Arrhythmias Flashcards
Long QT Syndrome Diagnosis
Diagnosis -LQTS (QTc >470 milliseconds in males or >480 milliseconds in females)
Pro-arrhythmia due to flecanide
Conduction abnormalities — Due to its significant effect on sodium channels, flecainide prolongs depolarization and can slow conduction in the AV node, the His-Purkinje system, and below. These changes can lead to prolongation of the PR interval, increased QRS duration, and first- and second-degree heart block. In addition, profound sinus bradycardia can be induced in patients with preexisting sinus node disease. In contrast, flecainide does not affect repolarization and therefore has little effect on the QT interval.
Proarrhythmia — Flecainide was one of two class IC antiarrhythmic medications included in the CAST trial, which evaluated patients with asymptomatic, non-life-threatening ventricular arrhythmias who were six days to two years after an acute myocardial infarction (MI). Flecainide had an apparent proarrhythmic effect with a significantly increased incidence of mortality plus nonfatal cardiac arrest (6.1 percent versus 2.3 percent in the placebo group).
It has been proposed that the increase in malignant arrhythmias was due to the use of flecainide in the setting of ischemia and/or cardiac structural abnormalities (eg scar from the prior infarction).
Catecholaminergic polymorphic VT Diagnosis
Diagnosis -
The primary diagnostic test and means of making the diagnosis of CPVT is the exercise stress test. Another alternative for patients who are unable to exercise is infusion of epinephrine.
CPVT can also be diagnosed in individuals with appropriate clinical presentation who have a pathogenic mutation. It may be diagnosed in family members of an index case with normal hearts that develop exercise-induced ventricular premature depolarizations (VPDs).
Bidirectional VT Causes
Bidirectional VT has been considered virtually pathognomonic for digitalis intoxication. However, it may also occur in patients with CPVT. Of note, in both cases, the arrhythmia is thought to result from intracellular calcium overload leading to delayed afterdepolarizations (DADs) causing triggered activity.
Brugada Syndrome Diagnosis
Brugada pattern findings on a surface ECG have some form of a pseudo-right bundle branch block and persistent ST segment elevation in leads V1 to V2. The characteristic ECG changes of the Brugada pattern can be transient or variable over time that may be exposed by a sodium channel blocker, such as flecainide, ajmaline, or procainamide.
•In the type 1 Brugada ECG pattern, the elevated ST segment (≥2 mm) descends with an upward convexity to an inverted T wave (figure 1). This is referred to as the “coved type” Brugada pattern.
•In the type 2 Brugada ECG pattern (combined from the original designation of types 2 and 3 patterns), the ST segment has a “saddle back” ST-T wave configuration, in which the elevated ST segment descends toward the baseline, then rises again to an upright or biphasic T wave.
Arrhythmogenic RV Dysplasia
- Diagnosis
- Genetic Screening
- Diagnosis
We recommend CMR imaging in all patients with suspected ARVC
- Genetic Screening
Screening of first-degree relatives over 10 years of age with a history, physical examination,
-ECG, and echocardiogram and/or CMR is recommended every 2 - 5 years depending on their exercise levels
Hypertrophic Obstructive Cardiomyopathy Afib Management
In patients with hypertrophic cardiomyopathy (HCM), the prevalence of atrial fibrillation (AF) appears to be four- to sixfold higher than in similarly aged patients in the general population, with an incidence in the range of 2 percent per year. For patients with HCM and AF, we recommend chronic oral anticoagulation
Myotonic Dystrophy
- Diagnosis
- Management
- Diagnosis
Myotonic dystrophy type 1 (DM1) and myotonic dystrophy type 2 (DM2) are multisystem disorders characterized by skeletal muscle weakness and myotonia, cardiac conduction abnormalities, cataracts, and other abnormalities. The age of onset, presentation, and severity and progression of symptoms vary according to DM phenotype.
- Management
Patients with palpitations, dizziness, syncope, non-sinus rhythm, PR interval >240 msec, QRS duration >120 msec, or second- or third-degree atrioventricular (AV) block should be evaluated at least annually and also considered for invasive electrophysiology study in anticipation of possible pacemaker or implantable cardioverter-defibrillator (ICD) placement. Permanent pacemaker placement is indicated for most patients with second- and third-degree AV block and all patients with symptoms related to the resulting bradycardia.
Indications to anticoagulate in atrial fibrillation
CHA2DS2-VASc Score
Congestive HF 1
Hypertension 1
Age ≥75 years 2
Diabetes mellitus 1
Stroke/TIA/TE 2
Vascular disease (prior MI, PAD, or aortic plaque) 1
Age 65 - 74 years 1
Female sex. 1
Maximum score 9
- Patients with HOCM should be anti-coagulated due to exclusion in CHADSVASC studies.
