Cardiac arrhythmias nursing: recognition, interventions, and NCLEX review

Cardiac arrhythmias — also called dysrhythmias — are disturbances in the rate, rhythm, origin, or conduction of the heart’s electrical impulse. They range from benign variants discovered incidentally to immediately life-threatening emergencies requiring defibrillation within minutes. For nursing students, arrhythmias are high-yield across every clinical setting: med-surg patients develop new-onset supraventricular tachycardia (SVT) postoperatively, ICU patients deteriorate into pulseless ventricular tachycardia, and outpatients with pacemakers present with failure-to-capture on a routine EKG strip. This article covers the arrhythmias most likely to appear on the NCLEX and in clinical practice — SVT, ventricular tachycardia, ventricular fibrillation, torsades de pointes, bradyarrhythmias, and heart block — along with pacemaker nursing, cardioversion and defibrillation, antiarrhythmic pharmacology, and ACLS priorities. For atrial fibrillation specifically, see the dedicated atrial fibrillation nursing reference; this article treats it as context rather than primary subject matter.

Quick reference: major arrhythmias at a glance

Classification framework

Arrhythmias are organized by origin and mechanism:

By origin:

• Supraventricular — originate above the bundle of His (SA node, atria, AV node). QRS is typically narrow because ventricular conduction follows the normal His-Purkinje pathway.
• Ventricular — originate below the bundle of His. QRS is wide and bizarre because ventricular depolarization spreads slowly through muscle rather than fast-conducting Purkinje fibers.
• Conduction system disorders — SA node dysfunction (sick sinus syndrome, sinus bradycardia) or AV nodal/infranodal block (1st, 2nd, 3rd degree).

By mechanism:

• Abnormal automaticity — a cell outside the SA node fires spontaneously (ectopic foci in VT, accelerated junctional rhythm).
• Re-entry — an impulse circles repeatedly through a closed loop of conductive tissue (SVT, AF, atrial flutter, most VTs in structural heart disease).
• Triggered activity — afterdepolarizations following a normal action potential (torsades de pointes, digoxin toxicity arrhythmias).

Robust EKG interpretation is the foundation of arrhythmia recognition. For a systematic approach to reading a rhythm strip, see the EKG interpretation cheat sheet.

Supraventricular tachycardias

SVT (paroxysmal supraventricular tachycardia)

Paroxysmal supraventricular tachycardia (PSVT) is the most common sustained tachyarrhythmia in patients without structural heart disease. Most cases result from AV nodal re-entry (AVNRT) — a re-entry circuit confined to or near the AV node — or from an accessory pathway (AVRT, as in Wolff-Parkinson-White syndrome). The atrial rate is 150–250 bpm with narrow QRS complexes (unless aberrant conduction is present). P waves are buried in the T wave or just after the QRS (retrograde conduction), making them invisible on a standard 12-lead in many cases.

Clinical presentation: Sudden-onset palpitations, lightheadedness, chest discomfort, and dyspnea. The episode stops as abruptly as it starts — this hallmark distinguishes PSVT from sinus tachycardia.

Nursing management:

1. Establish IV access and apply continuous telemetry monitoring.
2. Instruct the patient to perform a Valsalva maneuver (bear down, cough) or apply carotid sinus massage (contraindicated in carotid bruit or CVA history). Vagal stimulation increases vagal tone and may terminate AVNRT.
3. If vagal maneuvers fail, administer adenosine 6 mg rapid IV push followed immediately by a 20 mL saline flush through the most proximal large vein available. Adenosine has a half-life of under 10 seconds — injection must be fast.
4. If 6 mg fails, repeat with adenosine 12 mg (may repeat once more at 12 mg).
5. Have the crash cart available. Adenosine can cause a transient complete heart block, bronchospasm, and a brief period of asystole — warn the patient and document the rhythm strip during administration.
6. For hemodynamically unstable SVT (hypotension, chest pain, altered mental status), synchronized cardioversion is indicated over medication trials.
7. For recurrent SVT in Wolff-Parkinson-White: avoid AV nodal blockers (adenosine, beta blockers, verapamil, digoxin) if the patient is in pre-excited AF — these can paradoxically accelerate accessory pathway conduction and precipitate ventricular fibrillation.

