II,III or aVF (P pulmonale).

Mean P wave axis shifted to the right (more than +70 degrees).


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Ventricular Hypertrophy

Left Ventricular Hypertrophy

"Voltage criteria":

R or S wave in limb lead equal or more than 20mm

S wave in V1, V2 or V3 equal or more than 30mm

R wave in V4, V5 or V6 equal or more than 30mm.

Depressed ST segment with inverted T waves in lateral leads

(strain pattern; more reliable in the absence of digitalis therapy.

Left axis of -30 degree or more.

QRS duration equal or more than 0.09 sec.Time of onset of the intrinsicoid deflection (time from the

beginning of the QRS to the peak of the R wave) equal or more

than 0.05 sec in lead V5 or V6.

Tall Rs in V5 and V6

Deep S in V1 and V2

Sinus tachycardia, Left Axis deviation, LVH, No PR prolongation, No

AV blocks (pic below)

Right Ventricular HypertrophyTall R waves over the right precordium and deep S waves over

the left precordium ( R:S ratio in lead V1 > 1.0)

Normal QRS duration (if no bundle branch block)

Right axis deviation.

ST-T "strain" pattern over the right precordium.

Late intrinsicoid deflection in lead V1 or V2.

Tall Rs in V1 and V2

Deep S in V5 and V6


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Below: normal sinus rhythm (NSR), HR = 88, RA deviation (RAD), R

atrial enlargement (RAE), RVH

NSR, 80bpm, RAD, PR interval normal, RAE, RVH

Sinus tachycardia, RAD, LAE, RVH

Step 7: QRS DURATION

Left Bundle Branch Block

QRS duration equal or more than 0.12 sec.

Broad , notched or slurred R wave in lateral leads(I, aVL , V5,V6)

QS or rS pattern in the anterior precordium.

Secondary ST-T wave changes (ST and T wave vectors are

opposite to the terminal QRS vectors).

Late intrinsicoid deflection in lead V5 and V6.

Wide QRS due to prolonged ventricular depolarization (>0.12;

N: 0.08-0.1)

V5 and V6 wide, notched R wave

V1 and V2 deep S wave

With P-wave

o If w/o P-wave sinus tachycardia


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Right Bundle Branch Block

QRS duration equal or more than 0.12 sec.

Large R' wave in lead V1 (rsR').

Deep terminal S wave in lead V6.

Normal septal Q wave.

Inverted T wave in lead V1 (secondary T wave changes).

Late intinsicoid deflection in lead V1 and V2.

Step 8: ST SEGMENT ABNORMALITIES

ECG Changes in Acute Ischemia, Injury and Infarction.

Typically, three phenomena may occur on the ECG that are

characteristic of the evolution of a myocardial infarction (MI):

T wave inversion, indicating ischemia.

S-T segment elevation, indicating injury and the acuteness of

myocardial infarction (MI).

The presence of an abnormal Q wave, indicating tissue death

(necrosis).

The above abnormalities are usually seen in the ECG leads

representing the area of damage.


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Localization of Infarction

Leads I, V2, V3, V4

V1-V4: Q-wave and ST elevation (Anterior Wall infarction); T

inversion (Anterior wall ischemia)V1-V6 involement: extensive anterior extending to the lateral

wall

Leads V2, V3 and AVF

Leads I, V5, V6 and AVL

ST elevation in I, V5-V6, AVL: acute lateral wall infarction

Rare

V1: tall R

Localization of MI through ECG

Anterior wall V1 through V6

Anteroseptal V1 through V3

Inferior II, III, aVF

Right ventricular V4R, V3R

Posterior Wall V7 through V9

V1 through V3 ( ST depression)

Anterior wall

Anteroseptal

Inferior

Right ventricular

Posterior wall

Anterior wall infarct (V1-V4)


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Inferior Wall infarct (V2, V3, AVF)

