Arrhythmia Flashcards

Question

What is AVNRT ?

Answer 1

Atrioventricular Nodal Reentrant Tachycardia Most Common SVT (60%) and is due to re-entrant circuit within or near the AV node -Mechanism: Dual AV nodal pathways (fast & slow) -Typical: Slow pathway conduction, fast pathway retrograde -Symptoms: Sudden palpitations, can terminate abruptly -Trigger: Often Premature Atrial Contraction | slow and fast pathways

Answer 2

Trigger: Often Premature Atrial Contraction caused by ectopic beat

Answer 3

AVNRT -Rate: 140-250 bpm, very regular -QRS: Narrow (normal conduction down ventricles) -P wave: Often buried in QRS or just after it (retrograde) -Characteristic: RP' interval very short (P at or after QRS) | Look at II, III aVF and V1

Answer 4

-Acute termination: Vagal manoeuvres (Valsalva), adenosine IV -Chronic: Beta-blockers, CCBs, antiarrhythmics if frequent -Definitive: Slow pathway ablation (cure rate >95%) -Excellent prognosis, benign condition

Answer 5

Atrioventricular Reciprocating Tachycardia; Re-entrant circuit uses accessory pathway + AV node -Mechanism: Extra connection between atrium and ventricle -Orthodromic: Down AV node, back up accessory pathway (90% cases) -Antidromic: Down accessory pathway, back up AV node (wide QRS) -Association: Wolff-Parkinson-White (WPW) syndrome | Two connections between atria and ventricles; acceory quicker

Answer 6

Congenital accessory pathway causing preexcitation -ECG finding: Short PR interval + delta wave (slurred QRS onset) -Danger: AF with rapid conduction risk = VF -Management: Avoid AV node blockers in AF (use IV flecainide) -Definitive: Accessory pathway ablation | Preexitation; part of ventricle goes before rest ## Footnote Called ‘WPW Pattern’ rather ‘WPW Syndrome’ if asymptomatic

Answer 7

Wolff-Parkinson-White -ECG finding: Short PR interval + delta wave (slurred QRS onset) | delta looks like triangle going up

Answer 8

Abnormal atrial focus firing faster than SA node -Mechanism: Enhanced automaticity or re-entry -Rate: 100-250 bpm -ECG: P wave morphology different from sinus P waves -Often: Associated with underlying heart disease

Answer 9

Atrial Tachycardia -P wave morphology different from sinus P waves

Answer 10

Macro re-entrant circuit in the atrium, usually around the cavo-tricuspid isthmus -Rate: Atrial rate 250-350 bpm (usually ~300) -Ventricular rate: Depends on AV block(usually 2:1 = ~150 bpm) -ECG: Characteristic "sawtooth" or "flutter waves" -Regular rhythm (if fixed AV block so coduction ratio is fixed) ## Footnote Cavo-tricuspid isthmus = fibrous band in lower right atrium, between (IVC and tricuspid valve

Answer 11

Atrial flutter -ECG: Characteristic "sawtooth" or "flutter waves"

Answer 12

Three or more consecutive ventricular beats at rate >120 bpm -ECG: Wide QRS (≥120ms), AV dissociation often present -Clinical: Can cause syncope, haemodynamic collapse, death -Can be mono or polymorphic | Broad, regular QRS

Answer 13

Monomorphic: Same QRS morphology (usually from scar) Polymorphic: Changing QRS morphology (e.g. Torsades)

Answer 14

VT -Wide QRS (≥120ms), AV dissociation often present -Broad, regular

Answer 15

Polymorphic VT with long QT interval -Causes: Long QT (congenital or acquired) -Triggers: Hypokalaemia, hypomagnesaemia, drugs, bradycardia -Management: IV magnesium, correct electrolytes, pacing -Avoid QT-prolonging drugs | Twisting of Points

Answer 16

TdP Polymorphic VT long QT interval

Answer 17

Chaotic, uncoordinated ventricular activity -ECG: Disorganised, irregular baseline ("coarse" or "fine") -Clinical: Loss of pulse, unconsciousness, cardiac arrest -Management: Immediate defibrillation (CPR + shock)

Answer 18

Holter Monitor or R-test -24-48 hours, continuous Event or Patch Recorder -Weeks to months, activated by patient

Answer 19

Invasive cardiac catheter study to diagnose and treat arrhythmias -Multi-electrode catheters map electrical activity -Programmable stimulation induces arrhythmias -Allows precise localisation of arrhythmia origin -Ablation performed during same procedure | Like a really up close and personal ECG

