488 Appendix D

Less commonly, the posterior surface is damaged. The

ischemic changes of posterior infarctions are seen in the

anterior leads (V –V ), 1 4 but since those leads face the back

side of the damaged area, the changes will be reciprocal,

or the reverse of what you would see in an anterior MI.

Specifically, a posterior infarction will present ST depression

(rather than elevation), an upright T wave, and a tall, broad

R wave (the Q wave seen in reverse).

When ischemic changes are random across the

12 leads—that is, they fail to correlate readily with coronary

artery distribution—it may indicate something other than

myocardial ischemia or infarction. Pericarditis is the most

common cause of widespread or random ischemic changes.

Chamber Enlargement

Excesses of either volume or pressure can cause any of the

four heart chambers to enlarge. Chamber enlargement can

be due either to dilation (increase in internal size of chamber)

or to hypertrophy (increase in mass of chamber walls). When

either happens, the abnormal depolarization waves produce

vectors of longer duration and greater magnitude. Atrial

enlargement affects P waves, whereas ventricular enlargement affects QRS complexes.

Atrial Enlargement

Atrial enlargement will produce a biphasic P wave in V .1

Right atrial enlargement produces a sharply biphasic P,

with an initial upright deflection that is larger than the

terminal deflection. With left atrial enlargement, the P is

broad and the terminal, downward deflection is larger than

the initial deflection (Figure D11).

In Lead II, the P wave of right atrial enlargement will

characteristically be tall (amplitude >7.25 mm) and peaked,

with a normal duration (0.10 second or less). This distinctive P wave is called P pulmonale. Left atrial enlargement

produces a broad, notched P (0.11 second or more) in Lead II,

commonly called P mitrale.

Ventricular Enlargement

Ventricular enlargement will be seen as unusually high

amplitude QRS complexes across all the V leads. Right

ventricular enlargement has tall R waves in V1 and deep

S waves in V . 6 Left ventricular enlargement produces deep

S waves in V1 and tall R waves in V6 (Figure D12).

Rule of 35: To verify the presence of left ventricular

enlargement, measure the deepest wave in V1 or V2 and the

tallest wave in V5 or V . 6 If the sum of the two measurements

is greater than 35 mm in a patient over 35 years old, the

criteria for LVE are satisfied (Figure D13).

Bundle Branch Block

In Chapter 7 of this book, you learned about AV Heart Blocks,

a type of heart block that originates in the area of the AV node

and can be identified on a single-lead monitoring strip.

There is another kind of block, called bundle branch

block (BBB), that originates below the AV node within the

Figure D11 Atrial Enlargement

II V1

Tall, peaked

P wave

(P pulmonale)

First deflection

is largest.

RIGHT

Atrial Enlargement

RIGHT atrial activity is reflected in

first half of P wave.

II V1

Broad P wave

(P mitrale)

Last deflection

is largest.

LEFT

Atrial Enlargement

LEFT atrial activity is reflected in

second half of P wave.

Basic 12-Lead Interpretation 489

Figure D12 Ventricular Enlargement

V1 V6

Tall R wave Deep S wave

RIGHT

Ventricular Enlargement

V6

Deep S wave Tall R wave

LEFT

Ventricular Enlargement

V1

bundle branches. Since conduction above the ventricles is

normal, the only abnormal feature of BBB is an unexpectedly

wide QRS complex. You’ll recall that many of the strips in

this book had unexpectedly wide QRS complexes, and you

were directed to identify the underlying rhythm and note

that it had a “wide QRS.” That’s because you need more

than one lead to determine which of the bundle branches is

causing the problem.

A prolonged QRS measurement (> 0.12 second) suggests defective conduction within the bundle branches. This

feature will be apparent across all leads, but you look at V1

and V6 to determine whether the blockage is in the right or

left bundle branch. The normal QRS complex in V1 has a

small R wave and a deep S wave. The normal QRS complex

in V6 has a very small Q wave and a large R wave.

Right Bundle Branch Block (RBBB): In V , 1 RBBB

produces a notched QRS complex, commonly

referred to as “rabbit ears.” With RBBB, the QRS

complex in V6 is characterized by a very broad

S wave (Figure D14a).

Left Bundle Branch Block (LBBB): In V , 1 LBBB produces

a small initial R wave, followed by a wide, deep

S wave; the QRS complex is predominantly negative

in V . 1 In V , 6 the R wave is large, very broad, and

often notched. There is no Q wave or S wave, so the

QRS complex is totally positive in V6 (Figure D14b).