Questions

The ECG rhythm is called:

a. Sinus bradycardia changing to ventricular tachycardiab. Junctional rhythm with a run of ventricular tachycardiac. Sinus rhythm terminating in ventricular fibrillation

d. Sinus bradycardia changing to junctional tachycardia

This ECG rhythm is called:

a. Sinus rhythm with multifocal premature ventricularcomplexes (PVCs)

b. Sinus bradycardia with ventricular paced beatsc. Sinus rhythm with paced ventricular beatsd. Junctional rhythm with unifocal PVCs


a. Junctional rhythm with a premature atrial complex (PAC)b. Sinus bradycardia with a premature atrial complex (PAC)c. Sinus arrhythmiad. Sinus arrhythmia with a PVC


a. Sinus tachycardia with a PVCb. Atrial fibrillation with rapid ventricular responsec. Sinus tachycardia with a PACd. Sinus arryhtmia with a PVC


a. Sinus arrhythmiasb. Atrial fibrillation with ectopic atrial beatsc. Sinus tachycardia with ventricular couplets

d. Sinus rhythm, with ectopic atrial beats***

Hello 2012! Hello 2nd

sem!

As usual, hi sa mga Alphan brods and sisses ko Taktak, Kenji, Tel,

Rors, Charm, Tristan and especially sa mga batchmates ko na sina

Faith, Jes, Vin, and Mel. Also, sa mga brods and sisses ko from 2013

and 2014, wholl read this soon.

Hi rin sa PPG...so dilemma parin naten kung saan tayo kakain. Lapit

na Christmas!

Hi sa mga Med, Pedia, Surge, Psych (and ComMed?) groupmates

kotsismisan ulet lalo na si Dencyo hahaha!

Happy aral! I hope this helps (though this looks like a photo album.

Sorry!)hayzle

GRABE! Good luck sa topic na ito!

Isapuso natin ang pag-aaral nito. Magagamit natin ito next year.

Goodluck 2012!

There are only two questions that human beings have ever fought

over, all through history: How much do you love me? and Whos

in charge?

~Liz Gilbert in E.P.L.

Abby

*hello to all the hardworking members of 2012 trans4med!!

especially to those i worked with in this trans: hayz, abby, and to our

leader, senator peaches

*hugs to ms cathy, jo, darling vin, grandmere joie, twin monique,

therapeutic friend joey-gurl, riese-pieces, my inaanak andtweetmate charmy, melissa marie, sexy jessa, tellyteltel, faith,

POLARIS...and a special greeting to my mommy cyll who will be

getting married next month

*to my enchantmates: miriam, queen seon-dok, GA, fake, diyes,

ampatuan, los ohos, really?, brake fluid, claire dela fuente, senator,

train, elbow, and yamashita: only 5 meetings to go! we made it!!

*2012B, please support the vote for your Lantern Queen and escort

project by our class officers! Lantern Queen 2010 will be on

December 14, UERM Gym, 6pm-10pm

* Regina Iustitiae Sorority, Ateneo Law, in cooperation with Phi

Alpha Sigma Sorority and Alpha Sigma Phi Fraternity, are proud to

present to you vERdict, the first and biggest medical-law school

batch on December 11, 2010 (let's unwind after exams!), 8pm,Ascend Bar, The Fort. Tickets are priced at P250, inclusive of

drinks

*Medicine 2012, we only have four short months to go before we

become JIs...let's do this!

--ANAtomy amphitheater (inspired by daisy duck )

OMARISM (because you know this was coming...)

Alomar: nung narinig ko na ang lec ay EKG for dummies, i almost left!"

OMAR: Im no escort. Im either the host or the star. Armand has been

bugging me about wanting to be an escort again, he claims he is the key to

another victory.

DELOICIOUS: Ngeeeee... Can you believe this guy? Hahaha! wala na Omar.You have escaped you're rightful throne as the escort of the lantern queen

for 2 years! pinoproject mo lang sa ibang lalake kaya kmi nlang ni Glen last 2

years. Pero ngayon, there is no escape my friend

CARLOTACIOUS: Sabi ni Omar he is either the host or the star. Pero diba it's

not a star. IT'S OMAR! :) kaya yun na ang theme the Lantern natin. Hahaha

DELOICIOUS: Tama carlo. At ung mas ok pa. Dba c lanter queen

magddescribe ng lantern? eh, what's more, C escort is the lantern!!!

wahahahahaha! It's not a star, it's freakin OMAR!!!

Basic ECG and Arrhythmia FINAL

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