Atrial flutter

Atrial flutter is a macro-re-entry circuit typically in the right atrium. The atrial rate is 250–350 bpm, producing the characteristic sawtooth flutter waves (F waves) most visible in leads II, III, aVF, and V1. The AV node cannot conduct each atrial impulse, creating physiologic block — typically 2:1, 3:1, or 4:1. The clinical clue: a regular ventricular rate of exactly 150 bpm should raise immediate suspicion for atrial flutter with 2:1 block, even when sawtooth waves are not immediately obvious.

Management priorities mirror AF: rate control (diltiazem, beta blockers), anticoagulation following the same 48-hour rule as AF, and cardioversion or ablation for rhythm control. Atrial flutter is more reliably converted by electrical cardioversion than AF and is highly amenable to catheter ablation. For the shared anticoagulation logic and cardioversion principles, see the atrial fibrillation nursing article.

Ventricular arrhythmias

Ventricular tachycardia

Ventricular tachycardia (VT) is a series of three or more consecutive ventricular beats at a rate of 100 bpm or faster, arising from a ventricular ectopic focus or re-entry circuit below the bundle of His. QRS complexes are wide (≥0.12 s) and bizarre.

Classification dimensions:

Monomorphic VT most commonly results from re-entry around a prior myocardial infarction scar. AV dissociation — P waves marching independently from the QRS — is diagnostic when present. Capture beats (a normally conducted P wave briefly depolarizes the ventricle, producing a narrow QRS amid the wide complexes) and fusion beats (partial ventricular capture producing a hybrid QRS morphology) are also diagnostic features.

Pulsed monomorphic VT with a pulse:

• Assess hemodynamic stability. If the patient is stable (no hypotension, chest pain, or altered consciousness): administer amiodarone 150 mg IV over 10 minutes, followed by 1 mg/min infusion for 6 hours, then 0.5 mg/min.
• If unstable: prepare for immediate synchronized cardioversion starting at 100 J (biphasic).
• Correct electrolyte imbalances (hypokalemia and hypomagnesemia are common precipitants).

Pulseless VT:

• Treat identically to ventricular fibrillation: immediate unsynchronized defibrillation, CPR, epinephrine, and amiodarone per ACLS protocol. There is no time to deliver synchronized shocks when no pulse is present.

Ventricular fibrillation

Ventricular fibrillation (VFib) is the most immediately lethal cardiac arrhythmia. There are no organized QRS complexes — only chaotic, irregular electrical activity with no effective mechanical contraction and no cardiac output. The patient is unconscious and pulseless within seconds.

EKG appearance: Coarse VFib shows large, irregular undulations. Fine VFib shows small-amplitude oscillations that can be mistaken for asystole — if uncertain on a single lead, verify on a second lead before withholding defibrillation.

Immediate management:

1. Call for help and confirm pulselessness — begin CPR immediately.
2. Apply defibrillator pads. Shock immediately — unsynchronized defibrillation at 200 J biphasic (follow device manufacturer guidance).
3. Resume CPR for 2 minutes after each shock before rhythm check.
4. Establish IV/IO access during CPR.
5. Epinephrine 1 mg IV/IO every 3–5 minutes.
6. After the third shock, administer amiodarone 300 mg IV/IO bolus (second dose 150 mg if VFib persists).
7. Lidocaine is an alternative to amiodarone: 1–1.5 mg/kg IV first dose, then 0.5–0.75 mg/kg every 5–10 minutes (max 3 mg/kg).
8. Identify and treat reversible causes (the H’s and T’s — hypovolemia, hypoxia, hydrogen ion acidosis, hypo/hyperkalemia, hypothermia; tension pneumothorax, tamponade, toxins, thrombosis pulmonary/coronary).

