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INTERPRETATIONS OF EKG AND ECG

Notice

Medicine is an ever-changing science. As new research and clinical


experience broaden our knowledge, changes in treatment and drug
therapy are required. The author and the publisher of this work have
checked with sources believed to be reliable in their efforts to provide
inronnation that is complete and generally in accord with the standards
accepted at the time of publication. However, in view of the possibility
of human error or changes in medical sciences, neither the author nor the
publisher nor any other party who has been involved in the preparation
or publication or this work warrants that the infomlation contained
herein is in every respect accurate or complete, and they disclaim all
responsibility for any error.; or omissions or for the results obtained
from usc of the information contained in Ihis work. Readers arc
encouraged to contiml the infonnation containcd herein with other
sources. For example and in particular, readers arc advised to check thc
product infomlation sheet includcd in the package of each drug they
plan to administer to be certain that the information contained in this
work is accuratc and that changes have not been made in the
recommended dosc or in thc eontraindications for administration. This
recommendation is of particular importance in connection with new or
infrequently used drugs.
Contents

Preface ix
Acknowledgments xi

1. BASIC

2. RATE 11

3. RHYTHM 13

4. AXIS 15

5. HYPERTROPHY 25

6. ISCHEMIA, INJURY, ANO INFARCTION 31

7. CONDUCTION BLOCKS 35

8. ARRHYTHMIAS 51

9. ELECTROLYTE AND DRUG EFFECTS 85

10. OTHER CONDITIONS 91

11. CARDIAC TESTING 97

v
vi CONTENTS

12. CARDIAC PACEMAKER 119

13. IMPLANTABLE CARDIAC DEFIBRILLATOR 125

14. ACUTE CARDIAC LIFE SUPPORT (ACLS) PROTOCOLS 127

15. SUMMARY 137

Index 145
Preface

Despite the advancement of new technologies the EKG remains an


absolute staple of medical practice and education. Clinicians, residents,
and students are eager to review sample tracings, as they know the value
of a timely EKG lest and understand the importance of the test to everyday
clinical practice.
This book was written to assist clinicians, interns, residents, medical
students, or anyone in the health care profession who is likely to encounter
EKGs in clinical practice. While there are many EKG resources available
in print, we continually hear from students and residents that there is room
for improvement, and we believe none of these resources arc as detailed
nnd user-friendly as Lange llllitani Access: EKGs alld Cardiac Studies.
The book includes evidence-based information that is essential in
practicing medicine. All the information in the manual was acquired
from respected references in the medical literature.
This manual is the final product of two and a half years of hard work
and was reviewed by some of the most recognized and respected
physicians in cardiology and family medicine. We trust that you will find
it helpful in your own educational or clinical activities.

ix
Acknowledgments

Lange illstant Access: EKGs alld Cardiac Studies is dedicated to two


individuals. One is my grandmother, who inspired me to reach for the slars
and nothing less. The second is the someone special to whom my heart will
always belong.
I would like to thank all of my tcachers and colleagues for their
support throughout my years of education and training. Special thanks
go out to my best friends, Ray Glover and Pam Gross.

xi
1
Basic

1!iillmif
A Anatomy of Cardiac Conduction System 2
B Cardiac Action Potential and EKG Tracing 3
C EKG Lead Placement 4
D EKG Tracing 7
2 BASIC

A ANATOMY OF CARDIAC CONDUCTION SYSTEM


The ncnnal cardiac conduction pathway is

Sinoatrial (SA) node -7 atrioventricular (A V) node -7


bundle of HIS -7 right and left bundle branches -7 Purkinjc system

FIGURE 1-1 Cardiac Conduction System

SA node ""-,"""",, Bachmann bundle

Right atrium
Internodal
tract -~~==~~1~~;~~~~f~~~~~~~ Internodal tract
Left of
Bundle atrium
HIS
Left ventricle
AV node Left
Right ventricle bundle branch
\I'\o..-t'--;If-+-- Left posterior
Right bundle --'<-'~:--\\\ fascicular branch
branch
~#'--,I- ____ Purkinje
Purkinje -------''<:-''''';!) fibers
fibers
Left anterior
fascicular branch
BASIC 3

B CARDIAC ACTION POTENTIAL ANO EKG TRACING

FIGURE 1-2 Action Potential Generation and Conduction


in Myocardium
- - - Myocyte and Purkinje cells

~
~Ph~'~"~'~~~~~~~='~"~".~"~".~'~S~i"~"'~'~"~d~AV~"'~d~'====
~ Phase II plateau
" 40
~ 30
- 20

~
~ o ~~'--~
- 20
-30
ll)
E -40
~ - 50
f!'. . . ." " ~~/'~""' ~ '''1'-
, "' -

- -60
~ - 70
~ =:g
N";;rmal resting potential '" Ph~e IV

Phase 0: Depolarization
- Sodium influx in myocyte and Purkinje cells
- Calcium influx in sinus and A V node
Phase I: Initial repoiarization
Phase II: Plateau (sustained calcium influx)
Phase III: Restoration of membrane resting potential (potassiwn
efflux)
Phase IV: Restoration of ion gradient by the Na/K pump in
myocyte and Purkinje cells
Automatic cell depolarization in sinus and A V node
4 BASIC

FIGURE 1-3 Cardiac Action Potential

SA node

I V\
-= .~t:i::t, 1\ r--. I
f/ \ -.............. I
I- I
~
, AV node

Bundle of I

Bundle lranch. ..........


....-c . .
I
I
I
t'-r--.
i'-
I
I
I
/~ I I
1,~ 1
~ ~~/ m,,,t, I@ 11111
EKG tracing

C EKG LEAD PLACEMENT


Precordial Lead Placement
VI: Right of sternum, fourth intercostal space
V 2: Left of sternum, fourth intercostal space
V3: Midway between Vz and V 4
V 4: Midc1avicular line, fifth intercostal space
Vs: Midway between V4 and V6
V 6: Midaxillary line, fifth intercostal space
BASIC 5

FIGURE 1-4

~"--+""'-"""'<"- Clavicular line

Right _-+---1'-'
nipple

line

Right leg 0 o Left leg


(ground)
6 BASIC

FIGURE 1-5

Midaxil\ary line

1
1
1
1
1
1
1
1
1
1
1
1
1

q
1
1
1
1
1
1

0
C/'
1
1
Vs 1
1
1
1
1
1
1
1
1
BASIC 7

D EKG TRACING

FIGURE 1-6 Cardiac Conduction System

0 .25
1 mm

.L
1 mm
0.04 s

T
i. Vertical axis:
1 small box = 1 mm
• 1 large box = 5 mm
·lO mm = l mV
ii. Horizontal axis:
1 small box = 0.04 seconds
1 large box = 0.20 seconds
5 large boxes = 1 second
30 large boxes = 6 seconds
8 BASIC

FIGURE 1-7

Normal Sin~s Rhythm


PR interval
I
I, aTI I
interval

QRS interval
I 8T interval I
~ ;
,
\ ;
[~ I \ ,;
,, :J:t ~-
/ 1'- I r--..
~-tt
,,; :~pOint ;
;
; ; !
~ ill
~ i 5T s~gmenl
i GGgman!
!~~ QRS interval ; I I •i
BASIC 9

TABLE 1-1: EKG: Waves and Inlervals


• P wave = depolarization of the atria
• QRS = depolarization of the ventricle
• T wave = repoiarization of the ventricle
Normal Values
Duration Height
(horizontal axis) (vertical axis)
Pwave <0.12 s <2 .5 mm
P· R interval 0.12-0.20 s
QRS interval 0.08-0.10 s
QT interval 0.35-0.44 s
QTc interval = QT interval divided by the square root
of R-R interval
Age group QTc interval by age
0-2 yrs 0.37-0.53
2-10 yrs 0.39-0.42
10-14 yrs 0.40-0.42
>15 yrs 0.35-0.44
2
Rate

IUliI.lllt
IA Rate Calculat;on 12

II
12 RATE

A RATE CALCULATION
i. Rate is cycles or beats per minute.
ii. Nonnal rate ror the sinoatrial (SA) node is 60 to 100 beats per minute.
iii . Less than 60/minute "" sinus bradycardia.
iv. Greater than 100/minute = sinus tachycardia.

Count number of complete QRS complexes in 6 seconds


(30 large boxes) multiplied by 10 (lOx 8 = 80).

Per big boxes: 300-150-100-75-60.


(Take an R wave on a heavy line or close to heavy line. The next
heavy line that is encoun tered is rate of300. The next one is 150
fo llowed by 100,75, and 60 and ending with 50. [See example
below}.)
E xample
3
Rhythm

IUliI.lllt
IA Rhythm Guidelines 14

13
14 RHYTHM

A RHYTHM GUIDELINES
i. Check for a P wave before each QRS (known as sinus rhythm).
ii. Check the rhythm strip for regularity (regular, regularly irregular,
and irregularly irregular).
iii. Check PR interval (for atrioventricular [A V] blocks).
iv. Check QRS interval (for block, widening).
v. Check for QT interval prolongation.

FIGURE 3-1 Normal Sinus Rhythm Pathway

SA node
Left atrium
Right atrium -I-J',,"'

AvnOde-~~~~~~~~==~,- Bundle of HIS

Right bundle --\---\:---t1 -f--+- Left


branch bundle branch
Purkinje _ _--',,_"'\ o---;f-- Purkinje
fibers fibers
4
Axis

lililimif
A Axis and Vectors 16
B Normal Axis 20
C Left Axis Deviation 21
D Right Axis Deviation 22

15
16 AXIS

A AXIS AND VECTORS

FIGURE 4-1

aVA aVL
AXIS 17

FIGURE 4-2

Posterior

Right

,,
,,,

~-~==~~ +V3
+V +V2
1

Anterior

Direction of depolarization (vector) of the QRS complex:


i. The left ventricle is thicker, so the mean QRS vector is down and
to the left. (The origin of the vector is the AV node with the left
ventricle being down and to the left of this.)
ii. The vector will point toward hypertrophy (corresponding to
electrocardiogram [EKG] deflections above the electrical
baseline) and away from the infarct (corresponding to EKG
deflections below the electrical baseline).
18 AXIS

FIGURE 4-3

aVR aVL

III aVF II

FIGURE 4-4

- 90

aVR
~150 aVL

+60

II
aVF
AXIS 19

TABLE 4-1 Axis Devi ation


Degree
Axis (angle) Lead ] Lead aVF
Normal axis 010+90 Positive Positive
Left axis deviation - 3010 - 90 Positive Negative
(LAD)
Right axis deviation +9010+180 Negative Positive
(RAD)
Indctenninate - 9010 - 180 Negative Negative
(extreme)
axis deviation
Etiology
Left axis LVH Left anterior Inferior wall M I
deviation fascic ul ar block
Right axis RV H Left posterior Lateral wall MI
deviation fascicular block
20 AXIS

B NORMAL AXIS

FIGURE 4-5 Normal Axis

~"
_'-'II. . ._ I: Positive

_LJII. . ._ aVF: Positive

+aVF

Example

FIGURE 4-6 Normal Axis EKG


AXIS 21

C LEFT AXIS DEVIATION

FIGURE 4-7 Left Axis Deviation

_ ....11'-',.-,_ _ I: Positive

-1 "-- aVF: Negative


A

V
+aVF

Example

FIGURE 4-8

aVR V,
1

II aV'=

11
22 AXIS

o RIGHT AXIS DEVIATION

FIGURE 4-9 RighI Axis Deviation

_O"'v-'--- I: Negative
-1.1\->,-.__ aVF: Positive

+aVF

FIGURE 4-10 Exlreme RighI Axis Deviation

--'l:'y.---I: Negative
--'l:'y.---aVF: Negative
+aVF
AXIS 23

Example

FIGURE 4-11 Right Axis Deviation

.VR v,I v,I


l I ,
• r'l
i
• I' I • I Y

~
r-_(,v,
I
.¥L v2
I
Vs
, I
Iv-! I I I

~H I a~f ,I V(
I
, I

~
I I II

I I I ~ L..!I l+.
i'
5
Hypertrophy

A Atrial Hypertrophy 26
B Ventricular Hypertrophy 29

25
26 HYPERTROPHY

A ATRIAL HYPERTROPHY
i. Right atrial hypertrophy
Lead II: P wave (>3 mm amplitude)
• Lead V I : Upright and biphasic P wave

FIGURE 5-1

-l Right Atrial Hypertrophy (P Pulmonale) I


/

Lead II
peaked wave
) \ >3mm

( '\
Lead V I
\
I Upright and biphasic

/ \
(peaked and broad)

IV I I
HYPERTROPHY 27

Example

FIGURE 5-2 Righi Atrial Enlargement

8'1

II aVL
I, ,,

III aVF 3
1

II
28 HYPERTROPHY

ii. Left atrial hypertrophy


Lead II: Broad and notched P wave (>0.12 mm)
• Lead V I : Biphasic P wave with broad negative phase

FIGURE 5-3

Left Atrial Hypertrophy (P Mitrafe)

I
Broad
Lead" I I and

V "\ notched
>0.12

ft ""-f-'iI ;nVj"ed
"""
HYPERTROPHY 29

B VENTRICULAR HYPERTROPHY
i. Right ventricular hypertrophy
Right axis deviation
Possibly a predominant R wave in lead VI (in a nonnal EKG, the
S wave is dominant in VI)
Deep S in V 6 (in a nonnal EKG, the QRS complex is
predominantly upward in V6)
Inverted T waves in leads V 2, V3
Peaked P waves may also occur due to right atrial hypertrophy
QRS < 0.12 second

