The patient's presentation of sudden-onset palpitations with a regular, narrow-complex tachycardia at a rate of 170/min and absent P waves is classic for atrioventricular nodal reentrant tachycardia (AVNRT), a type of supraventricular tachycardia. Atrial fibrillation would be irregularly irregular. Ventricular tachycardia would typically show a wide QRS complex. Sinus tachycardia is a physiologic response and would have visible P waves preceding each QRS complex.

This hemodynamically stable patient presents with a supraventricular tachycardia (SVT), most likely AVNRT. The initial management for stable SVT should be vagal maneuvers, such as carotid sinus massage or the Valsalva maneuver. If these are unsuccessful, intravenous adenosine is the next step. Diltiazem is a second-line pharmacologic agent. Synchronized cardioversion is reserved for hemodynamically unstable patients.

For a hemodynamically stable patient with monomorphic ventricular tachycardia, the first-line treatment is an intravenous antiarrhythmic agent. Amiodarone is a preferred agent according to ACLS guidelines. Procainamide or sotalol are also options. Adenosine is used for diagnosing and treating supraventricular tachycardia, not VT. Magnesium sulfate is the treatment of choice for torsades de pointes (polymorphic VT). Verapamil (a calcium channel blocker) is contraindicated in wide-complex tachycardias of unknown origin as it can cause hemodynamic collapse if the rhythm is VT.

This patient's CHA2DS2-VASc score is 4 (Age ≥75=2 points, Hypertension=1 point, Diabetes=1 point). A score of 2 or greater in men or 3 or greater in women is a clear indication for long-term oral anticoagulation. Direct oral anticoagulants (e.g., apixaban, rivaroxaban) or warfarin are recommended over antiplatelet agents like aspirin or clopidogrel, which are less effective for stroke prevention in atrial fibrillation. No therapy would leave her at significant risk for stroke.

An implantable cardioverter-defibrillator (ICD) is indicated for primary prevention of sudden cardiac death in patients with ischemic cardiomyopathy, an LVEF ≤35%, and NYHA class II or III symptoms, provided they are at least 40 days post-MI and are on optimal medical therapy. A pacemaker is for bradyarrhythmias. Prophylactic amiodarone has not been shown to improve survival in this population and has significant side effects. Bypass grafting is for revascularization and would have been considered earlier if appropriate.

The ECG finding of progressive PR interval prolongation followed by a non-conducted P wave ('dropped beat') is the classic description of second-degree AV block, Mobitz type I (also known as Wenckebach phenomenon). First-degree AV block involves a constantly prolonged PR interval with no dropped beats. Mobitz type II involves dropped beats without preceding PR prolongation. Third-degree AV block involves complete dissociation between P waves and QRS complexes.

The patient has developed torsades de pointes (TdP), a polymorphic ventricular tachycardia occurring in the setting of a prolonged QT interval. Her alcoholism and malnutrition put her at risk for electrolyte abnormalities like hypomagnesemia and hypokalemia, common causes of QT prolongation. The first-line treatment for TdP (both stable and unstable) is intravenous magnesium sulfate, which helps stabilize the cardiac membrane. Amiodarone can further prolong the QT interval and should be avoided. Calcium is for hyperkalemia, and bicarbonate is for specific toxicities or acidosis.

Atrial flutter carries a similar thromboembolic risk to atrial fibrillation. Therefore, the management of stroke prevention is identical. The decision to initiate anticoagulation should be based on the CHA2DS2-VASc score, regardless of whether the arrhythmia is atrial flutter or atrial fibrillation. The ventricular rate and future plans for ablation do not change the need for risk stratification and appropriate anticoagulation.

The ECG findings describe complete atrioventricular (AV) dissociation, where the atria (P waves at 90/min) and ventricles (QRS complexes at 40/min) are beating independently. This is the definition of third-degree, or complete, AV block. The narrow QRS indicates the escape rhythm is originating from the AV junction. Mobitz II would show some relationship between P waves and QRS complexes (e.g., 2:1 or 3:1 block). Sick sinus syndrome can cause bradycardia but not necessarily complete AV dissociation.

This patient has symptomatic, high-degree AV block causing hemodynamic instability (hypotension, altered mental status). The immediate priority is to increase the heart rate and restore cardiac output. Transcutaneous pacing is the fastest and most reliable method to achieve this in an unstable patient. Atropine is unlikely to be effective for a high-degree (infranodal) block and should not delay more definitive therapy. While a permanent pacemaker will be needed, it is not the immediate intervention. Vasopressors like dopamine can be used as a bridge but pacing is the primary treatment.