See also: [[Long QT]], [[Ventricular Tachycardia]] See [goldfrank QT interval](x-devonthink-item://2F041FBD-FF1C-4E21-9CD5-5550C288F006?page=277&istart=7959&ilength=10&search=QT%2520Interval), [Dunn - Ventricular arrhythmias](x-devonthink-item://747079B5-0629-433D-A6A2-5282259F31B6) > [!pearl] definitions > **Polymorphic ventricular tachycardia (PVT)** is a form of [[Ventricular Tachycardia]] in which there are multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration. The most common cause of PVT is myocardial ischaemia/infarction. > > **Torsades de pointes (TdP)** is a specific form of PVT occurring in the context of [[Long QT|QT prolongation]] — it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line. The tachycardia is often nonsustained and self-terminating, but it may recur frequently and may require preventive therapy and correction or removal of any precipitating factor # Treatment > [!treatment] > - [[Cardioversion|DCCV]] if unstable 200j (may not be able to synchronise) > - IV [[Magnesium]] 2 - 2.47g (8-10 mmol) > - Isoprotenerol infusion overdrive pace (starting at 5mcg/min max 15mcg/min) target HR 100 -120 > - or external overdrive pacing > - or atropine > - ==Do **not** give class Ia or Ic antiarrhythmics or amiodarone!== can worsen condition (lignocaine may be ok b/c it shortens QT interval) # Causes > Drug (selected) causes of long QT mnemonic: **QT CODASS** - cipro, ondansetron, droperidol, amiodarone, sertraline, sotalol - Antiarrhythmics - Class ia (quinidine, disopyramide, procainamide) - Class iii (sotalol, ibutilide, dofetilide, dronedarone) - Antibiotics - (erythromycin, azithromycin, ciprofloxacin, clarithromycin, levofloxacin, trimethoprim-sulfa ) - Antihistamines (terfenadine, astemizole) Antianginals (bepridil) - Antimalarials (halofantrine, chloroquine) Antifungals (ketoconazole) - Antilipemics (probucol) - Tricyclic antidepressants (amitriptyline, imipramine, nortriptyline) - neuroleptics (haloperidol, chlorpromazine, risperidone, thioridazine) narcotics (methadone) - stimulants (cocaine) - Gastrointestinal stimulants (cisapride) - Hypocholesterolemics (probucol) - Electrolyte abnormalities - [[hypokalemia]] -- but more ↓ Mg - [[Hypomagnesemia]] - [[Hypocalcemia|hypocalcaemia]] — much less common torsades than with ↓ Mg and ↓ K - ion channel defects (congenital long QT syndrome) Bradycardia ***Causes:*** - Drug-induced—class IA and IC antidysrhythmics; many phenothiazines and butyrophenones (notably haloperidol and droperidol), cyclic antidepressants, antibiotics (especially macrolides), organophosphates, antihistamines, anti-fungals, antiseizure and antiemetic agents - Electrolyte abnormalities—hypokalemia, hypomagnesemia, hypocalcemia (rarely) - Diet-related—starvation, low protein - Severe bradycardia or atrioventricular block - Hypothyroidism - Contrast injection - Cerebrovascular accident (especially intraparenchymal) - Myocardial ischemia # Deep Dive ## Physiology of drug-induced QT prolongation and TdP > [!tldr] > Prolonged action potentials lead to early afterdeoplarisations (EADs) which in turn can cause polymorphic VT/torsades. Prolonged action potential is manifest on ECG by *prolonged QT interval* see: [Braunwald - electrophysiology of arrhythmias](x-devonthink-item://A45FDA08-6B2C-446C-8756-C67F9F1A45BD?page=8), [Mechanisms of drug-induced QT prolongation and Torsades de pointes](https://pmc.ncbi.nlm.nih.gov/articles/PMC1767957/) - Repolarisation of cardiac myocytes is driven by outward movement of K+ ions through rapid and slow channels. Block of either of these outward K+ currents can *prolong the action potential*. - rapid channels are the most susceptible to drugs - blockage of rapid K+ channels during myocardial repolarisation *prolongs the QT interval* and