15.1 Acute Atrial & Ventricular Arrhythmias

ACLS Tachycardia Evaluation & Hemodynamic Stability Assessment

The initial assessment of any patient presenting with an acute tachyarrhythmia (heart rate generally ≥150 beats/min) begins with a rapid, focused evaluation of hemodynamic stability. The fundamental principle of Advanced Cardiovascular Life Support (ACLS) is that clinical instability dictates immediate electrical therapy, whereas clinical stability affords time for diagnostic electrocardiography and targeted pharmacotherapy.

The Five Cardinal Signs of Hemodynamic Instability

A patient is classified as hemodynamically unstable if the tachyarrhythmia directly precipitates any of the following five cardinal features:

1. Hypotension: Systolic blood pressure <90 mm Hg or mean arterial pressure (MAP) <65 mm Hg, or a precipitous drop from baseline.
2. Acute Altered Mental Status: Lethargy, acute confusion, somnolence, agitation, or syncope resulting from cerebral hypoperfusion.
3. Signs of Shock: Diaphoresis, cold and clammy extremities, peripheral cyanosis, delayed capillary refill (>3 seconds), or elevated serum lactate (>2.0 mmol/L).
4. Ischemic Chest Discomfort: Squeezing substernal chest pressure, angina, or dynamic ST-segment depressions/elevations reflecting supply-demand myocardial ischemia.
5. Acute Heart Failure / Pulmonary Edema: Acute respiratory distress, tachypnea, diffuse pulmonary rales, jugular venous distention, or hypoxemia (SpO2 <90%).

Emergent Electrical Management

• Immediate Synchronized Cardioversion: If any of the five signs of instability are present, synchronized cardioversion must be performed immediately. In conscious patients, administer rapid intravenous procedural sedation and analgesia (e.g., etomidate 0.1–0.2 mg/kg IV, fentanyl 25–50 mcg IV, or midazolam 1–2 mg IV) without delaying lifesaving shock delivery.
• Synchronization Mechanism: The "sync" function must be activated on the defibrillator so that the energy discharge is delivered synchronously with the peak of the R wave. This avoids delivering energy during the vulnerable repolarization phase of the cardiac cycle (the T wave), which would precipitate ventricular fibrillation (the "R-on-T phenomenon").
• Energy Recommendations (Biphasic):
  • Narrow Regular (SVT, Atrial Flutter): 50 to 100 Joules.
  • Narrow Irregular (Atrial Fibrillation with RVR): 120 to 200 Joules biphasic (or 200 Joules monophasic).
  • Wide Regular (Monomorphic VT with a pulse): 100 Joules.
  • Polymorphic VT or Pulseless Tachycardia: Do NOT synchronize (machine cannot track varying R waves). Deliver immediate high-energy unsynchronized defibrillation (200 Joules biphasic or 360 Joules monophasic).

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Narrow-Complex Regular Tachycardias (QRS <120 ms)

Narrow-complex regular tachycardias originate at or above the bundle of His. The most common etiology encountered in primary care and emergency settings is paroxysmal supraventricular tachycardia (PSVT), which predominantly comprises Atrioventricular Nodal Reentrant Tachycardia (AVNRT, ~60%) and Atrioventricular Reentrant Tachycardia (AVRT, ~30%) involving an accessory pathway.

Step 1: Vagal Maneuvers

In a hemodynamically stable patient with regular narrow-complex tachycardia, vagal maneuvers represent the first-line non-pharmacological intervention by increasing parasympathetic tone via the vagus nerve, slowing AV nodal conduction and breaking the reentrant loop.

• Modified Valsalva Maneuver (The REVERT Trial Protocol): Standard Valsalva (forced expiration against resistance) has a low success rate of approximately 17%. The landmark REVERT trial demonstrated that the modified Valsalva maneuver achieves a cardioversion success rate of 43%:
  1. Position the patient in a semi-recumbent, seated position (45°).
  2. Have the patient blow forcefully into a 10-mL or 20-mL syringe to generate an expiratory pressure of 40 mm Hg for 15 seconds (enough pressure to just move the plunger).
  3. Immediately upon completion of the 15-second strain, lay the patient flat on their back (supine) and simultaneously have an assistant raise the patient's legs to a 45° angle for 15 seconds.
  4. Return the patient to the seated position for 45 seconds before re-evaluating rhythm.
• Carotid Sinus Massage: Perform only after auscultating for carotid bruits. Massage the carotid bulb at the superior border of the thyroid cartilage for 5 to 10 seconds. Never perform bilateral carotid massage simultaneously, and avoid in patients with prior stroke, TIA, or carotid stenosis.

