Hrev_master Introduction The Electrocardiogram (ECG) plays a crucial role in initial syncope evaluation. After a careful clinical history evaluation and an accurate physical examination including supine and standing BP measurements, the ECG features represent a pivotal moment to stratify the risk of patients. The presence of ECG findings suggest- ing arrhythmic syncope put the patient at relevant risk. This could mean the necessity to perform further specific invasive and non- invasive diagnostic procedures (echocardiogram, effort test, ECG monitoring, transoesophageal study, electrophysiological study, external and implantable loop recorder, magnetic resonance, coro- nary angiography). Furthermore, some ECG features already rep- resent an indication for a therapeutic strategy (pharmacological treatment, radio-frequency ablation or device implantation like pacemaker and permanent autonomous defibrillator) (Tables 1 and 2).1-9 On one hand a normal ECG1-4 with no pathological findings in clinical evaluation stratifies the syncopal events at low risk, on the other hand ECG findings can represent red flags in identifying high-risk patients.5 Sinus bradycardia, recurrent sinoatrial block and prolonged sinus arrest The first important aspect to interpret correctly the ECG is the recognition of sinus rhythm (SR). The depolarization wave of SR has an electric axis of approximately 60° and is positive in D1. Every P wave is followed by a QRS complex with constant PQ interval. Figure 1A shows a bradycardic SR with a heart rate (HR) of 45 bpm, which should be interpreted in the context of the clini- cal features of the patient: in athletes, this condition represents the normality. In some case further diagnostic investigation is needed. Clinical advice: effort test to verify the appropiate increase of HR (chronotropic competence) and the AV conduction. Echocardiogram for the exclusion of an organic cardiomyopathy; sinus node recovery time (SNRT)10 and nodal AV system (Wenckebach point and 1:1 AV conduction)11 using a simple tran- soesophageal study. It is not necessary to perform an invasive elec- trophysiological study. Clinical advice (Figure 1B): this is a clear example of signifi- cant sinus bradycardia which represents in most cases an accepted indication for cardiac pacing in a patient with syncope. Clinical advice (Figure 1C): investigate sinus node function with transoesophageal electrophysiological study (EPS) or inva- sive EPS. Clinical advice (Figure 1D): this is an indication for cardiac pacing in patients with syncope. Clinical advice (Figure 1E): this diagnosis in a patient affected by syncope is almost always treated using a pacemaker implantation in addition to pharmacological antiarrhythmic prophylaxis.12-16 Second and third degree atrio-ventricular block: bundle branch blocks Bundle branch conduction disturbances reflect a deficiency which involves the part of the system under the AV node (infrahis system) (Figure 2). In patients affected by syncope the evidence of BBB is highly suggestive for cardiac syncope. Second degree AV block Mobitz 2, third degree AV block and alternating bundle branch blocks (BBB) are a clear indication for cardiac pacing. Patients with syncope and left bundle branch block, right bundle branch block, left anterior hemiblock or 2nd degree AV block Mobitz 1 (Luciani- Wenckebach) must undergo further diagnostic investigation.17-23 Clinical advice (Figure 3A): in patients with unexplained syn- cope and left bundle brunch block (LBBB) at basal ECG an inva- sive electrophysiological study must be performed: the presence of a prolonged infrahis interval (HV>70ms) stratifies to a high risk to develop a third degree AV block. Pacemaker implantation is indi- cated. Typical ECG features of left bundle brunch block are the large QRS complex (more than 120ms), RR’ aspect in V6 deriva- tion. Clinical advice (Figure 3B): invasive electrophysiological study. The final report is: atrial fibrillation with aberrant AV con- duction characterized by right bundle brunch block (RBBB) and left anterior hemiblock, in sum bifascicular block. Clinical advice (Figure 3C): in a patient with syncope this find- ing is a clear indication to permanent cardiac pacing. The 4th P- Emergency Care Journal 2018; volume 14:7570 Correspondence: Marco Tomaino, Regional Hospital of Bolzano, Via Lorenz Böhler 5, 39100 Bolzano, Italy