Survival from VFib is directly proportional to time-to-defibrillation. Every minute without defibrillation reduces survival by approximately 7–10%. For patients who survive, therapeutic hypothermia (targeted temperature management, 32–36°C) may be indicated post-arrest to reduce neurological injury. These patients often require mechanical ventilation in the ICU setting.

Torsades de pointes

Torsades de pointes (TdP) is a form of polymorphic VT occurring in the setting of prolonged QT interval. The QRS complexes appear to rotate or “twist” around the isoelectric baseline — the hallmark feature giving the arrhythmia its French name (“twisting of the points”). TdP is triggered by early afterdepolarizations, a form of triggered automaticity promoted when the QT interval is lengthened.

Causes of QT prolongation (acquired):

• Medications: antiarrhythmics (sotalol, quinidine, procainamide), antibiotics (azithromycin, fluoroquinolones), antipsychotics (haloperidol, quetiapine), methadone
• Electrolyte disorders: hypokalemia, hypomagnesemia, hypocalcemia
• Hypothyroidism, bradycardia, intracranial events
• Congenital long QT syndrome (Romano-Ward, Jervell-Lange-Nielsen)

Normal QTc values: ≤440 ms in men, ≤460 ms in women. QTc ≥500 ms markedly increases TdP risk. Nurses must recognize prolonged QTc on telemetry before the arrhythmia occurs.

Treatment of torsades de pointes:

1. Magnesium sulfate 2 g IV over 1–2 minutes — first-line pharmacologic therapy regardless of serum magnesium level. Magnesium suppresses early afterdepolarizations by blocking calcium influx. Follow with an infusion of 1–2 g/hr if TdP recurs.
2. Discontinue all QT-prolonging medications immediately.
3. Correct electrolytes: maintain potassium 4.5–5.0 mEq/L and replete magnesium to normalize the QT.
4. Overdrive pacing (transvenous or transcutaneous) at 90–110 bpm shortens the QT by increasing heart rate — indicated for bradycardia-associated TdP or TdP refractory to magnesium.
5. If TdP degenerates into pulseless VFib: defibrillate immediately.
6. Isoproterenol infusion (increases heart rate, shortens QT) may be used as a bridge to pacing in acquired TdP.

Bradyarrhythmias

Sinus bradycardia

Sinus bradycardia is a sinus rhythm at a rate below 60 bpm. It is normal in well-conditioned athletes and during sleep. Pathological causes include inferior myocardial infarction (right coronary artery supplies the SA node in 60% of people), hypothyroidism, increased vagal tone, and medications (beta blockers, calcium channel blockers, digoxin, amiodarone).

When treatment is needed: Bradycardia causing symptoms — hypotension, syncope, altered consciousness, chest pain, or acute heart failure. Asymptomatic sinus bradycardia in an athlete requires no treatment.

Management:

• Atropine 0.5 mg IV — blocks vagal inhibition of the SA node. May repeat every 3–5 minutes to a maximum dose of 3 mg. Doses below 0.5 mg can paradoxically worsen bradycardia (partial vagolytic effect).
• If atropine fails: transcutaneous pacing while preparing transvenous access.
• Dopamine 2–10 mcg/kg/min or epinephrine 2–10 mcg/min as a bridge.
• Treat reversible causes: reverse offending medications, correct hypothyroidism, replete electrolytes.

Heart blocks

Heart blocks are disorders of AV conduction. A thorough review of first-degree, second-degree (Mobitz I and Mobitz II), and third-degree heart block is available in the heart block poem article, which also covers clinical mnemonics for distinguishing Wenckebach from Mobitz II.

Key points for NCLEX:

• First-degree AV block: PR >0.20 s. Every P wave conducts. Usually no treatment required — monitor and identify cause.
• Mobitz I (Wenckebach): Progressive PR lengthening until a QRS is dropped, then the cycle resets. Generally benign — most commonly inferior MI, AV node medication effect, or increased vagal tone. Atropine if symptomatic.
• Mobitz II: Constant PR interval with intermittent, unpredictable dropped QRS complexes. The block is infranodal (His bundle or bundle branches). Atropine is often ineffective. Mobitz II can deteriorate abruptly to complete heart block — transvenous pacing is usually indicated.
• Third-degree (complete) heart block: No relationship between P waves and QRS. The ventricles beat at an escape rate (20–40 bpm ventricular escape; 40–60 bpm junctional escape). This is hemodynamically critical — requires transcutaneous pacing immediately and transvenous pacing followed by permanent pacemaker implantation.