Example

FIGURE 5-4 Righi Venlricular Hypertrophy


30 HYPERTROPHY

ii. Left ventricular hypertrophy


aVL: Rwavc>12mm
V 1 or V2 and Vs or V6: S wave in V 1 orV2 + R wave in Vs or
V6~=35mm
V 5 0rV6: R wave> 27 mm
Example

FIGURE 5-5 Left Venlric"lar Hypertrophy


6
Ischemia, Injury, and Infarction

lililimif
A Ischemia 33
B Injury 33
C Infarct 34

31
32 ISCHEMIA, INJURY, AND INFARCTION

TABLE 6-1 Ischemia, Injury, and Infarct


Ischemia Is a relative lack of T-wave inversion or
blood supply ST-segment depression
(commonly seen in I, II,
V 2-V6 )
Acute injury Acute damage to Elevated ST-scgmcnts with
myocardium or without Q waves
Old inrarct Dead myocardium Q waves without ST-
segment elevation

TABLE 6-2 Leads and Its Location


V 1-V 2 Anleroseptai wall
V 3-V4 Anterior wall
V5- V 6 Anterolateral wall
II, III , aVF Inferior wall
I, aVL Lateral wall
V 1- V 2 orV,V9 Posterior wall
V,R Right ventricle wall
ISCHEMIA, INJURY, AN D INFARCTION 33

A ISCHEMIA

FIGURE 6-1 Ischemia

No tc: Symmetric T-Wave Inversions in Leads r, V2 to V5

B INJURY

FIGURE 6-2 Injury

IIHI

No te: ST-Segment Elevation in Leads V2 to V3 (Anteroseptall


Anterior Wall)
34 ISCHEMIA, INJURY, ANDINFARCTION

C INFARCT
FIGURE 6-3 Recenllnfarcl

Note: Q Waves with ST-Scgment Elevation in Leads II, III ,


and aVF (Inferior Wall)

FIGURE 6-4 Infe,opo,le,;o, Waif fnfarcl

Note: Tall R wave in VI posterior wall infarcts are often associ-


ated with inferior wall infarcts (0 waves in 11 , III , and aVF).
Acute posterior wall infarcti on-related EKG changes can also
have tall R waves and ST segment depression in VI and V2.
7
Conduction Blocks

1!iillmif
A Bundle Branch Blocks 36
B First-Degree A V Blocks 40
C Second-Degree Blocks 41
D Third-Degree AV Blocks (Complete Heart Block) 43
E Fascicular Blocks 44
F Sinus Pause 48
G Wolff-Parkinson-White Syndrome 49

35
36 CONDUCTION BLOCKS

A BUNDLE BRANCH BLOCKS


i. Complete right bundle branch block
QRS complex: ;::0.12 seconds
S wave: Wide in lead I, wide and slurred in Vs to V6
rsR': VI and V 2
Secondary ST- and T-wave changes in V I and V 2

ii. Incomplete right bundle branch block


QRS complex: Between 0.09 to 0.12 seconds
• Axis: Mayor may not have right axis deviation

FIGURE 7-1 Right Bundle Branch Block (RBBB)

SA node
Right atrium Left atrium
AV node

JIH---'''''''-+f- Bundle of HIS

Right bundle ---'t-\---/i/ 1If----;;.L--+- Left


branch bundle branch

Purkinje ----',,---:.j) ~_---,'-__ Purkinje


fibers fibers
CONDUCTION BLOCKS 37

Example: RBBB

FIGURE 7-2

II
38 CONDUCTION BLOCKS

iii. Complete left bundle branch block


QRS complex: 2!::O .1 2 seconds
R wave: Wide and s lurred in V 5 to V 6
Leads J, V s, V6: ST depression and inverted T wave and lack of
Q waves
iv. Incomplete left bundle branch block
QRS complex: Between 0.09 and 0.12 seconds
R wave: Tall R waves in V5 to V6
Lack ofQ wave: I, aVL, Vs to V6

FIGURE 7-3 Lell Bundle Branch Block (LBBB)

SA node - -,"-1
Right atrium ---1--'--
Left arium
AV node -1~:::;:¥
1I1+---"""-- H '--- Bundle of HIS

Right bundle --\---'l,----HllfI----.,.L----;/--- Left


branch bundle branch
Purkinje --'<----'VJI ,\''---_f-__ purkinje
fibers \: fibers
CONDUCTION BLOCKS 39

Example: LBBB

FIGURE 7-4
40 CONDUCTION BLOCKS

B FIRST-DEGREE AV BLOCKS
i. PR intervals: ;;::0.20 seconds or 200 ms
ii. Etiology:
Medications
Beta blocker
Calcium channel blocker
Digitalis
Quinidine
Excessive vagal tone
Intrinsic disease in the A V junction

FIGURE 7-5 First-Degree AV Block

P wave: P wave prior to QRS wave


PR interval: >0 .20 seconds
QRS complex: >0.12 seconds
Rhythm: Normal
CONDUCTION BLOCKS 41

C SECONO-OEGREE BLOCKS
i. Mobitz type I (Wcnckcbach)
Rate: 60 to 100 beats/minute
Atrial rhythm: Regular
Ventricular rhythm: Progressive shortening of the R~R interval
until the QRS is dropped
P-wave configuration: Nonnal
PR interval: Prolonged with each beat until QRS is dropped
QRS complex: Normal
ST segment: Nonnal
T wave: Nonnal
Etiology: Inferior wall MI, digitalis, beta blocker, calcium
channel blocker, rheumatic fever, myocarditis, and excessive
vagal tone

FIGURE 7-6 Second-Degree Type 1 Block


42 CONDUCTION BLOCKS

ii. Mobitz type II (2:1, 3:1 AV block)


Rate: Ventricular rate is variable.
Atrial rhythm: Regular (the P-P interval is constant).
Ventricular rhythm: Irregular.
P wave: 2: 1, 3: 1, or 4: 1 conduction with QRS.
PR interval : Constant (PR intervals are constant until a
nonconducted P wave occurs).
Etiology: Anterior or anteroseptal MI, cardiomyopathy,
rheumatic heart disease, coronary artery disease, beta blocker,
calcium channel blocker, digitalis.

FIGURE 7-7 Second-Degree Type 2 Block


CONDUCTION BLOCKS 43

D THIRD-DEGREE AV BLDCKS
(CDMPLETE HEART BLDCK)
i. There is no relationship with P wave and QRS complex because
there is complete A V dissociation .
ii. The dissociation is due to atria and ventricles being controlled by
separate foci .
Atrial rhythm: Regular
P~wave configuration: Normal
PR interval: No relationship between P wave and QRS complexes
QRS complex: Variable (depends on the intrinsic rhythm)
ST segment: Nannal
T wave: Nonnal
Etiology: Anterior and inferior MI, coronary artery disease,
excessive vagal tone, myocarditis, endocarditis, digitalis, beta
blocker, calcium channel blocker.

FIGURE 7- 8 Third-Degree AV Block


44 CONDUCTION BLOCKS

E FASCICULAR BLOCKS
Fascicular blocks are blocks on part oflhe left bundle, either the poste-
rior or the anterior division.

I. Left anterior fascicular block (the most common intraventricular


conduction defect)
Left axis deviation (-30 to -90 degrees).
rS complexes in II, III, aVF.
Small q in I and/or aVL.
The QRS will be slightly prolonged (0.1-0.12 seconds).