Step 2: Pharmacotherapy with Intravenous Adenosine

If vagal maneuvers fail, adenosine is the drug of choice for regular narrow-complex tachycardia.

• Mechanism: Endogenous purine nucleoside that binds to cardiac A1 adenosine receptors, inhibiting adenylyl cyclase, opening inward rectifier potassium channels (I[K,Ado]), and blocking calcium influx. This produces profound transient hyperpolarization and blocks conduction through the AV node for several seconds.
• Dosing & Administration Protocol:
  • Initial Dose: 6 mg rapid IV push through a large peripheral vein (preferably the antecubital fossa) over 1 to 2 seconds.
  • Saline Flush: Follow immediately with a 20 mL rapid normal saline flush using a dual-port stopcock or two-syringe technique, with the arm elevated.
  • Second Dose: If the tachycardia does not convert within 1 to 2 minutes, administer 12 mg rapid IV push followed by a 20 mL saline flush.
  • Third Dose: A final dose of 12 mg rapid IV push may be administered if needed.
• Dose Adjustments & Drug Interactions:
  • Reduce Dose to 3 mg: If administered via a central venous line (femoral, internal jugular, or subclavian), in cardiac transplant recipients (denervated hearts exhibit extreme receptor hypersensitivity), or with concurrent dipyridamole or carbamazepine (potentiate adenosine).
  • Increase Dose: In patients with heavy caffeine consumption or chronic theophylline / aminophylline therapy (competitive methylxanthine antagonists at A1 receptors).
• Patient Anticipatory Guidance: Counsel the patient that adenosine causes a transient, alarming sensation of intense facial flushing, chest tightness, dyspnea, and impending doom lasting 10 to 15 seconds, accompanied by several seconds of sinus pause or asystole on the cardiac monitor before normal sinus rhythm resumes.
• Contraindications: Severe active bronchospastic asthma (can precipitate lethal bronchoconstriction), second- or third-degree AV block, sick sinus syndrome, and pre-excited atrial fibrillation (Wolff-Parkinson-White syndrome).

Step 3: Second-Line Pharmacotherapy

If adenosine fails to convert the rhythm or if tachycardia recurs rapidly, the underlying rhythm may be atrial flutter or atrial tachycardia unmasked by AV nodal blockade. Second-line agents include:

• Intravenous Diltiazem: Non-dihydropyridine calcium channel blocker. Dose: 0.25 mg/kg IV bolus over 2 minutes (typical dose 15–20 mg); if no response after 15 minutes, repeat with 0.35 mg/kg IV (typical dose 20–25 mg). May follow with continuous infusion at 5 to 15 mg/h.
• Intravenous Verapamil: 2.5 to 5 mg IV bolus over 2 minutes; repeat with 5 to 10 mg after 15 to 30 minutes if needed (maximum cumulative dose 20 mg).
• Intravenous Metoprolol: 2.5 to 5 mg IV bolus every 5 minutes up to 3 doses (maximum 15 mg).

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Narrow-Complex Irregular Tachycardia: Atrial Fibrillation & Flutter

Atrial fibrillation (AF) is characterized by chaotic, disorganized atrial electrical activity (350–600 depolarizations/min) resulting in no discernible P waves, an irregularly irregular ventricular response, and variable QRS amplitude. Atrial flutter is characterized by a macroreentrant circuit within the right atrium (sawtooth flutter waves at ~300 bpm) with variable AV conduction (commonly 2:1 block producing a regular rate of 150 bpm, or variable block producing an irregular rhythm).

Rate Control vs Rhythm Control in Acute AF

In the acute setting for stable patients, the primary objective is rate control to relieve symptoms and prevent tachycardia-induced cardiomyopathy.

