Jorge Velsquez, MD y Julin Aristizbal, MD

6:30 -7:00 pm: Electrocardiografa y principios bsicos de los dispositivos de

estimulacin elctrica cardaca
Ral Garillo, MD

Arritmias en
Reanimacin
Jueves 11 de septiembre
SALONES 5 y 6

Coordinador: Mauricio Duque, MD.

8:30 - 8:55 am:

Instalacin.
9:00 - 9:20 am: Conferencia: Dr. Nelson Giraldo: De la Electrocardiografa a la
Electrofisiologa: El futuro se adelant
William Uribe, MD.

Julin Miguel Aristizbal A.

Estatinas despus de la GUIAS

Coordinador: Eduardo Medina, MD.

Internista - Cardilogo - Electrofisilogo

julianaristi1@gmail.com

Objetivos

Contexto

Definiciones

Identificacin electrocardiogrfica

Manejo

Contexto
100

Ventricular Tachycardia (VT): Monomorphic

02ECG-Tab 02 2/4/05 3:58 PM Page 54

QRS complexes in monomorphic VT have the same shape and amplitude.

75

75-84%

54

Taquicardia Ventricular sin Pulso!

Fibrilacin Ventricular
Rate: 100250 bpm
Rhythm: Regular
P Waves: None or not associated with the QRS
PR Interval: None
QRS: Wide (!0.10 sec), bizarre appearance

ECGs

50

Clinical Tip: It is important to confirm the presence or absence of pulses because

monomorphic VT may be perfusing or nonperfusing.
Clinical Tip: Monomorphic VT will probably deteriorate into VF or unstable VT if sustained
and not treated.

Actividad Elctrica sin Pulso!

Asistolia

25

>50%
Asystole

3
59

4/05 3:58 PM Page 59

Electrical activity in the ventricles is completely absent.

Rate: None

TV Monomrfica

54

QRS complexes in polymorphic VT vary in shape and amplitude.

The QT interval is normal or long.
Rate: 100250 bpm
Rhythm: Regular
P Waves: None or not associated with the QRS
PR Interval: None
QRS: Wide (!0.10 sec), bizarre appearance

ECGs

57

Fibrilacin Ventricular

ECGs

Rate: 100250 bpm

Rhythm: Regular or irregular
P Waves: None or not associated with the QRS
PR Interval: None
QRS: Wide (!0.10 sec), bizarre appearance
Ventricular Fibrillation (VF)
Clinical Tip: It is important to confirm the presence or absence of pulses because
or nonperfusing.
be perfusing
VT may
no ventricular depolarization or contraction.
occurs with
activity
polymorphic
Chaotic electrical
fibrillatory
the
of
used to define the type of
frequency
and
can be etiology.

amplitude
The
as a possible
Clinical Tip: Consider electrolyte abnormalitiesactivity
fibrillation as coarse, medium, or fine.

Torsade de Pointes

de Pointes
Torsade
or absence of pulses because
the presence
Clinical Tip: It is important to confirm
monomorphic VT may be perfusing or nonperfusing.
The QRS reverses polarity and the strip shows a spindle effect.
VF ororunstable
deteriorate
VT will
if sustained
Tip:isMonomorphic
This
Clinical
intervals.
long QTVT
normal
VT withinto
polymorphic
ofprobably
an unusual variant

rhythm
not treated.
the term means twisting of the points.
and
In French

56

55

ECGs

Rate: 200250 bpm

Rhythm: Irregular
P Waves: None
PR Interval: None
QRS: Wide (!0.10 sec), bizarre appearance
Pulseless Electrical Activity (PEA)
Clinical Tip: Torsade de pointes may deteriorate to VF or asystole.
is detected.
but no
electrical
an identifiable

Monitor shows
and electrolyte
interval
QTpulse
that prolong
drugs rhythm,
causes are
Tip: Frequent
Clinical
atrial, junctional, or ventricular in origin.
be sinus,
abnormalities
Rhythm may such
as hypomagnesemia.
PEA is also called electromechanical dissociation (EMD).