E-mail: marco.tomaino@sabes.it Key words: High-risk electrocardiogram patterns; Syncope; emergency department. Contributions: the authors contributed equally. Conflict of interest: the authors declare no potential conflict of interest. Funding: none. Received for publication: 18 May 2018. Revision received: 29 June 2018. Accepted for publication: 29 June 2018. This work is licensed under a Creative Commons Attribution 4.0 License (by-nc 4.0). ©Copyright M. Tomaino et al., 2018 Licensee PAGEPress, Italy Emergency Care Journal 2018; 14:7570 doi:10.4081/ecj.2018.7570 [Emergency Care Journal 2018; 14:7570] [page 37] High-risk electrocardiogram patterns in patients with syncope managed in the emergency department Marco Tomaino,1 Matthias Unterhuber,1 Attilio Del Rosso2 1Regional Hospital of Bolzano; 2Regional Hospital of Empoli, Italy Non -co mmerc ial us e o nly wave is not followed by a QRS complex, there is a sudden AV block without progressive elongation of PR interval in the beats before. The AV block Mobitz 2 is related to a serious disorder of the infrahis system and results in a worse prognosis for develop- ment of total AV block. Clinical advice (Figure 3D): a patient with syncope and these ECG features should undergo a thorough diagnostic investigation (effort test, electrophysiological study) in order to decide for per- manent cardiac pacing. This condition is an AV node difficulty to conduct all beats, and is characterized by a progressive elongation of PR interval before the AV block. Basal ECG shows SR, narrow QRS, PR 200ms and evidence of second degree AV block Luciani- Wenckebach (LW) or Mobitz 1-type. Clinical advice (Figure 3E): alternating BBB is an indication for cardiac pacing irrespective of syncope. In this ECG you can see an alternating LBBB and RBBB. On top, confirming the important infrahis system disorder in presence of a 2nd degree AV block Mobitz 2. Clinical advice (Figure 4 A): Pacemaker implantation. Clinical advice (Figure 4B and C): E.v. Atropine will block Educational paper Figure 1. A) Observe the prolonged PR interval (280 ms); the upper limit is 200 ms, thus representing an atrioventricular (AV) block first degree. Considering the narrow QRS complex, the most probable hypothesis is an AV node delay; B) In patients affected by syncope the evidence of a sinus bradycardia with HR<40 bpm in waking hours is highly suggestive for arrhythmic syncope; C) Sinoatrial block. Note the missing beat at the end of the P-wave cycle (expected beat), in absence of a significant pause (<3 sec); D) Sinoatrial block with 4 missing beats and resultant significant pause (>3 sec); E) Evidence of significant asystolic pause due to sinus arrest and concomitant atrial fibrillation with high ventricular response rate, i.e. brady-tachy Syndrome. In patients affected by syncope the evidence of recurrent sinus atrial block and sinus pauses>3s is highly suggestive of arrhythmic syn- cope.13-16 [page 38] [Emergency Care Journal 2018; 14:7570] A B C E D Non -co mmerc ial us e o nly parasympathetic efferents thus increasing temporarily the AV con- ducting ability. Clinical advice (Figure 4D): Being an infrahis conducting tis- sue disturbance, atropine will not increase the heart rate. By block- ing parasympathetic efferents it has no effect on the infrahis sys- tem (which is not influenced by the parasympathetic nervous sys- tem). Paroxysmal supraventricular and ventricular tachycardia Paroxysmal supraventricular tachycardia (SVT) is an episodic condition with abrupt onset and termination. It requires underlying atrial and/or AVN and/or Wolff-Parkinson-White (WPW) condi- tions. In patients with a syncope the suspected SVT must be inves- Educational paper Figure 2. Bundle branch conduction disturbances reflect a defi- ciency which involves the part of the system under the AV node (infrahis system). Taken from: https://en.wikipedia.org/ wiki/Bundle_of_His#/media/File:Conductionsystemoftheheartw ithouttheHeart-en.svg Figure 3. A) SR characterized by normal AV conduction with a left bundle branch block; B) the bundle branch abnormality con- cerns the right bundle (tipical ECG aspect of RR' in V1 deriva- tion) and the left anterior branch (negative D2 and D3 that means left axis deviation>30°, and deep s of ventricular complex in V6 derivation). Observe the absence of the P-wave and the irregularity of ventricular