Rate Control Agents

• Target Heart Rate: The landmark RACE II trial demonstrated that lenient rate control (resting heart rate <110 beats/min) is as clinically effective as strict control (<80 bpm) in reducing cardiovascular morbidity and mortality.
• First-Line Pharmacotherapy:
  • Intravenous Diltiazem: 0.25 mg/kg IV over 2 minutes, then 0.35 mg/kg at 15 minutes, followed by continuous infusion at 5–15 mg/h. Most rapid and reliable onset among rate-control agents.
  • Intravenous Metoprolol: 2.5 to 5.0 mg IV push every 5 minutes up to 15 mg.
  • Intravenous Esmolol: Ultra-short-acting beta-blocker. Loading dose 500 mcg/kg over 1 minute, followed by maintenance infusion at 50 to 200 mcg/kg/min.
• CRITICAL CONTRAINDICATION IN HFrEF: Non-dihydropyridine calcium channel blockers (diltiazem and verapamil) exert potent negative inotropic effects. They are strictly contraindicated in patients with heart failure with reduced ejection fraction (HFrEF, LVEF <40%) or acute decompensated heart failure, as they can precipitate severe pulmonary edema and cardiogenic shock. In HFrEF, use intravenous beta-blockers (cautiously if compensated), intravenous digoxin (0.25–0.5 mg IV), or intravenous amiodarone (150 mg IV over 10 minutes).

Thromboembolic Risk Stratification & Cardioversion Rules

The decision to perform electrical or chemical rhythm conversion depends strictly on the duration of atrial fibrillation:

                         ATRIAL FIBRILLATION DURATION & CARDIOVERSION
                                              
                    ┌────────────────────────────────────────────┐
                    │ Acute Atrial Fibrillation / Atrial Flutter │
                    └─────────────────────┬──────────────────────┘
                                          │
                      ┌───────────────────┴───────────────────┐
                      ▼                                       ▼
        ┌───────────────────────────┐           ┌───────────────────────────┐
        │    Duration <48 Hours     │           │ Duration ≥48 Hours or     │
        │    and Hemodynamically    │           │ Unknown Duration          │
        │          Stable           │           └─────────────┬─────────────┘
        └─────────────┬─────────────┘                         │
                      │                                       ▼
                      │                     ┌───────────────────────────────────┐
                      │                     │  TWO EVIDENCE-BASED PATHWAYS:     │
                      │                     │  1. Anticoagulate for ≥3 weeks    │
                      │                     │     prior to cardioversion, OR    │
                      │                     │  2. Perform Transesophageal Echo  │
                      │                     │     (TEE) to exclude LAA thrombus │
                      │                     └─────────────────┬─────────────────┘
                      │                                       │
                      │      ┌────────────────────────────────┘
                      ▼      ▼
        ┌───────────────────────────────────────────────────────────────────┐
        │ Perform Electrical or Pharmacological Cardioversion               │
        │ • Mandatory: Therapeutic Oral Anticoagulation for at least        │
        │   4 WEEKS post-cardioversion regardless of baseline CHA2DS2-VASc  │
        │ • Atrial stunning post-conversion creates high thrombus risk      │
        └─────────────────────────────────┬─────────────────────────────────┘
                                          │
                                          ▼
        ┌───────────────────────────────────────────────────────────────────┐
        │ Long-Term Anticoagulation Decision: Guided by CHA2DS2-VASc Score  │
        │ • Men ≥2, Women ≥3: Indefinite DOAC (Apixaban, Rivaroxaban)       │
        └───────────────────────────────────────────────────────────────────┘

