NSG210 September 30 Lecture: Management of Patients With Arrhythmias and Conduction Problems

Sources: Hinkle & Cheever, Brunner & Suddarth’s Textbook of Medical-Surgical Nursing, Ch. 22 “Management of Patients with Arrhythmias and Conduction Problems” (textbooks/HINKLE_MS_CH22.pdf), and the lecture deck “Management of Patients With Dysrhythmias and Conduction Problems” (raw/nsg210_wk04_Dyshythmias.pptx, text extract at raw/nsg210_wk04_Dyshythmias.md).

Placement: delivered September 30 as part of the “Alterations in Perfusion” lecture (calendar Week 06, Sep 28-Oct 2). This material is on Exam 2 (Oct 12; content cutoff October 7). This page is labeled by date. The reading list assigns Ch. 23 for arrhythmias, but Ch. 22 is the arrhythmia chapter in the 15th edition (see nsg210-textbook-chapter-crosswalk), and the “wk04” raw filename prefix only reflects when the file was added to raw/.

Relationship to Week 06: nsg210-week-06-summary already summarizes the lecture slides in prose (conduction, ECG components, sinus/atrial/ventricular rhythms, first- and third-degree block, nursing process, cardioversion, pacemakers, ICDs). This page is organized around the textbook chapter, uses tables for rhythm criteria, and marks content that is in Ch. 22 but not on the slides with “(chapter only)”. Slide-only emphasis is noted where it exists.

Lecture Objectives

From the slide deck:

1. Correlate the components of the normal ECG with the physiologic events of the heart.
2. Analyze the elements of an ECG rhythm strip.
3. Identify the ECG criteria, causes, and management of dysrhythmias and conduction disturbances.
4. Describe the methods used to diagnose and treat dysrhythmias and the nursing implications.

The chapter adds three more: compare pacemaker types, uses, and complications; describe key points of defibrillator use and ICD types; and describe nursing management of patients with implantable cardiac devices.

Key Terms

• Arrhythmia (dysrhythmia) - disorder of impulse formation, conduction, or both, altering heart rate, rhythm, or both
• Automaticity - ability of cardiac cells to initiate an impulse
• Conduction - transmission of the impulse from cell to cell
• Chronotropy / dromotropy / inotropy - rate of impulse formation / conduction velocity / force of contraction
• Depolarization - cells become more positively charged (electrical stimulation; mechanical result is systole)
• Repolarization - cells return to negative resting state (electrical relaxation; mechanical result is diastole)
• Paroxysmal - sudden onset, spontaneous termination, may recur
• Artifact - distorted, extraneous ECG waveforms (often from poor electrode contact)
• Cardioversion - shock synchronized to the patient’s QRS
• Defibrillation - shock not synchronized to the QRS
• Ablation - purposeful destruction of heart muscle cells to eliminate an arrhythmia
• Cardiac resynchronization therapy (CRT) - biventricular pacing for heart failure conduction delays
• ICD - implanted device that detects and treats tachyarrhythmias

Autonomic Influence on Rate (chapter only)

Sympathetic (adrenergic) stimulation produces positive chronotropy, dromotropy, and inotropy and constricts peripheral vessels (raises BP). Parasympathetic stimulation does the opposite for rate, AV conduction, and atrial contraction force. Clinical tie-in: exercise, anxiety, fever, and catecholamines (dopamine, aminophylline, dobutamine) increase arrhythmia incidence; rest, anxiety reduction, and beta-blockers decrease it. This is why “reduce anxiety” is a real arrhythmia intervention, not just comfort care.

Obtaining the ECG

Electrode prep matters: wash skin with soap and water (alcohol increases impedance), gently abrade with dry gauze, and clip chest hair if needed. Poor adhesion produces artifact.

Monitoring modes: standard 12-lead at the bedside; hardwire continuous monitoring (ICU); telemetry (transmits by radio to a central station); Holter or patch monitor (worn, analyzed later); loop recorder (implanted or wrist-worn, records on demand when symptomatic); electrophysiology study (intracardiac ECG, invasive).

A standard 12-lead uses 10 electrodes (4 limb, 6 chest). Limb leads give I, II, III, aVR, aVL, aVF; chest leads give V1-V6. Chest placement:

A 12-lead mainly reflects the left ventricle; right-sided precordial leads are needed for suspected right ventricular damage. A lead is “like a camera eye,” so a waveform change can mean a change in the impulse or a change in the lead.