Rate: Indeterminate
Rhythm: Chaotic
P Waves: None
PR Interval: None
QRS: None

AESP

Clinical Tip: There is no pulse or cardiac output. Rapid intervention is critical. The longer the
delay, the less the chance of conversion.
Asystole
Electrical activity in the ventricles is completely absent.
Rate, rhythm, P waves, P-R interval, and QRS: Reflect underlying rhythm.

ECGs

Clinical Tip: Potential causes of PEA are pulmonary embolism, MI, acidosis, tension
pneumothorax, hyper- and hypokalemia, cardiac tamponade, hypovolemia, hypoxia,
hypothermia, and drug overdose (i.e., cyclic antidepressants, beta blockers, calcium channel
blockers, digoxin).

59

Asistolia

ECGs

TV Polimrfica

Ventricular Tachycardia (VT): Polymorphic

58

02ECG-Tab 02 2/4/05 3:58 PM Page 55

/05 3:58 PM Page 59
02ECG-Tab 02 2/4/05 3:58 PM Page 57
02ECG-Tab 02 2/4/05 3:58 PM Page 58
02ECG-Tab 02 2/4/05 3:58 PM Page 02ECG-Tab
56
02 2/4/05 3:58 PM Page 54

QRS complexes in monomorphic VT have the same shape and amplitude.

Activar servicio emergencias

1
Iniciar RCP
-Oxgeno
-Monitorizacin

Si

Ritmo desfibrilable?

No

FV/TVsP

Asistolia / AESP
Pulseless Electrical Activity (PEA)

-Acceso IV/IO

TVM

54

Ventricular Tachycardia (VT): Polymorphic

QRS complexes in polymorphic VT vary in shape and amplitude.
The QT interval is normal or long.

Ritmo desfibrilable?

Rate: 100250 bpm

Rhythm: Regular
P Waves: None or not associated with the QRS
PR Interval: None
QRS: Wide (!0.10 sec), bizarre appearance

RCP 2 min

10

Clinical Tip: Always confirm asystole by checking the ECG in two different leads. Also,
search to identify underlying ventricular fibrillation.
Clinical Tip: Seek to identify the underlying cause as in PEA.

RCP 2 min

Ritmo desfibrilable?
Si

Si

No

11
ECGs

57

Rate: None
Rhythm: None
P Waves: None
PR Interval: None
QRS: None

No

Clinical Tip: Torsade de pointes may deteriorate to VF or asystole.

Clinical Tip: Frequent causes are drugs that prolong QT interval and electrolyte
abnormalities such as hypomagnesemia.

Clinical Tip: There is no pulse or cardiac output. Rapid intervention is critical. The longer the
delay, the less the chance of conversion.

Clinical Tip: Potential causes of PEA are pulmonary embolism, MI, acidosis, tension
pneumothorax, hyper- and hypokalemia, cardiac tamponade, hypovolemia, hypoxia,
hypothermia, and drug overdose (i.e., cyclic antidepressants, beta blockers, calcium channel
blockers, digoxin).

-Acceso IV/IO, Adrenalina cada 3-5

min, monitorizacin avanzada

Ritmo desfibrilable?

Rate: 200250 bpm

Rhythm: Irregular
P Waves: None
PR Interval: None
QRS: Wide (!0.10 sec), bizarre appearance

Rate: Indeterminate
Rhythm: Chaotic
P Waves: None
PR Interval: None
QRS: None

-Adrenalina 3-5 min

-Monitorizacin avanzada

ECGs

TdP

Rate, rhythm, P waves, P-R interval, and QRS: Reflect underlying rhythm.

Asistolia

Si

de Pointes
Torsade
or absence of pulses because
the presence
Clinical Tip: It is important to confirm
monomorphic VT may be perfusing or nonperfusing.
The QRS reverses polarity and the strip shows a spindle effect.
VF ororunstable
deteriorate
VT will
if sustained
Tip:isMonomorphic
This
Clinical
intervals.
long QTVT
normal
VT withinto
polymorphic
ofprobably
an unusual variant

rhythm
not treated.
the term means twisting of the points.
and
In French
Rate: 100250 bpm
Rhythm: Regular or irregular
P Waves: None or not associated with the QRS
PR Interval: None
QRS: Wide (!0.10 sec), bizarre appearance
Ventricular Fibrillation (VF)
Clinical Tip: It is important to confirm the presence or absence of pulses because
or nonperfusing.
perfusing
be
may
VT
polymorphic
no ventricular depolarization or contraction.
Chaotic electrical activity occurs with
fibrillatory activity
of the
used to define the type of
and frequency
can be etiology.

