2.1 Cardiac Dysrhythmias, Conduction Blocks & Device Management
Key Takeaways
Vagal maneuvers and rapid IV push adenosine (6 mg, followed by 12 mg if refractory) are first-line interventions for stable narrow-complex reentrant supraventricular tachycardias (AVNRT/AVRT).
In atrial fibrillation with Wolff-Parkinson-White (WPW) syndrome, AV nodal blocking agents (adenosine, beta-blockers, diltiazem, digoxin, IV amiodarone) are strictly contraindicated due to the risk of precipitating ventricular fibrillation; intravenous procainamide or electrical cardioversion is required.
Stable monomorphic VT may be treated with amiodarone or procainamide. Sustained polymorphic VT requires immediate unsynchronized high-energy shock; magnesium and correction of long-QT triggers help prevent recurrent torsades.
Mobitz II is usually infranodal. Complete AV block may be nodal or infranodal; unstable high-grade block requires prompt pacing, and atropine must not delay pacing when infranodal block is suspected.
Device interrogation distinguishes failure to pace, failure to capture, oversensing and undersensing. A magnet usually makes a transvenous pacemaker pace asynchronously. In a transvenous ICD, it generally suspends tachyarrhythmia therapies without changing pacing.
Cardiac Dysrhythmias, Conduction Blocks & Device Management
Acute care nurse practitioners manage life-threatening dysrhythmias and conduction failures in the intensive care unit. Immediate recognition of instability and lethal pharmacologic contraindications is paramount.
Supraventricular Tachycardias & Reentrant Pathways
Supraventricular tachycardias (SVTs) arise above the bundle of His. Atrioventricular nodal reentrant tachycardia (AVNRT) utilizes dual intranodal pathways (slow and fast), whereas atrioventricular reentrant tachycardia (AVRT) involves an extranodal accessory pathway.
Hemodynamic Assessment & Resuscitation
Rate-related hypotension, shock, altered mentation, ischemic chest pain or acute heart failure requires immediate electrical treatment. With a pulse, synchronize regular narrow-complex tachycardia or monomorphic VT at 100 J and AF/flutter at 200 J. Sustained polymorphic VT requires an immediate unsynchronized high-energy shock, even with a pulse. Pulseless VT/VF requires defibrillation and CPR. Sedate when feasible without delaying treatment.
Stable Narrow-Complex SVT Protocol
- Modified Valsalva Maneuver: 40 mmHg strain for 15 seconds semi-recumbent, followed immediately by supine repositioning and 45-degree passive leg elevation for 15 seconds (doubles conversion success over standard maneuvers).
- Adenosine: Binds cardiac A1 receptors, opening potassium channels and inhibiting cAMP-mediated calcium influx to induce transient AV nodal arrest (half-life <10 seconds).
- Dosing: 6 mg rapid IV push (1-2 seconds) via proximal IV with immediate 20 mL saline flush and arm elevation. If unconverted in 1-2 minutes, administer 12 mg rapid IV push.
- Adjustments: Consider a lower initial dose with central administration or after heart transplantation. AHA notes that 1 mg IV may suffice. Dipyridamole potentiates adenosine, and carbamazepine increases the risk of AV block. Theophylline and caffeine can blunt the response. Avoid adenosine in patients with asthma.
- Second-Line Pharmacotherapy: IV diltiazem (0.25 mg/kg over 2 minutes; repeat 0.35 mg/kg after 15 minutes; infusion 5 to 15 mg/hr) or IV metoprolol (2.5 to 5 mg every 5 minutes up to 15 mg).
Atrial Fibrillation & Atrial Flutter with RVR
Atrial fibrillation (AF; 400-600 atrial bpm, irregularly irregular) and atrial flutter (250-350 bpm, regular flutter waves):
- Rate Control (without pre-excitation): In stable AF, IV metoprolol is an option; use IV diltiazem only when LVEF >40%. Avoid IV diltiazem/verapamil in moderate or severe LV systolic dysfunction. IV digoxin (0.25–0.5 mg, with subsequent dosing adjusted for renal function and response) is an option when beta-blockers or calcium channel blockers are ineffective or contraindicated. IV amiodarone may be used in selected critically ill or decompensated-HF patients; consider its potential to cardiovert and the associated stroke risk.