ECG Components and Normal Values

Graph paper: time on the horizontal axis, amplitude on the vertical. Each small box is 0.04 seconds; each large box is 0.20 seconds and 5 mm (0.5 mV). Upward is a positive deflection, downward is negative.

Wave labeling (chapter only): lowercase q, r, s for waves under 5 mm; capitals for over 5 mm. Atrial repolarization is hidden inside the QRS.

Safety point: many common hospital medications prolong the QT, which puts the patient at risk for torsades de pointes.

Analyzing a Rhythm Strip

Heart rate:

• Regular rhythm: 1,500 divided by the number of small boxes in one RR interval (10 boxes is 150 bpm; 25 boxes is 60 bpm; 17.5 boxes is about 86 bpm).
• Irregular rhythm: count RR intervals in a 6-second strip and multiply by 10. Count intervals, not QRS complexes, to avoid overestimating. The top of the paper is usually marked every 3 seconds (15 large boxes).
• Use the PP interval the same way for atrial rate.

Rhythm: intervals that are the same, or differ by less than 0.8 seconds across the strip, are regular.

Systematic 12-step analysis (Chart 22-1): ventricular rate, ventricular rhythm, QRS duration, QRS duration consistency, QRS shape, P waves (a P before every QRS?), P-wave shape and consistency, atrial rate, atrial rhythm, each PR interval, PR consistency, P:QRS ratio.

Treat the patient, not the monitor: treatment is based on the clinical evaluation, cause, and hemodynamic effect, not the ECG alone.

Alarm fatigue (chapter only): frequent clinically insignificant alarms lead nurses to ignore or silence them. The nurse should individualize alarm limits and confirm with the provider that continuous monitoring is still needed.

Rhythm Criteria Quick Reference

Arrhythmias are named by site of origin and mechanism. Sinus rhythms start in the SA node, atrial rhythms in atrial foci, junctional rhythms in AV nodal tissue, ventricular rhythms in ventricular foci.

Sinus Node Arrhythmias

Sinus bradycardia. Causes: lower metabolic need (sleep, athletes, hypothyroidism), vagal stimulation (vomiting, suctioning, severe pain, bearing down), medications (calcium channel blockers, amiodarone, beta-blockers), sinus node dysfunction (formerly sick sinus syndrome), increased ICP, CAD especially inferior wall MI. Unstable symptomatic bradycardia is frequently due to hypoxemia. Tachy-brady syndrome is alternating bradycardia and tachycardia. First steps: prevent further vagal stimulation, hold the causative medication. If unstable (altered mental status, chest discomfort, hypotension): atropine 0.5 mg rapid IV, repeated every 3-5 minutes to a 3 mg maximum; if unresponsive, transcutaneous pacing, or dopamine, isoproterenol, or epinephrine.

Sinus tachycardia. Causes: physiologic or psychological stress (blood loss, anemia, shock, hypo- or hypervolemia, HF, pain, fever, exercise, anxiety), sympathomimetic meds (catecholamines, aminophylline, atropine), stimulants (caffeine, nicotine), illicit drugs (amphetamines, cocaine, ecstasy), inappropriate sinus tachycardia, and POTS (tachycardia without hypotension, presyncope on posture change). Nonparoxysmal: it does not start or stop suddenly. Faster rate shortens diastolic filling, which can drop cardiac output and lead to syncope, hypotension, or pulmonary edema. Treatment: find and remove the cause; vagal maneuvers (carotid massage by a physician, gagging, bearing down, forceful coughing, cold wet towel on face); adenosine; synchronized cardioversion if unstable and the above fail; IV beta-blockers or calcium channel blockers if stable; ablation for persistent inappropriate sinus tachycardia; fluids and sodium for POTS.

Sinus arrhythmia. Rate rises with inspiration and falls with expiration. No hemodynamic effect; not treated.

Atrial Arrhythmias

Premature atrial complex (PAC). Causes: caffeine, alcohol, nicotine, stretched atrium (hypervolemia), anxiety, hypokalemia, hypermetabolic states (pregnancy), atrial ischemia. Patient may say “my heart skipped a beat”; a pulse deficit may be present. Infrequent PACs need no treatment. More than six per minute may herald worsening disease or atrial fibrillation; treat the cause.

