arritmias en reanimacion

Arritmias en Reanimación

Julián Miguel Aristizábal A. Internista - Cardiólogo - Electrofisiólogo

[email protected]

Jorge Velásquez, MD y Julián Aristizábal, MD 6:30 -7:00 pm: Electrocardiografía y principios básicos de los dispositivos de estimulación eléctrica cardíaca Raúl Garillo, MD Jueves 11 de septiembre SALONES 5 y 6 Coordinador: Mauricio Duque, MD. 8:30 - 8:55 am: Instalación. 9:00 - 9:20 am: Conferencia: Dr. Nelson Giraldo: De la Electrocardiografía a la

Electrofisiología: El futuro se adelantó William Uribe, MD.

Estatinas después de la GUIAS Coordinador: Eduardo Medina, MD. 9:25 - 9:45 am: Estatinas en prevención primaria; ¿Son muchos los tratados? Juan Carlos Díaz, MD 9:50 - 10:10 am: Metas de tratamiento con estatinas en prevención secundaria Julián Aristizábal, MD 10:10 - 10:40 am: Descanso. 10:40 - 11:30 am: Debates en dislipidemia: Estatinas y diabetes Alejandro Arroyave, MD Estatinas y miopatías Cesar Hernández, MD Medicamentos diferentes a las estatinas en Dislipidemia Carolina Saldarriaga, MD Discusión Debates en Diabetes Mellitus Coordinador: César Hernández, MD. 11:30 - 11:50 am Diabetes y riesgo cardiovascular; ¿La terapia cambia el riesgo? José F Botero, MD.

mailto:[email protected]

Objetivos

• Contexto

• Definiciones

• Identificación electrocardiográfica

• Manejo

Contexto

Taquicardia Ventricular sin Pulso!Fibrilación Ventricular

Actividad Eléctrica sin Pulso!Asistolia

75-84%

>50%

⚡️⚡️⚡️

0

25

50

75

100

1 2 3 4

54

Ventricular Tachycardia (VT): Monomorphic

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

Rate: 100–250 bpmRhythm: RegularP Waves: None or not associated with the QRSPR Interval: NoneQRS: Wide (!0.10 sec), bizarre appearance

♥ Clinical Tip: It is important to confirm the presence or absence of pulses becausemonomorphic VT may be perfusing or nonperfusing.

♥ Clinical Tip: Monomorphic VT will probably deteriorate into VF or unstable VT if sustainedand not treated.

ECGs

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

59Asystole

■ Electrical activity in the ventricles is completely absent.

Rate: NoneRhythm: NoneP Waves: NonePR Interval: NoneQRS: None

♥ 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.

ECGs

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

55

Ventricular Tachycardia (VT): Polymorphic

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

Rate: 100–250 bpmRhythm: Regular or irregularP Waves: None or not associated with the QRSPR Interval: NoneQRS: Wide (!0.10 sec), bizarre appearance

♥ Clinical Tip: It is important to confirm the presence or absence of pulses becausepolymorphic VT may be perfusing or nonperfusing.

♥ Clinical Tip: Consider electrolyte abnormalities as a possible etiology.

ECGs

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

56

Torsade de Pointes

■ The QRS reverses polarity and the strip shows a spindle effect.■ This rhythm is an unusual variant of polymorphic VT with normal or long QT intervals.■ In French the term means “twisting of the points.”

Rate: 200–250 bpmRhythm: IrregularP Waves: NonePR Interval: NoneQRS: Wide (!0.10 sec), bizarre appearance

♥ Clinical Tip:Torsade de pointes may deteriorate to VF or asystole.♥ Clinical Tip: Frequent causes are drugs that prolong QT interval and electrolyteabnormalities such as hypomagnesemia.

ECGs

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

57

Ventricular Fibrillation (VF)

■ Chaotic electrical activity occurs with no ventricular depolarization or contraction.■ The amplitude and frequency of the fibrillatory activity can be used to define the type of

fibrillation as coarse, medium, or fine.

Rate: IndeterminateRhythm: ChaoticP Waves: NonePR Interval: NoneQRS: None

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

ECGs

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

58

Pulseless Electrical Activity (PEA)

■ 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).

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

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

ECGs

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

59

Asystole





ECGs

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

54






ECGs

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

TV Monomórfica

TV Polimórfica

Torsade de Pointes

Fibrilación Ventricular

AESP

Asistolia

⚡️⚡️⚡️

⚡️⚡️⚡️

⚡️⚡️⚡️

⚡️⚡️⚡️

👐

👐

Activar servicio emergencias

Iniciar RCP-Oxígeno-Monitorización

Ritmo desfibrilable?

FV/TVsP Asistolia / AESP

⚡️

RCP 2 min-Acceso IV/IO

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

⚡️

⚡️

RCP 2 min-Acceso IV/IO, Adrenalina cada 3-5 min, monitorización avanzada




Ritmo desfibrilable? Ritmo desfibrilable?


No hay ROSC? Pasar a 10 u 11Hay ROSC ? Cuidados post RCP Pasar a 5 ó 7

1

2

3

4

9

510

6

7

811

12

Si No

Si

Si

Si

No

No

No

Si

No

55

Ventricular Tachycardia (VT): Polymorphic

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

Rate: 100–250 bpmRhythm: Regular or irregularP Waves: None or not associated with the QRSPR Interval: NoneQRS: Wide (!0.10 sec), bizarre appearance

♥ Clinical Tip: It is important to confirm the presence or absence of pulses becausepolymorphic VT may be perfusing or nonperfusing.

♥ Clinical Tip: Consider electrolyte abnormalities as a possible etiology.

ECGs

02ECG-Tab 02 2/4/05 3:58 PM 5

56Torsade de Pointes

■ The QRS reverses polarity and the strip shows a spindle effect.■ This rhythm is an unusual variant of polymorphic VT with normal or long QT intervals.■ In French the term means “twisting of the points.”

Rate: 200–250 bpmRhythm: IrregularP Waves: NonePR Interval: NoneQRS: Wide (!0.10 sec), bizarre appearance

♥ Clinical Tip:Torsade de pointes may deteriorate to VF or asystole.♥ Clinical Tip: Frequent causes are drugs that prolong QT interval and electrolyteabnormalities such as hypomagnesemia.