The QRS changes associated with LBBB obscure the ST

changes associated with myocardial injury. Thus, the presence of LBBB greatly reduces the value of the EKG in diagnosing acute MI.

Miscellaneous EKG

Abnormalities

A number of drug and electrolyte imbalances cause EKG

changes that are detectable on a 12-lead EKG (Figure D15).

Some common anomalies are outlined below:

Pericarditis: The injury caused by an inflamed

pericardium produces ST changes similar to those

of ischemia/infarction. However, they will not

correlate with coronary artery distribution.

Digitalis: Digitalis toxicity produces ST changes

characterized by a “scooped” appearance. The QT

interval is also shortened.

Potassium: Hyperkalemia produces characteristic

peaked T waves and merging of the QRS and

T waves. Hypokalemia is reflected in flat T waves,

widening of QRS complexes, and appearance of

U waves.

Calcium: Hypercalcemia produces QT intervals that

are unexpectedly short for the rate, whereas in

hypocalcemia, the QT intervals are longer than

expected.

The types of EKG changes suggestive of these various effects

are outlined in Figure D16.

Figure D13 Rule of 35

RULE OF 35

Criteria for Left Ventricular Enlargement

1 Measure depth of deepest wave in V1

 or V . 2

2 Add height of tallest wave in V5 or V . 6

3 If sum is >35mm and patient is >35 years old,

criteria for LVE are met.

490 Appendix D

Analysis Format

As with arrhythmia interpretation, the key to easy and

effective analysis of 12-lead EKGs is use of a methodical

process (Figure D17). There are many acceptable formats,

and you will adjust your approach in response to the context.

However, it is advisable to develop a routine approach

and use it regularly until it becomes second nature to you.

One such approach is outlined below.

Context: Before beginning analysis, consider the

context in which you are looking at the EKG.

Figure D14 (a) Right Bundle Branch Block; (b) Left Bundle Branch Block

V1 Examples of Left Bundle Branch Block

V6

•

•

•

Small initial

R wave

Wide, deep

S wave

Primarily

negative

complex

•

•

•

Broad R

wave, often

notched

No Q or S

waves

Totally

positive

complex

Examples of Left Bundle Branch Block

V1 Examples of Right Bundle Branch Block

V6

•

•

Small

Q wave

Broad

S wave

• Notched

R wave

Examples of Right Bundle Branch Block

(a)

(b)

Deep S

RSR

RSR

Deep S

Basic 12-Lead Interpretation 491

Why was it ordered? Is this a middle-aged patient

with sudden onset of chest pain, diaphoresis, and

shortness of breath? Is this a repeat EKG on a postoperative orthopedic patient whose pre-op EKG

had non-specific changes? Is it a pre-admission

Figure D15 Miscellaneous Changes

PERICARDITIS

• Elevated, concave

ST segment

DIGITALIS EFFECT

•

•

•

Depressed, “scooped” ST

segments

Flat, inverted, or biphasic

T waves

Short QT intervals

HYPERKALEMIA

•

•

•

•

•

Tall, peaked T waves

Wide, flat P waves

Widening QRS

Disappearing ST segment

Merging QRS and T waves

HYPOKALEMIA

•

•

•

•

Appearance of U waves

Depressed ST segments

Flattening T waves

Widening QRS

HYPERCALCEMIA

• Short QT intervals

HYPOCALCEMIA

• Prolonged QT intervals

Figure D16 Miscellaneous Abnormalities

Abnormality . . .  Suggestive of . . . 

P Waves • wide, flat P waves

• no P waves

Hyperkalemia

QRS Complexes

• widening of QRS

• merging QRS and T

• widening of QRS

• prolonged QT interval

• short QT interval

• short QT interval

Hyperkalemia

Hypokalemia

Hypocalcemia

Hypercalcemia

Digitalis Toxicity

ST Segments

• disappearing ST segments

• ST depression

• sloping ST segments

• depressed, “scooped” ST segments

• elevated, concave ST segments

Hyperkalemia

Hypokalemia

Digitalis Toxicity

Pericarditis

T Waves

• tall, peaked T waves

• flattening of T wave

• diphasic or inverted T waves

Hyperkalemia

Hypokalemia

Digitalis Toxicity

U Waves • development of U waves Hypokalemia

EKG for an elective admission? Is the patient

stable or coding? Are you looking for something

specific, or just “fishing”? The context often guides

the order in which you approach the tracing and

may dictate the depth of your analysis.