beats; C) dangerous manifestation of second degree AV block Mobitz type 2, in a patient with RBBB in the basal ECG and an upper limit PR interval (200msec); D) Second degree AV block related to a good prognosis; E) Very seri- ous AV abnormality, to be considered as a prelude to total AV block. A B C E D [Emergency Care Journal 2018; 14:7570] [page 39] Non -co mmerc ial us e o nly [page 40] [Emergency Care Journal 2018; 14:7570] Educational paper Figure 4. A) This ECG was recorded 24 hours later in the same patient: 3rd degree AV block, in which notice the complete dissociation between P-waves and QRS-complexes; B) AV-Block II° Type I Luciani-Wenckebach. before atropine; C) AV-Block II° Type I Luciani- Wenckebach. afterwards atropine; D) AV-Block II° Mobitz II. A B A B C D Figure 5. A) Wolff-Parkinson-White (WPW) conditions; B) left bundle brunch block. Non -co mmerc ial us e o nly tigated, first of all using prolonged ECG monitoring. There is an ECG presentation which is highly suggestive for atrioventricular reentrant tachycardia or reciprocating tachycardia (AVRT). Figure 5A is a typical example of WPW, a congenital syn- drome involving abnormal conductive cardiac tissue between the atria and the ventricles that provides a pathway for a reentrant tachycardia circuit, in association with supraventricular tachycar- dia (SVT). Features of WPW are short PR interval, QRS<120ms and delta waves (not to be confounded with SR and LBBB, Figure 5B).24 Clinical advice (Figure 5): Careful risk assessment with pro- longed ECG monitoring, stress testing and electrophysiological study. QT duration abnormalities Long QT syndrome (LQTS) is a genetic or drug-induced dis- order which affects repolarization of the cardiomyocytes. This results in an increased risk of torsade de pointes which can result in loss of consciousness, drowning or sudden death. Significant pathologic QTc intervals include values>480ms, QTc durations of >500ms are highly associated with sudden cardiac death in patients with syncope. Pay attention to patients treated with amiodarone, sotalol, psychiatric drugs, antibiotics (especially macrolides and quinolones which are often used) and ondansetron. Precipitating factors can be electrolyte disorders like hypokalaemia, hypocal- caemia, hypomagnesaemia in vomiting, diarrhoea or other metabolic conditions. For a correct measurement of the QT inter- val it is important to pay attention at the U-wave. If the QT interval involves a U-wave or there is a notched T-wave, the U-wave takes part in the measurement. If the U-wave is separated (with clear space in the isoelectric line between T and U wave), it has not to be involved in the measurement of QT interval. The method to clarify this is the intersection between isoelectric line and the tan- gent of the descending T-wave part (maximum slope intercept method) (Figure 6). Clinical advice (Figure 7A and B): 74-year-old male, affected by hypertension treated with ACE-inhibitor and thiazide diuretic, permanent atrial fibrillation treated with digitalis, depression treat- ed using two non-tricyclic antidepressants. The patient was admit- ted because of a sudden syncopal episode in supine position, the blood tests showed hypokalaemia (2mEq/l). In the clinical evalua- tion the most important point regards the medication of the patient. This patient is at high risk of sudden death. Hospitalization and continuous ECG monitoring are mandatory. 25,29,38 This happened in the following hours during ECG monitoring: a torsade de pointes, which typically occurs in long QT conditions. It is characterized by continuous axis variation, and can be self- Educational paper Figure 6. Intersection between isoelectric line and the tangent of the descending T-wave part (maximum slope intercept method). [Emergency Care Journal 2018; 14:7570] [page 41] Figure 7. A) QT: 600 msec, QTc: 537 msec; the QT interval is particularly prolonged and most likely the cause of syncope; B) torsade de pointes, which typically occurs in long QT conditions, is characterized by continuous axis variation, and can be self-lim- iting. Often it can degenerate in ventricular fibrillation; C) the same careful management should be guaranteed for patients admitted with syncope and evidence of short QT interval. A B C Non -co mmerc ial us e o nly limiting. Often it can degenerate in ventricular fibrillation (Figure 7B). The same