Atrial fibrillation. The most common sustained arrhythmia (2.7-6.1 million Americans). Hyperactive ganglia of the intrinsic cardiac autonomic nervous system fire impulses from the pulmonary veins into the atria.

Risk factors (Chart 22-2): increasing age, hypertension, diabetes, obesity, valvular heart disease, heart failure, obstructive sleep apnea, alcohol abuse, hyperthyroidism, MI, smoking, exercise, cardiothoracic surgery, increased pulse pressure, European ancestry, family history.

Classification (Chart 22-3; “chronic” is no longer used):

Why it matters: loss of AV synchrony means loss of atrial kick (25-30 percent of cardiac output); a fast irregular ventricular response shortens filling and coronary perfusion time (HF symptoms, ischemia, angina); sustained ventricular rates over 80 can eventually cause mitral dysfunction and dilated cardiomyopathy; stasis forms thrombi, mostly in the left atrial appendage, raising stroke risk. Assess for a pulse deficit (apical minus radial).

Diagnostics: 12-lead ECG; TEE for valve disease, chamber size, and left atrial thrombus; thyroid, renal, and hepatic labs; chest x-ray, stress test, Holter or event monitor, EPS as needed.

Stroke risk: CHA2DS2-VASc (Chart 22-4):

Antithrombotic choice (nonvalvular AF): score 0, may choose no therapy; score 1, no therapy, oral anticoagulant, or aspirin; score 2 or more in men or 3 or more in women, warfarin, a direct thrombin inhibitor (dabigatran), or a Factor Xa inhibitor (rivaroxaban, apixaban, edoxaban). Mechanical valve: warfarin. Short-term bridging: IV heparin or LMWH until INR is therapeutic (2.0-3.0). Warfarin needs weekly INR during initiation; DOACs and Xa inhibitors need baseline Hgb, Hct, liver and renal function, but avoid frequent INR checks and have fewer interactions.

Rate control: target resting HR under 80 using a beta-blocker (Class II) or non-dihydropyridine calcium channel blocker (Class IV).

Rhythm control: AF lasting 48 hours or longer needs anticoagulation before any cardioversion attempt, or a TEE to rule out atrial thrombus. Pharmacologic conversion: flecainide, dofetilide, propafenone, amiodarone, IV ibutilide (most effective within 7 days of onset). Dofetilide requires hospitalization to monitor QT and renal function. “Pill in the pocket” is flecainide self-administered at home for recurrent AF. Preoperative beta-blockers and statins reduce post-cardiac-surgery AF. Electrical cardioversion for unstable AF unresponsive to meds; antithrombotic therapy continues at least 4 weeks afterward because atrial function stays impaired.

Rhythm therapies (chapter only):

• Catheter ablation - radiofrequency (heat) or cryoablation isolates the pulmonary veins. Done with moderate sedation and IV heparin. Risks: pericardial effusion or tamponade, phrenic nerve injury, stroke, hematoma, retroperitoneal bleeding, pulmonary vein stenosis, atrioesophageal fistula. Post-care is like cardiac cath: monitor for arrhythmias, stroke signs, access site complications; relieve back pain from prolonged bedrest with rolled towels under knees and waist.
• Maze - open-heart atrial incisions create scar that blocks reentry; reserved for patients already having cardiac surgery; may need a pacemaker afterward. Mini-maze uses small intercostal incisions and video guidance, avoiding sternotomy and bypass.
• Convergent procedure - hybrid surgeon plus electrophysiologist ablation through small abdominal incisions; lower recurrence but more 30-day complications; about 3-day stay; mild chest pain (acetaminophen) and possible dyspnea from phrenic nerve irritation.
• Left atrial appendage occlusion (WATCHMAN) - parachute device seals the LAA via femoral catheter; alternative to long-term anticoagulation for CHA2DS2-VASc 1 or higher. Post-procedure: aspirin plus warfarin, TEE at about 6 weeks, then switch warfarin to clopidogrel, stop clopidogrel at 6 months, aspirin indefinitely.

Wolff-Parkinson-White syndrome (chapter only). Suspect an accessory pathway when AF has a wide QRS and a very fast, irregular ventricular rate. Avoid AV nodal blockers (digoxin, diltiazem, verapamil), which can speed the ventricular rate. Unstable: electrical cardioversion. Stable: procainamide, propafenone, flecainide, or amiodarone. Long-term: ablation.