492 Appendix D

Ischemia and Infarction: This step has many

components and involves virtually all leads.

The major clusters are the anterior leads V –V , 1 4 ( )

the inferior leads (II, III, and aVF), and the lateral

leads (I, aVL, and V –5 6 V ).

Chamber Enlargement: A thorough 12-lead analysis will

include inspection for both atrial and ventricular

enlargement. The best leads for analyzing atrial

enlargement are V1 and Lead II, while ventricular

enlargement is best viewed in V1 and V . 6

Miscellaneous Changes: The final inspection goes back

over all leads to look for fine points indicative of

chemical, metabolic, or mechanical disorders.

Summary of Findings

Your summary analysis should answer these questions:

1. What’s the rhythm? Is it a threat to perfusion?

2. Are there any ischemic changes? If so, which leads?

Which wall is involved?

3. Is the axis normal? If not, what is the deviation?

4. Is there a ventricular conduction defect? If so, which

branch?

5. Are there signs of hypertrophy? If so, which chambers?

6. Are there any other unusual findings that might indicate

drug toxicity, electrolyte imbalance, pericarditis, etc.?

Never forget that it’s the patient you treat, not the EKG.

All findings should be considered in context of the patient’s

overall status. See Figure D18.

Rhythm: Look first at the rhythm strip at the bottom

of the page to identify the underlying rhythm and

rate. Name the arrhythmia and note its potential

to impact perfusion.

Axis Deviation: Check Lead I and aVF to determine

axis. An underlying axis abnormality affects

vectors of all leads, so it should be ruled out

before drawing conclusions from the remainder

of the tracing.

Bundle Branch Block: Look at V1 and V6 to detect

bundle branch block. It’s useful to identify

conduction defects before looking for ischemic

changes because the ST pattern of left bundle

branch block can obscure the ST changes

associated with myocardial ischemia and

infarction.

Figure D17 Analysis Format for 12-Lead EKG

Interpretation

STEP LOOK FOR LOOK AT

1 Rhythm Rhythm strip

2 Axis deviation I, aVF

3 Bundle branch block V ,1 V6

4 Ischemia/infarction

V ,1 V4

II, III, aVF

I, aVL, V , 5 V6

5 Chamber enlargement V ,1 II

6 Miscellaneous changes All leads

Figure D18 Summary of EKG Features

ASSESSMENT LOOK AT LOOK FOR

Context Patient, chart • Clinical condition

• Changes over time

Rhythm and Rate Rhythm strip (Lead II) • Arrhythmias

• Threats to perfusion

Ischemia/Infarction

All leads

• V1 4 –V (anterior)

• V , 5 V , 6 aVL, I (lateral)

• II, III, aVF (inferior)

• ST changes

• T wave changes

• Q waves

• Loss of R waves

Axis Leads I and aVF

• QRS upright in I and aVF (normal axis)

• QRS up in I, down in aVF (LAD)

• QRS down in I, up in aVF (RAD)

• QRS down in I and aVF (ERAD)

Chamber Enlargement

Atrial enlargement

V1

II

Ventricular enlargement V1

Diphasic P:

• Initial deflection is larger (RAE)

• Terminal deflection is larger (LAE)

Unusual P morphology:

• Tall, peaked P wave (RAE)

• Notched P wave (LAE)

High-amplitude QRS complexes:

• R wave longer than S (RVE)

• Extremely deep S (LVE)

V6 • S wave larger than R (RVE)

• Extremely tall R (LVE)

Intraventricular Conduction

Defects

V1

V6

Wide QRS:

• Notched R wave (RBBB)

• Deep, slurred S wave (LBBB)

• Broad S wave (RBBB)

• Broad notched R wave (LBBB)

Miscellaneous Abnormalities

• Hyperkalemia All leads

• Tall, peaked T waves

• Wide, flat P waves

• Widening of QRS

• Disappearing ST segment

• Merging QRS and T

• Hypokalemia All leads • Flat T waves

• Increasingly prominent U waves

• Hypocalcemia All leads • Prolonged QT interval (for rate)

• Hypercalcemia All leads • Short QT interval (for rate)

• Digitalis Toxicity All leads

• Sloping ST segment

• ST depression

• Diphasic or inverted T wave

• Short QT interval

• Pericarditis All leads

• Elevated, concave ST segment

• Diffuse ST changes not correlated to

coronary vessels

493

494

SECTION 1 Introduction

Practice 12-Lead EKGs

In this section, you will find 18, 12-lead EKGs for you to practice applying the things

you’ve learned up to this point. These 18 tracings are intentionally “simplified” to get

you used to looking at 12-leads. That means that each of the 12 leads has been reduced

to a single complex, rather than the usual 2-4 complexes. This helps you get the feel of

a 12-lead without becoming overwhelmed.