ECGs

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

57

Ventricular Fibrillation (VF)

■ Chaotic electrical activity occurs with no ventricular depolarization or contraction.■ The amplitude and frequency of the fibrillatory activity can be used to define the type of

fibrillation as coarse, medium, or fine.

Rate: IndeterminateRhythm: ChaoticP Waves: NonePR Interval: NoneQRS: None

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

ECGs

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

54






ECGs

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

TVM

TVP

TdP

FV

58

Pulseless Electrical Activity (PEA)

■ 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).

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

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

ECGs

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

59

Asystole





ECGs

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

AESP

Asistolia

Definiciones

• Taquicardia ventricular sin pulso

• Es una arritmia ventricular generalmente regular, monomófica que representa una actividad eléctrica organizada del miocardio ventricular pero que no produce actividad contráctil suficiente para mantener la perfusión, que puede degenerar en fibrilación ventricular

• TV monomórfica, Flutter ventricular,

• TV polimórfica, Taquicardia puntas torcidas

Taquicardia Complejos Anchos: TV vs TSV

80%

15%

<5%

<1%

Taquicardia Ventricular

Bloqueo Rama previo Fenómeno de aberrancia

Preexcitación

Marcapaso ventricular Antiarrítmicos, Hiperkalemia

Wellens

and are followed by a fully compensatory pause; the authors werewell aware that such beats are indistinguishable from AV nodalextrasystoles with aberration and no retrograde conduction. Mar-riott15 and Marriott and Sandler18 also noticed that ‘concordant’precordial patterns, whether entirely upright or entirely inverted,were almost diagnostic for ventricular origin. Positive concordancemay also occur during antidromic tachycardia using a left posterioror left lateral accessory pathway. Negative concordance is nearlyalways VT. However, Volders et al.23 published a case report ofa 17-year-old male with pectus excavatum and SVT with leftBBB (LBBB) resulting in a BCT with negative concordance. Mar-riott also introduced in 1971 the term ‘Rabbit ears’ for a double-peaked R-wave in lead V1. Whereas a ‘good rabbit’ with a tallerright peak being typical for RBBB aberrancy, a ‘bad rabbit’ with ataller left peak suggests ventricular origin. In 1972, Swanicket al.24 continued the differentiation between right VEB and supra-ventricular beats showing LBBB and found that (i) the presence ofS-wave in V4 greater in depth than the S in lead V1, (ii) a wider-wave ≥0.03 s in lead V1, and (iii) negative QRS polarity in leadI, all favour ventricular origin. In 1978, Wellens et al.12,13 used His-bundle recording for the first time to determine the site of originof tachycardia with broad QRS complex and create the so-called‘classical criteria’ (Figure 3).25 Later, Coumel et al.26 showed thata QR pattern in leads other than aVR or a QS pattern in V5–6during VT was present in 89% of the patients with old MI, whileconstantly absent in patients with idiopathic VT.

The Brugada algorithmIn 1991, Brugada et al.27 analysed 554 BCTs and produced simplecriteria in a stepwise approach irrespective of the QRS complexmorphology, whether RBBB- or LBBB-like, with a sensitivity andspecificity of 0.987 and 0.965, respectively. The algorithm(Figure 4) begins with the identification of an RS complex in anyprecordial lead, if failed the diagnosis of VT is made. If an RS

complex is present in one or more precordial leads, the nextstep is to measure the longest RS interval. If an RS interval islonger than 100 ms, the diagnosis of VT is made. If not, the nextstep of the algorithm is to consider whether AV dissociation ispresent. If so, the diagnosis of VT is made. If absent, the classicalmorphology criteria for VT are used (Figure 3). If both lead V1and V6 fulfil the criteria for VT, the diagnosis of VT is made. Ifnot, the diagnosis of SVT with aberrant conduction is made byexclusion of VT.

The aVR ‘Vereckei’ algorithmIn 2007, a new algorithm analysed in 287 patients with a high accu-racy27 has been proposed by Vereckei et al.28 They found that thefollowing criteria were suggestive of VT: (i) the presence of AV dis-sociation; (ii) the presence of an initial R-wave in lead aVR, and (3)measuring the voltage during the initial 40 ms (Vi), the terminal40 ms (Vt), their ratio (Vi/Vt), and that Vi/Vt ≤ 1 was suggestive ofVT (Figure 5). In 2008, the same group presented a simplified algor-ithm using only lead aVR, analysed in 313 patients with the sameaccuracy29 as their first algorithm. Criteria for VT in lead aVRwere (i) the presence of an initial R-wave, (ii) width of an initialr- or q-wave .40 ms, (iii) notching on the initial downstroke ofa predominantly negative QRS complex, and (4) Vi/Vt ≤ 1(Figure 6).

Other criteriaGriffith et al.30,31 performed in 1991 a multivariate analysis in 102patients to identify which of 15 clinical or 11 ECG variables are inde-pendent predictors of VT. They found that (i) the history of previousMI, (ii) in lead aVF, a predominant negative deflection was suggestiveof VT especially when Q-wave was present in RBBB pattern tachy-cardia. In LBBB pattern tachycardia, a QS or qR waveform in leadaVF is highly suggestive for VT, whereas an Rs complex was specificfor SVT, (iii) in RBBB pattern tachycardia, a monophasic or biphasic

Figure 3 Classical ‘Wellens’ criteria favouring VT in patients without AAD.1,12 One hundred VTs (68 ischaemic, 18 idiopathic, and 14 mis-cellaneous) and 100 SVTs with aberrant conduction were included in the comparison.

Diagnostic criteria of BCT 467

by guest on August 7, 2013

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E 100% S E 100% S

Am J Med 1978;64: 27–33

Diagnósticos

RS ≥100 ms

R monofásica V1 QS V6

R monofásica V1 S mayor que R en V6

Sin pulso Debo asumir TV

30 ECG and diagnosis/management of WCT | 257

but any part of the His-Purkinje system may be involved[14].