careful management should be guaranteed for patients admitted with syncope and evidence of short QT interval. Short QT syndrome is an inherited cardiac channelopathy charac- terized by an abnormally short QT interval and increased risk of ventricular fibrillation. Diagnosis is based on the evaluation of symptoms, patient’s family history for sudden cardiac death and 12-lead ECG.26 ICD is the first line therapeutic strategy (Figure 7C). Diagnostic criteria for short QT syndrome are: i) QTc ≤ 330 ms; ii) QTc < 360 ms in the presence of one or more of the follow- ing elements: a) Pathogenetic mutation; b) Family history of short QT syndrome; c) Family history of sudden death < 40 aa; d) VT or VF in absence of organic cardiopathy. Educational paper Figure 8. A) the evidence of AV dissociation means to find out a P-wave dissociated from the ventricular activity (you can see it in V1 derivation, in the last two beats); B) typical example of wide complex tachycardia; C) The transformation of QRS from wide to narrow QRS after e.v. adenosine. If adenosine does not influence the arrhythmia, the VT as diagnosis is confirmed;30-35 D), E) negative T-wave in precordial derivations; F) Type-1 Brugada pattern, characterized by coved ST-segment elevation V1-V2. A B C D E F [page 42] [Emergency Care Journal 2018; 14:7570] Non -co mmerc ial us e o nly [Emergency Care Journal 2018; 14:7570] [page 43] Wide complex tachycardia During wide complex tachycardia (HR > 100/min, QRS > 120ms) the differentiation between supraventricular and ventricu- lar origin of the arrhythmias is important to guide therapy. Several algorithms have been developed to aid in this differentiation. The evidence of a fusion beat or/and the AV dissociation estab- lishes the diagnosis of VT. The fusion beat is a fusion in the ven- tricular depolarization between the VT and a rare SR beat, which is able to overstep the AVN and give a contribution in a part of ven- tricular depolarization (fourth beat in aVR, aVL and aVF deriva- tion). The evidence of AV dissociation means to find out a P-wave dissociated from the ventricular activity (you can see it in V1 derivation, in the last two beats). In Figure 8A there are both fea- tures. A third feature is the capture beat, which consists in a normally conducted P-wave followed by a QRS with normal duration. A transoesophageal detection of atrial activity would allow to confirm AV dissociation, but it could be difficult to organize a pro- cedure like this in the Emergency Department. A useful trick to unhide the nature of arrhythmias can be the use of adenosine, a medical treatment with very short life of few seconds, blocking the AVN. The ECG showed in Figure 8B is a typical example of wide complex tachycardia, in which the diagnosis is very difficult con- sidering the impossibility to find out the two characteristics men- tioned before. If adenosine produces a modulation in AV conduc- tion as in Figure 8C (2:1,3:1, 4:1...), there is an underlying supraventricular arrhythmia with aberrant conduction.30-35 Figure 8D and E show the negative T-wave in precordial derivations. It is possible to identify a pathognomonic feature of right ventricular arrhythmogenic cardiomyopathy in V1 derivation at the end of QRS: the epsilon wave. In a patient affected by syncope, the clinical and ECG features put him at high risk of sudden death. Clinical advice: pharmaco- logical treatment or RF-Ablation could be useful to reduce the recurrences, but in context of high risk of sudden death, the ICD represents first line therapy.8,27,28,36,37 Figure 8F: type-1 Brugada pattern, characterized by coved ST- segment elevation V1-V2. In case of symptoms related to this ECG, we talk about Brugada Syndrome: a genetic condition that results in abnormal electrical activity within the heart, increasing the risk of sudden cardiac death. The condition is often inherited from a person´s par- ent with about a quarter of people having a family history. Some case may be due to a new mutation or certain medications. The most commonly involved gene is SCN5A which codes for the car- diac sodium channel. Diagnosis is typically made by ECG. Educational paper A B Figure 9. A) normal function of a pacemaker in sequential modality; B) pacemaker malfunction. Table 1. Major ECG findings suggesting arrhythmic syncope. Patients with syncope and one or more of this ECG