Ventricular tachycardia Notes


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Long QT syndrome and Torsade de pointes

Ventricular tachycardia

NOTES NOTES VENTRICULAR TACHYCARDIA GENERALLY, WHAT IS IT? PATHOLOGY & CAUSES ▪ Depolarization wavefronts originate in ventricles → ventricles pump > 100 beats per minute ↓ stroke volume ▪ Premature ventricular contractions (PVCs): single instance of ventricle contracting prematurely ▫ ≥ three PVCs consecutively defined as ventricular tachycardia (VT) COMPLICATIONS ▪ Sustained VT may result in sudden cardiac death due to insufficient blood perfusion/ rapid ventricular fibrillation SIGNS & SYMPTOMS ▪ Chest pain, syncope, dizziness, shortness of breath, palpitations DIAGNOSIS TYPES Monomorphic VT ▪ Ventricular contractions have typical, uniform shape ▪ Typical for reentrant circuits ▫ Depolarizations begin from same spot, for focal VT because one area of cells in ventricle is responsible ▫ Often caused by reentry around scar in ventricular wall; e.g. from previous myocardial infarction (MI) Polymorphic VT ▪ > One QRS complex morphology type ▫ Includes Torsades de pointes ▪ Shape of contractions from each beat changes as signal begins in different areas of ventricle ▪ May occur when pacemaker cells stressed, increasing automaticity rates, including from severe hypoxia RISK FACTORS ▪ Ventricular muscle ischemia, structural heart disease, coronary artery disease (CAD), electrolyte abnormalities LAB RESULTS ▪ Serum electrolytes ▪ Toxicology studies (therapeutic/recreational drug use) ▫ E.g. digoxin, tricyclic antidepressants, methamphetamine, cocaine OTHER DIAGNOSTICS ECG ▪ Determines cardiac rhythm TREATMENT MEDICATIONS ▪ Pharmacotherapy ▫ Depending on cause SURGERY ▪ Implanted devices OTHER INTERVENTIONS ▪ Cardioversion, pacing ▪ Correct underlying cause OSMOSIS.ORG 185
Figure 27.1 Illustration depicting ECG of monomorphic ventricular tachycardia. Figure 27.2 Illustration depicting focal ventrical tachycardia. 186 OSMOSIS.ORG
Chapter 27 Ventricular Tachycardia LONG QT SYNDROME (LQTS) PATHOLOGY & CAUSES ▪ Cardiac rhythm disorder characterized by prolonged ventricular repolarization ▪ Characterized by abnormally long QT interval ▫ QT interval: total time from ventricular depolarization (QRS complex) to complete repolarization (T wave); measured from beginning of QRS to end of T wave ▫ QTc (corrected) accounts for changes in heart rate: QTc = QT interval ÷ √RR interval (in sec); AKA Bazett formula ▫ Adult normal = 420 ± 20 msec ▪ Results in ↑ risk of polymorphic ventricular arrhythmias (TdP), which can deteriorate into ventricular fibrillation TYPES Inherited ▪ Caused by mutations in genes associated with cardiac potassium, sodium channels ▪ Triggered by exertion, emotional events, stress, postpartum events, noise ▪ ≥ 13 types identified; associated with mutations in genes encoding myocyte ion channels ▪ KCNQ1, KCNH2, KCNE1, KCNE2 affect potassium channels → ↓ outward potassium current ▪ SCN5A affects sodium channels → ↑ inward sodium current ▫ Two distinct LQT phenotypes due to mutant alleles in same locus: ▫ Romano–Ward syndrome: autosomal dominant; LQTS without hearing loss ▫ Jervell and Lange–Nielsen syndrome: autosomal recessive; LQTS with congenital sensorineural hearing loss Acquired ▪ Usually caused by certain drugs (e.g. antiinfectives, psychotropics, antiarrhythmics, antineoplastics, bronchodilators, gastric motility agents) ▫ Common mechanism involves blockage of rapidly activating potassium channels (IKr) current in potassium