Following these 18 “simplified” tracings, you’ll find another 20 tracings in Section 2.

The tracings in Section 2 have not been simplified. They are just the way they come

out of the EKG machine. By the time you get to Section 2, you should be comfortable

enough to find your way around the format.

Approach each tracing in the methodical format you learned in Figure D17. Look

at Rhythm, Axis, Bundle Branch Block, Ischemia/Infarction, Chamber Enlargement,

and finally Miscellaneous Changes.

495

Figure D19 12-Lead EKG—Practice Tracing #1

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

•

•

•

•

Sinus Rhythm, rate

72 bpm

Left Atrial

Enlargement

Left Ventricular

Enlargement

Acute anterior

ischemia

496

Figure D20 12-Lead EKG—Practice Tracing #2

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

•

•

•

•

Sinus rhythm, rate

60 bpm

Left axis deviation

Inferior wall

ischemia

(acute evolving

inferior wall MI)

Right bundle

branch block

497

Figure D21 12-Lead EKG—Practice Tracing #3

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

•

•

•

NOTE: The underlying

 rhythm is potentially

 lethal, making it the

most important feature

 of this EKG.

Third-degree AV

block (CHB) with

junctional escape

pacemaker

—atrial rate: 84 bpm

—ventricular rate:

50 bpm

 (irregular rhythm)

Left bundle branch

block

Left axis deviation

498

Figure D22 12-Lead EKG—Practice Tracing #4

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate

67 bpm

• Premature atrial

complex

• Inferior infarct, age

indeterminate

• Anterolateral infarct,

age indeterminate

499

Figure D23 12-Lead EKG—Practice Tracing #5

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate

69 bpm

• Right bundle branch

block

• Possible lateral

infarct

500

Figure D24 12-Lead EKG—Practice Tracing #6

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus bradycardia

rate 54 bpm

• Possible left atrial

enlargement

• Anterolateral

ischemia, possibly

acute

501

Figure D25 12-Lead EKG—Practice Tracing #7

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate

77 bpm

• First-degree heart

block

• Incomplete right

bundle branch block

•

•

Biatrial enlargement

Probable anteroseptal

MI, age indeterminate

502

Figure D26 12-Lead EKG—Practice Tracing #8

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate

76 bpm

• Left atrial

enlargement

• Inferior infarct

503

Figure D27 12-Lead EKG—Practice Tracing #9

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate is

86 bpm

• Acute inferior

subepicardial injury

504

Figure D28 12-Lead EKG—Practice Tracing #10

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate

72 bpm

• Anterior myocardial

ischemia

505

Figure D29 12-Lead EKG—Practice Tracing #11

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate

100 bpm

• Recent inferior wall

MI

• Possible previous

anterior MI

506

Figure D30 12-Lead EKG—Practice Tracing #12

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate

82 bpm

• Anterolateral

ischemia

507

Figure D31 12-Lead EKG—Practice Tracing #13

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate

79 bpm

• Less-than-transmural

MI is possible

• Actual anterolateral

ischemia

508

Figure D32 12-Lead EKG—Practice Tracing #14

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus tachycardia,

rate 107 bpm

• Old inferior infarct

• Repolarization

abnormality

consistent with

pericarditis following

recent surgery

509

Figure D33 12-Lead EKG—Practice Tracing #15

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate

85 bpm

• Anterior infarct, age

indeterminate

• Diffuse

non-diagnostic T

wave changes

510

Figure D34 12-Lead EKG—Practice Tracing #16

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus rhythm, rate

73 bpm

• Left axis deviation

• Inferior infarct, age

indeterminate

• Non-diagnostic

anterolateral T wave

changes

511

Figure D35 12-Lead EKG—Practice Tracing #17

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus tachycardia,

rate 107 bpm

• Left axis deviation

• Left atrial

enlargement

• Non-diagnostic lateral

T wave changes

• Inferior infarct

512

Figure D36 12-Lead EKG—Practice Tracing #18

aVR V1 V4

aVL V2 V5

aVF V3 V6

SIGNIFICANT

FINDINGS

• Sinus tachycardia,

rate 115 bpm

• Right axis deviation

• Inferior infarct, age

indeterminate

• Recent anterolateral

infarct

513

SECTION 2 Introduction

Practice 12-Lead EKGs

In this section, you’ll have an opportunity to practice reading 12-Lead EKGs as they