• Duration <48 Hours: If the patient has documented onset <48 hours ago and no high-risk stroke features, cardioversion can be performed acutely without prolonged pre-anticoagulation. Administer therapeutic low-molecular-weight heparin (enoxaparin 1 mg/kg SC) or a DOAC prior to cardioversion.
• Duration ≥48 Hours or Unknown: Cardioversion is associated with a 1% to 5% risk of thromboembolism due to dislodgement of a left atrial appendage (LAA) thrombus. Two clinical strategies are accepted:
  1. Delayed Cardioversion: Therapeutic anticoagulation with a Direct Oral Anticoagulant (DOAC) or warfarin (INR 2.0–3.0) for at least 3 consecutive weeks prior to cardioversion, followed by at least 4 weeks of anticoagulation post-cardioversion.
  2. TEE-Guided Cardioversion: Perform Transesophageal Echocardiography (TEE) to directly visualize and exclude thrombus in the left atrial appendage. If no thrombus is present, cardioversion is performed immediately, followed by at least 4 weeks of therapeutic anticoagulation.
• POST-CARDIOVERSION MANDATE: Because the atria experience "atrial stunning" (impaired mechanical contractility despite restoration of sinus rhythm on ECG) lasting days to weeks after cardioversion, all patients undergoing cardioversion must receive at least 4 weeks of therapeutic oral anticoagulation, regardless of their baseline CHA2DS2-VASc score.

The CHA2DS2-VASc Score for Long-Term Anticoagulation

Long-term oral anticoagulation is determined by the CHA2DS2-VASc score:

• Clinical Indications:
  • Score ≥2 in Men or ≥3 in Women: Oral anticoagulation is strongly recommended (Class I).
  • Score = 1 in Men or 2 in Women: Oral anticoagulation should be considered based on individual shared decision-making.
  • Score = 0 in Men or 1 in Women: No antithrombotic therapy recommended.
• Preferred Agents: Direct Oral Anticoagulants (DOACs: apixaban, rivaroxaban, dabigatran, edoxaban) are preferred over warfarin due to a 50% lower rate of intracranial hemorrhage and comparable or superior stroke reduction. Warfarin remains indicated exclusively in patients with mechanical prosthetic heart valves or moderate-to-severe mitral stenosis (target INR 2.0–3.0 for aortic, 2.5–3.5 for mitral mechanical valves).

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Wolff-Parkinson-White (WPW) Syndrome with Pre-Excited Atrial Fibrillation

Wolff-Parkinson-White (WPW) syndrome is characterized by an accessory pathway (the Bundle of Kent) that provides an alternative conduction route connecting the atria directly to the ventricles, bypassing the physiological conduction delay of the AV node.

The Lethal Clinical Presentation

When a patient with WPW develops atrial fibrillation, chaotic atrial impulses (350–600 bpm) conduct rapidly down both the normal AV node and the accessory pathway. Because accessory pathways lack the decremental conduction properties of the AV node, ventricular rates can reach 250 to 350 beats/min.

• ECG Characteristics:
  1. Irregularly irregular ventricular rhythm.
  2. Wide and bizarre QRS complexes (>120 ms) with dramatic beat-to-beat variability in morphology and width (due to varying proportions of ventricular myocardium activated by the accessory pathway versus the AV node).
  3. Extremely rapid ventricular rates, frequently exceeding 200–250 bpm (rates that the AV node cannot physiologically conduct).

THE "ABCD" CONTRAINDICATION: Fatal Pharmacological Pitfalls

Administering AV nodal blocking agents to a patient with pre-excited atrial fibrillation is a catastrophic medical error that frequently triggers ventricular fibrillation and sudden cardiac death.

                       THE FATAL PHARMACOLOGICAL SHORT-CIRCUIT
                       
                 ┌────────────────────────────────────────────────┐
                 │   Chaotic Atrial Fibrillation (350-600 bpm)    │
                 └───────────────┬────────────────┬───────────────┘
                                 │                │
                        Normal   │                │ Accessory Pathway
                       AV Node   │                │ (Bundle of Kent: NO decremental delay)
                                 ▼                ▼
                 ┌────────────────────────┐      ┌────────────────────────┐
                 │    AV Nodal Blockers   │      │ 100% of impulses shunted│
                 │   "ABCD" CONTRAINDICATED│      │ straight to ventricles │
                 │  • Adenosine           │      │ at >300 bpm            │
                 │  • Beta-blockers       │      └───────────┬────────────┘
                 │  • Calcium blockers    │                  │
                 │  • Digoxin             │                  ▼
                 └────────────────────────┘      ┌────────────────────────┐
                                                 │ VENTRICULAR FIBRILLATION│
                                                 │   AND CARDIAC ARREST   │
                                                 └────────────────────────┘