characteris- tics are considered at high risk.1-8 Major ECG criteria suggesting arrhythmic syncope Acute ischaemia Q- Waves consistent with ischaemic heart disease AV- Block II° type Mobitz II or higher Atrial fibrillation <40bpm Persistent sinus bradycardia <40bpm Repetitive sinoatrial block or sinus pauses >3s in waking hours Bundle branch blocks Intraventricular conduction disturbances Signs of ventricular hypertrophy (Sokolow-Lyon Index >35mm) Sustained or non-sustained ventricular tachycardia Implanted cardiac device malfunction ST- Segment elevation of Brugada I type-pattern QTc >460ms indicating Long-QT Syndrome Table 2. Minor criteria which put the patient at high risk profile if there is a history suggesting an arrhythmic syncope.7-9 Minor criteria suggesting arrhythmic syncope AV-Block I° with markedly prolonged AV- Interval or AV-Block II° Mobitz I Asymptomatic inappropriate sinus bradycardia (40-50bpm) Slow atrial fibrillation with 40-50bpm Paroxysmal supraventricular tachycardia or atrial fibrillation Pre-excited QRS complex Short QTc interval (<340ms) Atypical Brugada patterns Negative T-waves in right precordial leads, epsilon waves suggesting arrhythmogenic right ventricular cardiomyopathy (ARVC)Non -co mmerc ial us e o nly [page 44] [Emergency Care Journal 2018; 14:7570] However, the abnormalities may not be consistently present. Medications such as ajmaline may be used to reveal the ECG changes. Fever can unmask the ECG Brugada pattern. Similar ECG patterns may be seen in certain electrolyte disturbances or due to a reduced blood supply to the heart. Clinical advice: risk stratification in individuals with type 1 Brugada ECG pattern for primary prevention of sudden death is an unsolved issue. Patients with unexplained Syncope and evidence of type 1 Brugada ECG must be thoroughly investigated. Verify the family history of sudden death and perform an electrophysio- logic study for the induction of ventricular arrhythmias. According to a consensus statement of experts the presence of two out of three criteria (unexplained syncope, family history of sudden death and induction of ventricular arrhythmias) represent an indication for ICD implantation. Anyway we suggest to monitor (with Implantable Loop Recorder) patients with unexplained syncope and type 1 Brugada ECG pattern.39-43 Supraventricular and ventricular tachycardia are suggestive of cardiac syncope in class 1 according to the guidelines of the European Society of Cardiology. Pharmacologic treatment or catheter ablation are indicated as first line therapy. In case of ven- tricular arrhythmias an accurate risk stratification of sudden death, which aims to verify the indication for an ICD implantation, is nec- essary. Device malfunction Pacemaker and ICD defects in patients affected by syncope are not uncommon. Figure 9A: normal function of a pacemaker in sequential modality (synchronized atrial and ventricular pacing): atrial spikes generate an atrial depolarization and the ventricular spikes produce a ventricular depolarization, with wide QRS as as consequence of the fact that the ventricular catheter is located in apical position. Figure 9B: pacemaker malfunction. The device can recognize the P-wave, but the ventricular spike is not followed by any depo- larization (QRS complex): there is a working detection of the atrial catheter and a pacing defect of the ventricular catheter. This condi- tion produces an asystolic pause which is cause of the syncope. Clinical advice: all patients with previous pacemaker or ICD implantation affected by syncope must undergo a device control to verify its proper function. Conclusions An accurate clinical evaluation of patients affected by syncope involves the clinical history, physical examination, blood pressure measurement and careful ECG interpretation (Table 3). The pre- sence of an abnormal ECG classifies the patient at moderate or high risk. This implies the necessity to perform further diagnostic procedures or to decide for a specific cardiologic treatment. References 1. Quinn J, McDermott D, Stiell I, et al. Prospective validation of the San Francisco Syncope Rule to predict patients with seri- ous outcomes. Ann Emerg Med 2006;47:448-54. 2. Colivicchi F, Ammirati F, Melina D, OESIL (Osservatorio Epidemiologico sulla Sincope nel Lazio) Study Investigators. 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