FIGURE 7-9 Anterior Fascicular Block

SA node Left atrium


Right atrium
AV node-\+-;;;:~~.(
~\'\---+-+- Bundle of HIS

Left
Right bundle --\---\__-11/ \\LlI-I---J~bundre branch
branch Posterior fascicle
~~~+- Anterior fascicle
CONDUCTION BLOCKS 45

Example

FIGURE 7-10 Anterior Fascicular Block


46 CONDUCTION BLOCKS

ii. Left posterior fascicular block (less common)


Right axis deviation (usually >+100 degrees)
• rS in lead I
• Q in lead III (S IQ3)
• The QRS will be slightly prolonged (0.1-0.12 seconds)

FIGURE 7-11 Posterior Fascicular Block

SA node Left atrium


Right atrium

AV nOde-\:~~~~~~~L1~ Bundle of HIS

Right bundle \\\-'1-+---;f- Left bundle branch


branch -\--\---Ili Posterior fascicle
~..-+-Anterror fascicle

Example

FIGURE 7-12 Posterior Fascicular Block


, ,.."
aVi
J. • .~4 A " A,I
• • I I
11111
I'
-, -,'I"L
, , ~, .~ ,
~; ,

'v ~ r v' -y -y -1 I

"' aVF
, c, -,
v~ A A Vs ,,
j~ 11' ~I
II
, ,
, , 'v 'v , -, 'v -v' v v -v -v,
CONDUCTION BLOCKS 47

iii. Bifascicular block


• Represents block of two of the three fascicles .
• The most common of them is RBBB plus left anterior fascicular
block (LAFB) or left posterior fascicular block (LP FB) .

FIGURE 7-13 Bilascicular Block

SA node Left atrium


Right atrium

Avnooe1i~::~~~~~=z~ Bundle of HIS


\/~I<),,,,-f---+ l eft
bundle branch
Righi bundle -'\--\_-+11 "I------,~ Posteri or fascicle
branch
~Qr-l'-- Anterior fascic le

Example

FIGURE 7-14 Right Bundle Branch Block and


Left Anterior Fascicular Block

'IT ""1 n '\if ~) ±~ ]


;,,~r~' ravR" I ~ t V, " -~
, II! 'II'VL v, ~~
:~

.., tl
II I

I lc~ v,
' I'';~.
,~j
~'~"'. . I""

~
- i I-~ ~ i ""if'
48 CONDUCTION BLOCKS

F SINUS PAUSE
i. Rate: Variable
ii. Rhythm: Sinus
iii. P wave: Conducted P wave occurs later in time than expected
based on previous sinus rhythm (P~P interval is disturbed)
iv. PR interval: 0.12 to 0.20 seconds
v. QRS complex: <0.12

FIGURE 7-15
CONDUCTION BLOCKS 49

G WOLFF-PARKiNSON-WHITE SYNOROME
i. Rhythm: Sinus
ii. P wave: Nonna]
iii. P-R interval: Short «0.12 second)
iv. QRS complex: Slurred (delta wave), prolonged with ST
segment and T wave changes

FIGURE 7-16 Wolff-Parkinson-While Syndrome

SA node Left atrium


Right atrium
AV node -I*--,~,{
Bundle of Kenll~':::;:::-:;fr~
\\\-\-- --/-1-'1- Bundle of HIS

Right bundle --\-~'<---H \ \\\-f--!JLf- bundle


Left
branch branch
Myocardium
Purkinje _ _-''''-'''':::~) ~=",'-f-- Purkinje
fibers fibers
so CONDUCTION BLOCKS

Example

FIGURE 7-17 WPW Syndrome

"

'"
8
Arrhythmias

lililimif
A Supraventricular Arrhythmia 52
B Ventricular Rhythm 73
C Paced Rhythm 83
D Miscellaneous 84

51
52 ARRHYTHMIAS

A SUPRAVENTRICULAR ARRHYTHMIA
i. Sinus tachycardia
Rate: > 100 beats/minute
Rhythm: Sinus
P wave: Normal prior to each QRS complex
PR interval: 0.12 to 0.20 seconds
QRS complex: <0.12 seconds

FIGURE 8-1

Example

FIGURE 8-2

aVR
ARRHYTHMIAS 53

ii. Sinus bradycardia


Rate : <60 beats/minute
Rhythm: Sinus
P wave: Nannal prior to each QRS complex
PR interval: 0. 12 to 0.20 seconds
QRS complex : <0. 12 seconds

FIGURE 8-3

Exa mple

FIGURE 8-4

e--,\ 1= I s==::fi"Pt •
~I a~H V,
c

aVL

11" aVF
1

II

~
S4 ARRHYTHMIAS

iii. Sinus arrhythmia


Rate: 60 to 100 beats/minute
Rhythm: Irregular (10% variation in P-P interval)
P wave: Nonnal prior to QRS complex
P-R interval: 0.12 to 0.20 seconds
QRS complex: <0.12 seconds

FIGURE 8-5
ARRHYTHMIAS 55

iv. Atrial bigeminy: Each sinus beat is followed by an atrial


premature beat.
Rate: N/A
Rhythm: Irregular
P wave: Premature and abnonnal or hidden
PR interval: <0.20 seconds
QRS complex: <0.12 seconds
Note premature beats below

FIGURE 8-6

Example

FIGURE 8-7 Alrial Bigeminy


S6 ARRHYTHMIAS

v. Premature atrial contraction (PAC)


Rate: N/A
Rhythm: Irregular
P wave: Ectopic
PR interval : May be nonnal or >0.20 seconds
QRS complex: <0.12 seconds
Nonnal ventricular complex

FIGURE 8-8 Premature Atrial Contraction

SA node ----t<-t"-
AVnode-i-~~~2\

Right -+- +-- -+11


bundle
branch
ARRHYTHMIAS 57

vi. Premature junctional beat or complex


Rate: 60 to 100 beats/minute
Rhythm: Irregular
P wave: Can occur prior, during, and after QRS complex
PR interval: <0.12 seconds
QRS complex: <0.12 seconds
Is an ectopic foci in the A V junction

FIGURE 8-9 Premature Junction Beat

SAnade ~-+/

Stimuli
AV node li:2~::::~.\ initiation
\11'1-- -++- Bundle
of HIS

Right -\---\---~I 11l---tt- Left


bundle bundle
branch branch
S8 ARRHYTHMIAS

Vl1 . Atrial escape beat


Sinus P wave QRS complex that is followed by a P-QRS complex
in wh ich the P wave appears later and may have slightly different
morphology than the sinus P wave

FIGURE 8-10 Atrial Escape Beat

SA",de~ LJ
AvnOde-lIi~::~~~~~~:=:L-'- Bundle
of HIS

Right -Ir--\----il \\\-- - -H - Left


bundle bundle
branch branch

illlllllliJ tll l lE
ARRHYTHMIAS 59

viii. Junctional escape beat


An escape beat that occurs after a pause in the normal sinus
rhythm.
Atrial pacing usually resumes after the junctional beat.
P wave is missing prior to junctional beat.

FIGURE 8-11 Junctional Escape Beat

SA node

AV node -t~::::::~~~S~-:~l- Bundle


of HIS

Right- \---\-- -J+-Left


bundle bundle
branch branch
60 ARRHYTHMIAS

ix. Supraventricular tachycardia (SVT)


Regular rhythm
Rate 140 to 220 beats/minute
Abnonnal P wave (not easily identified)
Nonspecific ST- and T-wave changes
QRS complex can be narrow or wide depending on whether
there is aberrant conduction

FIGURE 8-12 Supraventricular Tachycardia (SVT)

Left atrium
SAnOdetfl..

Right
atrium
""" AV node

Bundle
of HIS

~
Right Left
bundle bundle
branch branch

Purkinje Purkinje
fibers fibers
ARRHYTHM IAS 61

Example

FIGURE 8-13 SVT

I - ~ p

?- - ' ,
- t
-
•, , ,
-f .-

r l:-
" a--Fr
" ,

Q~!i!ID![;!ii!3IIDll:i~!~lillif!;jm~!!!3lififf11lli!bI~§
62 ARRHYTHMIAS

FIGURE 8-14 Paroxysmal Atrial Tachycardia (PAT) or Paroxysmal


Supraventricular Tachycardia

SA node

AV node

Bundle
of HIS

Right Left
bundle bundle
branch
ARRHYTHMIAS 63

Example

FIGURE 8-15 PAT/PSVT

i. Rate exceeds 100 beats/minute


ii. Negative P waves can be seen
64 ARRHYTHMIAS

FIGURE 8-16 Paroxysmal Junctional Tachycardia

SA node

AV node
Bundle
of HIS

Right Left
bundle bundle
branch branch
ARRHYTHMIAS 65

X. Multifocal atrial tachycardia (MAT)


Rate: > 100 beats/minute (if <100 beats/minute ~ it is called
multifocal atrial rhythm)
P wave: At least three different shapes of P waves in onc lead
Rhythm: Irregularly irregular with varying PR, R-R, and PR
intervals
Etiology: COPD or other underlying lung disease

FIGURE 8-17 Multi!ocal Atrial Tachycardia (MAT)

SAnOde~

AV node +f.~::5~~:c~~/::::l
\\\~--='-----I-1r- Bundle
of HIS

Right - 'l--\-- ---\l1 \\\-- - -H - Left


bundle bundle
branch branch
66 ARRHYTHMIAS

Example

FIGURE 8-18 MAT

r- IV'
aVR . v; , ('; I y,

th . v, ,v,
-

'II , l l
aVL

.LI l • ....,.,
"I aVF
PJ31V; lv, ,
frree different morphologies 01

I' =1 ' ' ' ' - ' ' ' · ' -,


, -"
, ' I
...II _1.L1 1.1 _I .1 ,I .1 I .11 . 1

XI. Junction al rhythm


Rate: 40 to 60 beats/minute
Rhythm: Regular
P wave: Inverted or absent or after QRS complexes or
<0. 10 seconds
PR interval: <0. [2 seconds
QRS complex: <0.12 seconds
Etiology: Inferior wall MI, hypoxia, electrolyte disturbance,
CHF. cardiomyopathy

FIGURE 8-19 Juneli.n.1 Rhythm


68 ARRHYTHMIAS

xiii. Atrial fibrillation


Rate: >350 beats/minute
Rhythm: Irregularly irregular
P wave: Absent/fibrillatory waves
PR interval: N /A
QRS complex: <0. 12 seconds

FIGURE 8-21 Atrial Fibrillation (A.Fib)

SA node

AV node
Bundle
of HIS

Right Left
bundle bundle
branch branch

~ or,. - . .A _
ARRHYTHMIAS 69

FIGURE 8-22 A-Fib

I
70 ARRHYTHMIAS

xiv. Atrial flutter


Rate: 200 to 350 beats/minute (if rate is 150 beats/minute, it may
flutter with 2: 1 block)
Rhythm: Regular, sawtooth pattern (best noted in II, III, aYF)
P wave: Absent/sawtooth pattern
PR interval: N/A
QRS complex: <0.12 seconds (conduction ratio--P wave to
QRS-may be 2: 1,3: 1, etc)

FIGURE 8-23 Alrial Flutter

SA node

AV node
Bundle
of HI S

Right Left
bundle bundle
branch branch
ARRHYTHM IAS 71

Example

FIGURE 8-24 Alrial Flutter

iI ~
,
11
72 ARRHYTHMIAS

xv. Wandering atrial pacemaker


Rate: <100 beats/minute
Rhythm: Irregular
p wave: 2:3 morphologies
PR interval: Variable
QRS complex: <0. 12 seconds

FIGURE 8-25 Wandering Pacemaker

SAnOde/O
'*
AvnOde~~~~~~~;;::~===!~
I Bundle
of HIS

Right --\-- \-- --\11 \\-- - -;-/- Left


bundle bundle
branch branch
ARRHYTHMIAS 73

B VENTRICULAR RHYTHM
i. Idiovcntricular rhythm: Benign rhythm commonly associated
with reperfusion
Rate: 301040 beats/minute
Accelerated idioventricular rhythm rate (A1VR): 40 to 60
beats/minute
Benign and commonly associated with reperfusion in the
setting of acute myocardial infarction
Rhythm: Regular without P wave or no relationship between P
wave and QRS complexes
P wave: May be absent
QRS complex: Wide (>0. 12 seconds)

FIGURE 8-26

Example

FIGURE 8-27
74 ARRHYTHMIAS

ii. Premature ventricular contraction (PVC)


Is an ectopic foci originating in the ventricles.
Three pyes are considered a run of ventricular tachycardia.
Bigeminy: pves that occur in every other beat.
Trigeminy: pves that occur with evcl)' third beat.
Rate: Variable.
Rhythm: Regular except for the PVC .
P wave: Absent.
PR interval: None.
QRS complex: >0.12 seconds.

FIGURE 8-28 Premalure Venlrieular Conlraelion (PVC)

SA node

AV node it:::::::3~~
\\Vf----t-l- Bundle
of HIS

Right -\--\--111
bundle \\\---+--+- Left
branch bund le
branch

~I
If! v
I
ARRHYTHMIAS 75

Example

FIGURE 8-29 PVC

iii. Ventricular bigeminy


• Bigeminy: PVC followed by a nonnal QRS complex
<)Rate: 60 to 100 beats/minute
o Rhythm : Irregular
o P wave: Normal
PR interval: Normal
QRS complex: Nannal QRS complex followed by a wide
QRS complex
Etiology: Electrolyte disturbance, hypox ia, medication
toxicity, acute MI

FIGURE 8-30
76 ARRHYTHMIAS

iv. Ventricular trigeminy


• Trigeminy: PVC followed by a two normal QRS complexes
Rate: 60 to 100 beats/minute
Rhythm: Irregular
P wave: Normal
PR interval: Normal
QRS complex: Normal QRS complex followed by a wide
QRS complex
Etiology: Electrolyte disturbance, hypoxia, medication
toxicity, acute MI

FIGURE 8-31
ARRHYTHM IAS 77

v. Ventricular escape beat


Rate: N/A.
Rhythm: Beat occurs later than expected.
P wave: Absent.
PR interval: N /A.
QRS complex: 2:0. 12 seconds.

FIGURE 8--32 Ventricular Escape Beat

SA node

AV node -~~~~~~;;~:l- Bundle of HIS

bundle
Right
branch
-+--k*-+-- bundle branch
Left

. 11-
78 ARRHYTHMIAS

vi. Ventricu lar tachycardia (VT)


Rate: 150 to 250 beats/minute
Rhythm: Regular
P wave: Absent or invcI1ed and is not associated with QRS
complex
PR interva l: N/A
QRS complex: ;:: 0.12 seconds (wide)
Etiology: MI , cardiomyopathy, CHF, hypokalemia,
hypomagnesem ia, medication tox icity, reperfusion
following thrombolytic therapy

FIGURE 8-33 Venlricular Tachycardia

SA node

AV node \t:::::::::f:~~
\\\+----+-+ Bundle
of HIS

>T++- Left
bundle
Right ---'\---\---
branch
bundle
branch
ARRHYTHM IAS 79

Example

FIGURE 8-34 V. Tach


80 ARRHYTHMIAS

vii. Ventricular flutter


Rate: 250 to 350 beats/minute
P wave: Absent
PR interval: N/A

FIGURE 8-35 Ventricular Flutter

SAnOde
w
AV node -ttc~~~~:::::"~~=f-t- Bundle
of HIS

\\\----.-.t-+ Left
bundle
Right - -\--'\-- -1\\ branch
bundle
branch
ARRHYTHMIAS 81

viii. Ventricular fibrillation (V. Fib)


Rate: 2!300 beats/minute
Rhythm: Irregular
P wave: Unrecognized
PR interval: N/A
QRS complex: Fibrillatory waves
Etiology: Coronary artery disease, MI, cardiomyopathy,
cardiac trauma, medication toxicity, hypoxemia,eieclrolyte
imbalance

FIGURE 8-36 Venlricular Fibrillalion (V. Fib)

SAnOde~

AV node -t-t---:::;::G:~

Bundle of HIS -+~=T~"-:'\\\


82 ARRHYTHMIAS

Example

FIGURE 8-37 V. Fib

ix. Torsadcs de pointes: Usually associated with electrolyte


abnormalities or medications that may excessively prolong the
QT interval

FIGURE 8-38 Torsades de Pointes


ARRHYTHMIAS 83

C PACED RHYTHM
i. Ventricular demand pacemaker

FIGURE 8-39

; ;tt-'

ii. Dual chamber pacemaker

FIGURE 8-40
84 ARRHYTHMIAS

o MISCELLANEOUS
i. Sick sinus syndrome (S88), also known as tachycardia-
bradycardia syndrome
Rate: Variable
Rhythm: Regular or irregular
P wave: Nannal
PR interval: Nonnal
QRS complex: Normal
Etiology: Damage to conduction system
Cardiomyopathies, sarcoidosis, amyloidosis, Chagas disease
SSS worsened by following medications:
• Digitalis
• Calcium channel blocker
• Beta blocker
• Sympathomimetics

FIGURE 8-41
9
Electrolyte and Drug Effects

lililimif
A Hypokalemia 86
B Hyperkalemia 87
C Hypocalcemia 88
D Digitalis Effect 89

85
86 ELECTROLYTE AND DRUG EFFECTS

A HYPOKALEMIA
i. Prolonged PR interval
ii . T-wave flattening
iii. Prominent U waves displayed by arrows

FIGURE 9-1
ELECTROLYTE AND DRUG EFFECTS 87

B HYPERKALEMIA
i. K+ level: 5.5 to 6.5 meq ~ tall peaked T waves, more prominent
inV3toV5
ii. K+ level : 6.5 to 7.5 meq ~ flattening ofP wave and QRS
widening
iii. K+ level: >7.5 meq ~ sinus arrest and possible sine wave pattern
due to marked intraventricular conduction delay

FIGURE 9-2 Hyperkalemia


88 ELECTROLYTE AND DRUG EFFECTS

C HYPOCALCEMIA
i. QT prolongation

FIGURE 9-3
ELECTROLYTE AND DRUG EFFECTS 89

D DIGITALIS EFFECT
i. Commonly seen in use of digitalis and not with digitalis toxicity
ii. Prolonged PR interval
iii. Depressed and concave (scooped) ST segment: Most prominent
in I, II, aVF, and V2 to V6

FIGURE 9-4 Digitalis Toxicity

No te: Digitalis toxicity

iv. Induces arrhythmias such as paroxysmal atrial tachycardia (PAT)


with block, atrial fibrillation (A. Fib) with complete heart block,
accelerated junctional rhythm
10
Other Conditions

lililimif
A Hypothermia 92
B Pulmonary Embolism 93
C Pericarditis 94
D Pericardial Effusion 95

91
92 OTHER CONOITIONS

A HYPOTHERMIA
i. J wave or Osborne wave: Noted immediately after QRS complex,
common in lead r.
ii. J wave disappears after wanning of body temperature.

FIGURE 10-1

Osborn wave at J point

- Z
OTHER CONDITIONS 93

B PULMONARY EMBOLISM
i. Prominent S wave in lead I
ii. Q wave in lead III
iii. T wave invers ion in lead III
iv. Note: Most commonly seen rhythm in pulmonary embolism in
sinus tachycardia

FIGURE 10-2 Pulmonary Embolism


94 OTHER CONDITIONS

C PERICARDITIS
i. ST segment elevation in leads T, II, aVL, aYF, V 2 to V 6 .
ii. A clue that the EKG may be pericarditis is early PR depression
and ST segments return to nonna! before T waves invert .

FIGURE 10-3
OTHER CONDITIONS 95

D PERICARDlAl EFFUSIDN
i. Electrical altemans noted on EKG .
ii. The amplitude (height) of the R wave alternately varies in every
other beat.