• Strictly Contraindicated "ABCD" Agents:
  • A - Adenosine
  • B - Beta-blockers (metoprolol, atenolol, esmolol)
  • C - Calcium channel blockers (diltiazem, verapamil)
  • D - Digoxin
• Electrophysiological Mechanism: In pre-excited AF, the AV node normally conducts some impulses that collide with accessory pathway impulses, generating retrograde refractory barriers (concealed conduction) that limit how many impulses can traverse the accessory pathway. When an AV nodal blocker is administered, AV nodal conduction is abolished. This eliminates concealed retrograde conduction, allowing 100% of the 350–600 chaotic atrial impulses to conduct unopposed down the accessory pathway into the ventricles, instantly degenerating into ventricular fibrillation.

Management of Pre-Excited Atrial Fibrillation

• Hemodynamically Unstable: Immediate synchronized electrical cardioversion (120–200 Joules biphasic).
• Hemodynamically Stable: First-line pharmacological therapy is Intravenous Procainamide:
  • Dose: 20 to 50 mg/min IV infusion until the arrhythmia is suppressed, hypotension develops, the QRS widens by >50%, or a maximum dose of 17 mg/kg is reached.
  • Alternative: Intravenous Ibutilide (1 mg IV over 10 minutes; class III antiarrhythmic).
  • Mechanism: Class Ia (procainamide) and class III (ibutilide) agents block sodium and potassium channels, directly prolonging the refractory period of the accessory pathway and terminating conduction.
• Definitive Treatment: Catheter-directed radiofrequency ablation of the accessory pathway.

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Wide-Complex Regular Tachycardia: VT vs SVT with Aberrancy

A wide-complex tachycardia (QRS duration ≥120 ms, heart rate >100 bpm) presents a critical diagnostic challenge: differentiating Ventricular Tachycardia (VT, ~80–85% of cases) from Supraventricular Tachycardia with aberrant ventricular conduction (SVT with bundle branch block, ~15%).

Clinical Heuristic: Assume VT Until Proven Otherwise

In board examinations and clinical practice, all wide-complex tachycardias must be treated as ventricular tachycardia until proven otherwise. The presence of a prior myocardial infarction, ischemic cardiomyopathy, or structural heart disease increases the statistical probability of VT to >95%. Presuming SVT and administering AV nodal blockers (such as verapamil or diltiazem) to a patient with VT frequently causes hemodynamic collapse and cardiac arrest.

Diagnostic Criteria (Brugada Algorithm for VT)

The Brugada algorithm evaluates four sequential questions; answering "YES" to any single question confirms Ventricular Tachycardia:

1. Absence of an RS complex in all precordial leads (V1–V6): Are all precordial leads entirely positive (concordant R) or entirely negative (concordant QS)? If YES → VT.
2. RS interval >100 ms in any precordial lead: Is the duration from the onset of the R wave to the deepest nadir of the S wave >100 ms (2.5 small boxes)? If YES → VT.
3. Atrioventricular (AV) Dissociation: Are there independent, non-conducted P waves marching through the wide QRS rhythm? Are there capture beats (a normal narrow QRS beat occurring when a supraventricular impulse captures the ventricle) or fusion beats (Dressler beats) (a hybrid beat resulting from the simultaneous activation of the ventricle by both a supraventricular and ventricular impulse)? The presence of AV dissociation, capture beats, or fusion beats is pathognomonic for VT.
4. Morphological Criteria for VT in Leads V1/V2 and V6:
   • RBBB Morphology (dominant R in V1): Monophasic R, qR, or classic "rabbit ear" with a taller left rabbit ear in V1; R/S ratio <1 in V6.
   • LBBB Morphology (dominant S in V1): Wide R wave >30 ms in V1, notched S wave descent, or qR pattern in V6.