The amplitude
as a possible
abnormalities
electrolyte
Tip: Consider
Clinical
fibrillation as coarse, medium, or fine.

No

Asystole
Electrical activity in the ventricles is completely absent.

56

55

ECGs

TVP

FV

AESP

RCP 2 min

59

ECGs

02ECG-Tab 02 2/4/05 3:58 PM Page 55

02ECG-Tab 02 2/4/05 3:58 PM Page 57
02ECG-Tab 02 2/4/05 3:58 PM Page 02ECG-Tab
56
02 2/4/05 3:58 PM Page 54

QRS complexes in monomorphic VT have the same shape and amplitude.

ECGs

Ventricular Tachycardia (VT): Monomorphic

02ECG-Tab 02 2/4/05 3:58 PM Page 59

02ECG-Tab 02 2/4/05 3:58 PM Page 58

Monitor shows an identifiable electrical rhythm, but no pulse is detected.

Rhythm may be sinus, atrial, junctional, or ventricular in origin.
PEA is also called electromechanical dissociation (EMD).

RCP 2 min
-Adrenalina 3-5 min
-Monitorizacin avanzada

RCP 2 min
-Adrenalina 3-5 min
-Monitorizacin avanzada

Ritmo desfibrilable?

12

No
No hay ROSC? Pasar a 10 u 11
Hay ROSC ? Cuidados post RCP

Si
Pasar a 5 7

Definiciones

Taquicardia ventricular sin pulso

Es una arritmia ventricular generalmente regular, monomfica

que representa una actividad elctrica organizada del miocardio
ventricular pero que no produce actividad contrctil suficiente
para mantener la perfusin, que puede degenerar en fibrilacin
ventricular

TV monomrfica, Flutter ventricular,

TV polimrfica,Taquicardia puntas torcidas

Taquicardia Complejos Anchos:TV vs TSV

80%

Taquicardia Ventricular

15%

Bloqueo Rama previo

Fenmeno de aberrancia

<5%

Preexcitacin

<1%

Marcapaso ventricular

Antiarrtmicos, Hiperkalemia

Wellens

criteria of BCT

E 100% S
E 100% S

Diagnsticos

J Med 1978;64: 2733

e 3 Am
Classical
Wellens criteria favouring VT in patients without AAD.1,12 One hundred VTs (68 ischaemic, 18 idiopathic, and

R monofsica V1

QS V6

RS 100 ms

R monofsica V1

S mayor que R en V6

Sin pulso

Debo asumir TV

(a)

TVm
(b)

TVp
(c)

TdP

Figure 30.9 (a) Monomorphic VT. (b) Polymorphic VT. (c) Polymorphic
VT with undulating pattern, suggestive
of torsade
deAcute
pointes.
Brady. Critical Decisions
in Emergency and
Care Electrocardiography 2009
Reprinted from Hudson KB et al. Electrocardiographic manifestations:

This EGG was recorded in a coronary care unit from a patient admitted 2 h previously with an acute anterior
myocardial infarction. The patient was cold and clammy, and confused, and his blood pressure was unrecordable. What
does the ECG show and what would you do?

TDP

FIGURE 26-13 Torsades des pointes. This rhythm strip demonstrates the initiation of
torsadesECG
des pointes
by a series ofMEDICINE
ectopic beatsAND
that begin
withCARE 2005
ROSEN.
IN EMERGENCY
ACUTE
a premature ventricular beat or salvo of ventricular beats, followed by a pause, and then a supraventricular beat. Another premature ventricular beat arrives at
a relatively short coupling interval and falls on the preceding T wave, precipitating the rhythm. The baseline corrected QT interval was 0.64 sec.