Pre-excited tachycardia: With this type of rhythm, AVconduction occurs over two paths – the AV nodal His path-way and an accessory pathway (AP). Accessory pathways are abnormal extranodal tissues that connect the epicardialsurface of the atrium and ventricle along the AV groove.Because conduction through the AP does not encounter theusual slowing of conduction that occurs in the AV node, theventricle begins depolarization early through the AP, i.e. the ventricle becomes “pre-excited.” The WPW syndrome isthe most common cause of pre-excitation. Patients with thissyndrome frequently develop symptomatic tachyarrhyth-mias [11,15]. Common forms of pre-excited tachycardia inpatients with WPW syndrome are atrial fibrillation andparoxysmal SVT with ventricular activation over an AP [10].Patients who have APs may have atrioventricular re-entranttachycardia (AVRT). In patients with WPW, AVRT is themost common arrhythmia, occurring in 75% [15]. Atrio-ventricular re-entrant tachycardia may be orthodromic orantidromic. In orthodromic conduction, the anterograde(atrium to ventricle) conduction occurs over the AV nodeand retrograde (ventricle to atrium) conduction occurs overthe AP. The QRS complex is regular and narrow, as the con-duction is occurring in the normal manner, unless there is a pre-existing BBB. In contrast, in antidromic conduction,anterograde conduction occurs through the AP, and retro-grade conduction is through the AV node, manifesting asregular WCT that is virtually indistinguishable from mono-morphic VT. Orthodromic AVRT is more common, even inpatients with WPW syndrome; antidromic tachycardia isseen in 10% of individuals with WPW syndrome [16]. Atrialfibrillation is an uncommon arrhythmia in patients withWPW syndrome, occurring in approximately 20% (Figure30.3) [16], but it is much more deadly, as its rapid rates can

degenerate into ventricular fibrillation [15]. In the treatmentof this subgroup of WCT, AV nodal blocking agents must bestrictly avoided, because they can worsen the tachycardia by increasing conduction through the AP. A more detaileddiscussion of the tachyarrhythmias associated with WPWsyndrome can be found in Chapter 34.

Other causes of regular WCT: Several other importantcauses of WCT should also be considered. Sinus tachycardiawith pre-existing BBB (Figure 30.10) produces WCT. In thissetting, close scrutiny of all leads for evidence of a regular P-QRS association confirms the diagnosis. Note that in thepresence of tachycardia, P waves are not always obvious inall 12 leads, because they may become fused with or “buriedwithin” the preceding T wave.

Wide complex tachycardias can be caused by medicationsthat induce sodium channel-blockade (Table 30.1), such astricyclic depressants (Figure 30.11). The cardiac effects of

(a)

(b)

(c)

Figure 30.9 (a) Monomorphic VT. (b) Polymorphic VT. (c) PolymorphicVT with undulating pattern, suggestive of torsade de pointes.Reprinted from Hudson KB et al. Electrocardiographic manifestations:ventricular tachycardia. J Emerg Med 2003;25:303–14. Copyright2003, with permission from Elsevier.

Table 30.1 Sodium channel–blocking drugs that can cause widecomplex tachycardia

CarbamazepineChloroquineClass IA anti-arrhythmics

DisopyramideQuinidineProcainamide

Class IC anti-arrhythmicsEncainideFlecainidePropafenone

CitalopramCocaineCyclic anti-depressants

AmitriptylineAmoxapineDesipramineDoxepineImipramineNortriptylineMaprotiline

DiphenhydramineHydroxychloroquineLoxapineOrphenadrinePhenothiazines

MesoridazineThioridazine

PropoxypheneQuinineVenlafaxine

Reprinted with permission from Hollowell H et al. Wide-complextachycardia: beyond the traditional differential diagnosis of ventriculartachycardia vs supraventricular tachycardia with aberrant conduction.Am J Emerg Med 2005;23:876–89. Copyright 2005, with permissionfrom Elsevier.

C30.qxd 10/17/08 7:08 PM Page 257

Brady. Critical Decisions in Emergency and Acute Care Electrocardiography 2009

TVm

TVp

TdP

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

nO

ROSEN. ECG IN EMERGENCY MEDICINE AND ACUTE CARE 2005TDP

with supraventricular rhythm and BBB, including:18

1. RSr′ or Rr′ pattern in lead V1 in setting of RBBB2. QS, QR, or R pattern in lead V6 in the presence of an RBBB3. Any Q wave in lead V6 in the presence of an LBBB4. Concordance in precordial leads5. Absence of RS complex in all precordial leads

Torsades de Pointes. Torsades de pointes (TdP) is a rapidform of polymorphic VT that is characterized by beat-to-beatvariability in the QRS complexes, which vary in both ampli-tude and polarity. The resultant QRS complexes appear to“twist” around the isoelectric line. A prerequisite for therhythm is baseline prolongation of the QT interval, whichmay be congenital or acquired, such as can occur with med-ications (type Ia antidysrhythmics) and electrolyte imbalances(hypokalemia, hypomagnesemia). TdP is initiated by a seriesof ectopic beats that begin with a premature ventricular beat

or salvo of ventricular beats, followed by a pause, and then asupraventricular beat. Another premature ventricular beatarrives at a relatively short coupling interval and falls on thepreceding T wave, precipitating the rhythm.

TdP is usually paroxysmal in nature and the underlyingrhythm and intervals can be identified during “breaks” in therhythm. Typically, 5 to 20 complexes are seen in each cycle;the rhythm may either self-terminate or degenerate into ven-tricular fibrillation. The ventricular rate is usually between 200and 250 bpm, and the amplitude of the QRS complexes variesin a sinusoidal pattern (Fig. 26-13). The baseline ECG usuallyprovides important clues to diagnosis, including corrected QTinterval prolongation and ST segment and T wave changesrelated to the underlying metabolic abnormality (Fig. 26-14).