are typically found. Unlike SECTION 1, the EKGs in this section are not simplified as

single complexes, but are left in their original state of a running EKG. This will help you

transition from a textbook to the “real” EKGs you will find in your work. The purpose

of this section is to get you used to “real life” EKGs.

Some of the EKGs are normal while others have various abnormalities. Approach

each strip according to the format shown in Figure  D17. Consider the context—

why was the EKG taken? Then analyze Rhythm, Axis Deviation, Bundle Branch Block,

Ischemia/Infarction, Chamber Enlargement, and Miscellaneous Changes.

514

Figure D37 12-Lead EKG—Practice Tracing #19

I aVR V1

II aVL V2

III

V1

II

V5

aVF V3

V4

V5

V6

Ventricular Rate 76 bpm Normal Sinus Rhythm

PR Interval 0.20 sec Inferior infarct, age undetermined

QRS Duration 0.08 sec Abnormal EKG

515

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D38 12-Lead EKG—Practice Tracing #20

Ventricular Rate 113 bpm Sinus Tachycardia

PR Interval 0.16 sec Otherwise normal EKG

QRS Duration 0.08 sec

516

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D39 12-Lead EKG—Practice Tracing #21

Ventricular Rate 85 bpm Sinus Rhythm with First-Degree Heart Block

PR Interval 0.24 sec Inferior infarct, age undetermined

QRS Duration 0.08 sec Abnormal EKG

517

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D40 12-Lead EKG—Practice Tracing #22

Ventricular Rate

PR Interval

QRS Duration

48 bpm

0.24 sec

0.10 sec

Marked Sinus Bradycardia with First Degree

Heart Block

Abnormal EKG

518

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D41 12-Lead EKG—Practice Tracing #23

Ventricular Rate 73 bpm Sinus Rhythm with First-Degree Heart Block

PR Interval 0.24 sec Otherwise normal EKG.

QRS Duration 0.10 sec

519

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D42 12-Lead EKG—Practice Tracing #24

Ventricular Rate 94 bpm Sinus Rhythm with occasional PVCs

PR Interval 0.20 sec Possible left atrial enlargement

QRS Duration 0.10 sec Right Bundle Branch Block

Abnormal EKG

520

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D43 12-Lead EKG—Practice Tracing #25

Ventricular Rate 124 bpm Sinus Tachycardia

PR Interval 0.20 sec ST abnormality, possible digitalis effect

QRS Duration 0.08 sec Abnormal EKG

521

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D44 12-Lead EKG—Practice Tracing #26

Ventricular Rate 116 bpm Sinus Tachycardia

PR Interval 0.12 sec Voltage criteria for Left Ventricular Hypertrophy

QRS Duration 0.08 sec Abnormal EKG

522

I aVR V1 V4

II aVL V2 V5

III

II

aVF V3 V6

Figure D45 12-Lead EKG—Practice Tracing #27

Ventricular Rate 76 bpm Sinus Arrhythmia with occasional PVCs

PR Interval 0.20 sec Left Axis Deviation

QRS Duration 0.12 sec Left Ventricular Hypertrophy

Cannot rule out Septal infarct

Abnormal EKG

523

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D46 12-Lead EKG—Practice Tracing #28

Ventricular Rate 95 bpm Normal Sinus Rhythm

PR Interval 0.12 sec Incomplete Right Bundle Branch Block

QRS Duration 0.08 sec Inferior infarct, age undetermined

Abnormal EKG

524

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D47 12-Lead EKG—Practice Tracing #29

Ventricular Rate 84 bpm Normal Sinus Rhythm

PR Interval

QRS Duration

0.16 sec

0.08 sec

Cannot rule out Anterior infarct, age

undetermined

T wave abnormality, consider inferior ischemia

Abnormal EKG

525

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D48 12-Lead EKG—Practice Tracing #30