126

SECTION III: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE

FIGURE 26-14 Polymorphic ventricular tachycardias with hypokalemia. Paroxysms of multifocal ventricular ectopy are seen in this ECG from a patien

with a serum potassium of 1.9 mEq/dL. Note the ST segment depression and giant U waves (arrows).
ROSEN. ECG IN EMERGENCY MEDICINE AND ACUTE CARE 2005

TVP

V5
FIGURE 8-11 Irregular tachydysrhythmias with aberrancy. Atrial fibrillation with left bundle branch block demonstrating an irregular, wide-complex
tachycardia.

FIGURE 8-12 Preexcited atrial fibrillation (AF). ECG and rhythm strip demonstrate AF with preexcitation and conduction down the accessory pathway, pro-

ducing runs of rapid, irregular, wide-complex tachycardia. Note the intermittent narrow QRS complexes resulting from occasional normal AV conduction (arrows).

FA Y WPW

ROSEN. ECG IN EMERGENCY MEDICINE AND ACUTE CARE 2005

FIGURE 25-6 Orthodromic reentry tachycardia. This electrocardiogram shows orthodromic reentry tachycardia with a rate of approximately 250 bpm.
This rhythm exhibits regular, narrow complexes and the absence of discernible P waves.

FIGURE 25-7 Antidromic reentry tachycardia. This electrocardiogram shows antidromic reentry tachycardia with a rate of approximately 300 bpm. Note
the wide-complex regular tachycardia.

TMCA

ROSEN. ECG IN EMERGENCY MEDICINE AND ACUTE CARE 2005

FIGURE 26-11 Ventricular tachycardia. The QRS complex width is greater than 140 msec in lead V1, which is positive. The axis is superior with no
RS complexes seen in the precordial leads.

FIGURE 26-12 Right ventricular outflow tract ventricular tachycardia (VT). This rhythm strip demonstrates right ventricular outflow tract VT with

typical left bundle branch block morphology and right inferior axis.

TV TSVD

ROSEN. ECG IN EMERGENCY MEDICINE AND ACUTE CARE 2005

Definiciones

Fibrilacin Ventricular

Es una arritmia ventricular que representa una actividad

elctrica desorganizada y compromete la capacidad contrctil
del corazn

Diferenciar: Interferencia, Flutter ventricular,TV polimrfica, FA

3. Open the airway with a head tilt and chin lift.

4. Perform CPR with a 30:2 sternal compression to
breath ratio.
5. Continue until paramedics arrive or the victim
becomes responsive.

BOX 19-2

Three Basic ECG Patterns with

Cardiac Arrest

Ventricular tachyarrhythmia, including ventricular

fibrillation (VF) or a sustained type of pulseless
ventricular tachycardia (VT)
Ventricular asystole or a brady-asystolic rhythm
with an extremely slow rate
Pulseless electrical activity (PEA), also referred to
as electromechanical dissociation (EMD)

magnesium sulfate (in cases of torsades de pointes

and when hypomagnesemia is present).

Ventricular Asystole and Brady-Asystolic

Rhythms

The normal pacemaker of the heart is the sinus

node, which is located in the right atrium. Failure o
the sinus node to function (sinus arrest) leads to
ventricular standstill (asystole) if no other subsid
iary pacemaker (e.g., in the atria, atrioventricula
[AV] junction, or ventricles) takes over. In such cases
the ECG records a straight-line pattern (see Fig. 19-3)
indicating asystole. Whenever you encounter a
straight-line pattern, you need to confirm this find
ing in at least two leads (as seen in most conven
tional telemetry systems) and check to see that al
electrodes are connected to the patient. Electrodes

Figure 19-1. Ventricular fibrillation causing cardiac arrest.

A 50-year-old man who had come to the A & E department with chest pain, collapsed while his EGG was
being recorded. What happened and what would you do?
Hampton. ECG problems 2003

Figure 16-20. Accelerated idioventricular rhythm (AIVR) in a patient with an acute inferior wall infarction. The first four beats

show the typical pattern, followed by a return of sinus rhythm, then the reappearance of the AIVR. Notice that the fifth, sixth, twelfth,
and thirteenth QRS complexes are fusion beats because of the nearly simultaneous occurrence of a sinus beat and a ventricular
beat.