Polymorphic Ventricular Tachycardia (Normal QRS). Thisform of VT often appears similar to TdP, with the important dif-ference being the absence of QT prolongation. Patients with

CHAPTER 26: Ventricular Tachycardia and Ventricular Fibrillation 125

FIGURE 26-13 • Torsades des pointes. This rhythm strip demonstrates the initiation of torsades des pointes by a series of ectopic beats that begin witha premature ventricular beat or salvo of ventricular beats, followed by a pause, and then a supraventricular beat. Another premature ventricular beat arrives ata relatively short coupling interval and falls on the preceding T wave, precipitating the rhythm. The baseline corrected QT interval was 0.64 sec.

ROSEN. ECG IN EMERGENCY MEDICINE AND ACUTE CARE 2005TVPthis rhythm are often found to have unstable coronary arterydisease, and acute coronary ischemia is thought to be an impor-tant prerequisite for this dysrhythmia1,19 (see Fig. 26-14).Ventricular Flutter/Fibrillation. Both ventricular flutterand fibrillation are fatal unless terminated abruptly. The ECGin flutter appears as a continuous sine wave, with no distinc-tion between the QRS complex, ST segment, and T waves(see Fig. 26-5). Ventricular fibrillation is unmistakable—thecomplexes are chaotic and irregular, without discrete QRScomplexes (Fig. 26-15). The patient is always unconsciousbecause this rhythm is unable to generate synchronous ventric-ular contractions.

Digoxin-Toxic Fascicular Tachycardia. This unusual formof ventricular tachycardia is usually a monomorphic VT thathas a relatively narrow QRS and can be mistaken for SVT. Itcan also present as a bidirectional tachycardia, where the QRSusually has a baseline RBBB morphology and alternates itselectrical axis with alternating beats. This VT subtype isthought to be due to alternating block in anterior and posteriorfascicles of the left bundle branch.Brugada Syndrome. Brugada and Brugada described asyndrome that was associated with sudden death in individualswith a structurally normal heart and no evidence of athero-sclerotic coronary disease.20 Patients with this syndrome,

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 patientwith a serum potassium of 1.9 mEq/dL. Note the ST segment depression and “giant” U waves (arrows).

FIGURE 26-15 • Ventricular fibrillation. Ventricular fibrillation is characterized by chaotic, irregular complexes without discrete QRS complex morphology.

FIGURE 8-10 • Torsades de pointes. Rhythm strip of torsades de pointes demonstrates irregular, wide-complex rhythm with oscillating QRS complexamplitude and polarity.

I a VR V1 V4

II

II

a VL V2 V5

III

V1

V5

a VF V3 V6

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

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).

ROSEN. ECG IN EMERGENCY MEDICINE AND ACUTE CARE 2005FA 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. Notethe 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 noRS 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 withtypical left bundle branch block morphology and right inferior axis.

TV TSVD

Definiciones

• Fibrilación Ventricular

• Es una arritmia ventricular que representa una actividad eléctrica desorganizada y compromete la capacidad contráctil del corazón

• Diferenciar: Interferencia, Flutter ventricular, TV polimórfica, FA

CHAPTER 19 Basic ECG Patterns in Cardiac Arrest 177

Ventricular Tachyarrhythmia (Ventricular Fibrillation or Pulseless VT)With ventricular fibrillation (VF) the ventricles do not contract but instead twitch rapidly in a com-pletely ineffective way. No cardiac output occurs, and the patient loses consciousness within seconds. The characteristic ECG pattern, with its unmistakable fast oscillatory waves, is illustrated in Figure 19-1.

VF may appear spontaneously, as noted in Chap-ter 14, but is often preceded by another ventricular

arrhythmia (usually ventricular tachycardia [VT] or premature ventricular beats). Figure 19-2 shows a run of VT degenerating into VF during cardiac arrest.

The treatment of VF was described in Chapter 16. The patient should be immediately defibril-lated, given a direct current electric shock (360 joules) to the heart by means of paddles or pads placed on the chest wall (usually in an anterior-posterior position).

VT and VF are the only “shockable” sudden cardiac arrest rhythms. An example of successful defibrilla-tion is presented in Figure 19-6D.

Success in defibrillating any patient depends on a number of factors. The single most important factor in treating VF is haste: the less delay in defi-brillation, the greater the chance of succeeding.

Sometimes repeated shocks must be adminis-tered before the patient is successfully resuscitated. In other cases, all attempts fail. Finally, external cardiac compression must be continued between attempts at defibrillation.

In addition to defibrillation, additional measures include intravenous drugs to support the circula-tion (epinephrine or vasopressin) and antiarrhyth-mic agents such as amiodarone or lidocaine, and magnesium sulfate (in cases of torsades de pointes and when hypomagnesemia is present).

Ventricular Asystole and Brady-Asystolic RhythmsThe normal pacemaker of the heart is the sinus node, which is located in the right atrium. Failure of the sinus node to function (sinus arrest) leads to ventricular standstill (asystole) if no other subsid-iary pacemaker (e.g., in the atria, atrioventricular [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 all electrodes are connected to the patient. Electrodes

Untrained Bystanders 1. Call 911. 2. Begin manual chest compressions at the ster-

num, at 100 compressions per minute and at a depth of approximately 2 inches.

3. Continue compressions-only CPR until trained professionals arrive, or the victim becomes responsive.

Bystanders Trained in CPR 1. Call 911. 2. Deliver 30 forceful, manual chest compressions

of the sternum, at a rate of 100 compressions per minute and at a depth of approximately 2 inches.

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 19-1 Cardiopulmonary Resuscitation (CPR) Guidelines

␣ • 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)

BOX 19-2 Three Basic ECG Patterns with Cardiac Arrest

Figure 19-1. Ventricular fibrillation causing cardiac arrest.

Hampton. ECG problems 2003

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

178 PART II Cardiac Rhythm Disturbances

often become disconnected during a cardiac arrest, leading to the mistaken diagnosis of asystole. Very low amplitude VF (so-called “fine VF”) may also mimic a straight-line pattern. Increasing the gain on the monitor may reveal this “hidden” VF pattern.

