Basic Physiology/ Anatomy Flashcards
Long QT Syndrome Diagnosis
Diagnosis -LQTS (QTc >470 milliseconds in males or >480 milliseconds in females)
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 %.
Mechanism of proarrhythmia slow conduction
- Class 1c agents
- promotes reentry
Mechanism of proarrhythmia prolong repoloarization
Class III drugs
- Triggered early after depolarizations
- Torsades de pointe
Mechanism of proarrhythmia calcium overload
- Digoxin
- Delayed after depolarizations
- Bidirectional VT (increased automaticity)
Delayed afterdepolarization definition
A DAD is an oscillation in membrane voltage that occurs after completion of repolarization of the AP (during phase 4).
These oscillations are caused by a variety of conditions that raise the diastolic intracellular Ca2+ concentration, which cause Ca2+ mediated oscillations that can trigger a new AP if they reach the stimulation threshold.
A critical factor for the development of DADs is the duration of the AP. Longer APs are associated with more Ca2+ overload and facilitate DADs. Therefore, drugs that prolong AP (eg, Class IA antiarrhythmic agents) can occasionally increase DAD amplitude.
Causes of DADs
Toxic concentration of digitalis. This occurs via inhibition of the Na/K pump, which promotes the release of Ca2+ from the sarcoplasmic reticulum. Clinically, digoxin toxic bidirectional fascicular tachycardia is felt to be an example of triggered activity.
Catecholamines (i.e. catecholaminergic polymorphic VT) can cause DADs by causing intracellular Ca2+ overload via an increase in ICa-L and the Na+-Ca2+ exchange current, among other mechanisms.
Ischemia-induced DADs are thought to be mediated by the accumulation of lysophosphoglycerides in the ischemic tissue, with subsequent elevation in Na+ and Ca2+.
Abnormal sarcoplasmic reticulum function (e.g. mutations in ryanodine receptor) can also lead to intracellular Ca2+ overload, facilitating clinical arrhythmias, such as catecholaminergic polymorphic VT.