Atrial flutter (chapter only). A conduction defect in the atrium produces rapid, regular saw-tooth F waves. The AV node cannot conduct every impulse, which creates a protective “therapeutic block”; if all 250-400 impulses were conducted, the result would be VF. Can cause chest pain, dyspnea, and hypotension. Vagal maneuvers or adenosine (rapid IV push, 20 mL saline flush, raise the arm) slow AV conduction and reveal flutter waves. Otherwise managed like AF (antithrombotics, rate and rhythm control); cardioversion is often successful.

Junctional Arrhythmias (chapter only)

Originate in AV nodal tissue. Only junctional rhythm is mentioned by name on the slides.

• Premature junctional complex - like a PAC but the P wave is absent, after the QRS, or before it with PR under 0.12. Causes: digitalis toxicity, HF, CAD. Rarely symptomatic.
• Junctional (idionodal) rhythm - the AV node takes over as pacemaker when the sinus node slows or the impulse is blocked. Rate 40-60; P waves often inverted in lead II. If cardiac output drops, treat like sinus bradycardia; may need pacing.
• Nonparoxysmal junctional tachycardia - same rhythm at 70-120; usually not hemodynamically significant but may signal digitalis toxicity, ischemia, hypokalemia, or COPD.
• AVNRT (paroxysmal atrial tachycardia, PSVT) - a reentry loop in the AV node fires rapidly. Associated with caffeine, nicotine, hypoxemia, stress; more common in females without structural disease. Usually just palpitations; a fast rate can cause chest pain, dyspnea, hypotension, syncope. Catheter ablation is the treatment of choice long-term. Acute: vagal maneuvers (carotid massage contraindicated in carotid disease), then adenosine (up to three doses), then IV verapamil, beta-blocker, or digoxin; cardioversion if unstable.
• SVT or PSVT is a placeholder label when P waves cannot be identified; it only means “not VT” and could be AF, flutter, or AVNRT.

Tachycardia vs. SVT vs. VT

“Tachycardia” is not a diagnosis by itself. It only means a heart rate over 100. The rhythm name says where the fast impulses start:

• Sinus tachycardia - the SA node itself is firing fast, usually because the body needs it to (fever, pain, hypovolemia, anxiety, anemia).
• Supraventricular tachycardia (SVT) - “supra” means above the ventricles. The fast rhythm starts in the atria or the AV node but not in the SA node. SVT is an umbrella term; the chapter uses it when P waves cannot be seen and the rhythm could be AF, atrial flutter, or AVNRT. PSVT is SVT that starts and stops suddenly (paroxysmal).
• Ventricular tachycardia (VT) - starts in the ventricles.

Sinus tachycardia is technically above the ventricles too, but in practice “SVT” means a fast rhythm that is not sinus. The clinically important distinctions:

Why it matters for nursing:

• Sinus tachycardia is a symptom. Slowing it with drugs without treating the cause (bleeding, fever, pain, dehydration) hides the problem. The bedside question is “why is this patient tachycardic?”
• SVT is the rhythm itself causing the problem. The reentry loop has to be broken, which is why vagal maneuvers and adenosine work: they slow AV node conduction. Adenosine is given as a rapid IV push with a 20 mL saline flush and the arm raised.
• A diagnostic clue: vagal maneuvers or adenosine may slow sinus tachycardia briefly, but it gradually returns. In AVNRT they often stop the rhythm abruptly. In flutter or AF they slow the ventricular rate enough to expose the flutter or fibrillatory waves.
• A wide-QRS tachycardia is treated as VT until proven otherwise, because VT can quickly become pulseless.

When Sinus Tachycardia Hides Its P Waves

No, sinus tachycardia does not become SVT when the P waves disappear. The rhythm is named by where the impulse starts, not by what is visible on the strip. As the rate rises, diastole shortens and the P wave slides back into the preceding T wave (“P on T”). The P wave is still there, and still before every QRS, just hidden. Ch. 22 notes this directly: in sinus tachycardia the P wave “may be buried in the preceding T wave.”

The problem is that at that point the strip alone may not tell you which it is. The chapter’s answer is to call it SVT as a descriptive label (“not VT”) until the underlying rhythm is determined, then rename it once you know.

How to tell them apart:

The chapter supports using vagal maneuvers and adenosine partly as a diagnostic step: they slow AV node conduction “to allow visualization of the P waves.” Whatever shows up once the rate slows tells you the real rhythm.