The treatment of asystole also requires contin-ued external cardiac compression; however, unlike VT or VF, defibrillation is not appropriate, nor effective. Sometimes spontaneous cardiac electrical activity resumes. Drugs such as vasopressin or epinephrine

VT VF

Figure 19-2. Ventricular tachycardia (VT) and ventricular fibrillation (VF) recorded during cardiac arrest. The rapid sine wave type of ventricular tachycardia seen here is sometimes referred to as ventricular flutter.

Figure 19-3. Complete ventricular standstill (asystole) producing a straight-line pattern during cardiac arrest.

A

B

Cardiac Arrest: Brady-Asystolic Patterns

Figure 19-4. Escape rhythms with underlying ventricular standstill. A, Junctional escape rhythm with narrow QRS complexes. B, Idioventricular escape rhythm with wide QRS complexes. Treatment should include the use of intravenous atropine and, if needed, sympathomimetic drugs in an attempt to speed up these bradycardias, which cannot support the circulation. If hyperkalemia is pres-ent, it should be treated.

C QRSII

Figure 19-5. External cardiac compression artifact. External cardiac compression during resuscitation produces artifactual ECG complexes (C), which may be mistaken for QRS complexes.

aVF-Continuous stripAccelerated Idioventricular Rhythm

P P P

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.

AIVRVT

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.

Coarse VF Fine VF Coarse VF

Ventricular Fibrillation

Figure 16-22. Ventricular fibrillation (VF) may produce both coarse and fine waves. Immediate defibrillation should be performed.

VT VF

Cardiac Arrest

Figure 16-23. Ventricular tachycardia (VT) and ventricular fibrillation (VF) recorded during the onset of cardiac arrest. The rapid sine wave type of VT seen here is sometimes referred to as ventricular flutter.

Goldberger. Clinical Electrocardiography 2012

ECG 148 The 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?

Hampton. ECG problems 2003Interferencia


CHAPTER 16 Ventricular Tachycardias 155

to the slight pause. TdP can occur with congenital (hereditary) or acquired QT interval prolongation, and can deteriorate into VF, causing sudden car-diac arrest (see Chapter 19).

QT prolongation syndromes that may give rise to TdP are usually classified as acquired or congenital (hereditary) (also see Chapter 24 for a more com-plete list).

Acquired Long QT Syndrome Causes of acquired long QT syndrome include the following: • Drugs, particularly quinidine (see Chapter 10

and Fig. 19-7) and related antiarrhythmic agents (disopyramide and procainamide), as well as ibu-tilide, dofetilide, sotalol, amiodarone, psycho-tropic agents (phenothiazines and tricyclic antidepressants), and many other noncardiac drugs (e.g., pentamadine, erythromycin, and cer-tain other antibiotics) • Electrolyte imbalances, especially hypokalemia and hypomagnesemia, and, less commonly, hypocalcemia, which prolong repolarization

• Severe bradyarrhythmias (especially high-grade AV heart block syndromes) • Miscellaneous factors, such as liquid protein diets

Hereditary Long QT Syndromes: Hereditary forms of long QT syndrome are related to abnormal ion channel function in the heart (related to potassium or sodium) that result in prolonged repolarization. For a discussion of these “channel-opathies,” an important but more advanced concept, see the Bibliography.

Sometimes, TdP is due to a combination of fac-tors that “create a perfect storm” (e.g., hypokale-mia, drug administration, and an unrecognized hereditary ion channel dysfunction that may become unmasked).

General principles of management of TdP include review and discontinuation of any possi-ble QT-prolonging medications and correction of relevant electrolyte abnormalities (especially hypokalemia or hypomagnesemia). Intravenous magnesium may be helpful to shorten the QT

T-U T-U

Torsades de pointes

Torsades de Pointes: NonsustainedMonitor lead

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).

Monitor leadTorsades de Pointes: Sustained

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 arrhyth-mia, which occurs in the setting of QT(U) prolongation.

CHAPTER 16 Ventricular Tachycardias 155

to the slight pause. TdP can occur with congenital (hereditary) or acquired QT interval prolongation, and can deteriorate into VF, causing sudden car-diac arrest (see Chapter 19).

QT prolongation syndromes that may give rise to TdP are usually classified as acquired or congenital (hereditary) (also see Chapter 24 for a more com-plete list).

Acquired Long QT Syndrome Causes of acquired long QT syndrome include the following: • Drugs, particularly quinidine (see Chapter 10

and Fig. 19-7) and related antiarrhythmic agents (disopyramide and procainamide), as well as ibu-tilide, dofetilide, sotalol, amiodarone, psycho-tropic agents (phenothiazines and tricyclic antidepressants), and many other noncardiac drugs (e.g., pentamadine, erythromycin, and cer-tain other antibiotics) • Electrolyte imbalances, especially hypokalemia and hypomagnesemia, and, less commonly, hypocalcemia, which prolong repolarization

• Severe bradyarrhythmias (especially high-grade AV heart block syndromes) • Miscellaneous factors, such as liquid protein diets

Hereditary Long QT Syndromes: Hereditary forms of long QT syndrome are related to abnormal ion channel function in the heart (related to potassium or sodium) that result in prolonged repolarization. For a discussion of these “channel-opathies,” an important but more advanced concept, see the Bibliography.

Sometimes, TdP is due to a combination of fac-tors that “create a perfect storm” (e.g., hypokale-mia, drug administration, and an unrecognized hereditary ion channel dysfunction that may become unmasked).

General principles of management of TdP include review and discontinuation of any possi-ble QT-prolonging medications and correction of relevant electrolyte abnormalities (especially hypokalemia or hypomagnesemia). Intravenous magnesium may be helpful to shorten the QT

T-U T-U

Torsades de pointes

Torsades de Pointes: NonsustainedMonitor lead

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).

Monitor leadTorsades de Pointes: Sustained

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 arrhyth-mia, which occurs in the setting of QT(U) prolongation.

254 | Part 4 The Dysrhythmic ECG

I aVR V1

II

II

aVL V2

III aVF V3

V4

V5

V6

Figure 30.4 Atrial fibrillation with non-specific intraventricular conduction delay ventricular rate, 145 bpm. In contrast to atrial fibrillation withWolff-Parkinson-White syndrome (Figure 30.3), atrial fibrillation with aberrant conduction demonstrates slower ventricular rates and minimalvariation in the QRS complex morphologies.