PART II Cardiac Rhythm Disturbances

78

VT

AIVR
II

Figure 16-21. Accelerated idioventricular rhythm (AIVR) and nonsustained polymorphic ventricular tachycardia (VT) occurring
together. Notice the VPB on T beats that initiate both the AIVR and the VT episodes. VPB, ventricular premature beat.

VT

VF

Ventricular Fibrillation
gure 19-2. Ventricular tachycardia (VT) and ventricular fibrillation (VF) recorded during cardiac arrest. The rapid sine wave typ

ventricular tachycardia seen here is sometimes referred to as ventricular flutter.

Coarse VF

Fine VF

Coarse VF

Figure
16-22.
Ventricular
fibrillation
(VF)
may produce
both
coarse and
fine waves. pattern
Immediate
defibrillation
should be
Figure
19-3.
Complete
ventricular
standstill
(asystole)
producing
a straight-line
during
cardiac arrest.

performed.

Cardiac Arrest: Brady-Asystolic Patterns

Cardiac Arrest

Goldberger. Clinical Electrocardiography 2012

ECG148The houseofficer from the health care of the elderly ward is puzzled by this ECG and asks for your help.
What questions would you ask him?

Interferencia

Hampton. ECG problems 2003

Torsades de Pointes: Nonsustained

Monitor lead
T-U

T-U

CHAPTER 16 Ventricular Tachycardias

Figure 30.5 Polymorphic ventricular tachycardia. The rate is extremely rapid, with changing QRS morphologies and axis.

Monitor lead

155

Torsades de pointes
Torsades
de Pointes: Nonsustained

Figure 16-17. Notice the shifting polarity and amplitude of the QRS complexes during an episode of nonsustained torsades de

pointes. QT(U) prolongation (0.52 sec) is also present in the supraventricular beats (possible underlying atrial fibrillation).
T-U
T-U

Monitor lead

Torsades
de Pointes:
Sustained
Torsades
de pointes

Figure 16-17. Notice the shifting polarity and amplitude of the QRS complexes during an episode of nonsustained torsades de

pointes. QT(U) prolongation (0.52 sec) is also present in the supraventricular beats (possible underlying atrial fibrillation).

Torsades de Pointes: Sustained

Figure 30.6
Torsade de pointes. The rhythm is initiated by an R-on-T phenomenon. The rate is extremely fast, with changing QRS morphologies and
Monitor
lead
axis. The QRS complexes change smoothly in amplitude, giving the appearance they are twisting around a central axis.

Figure 16-18. Classic pattern of the sustained torsades de pointes type of ventricular tachycardia. Notice the pattern of beats in

which the QRS axis appears to rotate or turn in a systematic way. Figure 16-17 shows a short, nonsustained run of the same arrhythmia, which occurs in the setting of QT(U) prolongation.

to the slight pause. TdP can occur with congenital

Severe bradyarrhythmias (especially high-grade
(hereditary) or acquired QT interval prolongation,
AV heart block syndromes)
Figure 16-18. Classic pattern of the sustained torsades de pointes type of ventricular tachycardia. Notice the pattern of beats in
and
deteriorate
into
VF, or
causing
factors,
suchrun
asofElectrocardiography
liquid
whichcan
the QRS
axis appears
to rotate
turn in asudden
systematiccarway. FigureMiscellaneous
16-17 shows a short,
nonsustained
the sameprotein
arrhythGoldberger. Clinical
2012
diac
arrestoccurs
(see in
Chapter
19).
diets
mia, which
the setting
of QT(U) prolongation.

Definiciones

Actividad elctrica sin pulso

Es la despolarizacin elctrica organizada del corazn sin actividad

mecnica cardaca suficiente para generar un ritmo que permita la
perfusin corporal adecuada. Debe diferenciarse de la pseudo AESP la cul
describe un estado de choque cardiognico profundo que resulta
inadecuado para mantener la presin de perfusin, pero no presenta una
verdadera disociacin electromecnica

Pueden observarse ritmo sinusal, ritmos atriales, ritmos ventriculares e

idioventriculares, bloqueos cardacos de diversos grados, arritmias
supraventriculares, pero todos ellos asociados con las ausencia de presin
arterial y pulso que reflejan una contraccin cardaca ineficaz.