FIGURE 10-4 Pericardia I EIf"sion


11
Cardiac Testing

llliillillf
A Cardiac Stress Test 98
B Exercise Stress Test 100
C Cardiac Stress Echocardiography 105
D Pharmacological Stress Test 106
E Nuclear Imaging 109
F Cardiac Echocanliography 111
G Cardiac Catheterization 113
H Holter Monitoring 115
I Electrophysiologic Study 115

97
98 CARDIAC TESTING

A CARDIAC STRESS TEST


i. Pretest probability for coronary artery disease (CAD)

TABLE 11-1 Pretest Probabilitv for Coronary Artery Disease: Male


Condition 30-39 yrs 40-49 yrs 50-59 yrs 60-69 yr.
Classic Inter- High High High
angina mediate
pectoris
Atypical Inter- Inter- Inter- Inter-
angina mediate mediate mediate mediate
pectoris
Nonanginai Low Inter- Inter- Inter-
chest pain mediate mediate mediate
Asymptomatic Very low Low Low Low
CARDIAC TESTING 99

TABLE 11-2 Pretest Probability for Coronary Artery


Disease: Female
Condition 30-39 yrs 40-49 yrs 50-59 yrs 60-69 yrs

Classic angina Inter- Inter- Inter- High


pectoris mediate mediate mediate

Atypical Very low Low Inter- Inter-


angina mediate mediate
pectoris

Nonanginal Very low Very low Low Inter-


chest pain mediate

Asymptomatic Very low Very low Very low Low

Source: Gibbons RJ, 8alady GJ, Beasley JW, et al. ACe/AHA


guidelines for exercise testing: Executive summary. A report of the
American College of Cardiology/American Heart Association Task
Force on Practice Guidelines (Committee on Exercise Testing). Circu-
lation. 1997; 96 :345- 354.

High: >90% probability ofeAD


Intennediate: 10% to 90% probability of CAD
Low: <10% probability of CAD
Very low: <5% probability of CAD

ii. Coronary artery disease and cardiac testing modalities


Treadmill exercise testing
Cardiac nuclear imaging
Cardiac angiography
Cardiac echo
100 CARDIAC TESTING

B EXERCISE STRESS TEST

FIGURE 11-1 Exercise Treadmill Testing (Err)

• •
o~o
o 0

i. Class types: Ace/AHA classification


Class I: Agreement/evidence of a condition that a procedure
or treatment is useful and effective.
Class II: Discrepancy/conflicting evidence of a condition that
a procedure or treatment is useful and effective.
Class llA: Data/opinion is in support of usefulnessl
efficacy
Class liB: Data/opinion is less well established to
support usefulness/efficacy
Class III: Agreement/evidence of a condition that a procedure
or treatment is not useful or effective. It may even be
hannfuL
CARDIAC TESTING 101

ii. Indications for exercise testing for detection of coronary artery


disease
Class I: Individual with intennediate pretest probability of CAD
Class IIA: Individual with vasospastic angina
Class rrB: Individual with high or low pretest probability
Class III: Individual with
Wolf-Parkinson-White syndrome
Paced ventricular rhythm
> 1 mm of resting S-T depression
Complete left bundle branch block
iii. Indications for ETT for risk stratification in patients with
known CAD
Class I: Initial testing
Change in clinical status post-revascularization
(combine with cardiac imaging)
Class I1A: None
Class lIB: Stable symptoms and periodic monitoring to guide
treatment
iv. Indications for ETT post-m)'ocardial infarction
Class I: Submaximal stress test 4 to 7 days post-uncomplicated
myocardial infarction prior to hospital discharge for
prognosis, activity prescription, or evaluation of medi-
cal treatment
Class II: Post-revascularization for activity prescription or
periodic monitoring of high-risk patients
Class III: Routine monitoring after revascularization
v. Indications in asymptomatic patients with no known CAD
Class I: None
Class liB: Multiple risk factors, diabetes
Class III: Routine screening
vi. Disadvantages
Specificity decreases with
Marked baseline ST abnormalities
Usc of dioxin
Left bundle branch block
Pacemaker
102 CARDIAC TESTING

vii. Baseline EKG changes that may lead to difficulty in


interpreting stress test
• ST depression or elevation (2:1 mm)
• Ventricular strain pattern (secondary from right or left
ventricular hypertrophy)
• T-wave inversion (from strain or previous injury)

Exercise Stress Test

1.5 1.5
1.0 HOjOntal 1.0
mV +0.5
0
~
-0.1 mV
). mV +0.5
0
U\
-0.5
~ Downsloping - 0.5

Horizontal downsloping 51-segment ST-segment elevation <! 0.1 mV


depression, <: 0.1 mV

0.08 seconds
1.5 1.5
,(
1.0 1.0
mV +0.5
0
II A mV +0.5
0
/\ ~

-0.5 'I "--0.2 mV -0.5

Upsloping ST-segment depression, U-wave inversion


<: 0.2 mY, 0.08 seconds from the
J point

(continued)
CARDIAC TESTING 103

Exercise Stress Test (Continued)


Electrocardiographic (EKG) findings suggestive of a positive
exercise stress test. In addition to the EKG findings depicted here,
the occurrence of frequent premature ventricular contractions
(pyes), multi focal pyes, or ventricular tachycardia at mild
exercise «70% of maximal heart rate) is suggestive of an exercise
stress test positive for myocardial ischemia.

Reproduced with pennission from Darrow MD. Ordering and understanding


the exercise stress test. Alii Fam PhYSician. 1999;59:401-410.

Exercise Testing Contraindications


Absolute
i. Acute aortic dissection
ii. Acute myocardial infarction within 2 days
iii. Acute myocarditis
iv. Acute pericarditis
v. Pulmonary embolism/infarction
vi. Recent lower extremity DVT
vii. Severe symptomatic aortic stenosis
viii. Uncontrolled heart failure
ix. Uncontrolled symptomatic cardiac arrhythmia
x. Unstable angina
xi. Third-degree A V block

Relative
i. Stenotic valvular disease
ii. Electrolyte imbalance
iii. Uncontrolled hypertension
iv. Tachycardia or bradycardia
v. Hypertrophic cardiomyopathy
vi. Inability to exercise
vii. High grade of AV block
104 CARDIAC TESTING

Stress Test Protocols


i. There are several protocols in existence for exercise stress testing.
ii. Majority arc aimed at obtaining 85% to 100% of age-predicted
heart rate.
iii. Maximum predicted heart rate = 220 - age (years).
iv. Metabolic equivalents of tasks (METs) = actual metabolic expense
during exercise (resting O2 consumption [V0 2]) = 3.5 mLlkg/min
Functional capacity in METs
Poor: <4
Moderate: 4 to 7
Good: 7 to 10
Excellent: >10
i. Bruce protocol: 8 stages, each stage is 3 minutes, substantial
increase in incline and speed .
Test is considered correct if;::6 METs have been obtained.
(Note: The test is usually continued even if 6 METs have been
reached.)
Certainty of MET levels achieved:
Less than or equal to 5 METs = Poor prognosis in individual
of age :5:65 years
10 METs = Good prognosis with medical
therapy
Less than or equal to 13 METs = Good prognosis despite abnormal
exercise test
ii . Report of exercise should include the following in its interpretation:
Baseline EKG
EKG changes noted during thc test
Blood pressure during the test
Arrhythmia or abnormal beats noted during the test
Symptoms observed during the test
Approximate exercise capacity of the individual in METs (most
important prognostic indicator)
Whether test was ended prematurely and reason
CARDIAC TESTING 105

iii. Conclusion of the report should include


Positive
Negative
Equivocal
Nondiagnostic
Goal achieved (maximal, submaximal)

iv. Clinical findings for positive stress test


Hypotension
Angina
83, S4, or murmur during exercise

Positive stress test


Less than or equal to I-mm ST elevation in leads without prior Q
waves
Less than or equal to I-mm horizontal or downs loping
ST depression
(Note: All ST segment changes have to occur in at least two
consecutive leads and three consecutive beats per lead.)
Less than or equal to I.S-rum upsloping ST depression
T inversion
Uwave
Ventricular tachycardia (VT)

v. False-positive results on exercise stress testing


Coronary artery spasm
Left bundle branch block
Cardiomyopathy
Left ventricular hypertrophy with strain at baseline
Use of digitalis or antidepressants

C CARDIAC STRESS ECHOCARDIOGRAPHY


i. Is perfonned to make observation of the wall motion at rest and with
stress.
ii. Baseline echocardiography is performed to rule out any
abnonnalities at rest.
106 CARDIAC TESTING

iii. Increases the sensitivity and specificity oflhc exercise stress testing
alone.
iv. If individual is unable to exercise, a pharmacological agent can be
useful.

i. Indications:
Assessment of ventricular function
Chamber size
Wall thickness
Valvular function

ii. Diagnosis of coronary artery disease in presence of EKG


abnormalities that may make stress test uninterruptible such as
Left bundle branch block (Note: Specificity for detecting
ischemia decreases in patients with LBBB.)
Left ventricular hypertrophy
Early repolarization or conduction abnormalities
Determine extent and location of ischemia

iii. Restrictive factors: Individual with COPD and obesity.


iv. Disadvantages: Interpretation is very subjective especially if there
is a baseline wall motion abnormality.

o PHARMACOLOGICAL STRESS TEST


i. Indications:
Individual is unable to exercise.
Abnormal baseline EKG such as LBBB (Note: Should be
combined with imaging component).

ii . Disadvantages: Specificity is reduced in individual with right


ventricular pacemaker.

i. Dobutamine
Useful alternative to adenosine and dipyridamole in individuals
with conditions associated with bronchospasm (asthma, COPD, etc)
Useful in individual taking Aggrenox or Persantine
Useful in individual with severe carotid stenosis
CARDIAC TESTING \07

Increases heart rate and blood pressure


Enhances contractility
Half-life is about 2 minutes
Contraindications
Ventricular tachycardia
Myocardial infarction within past 3 days
Unstable angina
• Severe left ventricular outflow obstruction
Aortic aneurysm
Aortic dissection
Systemic hypertension
Discontinuation of the dobutamine infusion is as follows:
BP: 2301130
• SBP: <80
• Patient becomes symptomatic such as chest pain, SOB
• Less than 2 mm of ST depression from baseline
Ventricular tachycardia
Supraventricular tachycardia
Atrial fibrillation
A V block (2: I , complete)
Attainment of>85% of predicted heart rate
Side effects: Palpitation, chest pain, nausea, anxiety,
arrhythmias (SYTNTNF), tremors
ii. Dipyridamole
Onset is about 3 minute after infusion for 4 minutes, peaks at
approximate 7 to 12 minutes.
Half-life is >20 minutes.
Commonly used agent for performing nuclear imaging.
It may increase the efficacy or antihypertensive medications.
Individual should avoid caffeine-containing product 24 hours
prior to test.
Individual should avoid theophylline-containing product 72 hours
prior to test.
Contraindications
Myocardial infarction within 72 hours
• Severe lung disease or asthma
108 CARDIAC TESTING

Severe left ventricle systolic dysfunction


Second- or third-degree heart block
Baseline hypotension
Side effects: Chest pain, dizziness, headache, shortness of
breath, flushing myocardial infarction, stroke
Antidote: Aminophylline

iii. Adenosine
Rapid onset (seconds)
Short half-life for elimination (few seconds).
Most commonly used agent for performing nuclear imaging.
Very powerful vasodilator of coronaries; requires controlled
infusion.
Individual should avoid caffeine-containing product 24 hours
prior to test.
Individual should avoid theophylline-containing product 72 hours
prior to test.
Indications
Left bundle branch block
• Paced rhythm
• Wolff-Parkinson-White syndrome
Contraindications
High-grade A V block
Condition that can causc bronchospasm (asthma, COPD, etc)
Sick s inus syndrome
Hypotension
Individual on Aggrenox/Persantine
Caffeine ingestion in past 24 hours (blocks adenosine
receptors)
Side effects: Chest pain, flushing, shortness of breath, nausea,
and headache; arrhythmias (VT IVF)

iv. Arbutamine
Is a strong beta-adrenergic agonist and mild alpha-
sympathomimetic agent.
It increased heart rate and contractility of the myocardium.
High cost limits its use.
CARDIAC TESTING 109

E NUCLEAR IMAGING

FIGURE 11-2 Nuclear Imaging

i. Indications for nuclear imaging


Equivocal stress test or intermediate probability.
Evaluation of viability of myocardium after myocardial
infarction or revascularization.
Evaluation of preoperative risk .
Evaluate recurrent symptoms after coronary artery bypass
grafting (CABG) or balloon angioplasty (PTCA).
Chest pain in association with bundle branch block, early
repoiarization, nonspecific ST changes, post- myocardial
infarction, pre-excitation.
110 CARDIAC TESTING

ii. Radioisotopes
Teclmetium-m99
Thallium-201

iii. Pharmaceutical agents


Tetrofosmin
Sestamibi
Technetium-m99 scstamibi (Cardiolitc)
It is deposited into mitochondria and provides enhanced
image quality.
Superior image acquired in female and obese patient.
Thallium
Replaces K+ in the cell
Longer half-life than technetium (Note: Areas which are
ischemic/necrotic take up less/no blood flow. Thus there is
lack of or less uptake of tracer compared to normally
perfused areas.)

iv. Disadvantages: Artifact may be due to soft tissue li ke breast.


CARDIAC TESTING III

F CARDIAC ECHOCARDIOGRAPHY

FIGURE 11-3 Ecocardiogram

i. Echocardiography is an imaging modality used for assessing


cardiac anatomy and function by using high-frequency sound waves.
ii. There are two routine ways of performing the cardiac
cchocardiogram .
• Transthoracic echocardiogram
• TransesophageaJ echocardiogram

iii. There are three modalities for the echocardiogram.


"M"- modc cchocardiography: It provides single-dimension
images that allow measurement of the heart chambers. Displays
onc-dimensional image.
112 CARDIAC TESTING

Two-dimensional echocardiography: It provides cross-sectional


slices of the heart. Displays two-dimensional image.
Color flow echocardiography: It provides visualization of the
blood flow across valves and congenital anomalies.
iv. Indications:
Aortic aneurysm
Atrial function
Cardiomyopathy
Congenital heart disease
Endocarditis
Great vessel disease
Heart failure assessment
Hypotension
Intracardiac thrombus
Penetrating/blunt trauma
Pericarditis
Unexplained syncope
Valvular dysfunction/valvular disease
Ventricular function

v. Specific clinical indications for transcsophagcal cchocardiogram:


Embolism of cardiac source
Endocarditis
Prosthetic heart valve function
Native valvular disease
Aortic dissection
Aortic aneurysm
Intracardiac tumor, mass, or thrombus
Congenital heart disease
CARDIAC TESTING 113

G CARDIAC CATHETERIZATION
i. Technique: A catheter is inserted from groin or an11 into the heart and
then eventually into the coronary arteries and appropriate area.

FIGURE 11-4

Catheter flow direction


.«<- ---"' T - in ascending aorta
)-- - \- --Heart

f---+---\---\- Abdominal aorta

Catheter 11-+- - - - Femoral artery


insertion - +-::f,lJ
site
114 CARDIAC TESTING

FIGURE 11-5

" " ' , - - - - - - Aorta


Superior vena
cava
~,,-'.I,-- Left coronary artery