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

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 andaxis. The QRS complexes change smoothly in amplitude, giving the appearance they are “twisting” around a central axis.

C30.qxd 10/17/08 7:08 PM Page 254

Definiciones

• Actividad eléctrica sin pulso

• Es la despolarización eléctrica organizada del corazón sin actividad mecánica cardíaca suficiente para generar un ritmo que permita la perfusión corporal adecuada. Debe diferenciarse de la pseudo AESP la cuál describe un estado de choque cardiogénico profundo que resulta inadecuado para mantener la presión de perfusión, pero no presenta una verdadera disociación electromecánica

• Pueden observarse ritmo sinusal, ritmos atriales, ritmos ventriculares e idioventriculares, bloqueos cardíacos de diversos grados, arritmias supraventriculares, pero todos ellos asociados con las ausencia de presión arterial y pulso que reflejan una contracción cardíaca ineficaz.

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

MESA GOMEZ GLORIA C 1.0x 1.0x 1.0x of 10 mm/mv 25mm/secRegistrando fecha de inicio31/10/2012

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msmsmsms

103103103103

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828828828828

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99999999

601601601601

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578578578578

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15:21:49

Copyright 1994-2008, All Rights Reserved. Version: 4.0052.Physician Must Review Data Printed: 2/11/2012 11:56:52 2012Copyright 1994-2008, All Rights Reserved. Version: 4.0052.Physician Must Review Data Printed: 2/11/2012 11:56:52 2012Copyright 1994-2008, All Rights Reserved. Version: 4.0052.Physician Must Review Data Printed: 2/11/2012 11:56:52 2012Copyright 1994-2008, All Rights Reserved. Version: 4.0052.Physician Must Review Data Printed: 2/11/2012 11:56:52 2012Page 11Page 11Page 11Page 11

Definiciones

• Asistolia

• Definición: representa la ausencia de actividad eléctrica ventricular con sin actividad eléctrica atrial.

• Características electrocardiográficas: en el electrocardiograma se observa una línea plana de registro sin actividad eléctrica alguna.

• Debe verificarse la adecuada conexión de los electrodos para no pasar por alto un ritmo susceptible de desfibrilación y debe confirmarse en al menos dos derivaciones diferentes.

• Una FV muy fina podría también ser tomada erróneamente como asistolia, por lo que si existe la duda debe incrementarse la ganancia del monitor.

CHAPTER 19 Basic ECG Patterns in Cardiac Arrest 179

may help support the circulation or stimulate car-diac electrical activity. Patients with refractory ven-tricular standstill require a temporary pacemaker, inserted into the right ventricle through the internal jugular or femoral veins. Noninvasive, transcutaneous pacing uses special electrodes that are pasted on the chest wall. However, transcutaneous pacing may only be effective with bradycardia, not frank asystole, and it may be quite painful in conscious patients.

Not uncommonly with ventricular standstill, you also see occasional QRS complexes appearing at infrequent intervals against the background of

the basic straight-line rhythm. These are escape beats and represent the attempt of intrinsic cardiac pace-makers to restart the heart’s beating (see Chapter 14). Examples of escape rhythms with underlying ventricular standstill are shown in Figure 19-4. In some cases the escape beats are narrow, indicating their origin from either the atria or the AV junction (see Fig. 19-4A). In others they come from a lower focus in the ventricles, producing a slow idioventric-ular rhythm with wide QRS complexes (see Fig. 19-4B). The term brady-asystolic pattern is used to describe this type of cardiac arrest ECG.

Asystole

External cardiac compression

Ventricular fibrillation

Ventricular fibrillation DC shock given

R

V

V

1 sec

V

R R R

R

C

External cardiac compressionstartedIntravenous atropine andepinephrine given

DC shock given by electricaldefibrillator

Intravenous lidocaine givento suppress ventricular ectopyand possibly to prevent furtherepisodes of ventricularfibrillation

ECG shows ventricularstandstill (asystole)

ECG now showsventricular fibrillation

ECG now shows sinus rhythmwith ventricular premature beats

A

B

C

D

E

F

G

Figure 19-6. ECG “history” of cardiac arrest and successful resuscitation. The left panel shows the ECG sequence during an actual cardiac arrest. The right panel shows sequential therapy used in this case for the different ECG patterns. A and B, Initially the ECG showed ventricular asystole with a straight-line pattern, which was treated by external cardiac compression, along with intravenous medications. Intravenous vasopressin may also be used here. C and D, Next ventricular fibrillation was seen. Intravenous amiodarone and other medications may also be used in this setting (see text and Bibliography). E to G, Sinus rhythm appeared after defibrillation with a direct current electric shock. C, external cardiac compression artifact; R, R wave from the spontaneous QRS complex; DC, direct current; V, ventricular premature beat.


5H!Hipovolemia Hipoxemia

Hiperkalemia Hipotermia

Hidrogeniones

5T!Trombosis miocárdica

TEP Taponamiento

Tensión Neumo Tóxicos /Tablets

5H!Hipovolemia Hipoxemia

Hiperkalemia!Hipotermia

Hidrogeniones


Medication overdose

Tricyclic anti-depressants (TCA): Patients who overdoseon TCAs are well known to develop rapid neurologic and hemodynamic decompensation: they may be alert andtalking one moment and may develop status epilepticus or

complete cardiovascular collapse moments later. Pulselesselectric activity may be the result of profound vasodilationalong with direct toxic effects on the myocardium.

Tricyclic anti-depressants have many complex pharmaco-logic actions, many of which have cardiovascular implications.The most important for this discussion are anti-cholinergiceffects, and blockade of cardiac fast sodium channels. These

I aVR V1

II aVL V2

III

V1

II

aVF V3

V4

V5

V6

Figure 35.6 Mild hyperkalemia. Peaked T waves are present, but the P waves and intervals are normal.

I aVR V1 V4

II aVL V2 V5II

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.

C35.qxd 10/17/08 7:08 PM Page 308

5H!Hipovolemia Hipoxemia Hiperkalemia!Hipotermia!

