Advanced Diagnosis and Management of Ventricular Arrhythmias

Wide complex tachycardia can be caused by a variety of arrhythmias such as Ventricular Tachycardia, Supraventricular Tachycardia with pre-existing bundle branch block, SVT with aberrancy, WPW (antidromic reciprocating tachycardia), artifacts, and paced rhythms. Atrial flutter, Ventricular Fibrillation, and Sinus Bradycardia are not typically associated with wide complex tachycardia.

When looking at a baseline EKG in SR for a patient with WPW or a preexisting BBB, you would be looking for signs of pre-excitation, which can help differentiate SVT from VT. Prolonged QT interval, narrow QRS complex, ST segment elevation, T wave inversion, atrial fibrillation, and sinus tachycardia are not specific markers for WPW or preexisting BBB related to WCT etiology.

The correct answer provides key EKG characteristics that help differentiate between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) based on various findings such as dissociation, axis, conduction delays, and heart irregularities. The incorrect answers do not accurately reflect the distinguishing features of VT from SVT.

Fusion and capture beats have distinct characteristics as described in the answer. The incorrect answers provided go against the established characteristics of fusion and capture beats.

The correct answer explains that in VT, a NW axis is characterized by the stimulus moving away from lead I and away from lead aVF, suggesting the exit site is in the lateral left ventricle. The incorrect answers provide misinformation about the causes and implications of the NW axis in VT.

SVT with aberrancy and VT can have distinct QRS morphologies that can help differentiate between the two arrhythmias. Typical RBBB patterns and atypical RBBB patterns in specific leads can provide important clues in making the correct diagnosis.

The correct answer highlights that in the setting of WCT with LBBB morphology, the finding of diseased myocardium not conducting efficiently is indicative of VT. The incorrect options provide distractors that do not accurately point towards the likelihood of VT.

In the setting of WCT with LBBB morphology, the presence of a QS or rS complex in lead V6 suggests ventricular tachycardia (VT) rather than supraventricular tachycardia.

Precordial concordance refers to a specific pattern where all the QRS complexes in the precordial leads V1-V6 have the dominant deflection in the same direction. This pattern is important in electrocardiogram interpretation.

In patients with prior MI or heart disease, the likelihood of a wide-complex tachycardia (WCT) being ventricular tachycardia (VT) is high at 95%. This is due to the increased risk of ventricular arrhythmias in individuals with a history of heart conditions.

RVOT VT typically presents with characteristic EKG features such as AV dissociation, LBBB morphology, positivity in II, III, aVF, negativity in I and aVR, absence of notching or slurring, and a negative to positive transition after V3. Inverted T waves in leads V1-V3, prolonged PR interval, and ST-segment elevation in leads II, III, aVF are not consistent with the EKG characteristics of RVOT VT.

ICD therapy is not indicated for RVOT VT as it can potentially worsen the condition by causing inappropriate shocks or increasing the risk of arrhythmias.

Radiofrequency catheter ablation is the preferred treatment for RVOT VT due to its high success rate of over 90% in eliminating the arrhythmia. Pharmacological management is not as effective as ablation, surgical resection is typically reserved for specific cases, and observation without intervention may lead to complications.

PVC-induced cardiomyopathy is a specific condition that can lead to low EF in the setting of RVOT VT when the number of PVCs exceeds 20K/day. The incorrect answers are not directly related to this specific condition and do not explain the observed low EF in the context of RVOT VT.

RVOT VT is typically triggered by exercise and fluctuating catecholamine levels, not caffeine, sodium intake, or lack of sleep.

Patients with RVOT VT typically have normal EKG findings between episodes, with a normal signal averaged ECG. This helps differentiate RVOT VT from conditions like ARVD, where EKG changes may be present even between episodes.

Patients with RVOT VT on exercise stress test may show possible VT without ischemia, not abnormal ECG changes indicating ischemia, decreased exercise capacity, or normal exercise stress test results.

RV biopsy is not commonly used to diagnose RVOT VT because it is usually diagnosed through other methods such as imaging studies and electrophysiology testing.

RVOT VT generally responds well to medications that target intracellular calcium/cAMP levels or alter the electrical properties of the heart. Surgical resection and high-dose corticosteroid therapy are not commonly used for RVOT VT management, and antibiotics would not typically be indicated for this condition.

RVOT VT (Right Ventricular Outflow Tract Ventricular Tachycardia) is best treated with catheter ablation due to its high success rate. Medication therapy, surgical resection, and watchful waiting are not the preferred treatment modalities for RVOT VT.

ARVD, or Arrhythmogenic Right Ventricular Dysplasia, is primarily inherited in an autosomal dominant pattern, meaning that an affected individual has a 50% chance to pass on the mutated gene to each of their offspring.

Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by fibrofatty infiltration of the right ventricle (RV), leading to structural abnormalities in the heart. This infiltration is a hallmark finding in ARVD.

ARVD (Arrhythmogenic Right Ventricular Dysplasia) is more commonly found in the Veneto region of Italy and on the island of Naxos in Greece. It is not associated with Tokyo, Japan; Sydney, Australia; or New York, USA.

The variant of ARVD found in Naxos, Greece is characterized by black wooly hair and palmar/plantar keratoderma.

In Arrhythmogenic Right Ventricular Dysplasia (ARVD), there is abnormality in the desmosomes which are the structures that help cells adhere to each other in tissues.

Arrhythmogenic right ventricular dysplasia (ARVD) is a genetic condition mainly involving mutations in desmosomal genes such as Desmoplakin (DSP), Plaskoglobin (JUP), and Ryanodine (RyR2). Desmin (DES), Titin (TTN), and Lamin A/C (LMNA) are not directly associated with ARVD.

The correct answer highlights specific ECG findings associated with arrhythmogenic right ventricular dysplasia (ARVD), which include epsilon waves, T wave inversions in specific leads, and specific QRS duration differences between V1 and V6 due to RV involvement. The incorrect answers do not align with the characteristic findings of ARVD on ECG.

The correct answer explains how fibrofatty changes in the right ventricle of the heart affect conduction, resulting in the Epsilon wave characteristic of Arrhythmogenic Right Ventricular Dysplasia (ARVD). The incorrect answers provide plausible but inaccurate explanations for the Epsilon wave.