results in other T or U wave abnormalities on the ECG - the prolongation of repolarisation may result in activation of an inward depolarisation current known as **early after-depolarisation** (i.e. cell membrane becomes less-negative again), which can lead to a phenomenon called **triggered activity** - Triggered activity is impulse initiation in cardiac fibres caused by after-depolarisations - Any factor that shifts the net current of cations inward during repolarisation can lead to early afterdepolarisations and arrhythmias - decreased outward (repolarising) currents of K+ - increased inward (depolarising) currents of Na or Ca - After opening, most Na+ channels qwuickly inactivate to prevent further depolarisation - However, in pathology eg type 3 long-QT syndrome, heart failure, cardiomyopathy, ischemia, drugs, Na+ channel inactivation may be either *delayed* or reversed, allowing channel reopenings before repolarisation of the action pptential, resulting in smal residual inward Na channel (called late INa) → promotes early afterdeploarisations - Under certain conditions, when an EAD is large enough, the decrease in membrane potential leads to an increase in net inward (depolarising) current and a **second action potential is triggered** before complete repolarisation of the first - EADs can make tissue vulnerable to re-entry and result in reentrant arrhythmias, multiple shifting foci, and a mixture of multipel shifting foci and re-entry - **action potential prolongation** is a fundamental phenomenon that underlies development of EADs, which is ==manifest by prolonged QT prolongation on ECG== - heart failure, long QT syndrome, [[hypokalemia|hypo-k]], [[Hypomagnesemia|hypo-mg]], acidosis, [[Bradycardia]], catecholamines, and drugs that block K+ channels can also prolong action potential and lead to early after-deoplarisations A- phase 2 early afterdepolarisations (EADs) B- phase 3 EADs, C - delayed afterdepolarisations. ![[Pasted image 20250327155108.png]] ### Drugs that prolong QT - Class IA and III [[Anti-arrhythmic drugs|Antiarrhythmic]] agents prolong the action potential duration and QT interval - other non-cardiac drugs: phenothiazines, some antihistamiens, some abx can also prolong action potential and predispose ot EAD-mediated triggered arrhythmias, *particularly when there is hypokalemia or bradycardia* - decreased extracellular K paradoxically decreases some membrane K current, especially in ventricle - this explains why hypokalemia causes action potential prolongation and EADs - **EADs are opposed** by ATP-dependent K channel openers (pinacidil, nicorandil, some other drugs I've never heard of), ==magnesium==, antiarrhythmics that shorten AP (lidocaine and mexiletine) - alpha adrenergic stimulation can **exaerbation** EADs ### Why bradycardia is bad - amplitude of an of an EAD is augmented at slow rates when action potentials are longer in duration - [[Transcutaneous pacing|pacing]]-induced increases in rate **shorten the action potential duration** and reduce EAD amplitude - likely result of augmenting delayed rectivier K currents and possibly hastening Ca=induced inactivation of calcium channels - ∴ EADs are more likely to trigger arrhythmia when HR is slow because bradycardia is associated with prolongation of the QT interval and AP duration - similarly, catecholamiens increase HR and decrease action potential duration and EAD amplitude, depsite the effect of beta-adrenergic stimulation to increase L-type calcium currents ### Why does magnesium help treat TdP? - maybe to suppress triggered activity - doesn't do anything for sustained monoprophic VT ### What about non-prolonged QT polymorephic VT? ==This is a totally different thing!