El ms frecuente es un ritmo ventricular muy lento con un QRS 120 ms.

15:20:27
HR 160
ms 375
V

160
375
V

:
156
382
V

163
367
V

163
367
V

160
375

163
367
V

160
375
V

166
359

163
367
V

163
367
V

166
359

166
359
V

166
359
V

166
359
V

166
359

166
359
V

166
359
V

102
585

137
437
V

128
468
V

15:21:23
HR 103
ms 578

102
585

70
851

72
828

76
781

99
601

108
554

103
578

76
781

76
789

76
789

85
703

Definiciones

Asistolia

Definicin: representa la ausencia de actividad elctrica ventricular

con sin actividad elctrica atrial.

Caractersticas electrocardiogrficas: en el electrocardiograma se

observa una lnea plana de registro sin actividad elctrica alguna.

Debe verificarse la adecuada conexin de los electrodos para no pasar

por alto un ritmo susceptible de desfibrilacin y debe confirmarse en al
menos dos derivaciones diferentes.

Una FV muy fina podra tambin ser tomada errneamente como

asistolia, por lo que si existe la duda debe incrementarse la ganancia del
monitor.

CHAPTER 19 Basic ECG Patterns in Cardiac Arrest

ECG shows ventricular

standstill (asystole)
External cardiac compression
started
Intravenous atropine and
epinephrine given

Asystole
R

External cardiac compression

179

B
C

ECG now shows

ventricular fibrillation
Ventricular fibrillation
DC shock given by electrical
defibrillator
Ventricular fibrillation

DC shock given

D
R

Intravenous lidocaine given

to suppress ventricular ectopy
and possibly to prevent further
episodes of ventricular
fibrillation

ECG now shows sinus rhythm

with ventricular premature beats

1 sec

Clinical Electrocardiography 2012

Figure 19-6. ECG history of cardiac arrest and successful resuscitation. The left panel shows theGoldberger.
ECG sequence during an actual

5H!

5T!

Hipovolemia
Hipoxemia
Hiperkalemia
Hipotermia
Hidrogeniones

Trombosis miocrdica
TEP
Taponamiento
Tensin Neumo
Txicos /Tablets

aVF

III

V3

V6

5H!
Hipovolemia
V1
Hipoxemia
Hiperkalemia!
Hipotermia
II
Hidrogeniones
Figure 35.6 Mild hyperkalemia. Peaked T waves are present, but the P waves and intervals are normal.

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Figure 35.7 Severe hyperkalemia. Peaked T waves, flattened P waves with PR segment prolongation, and marked QRS widening are all evident.

5H!
Hipovolemia
35.qxd 10/17/08 7:08 PM
Hipoxemia
Hiperkalemia!
Hipotermia!
Hidrogeniones

Page 309

35 ECG in PEA cardiac arrest scenarios

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

| 309

Figure 35.8 Hypothermia. Upward deflections at the terminal portion of the QRS complexes, termed Osborn waves or J waves, are noted. These

5T!
Trombosis miocrdica!
TEP
Taponamiento
Tensin Neumo
Txicos /Tablets

xd 10/17/08 7:12 PM Page 328

328 | Part 5 The ECG in Critical Care

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Figure 37.2 ECG demonstrating significant ST segment elevation in leads I, aVL, and V2V5 with reciprocal ST segment depression in leads III and
aVF consistent with a large anterior MI.