channel encoded by KCNH2 gene RISK FACTORS ▪ Electrolyte imbalances (e.g. hypokalemia, hypomagnesemia, hypocalcemia) ▪ Underlying heart disease (e.g. HF, hypertrophic left ventricle, history of myocardial infarction) ▪ Bradyarrhythmias ▪ Biological females > biological males ▪ ↑ age ▪ Inherited genetic mutation ▪ Postpartum period ▫ Related to physiologic stress, altered sleep patterns ▪ Anorexia nervosa COMPLICATIONS ▪ Malignant arrhythmias (TdP, VF), syncope, seizures, sudden death SIGNS & SYMPTOMS ▪ Palpitations, lightheadedness, hypotension DIAGNOSIS LAB RESULTS ▪ Serum electrolytes ▫ Hypokalemia, hypomagnesemia, hypocalcemia may be present OSMOSIS.ORG 187
OTHER DIAGNOSTICS SURGERY 12-lead ECG ▪ Prolonged QTc (> 470msec in males, > 480msec in females); presence of tachyarrhythmias (TdP); altered T-wave morphology Congenital LQTS ▪ Left cervicothoracic sympathectomy (LCTS), left cardiac sympathetic denervation; implantable cardioverter-defibrillator (ICD); pacemaker Bicycle/treadmill stress test ▪ Presence of exercise-associated arrhythmias Acquired LQTS ▪ Pacemaker → if bradycardia triggers arrhythmia Catecholamine drug testing ▪ Differentiates etiology ▫ Provocative testing with catecholamine; e.g. epinephrine ▫ Measure effect on QT interval Clinical/family history, physical examination ▪ With compatible findings Genetic testing Schwartz score ▪ Diagnosis of congenital LQTS by scoring QTc, clinical factors, individual history ▪ Scoring: probability of congenital LQTS ▫ ≤ 1: low ▫ 1.5–3: intermediate ▫ ≥ 3.5: high TREATMENT MEDICATIONS Congenital LQTS ▪ Beta-blockers: blunt adrenergic response ▪ Mexiletine: for sodium-channel mutations ▪ Flecainide: if SCN5A mutation Acquired LQTS ▪ Magnesium sulfate: treatment, prevention of recurrence of long QT-related ventricular ectopic beats ▪ Isoproterenol: increase sinus rate, decrease QT interval ▪ Lidocaine/phenytoin: shorten duration of the action potential 188 OSMOSIS.ORG OTHER INTERVENTIONS Acquired LQTS ▪ Address underlying cause; e.g. correct electrolyte abnormalities, discontinue offending drug; temporary transvenous overdrive pacing, electrical cardioversion/ defibrillation Lifestyle modifications ▪ Avoidance of triggering drugs, avoidance adrenergic stimuli; e.g. strenuous exercise, emotional stress
Chapter 27 Ventricular Tachycardia Figure 27.3 ECG trace demonstrating long-QT syndrome. OSMOSIS.ORG 189
Figure 27.4 ECG trace demonstrating long-QT syndrome. TORSADES DES POINTES (TdP) PATHOLOGY & CAUSES ▪ Literally means “twisting of the points” ▪ The peaks of QRS complex “twist” around isoelectric line on electrocardiogram ▪ Lengthening QT interval → early afterdepolarizations (EADs) → premature ventricular depolarizations → polymorphic VT (TdP) ▫ May resolve spontaneously ▫ Transmural reentry/abnormal automaticity may perpetuate TdP ▫ May degenerate into ventricular fibrillation RISK FACTORS ▪ ▪ ▪ ▪ ▪ LQTS, drugs associated with LQTS Bradycardia Electrolyte imbalance Biologically female Anorexia nervosa COMPLICATIONS ▪ Ventricular fibrillation, seizures, sudden cardiac death 190 OSMOSIS.ORG MNEMONIC: TO4SADE Drugs that may induce QT prolongation Thiazides O4 - Oanzapine, Opioids, Quinidine, Quinolones Sotalol/SSRIs Antihistamines/antipsychotics AntiDepressants like TCAs Erythromycin (Macrolide antibiotics SIGNS & SYMPTOMS ▪ Palpitations, lightheadedness, syncope DIAGNOSIS LAB RESULTS ▪ Serum electrolytes ▫ Hypokalemia, hypomagnesemia, hypocalcemia may be present