== **Magnesium probably doesn't work** # Related Questions ## bradycardia - [ ] 3Q: [ECG in Syncope](x-devonthink-item://40F10AFA-5F29-4EE4-B149-300627B498B0?page=14) -- [Answer](x-devonthink-item://2088AEED-9FCF-4CF0-B58D-E4279D4BCC76?page=36) -- [prop](x-devonthink-item://5F365535-E019-4C8D-8402-2E764B328988?page=7) ## long qt - [ ] 5Q: [Syncope](x-devonthink-item://4134DDB3-6E12-474A-9F6F-64135C0C6048?page=34) -- [Answer](x-devonthink-item://AC92B5F1-8EE6-461A-B03E-F70AE7DC1275?page=34) -- [prop](x-devonthink-item://68EA6F60-334D-4A94-8327-78286C5F1AED?page=8) - [ ] 6Q: [Syncope, abnormal ECG](x-devonthink-item://2F267333-5FEC-47E5-83D1-CC05B23EB91A?page=1) -- [Answer](x-devonthink-item://C6CAC39D-CAE8-4F76-9C45-689A0464D936?page=0) -- [prop](x-devonthink-item://C5EFC1EA-802B-49BC-824D-CFF7C6FFDBD8?page=2) - [ ] 7Q: [Syncope with Abnormal ECG](x-devonthink-item://7061D1B4-0AB9-4963-B3B0-23BDD975B2CD?page=20) -- [Answer](x-devonthink-item://3F30C77E-E23E-4200-89FE-48A41618E0C2?page=13) ## qt prolongation - [ ] 10Q: [Syncope](x-devonthink-item://9C485EF0-3985-4EBA-B9DC-9CDF8A6E2F45?page=7) -- [Answer](x-devonthink-item://A0D348CE-FCD4-4ECD-BE21-6CA73F6DE8CD?page=11) - [ ] 11Q: [Large Citalopram Overdose](x-devonthink-item://834C484F-DDAA-4819-8DF0-84AE5E70DA1D?page=36) -- [Answer](x-devonthink-item://D46998FE-62E2-4A3A-860D-C32C94B86E42?page=17) -- [prop](x-devonthink-item://834C484F-DDAA-4819-8DF0-84AE5E70DA1D?page=77) ## torsades - [x] DUPLICATE Q: [Syncope](x-devonthink-item://9C485EF0-3985-4EBA-B9DC-9CDF8A6E2F45?page=7) -- [Answer](x-devonthink-item://A0D348CE-FCD4-4ECD-BE21-6CA73F6DE8CD?page=11) ## torsades de pointes - [ ] 23Q: [Dizziness and Abnormal ECG](x-devonthink-item://27CD16C2-557A-4CB1-B3CF-D01330708170?page=13) -- [Answer](x-devonthink-item://00427DF6-6D28-4FEB-A0CA-DF96DBBBCE97?page=17) -- [prop](x-devonthink-item://AB9BDA6D-9CA8-4E73-9D15-B6105225A1B4?page=8) - [x] 24Q: [Collapse with Abnormal Rhythm Strip](x-devonthink-item://73409C77-B2FA-4E0A-AEB3-5EB284457F0C?page=46) -- [Answer](x-devonthink-item://5A848952-80E3-4184-B553-368412A69917?page=31) -- [prop](x-devonthink-item://2A1F4A99-92AE-4C8E-B325-AE448BD46AC6?page=10) - [ ] 25Q: [ECG for Lightheadedness](x-devonthink-item://CDB16617-3785-40E5-B8BE-5668D2D7A3E7?page=6) -- [Answer](x-devonthink-item://A6CA01E8-9551-45E7-8617-441BE3DBB5D7?page=5) -- [prop](x-devonthink-item://B892F073-9AD2-46E4-98D6-B0574CAA73A3?page=8) ## ventricular tachycardia - [x] 26Q: [VT](x-devonthink-item://2CB6E202-E7C1-46E8-B49F-435AB6C937F0?page=16) -- [Answer](x-devonthink-item://78503782-404C-41A2-A3AE-B1A26F578DF5?page=19) -- [prop](x-devonthink-item://51B63B5B-D684-4BF3-8B62-95FCA5EF7503?page=7) - [ ] 27Q: [Arrhythmia](x-devonthink-item://5DC0999B-D537-4002-86AF-FD7B54B45E2E?page=1) -- [Answer](x-devonthink-item://406AF611-5CD4-4B3B-9795-327E8F4E3626?page=0) - [ ] 28Q: [Ventricular Tachycardia](x-devonthink-item://834C484F-DDAA-4819-8DF0-84AE5E70DA1D?page=53) -- [Answer](x-devonthink-item://D46998FE-62E2-4A3A-860D-C32C94B86E42?page=23) - [x] DUPLICATE Q: [Abnormal ECG](x-devonthink-item://FE3157C2-07B3-43F2-9ECE-AFACE1355E13?page=26) -- [Answer](x-devonthink-item://DDC959EB-0C1E-448A-8380-C397BF734322?page=12) - [ ] 29Q: [Broad Complex Tachycardia](x-devonthink-item://A8F2D7A0-9A26-4012-AF42-19D640D674B4?page=18) -- [Answer](x-devonthink-item://A10DE51E-92FA-42D1-8AA0-7AE68C2FA743?page=9) -- [prop](x-devonthink-item://B864660E-6598-4555-ACA9-B87F41ED4C3A?page=5) - [x] 30Q: [Arrhythmia and Chest Pain](x-devonthink-item://09CFA1A7-00F1-4151-979E-8F3984924D54?page=17) -- [Answer](x-devonthink-item://CF5E9C2B-42F9-4F9C-AC29-877E20134927?page=11) - [ ] 31Q: [Ventricular Tachycardia](x-devonthink-item://7E9EF652-F67B-42C5-A536-2EE85BA1954F?page=12) -- [Answer](x-devonthink-item://2DE5FACA-6D8F-41A2-8EAA-8DFE1E76FA61?page=7)