Hidrogeniones35 ECG in PEA cardiac arrest scenarios | 309

effects create the ECG changes seen in TCA poisoning [14](Table 35.6 and Figure 35.9). The most specific ECG findingin TCA overdose is the presence of a rightward deviation ofthe vector of the terminal 40 ms of the QRS complex; thisrightward shift occurs between 130° and 207°. This right-ward shift produces an R or R′ wave in the terminal 40 ms ofthe QRS in lead aVr and an S wave in lead I. It is postulatedthat the right ventricular conduction system is more suscep-tible than the left to TCA effects. The presence of this findinghad shown a sensitivity for TCA toxicity ranging from 83 to100% and a specificity of 63 to 98% [15]. The treatment ofTCA overdose with sodium bicarbonate leads to fairly rapidreversal of many of the ECG findings and their clinical conse-quences [16]. The presence of a wide QRS complex, ratherthan tachycardia, is the indication for sodium bicarbonateadministration.

Digoxin: Although death from massive digoxin (and otherdigitalis preparations and plant sources) overdose is usuallyfrom conduction system impairment and ventricular arrhy-thmias, approximately 10% of deaths result from acute leftventricular dysfunction – resulting in PEA arrest. Owing to itsprimary inhibition effect of the Na/K-ATPase on myocardialcalcium channels, potassium moves to the extracellularspace resulting in hyperkalemia. Electrocardiogram changescharacteristic of hyperkalemia may also be seen, further

Table 35.6 Possible ECG findings in TCA Overdose

Rhythm problemsSinus tachycardiaAtrial dysrhythmias

Atrial and AV junctional tachycardiasAtrial fibrillationAtrial flutterBradycardia

Ventricular dysrhythmiasPVCsIdioventricular rhythmVentricular tachycardiaVentricular fibrillationTorsade de pointes

Asystole

Other ECG findingsNon-specific ST or T wave changesPR, QRS, QT interval prolongationRight bundle branch blockRight axis deviation

R wave in AVR with S wave in IAV nodal blockBrugada-type changes (ST elevation in V1–V3 and right bundle branch

block)

I aVR V1 V4

aVL V2 V5II

III aVF V3 V6

Figure 35.8 Hypothermia. Upward deflections at the terminal portion of the QRS complexes, termed Osborn waves or J waves, are noted. TheseOsborn waves are most obvious in the precordial leads and resolve with warming.

C35.qxd 10/17/08 7:08 PM Page 309

5T!Trombosis miocárdica!

TEP Taponamiento


328 | Part 5 The ECG in Critical Care

The diagnostic use ofelectrocardiography in theevaluation of coronary versusnon-coronary diagnoses in thecritically illThese four cases illustrate a sampling of scenarios that canpresent to ICUs and, either on presentation or during their

care, may have clinical evidence suggestive of an acute cor-onary syndrome (ACS). While coronary events are a majorconcern, alternate diagnoses can often present with similarfeatures. Given the variety of pathologies that may produceECG abnormalities, how can the ECG be used to distinguishcoronary from non-coronary etiologies in the ICU?

The ECG has become a powerful diagnostic tool in themanagement of critically ill patients. Since its introduction by Willem Einthoven [1], the ECG has consistently demon-strated its utility in providing information regarding the heart

I 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 V2–V5 with reciprocal ST segment depression in leads III andaVF consistent with a large anterior MI.

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Figure 37.3 ECG demonstrating tachycardia with a heart rate of approximately 140 bpm, left ventricular hypertrophy, non-specific intraventricularconduction delay, poor R wave progression, and Q waves in V1 and V2. Upon closer examination with calipers, irregularity is noted in the R to Rinterval, consistent with atrial fibrillation with rapid ventricular response. Following fluid resuscitation, the patient’s heart rate slowed anddemonstrated clear atrial fibrillation.

C37.qxd 10/17/08 7:12 PM Page 328


TEP!Taponamiento



Similarly, the right ventricular dilatation and the resultingrotation pushes the terminal portion of the QRS vector towardthe right and away from lead I, producing an S wave. Otherspropose the S1Q3T3 pattern results from acute left posteriorhemiblock.6 T wave inversion may be caused by subendocar-dial ischemia in the right ventricle and inferior septal wall inthe presence of high right-sided pressures.7

Axis Deviation. As noted previously, the S1Q3T3 patternmay be in part due to a change to the QRS axis. Althoughright axis deviation is described as the classic axis changeassociated with PE, left axis deviation as well as indeterminateQRS axis changes have been reported with variablefrequency.2 Part of this variability may be related to thespecific definitions of right, left, and indeterminate axisdeviations. Preexisting cardiopulmonary disease may affectaxis changes as well.8

Anterior T Wave Inversions. Inversion of the T waves inleads V1 to V4 has been reported to be closely related to theseverity of PE (Figs. 59-3 through 59-5). Ferrari and col-leagues demonstrate a relationship between T wave inversion

in the anterior leads and both the Miller index (a measure ofvascular blockage derived from the ventilation–perfusionscan) and the degree of pulmonary hypertension.9 Thus, itmay be useful in risk-stratifying patients with PE (see later).The morphology of the inverted T waves is typically sym-metric, and may be found in a wider anatomic range and withdeeper inversion, depending on the severity of PE. An isolatedinverted T wave in lead V1 can be normal.

Several mechanisms have been proposed to explain thisphenomenon, including ischemia in the setting of preexistingright coronary artery stenosis, neurohumorally mediatedchanges in myocardial repolarization, and myocardial shearinjury from increased intramural tension and microvascularcompression. Regardless of mechanism, the finding of sym-metrically inverted T waves in the precordial leads often signifiesprofound right ventricular strain and the potential for clinicaldeterioration in a patient with respiratory distress and hypoxia.

Global T Wave Inversion. Global T wave inversion(Fig. 59-4) in acute PE has been reported in a case report fromthe literature. Although the differential diagnosis for global

FIGURE 59-3 • Anterior T wave inversions. Note the deeply inverted T waves throughout leads V1 to V4 in this patient who was found to have profoundlyelevated pulmonary artery pressures.