Bottom line for the bedside: if you cannot see P waves, do not assume. Look at the trend, get a 12-lead, look for a cause, and report it as a narrow-complex tachycardia (or SVT) while the rhythm is being identified.

Ventricular Arrhythmias

Premature ventricular complex (PVC). Causes: caffeine, nicotine, alcohol, ischemia or infarction, increased cardiac workload (HF, tachycardia), digitalis toxicity, hypoxia, acidosis, electrolyte imbalance especially hypokalemia. Patterns (chapter only): bigeminy (every other beat), trigeminy (every third), quadrigeminy (every fourth); unifocal if all PVCs look alike, multifocal if two or more shapes. PVCs are common and increase with age; they are not considered a warning of impending VT, but are associated with adverse outcomes, so look for underlying causes. Frequent persistent PVCs may be treated with amiodarone or beta-blockers.

Slide review question: the characteristic of PVCs is an irregular rhythm due to early QRS (not a regular rhythm, not a rate of 100-200, not a rate over 300, not absent QRS).

Ventricular tachycardia. Three or more PVCs in a row at over 100 bpm. Highest risk with large MIs and low ejection fraction. Management depends on monomorphic versus polymorphic, a prolonged QT before onset, comorbidities, and heart function. Stable: continue assessment, 12-lead ECG; antiarrhythmics (procainamide, amiodarone, sotalol, lidocaine), antitachycardia pacing, or cardioversion. Symptomatic monomorphic VT: cardioversion. Pulseless VT: treat like VF, immediate defibrillation. Long-term: ICD if EF under 35 percent; antiarrhythmics if over 35 percent.

Torsades de pointes (chapter only). Polymorphic VT preceded by a prolonged QT. Causes: CNS disease, ciprofloxacin, erythromycin, haloperidol, lithium, methadone, low potassium, calcium, or magnesium, congenital long QT. Likely to deteriorate to pulselessness; treat immediately with IV magnesium and electrolyte correction, plus isoproterenol or pacing if bradycardic.

Ventricular fibrillation. Most common rhythm in cardiac arrest; most often from CAD and acute MI. Also untreated VT, cardiomyopathy, valve disease, proarrhythmic drugs, acid-base or electrolyte problems, electrical shock, and Brugada syndrome (structurally normal heart, family history of sudden death, frequently Asian descent). No heartbeat, pulse, or respirations. Immediate bystander CPR and early defibrillation; amiodarone and epinephrine for refractory VF.

Idioventricular (ventricular escape) rhythm (chapter only). Purkinje fibers take over when higher pacemakers fail. Often causes loss of consciousness; treat like asystole or PEA if in arrest, like bradycardia if not (epinephrine, atropine, vasopressors, transcutaneous pacing).

Ventricular asystole. Flatline confirmed in two leads. High-quality CPR with minimal interruptions, then intubation and IV access, while rapidly assessing the Hs and Ts: hypoxia, hypovolemia, hydrogen ion (acidosis), hypo- or hyperglycemia, hypo- or hyperkalemia, hypothermia, trauma, toxins, tamponade, tension pneumothorax, thrombus (coronary or pulmonary).

Conduction Abnormalities (AV Blocks)

Identify the underlying rhythm first, then check the PR interval. Causes: digitalis, calcium channel blockers, beta-blockers, Lyme disease, ischemia or MI, hypothyroidism, increased vagal tone (athletes, sleep, coughing, suctioning, pressure on the eyes or large vessels, anal stimulation). The same block can be stable in one patient and unstable in another, so treat the patient, not the rhythm.

Management: stable and asymptomatic, remove the cause (hold the drug). Initial treatment of choice is IV atropine, but it does not work for second-degree type II or third-degree block. If no response, advanced block, or acute MI, start transcutaneous pacing. Pulseless, treat as asystole. Persistent block, permanent pacemaker (also if the causative drug is essential).

Nursing Process: The Patient With an Arrhythmia

Assessment: history of low-output episodes (syncope, lightheadedness, dizziness, fatigue, chest discomfort, palpitations); possible causes (heart disease, COPD); all medications including OTC, herbs, and supplements; antiarrhythmic adherence and side effects (some, like digoxin, cause arrhythmias); labs for drug levels and contributors like anemia; psychosocial assessment including whether anxiety is contributing. Physical exam: level of consciousness, pale cool skin, JVD, crackles or wheezes, apical and radial pulses with any pulse deficit, S3 and S4, murmurs, BP, and pulse pressure. A declining pulse pressure means falling cardiac output. Compare findings over time, with and without the arrhythmia.