- Thromboembolism & Anticoagulation: Stratified by CHA2DS2-VASc (CHF [1], HTN [1], Age >=75 [2], DM [1], Stroke/TIA [2], Vascular disease [1], Age 65-74 [1], Female [1]). Anticoagulation (DOAC preferred) is indicated for score >=2 in men or >=3 in women.
- Timing: If duration >=48 hours (or unknown), cardioversion requires 3 weeks of therapeutic anticoagulation or transesophageal echocardiogram (TEE) ruling out left atrial appendage (LAA) thrombus. All patients require 4 weeks post-cardioversion anticoagulation due to atrial stunning.
- WPW with AFib: Irregularly irregular wide-complex tachycardia (>200-300 bpm). AV nodal blockers, including adenosine, beta-blockers, diltiazem, verapamil, digoxin and IV amiodarone, are STRICTLY CONTRAINDICATED; blocking the AV node shunts impulses exclusively down the accessory pathway (bundle of Kent), precipitating VF and arrest. Treat with IV procainamide (15-18 mg/kg at 20-50 mg/min), IV ibutilide (1 mg), or synchronized cardioversion if unstable.
Ventricular Tachycardia: Monomorphic & Polymorphic
Wide-complex tachycardias (QRS >=120 ms at rate >100 bpm) are managed presumptively as VT.
- Monomorphic VT: Unstable with pulses requires immediate synchronized cardioversion at 100 J biphasic. Pulseless VT/VF mandates CPR, unsynchronized defibrillation (120-200 J biphasic), epinephrine 1 mg IV q3-5min, and amiodarone 300 mg IV (second dose 150 mg) or lidocaine 1-1.5 mg/kg. Stable VT is treated with IV amiodarone (150 mg over 10 min, then 1 mg/min for 6 hr, then 0.5 mg/min; max 2.2 g/24 hr) or IV procainamide (20-50 mg/min). IV lidocaine (1.0-1.5 mg/kg bolus, maintenance 1-4 mg/min) is preferred for acute ischemic VT.
- Polymorphic VT & Torsades de Pointes (TdP): Sustained polymorphic VT requires immediate unsynchronized high-energy defibrillation, even when a pulse is present. TdP occurs with a prolonged baseline QT, often from electrolyte depletion or QT-prolonging drugs. For recurrent long-QT TdP, give magnesium sulfate 1–2 g IV, stop culprit drugs and correct potassium and magnesium. Recurrent pause-dependent acquired TdP may require overdrive pacing or isoproterenol with expert guidance. Magnesium and rate acceleration prevent recurrence; they must not delay shock treatment of sustained polymorphic VT.
Conduction Blocks & Emergency Bradycardia Protocols
AV Block Differentiation
- First-Degree: PR >200 ms with 1:1 conduction. Usually asymptomatic.
- Second-Degree Mobitz I (Wenckebach): Progressive PR lengthening until a dropped QRS. Usually AV nodal. Assess symptoms and reversible causes.
- Second-Degree Mobitz II: Constant PR with intermittent nonconducted P waves. Usually infranodal, often with a wide QRS. Prepare for pacing and pace promptly if unstable. Persistent acquired block without a reversible cause warrants permanent pacing.
- Third-Degree (Complete): Complete AV dissociation. Nodal block may produce a narrow junctional escape at 40–60 bpm; infranodal block may produce a wide ventricular escape at 20–40 bpm. Instability or an unreliable escape rhythm requires immediate pacing.
Acute Bradycardia Algorithm
For bradycardia causing hemodynamic compromise, treat reversible causes and give atropine 1 mg IV every 3–5 minutes to a maximum of 3 mg when appropriate. Atropine often fails in infranodal block and must not delay pacing. For persistent instability, use transcutaneous pacing and/or dopamine (5–20 mcg/kg/min) or epinephrine (2–10 mcg/min). Confirm electrical and mechanical capture and provide analgesia/sedation when feasible. Arrange temporary transvenous pacing if instability persists.
Postural Orthostatic Tachycardia Syndrome
POTS combines chronic orthostatic intolerance with a sustained heart-rate rise of at least 30 beats/min within 10 minutes of standing or tilt in adults, without orthostatic hypotension. Lightheadedness, palpitations and exercise intolerance improve when supine. Measure supine and standing heart rate/blood pressure, obtain an ECG and assess alternative causes such as volume depletion, anemia, thyroid disease and medications. Acute sepsis-related or hemorrhagic tachycardia does not establish POTS. Management includes progressive reconditioning, compression and individualized fluid/salt intake when cardiac and renal status permit. Persistent disabling symptoms warrant specialist-directed medication. Routine long-term IV saline and central access are not recommended treatment.