Chapter 27 Ventricular Tachycardia OTHER DIAGNOSTICS ▪ 12-lead ECG ▫ Ventricular rate: 150–300 beats per minute ▫ RR interval: irregular ▫ P wave, PR interval: absent ▫ QRS duration: > 0.12 seconds; changes amplitude, shape, direction TREATMENT SURGERY ▪ Left cardio-thoracic sympathectomy OTHER INTERVENTIONS ▪ Treat underlying cause; e.g. correct electrolyte abnormalities, discontinue offending drug ▪ Temporary pacing, permanent dual chamber pacemaker, implantable cardioverter-defibrillator (ICD) MEDICATIONS ▪ For acquired LQTS/other causes of TdP ▫ Magnesium sulfate, isoproterenol, lidocaine, phenytoin ▪ For congenital LQTS ▫ Beta-blockers, mexiletine Figure 27.5 ECG demonstrating torsades de pointes. OSMOSIS.ORG 191
VENTRICULAR TACHYCARDIA PATHOLOGY & CAUSES ▪ Ventricular arrhythmia originating in ectopic ventricular pacemaker, resulting in ≥ three premature ventricular complexes (PVCs) occurring at ≥ 100 beats/min ▪ Dysrhythmia may be sustained (> 30 seconds)/nonsustained (< 30 seconds)/ paroxysmal ▪ Abnormally fast ventricular contractions → ↓ ability for ventricles to fill → ↓ cardiac output → ↓ perfusion → impaired hemodynamics TYPES Non-reentrant/focal ventricular tachycardia ▪ Triggered by abnormal automaticity of specific area of ventricle ▫ Ventricular pacemaker cells fire at high rate, preventing pacemaker cells in SA node from firing → heart rate driven by ventricular pacemakers ▫ May be caused by certain medications, illicit drugs (e.g. methamphetamine, cocaine), electrolyte imbalances, myocardial ischemia in ventricles Reentrant ventricular tachycardia ▪ More common than focal VT ▪ Reentry: perpetual electrical signal that occurs due to changes in refractory period length, rate of signal conduction ▫ Cardiomyocytes can be altered when stressed/irritated by external stimuli; e.g. medications/illicit drugs: change conduction speed, refractory period ▫ Dead cells in myocardial tissue create scar tissue → conduction signals go around scar → perpetual signal, AKA reentry 192 OSMOSIS.ORG RISK FACTORS ▪ ↑ age ▪ Cardiac disease ▫ Post-MI, cardiomyopathy, valve disease, HF ▪ Electrolyte imbalance ▪ Cardiac ion channelopathies resulting in long QT syndromes ▪ Infiltrative disease; e.g. amyloidosis ▪ Pericardial inflammation ▪ Blunt chest trauma ▪ Drugs; e.g. cocaine COMPLICATIONS ▪ Cardiac ischemia, infarction ▪ May degenerate into ventricular fibrillation ▪ Sudden cardiac death SIGNS & SYMPTOMS ▪ ▪ ▪ ▪ ▪ ▪ Chest pain Shortness of breath Dizziness Syncope Pallor Blood pressure: normal/↓ DIAGNOSIS LAB RESULTS ▪ Serum electrolytes ▫ Hypokalemia, hypomagnesemia, hypocalcemia may be present OTHER DIAGNOSTICS ECG ▪ Rate: >100 beats per minute, irregular ▪ P waves: may be absent ▫ If present, atrioventricular dissociation common (hallmark of VT)
Chapter 27 Ventricular Tachycardia ▫ May be positive/upright or negative/ inverted in Lead II ▪ PR interval: none ▪ QRS complex: wide ( > 0.12 seconds); ≥ 3 consecutive; distorted shape: may be monomorphic/polymorphic ▪ T-waves: large; polarity may be opposite of major QRS deflection; may be difficult to distinguish TREATMENT MEDICATIONS ▪ Chronic prevention ▫ Beta blockers, amiodarone, nondihydropyridine calcium channel blockers OTHER INTERVENTIONS ▪ Acute treatment ▫ Cardioversion ▪ Drug cardioversion ▫ Procainamide, lidocaine, amiodarone frequently used ▪ Electrical cardioversion ▫ Primary treatment for VT associated with hemodynamic instability/when drug cardioversion not immediately available ▪ Radiofrequency catheter ablation ▪ ICD OSMOSIS.ORG 193

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