~~~== Circumflex artery


Right coronary -f----'\\ .: Circumflex artery
artery Left anterior
descending artery
L-\\--1r Anastamosis
Left ventric le area ---t-df-,,,..~ ,,--lII-+- Posterior
interventricular
Inferior vena cava a rtery
Aorta
Marginal artery _ _ _ _ _ _J
H ___ Catheler flow
direction

ii. Indications:
Stenling and dilatation of the coronary arteries in acute
myocardial infarction
Stenting or dilatation of the coronary arteries to relieve symptoms
in chronic coronary disease patients
Diagnosis of coronary artery disease
Valvuloplasty
Measure pressure in the heart and aorta
Cardiac biopsies
Visualization of the atrium and ventricles
Electrophysiology which includes ablation of the aberrant
patbways

iii. Complications:
Allergic reaction to contrast medium
Angina
Myocardial infarction
CARDIAC TESTING 115

Arrhythmia
Hemorrhage from catheter insertion site
Pericardial tamponade
Renal damage from contrast medium
Stroke

H HOLTER MONITORING
i. It is a device designed to monitor and store electrical activities of
the heart (arrhythmia, blocks, etc) .
ii. The device can store activities for ;::24 hours.
iii. The Holter device is connected to the chest via series ofwiTes.

ELECTROPHYSIOLOGIC STUOY
It involves series of tests to help detennine the location and type of
electrical activity, as well as response to treatment.

i. Technique:
After sedating the patient, "multiple," specialized catheters are
inserted via fluoroscopy from groin or neck into specific areas of the
heart through which heart rhythm is recorded and the pathways of
arrhythmias are determined through small amounts of delivered
electricity. The study takes several hours for completion.
ii. It is a study performed to determine and manage the following
conditions:
Paroxysmal supraventricular tachycardia
Ventricular tachycardia
Atrial flutter
Risk of cardiac arrest
Bradycardia
Syncope
Effectiveness of medication to control arrhythmia
Assess the need for an implantable device (pacer, ICD)
116 CARDIAC TESTING

Electrophysiologic Study (EPS):


Normal Intracardiac Electrograms
Three surface EKG leads: J, aVF, and V 1

FIGURE 11-6

'KG
- 1- - - - - - - 'A A--
II V--
HRA

HBE p
~
A V
f A V

v v

----"",-'" -~-~
----'-:::;;;~--_A~ A~___
r r
~RV
A --------'; ~~ 100
~J\r-
..-;;;;-"1
11111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111111
CARDIAC TESTING 117

i. EPS study abbreviations


HRA = High right atrium
A=Atrium
HBE = Bundle of HIS
p = Proximal
m=Mid
d = Distal
exp = Exploratory catheter
CS = Coronary sinus
RVA = Right ventricular apex
V = Ventricle

ii. Complications associated with EPS


Secondary from procedure
o Bleeding
Infection
Pain
Allergic reaction
Thrombophlebitis
Aortic dissection
StrokerrIA
() Coronary sinus perforation
Cardiac tamponade
Secondary from programmed cardiac stimulation
Cardiac arrhythmia
a Myocardiac infarction
" Bundle branch block
Secondary from transcatheter ablation
Third-degree heart block
Thromboembolism
Cardiac arrhythmia
Pericarditis
Phrenic nerve paralysis
Radiation skin bum
Coronary artery thrombosis
Myocardial infarction
Cardiac perforation from excessive radiation to various cardiac
structures
12
Cardiac Pacemaker

1iiiilliTIf
A Indications for Permanent Cardiac Pacemaker: 120
ACe/AHA Classification
B Indications for Permanent Cardiac 120
Pacemaker Implantation
C Types of Pacemakers 122
D Pacing Codes 123

119
120 CARDIAC PACEMAKER

Cardiac pacemaker is a device that supplies electrical stimuli to cause


cardiac contractions when there is defect in the intrinsic cardiac electri-
cal activity. It functions by detecting intrinsic cardiac electric poten-
tials. Ifit senses the potentials arc too infrequent or absent, it provides
electrical impulses to the heart thus stimulating myocardial contraction.

A INDICATIONS FOR PERMANENT CARDIAC


PACEMAKER: ACC/AHA CLASSIFICATION
Class I: Agreement/evidence of a permanent pacing is definitely
beneficial, useful, and effective.
Class II: Discrepancy/conflicting evidence of penn anent pacing is
useful and effective.
Class IlA: Data/opinion is in support of use fulnessI
efficacy.
Class lID: Data/opinion is less well established to
support usefulness/efficacy.
Class nl: Agreement/evidence ofa pennanent pacing is not useful
or effective. It may even be hannful.

B INDICATIONS FOR PERMANENT CARDIAC


PACEMAKER IMPLANTATION
Class I:
• Symptomatic bradycardia (usually <40 beats per minute).
Complete A V block (third degree).
Advanced second-degree A V block.
Second-degree AV block in the HIS -Purkinje system with
bilateral bundle branch block.
Symptomatic Mobitz I or Mobitz II second-degree A V block.
Second-degree A V block that is symptomatic and persistent.
Mobitz II second-degree A V block associated with a wide QRS or
chronic bifascicular block regardless of symptoms.
CARDIAC PACEMAKER 121

Transient complex infranodal AV block with associated bundle


branch block.
Second· or third-degree block with associated myotonic muscular
dystrophy, peroneal muscular atrophy, Keams-Sayre syndrome,
or Erb dystrophy.
Individual with neurocardiogenic syncope: Syncope and >3 second
of asystole fo llowing minimal carotid sinus message.
Syncope and >3 seconds of asyslO[c or escape rhythm <40 beats
per minute in an awake patient.
Wide QRS escape rhythm.
Complex ventricular celepy.
Sustained ventricular arrhythmia that is pause dependent.
Less than or equal to I year arage: Ventricular ralc is <55 beats
per minute or <70 beats per minute and has associated congenital
ncan disease regardless of the symptom.
Long QT syndrome due to unknown etiology.
NYHA III or refractory heart failure (EF <35%) after optimization
of medical treaunenl and 3 months post-revascu larization, and
evid ence of ventricular dyssync hrony-indication for
biventricu lar pacemaker implantation.

C lass I I :
Sinus bradycardia with no clear association between symptoms
and bradycardia «40 beats per minute).
Sinus node dysfunction with unknown etiology of syncope.
Mobitz II second-degree AV block with symptomatic bradycardia.
First-degree AV block with hemodynamic compromise.
Asymptomatic second- or third-degree AV block post-Ml at the
level of AV node.
Bifascicular or trifascicular block with syncope that can be
contributed to transient high-grade AV block.
Syncope of unknown etiology where major abnonnalities of sinus
node function arc discovercd in clcetrophysiologic (EP) study.
Recurrent syncope of unknown etiology with abnonnal response
to carotid sinus message, but syncope is not due to carotid sinus
message.
122 CARDIAC PACEMAKER

Recurrent neurocardiogenic syncope with bradycardia


(spontaneously or noted during tilt-table testing).
Symptomatic hypertrophic cardiomyopathy despite optimal
medication and significant left ventricular outflow tract
obslnlction at rest or during exercise.
Class Ill:
Syncope of unknown etiology.
Sinus bradycardia without significant symptoms.
Sinoatrial block or sinus arrest without significant symptoms.
Transient ventricular pace.
Asymptomatic bradycardia in sleep.
Asymptomatic second-degree Mobitz I AV block (Wenckebach).
Intermittent A V block.
Right bundle branch block with left axis deviation without
symptom.
Reversible AV block (secondary for conditions such as sleep
apnea, Lyme disease, enhanced vagal tone, post·operative
medications (beta blocker, diltiazem, verapamil).
Long QT due to reversible etiology.
Torsades de pointes due to reversible etiology.

C TYPES OF PACEMAKERS
i. Single chamber: Only one wire is implanted into the atrium or
ventricle.
ii. Dual chamber: Wires are implanted into two chambers (atrium and
ventricle).
iii. Rate responsive: Is sensor sensitive to person's physical activity.
iv. Bivcntricular pacemaker: Three leads are implanted. One lead into
the atrium, one into the right ventricle, and one into the coronary
sinus which stimulates the left ventricle.
CARDIAC PACEMAKER 123

o PACING COOES
First letter: Chamber paced
Second letter: Chamber sensed
Third letter: Chamber response to sensing
Fourth letter: Programmability
Fifth letter: Antitachycardia function

i. Chamber paced
A = Atrium
V = Ventricle
D = Dual (both chambers)
o =None
ii. Chamber sensed
A = Atrium
V = Ventricle
D = Dual (both chambers)
o = None
iii. Response to sensing
T = Triggered pacing
I = Inhibited pacing
D = Dual (T+ I)
o = None
iv. Programmable function
P = Programmable rate and/or output
M = Multiprogrammability of rate,
output, sensitivity, and more
C = Communicating function (tclemctly)
R = Rate adaptive
0 = None

v. Antitachycardia function
P = Overdrive pacing
S = Shock
0= Dual
o = None
FIGURE 12-1 Pacer Classilicalion

Ventri cular demand


inhibited: VVI
(Triggered-VVT)
Atrial demand
inhibited: AAI
(Triggered-AAn
Atrial synchronous
(VeritricularinhiOited)
VDD
~ ~
Fully automatic

DOD
Antitachyarrhythl

WIMP

Sensor
Sensor
<l Sensing ci

Coo'
D Output cir(

o Sensing

Slimulatiol
A·V
VVIR M IR DVI DOOR

10:794-799.
13
Implantable Cardioverter Defibrillator

A Implantable Cardioverter Defibrillator Device \26

125
126 IMPLANTABLE CARDIOVERTER DEFIBRILLATOR

A IMPLANTABLE CARDIOVERTER
OEFIBRILLATOR OEVICE
The implantable cardioverter defibrillator (leO) is a device for treat-
ment of cardiac tachyarrhythmia.
Newer ICDs have the functionality to manage bradycardia, tachy-
cardia, low-energy cardioversion, high-energy defibrillation, and elec-
trogram storage. These devices have capacity to multiprogram and
respond differently to different rhythm.
i. leD device consists of the following four elements:
Sensing electrodes
Defibrillation electrodes
Pulse generator
Backup bradycardia pacing in the event afpost-defibrillation
bradycardia
Ii. Indications:
Secondary prevention in an individual with cardiac arrest due to
ventricular fibrillation or ventricular tachycardia that is not due to
reversible cause
Secondary prevention of individual with 2::2 episode of
spontaneous sustained ventricular tachycardia in the presence of
structural hemt disease
Primary prevention in individual with documented MI (at least 30
days post-MI) and impaired left ventricular systolic dysfunction
(EF <30%), I-month post-MI or 3 months post-CABG
Primary prevention in individual with llonischemic
cardiomyopathy, NYHA class 111111 heart failure, and left
ventricular ejection fraction ::;;30%
14
Acute Cardiac Life Support
(ACLS) Protocols