Ventricular Rate 48 bpm Marked Bradycardia

PR Interval 0.16 sec Abnormal EKG

QRS Duration 0.10 sec

526

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D49 12-Lead EKG—Practice Tracing #31

Ventricular Rate 107 bpm Sinus Tachycardia

PR Interval 0.16 sec Left Axis Deviation

QRS Duration 0.08 sec Possible Inferior infarct, age undetermined

Abnormal EKG

527

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D50 12-Lead EKG—Practice Tracing #32

Ventricular Rate 79 bpm Normal Sinus Rhythm

PR Interval 0.20 sec Inferior infarct, age undetermined

QRS Duration 0.08 sec Abnormal EKG

528

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D51 12-Lead EKG—Practice Tracing #33

Ventricular Rate 89 bpm Normal Sinus Rhythm

PR Interval 0.16 sec Possible Left Atrial Enlargement

QRS Duration 0.08 sec Borderline EKG

529

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D52 12-Lead EKG—Practice Tracing #34

Ventricular Rate 59 bpm Sinus Bradycardia

PR Interval 0.16 sec Left Bundle Branch Block

QRS Duration 0.16 sec Abnormal EKG

530

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D53 12-Lead EKG—Practice Tracing #35

Ventricular Rate 56 bpm Sinus Bradycardia

PR Interval 0.12 sec Low voltage QRS

QRS Duration 0.16 sec Right Bundle Branch Block

Abnormal EKG

531

I

aVR

V1 V4

II aVL V2 V5

III

II

aVF V3 V6

Figure D54 12-Lead EKG—Practice Tracing #36

Ventricular Rate 87 bpm Normal Sinus Rhythm

PR Interval

QRS Duration

0.08 sec

0.10 sec

ST elevation, consider inferolateral injury or

acute infarct

Abnormal EKG

532

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D55 12-Lead EKG—Practice Tracing #37

Ventricular Rate 122 bpm Sinus Tachycardia

PR Interval 0.12 sec Otherwise normal EKG

QRS Duration 0.08 sec

533

I aVR V1 V4

II aVL V2 V5

III

V1

II

V5

aVF V3 V6

Figure D56 12-Lead EKG—Practice Tracing #38

Ventricular Rate 74 bpm Normal Sinus Rhythm

PR Interval

QRS Duration

0.16 sec

0.08 sec

ST & T wave abnormality, consider lateral ischemia

Abnormal EKG

534

Overview

IN THIS APPENDIX, you will learn about artificial pacemakers, why and how they are used, and

the various ways they work. You will find out how different types of pacemakers produce different

wave forms on an EKG. You will learn to recognize pacemaker spikes and to differentiate between

functioning and malfunctioning pacemakers. You will learn how to interpret what is happening in

the heart based on what is seen on the rhythm strip.

Pacemakers

Appendix E

Artificial Pacemakers

When the heart’s normal pacemaker is unreliable and causes

bradyarrhythmias, it becomes essential to restore ventricular

function. This can be done by applying an artificial stimulus

to heart muscle, resulting in depolarization. Pacemakerinduced depolarization is called capture.

Pacemakers use three components to produce a repetitive

electrical stimulus and convey it directly to the myocardium:

1. Power Source: Battery unit called a pulse generator

2. Conducting Wire: Electrode that provides electrical

stimuli to the myocardium

3. Return Wire: Wire that returns to the battery unit to

complete the electrical circuit

Pacemakers 535

Pacemakers can be used temporarily or permanently.

• Temporary pacemakers are just that—they rarely stay

in place longer than a few days. They are used in acute

settings to stabilize and maintain the patient for short

periods. Temporary pacemakers are most often employed

using external pacing pads, or a special transvenous

pacing cannula if in controlled settings. In either case, the

pacing unit itself is positioned outside the body.

• Permanent pacemakers are indicated when long-term

support is needed. This generally requires an operating

room with anesthesia and imaging. The surgeon attaches

pacing wires directly to the myocardium, and implants

the pacemaker unit within the chest or abdominal cavity.

Classification of

Pacemakers

Pacemakers can be described according to the chamber paced,

the chamber sensed, and the response of the pacemaker to the

sensed impulse. A three-letter code correlating to these categories is used to describe pacemaker types. For example, a

VVI pacemaker paces the ventricles, senses the ventricles, and

is inhibited when it senses a beat. This classification scheme

is outlined in Figure E1a.