the presence of high right-sided pressures.7

Axis Deviation. As noted previously, the S1Q3T3 pattern
may be in part due to a change to the QRS axis. Although
right axis deviation is described as the classic axis change
associated with PE, left axis deviation as well as indeterminate
QRS axis changes have been reported with variable
frequency.2 Part of this variability may be related to the
specific definitions of right, left, and indeterminate axis
deviations. Preexisting cardiopulmonary disease may affect
axis changes as well.8
Anterior T Wave Inversions. Inversion of the T waves in
leads V1 to V4 has been reported to be closely related to the
severity of PE (Figs. 59-3 through 59-5). Ferrari and colleagues demonstrate a relationship between T wave inversion

deeper inversion, depending on the severity of PE. An isolated

inverted T wave in lead V1 can be normal.
Several mechanisms have been proposed to explain this
5T!of preexisting
phenomenon, including ischemia in the setting
right coronary artery stenosis,
neurohumorally
mediated
Trombosis
miocrdica
changes in myocardial repolarization, and myocardial shear
injury from increased intramural tension TEP!
and microvascular
compression. Regardless of mechanism,
the finding of symTaponamiento
metrically inverted T waves in the precordial leads often signifies
Tensin Neumo
profound right ventricular strain and the potential for clinical
Txicos
/Tablets
deterioration in a patient with respiratory
distress
and hypoxia.
Global T wave inversion
(Fig. 59-4) in acute PE has been reported in a case report from
the literature. Although the differential diagnosis for global

Global T Wave Inversion.

FIGURE 59-4 Global T wave inversion. This patient was thought to have had a nonQ wave myocardial infarction because of the presence of this pattern

along with elevated troponin levels. Pulmonary embolism turned out to be the lone culprit.

tude of electrical complexes on the ECG. While very specific

for the diagnosis of pericardial effusion, its sensitivity is only
around 30%. Likewise, the classic presentation of electrical
5T!
alternans, low voltage QRS complexes and PR
depression, is
very insensitive (117%), but Trombosis
highly specific for
diagnosing
miocrdica
effusion and tamponade [22] (Table 35.9 and Figure 35.11).
TEP
Sinus tachycardia and low voltage QRS complexes are the
most common findings in pericardialTaponamiento!
tamponade as the heart
rate increases to try to compensateTensin
for the lowNeumo
cardiac output. Any of these findings in the appropriate clinical scenario

to a tension pneumothorax, this high pressure can retard

cardiac return and produce progressive hypotension. Cases
of PEA have been reported as the result of aggressive ventilation during resuscitation [21]. Simply disconnecting the
patient from the ventilator or Ambu Bag will result in
restoration of pulse and blood pressure.
Pericardial tamponade: Pericardial tamponade prevents
normal ventricular filling and severely decreases cardiac
output. As the pressure in the pericardium increases, the

Txicos /Tablets

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Figure 35.11 Electrical alternans in a patient with a large pericardial effusion. Beat-to-beat variation in the amplitude of the QRS complexes is

5T!
Trombosis miocrdica
TEP
Taponamiento
Tensin Neumo
Txicos /Tablets

C35.qxd 10/17/08 7:08 PM Page 310

310 | Part 4 The Dysrhythmic ECG

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

V1

II

V5
Figure 35.9 Tricyclic antidepressant overdose. The classic findings of tachycardia, rightward axis, prominent S wave in lead I (large arrow) and tall R

Activar servicio emergencias

1
Iniciar RCP
-Oxgeno
-Monitorizacin

Si

Ritmo desfibrilable?

FV/TVsP

3
4

No
Asistolia / AESP

RCP 2 min

-Acceso IV/IO

Ritmo desfibrilable?

No

Si

5
6

10

RCP 2 min

RCP 2 min

-Adrenalina 3-5 min

-Monitorizacin avanzada

-Acceso IV/IO, Adrenalina cada 3-5

min, monitorizacin avanzada

No
Ritmo desfibrilable?

Ritmo desfibrilable?
Si

Si

No

11
8

RCP 2 min
-Adrenalina 3-5 min
-Monitorizacin avanzada

RCP 2 min
-Adrenalina 3-5 min
-Monitorizacin avanzada

Ritmo desfibrilable?

12

No
No hay ROSC? Pasar a 10 u 11
Hay ROSC ? Cuidados post RCP

Si
Pasar a 5 7

Conclusiones

Compromiso hemodinmico: asuma TV

Identifique ritmo:

Determina el tratamiento

Determina el pronstico