Sepsis and hypertensive emergencies are two systemic conditions that can precipitate or unmask conduction disorders through ischemia, metabolic derangement, or direct myocardial injury.

Cardioversion vs defibrillation

These two procedures both deliver electrical energy to the heart but differ in timing, indication, and energy delivery.

Critical NCLEX distinction: A patient in VFib needs unsynchronized defibrillation. If a nurse selects “synchronized” mode for VFib, the defibrillator cannot identify an R wave and the shock will not be delivered — resulting in a fatal delay. Always verify the mode before charging.

Elective cardioversion nursing checklist:

• Confirm NPO status (typically ≥6 hours solids, ≥2 hours clear liquids)
• Verify IV access and patent line
• Confirm consent obtained
• Confirm anticoagulation compliance (AF/flutter)
• Remove supplemental oxygen during shock delivery (fire hazard)
• Have airway equipment and resuscitation medications at bedside
• Administer sedation per order; monitor SpO2 and respiratory rate
• Document pre- and post-cardioversion rhythm strip, vital signs, energy levels used

Pacemaker nursing

Types and terminology

Pacemakers deliver an electrical stimulus to the myocardium when the heart’s intrinsic rate falls below the programmed threshold.

Temporary pacemakers:

• Transcutaneous pacing (TCP) — external pads applied to the anterior and posterior chest wall. Used in emergencies (symptomatic bradycardia, complete heart block). Rate and output (mA) are dialed in on the defibrillator/pacer unit. TCP is painful — IV analgesia and sedation are essential for conscious patients.
• Transvenous pacing — a pacing lead is threaded via central venous access (usually right internal jugular or subclavian) to the right ventricle. More reliable than TCP and better tolerated; used as a bridge to permanent pacemaker.

Permanent pacemakers:

• Subcutaneously implanted pulse generator (pocket in the chest wall) connected to leads in the right atrium, right ventricle, or both. The five-letter NASPE/BPEG code describes pacemaker programming (e.g., “DDD” = dual-chamber sensing and pacing with tracking).
• Cardiac resynchronization therapy (CRT/biventricular pacing): simultaneous left and right ventricular pacing to coordinate contraction in heart failure with left bundle branch block.
• Implantable cardioverter-defibrillator (ICD): combines pacemaker function with the ability to detect and shock VT/VFib. Indicated after cardiac arrest, sustained VT, or severely reduced ejection fraction (EF ≤35%).

Pacemaker malfunctions

Magnet response

Placing a ring magnet over a pacemaker converts it to asynchronous mode (paces at a fixed rate regardless of intrinsic rhythm). This is used during surgical/procedural electromagnetic interference to prevent oversensing-induced inhibition. Conversely, placing a magnet over an ICD temporarily disables tachyarrhythmia detection without affecting pacing — useful when an ICD is delivering inappropriate shocks.

Post-implant nursing care and patient education

Immediate post-implant:

• Arm sling on the ipsilateral arm for 24 hours; limit arm elevation above the shoulder for 4–6 weeks (prevents lead dislodgement).
• Incision care: keep dry for 48–72 hours; monitor for hematoma, erythema, or pocket swelling.
• Telemetry monitoring for 24 hours post-implant — detect early lead displacement (failure to capture/pace).
• Post-procedure chest X-ray to confirm lead position and exclude pneumothorax.