Nursing diagnoses: impaired cardiac output (inadequate filling or altered rate); anxiety (fear of unknown outcome); lack of knowledge about the arrhythmia and treatment.

Collaborative problems: cardiac arrest, heart failure, thromboembolic event (especially with AF).

Interventions:

• Maintain cardiac output - ongoing BP, pulse rate and rhythm, respirations, breath sounds; ask about lightheadedness or fainting; 12-lead and continuous ECG; keep antiarrhythmic serum levels steady; 6-minute walk test (record distance and pre/post HR); watch for QRS widening, QT prolongation, and rising rate; correct contributors (hypoxia, acid-base and electrolyte imbalance, caffeine, nonadherence).
• Reduce anxiety - stay with the patient during episodes, stay calm and reassuring (lowers sympathetic drive), encourage verbalizing fears, point out successes, help keep a diary of triggers and relieving factors.
• Educate - clarify misinformation without frightening; explain cause and treatment; why steady drug levels and blood tests matter; take pulse before each rate-altering dose and report abnormal values; link arrhythmia to cardiac output symptoms; anticoagulant teaching; recurrence prevention; emergency plan and family CPR training for lethal arrhythmias; AF patients should know embolic risk.
• Home referral usually unnecessary unless unstable, significant comorbidities, socioeconomic barriers, limited self-management, or a newly implanted device.

Expected outcomes: stable vitals and LOC with fewer episodes; reduced anxiety and confidence in emergency actions; can explain the arrhythmia, medication regimen, need for therapeutic levels, trigger avoidance, and emergency steps.

Antiarrhythmic Medications (Table 22-1)

Vaughan-Williams classification. This is the pharmacology-track entry for the week.

Also used acutely: atropine (bradycardia), adenosine (SVT, flutter diagnosis), epinephrine (arrest), magnesium (torsades), digoxin (rate control; withhold 48 hours before elective cardioversion).

Adjunct Modalities: Cardioversion and Defibrillation

Both use the same device and deliver current that depolarizes a critical mass of myocardium so the SA node can recapture control. Only biphasic defibrillators are now manufactured. Pads allow hands-off delivery and are what AEDs use.

Concept Mastery Alert: the difference is timing. Cardioversion is synchronized to the QRS; defibrillation is immediate and unsynchronized.

Safety checklist (Chart 22-5, chapter only):

• Use proper conductive medium (sheet, gel, or paste); never ultrasound gel.
• Keep pads off clothing, linens, medication patches, and out of oxygen flow.
• Place the left pad under or lateral to a large left breast.
• Paddles need 20-25 lb of pressure.
• Charge only when ready; announce “charging to (joules).”
• Call “Clear” three times: self, others (including ETT and equipment), final check.
• Record energy and resulting rhythm; resume CPR with compressions immediately; recheck rhythm after 5 cycles (about 2 minutes).
• Inspect skin for burns afterward; plug the defibrillator back in and restock.

Electrophysiology Study (chapter only)

Invasive catheter study in a cath lab with the patient lightly sedated. Uses: map impulse conduction, assess SA and AV node function, locate arrhythmogenic foci, test drug and device effectiveness, and ablate. Programmed stimulation tries to induce the arrhythmia; “inducible” means reproducible, and a later noninducible study means treatment worked. Overdrive suppression tests sinus node recovery time. Lasts about 2 hours (up to 6 with treatment). Teach the patient to lie still, report symptoms, and expect that the arrhythmia may occur and be cardioverted under controlled conditions. Post-care is like cardiac cath, with fewer vascular complications because an artery is not always used.

Pacemaker Therapy

Indications: slow impulse formation, symptomatic AV or ventricular conduction disturbances, some drug-resistant tachyarrhythmias; CRT for advanced HF.

Components: a pulse generator (sets rate in bpm, output in mA, and sensitivity in mV) and leads.