Chamber Paced

Pacemakers that stimulate only the ventricles are called

ventricular pacemakers. Since ventricular function is

essential, virtually all pacemakers have this capability.

In occasional patients, the pathology is within the atrial

conduction system while ventricular conduction is known

to be reliable. In such cases, an atrial pacemaker is used to

depolarize the atria, and the heart’s own conduction system

is relied upon to depolarize the ventricles.

Some pacemakers stimulate both atria and ventricles

in sequence. Called AV synchronous pacemakers, these

advanced pacemakers are physiologically superior because

they restore atrial kick.

Pacemakers that stimulate either the atria or the ventricles, but not both, are considered single-chamber pacemakers. Pacemakers that can stimulate both atrial and

ventricular chambers are considered dual-chamber pacemakers (Figure E1b).

Chamber Sensed

Advancing technologies enable tiny pacemakers to sense

intrinsic electrical activity and respond appropriately, either

by pacing or withholding stimulation in synchrony with the

patient’s rhythm. This technology enables them to manage

Figure E1a Pacemaker Classification

Chamber PACED Chamber SENSED Pacemaker RESPONSE

V Ventricle V Ventricle T Triggered (fires even when it senses a beat)

A Atrium A Atrium I Inhibited (holds back when it senses a beat; fires only on demand)

D Dual (both) D Dual (both) D Dual (atrial triggered and ventricular inhibited)

O Neither (no sensing)

Figure E1b Common Pacemaker Types

Single-Chamber

Pacemakers that can stimulate either atria

or ventricles, but not both

Dual-Chamber

Pacemakers that can stimulate both atria

and ventricles

Ventricular Demand Pacemaker (VVI):

• By far the most common type of pacemaker

• Senses spontaneous ventricular impulses

• Paces ventricles only when needed

Atrial Demand Pacemaker (AAI):

• Similar to VVI

• Except it senses and paces atria

• Maintains sequence of atrial and ventricular

contraction

AV Synchronous Pacemaker (VDD):

• Senses atrial and ventricular activity

• Paces only the ventricle

AV Sequential Pacemaker (DVI):

• Paces both chambers sequentially

• Senses only in the ventricle

Optimal Pacemaker (DDD):

• Referred to as fully automatic, universal,

and physiologic

• Senses both atrial and ventricular activity

• Paces atria, ventricles, or both in synchrony

as needed

536 Appendix E

complex information, making them “smart” devices that are

more responsive to changing patient needs.

Pacemaker Response

There are two basic ways in which pacemakers can initiate

impulses:

Triggered: These are fixed-rate pacemakers that fire

according to a predetermined plan, regardless of

the patient’s underlying cardiac activity.

Inhibited: These pacemakers are demand pacemakers—

they fire only when needed. They are capable

of inhibiting their stimulus when they sense a

patient’s complex.

It is possible for pacemakers to be both triggered and

inhibited. That is, they ignore atrial complexes but hold back

if they sense a ventricular beat.

Electrode Placement for

Temporary Pacemaker

When a patient is unstable and the EKG indicates that an

artificial pacemaker is needed, temporary pacing can be

initiated. The most common electrode placement for temporary pacemaker placement in acute settings is via external

pacing pads. Both pads can be placed on anterior chest wall,

or one pad can go on the front chest and the other on the

back. The key point when positioning the electrodes is to

ensure that the heart is well situated between the two pads

(Figure E2).

Temporary pacing can also be achieved transvenously

by inserting a special pacing wire cannula through a large

vein like the internal jugular or subclavian. Generally, this is

done only in settings where a sterile field can be maintained

and imaging is available to guide wire placement.

EKG Analysis

The electrical impulses produced by the pacemaker appear on

the EKG tracing as unnaturally sharp spikes superimposed

on the patient’s underlying rhythm. Pacemaker spikes can

be small and difficult to detect, so EKG machines often

augment the signal to make spikes more visible.

When the pacemaker captures, it produces an EKG

wave consistent with the chamber being paced. That is, if

it’s an atrial pacemaker, the spike will be followed immediately by a P wave, but if the pacemaker is stimulating the

ventricles, the spike will be followed immediately by a wide

QRS similar to a PVC. If both chambers are paced, there will

be two spikes for each cardiac cycle. See Figures E3–E5.

Properly Functioning

Pacemakers

In Figures E3–E7, the sharp spikes produced by pacemakers

are marked