Case Discussion < Brief History > A 68-year-old man was admitted to the intensive care unit (ICU) because of a witnessed collapse of sudden onset while he was waiting for excision of a lipoma on his right elbow in this hospital. He had had a history of hypertension for 10 years that had been treated with trichlormethiazide 1mg qd. He had an established diagnosis of chronic obstructive pulmonary disease (COPD) and reported having experienced brief episodes of lightheadedness without warning. This lightheadedness occurred occasionally, without any identifiable precipitating factor, and it abated without intervention. In addition, he had experienced episodes of shortness of breath on exertion, which he attributed to a long history of cigarette smoking. He had been otherwise healthy without having had any symptoms of nausea, vomiting, chest pain and pressure sensation, palpitations, diaphoresis, or syncope. He had no known family history of heart disease or diabetes mellitus. On physical examination, he was in no acute distress and his consciousness was clear and oriented. He was afebrile, and the blood pressure was 134/76 mm Hg, the pulse rate 65 beats per minute, and the respirations 16 breaths per minute. The oxygen saturation was 93% while he was breathing ambient air. The neck examination showed no jugular venous distension or carotid bruits. Auscultation of his chest revealed distant breath sounds with no wheezing, crackles, or rhonchi. Cardiac examination revealed a regular heart rhythm, with frequent skipped beats and slightly accentuated second heart sounds. There were no murmurs, rubs, or gallops. No peripheral edema of the lower extremities was observed and the remainder of the physical examination was normal. An electrocardiogram (ECG) and a panel of preoperative blood tests were ordered. The patient experienced an episode of severe lightheadedness while waiting for the operation. He became unconscious with a blood pressure of 84/48 mm Hg. An ECG was recorded (Figures 1 and 2 ). < Laboratory data > CBC/DC: (Time: 11:04am, June 26th, 2008, after collapse) WBC /μL 8400 Band % 0 RBC M/μL 3.36 Seg % 84 Hb g/dL 13.2 Lym % 4 Hct % 39.6 Mono % 6 MCV fl 90.3 Eos % 1 PLT. /μL 326000 Baso % 5.0 Biochemistry: (Time: 11:04am, June 26th, 2008, after collapse) Alb         g/dL 4.1 T-Bil   mg/dL 0.7 BUN      mg/dL 25 K        mmol/L 4.7 Cre        mg/dL 0.8 ALT    U/L 24 Glucose  mg/dL 116 Cla      mmol/L 104 Na          mmol/L 135 AST    U/L 26 Mg         mmol/L 1.1 Ca       mmol/L 8.2 Serial cardiac enzyme (after collapse)   11:04am 06/26/2008 3:15m 06/26/2008 9:12pm 06/26/2008 3:24am 06/27/2008 9:25am 06/27/2008 CK(U/L) 180 198 194 190 188 CK-MB(U/L) 8 12 10 8 12 Troponin-I (U/L) 0.08 0.02 0.04 0.08 0.04 Artery blood gas (10:28am, 06/26/2008, after collapse) : pH: 7.38, PaCO2: 48.3, PO2: 60, HCO3-: 25.6 CXR: Normal heart size and clear lung fields. Echocardiography (11:28am, 06/26/2008, after collapse): normal size of the left atria (LA) and left ventricles (LV) with good contractility; mild TR and mild pulmonary hypertension. Magnetic resonance imaging of the heart (8am, 06/27/2008, after collapse): normal LV and RV structures and systolic function. < Course and Treatment > A 200-J biphasic cardioversion shock was performed and the patient regained consciousness with blood pressure returning to 110/62 mm Hg. The patient was transferred to ICU. Sotalol (320 mg/day) and atenolol (100 mg/day) were administered. The follow-up ECG were normal, and his serial examinations of cardiac enzymes as well as serum electrolytes were within the normal ranges for the next 24 hours during the ICU stay. A coronary angiogram revealed patent coronary arteries. An electrophysiological study demonstrated an arrhythmogenic focus of myocardial irritability, which was thought to be caused by scar tissue from a previously unrecognized myocardial infarction, was identified. An automatic internal cardiac defibrillator was placed and, subsequently, his lipoma on the right elbow was successfully excised. < Case Discussion >      A wide-complex tachycardia is a form of cardiac dysrhythmia that originates from either a ventricular focus or a supraventricular focus associated with a conduction abnormality and presents with a ventricular rate that exceeds 100 bpm in the setting of a QRS duration greater than or equal to 120 milliseconds. In this case, a 12-leads ECG showed that the ventricular rate was greater than 100 bpm and the QRS duration was greater than 140 milliseconds with no regular P waves.      Ventricular tachycardia (VT) accounts for up to 80% of wide-complex tachycardias, which may be higher in patients with structural or ischemic heart disease. VT also occurs in patients with hypoxemia, acidemia and electrolyte abnormalities, such as hypokalemia and hypomagnesemia, as well as in patients with mitral valve prolapse and receipt of drugs that may prolong the QT interval, such as digitalis, antihistamine, tricyclic antidepressants. VT occasionally occurs in individuals without any identifiable risk factors.      Symptoms associated with a wide-complex tachycardia are typically caused conditions that result in a decreased cardiac output, namely presyncope, syncope, orthostasis, exercise limitation, dyspnea, and hypotension. However, clinical symptomatology is of limited value in the differentiation of VT from supraventricular tachycardia (SVT) since similar symptoms may be presented by patients with either of these conditions.      In order to accurately treat and manage patient with wide-complex tachycardia, it is critical that the underlying rhythm is accurately diagnosed, especially when the patient is hemodynamically unstable. A wide-complex tachycardia should be presumed to be a VT until the presence of SVT can be proven, because medications routinely used to treat SVT can cause severe hemodynamic deterioration by inducing a relatively stable rhythm of VT to degenerate into ventricular fibrillation. Patients with a wide-complex tachycardia in an unstable condition should receive immediate electrical cardioversion. In accordance with the ACLS guidelines[1], amiodarone, procainamide, or lidocaine may be used in patients with a stable VT or a wide-complex tachycardia of unclear origin.      