A Acute coronary syndrome 128

M Ventricular fibrillation/pulseless 136


ventricular tachycardia

127
128 ACUTE CARDIAC LIFE SUPPORT (ACLS) PROTOCOLS

A ACUTE CORONARY SYNDROME


i. Maintain airway, breathing, and circulation.
ii. 12-lead EKG.
iii. Intravenous (IV) noonal saline to keep (venous infusion saline)
open
iv. Administer nitroglycerine 0.3 to 0.4 mg sublingual, repeat in
5 minutes up to three times in total, check blood pressure (BP)
between administration; avoid ifBP < 100/60 mm Hg.
v. Aspirin 325 mg x I dose.
vi. Metoprolo15 mg IV slow push ifheart rate (HR) > 60 and systolic
blood pressure (SBP) > 110.
May repeat second administration ofS-rug metopro!ol IV push
in 5 minutes if HR > 60 and S8P > 110.
Caution: Consult medical directives if there is evidence of
asthma, emphysema, chronic obstructive pulmonary disease
(COPD), or other broncho-constricting conditions. Also, if
there exist cardiac blocks.
vii. Administer morphine sulfate 2 to 4 mg IV push, 10, or intranasal.
May repeat another dose ifno reliefis obtained (maximum dose:
10 mg); hold if HR < 60 or SBP < 100.
viii. Ifmorphine allergy, administer fentanyl 25 to 50 mcg slow IV
push, 1M, or intranasal.
ix. Continue monitoring for myocardial infarct and cardiac
dysrhythmia.
ACUTE CARDIAC LIFE SUPPORT (ACLS) PROTOCOLS 129

B STEMI (ST -SEGMENT ELEVATION


MYOCARDIAL INFARCT)
i. Maintain airway, breathing, and circulation.
ii. 12-1ead EKG.
iii. IV nonnal saline TKO.
iv. Administer nitroglycerine 0.3 to OA-mg sublingual, repeat in 5
minutes up to three times in total, check BP between
administration, avoid if BP < 100/60.
v. Aspirin 325 mg x I dose.
vi. Metopro\o\ 5-mg IV slow push if HR > 60 and SSP> 110.
May repeal second administration ofS-mg metopro!ol IV push
in 5 minutes if HR > 60 and SSP> 110.
Caution: Consult medical direction if there is evidence of
asthma, emphysema, COPD, or other broncho-constricting
conditions. Also if there exist cardiac blocks.
vii. Administer morphine sulfate 2-10 4-mg IV push, 10, or
intranasal. May repeat another dose ifno relief is obtained
(maximum dose: 10 mg), hold if HR < 60 or SSP < 100; if
morphine allergy, administer fentanyl 25-to 50-mcg slow IV
push, 1M or intranasaL
viii. Continue monitoring for myocardial infarct and cardiac
dysrhythmia.
ix. Heparin 50 unitslkg (maximum dose: 4000 units) slow IV push,
most institutes may have their own heparin protocol.
130 ACUTE CARDIAC LIFE SUPPORT (ACLS) PROTO COLS

C SINUS BRADYCARDIA (SYMPTOMATIC)


i. Maintain airway, breathing, and circulat ion.
ii. 12-1ead EKG.
iii. Atropine D.S-mg IV push every 3 to 5 minutes (maximum dose: 3
mg); chi ldren: 0.02 mg Ikg IV push, repeat every 5 minute
(maximum dose: 0.1 mg) .
iv. Ifnot responsive, then consider transcutaneous pacing; IV normal
saline TKO .
v. Consider sedation for comfort, such as Versed 2 mg.
ACUTE CARDIAC LIFE SUPPORT (ACLS) PROTOCOLS 131

D ASYSTDLE
i. Maintain airway, breathing, and circulation,
ii. 12-1ead EKG.
iii. IV nonnal saline TKO.
iv. Consider treating secondary causes.
v. Possible etiologies for asystole.
Acidosis
Acute myocardial infarct
Cardiac tamponade
Drug overdose
Hyperkalemia
Hypovolemia
Hypoxemia
Pulmonary embolism
Tension pneumothorax
vi. Epinephrine I-mg IV push, repeat every 3 to 5 minutes.
vii. Atropine I rug IV, every 3 to 5 minutes (maximum dose:
0.04 mglkg).
viii. Consider IV fluid bolus 500 cc (NS) if evidence of fluid loss.
ix. Consider bicarbonate 50-mEq IV push or 1 mEq/kg IV.
132 ACUTE CARDIAC LIFE SUPPORT (ACLS) PROTOCOLS

E THIRD-DEGREE BLOCK (SYMPTOMATIC)


i. Maintain airway, breathing, and circulation .
ii. 12-1ead EKG.
iii. Consider transcutaneous pacemaker.

F SECOND-DEGREE MOBITZ TYPE II HEART BLOCK


i. Maintain airway, breathing, and circulation .
ii. 12-1cad EKG.
Atropine 0.5 to I mg.
Transcutaneous pacing.
Dopamine 5 to 20 ).lglkglmin.
Epinephrine 2 to 10 ).1g1min.
Isoproterenol 2 to 10 ).lg/min.
Prepare for transvcnous pacemaker.
ACUTE CARDIAC LIFE SUPPORT (ACLS) PROTOCOLS 133

G ATRIAL FIBRillATION/ATRIAL FLUTTER


i. Management if duration is <48 hours
Maintain airway, breathing, and circulation.
12-lead EKG.
IV normal saline TKO.
Rate control:
If ventricular function preserved -7 diltiazcm (or another
CCB) or meloproioi (or another beta blocker).
If ventricular function is not preserved -7 diltiazcm
(only CCB) or digoxin or amiodarone
Convert to sinus rhythm
DC cardioversion
or
If ventricular function preserved: procainamidc,
amiodarone, flecainide, or propafenone
If ventricular function is not preserved: amiodarone

ii. Management if duration is >48 hours


Maintain airway, breathing, and circulation.
12-Iead EKG.
IV normal saline TKO.
Ratc control
If ventricular function preserved -7 diltiazem (or another
CCS) or metoprolol (or another beta blocker)
Ifventricular function is not preserved ~ diltiazem (only
CCS) or digoxin or amiodarone
Convert to sinus rhythm
Start IV heparin infusion.
() Perfonn transesophageal echocardiography to exclude
atrial clot.
Then perfonn cardioversion within 24 hours and
anticoagulate after >4 weeks.
134 ACUTE CARDIAC LIFE SUPPORT (ACLS) PROTOCOLS

H NARROW COMPLEX SUPRAVENTRICULAR


TACHYCARDIA
JUNCTIONAL TACHYCARDIA
i. Vagal stimulation or Adenosine
ii. EF>40%
Bcta blocker or
• Calcium channel blocker (CCB) or
• Amiodarone
iii. EF <40%
• Amiodarone

J ECTOPIC OR MULTI FOCAL ATRIAL


TACHYCARDIA
i. Vagal stimulation or adenosine
ii. EF >40%
Beta blocker or
• Calcium channel blocker or
• Amiodarone
iii. EF<40%
• Amiodarone
iv. Diltiazem

K PAROXYSMAL SUPRAVENTRICULAR
TACHYCARDIA
i. Vagal stimulation or adenosine
ii. EF>40%
Beta blocker or
Calcium channel blocker or
Digoxin or
Cardioversion or
ACUTE CARDIAC LIFE SUPPORT (ACLS) PROTOCOLS 135

Procainamide or
Amiodarone or
Sotalol
iii. EF<40%
Cardioversion
Digoxin or
Amiodarone or
Diltiazem

L VENTRICULAR TACHYCARDIA (STABLE)


i. Monomorphic
EF> 40%
o Procainamide or
o Sota101 or
o Amiodarone or
<)Lidocaine
EF<40%
() Amiodarone or
Lidocaine
() Synchronized cardioversion

ii. Polymorphic
Normal baseline QT interval
Beta blocker or
() EF>40%
o Lidocaine or
o Amiodarone or
o Procainamide or
() Sotalolor
Normal baseline QT interval
" Amiodarone or
EF <40%
Lidocaine or
() Synchronized cardioversion
136 ACUTE CARDIAC LIFE SUPPORT (ACLS) PROTOCOLS

Prolonged baseline QT interval


() Magnesium or
" Override pacing or
" Isoproterenol or
" Phenytoin or
" Lidocaine

M VENTRICULAR FIBRILLATION/PULSELESS
VENTRICULAR TACHYCAROIA
i. Maintain airway, breathing, and circul ation
ii. Defibrillation (maximum three times) (200 J, 200-300 J,
and 360 J)
iii. Epinephrine I-mg IV push (repeat every 3-5 minutes)
or
iv. Vasopressin 40-unit-IV single dose (one time only)
v. Defibrillation x 1 (360 J)
vi. Amiodarone or
lidocaine or
procainamide
vi. Magnesium (if known magnesium deficiency)
15
Summary

Tahle 15-1 EKG Reading: Normal EKG Intervals and 138


Segment Values

137
138 SUMMARY

Table 15-1 EKG Reading: Normal EKG Intervals


and Segment Values
Intervals and Lead Areas
I small box = 0.04 s or 1 mm Anteroseptal wall -7 V I and V2
1 large box = 0.2 s or 5 mm Anterior wall -7 V3 and V 4
P wave -7 <0. 11 s Anterolateral wall -7 V5
and V6
PR interval -7 0.12-0.2 s High lateral -7 I and aVL
QRS complex -7 <0.07-0.10 s Inferior wall -7 leads II ,
III, aVF
QTc interval -7 0.33-0.47 s Lateral1eads -7 t, aVL, Vs.
and V6
QTc (corrected QT interval) = QT interval/square root of R-R
interval (millisecond)

A. RATE
Count number of large boxes between RR and divide 300 by the
number of boxes.
Count number of large boxes between R-R in 10 seconds
multiplied by 6.
Per big boxes: 300-150-\ 00-75-60.

B. RHYTHM
P wave Regular <60 bpm Sinus
followed bradycardia
byQRS -7
SINUS
60·100 bpm Normal sinus
rhythm
>100 bpm Sinus
tachycardia
Irregular Sinus arrhythmia
(conflnued)
140 SUMMARY

Table 15-1 EKG Reading: Normal EKG Intervals and Segment


Values (Continued)
C. AXIS
Lead I Lead aVF Lead lIt Axis
(+) (+) (+) Nonnal
(+) (-) (-) Left
(- ) (+) (+) Right
(-) (-) (-) Right or indetenninate if aVR+
tUse lead II if a VF is isoelcctric
(+) ~ QRS upward deflection> downward deflection
(- ) -? QRS downward deflection> upward deflection

D. QRS DURATION
<0.10 s Normal
0.10-0.125 Incomplete BBB or LAFB/LPFB
LAFB (left anterior fascicular block) - LAD + 0 18 3
LPFB (left post-fascicular block) = RAD + Q3S 1
>0.125 Complete RBBB (rSR in V I)
LBSB; nonspecific intraventricular conduction
delay (qR or q)
Bifascicular block = RBBB + LAFB

E. HYPERTROPHIES
RAE Lead II p wave >2.5 mm (also known as "P"-pulmonale)
LAE V I p-wave negative deflection >1 block wide and >1
block deep (also known as P-mitrale)
(continued)
140 SUMMARY

Table 15-1 EKG Reading: Normal EKG Intervals and Segment


Values (Continued)
c. AXIS
Lead I Lead aVF Lead lIt Axis
(+) (+) (+) Nonnal
(+) (- ) (- ) Left
(- ) (+) (+) Right
(- ) (- ) (- ) Right or indeterminate if aVR+
t Use lead II if a VF is isoelcctric
(+) -7 QRS upward deflection> downward deflection
(-) -7 QRS downward deflection> upward deflection

D. Q RS DURATION
<0. 10 s Normal
0 .10-0. 12 s Incomplete BBB or LAFB/LPFB
LAFB (left anterior fascicular block) - LAD + 0 18 3
LPFB (left post-fascic ular block) = RAD + Q3S 1
>0. 125 Complete RBBB (rSR in V I)
LSBS; nonspecific intraventricular conduction
delay (qR or q)
Bifascicular block = REBB + LAFB

E. HYPERTRO PHIES
RAE Lead II p wave >2.5 mm (also known as "P"-pulmonale)
LAE V I p-wave negative deflection > 1 block wide and >1
block deep (also known as P-mitrale)
(continued)
SUMMARY 141

Table 15-1 EKG Reading: Normal EKG Inlervals and Segmenl


Values (Continued)
LVH I. R wave in aVL >12 mill
2. (8 wave in V I or V2- whichever is larger) + (R wave in
V5 or V6, whichever is larger) ~35 mm
RVH 1. R>SinV I
2. R decreases from VIto V6
RAE = right atrial enlargement LAE = left atrial enlargement
LVH = left ventricular RVH = right ventricular
enlargement enlargement