Management of Monomorphic Ventricular Tachycardia

• Unstable VT with a Pulse: Immediate synchronized cardioversion at 100 Joules biphasic.
• Pulseless VT: Treat as cardiac arrest with immediate unsynchronized CPR, defibrillation at 200 Joules biphasic, epinephrine 1 mg IV every 3–5 minutes, and amiodarone 300 mg IV push.
• Stable Monomorphic VT: Pharmacological antiarrhythmic infusion:
  • Intravenous Amiodarone: First-line. Administer 150 mg IV over 10 minutes (diluted in 100 mL D5W). Follow with a continuous maintenance infusion of 1 mg/min for 6 hours (360 mg), then 0.5 mg/min for the subsequent 18 hours (540 mg). Total 24-hour dose should not exceed 2.2 grams.
  • Intravenous Procainamide: Alternative first-line agent. 20 to 50 mg/min IV infusion up to 17 mg/kg.
  • Intravenous Lidocaine: Class Ib antiarrhythmic (1.0–1.5 mg/kg IV bolus). Second-line agent, especially effective in acute ischemia-mediated VT.

Polymorphic VT & Torsades de Pointes

Polymorphic ventricular tachycardia is characterized by continuously varying QRS amplitude and axis twisting around the isoelectric line. When polymorphic VT occurs in the setting of a prolonged baseline QT interval (QTc >500 ms), it is termed Torsades de Pointes (TdP).

• Etiologies: Electrolyte derangements (hypokalemia, hypomagnesemia, hypocalcemia), congenital long QT syndromes (Jervell and Lange-Nielsen, Romano-Ward), and QT-prolonging pharmacotherapy (macrolides, fluoroquinolones, antipsychotics, cyclic antidepressants, ondansetron, methadone, Class Ia and Class III antiarrhythmics).
• Emergency Management:
  1. Intravenous Magnesium Sulfate: First-line therapy regardless of baseline serum magnesium. Administer 2 grams IV push diluted in 10–20 mL D5W over 1 to 2 minutes, followed by an infusion at 1 to 2 grams/hour.
  2. Defibrillation: If the patient becomes pulseless or unstable, deliver immediate unsynchronized high-energy defibrillation (200 Joules biphasic).
  3. Overdrive Pacing: Temporary transvenous overdrive pacing at a rate of 90 to 110 beats/min shortens ventricular repolarization and prevents early afterdepolarizations (EADs).
  4. Isoproterenol Infusion: In the absence of pacing, infuse isoproterenol (beta-agonist) to drive sinus rate to 90–110 bpm and shorten the QT interval (strictly contraindicated in congenital long QT syndrome or acute myocardial ischemia).
  5. STRICT CONTRAINDICATION: Amiodarone and procainamide prolong the QT interval and will trigger recurrent, fatal Torsades de Pointes. Never administer amiodarone for polymorphic VT with prolonged QT.

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ACLS Bradycardia Algorithm & Conduction Block Classification

Symptomatic bradycardia is defined as a heart rate <50 beats/min associated with hypoperfusion (hypotension, acute altered mental status, chest pain, syncope, or signs of shock).