Answer 20

Class I: Sodium channel blockers (sub-divided by degree of blockade) Ia – e.g., Quinidine, Ajmaline, Procainamide Ib – e.g., Lignocaine, Mexiletine Ic – e.g., Flecainide, Propafenone Class II: Beta-blockers (e.g., Bisoprolol, Metoprolol, Atenolol) Class III: Potassium channel blockers (e.g., Amiodarone, Dronaderone, Sotalol) Class IV: Calcium channel blockers (e.g., Verapamil, Diltiazem) (Class V: Miscellaneous – e.g., Digoxin, Adenosine) | Sotalol does some class II as well ## Footnote Class I all slow the electrical conduction velocity in the heart

Answer 21

Symptomatic bradycardia unresponsive to drugs 2nd degree Mobitz II 3rd degree heart block Sinus node dysfunction with symptoms Atrial fibrillation with tachy/brady

Answer 22

Implantable cardioverter-defibrillators; Detect and treat dangerous ventricular arrhythmias -Pacemaker + defibrillator capability -Indicated for: Recurrent VT/VF, cardiomyopathy with low EF (poor contractibility) -Can deliver antitachycardia pacing or shock -CRT-D adds resynchronisation therapy | SICDs are subcutaneous

Answer 23

Destroys arrhythmia source by applying energy -Performed during EP study using catheters -AVNRT ablation: >95% success, very low complication rate -AF ablation: ~70% success, depends on AF type -Definitive treatment (no ongoing medication)

Answer 24

Radiofrequency: Original standard, point-by-point ablation (may or may not need a genreral) Cryoballoon: Single-shot, faster, less operator dependent Pulsed Field: NEW, nonthermal, safer profile (avoids oesophageal/phrenic injury) (needs a genreral)(give them hiccups to make sure phrenic ok) | Transeptal puncture or PFO used to get from RA to pulm vein in LA (Afib

Answer 25

AF -Absent P waves: Replaced by baseline undulation ("fibrillation waves") -Irregular ventricular rate: Chaotic AV node conduction -Narrow QRS: Normal ventricular conduction (unless BBB present, then is broad) -Baseline may appear fine or coarse

Answer 26

Chaotic, disorganised atrial electrical activity -Most common arrhythmia - affects >1 million people in UK -Prevalence increases with age 0.1% age 40s → 9% age 80s and male majority -Major cause of stroke (5x increased risk) -Haemodynamically significant (loss of atrial contraction) | Anticoagulation is critical for AF (stroke prevention)

Answer 27

Classification by Duration -Paroxysmal: Self-terminating (<7 days) -Persistent: Lasts >7 days, requires intervention -Long-standing persistent: >1 year -Permanent: Accepted as patient lifestyle

Answer 28

Cardiac: Hypertension, HF, IHD, valvular disease, cardiomyopathy Non-cardiac: Hyperthyroidism, COPD, sleep apnoea, obesity Triggers: Alcohol, (caffeine), stress, infection Lone AF: No structural disease (10-15% cases) | Check thyroid func, alcohol also big cause ## Footnote Mitral stenosis/regurg is big here as causes atrial dialtiom and overfilling

Answer 29

Two main mechanisms: -Focal mechanism: Ectopic beats from pulmonary veins (more common in younger patients) -Re-entrant mechanism: Multiple re-entry circuits in atria Often both mechanisms coexist

Answer 30

Absent P waves: Replaced by baseline undulation ("fibrillation waves") Irregular ventricular rate: Chaotic AV node conduction Narrow QRS: Normal ventricular conduction (unless BBB present; broad, irregular) Baseline may appear fine or coarse | Irregularly irregular

Answer 31

Common: Palpitation symptoms, dyspnoea, fatigue Severe: Chest pain, syncope, heart failure symptoms Incidental: Found on routine ECG or during monitoring, sometimes after stroke Very variable symptoms! | Fibrilations/tachycardias + coronary artery disease = ischaemic heart pa

Answer 32

CHA2DS2-VA ≥1: Anticoagulation recommended -DOACs: First-line (apixaban, dabigatran, edoxaban, rivaroxaban) -Warfarin: Alternative if DOAC contraindicated -Aspirin: Not recommended (insufficient for AF stroke prevention) | Anticoagulation is critical for AF (stroke prevention) ## Footnote Only warfain works if metal valves; cant use doac

Answer 33

Rate Control: Accept AF, slow ventricular rate to ≤110 bpm -Preferred for older patients with comorbidities Rhythm Control: Restore normal sinus rhythm -Often required for younger, symptomatic patients (younger peeps tend to be symptomatic more) | Studies show similar outcomes ## Footnote Rate control reasonable if patient asymptomatic or like didn’t even know they ahd it cause theyre chill