FIGURE 59-4 • Global T wave inversion. This patient was thought to have had a non–Q wave myocardial infarction because of the presence of this patternalong with elevated troponin levels. Pulmonary embolism turned out to be the lone culprit.


TEP Taponamiento!Tensión Neumo Tóxicos /Tablets


resulting in a substantially elevated level of auto-PEEP. Anend-expiratory pressure that is associated with a higher thanresting lung volume is called intrinsic or auto-PEEP. Similarto a tension pneumothorax, this high pressure can retard cardiac return and produce progressive hypotension. Casesof PEA have been reported as the result of aggressive ventila-tion during resuscitation [21]. Simply disconnecting thepatient from the ventilator or Ambu Bag will result inrestoration of pulse and blood pressure.

Pericardial tamponade: Pericardial tamponade preventsnormal ventricular filling and severely decreases cardiac output. As the pressure in the pericardium increases, the

pulse pressure narrows and a palpable pulse can be lost. Thedevelopment of this degree of tamponade is usually not sudden unless a traumatic injury is involved. If tamponade isthe result of pericarditis, some of the typical ECG changes ofpericarditis may be seen – diffuse ST segment elevation withPR depression.

Electrical alternans is a beat-to-beat variation in the ampli-tude of electrical complexes on the ECG. While very specificfor the diagnosis of pericardial effusion, its sensitivity is onlyaround 30%. Likewise, the “classic” presentation of electricalalternans, low voltage QRS complexes and PR depression, isvery insensitive (1–17%), but highly specific for diagnosingeffusion and tamponade [22] (Table 35.9 and Figure 35.11).

Sinus tachycardia and low voltage QRS complexes are themost common findings in pericardial tamponade as the heartrate increases to try to compensate for the low cardiac out-put. Any of these findings in the appropriate clinical scenario

Table 35.8 ECG changes in tension pneumothorax

Left-sided tension PTX

Sinus tachycardiaDecreased QRS voltagePoor R wave progressionT wave inversion in precordial leadsElectrical alternans

Right-sided tension PTX

Sinus tachycardiaS1Q3T3S wave in V1Decreased QRS voltageAnterior or posterior MI pattern (rare)

I 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 isnoted. Other findings typical of a large pericardial effusion include sinus tachycardia and low QRS voltage.

Table 35.9 ECG findings of pericardial tamponade*

Sinus tachycardiaLow voltage QRS complexesElectrical alternansPR depressionDiffuse ST segment elevationST segment depression in aVR and V1

*The absence of these findings cannot rule out significant effusion ortamponade

C35.qxd 10/17/08 7:08 PM Page 312


complicating the cardiovascular toxicity. Treatment of theresultant hyperkalemia with calcium in the face of digoxintoxicity may result in increased calcium influx intracellu-larly. There have been two human cases of reported myo-cardial tetany producing asystole – the so-called stone heart – with calcium boluses in digoxin toxicity. The cause of deathin these cases was unclear and inconclusive. “Stone heart” asa cause of PEA, if it occurs at all, is extremely rare and hasbeen highly inconsistent in studies looking at the interactionof digoxin and calcium, likely relegating this issue to themyth category [17].

Any arrhythmia is possible with digoxin toxicity [18] (seeTable 35.7). The most common abnormal finding on the ECGin digoxin overdose is premature ventricular contractions,and the most common arrhythmias are an accelerated junc-tional rhythm (often in the presence of atrial fibrillation and complete heart block; Figure 35.10) and paroxysmalatrial tachycardias with variable AV block. Multiple differentarrhythmias can occur simultaneously. The combination ofconduction blockade with enhanced automaticity clearlydescribes the rhythm disturbances seen in digoxin toxicity.Digoxin immune Fab (antigen binding fragments) should beconsidered in patients with PEA and digoxin toxicity.

Beta-adrenergic and calcium channel-blockers: Beta-adrenergic and calcium channel-blockers can be consideredtogether because of similar effects on the cardiovascular

system – hypotension and bradycardia with minimal impacton the QRS complex and QT intervals [19]. Ventriculartachydysrhythmias are uncommon, with the exceptionsoccurring with bepridil and sotalol. These agents have addi-tional anti-arrhythmic effects, which, in overdose, can bepro-arrhythmic: sotalol has both Class II and Class III effects,while bepridil has Class I anti-arrhythmic effects. Ventricularconduction disturbances are more likely to occur in patientswho have beta-blocker poisoning, because the drugs are able

I aVR V1 V4

aVL V2 V5II

III

V1

V5

II

aVF V3 V6

Figure 35.9 Tricyclic antidepressant overdose. The classic findings of tachycardia, rightward axis, prominent S wave in lead I (large arrow) and tall Rwave in aVR (small arrow) are present.

Table 35.7 ECG findings in digoxin overdose

ECG findings with digoxin usePR interval prolongationQT interval shorteningInverted/flattened T waves with “scooped” ST segments (often referred

to as the “Salvador Dali” or “digoxin effect” appearance at theterminal portion of the QRS complex.

ArrhythmiasPVCs, PACs, PJCsAny arrhythmia (increased automaticity + increased vagal tone lead to

both tachy and bradyarrhythmias)Paroxysmal atrial tachycardia with variable AV blockAccelerated junctional rhythm

Other findingsBundle branch blocksVarying AV nodal blocks

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


TEP Taponamiento


Activar servicio emergencias

Iniciar RCP-Oxígeno-Monitorización


FV/TVsP Asistolia / AESP

⚡️

RCP 2 min-Acceso IV/IO


⚡️

⚡️

RCP 2 min-Acceso IV/IO, Adrenalina cada 3-5 min, monitorización avanzada




Ritmo desfibrilable? Ritmo desfibrilable?


No hay ROSC? Pasar a 10 u 11Hay ROSC ? Cuidados post RCP Pasar a 5 ó 7

1

2

3

4

9

510

6

7

811

12

Si No

Si

Si

Si

No

No

No

Si

No

Conclusiones

• Compromiso hemodinámico: asuma TV

• Identifique ritmo:

• Determina el tratamiento

• Determina el pronóstico

arritmias en reanimacion

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