Rapid Review·Cardiovascular

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PATHOLOGY

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Narrow Complex Tachycardias

P310

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the ventricles were activated rapidly through the normal conduction system, so the tachycardia originates within or above the AV node, i.e. it is supraventricular. WPW is the exception, since its QRS is widened.
irregularly irregular rate and rhythm with NO discrete P waves, as on the atrial fibrillation tracing. It is often paroxysmal, so continuous monitoring may be needed to catch it. Patients may be asymptomatic, or notice palpitations, dyspnea, and fatigue.
arrhythmogenic foci usually sit near the pulmonary vein ostia in the left atrium, which is precisely what pulmonary vein ablation targets. The catheter enters the right heart through the SVC or IVC and crosses the interatrial septum at the foramen ovale to reach them. Alcohol and a high sympathetic drive can set the foci off.
anything that remodels the atria: age-related myocardial change (the strongest), atrial enlargement from heart disease (hypertension, mitral stenosis), coronary artery disease. AF begets AF: each episode shortens the atrial refractory period and slows conduction, so ectopic foci and reentry persist and later episodes come more easily.
thromboembolism from left atrial stasis, and the LA appendage is the commonest thrombus site.
Anticoagulation, Beta-blockers, Calcium channel blockers, Digoxin, plus cardioversion or ablation.
irregularly irregular with 3 or more distinct P wave morphologies, from multiple ectopic atrial foci, as on the MAT tracing. Associated with COPD, pneumonia, and heart failure.
rapid identical consecutive atrial depolarizations giving "sawtooth" P waves with a regular RR interval, as on the atrial flutter tracing. The reentry circuit runs around the tricuspid annulus through the cavotricuspid isthmus, as drawn on the flutter reentry circuit, and that isthmus is the ablation target. Otherwise treat as for AF.
any narrow-complex SVT with an abrupt onset (and termination), lasting seconds to days. Most often a reentrant tract, usually within the AV node. Sudden-onset palpitations, lightheadedness, diaphoresis; the ECG on the paroxysmal SVT tracing is regular with the retrograde P waves buried. Terminate by slowing AV nodal conduction with vagal maneuvers (carotid sinus massage, Valsalva, cold water immersion) or adenosine; cardiovert if unstable; definitive treatment is catheter ablation.
the commonest ventricular pre-excitation syndrome. All three of its states are on the WPW diagram.
an abnormally fast accessory pathway, the bundle of Kent, bypasses the rate-slowing AV node, so the ventricles partially depolarize early. That gives a delta wave, widened QRS, and shortened PR interval. The pathway can complete a reentry circuit, producing SVT.
procainamide or ibutilide. AVOID all AV nodal blockers (adenosine, calcium channel blockers, beta-blockers), because blocking the node forces conduction down the accessory pathway and can precipitate ventricular fibrillation.

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High-yield images8
Wolff-Parkinson-White in three states. Sinus rhythm with the WPW pattern: conduction runs down both the AV node and the accessory bundle of Kent, pre-exciting the ventricle to give a delta wave and short PR. Orthodromic AV-reentrant tachycardia: the circuit goes down the AV node and back up the accessory pathway, giving a narrow QRS with a retrograde P wave. Antidromic AV-reentrant tachycardia: the circuit goes down the accessory pathway and back up the AV node, giving a wide QRS with a delta wave.
Atrial fibrillation on ECG: successive RR intervals are all unequal (irregularly irregular) and the baseline is irregular with no discrete P waves.
Multifocal atrial tachycardia on ECG: an irregularly irregular rhythm in which the arrows mark P waves of at least three different morphologies, each from a separate ectopic atrial focus.
Atrial flutter on ECG: identical consecutive atrial depolarizations produce a sawtooth baseline, here conducting 4:1 so the RR intervals are equal and the ventricular rhythm is regular.
Paroxysmal supraventricular tachycardia on ECG: a regular narrow-complex tachycardia at a rapid rate with P waves buried in the preceding T waves and not separately visible.
ACLS algorithm for adult tachycardia with a pulse. Sinus tachycardia is treated by finding the cause. Hemodynamic instability goes straight to synchronized cardioversion. Otherwise the QRS width splits the tree: narrow and irregular is likely AF or flutter (rate control); narrow and regular is non-AF SVT such as AVNRT (vagal maneuvers then adenosine); wide and irregular is AF with aberrancy, pre-excited AF or polymorphic VT (procainamide for pre-excited AF, magnesium for PMVT); wide and regular is likely monomorphic VT (pharmacologic cardioversion with amiodarone, procainamide, lidocaine or sotalol).
Pulmonary vein ablation for atrial fibrillation: an ablation catheter is advanced into the left atrium and burns a circumferential lesion around the pulmonary vein ostia, electrically isolating the arrhythmogenic foci that sit there.
Reentrant circuit in atrial flutter: the wavefront circles the right atrium around the tricuspid valve annulus, passing through the cavotricuspid isthmus between the tricuspid annulus and the inferior vena cava. That isthmus is the target of catheter ablation. FO marks the fossa ovalis and CS the coronary sinus.

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Where are ablations commonly performed in the treatment of atrial fibrillation and in the treatment of atrial flutter?

Atrial fibrillation → (...) and (...)
Atrial flutter → Region between the (...) and the (...)

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