Ongoing patient education:

• Carry pacemaker ID card at all times; alert healthcare providers before any procedure.
• MRI: modern MRI-conditional pacemakers allow imaging with specific protocols — the patient should know the pacemaker model. Never assume MRI is safe without confirming MRI-conditional status.
• Cell phones: hold on the contralateral side; avoid placing phone directly over the device.
• Airport security/metal detectors: will set off detectors; use pacemaker card; the brief detector exposure is not harmful.
• Household appliances (microwave ovens, electric shavers, small power tools): generally safe with modern pacemakers — current guidance from major manufacturers does not restrict routine use of properly functioning household appliances.
• High-powered electromagnetic sources to avoid: arc welding equipment, large industrial generators, MRI scanners without conditional clearance, diathermy/electrocautery (surgical team must use bipolar mode; program pacemaker to asynchronous before major procedures).
• ICD patients: counsel on driving restrictions (typically 3–6 months post-implant or post-shock per state regulations), and what to do if a shock fires (sit down, call provider; call 911 if a second shock fires within minutes or if symptoms persist).

Antiarrhythmic medications

See the drug classifications nursing article for a broader overview of antiarrhythmic drug class pharmacology in the context of nursing pharmacology coursework.

ACLS context: shockable vs non-shockable rhythms

The most critical ACLS decision during cardiac arrest is determining whether the rhythm is shockable or non-shockable — because the interventions differ completely.

PEA (pulseless electrical activity): Organized EKG activity (sinus rhythm, bradycardia, IVCD) with no palpable pulse. The rhythm appears perfusing — the absence of a pulse is the critical finding. PEA is always secondary to a reversible cause. Systematic search for H’s and T’s (hypovolemia, hypoxia, hydrogen ion/acidosis, hypo/hyperkalemia, hypothermia; tamponade, tension pneumothorax, toxins, thrombosis) drives treatment.

Asystole: Flat line with no electrical or mechanical activity. Confirm in at least two leads (coarse VFib can mimic asystole). CPR and epinephrine are the only interventions — atropine is no longer included in current ACLS guidelines for asystole/PEA.

NCLEX tips

1. Ventricular rate of exactly 150 bpm in a regular tachycardia should immediately raise suspicion for atrial flutter with 2:1 block — not sinus tachycardia.

2. Adenosine must be given as a rapid IV push (followed immediately by a fast saline flush) through the largest, most proximal vein available. A slow push fails — the drug is inactivated before reaching the heart.

3. VFib and pulseless VT are the only cardiac arrest rhythms that respond to defibrillation. PEA and asystole require CPR and epinephrine — shocking them does nothing.

4. Torsades de pointes = first-line magnesium sulfate, regardless of the serum magnesium level. Also stop all QT-prolonging drugs.

5. Amiodarone toxicity targets: lungs (pulmonary fibrosis), liver (hepatotoxicity), thyroid (hypo- or hyperthyroidism), eyes (corneal microdeposits, optic neuropathy), skin (photosensitivity, blue-gray discoloration). Monitor all five systems.

6. Digoxin toxicity is precipitated by hypokalemia. Classic signs: bradycardia, heart block, yellow-green vision (xanthopsia), nausea and vomiting. Low potassium increases myocardial sensitivity to digoxin even at therapeutic serum levels.

7. Atropine is ineffective for Mobitz II and complete heart block — the block is infranodal (below the AV node), outside the reach of vagal blockade. Pacing is required.

8. Failure to capture vs failure to pace: Failure to capture = spikes present, no response. Failure to pace = no spikes when expected. These require different interventions (increase mA for capture; check connections/sensitivity for failure to pace).

9. Synchronized cardioversion requires a detectable R wave. Never select synchronized mode for VFib — there is no R wave, the machine cannot fire, and the patient deteriorates while the nurse waits for a shock that never comes.

10. Adenosine is contraindicated in WPW with pre-excited AF. Blocking the AV node in WPW forces conduction down the accessory pathway at maximum speed, which can precipitate VFib.

11. A paced rhythm on a 12-lead shows wide QRS complexes with LBBB morphology — this is expected because ventricular pacing from the right ventricular apex depolarizes the left ventricle late. Do not confuse this with pathological VT; look for the pacemaker spike before the QRS.