• Temporary - hospital only. Epicardial wires sutured during open-heart surgery (pulled out after a few days) or transvenous endocardial leads (femoral, subclavian, internal jugular). Generator is phone-sized and runs on a household battery; monitoring battery and function is a nursing responsibility. Pulmonary artery wedge pressure readings can dislodge PA-catheter pacing leads.
• Permanent - transvenous leads through the subclavian, axillary, or cephalic vein; generator in a pectoral subcutaneous pocket (below the clavicle in men, behind the breast in women). About 1 hour with local anesthetic and moderate sedation. Lithium battery lasts 5-15 years; the elective replacement indicator (ERI) warns months ahead; the whole generator is replaced.
• Leadless - 90 percent smaller, placed directly in the RV; fewer infections, hematomas, and lead problems, but single-chamber RV pacing only and no defibrillator.
• Transcutaneous - emergency pads on chest and back for symptomatic bradycardia with a pulse unresponsive to atropine. Painful (burning, muscle contraction): sedate and give analgesia if alert, inspect skin afterward. Not indicated for pulseless bradycardia.

NASPE-BPEG code (Chart 22-6, chapter only):

Example DVI: paces both chambers, senses the ventricle, inhibited when the ventricle beats on its own. On-demand pacing senses and responds; AOO or VOO is fixed-rate (asynchronous), and VOO may indicate battery failure. VVI loses atrial kick and can cause pacemaker syndrome (chest discomfort, dyspnea, fatigue, activity intolerance, orthostatic hypotension). AAI or DDD is preferred for sinus node dysfunction with an intact AV node; dual-chamber for AV conduction disturbances.

Reading a paced strip: a vertical pacemaker spike should be followed immediately by a P wave (atrial pacing) or a wide QRS (ventricular pacing). That is called capture.

Document: pacemaker model, generator type, insertion date and time, generator location, stimulation threshold, and settings (rate, mA, mV, AV delay).

Complications (Chart 22-7): infection at the lead or pocket site; pneumothorax or hemothorax; bleeding and hematoma (cold compresses, hold antiplatelets and antithrombotics); ventricular ectopy from lead irritation; lead dislodgment (most common early complication, so limit activity and immobilize the arm on the implant side); phrenic, diaphragm, or skeletal muscle stimulation (hiccups are a clue); cardiac perforation and tamponade; twiddler syndrome (patient manipulates the generator); pacemaker syndrome.

Pacemaker malfunction (Table 22-2, chapter only):

Malfunction presents as bradycardia and low-output signs (diaphoresis, orthostatic hypotension, syncope), depending on how pacemaker-dependent the patient is.

Electromagnetic interference: household appliances and tools are generally safe. Turn off gas engines before working on them. Keep magnets (phone earpieces, speakers, jewelry) away from the generator beyond a few seconds; phone 6-12 inches away or on the opposite side, not in a shirt pocket. Avoid MRI, transmitter towers, transmission lines, and substations; move away if dizzy or palpitating. Avoid welding and chainsaws (or limit to 60-130 amp welding and electric saws). Walk quickly through store and airport detectors; request a hand search instead of the handheld wand. Wear medical ID.

Surveillance: remote monitoring (transtelephonic, inductive wand, or wandless radiofrequency) transmits ECG, battery, lead, and sensing data; replaces frequent in-person visits and is associated with improved survival.

Implantable Cardioverter Defibrillator

Detects and terminates life-threatening tachycardia or fibrillation.

Indications: secondary prevention (survived sudden cardiac death or symptomatic VT not from a reversible cause); primary prevention (CAD at least 40 days post-MI with EF 35 percent or less; nonischemic dilated cardiomyopathy for at least 9 months with NYHA class II or III HF). A wearable vest defibrillator (LifeVest) bridges the waiting period: worn at all times including in the hospital, off only to bathe, battery changed daily, vibrates and alarms before a shock.

Device: gum-pack-sized generator in the upper chest with at least an RV lead. It senses rate and isoelectric changes, charges, takes a second “look,” then shocks. Battery about 9 years. Therapies can include antitachycardia pacing (fast pulses to break a reentry loop), low-energy cardioversion, and defibrillation, plus backup pacing (usually VVI) for post-shock bradycardia. Subcutaneous ICDs avoid vascular access and suit patients who do not need pacing or CRT. Antiarrhythmics are often continued to reduce shocks. ICD code (chapter only): chamber shocked, chamber antitachycardia-paced, detection method (E electrogram, H hemodynamics), chamber with antibradycardia pacing.