F. PROLONGED QTc ETIOLOGIES


QTc (corrected QT interval) = QT intervaVSquare root of
RR interval (millisecond)
Medications Miscellaneous Medications
Antibiotics Phenylamine
Azithromycin, erythromycin, Cisapride
cJarithromycin
Telithromycin Domperidone
Levofloxacin, moxifloxacin, Oroperidol
gatifloxacin
Sparfloxacin Probucol
Pentamidine Cocaine
Spiramycin, chloroquine, Terodiline
halofantrine, mefloquine
Antihistamines Papaverine
Astemizole Chloral hydrate
Terfenadine Arsenic
(continued)
142 SUMMARY

Table 15-1 EKG Reading: Normal EKG Intervals and Segment


Values (Continued)
Medications Miscellaneous Medications
Antiarrhythmics Cesium chloride
Amiodarone Levomethadyl
Disopyramide Metabolic etiology
Dofetilidc, scmatilide, ibutilidc, Hypokalemia
bepridil, mibefradil
Procainamidcl Hypomagnesemia
N-acetylprocainamide
Quinidine Hypocalcemia
80ta101 Hypothyroidism
Psychotropic Starvation
Bulorphanoi Miscellaneous
Haloperidol Idiopathic
Methadone (high dose) Mitral valve prolapse
Phenothiazine Myocardial ischemia!
infarction
Risperidone HIV
SSRI Hypothermia
TCA Connect ive tissue disease
Thioridazine Jervell- Lange- Nielsen and
Romano-Ward syndrome
(contlllued)
SUMMARY 143

Table 15-1 EKG Reading: Normal EKG Inlervals and Segmenl


Values (Continued)
G. MISCELLANEOUS
COPD pattern: Precordial leads RlS ratio <I
Chronic lung disease: Poor R-wave progression, P-pulmonale,
MAT (multi focal atrialt3chycardia)

T-w3ve flatte ning: Ischem ia, hypokalemia, or nonspecific


U wave: Hypokalemia, ischemia
QT shortening: Hypercalcemia
QT prolongation: Hypocalcemia, other metabolic abnormalities
Pulmonary embol ism : Tachycardia, T.L in V I-V 4 , rarely S in I, Q
in Ill, T inversion in III is seen

WPW: PR shortening, wide QRS, and delta wave


Index

A ST-segment elevation
ACe. See American College of myocardial infarct,
Cardiology 129
accelerated idioventricular rhythm third-degree block,
rate (AIVR), 73 132
accelerated junctional rhythm, ventricular fibrillation,
67,671 136
acidosis, asystole and, 131 ventricular tachycardia,
action potential generation, 3[ 135
acute cardiac life support (ACLS) acute coronary syndrome,
protocols, 127-136 128
acute coronary syndrome, acute inj ury, 32t, 33/
128 acute myocardial infarct,
asystole, 131 asystole and, 131
atrial fibrillation, 133 adenosine
atrial flultcr, 133 contraindications of, 108
ectopic atrial tachycardia, in ectopic atrial tachycardia,
134 134
junctional tachycardia, 134 indications, 108
multifocal atrial tachycardia, injunctional tachycardia,
134 134
narrow complex supraventricular in multifocal atrial tachycardia,
tachycardia, 134 134
paroxysmal supraventricular in paroxysmal supraventricular
tachycardia, 134 tachycardia, 134
pulseless ventricular side effects of, 108
tachycardia. 136 Aggrcnox, 106
second-degree Mobitz Iype II AHA. See American Heart
heart block. 132 Association
sinus bradycardia AIVR. See accelerated idioventric-
(symptomatic), 130 ular rhythm rate

145
146 INDEX

American College of Cardiology aspirin


(ACC) in acute coronary syndrome, 128
exercise stress test classification, in ST-segment elevation
100 myocardial infarction, 129
pacemaker classification, astemizole, 141t
120- 122 asthma. See bronchospasm
American Heart Association asymptomatic coronary artery
(AHA) disease, 98t, 991
exercise stress test classification, exercise stress test in, 101
100 asystole
pacemaker classification, acute cardiac life support
120- 122 protocol, 131
aminophylline, 108 etiologies, 131
amiodaronc, 1421 atrial bigeminy, 55, 55f
in atrial fi brillation/atrial flutter, atrial escape beat. 58, 58/
133 atrial fibrillation, 68, 68J, 69f
in ectopic atrial tachycardia, acute cardiac life support
134 protocol, 133
injunctional tachycardia. 134 rate control, 133
in multi focal atrial tachycardia, sinus rhythm conversion, 133
134 atrial flutter, 70, 70J, 71f
in paroxysmal supraventricular acute cardiac life support
tachycardia, 134 protocol, 133
in ventricular fibrillation! rate control, 133
pulseless ventricular sinus rhythm conversion, 133
tachycardia, 136 atrial hypertrophy, 26-28
in ventricular tachycardia I,ft, 28, 281
(stable), 135 right, 26-27, 26J, 27/
angina pectoris atrioventricular (A V) block(s),
atypical, 98/, 991 40-43
classic, 98t, 991 first-degree, 40, 40f
antiarrhythmics,1421 in PR interval, 14
antibiotics, 141 t second-degree, 41-42, 41J, 42f
antihistamines, 141 - 142r Mobitz type I (Wenckebach),
antitachycardia function, pacing 41,411
codes, 123 Mobitz type 11,42, 42f
arbutamine, J08 third-degree (complete heart
arsenic, 141/ block), 43, 43f
INDEX 147

atrioventricular (A V) node, 2, 2J right, 36J, 37J, 47, 471


atropine complete, 36
in asystole, 131 incomplete, 36
in second-degree Mobitz type II bundle of HIS, 2, 2f
heat block, 132 butorphanol, 142/
in sinus bradycardia
(symptomatic), 130 C
atypical angina pectoris, 98/, 991 CAD. See coronal)' artcl)' discasc
A V node. See atrioventricular calcium. See hypocalcemia
node, 16J, l8J cardiac action potential, EKG
axis, 16J tracing,4J
deviation, 191 cardiac angiography, 99
electrocardiogram tracing, cardiac catheterization, 113- 115
7, 7f compilcations, 114---115
indetenninate (extreme) indications, 114
deviation, 19t technique, 113, I13J, 114J
left deviation, 19/, 211 cardiac conduction pathway, 2
nonnai, 191, 20J cardiac conduction system,
right deviation, 19t, 22-23J anatomy, 2, 2[
extreme, 22[ cardiac echo, 99
vertical, electrocardiogram cardiac echocardiography. See
tracing, 7, 7f echocardiogram
azithromycin,14lt cardiac nuclear imaging, 99
cardiac pacemaker. See pace-
B makcr(s)
Bachmann bundle, 2J cardiac stress echocardiography,
bepridil, 142t 105-106
bicarbonate, in asystole, 131 disadvantages, 106
bifascicular fascicular block, indications, 106
47, 47f restrictive factors, 106
biventricular pacemaker, 122 cardiac strcss test, 98- 99
bronchospasm, dobutamine, coronal)' artcl)' discase
106 cardiac testing modalities,
Bruce protocol, 104 99
bundle branch blocks, 36--39 pretest probability, 981, 99,
I,ft, 38J, 39f 991
complete, 38 cardiac tamponade, asystole,
incomplete, 38 131
148 INDEX

cardioversion digitalis effect, 89, 89f


in paroxysmal supraventricular digitalis toxicity, 89f
tachycardia, 134 digoxin
synchronized, in ventricular in atrial fibrillation/atrial flutter,
tachycardia (stable), 135 133
cesium chloride, 1421 in paroxysmal supraventricular
chamber paced, pacing codes, tachycardia, 134
123 diltiazcm
chamber sensed, pacing codes, 123 in atrial fibrillation/atrial flutter,
chloral hydrate, 1411 133
chloroquine, 141 f in ectopic atrial tachycardia, 134
chronic lung disease, 143t in multifocal atrial tachycardia,
chronic obstmctive pulmonary dis- 134
ease (COPD). See also in paroxysmal supraventricular
bronchospasm tachycardia, 134
pattern, 143r dipyridamole, 107- 108
cisapride. 141 t antidote, 108
cJarithromycin, 1411 contraindications, 107- 108
classic angina pectoris, 981, 99t side effects, 108
cocaine, 1411 disopyramide, L421
color flow cchocardiography, 112 dobutamine, 106- 107
complete heart block, 43, 431 contraindications, 107
connective tissue disease, 1421 discontinuation, 107
COPD. See chronic obstmctive side effects, 107
pulmonary disease dofetilide, 142/
coronary artery disease (CAD) domperidone, 1411
asymptomatic, 98/, 99/, 101 dopamine, in second-degree
cardiac testing modalities, 99 Mobitz type [I heat block,
pretest probability for, 98(, 99, 132
991 droperidol, 141 (
corrected QT interval. See QTc drug overdose, asystole and, 13 I
dual chamber pacemaker, 83f, 122
o
defibrillation, in ventricular E
fibrillation/pulseless ven- echocardiogram (EKG), 11 If
tricular tachycardia, 136 color flow, 112
depolarization, 3, 3f indications, 112
ofQRS complex, 17, 17f "M"-mode, III
INDEX 149

trans esophageal, III, 112 pericardial effusion, 95f


transthoracic, III pericarditis,94f
two-dimensional, I 12 premature atrial contraction,
echocardiography. See cardiac 56J
stress echocardiography; premature ventricular contrac-
echocardiogram tion ,75f
ectopic atrial tachycardia, acute prolonged QTc etiologies, 1411
cardiac life support pulmonary embolism, 93/
protocol, 134 QRS duration, 1401
EKG. See electrocardiogram rate, 1381
electrocardiogram (EKG) reading recent infarct, 34f
atrial bigeminy, 55f rhythm, 138-\391
atrial fibrillation, 69f right axis deviation, 23f
atrial flutter, 71f right bundle branch block, 37J,
axis, 1401 47J
dual chamber pacemaker, 83f right ventricular hypertrophy,
first-degree AV block, 41/ 29J
hypertrophies, 140-1411 second-degree block, 42/
idioventricular rhythm, 73f sinus arrhythmia, 54f
infcroposterior wall infarct, 34f sinus bradycardia, 53/
injury,33f sinus pause, 48/
intervals, 9/, 138t sinus tachycardia, 52f
ischemia, 33/ supraventricular atrial
lead areas, 1381 contraction, 61f
lead placement, 4, 5f, 6f third-degree block, 43f
left anterior fascicular block, ventricular demand pacemaker,
45f, 47J 83J
left axis deviation, 21/ ventricular fibrillation, 82/
left bundle branch block, 38/ ventricular tachycardia, 791
left posterior fascicular block, waves,9t
46J Wolff-Parkinson-White
left ventricular hypertrophy, syndrome, 50f
30J electrocardiogram (EKG) tracing,
multifoeal atrial tachycardia, 7, 7f, 8J
66J cardiac action potential, 4f
nonnal axis, 20f horizontal axis, 7, 71
paroxysmal atrial tachycardia, normal sinus rhythm, 8f
63J vertical axis, 7, 7f
150 INDEX

electrophysiologic study (EPS), positive, 105


115-\17 protocols, 104--105
complications interpretation report, 104,
from procedure, t 17 105
from programmed cardiac exercise treadmill testing (ETT),
stimulation, J 17 100J
from transcatheter ablation, post-myocardial infarction,
117 101
nannal intracardiac clcctro- for risk stratification, 101
grams, 116-117, 116/ extreme right axis deviation, 22/
study abbreviations, 117
technique, 115 F
use, 115 fascicular blocks, 44-47
epinephrine bifascicular. 47. 47/
in asystole, 131 left anterior, 44, 44J, 45f,
in second-degree Mobitz type II 47,47J
heat block, 132 left posterior, 46, 46[
in ventricular fibrillation! fentanyl
pulsclcss ventricular in acute coronary syndrome,
tachycardia, 136 128
EPS. See clcctrophysiologic study in ST-segment elevation
erythromycin, \4\ t myocardial infarction, 129
ETT. See exercise treadm ill testing first-degree atrioventricular block,
exercise stress test. See also exercise 40,40J
treadmill testing flccainidc, in atrial fibrillation/
ACe/AHA classification of, atrial flutter, 133
100
in asymptomatic coronary artery G
disease, 101 gatif1oxacin, 141 t
baseline EKG changes and,
102- 103J H
contraindications of halofantrinc, 141 t
absolute, 103! haloperidol,142t
relative, 103! heparin
for coronary artery disease in atrial fibrillation/atrial flutter,
detection, 101 133
disadvantages of, 101 in ST-segment elevation
false-positive, 105 myocardial infarction, 129
INDEX 151