- Patients with cardiac amyloid should be anti-coagulated since the risk of intracardiac thrombus is very high
RV outflow tract premature ventricular contractions/ VT management
RMVT can be terminated with adenosine and beta blockers which interfere with cAMP-mediated slow inward calcium current.
For prevention Beta blockers are first line. Propranolol is preferred in some studies.
Radiofrequency ablation — There is evidence supporting RF ablation in patients with symptomatic idiopathic VT that is drug-refractory, or in such patients who are intolerant of drugs or do not desire long-term drug therapy
Indication for ICD primary prevention
Primary prevention —
●Patients with a prior MI (at least 40 days ago) and left ventricular ejection fraction (LVEF) ≤30 percent.
●Patients with a cardiomyopathy, New York Heart Association (NYHA) functional class II to III, and LVEF ≤35 %.
- Patients with a nonischemic cardiomyopathy generally require optimal medical therapy for 3 months with persistent LVEF ≤35 %.
Ibutelide uses and contraindications
Class III antiarrhythmic drug, blocks IKr, the rapid component of the cardiac delayed rectifier potassium current. This results in prolonged repolarization, increased action potential duration, and lengthening of the refractory period.
Ibutilide is approved for the acute termination of atrial fibrillation and atrial flutter and is most useful and effective for the pharmacologic cardioversion of atrial fibrillation less than or equal to seven days duration.
Proarrhythmia, particularly nonsustained or sustained polymorphic ventricular tachycardia (VT) (torsades de pointes) or monomorphic VT, is the most important toxicity associated with ibutilide. Because of the risk of VT, particularly torsades de pointes, patients treated with ibutilide should be observed with continuous ECG monitoring for at least four hours after the infusion is finished, or until the QTc interval has returned to baseline.
Long QT Syndrome Management
Our approach to treatment of symptomatic:
•Avoid medications known to prolong the QT interval and the aggressive treatment of electrolyte imbalances
•Most patients should receive an ICD and beta-blocker therapy if the initial presentation was SCA. Importantly, self-limiting syncope/seizures, even if assessed to be LQTS-triggered (ie, secondary to TdP) are not equivalent to SCA.
•For all patients with congenital LQTS and a history of syncope or seizures, we recommend treatment with a beta blocker (Grade 1B). We suggest propranolol or nadolol, given their superior efficacy in this patient population (Grade 2C).
•For patients with recurrent, LQTS-triggered arrhythmic events treatment intensification is pursued with either concomitant drug therapy, left cardiac sympathetic denervation, and/or an ICD
Our approach to treatment of asymptomatic patients:
•we suggest a beta blocker (Grade 2C). However, for asymptomatic patients with a QTc <470 milliseconds, beta-blocker therapy may not be required.
•We suggest either a prophylactic left cardiac sympathetic denervation (LCSD; PJS) or a prophylactic ICD (MJA) in an asymptomatic patient with either LQT2 or LQT3 whose resting QTc is >550 milliseconds (Grade 2C).
For postpubertal women with LQT2, either prophylactic LCSD (PJS) or a prophylactic ICD (MJA) at a lower QTc threshold (QTc >500 milliseconds) is reasonable. Importantly, an ICD is never indicated based solely on a family history of LQTS-associated SCD, as family history is not a personal risk factor for the patient.
Catecholaminergic polymorphic VT Management
- ICD and beta blockers for most patients (Never ICD by itself)
- Avoidance of competitive sports
- Addition of verapamil or flecainide in patients with ongoing ventricular arrhythmias despite initial therapy.
Propranolol is used for acute suppression of recurrent polymorphic VT. For long-term preventive therapy, nadolol (1 to 2 mg/kg) is preferred
Brugada Syndrome Management
•For patients who have survived sudden cardiac arrest or those with a history of syncope which is felt to be due to ventricular tachyarrhythmias, we recommend implantation of an ICD rather than antiarrhythmic drug therapy (Grade 1A).
•In patients who refuse ICD implantation or are not considered a candidate for ICD implantation due to reduced life expectancy or significant comorbidities, we suggest initial therapy with either quinidine or amiodarone (Grade 2C).
•In patients with an ICD who have recurrent arrhythmias resulting in ICD shocks, we suggest catheter ablation of arrhythmogenic substrate in the RVOT and right ventricular free wall. (Grade 2C). Therapy with quinidine or amiodarone is also an option.