Pacemakers, ICDs & Device Troubleshooting
NASPE/BPEG Code & Troubleshooting
- NASPE/BPEG Code: Position I (Paced: A, V, D, O), Position II (Sensed: A, V, D, O), Position III (Response: I-Inhibited, T-Triggered, D-Dual, O-None), Position IV (Rate modulation: R).
- Failure to Pace: Absence of pacing spikes below base rate (lead fracture, battery exhaustion, or oversensing).
- Failure to Capture: Spikes visible without evoked P or QRS (lead dislodgement, exit block, hyperkalemia, acidosis); increase output (mA).
- Undersensing: Fails to sense intrinsic beats; spikes fire randomly, risking R-on-T VT/VF; increase sensitivity by lowering threshold (mV).
- Oversensing: Misinterprets non-cardiac signals (myopotentials, cautery) as beats, inappropriately inhibiting pacing; decrease sensitivity by raising threshold (mV).
Clinical Magnet Application
- Pacemaker: Most transvenous pacemakers switch to asynchronous pacing with a magnet. Confirm the programmed response and rate first because response varies by device.
- ICD: Magnet suspends tachycardia detection and shocks (preventing inappropriate surgical shocks); pacemaker function is unaffected (does not become asynchronous). If VT/VF occurs, restore ICD therapies and provide external defibrillation promptly as indicated.
A 62-year-old male with a history of coronary artery disease presents with sudden palpitations, lightheadedness, and shortness of breath. Vital signs: blood pressure 118/76 mmHg, heart rate 188 bpm, respiratory rate 22/min, and SpO2 96% on room air. The 12-lead ECG reveals a regular narrow-complex tachycardia with no visible P waves. A modified Valsalva maneuver fails to convert the rhythm. The acute care nurse practitioner prepares to administer intravenous adenosine. Which administration technique and clinical consideration is most appropriate?
Administer adenosine 12 mg as a slow intravenous infusion over 5 minutes through a peripheral catheter to minimize bradycardic side effects.
Administer adenosine 6 mg as a rapid intravenous push over 1 to 2 seconds through a proximal large-bore IV, followed immediately by a 20 mL rapid saline flush.
Administer adenosine 3 mg through a peripheral IV, because patients with known coronary artery disease require a routine 50% dose reduction.
Administer adenosine 6 mg as a rapid IV push, followed by an immediate prophylactic bolus of intravenous aminophylline.
A 54-year-old male with a history of Wolff-Parkinson-White (WPW) syndrome presents to the intensive care unit with acute palpitations and diaphoresis. His blood pressure is 108/68 mmHg, heart rate is 210 bpm, and respiratory rate is 20/min. The 12-lead ECG demonstrates an irregularly irregular, wide-complex tachycardia with variable QRS morphologies and ventricular rates exceeding 200 bpm. Which pharmacologic agent is contraindicated in this patient's acute management?
Intravenous procainamide
Intravenous ibutilide
Intravenous diltiazem
Intravenous magnesium sulfate
An 82-year-old female with a dual-chamber permanent pacemaker (programmed DDD, lower rate limit 60 bpm) is admitted to the cardiac ICU following an elective right hip arthroplasty. On continuous cardiac telemetry, the nurse observes that the patient's intrinsic heart rate drops to 44 bpm, but no pacemaker spikes are visible on the monitor. The patient reports dizziness and mild presyncope. The ECG shows sinus bradycardia at 44 bpm without pacing artifacts. Device interrogation confirms an intact lead and shows that myopotentials are being sensed as intrinsic beats and inhibiting pacing. Which malfunction is occurring, and what is the initial troubleshooting step?
Failure to capture; increase the pacemaker output amplitude.
Undersensing; increase pacemaker sensitivity by lowering the millivolt threshold.
Pacemaker-mediated tachycardia; reprogram the post-ventricular atrial refractory period.
Failure to pace due to oversensing; decrease pacemaker sensitivity by raising the millivolt threshold.
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