HIV, 1421 inju!)" acute. 32(, 33/


Holter monitoring, 115 internodal tract, 2/
horizontal axis, electrocardiogram ischemia, 321, 33/
tracing, 7, 7/ isoproterenol
hyperkalemia, 87, 87/ in second-degree Mobitz type II
asystole, 131 heat block, 132
hypertrophy in ventricular tachycardia (stable),
atrial,26- 28 135
left, 28, 28/
right, 26-27, 26J, 271 J
ventricular, 29- 30 J wave, 92, 92/
left, 30, 301 lervell-Lange-Nie1sen syndrome,
right, 29, 29/ 1421
hypocalcemia, 88, 88f, 1421 junctional escape beat, 59, 59/
hypokalemia, 86, 86f, 1421 junctional rhythm, 66, 66/
hypomagnesemia, 1421 accelerated, 67, 67/
hypothermia, 92, 92f, 142t junctional tachycardia. acute
hypothyroidism, 1421 cardiac life support
hypovolemia, asystole, protocol, 134
131
hypoxemia, asystole, 131 l
LAD. See left axis deviation
LAFB. See left anterior fascicular
ibutilide, 142t block
lCD. See implantable cardioverter LBBB . See left bundle branch
defibrillator block
idiopathic, 142t lead(s)
idioventricular rhythm, 73, 73/ locations of, 321
implantable cardioverter placement, 4, Sf, 6/
defibrillator (lCD), 126 electrocardiogram, 4, Sf, 6/
indetenninate (extreme) axis precordial, 4, Sf, 6/
deviation, 191 left anterior fascicular block (LAFB),
infarct 44, 44J, 45J, 47, 471
inferoposterior wall, 341 left atrial hypertrophy, 28, 28/
old,32t left atrium, 2/
recent, 341 left axis deviation (LAD),
inferoposterior wall infarct. 191,2 11
34f left bundle branch, 2, 2/
152 INDEX

left bundle branch block (LBBB), metoprolol


38f, 39[ in acute coronary syndrome,
adenosine, 108 128
complete, 38 in atrial fibrillation/atrial flutter,
incomplete, 38 133
left posterior fascicular block in ST~segment elevation
(LPFB), 46, 46[ myocardial infarction,
left posterior fascicular branch, 2f 129
left ventricle, 2[ METs, See metabolic equivalents
left ventricular hypertrophy, of tasks
30,30[ mibefradil, 142t
levofloxacin, 141 t mitral valve prolapse, 142t
levomethadyl, 142t Mobitz type I (Wenckcbach),
lidocaine 41,41[
in ventricular fibrillation! Mobitz type II, 42, 42[
pulse less ventricular acute cardiac life support
tachycardia, 136 protocol, 132
in ventricular tachycardia monomorphic ventricular tachy-
(stable), 135 cardia, acute cardiac life
LPFB. See left posterior fascicular support protocol, 135
block morphine sulfate
in acute coronary syndrome,
M 128
"M"-mode echocardiography, in ST-segment elevation myo-
III cardial infarction, 129
magnesium moxifloxacin, 141 t
in ventricular fibrillation! multi focal atrial tachycardia, acute
pulse less ventricular cardiac Ii fe support protocol,
tachycardia, 136 134
in ventricular tachycardia multifocal atrial tachycardia (MAT),
(stable), 135 65, 65f, 66[
MAT. See multi focal atrial myocardial ischemia/infarction,
tachycardia 142t
mefloquine, 141 t myocardium, conduction in, 3[
metabolic equivalents of tasks
(METs),104 N
functional capacity, 104 narrow complex supraventricular
methadone (high dose), 142t tachycardia, 134
152 INDEX

left bundle branch block (LBBS), metoprolo!


38f, 39f in acute coronary syndrome,
adenosine, 108 128
complete, 38 in atrial fibrillationlatrial flu tter,
incomplete, 38 133
left posterior fascicular block in ST-segment elevation
(LPFB), 46, 46f myocardial infarction,
left posterior fascicular branch, 2/ 129
left ventricle, 2[ METs. See metabolic equivalents
left ventricular hypertrophy, of tasks
30,30f mibefradil,142t
levofloxacin,1411 mitral valve prolapse, 142t
lcvomethadyl,1421 Mobitz type I (Wcnckebach),
lidocaine 41,41f
in ventricular fibrillation! Mobitz type n, 42, 42[
pulse less ventricular acute cardiac life support
tnchycordi n, 136 protocol, 132
in ventricular tachycardia monomorphic ventricular tachy-
(stable), 135 cardia, acute cardiac lifc
LPFB. See left posterior fascicular support protocol, 135
block morphine sulfate
in acute coronary syndrome,
M 128
" M"- mode echocardiography, in ST-segment elevation myo-
III cardial infarction, 129
magnesium moxifloxacin, 141 t
in ventricular fibrillation! multi focal atrial tachycardia. acute
pulse less ventricular cardiac life support protocol,
tachycardia, 136 134
in ventricular tachycardia multifocal atrial tachycardia (MAT),
(stable), 135 65 , 65f, 66f
MAT. See multi focal atrial myocardial ischemia/infarction,
tachycardia 142t
mefloquine, 141 t myocardium, conduction in, 3[
metabolic equivalents of tasks
(METs),104 N
functional capacity, 104 narrow complex supraventricular
methadone (high dose), !42t tachycardia, 134
INDEX 153

nitroglycerine pacer classification, 1241


in acute coronal)' syndrome, 128 pacing codes, 123
in ST-segment elevation rate responsive, 122
myocardial infarction. 129 single chamber, 122
nonangina1 chest pain, 981. 991 transcutaneous, for third-degree
normal sinus rhythm, electrocar- block, 132
diogram tracing, 8f lransvenous, for second-degree
nuclear imaging, t09! Mobitz type II heat block,
disadvantages, 110 132
indications, 109 types, 122
radioisotopes, It 0 pacer classification, 1241
sestamibi. 110 pacing codes, 123
technetium-m99, 110 papaverinc. 14Jt
thallium, 110 paroxysmal atrial tachycardia
tetrofosmin, 110 (PAT), 62f, 63f
paroxysmal supraventricular
o tachycardia. acute cardiac
old infarct, 32t life support protocol,
Osborne wave, 92, 92f 134
override pacing, in ventricular paroxysmal supraventricular
tachycardia, 135 tachycardia (PSYT),
62f, 63f
p PAT. See paroxysmal atrial tachy-
P wave, 91 cardia
PAC. See premature atrial pentamidine, 141/
contraction pericardial effusion, 95, 95f
pace rhythm, adenosine, pericarditis, 94, 94{
108 Persantine, 106
paced rhythm pharmacologic stress test,
dual chamber pacemaker, 83f 106-108
ventricular demand pacemaker, adenosine, 108
83f arbutamine. 108
paccmaker(s) dipyridamole, 107-108
ACe/AHA classification of, disadvantages of, 106
120-122 dobutamine, 106-107
biventricular, 122 indications for, 106
dual chamber, 122 phenothiazine, 142(
indications, 120-122 phenylamine, 141(
154 INDEX

phenytoin, in ventricular psychotropics, 1421


tachycardia. 135 pulmonary embolism, 93, 93f,
plateau, 3, 3/ 143t
polymorphic ventricular tachycardia, asystole and, 13 I
135 pulseless ventricular tachycardia,
potassium. See hyperkalemia; 136
hypokalemia Purkinje fibers, 2f
potassium efflux, 3, 3/ Purkinjc system, 2
PR interval, 8f PVC. See premature ventricular
atrioventricular block, 14 contraction
nonnal value, 9t
PR segment, 8f Q
precordial lead placement, 4, 5f, 6/ QRS, 91
premature atrial contraction QRS complex, depolarization of,
(PAC), 56, 56J 17,17J
premature junction beat/complex, QRS interval, Sf
57,57J block, 14
premature ventricular contraction normal value, 9t
(PVC), 74, 74[, 75J widening, 14
probucol, 141 f QT interval, 8f
procainamidc nonnal value, 91
in atria! fibrillation/atrial flutter, prolongation, 14
133 QT prolongation, 1431
in paroxysmal supraventricular QT shortening, 1431
tachycardia, 134 QTc (corrected QT interval), 91
in ventricular fibrillation! quinidine, 1421
pulseless ventricular
tachycardia, 136 R
in ventricular tachycardia RAD, See right axis deviation
(stable), 135 radioisotopes, 110
procainamidelN-acetyl rate calculation, 12
procainamide, 142t rate responsive pacemaker, 122
programmable function, pacing RBBS, See right bundle branch
codes, 123 block
propafenone, in atrial fibrillation! repolarization, 3, 3f
atrial flutter, 133 response to sensing, pacing codes,
PSVT. See paroxysmal supraven· 123
tricular tachycardia rhythm guidelines, 14, 14f
INDEX 155

rhythm strip, regularity, 14 sinus tachycardia, 12,52, 52!


right atrial hypertrophy, 26-27, sotalol, 142t
26J, 27/ in paroxysmal supraventricular
right atrium, 2/ tachycardia, 134
right axis deviation (RAD), 19(, in ventricular tachycardia, 135
22-23/ spartloxacin, 141 (
extreme, 22/ spiramycin, 141 t
right bundle branch, 2, 2! SSRI, 1421
right bundle branch block (RBBB), SSS. See sick sinus syndrome
36J, 37J, 47, 47/ ST interval, 8/
complete, 36 ST segment, 8!
incomplete, 36 starvation, 1421
right posterior fascicular branch, 2! STEMI. See STwsegment elevation
right ventricle, 2/ myocardial infarct
right ventricular hypertrophy, STwsegment elevation myocardial
29,29/ infarct (STEM I), 129
risperidone, 142t supraventricular arrhythmia,
Romano· Ward syndrome, 142t 52-72
accelerated junctional rhythm,
S 67,67/
SA node. See sinoatrial node atrial bigeminy, 55, 55/
second·degree atrioventricular atrial escape beat, 58, 58f
block, 41-42, 41J, 42/ atrial fibrillation, 68, 68[, 69f
Mobitz type I (Wenckebach), atrial flutter, 70, 70[, 71/
41,41/ junctional escape beat, 59, 59/
Mobitz type IT, 42, 42J, 132 junctional rhythm, 66, 66/
sematilide,142t multi focal atrial tachycardia,
sestamibi, 110 65, 65J, 66/
sick sinus syndrome (SSS), paroxysmal atrial tachycardia,
84,84f 62J, 63/
single chamber pacemaker, 122 paroxysmal junctional tachycarw
sinoatrial (SA) node, 2, 2/ dia,64/
rate, 12 premature atrial contraction, 56,
sinus arrhythmia, 54, 54! 56/
sinus bradycardia, 12,53, 53! premature junction beat!
sinus bradycardia, 130 complex, 57, 57!
sinus pause, 48, 48/ sinus arrhythmia, 54, 54/
sinus rhythm, 14 sinus bradycardia, 53, 53!
156 INDEX

supraventricular arrhythmia transcutaneous pacemaker, for


(Continued) third-degree block, 132
sinus tachycardia, 52, 52f transesophageal echocardiogram,
supraventricular tachycardia, 111,112
60, 60J, 61f in atrial fibrillation/atrial flutter,
wandering atrial pacemaker, 133
72 , 72f transthoracic echocardiogram, Itt
supraventricular tachycardia transvcnous pacemaker, for sccond-
(SVT), 60, 60J, 61f degree Mobitz type II heat
narrow complex, 134 block, 132
paroxysmal,134 treadmill exercise testing, 99. See
SVT. See supraventricular also exercise stress test
tachycardia two-dimensional cchocardio-
synchronized cardioycrsion. 135 graphy, 112

T u
T wave, 9t U wove, 143t
flattening, 1431
tachyarrhythmia, ICD for, 126 V
tachycardia-bradycardia VI lead placement, 4, 5f
syndrome. See sick sinus V2lead placement, 4, 5f
syndrome V3lead placement, 4, 5f
TeA, 142t V4 lead placement, 4, 5f
technetium-m99 sestamibi V5lead placement, 4, 5f, 6f
(Cardiolite), 110 V 6 lead placement, 4, 6f
telilhromycin, 141 t vagal stimulation
tension pneumothorax, asystole, in ectopic atrial tachycardia, 134
131 injunctional tachycardia, 134
terfenadine, 141 t in multi focal atrial tachycardia,
tcrodilinc, 141 t 134
tetrofosmin, nuclear imaging, 110 in paroxysmal supraventricular
thallium, 110 tachycardia, 134
thioridazine, 1421 vasopressin, in ventricular fibrilla-
third-degree atrioventricular block, tionfpulseless ventricular
43,43f tachycardia, 136
symptomatic, acute cardiac life ventricular bigeminy, 75, 75f
support protocol for, 132 ventricular demand pacemaker, 83f
Torsadcs de Pointes, 82, 82f ventricular escape beat, 77, 77f
INDEX 157

ventricular fibrillation , 81, 8 If, ventricular tachycardia. pulselcss.


82}; 136 acute cardiac life support
ventricular flutter, SO, SO/ protocol for, 136
ventricular hypertrophy, 29-30 ventricular tachycardia, 135
ventricular rhythm, 73-82 monomorphic, 135
idioventricular rhythm, 73. 73/ polymorphic. 135
premature ventricular contraction. ventricular trigeminy, 76. 76/
74, 74[, 75} Versed, in sinus bradycardia, 130
Torsades de Pointes, 82, 8~r vertical axis. electrocardiogram
ventricular bigeminy. 75. 75/ tracing. 7, 7/
ventricular escape beat, 77, 77/
ventricular fibrillation, 8 1, 81f, W
82} Wenckebach block, 41 , 41/
ventricular flutter, SO, SO/ Wolff-Parkinson-White (WPW)
ventricular tachycardia, 7S, syndrome, 49, 49/. 50/.
78j, 79/ 1431
ventricular trigeminy, 76, 76/ adenosine. 108
ventricular tachycardia, 7S, 7Sf. WPW syndrome. See WolfT-
79/ Parkinson-White syndrome

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