12. Magnesium sulfate nursing antidote: calcium gluconate 1 g IV reverses magnesium toxicity. Always have it at the bedside. Signs of toxicity: loss of deep tendon reflexes (earliest sign), respiratory depression, hypotension, cardiac arrest.

13. Post-cardioversion nursing: Assess airway, breathing, and circulation first after sedation/cardioversion. Document the post-procedure rhythm. Maintain NPO until fully alert. Monitor for skin burns at pad sites.

14. R-on-T phenomenon: A premature ventricular contraction that falls on the T wave of the preceding beat (the vulnerable period) can trigger VFib. This is why synchronized cardioversion avoids the T wave and why undersensing (pacemaker firing randomly in the cycle) carries clinical risk.

15. Epinephrine is used in both shockable and non-shockable ACLS algorithms, but timing differs: in VFib/pulseless VT, give after the first or second shock; in PEA/asystole, give as soon as IV/IO access is established.

16. The QTc — not the raw QT — is the relevant interval. QT naturally shortens with faster heart rates; QTc corrects for rate. Bazett’s formula: QTc = QT ÷ √(R-R interval in seconds). Normal: ≤440 ms (men) / ≤460 ms (women). QTc ≥500 ms is high-risk for torsades.

Practice NCLEX questions

Question 1

A nurse is caring for a patient with a new permanent pacemaker implanted three hours ago for complete heart block. The patient’s telemetry now shows pacemaker spikes occurring regularly but without subsequent QRS complexes. Which action is the priority?

A. Administer atropine 0.5 mg IV per standing order
B. Increase the pacemaker output (mA) per protocol and notify the cardiologist
C. Place the patient in Trendelenburg position
D. Reassure the patient that this pattern is expected post-implant

Answer: B

Rationale: The rhythm description — pacemaker spikes without QRS response — is failure to capture. The most common cause in the immediate post-implant period is inadequate output relative to the pacing threshold, or early lead displacement. The intervention is to increase the output (mA). Atropine (option A) would address the intrinsic rate but does nothing for the pacemaker’s inability to stimulate the myocardium. Trendelenburg position (option C) is irrelevant. Failure to capture is never expected or normal in the post-implant period (option D).

Question 2

A nurse is preparing to administer adenosine to a patient in PSVT. Which action is most important before giving the medication?

A. Obtain a 12-lead EKG immediately after injection
B. Start a peripheral IV in the antecubital fossa and confirm patency
C. Administer with a slow push over 3–5 minutes to avoid hypotension
D. Pre-medicate with diphenhydramine to prevent flushing

Answer: B

Rationale: Adenosine must be given via rapid IV push through a large, proximal vein (antecubital or larger). Its half-life is under 10 seconds; a distal IV site allows the drug to be inactivated before reaching the AV node. A slow push (option C) is incorrect — adenosine given slowly is ineffective. A 12-lead EKG after injection (option A) is useful for documentation but is secondary. Diphenhydramine (option D) has no role in adenosine administration.

Question 3

A patient on telemetry develops a wide-complex tachycardia at 190 bpm. The QRS complexes vary in amplitude and appear to twist around the isoelectric baseline. The patient’s QTc was 530 ms on the morning EKG. Which medication does the nurse anticipate administering first?

A. Adenosine 6 mg rapid IV push
B. Amiodarone 150 mg IV over 10 minutes
C. Magnesium sulfate 2 g IV over 1–2 minutes
D. Lidocaine 1.5 mg/kg IV bolus

Answer: C

Rationale: The description — wide-complex tachycardia with QRS amplitude twisting around the baseline in the context of prolonged QTc (530 ms) — is torsades de pointes. First-line pharmacologic treatment is magnesium sulfate 2 g IV regardless of serum magnesium level. Adenosine (option A) is only effective for AV nodal re-entrant tachycardias (SVT) and is ineffective for ventricular arrhythmias. Amiodarone (option B) can actually prolong the QT interval further, potentially worsening torsades. Lidocaine (option D) is used for VFib and monomorphic VT, not torsades.