Atrioventricular (AV) Conduction Block Spectrum

                         ATRIOVENTRICULAR (AV) BLOCK SPECTRUM
                         
  ┌─────────────────────────────────────────────────────────────────────────────────────────┐
  │ 1. FIRST-DEGREE AV BLOCK: PR Interval >200 ms (>5 small boxes)                           │
  │ • Fixed delay at AV node; every P wave conducts to a QRS (1:1 conduction)               │
  │ • Benign, asymptomatic; no treatment required; watch for medication effects             │
  └───────────────────────────────────────────┬─────────────────────────────────────────────┘
                                              │
  ┌───────────────────────────────────────────┴─────────────────────────────────────────────┐
  │ 2. SECOND-DEGREE MOBITZ TYPE I (Wenckebach)                                             │
  │ • Progressive PR lengthening until a P wave fails to conduct (dropped QRS)              │
  │ • Block located at AV NODE; physiologic/vagal or inferior MI; responsive to atropine    │
  │ • Benign prognosis; rarely progresses to complete block; pacing rarely needed            │
  └───────────────────────────────────────────┬─────────────────────────────────────────────┘
                                              │
  ┌───────────────────────────────────────────┴─────────────────────────────────────────────┐
  │ 3. SECOND-DEGREE MOBITZ TYPE II                                                         │
  │ • Constant PR intervals in conducted beats; intermittent unheralded dropped QRS         │
  │ • Block located in INFRANODAL His-Purkinje system; anterior MI or structural fibrosis   │
  │ • High risk of sudden complete heart block and syncope (Stokes-Adams attacks)           │
  │ • Atropine INEFFECTIVE/harmful; REQUIRES immediate pacing and PERMANENT PACEMAKER       │
  └───────────────────────────────────────────┬─────────────────────────────────────────────┘
                                              │
  ┌───────────────────────────────────────────┴─────────────────────────────────────────────┐
  │ 4. THIRD-DEGREE (COMPLETE) HEART BLOCK                                                  │
  │ • Complete atrioventricular dissociation; regular atrial P waves, regular escape QRS    │
  │ • Atrial rate > ventricular rate; PR intervals completely variable; no relationship    │
  │ • Extreme hemodynamic instability; REQUIRES emergency pacing and PERMANENT PACEMAKER   │
  └─────────────────────────────────────────────────────────────────────────────────────────┘

Emergency Management Protocol for Symptomatic Bradycardia

When a patient exhibits symptomatic bradycardia with hypoperfusion, follow the stepwise ACLS escalation:

1. First-Line Pharmacotherapy: Intravenous Atropine:

   • Dose: 1 mg IV push every 3 to 5 minutes up to a maximum cumulative dose of 3 mg (0.04 mg/kg).
   • Mechanism: Antimuscarinic agent that blocks acetylcholine at M2 muscarinic receptors on the SA and AV nodes, increasing intrinsic automaticity and AV conduction velocity.
   • Limitations & Pitfalls:
     • Ineffective in Infranodal Block: Atropine acts strictly on the AV node. In Mobitz type II second-degree block or third-degree block with wide QRS escape, the conduction failure is in the His-Purkinje system. Atropine will NOT improve conduction and may paradoxically worsen ventricular rate by increasing atrial impulses hitting a blocked infranodal system.
     • Avoid Underdosing: Doses <0.5 mg can cause paradoxical bradycardia due to central vagal stimulation.
     • Heart Transplant Warning: Ineffective in denervated donor hearts lacking vagal innervation.

2. Second-Line Interventions (If Atropine Ineffective or in High-Grade Block): Do not delay second-line therapy while administering repeating doses of atropine in patients with Mobitz II or complete heart block.

   • Transcutaneous Pacing (TCP):
     • Apply anterior-posterior pacing pads immediately.
     • Set pacing mode to demand (synchronous), rate to 60 to 80 beats/min.
     • Increase current output (milliamperes, mA) until electrical capture is confirmed (characterized by a pacer spike followed immediately by a wide QRS complex and a broad, discordant T wave).
     • Confirm mechanical capture by simultaneously palpating a right femoral or radial pulse. Pacing artifact on the monitor does not guarantee myocardial contraction.
     • Provide IV analgesia and sedation (e.g., fentanyl and midazolam), as transcutaneous pacing causes painful skeletal muscle contraction.
   • Chronotropic / Vasopressor Infusions (While pacing is initiated or if TCP fails):
     • Dopamine Infusion: 5 to 20 mcg/kg/min continuous IV infusion (acts on beta-1 receptors at 5–10 mcg/kg/min; alpha-1 vasoconstriction at >10 mcg/kg/min).
     • Epinephrine Infusion: 2 to 10 mcg/min continuous IV infusion (potent combined beta-1 chronotrope and inotrope).

3. Definitive Treatment: Transvenous Pacing & Permanent Pacemaker (PPM):

   • Emergency transvenous temporary pacing wire insertion via internal jugular or subclavian vein.
   • Permanent pacemaker implantation is a Class I indication for:
     • Symptomatic sinus node dysfunction (Sick Sinus Syndrome).
     • Second-degree Mobitz type II AV block (regardless of symptoms, due to high sudden death risk).
     • Third-degree complete AV block (regardless of symptoms).
     • Alternating bundle branch block.