Answer 34

First-line: Beta-blockers (bisoprolol, atenolol) Second-line: Calcium channel blockers (diltiazem, verapamil) Adjunctive: Digoxin (especially if HF) Target: Ventricular rate <110 bpm at rest and on exertion | Rate limiting

Answer 35

Flecainide/Propafenone: -Class Ic, if structurally normal heart Sotalol: -Class III, needs QT monitoring Amiodarone: -Most effective but toxicity concerns Dronaderone: -Less effective than amiodarone but less toxicity (Ic) Often combined with AV nodal blocker Pill in the pocket option

Answer 36

Symptomatic AF refractory to drugs; drugs arent working Young patients seeking definitive treatment First-line option in paroxysmal AF (alternative to drugs) Failing rate/rhythm control despite drugs

Answer 37

Pulmonary Vein Isolation (PVI) Standard anatomic AF ablation technique -Isolates pulmonary veins (ectopic focus source) -Success: 70-80% paroxysmal AF, lower for persistent -May require additional atrial ablation for persistent AF

Answer 38

Synchronized electrical shock under sedation -Immediately restores sinus rhythm -Indications: Haemodynamic instability, failed drug conversion -Must anticoagulate first (unless <48 hrs symptom onset) -Risk of recurrence without antiarrhythmic drugs used to treat Afib | Defibrilation

Answer 39

Second most common arrhythmia after AF (flutter = organised, Afib = unorganised) -Often coexists with AF, similar risk factors (e.g., age, hypertension, infection) -Can degenerate to AF -Similar stroke risk and anticoagulation needs as AF -fixed rate (unlike Afib) | Narrow, regular QRS

Answer 40

Typical (cavo-tricuspid isthmus [CTI] dependent): 90% cases, reentry around tricuspid valve Atypical: Various locations in atria, rarer – more common after previous LA ablation | CTI = fibrous tissue in right atrium, between IVC and tricuspid valve

Answer 41

Flutter waves: Regular "sawtooth" pattern in baseline Atrial rate: ~300 bpm (range 250-350) Ventricular rate: Depends on AV conduction ratio 2:1 AV block most common: Results in ventricular rate ~150 bpm Regular ventricular rhythm (fixed conduction)

Answer 42

Atrial flutter -Flutter waves: Regular "sawtooth" pattern in baseline -Atrial rate: ~300 bpm (range 250-350) -Ventricular rate: Depends on AV conduction ratio -2:1 AV block most common: Results in ventricular rate ~150 bpm -Regular ventricular rhythm (fixed conduction) | check v1?

Answer 43

Often more symptomatic than AF (fixed, fast rate) Palpitation symptoms, dyspnoea, chest discomfort common Can precipitate heart failure if untreated (more common if asymptomatic) Risk of stroke similar to AF

Answer 44

Challenge: Flutter re-entrant circuit = regular rate; no chaos for us to target; cant meaningfully slow atrial rhythm -Rate control drugs less effective than AF -Often achieve 2:1 block rather than slowing atrial rate; hard to slow ventricles beyond this -Can paradoxically increase 1:1 conduction through AV node slowed (e.g., type Ic flutter); fast ventricle contraction | Afib easier to rate control than this ## Footnote Slowing Atrial rhythm a bit can make it possible for AV to conduct every beat, so ventricles contract more often than when atria were going faster but with less AV conduction e.g. Class Ic anti-arrhythmics: flecainide, propafenone

Answer 45

Very effective short-term treatment Acute option for haemodynamic instability Potential for recurrence unless underlying pathway ablated Anticoagulation same as AF

Answer 46

Ablation is an appropriate first-line treatment (not rate control) -CTI ablation: Interrupts re-entrant circuit -Cure rate >95% for typical flutter -Single procedure, minimal morbidity -Often preferred over lifelong drug therapy

Answer 47

Increase intrathoracic pressure to stimulate vagus nerve and get heart to chill out -Slows the SA node -Slows AV nodal conduction Can be used forerminating AV-nodal–dependent SVTs (like AVNRT) | aka vagal maneuvers

Answer 48

Pill-in-the-pocket -Beta blocker (or non-DHP CCB) → taken regularly -Flecainide → taken only at AF onset Beta blocker: -lecainide can organize AF into atrial flutter; so wthout AV nodal blockade → dangerous 1:1 conduction -lows AV nodal conduction for paroxysmal AF in otherwise healthy hearts. | Class Ic drugs should always be combined with AV nodal blockade. ## Footnote Beta-blockers can cause AV nodal blockade

Arrhythmia Flashcards

(74 cards)