Complications: surgical infection is primary (risk rises with replacements); battery depletion, lead problems; inappropriate shocks (oversensing, sinus or atrial tachycardia with fast ventricular response) are the most frequent long-term problem and need reprogramming.

Nursing Management After Device Implantation

• Monitor ECG against device settings; examine the pacing spike and surrounding complexes; assess cardiac output and hemodynamic stability; report new or increasing arrhythmias. With an ICD, record time from arrhythmia onset to shock or antitachycardia pacing.
• Incision: watch for bleeding, hematoma, infection (swelling, tenderness, drainage, warmth, persistent throbbing).
• Chest x-ray to confirm lead position and rule out pneumothorax.
• Medication effects on pacing threshold: antiarrhythmics, beta-blockers, and diuretics raise it; corticosteroids and alpha-adrenergic agents lower it; the opposite happens when stopped.
• Infection prevention: change dressings as needed; report redness, swelling, drainage, rising temperature, or WBC.
• Coping: expect anger, depression, fear, and anxiety; ICD patients are especially prone to helplessness and depression from unpredictable shocks. Help identify changes, emotional responses, and realistic goals; refer to support groups; teach relaxation; include family. Nursing research (Palese et al., 2019): most shocks happen at home, often with family present; teaching patients and families to recognize prodromal symptoms can guide reprogramming or drug titration.

Patient education checklist (Chart 22-9):

• Check pulse daily (pacemaker); report sudden slowing or speeding.
• Incision: leave uncovered, inspect daily, take temperature at the same time daily, avoid tight clothing, avoid tub soaking and lotions or powders initially.
• Activity: do not raise the arm above the head for 2 weeks; avoid heavy lifting for a few weeks; discuss driving with the provider; normal activity in 2-3 weeks except contact sports.
• EMI precautions as above; carry a provider letter and ID card for security.
• Keep a log of ICD shocks and what preceded them; bring it to follow-up.
• Call 911 for dizziness; family should take a CPR class.
• A shock will not harm someone touching the patient, but they may feel it; warn sexual partners.
• Medical ID with provider, device type and model, manufacturer, and implanting hospital.
• Keep follow-up appointments, especially in the first month and near end of battery life.

Review Questions From the Lecture

1. True or false: the PR interval represents sinus node stimulation, atrial depolarization, and AV node conduction. Answer: true.
2. Which is characteristic of PVCs? Answer: irregular rhythm due to early QRS.

Chapter critical-thinking prompts (worth rehearsing): a relative with alcohol use disorder and new AF who refuses warfarin because it is “rat poison” (evidence for adherence and risks of stopping); a post-hysterectomy patient whose HR rose from 65 to 98 while sleeping (causes and assessment priorities, think sinus tachycardia triggers such as bleeding, pain, fever, hypovolemia); a post-MI patient with frequent PVCs and a four-beat run of VT who remains stable (leading an interprofessional huddle).

Unfolding case tie-in: Kenneth Bronson (27, RLL pneumonia, sinus tachycardia with unifocal PVCs) - consider fever, hypoxemia, dehydration, pain, and sympathomimetic medications as causes.

Memory Anchors

• 1,500 divided by small boxes for a regular rate; 6-second count times 10 for irregular.
• PR over 0.20 is first-degree; lengthening then dropped is Wenckebach; constant then dropped is type II; no relationship at all is third-degree. Atropine fails for type II and third-degree, so pace.
• Wide, bizarre QRS (0.12 or more) means ventricular origin.
• Tachycardia is just a rate. Sinus tach is gradual, has P waves, and needs its cause fixed. SVT is abrupt, narrow, often has no visible P waves, and is broken with vagal maneuvers or adenosine. Wide and fast is VT until proven otherwise.
• AF: no P waves, irregularly irregular, CHA2DS2-VASc for anticoagulation, anticoagulate or TEE before cardioverting anything over 48 hours, and 4 weeks of anticoagulation afterward.
• Flutter: saw-tooth. WPW with AF: no digoxin, diltiazem, or verapamil.
• Prolonged QT leads to torsades; the fix is magnesium.
• Synchronized for a pulse, unsynchronized for no pulse.
• Pacemaker spike followed by a complex is capture; spike without a complex is loss of capture; spikes ignoring intrinsic beats is undersensing; no spikes when needed is oversensing.
• Hiccups after a pacemaker may mean phrenic stimulation or perforation.

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