To date, several studies have attempted to improve the diagnostic accuracy of differentiating VT from SVT in the evaluation of wide-complex tachycardia. Of these, Brugada proposed one of the most well-recognized 4 characteristics [2]: If an RS complex cannot be identified in any precordial lead, VT can be diagnosed with a specificity of 100% and a sensitivity of 21%. If an RS complex is clearly distinguished in one or more precordial leads, the interval between the onset of the R wave and the deepest part of the S wave (RS interval) is measured. If the RS interval is greater than 100 milliseconds, VT can be diagnosed with a specificity of 98% and a sensitivity of 66%. If the RS interval is less than 100 milliseconds, the presence or absence of atrioventricular (AV) dissociation must be determined. Evidence of AV dissociation is 100% specific and 82% sensitive for VT. This is because AV dissociation does not occur in SVT. If the RS interval is less than 100 milliseconds, and if AV dissociation cannot be clearly demonstrated, the QRS morphology may be evaluated. Morphologic criteria suggestive of VT are extensive and complex, and they should be evaluated in conjunction with a cardiologist, if necessary. Other characteristic ECG findings that may assist in the quick differentiation of VT from SVT include the following[3,4]: • An extreme rightward axis (-90 to -180 degrees) is often more suggestive of VT. A slight irregularity of the RR intervals, especially in the early stages before settling into a regular rhythm, can be suggestive of VT. The width of the QRS complex can also be useful for distinguishing SVT from VT. In general, a wide QRS complex greater than 140 milliseconds suggests VT; however, a QRS duration of less than 140 milliseconds is not helpful for excluding ventricular tachycardia, because VT is sometimes associated with a relatively narrow QRS complex. If the degree of voltage change in the first 40 milliseconds of the QRS complex is less than the degree of voltage change in the last 40 milliseconds of the complex, this finding is suggestive of VT. "Fusion" occurs when a supraventricular impulse reaches the AV node simultaneously with a ventricular impulse. Intermittent fusion beats during a wide-complex tachycardia indicate atrioventricular dissociation and, therefore, also indicate VT. A "capture beat" occurs when a supraventricular rhythm briefly conducts in a normal fashion, with a resultant normal QRS complex. The term "capture beat" implies that the normal conduction system has momentarily replaced the control of a ventricular focus; hence, VT is present. In addition, more recently, a study found that VT mechanism was predicted by the following[5]: Presence of an initial R wave in aVR Width of an initial r or q wave >40 ms in aVR Notching on the initial downstroke of a predominantly negative QRS complex in aVR In conclusion, this patient with ventricular tachycardia; as diagnosed through a ventricular rate of greater than 100 bpm and wide QRS morphology with no regular P waves, as indicated with a 12-leads ECG; presented with an episode of severe lightheadedness, unconscious and low blood pressure. An electrophysiological study was performed, and an arrhythmogenic focus identified. As a result the patient had an automatic internal cardiac defibrillator placed and was followed up as an outpatient. < References > Wellens HJ. Electrophysiology: Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart. 2001;86:579-585. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83:1649-1659. Akhtar M, Shenasa M, Jazayeri M, Caceres J, Tchou PJ. Wide QRS complex tachycardia. Reappraisal of a common clinical problem. Ann Intern Med. 1988;109:905-912. Gupta AK, Thakur RK. Wide QRS complex tachycardias. Med Clin North Am. 2001;85:245-66. Vereckei A, Duray G, Szenasi G, et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm. Jan 2008;5(1):89-98. 繼續教育考題 1. (C) What rhythm is demonstrated by the ECG strip? A Atrial Flutter B Supraventricular tachycardia (SVT) with aberrant conduction C Non-sustained ventricular tachycardia D Torsade de Pointes 2. (C) What rhythm is demonstrated by the 12-lead ECG?  A Atrial Flutter B Supraventricular tachycardia (SVT) with aberrant conduction C Ventricular tachycardia D Torsade de Pointes 3. (E) Which of the following symptoms is NOT a presentation of ventricular tachycardia?  A Syncope B Lightheadedness C Palpitation D Cold sweating E Tremor 4. (D) Which of the following statements concerning wide-complex tachycardias is NOT true? A 80% of the cases of wide-complex tachycardia are VT. B The presumptive diagnosis of VT guards against inappropriate and potentially dangerous therapies. C Mistreatment of SVT as VT is safe and frequently effective at restoring a sinus rhythm. D The presence of hemodynamic stability can be used as a sign in the diagnosis of SVT with aberrancy. E Structural heart disease is the most common cause of VT. 5. (B) Which of the following ECG findings is NOT suggestive of ventricular tachycardia?  A An RS complex is not present in any precordial lead B Regularity of the RR interval C The RS interval is greater than 100 milliseconds D Atrioventricular dissociation E The presence of capture beats 6. (D) Which of the following treatment is the best choice for treating patients with loss of consciousness and ventricular tachycardia initially in the hospital? A Immediate intubation B Oxygen supply C Set intravenous fluid D Cardioversion shock E Intravenous antiarrhythmic drugs