Dysrhythmias and Electrical Problems

Clinical Orientation

A patient on telemetry suddenly has a run of wide-complex tachycardia at 180 bpm. The nurse rushes in. The patient is awake but diaphoretic, BP 82/50, complaining of chest pressure. Is this VT or SVT with aberrancy? The answer determines treatment, but both are dangerous when hemodynamically unstable. This chapter answers: What mechanism links dysrhythmias to bedside findings, tests, red flags, and nursing priorities?

What Is Normal?

Cardiac conduction system: SA node (60-100 bpm, primary pacemaker) → AV node (delays impulse, allows ventricular filling) → Bundle of His → right and left bundle branches → Purkinje fibers. The AV node protects the ventricles from excessively rapid atrial rates (e.g., atrial fibrillation with 400 atrial impulses/minute → only some conduct to ventricles).

Action potential phases:

• Phase 0: Rapid depolarization (Na+ influx in working myocytes; Ca2+ in SA/AV nodes)
• Phase 1: Early repolarization
• Phase 2: Plateau (Ca2+ influx balanced by K+ efflux)
• Phase 3: Repolarization (K+ efflux)
• Phase 4: Resting membrane potential

Determinants of cardiac output with rhythm: CO = HR × SV. Extremely fast rates → inadequate diastolic filling → decreased SV → decreased CO. Extremely slow rates → inadequate beats/minute → decreased CO. Loss of atrial contraction ("atrial kick") → loss of ~15-30% of LV filling — significant in patients with impaired diastolic function.

What Goes Wrong?

Mechanisms of arrhythmogenesis:

• Abnormal automaticity: Cells that shouldn't initiate impulses start doing so (ischemia, electrolyte abnormalities, stretch, catecholamines).
• Triggered activity: Afterdepolarizations (early or delayed) reach threshold, triggering extra beats.
• Reentry: The most common mechanism of sustained arrhythmias. An impulse circles around an obstacle (scar, functional block) and re-excites tissue that has recovered. Requires: two pathways with different conduction velocities and refractory periods, plus a unidirectional block.

Common dysrhythmias:

• Atrial fibrillation: Chaotic atrial activity → irregularly irregular ventricular response. Risk: thromboembolism (stasis in left atrial appendage), rapid ventricular rate → decreased CO.
• Atrial flutter: Sawtooth atrial pattern, typically 2:1, 3:1, or 4:1 conduction.
• Supraventricular tachycardia (SVT): Regular narrow-complex tachycardia, usually AV nodal reentry or AV reentry (accessory pathway).
• Ventricular tachycardia (VT): Wide-complex tachycardia from ventricular focus. May be stable or unstable. Sustained VT (>30 sec) is a medical emergency.
• Ventricular fibrillation (VF): Chaotic ventricular activity → no effective contraction → cardiac arrest.
• Bradyarrhythmias: Sinus bradycardia, junctional escape, heart blocks (first-degree, second-degree type I/II, third-degree/complete).

What the Nurse May See

Stable vs unstable: If the patient has chest pain, dyspnea, hypotension, altered mental status, or signs of shock → the rhythm is UNSTABLE → immediate synchronized cardioversion (if pulse present) or defibrillation (if pulseless).

Atrial fibrillation: Irregularly irregular pulse. Pulse deficit (apical rate > radial rate because some beats don't generate enough SV for a peripheral pulse). Rapid AF → hypotension, heart failure.

VT: Wide QRS (>0.12 sec), rate 100-250. May be hemodynamically stable or unstable. Sustained VT → always treat.

Bradycardia: HR <60. Assess whether the patient is symptomatic: hypotension, confusion, chest pain, dyspnea. Asymptomatic bradycardia in a healthy person (athlete) may not need treatment.

Nursing Priorities

1. Determine stability FIRST: Is the patient symptomatic? Chest pain? Hypotension? Altered mental status? Signs of shock? If UNSTABLE → synchronized cardioversion (narrow or wide complex with pulse) or defibrillation (pulseless VT/VF).

1. For stable tachyarrhythmias: 12-lead ECG. Determine narrow vs wide complex. Narrow complex = supraventricular origin. Wide complex = ventricular origin (or SVT with aberrancy — assume VT if uncertain in a patient with heart disease).

1. For AF with RVR: Rate control (beta-blocker, calcium channel blocker) or rhythm control (cardioversion, antiarrhythmics). Anticoagulation based on CHA2DS2-VASc score.

1. For bradycardia with symptoms: Atropine 0.5 mg IV (may repeat to 3 mg total). If ineffective: transcutaneous pacing, then transvenous pacing. Identify reversible causes (Hs and Ts: hypoxia, hypovolemia, hypo/hyperkalemia, hydrogen ions/acidosis, hypothermia, toxins, tamponade, tension pneumothorax, thrombosis).

1. Post-cardioversion: Check for return of normal rhythm, assess hemodynamics, monitor for thromboembolism if AF was not anticoagulated.

Red Flags

Common Student Mistakes

1. Treating the monitor instead of the patient: Asymptomatic PVCs or sinus bradycardia in a healthy patient usually need no treatment. Treat the patient, not the strip.
2. Giving AV nodal blockers in atrial fibrillation with WPW: These can paradoxically increase conduction down the accessory pathway → VF.