Dysrhythmias: Recognition, ECG Interpretation, Emergency Treatment and Nursing Care

Add a labelled ECG or resuscitation image here.

Learning objectives

By the end of this lesson, the learner should be able to define dysrhythmia, describe normal cardiac impulse formation and conduction, obtain and interpret a systematic ECG, distinguish stable from unstable tachycardia and bradycardia, select appropriate electrical or pharmacological treatment, support a patient before and after cardioversion or pacing, and document and communicate rhythm changes safely.

• Assess the patient first: a rhythm is clinically important when it compromises oxygen delivery, cardiac output or the risk of cardiac arrest.
• Recognise shockable rhythms, non-shockable arrest rhythms, high-risk AV block, pre-excited atrial fibrillation and torsades de pointes.
• Apply local Uganda Ministry of Health, ambulance and hospital protocols and involve a senior clinician early.

1. Meaning and electrical basis of dysrhythmias

A dysrhythmia (often called an arrhythmia) is an abnormality of impulse formation, impulse conduction, heart rate, rhythm or the relationship between atrial and ventricular activity. It may be too fast, too slow, irregular, prematurely triggered, conducted by an abnormal pathway, or absent during cardiac arrest. “Normal” does not mean that every pulse is identical: respiratory sinus variation may be normal in a young person, while a regular-looking rhythm can still be life-threatening if it is ventricular tachycardia.

Normal impulse formation and conduction

• Sinoatrial (SA) node: the usual pacemaker in the right atrium; its automaticity normally produces 60–100 impulses/minute.
• Atrial myocardium: depolarises and contracts, producing the P wave.
• Atrioventricular (AV) node: briefly delays conduction, allowing ventricular filling. It can provide a slower escape rhythm when higher pacemakers fail.
• His bundle, right and left bundle branches, and Purkinje fibres: rapidly spread the impulse through the ventricles, producing a coordinated QRS contraction.
• Re-entry, abnormal automaticity and triggered activity: common mechanisms of tachyarrhythmia. Fibrosis, ischaemia, scar and accessory pathways can create circuits that sustain re-entry.

The ECG language

Electrical treatment terms: synchronized cardioversion delivers a shock timed to the R wave and is used for an organised tachycardia with a pulse. Defibrillation is an unsynchronized shock used for ventricular fibrillation or pulseless ventricular tachycardia. Pacing provides electrical impulses when the intrinsic rate is too slow or conduction is blocked.

2. Causes and risk factors

Ask “why now?” A new rhythm in an ill patient is often a marker of hypoxia, shock, infarction, sepsis, electrolyte disturbance or drug toxicity. Treating the cause may terminate the rhythm and prevents recurrence.

The reversible Hs and Ts

• Hs: hypovolaemia, hypoxia, hydrogen ion (acidosis), hypo-/hyperkalaemia, hypothermia and hypoglycaemia.
• Ts: tension pneumothorax, cardiac tamponade, toxins, thrombosis (coronary or pulmonary) and trauma.

3. First contact: ABCDE and stability

1. Safety and response: use PPE, identify hazards, call for help, bring the defibrillator, confirm identity and ask for a brief history from the patient or witness.
2. Airway: open and protect the airway. Suction secretions and prepare airway equipment if consciousness is falling.
3. Breathing: assess respiratory rate, effort, chest movement, cyanosis and SpO2. Give oxygen when hypoxaemic or in respiratory distress; avoid indiscriminate high-flow oxygen in patients with normal saturation unless a protocol indicates it.
4. Circulation: palpate a pulse for no more than 10 seconds if unresponsive, check blood pressure, skin temperature, capillary refill and urine output. Apply ECG monitoring and defibrillator pads, establish IV access (or IO access in arrest), and take blood samples without delaying treatment.
5. Disability: assess mental status using AVPU or GCS, check bedside glucose, pupils and new focal neurological signs.
6. Exposure: look for fever, rash, bleeding, medication patches, implanted devices, trauma and signs of heart failure while preventing hypothermia.

Features of an unstable tachycardia or bradycardia

• Hypotension or signs of shock: weak pulse, clammy skin, confusion, oliguria or collapse.
• Acute altered mental status or syncope caused by the rhythm.
• Ischaemic chest pain or dynamic ischaemic ECG changes.
• Acute heart failure, severe dyspnoea, pulmonary oedema or inability to lie flat.
• Peri-arrest appearance, severe cyanosis or recurrent pauses.

When instability is caused by a tachyarrhythmia with a pulse, prepare immediate synchronized cardioversion. When instability is caused by bradycardia, prepare atropine and pacing. If there is no pulse, start the cardiac-arrest algorithm.

4. Systematic ECG assessment

1. Confirm patient, date, calibration, lead placement and artefact. Repeat leads if the tracing is unclear.
2. Calculate ventricular rate and atrial rate when they differ.
3. Describe regularity and identify whether every P wave conducts.
4. Inspect P-wave morphology and the PR relationship.
5. Measure QRS width. A wide QRS may be ventricular in origin, a bundle-branch block, a paced rhythm, hyperkalaemia or pre-excitation.
6. Inspect QT and correct it for rate. Recheck a prolonged QT before giving further QT-prolonging medicine.
7. Assess ST and T waves and compare with previous ECGs. Obtain serial 12-leads if pain, shock or intermittent symptoms continue.
8. Document the rhythm, rate, patient symptoms, blood pressure, intervention and response. Never label an ECG as “just AF” without checking for ACS, heart failure, sepsis and pre-excitation.

5. Tachyarrhythmias

5.1 Unstable tachycardia with a pulse

Call the resuscitation team, attach pads, provide airway and breathing support, obtain IV access and perform synchronized cardioversion according to the defibrillator and local protocol. Use analgesia and conscious sedation when the patient can be safely sedated, but do not delay lifesaving shock in severe shock or peri-arrest deterioration. Recheck rhythm and pulse after each attempt, treat hypoxia/electrolytes/ischaemia and escalate early if the rhythm persists.

5.2 Stable narrow-complex regular tachycardia (often SVT)

• Record a 12-lead ECG if this does not delay treatment and look for sudden onset/termination, retrograde P waves and a regular narrow QRS.
• Try a monitored vagal manoeuvre, usually a modified Valsalva. Do not use carotid sinus massage in a carotid bruit, previous stroke/TIA or significant vascular disease.
• If it persists, give adenosine using the local emergency protocol through a large proximal IV with a rapid flush; explain the transient flushing, chest tightness and frightening sensation beforehand. Have the defibrillator attached because adenosine can reveal or precipitate serious conduction problems.
• If adenosine fails or is contraindicated, obtain expert help for a suitable AV-nodal blocker or synchronized cardioversion. Avoid AV-nodal blockade when pre-excited AF is suspected.

5.3 Atrial fibrillation and atrial flutter

AF is an uncoordinated atrial rhythm producing an irregularly irregular ventricular response; flutter often has saw-tooth atrial activity with a regular or variable ventricular response. Assess onset, haemodynamic stability, heart failure, myocardial ischaemia, infection, thyroid disease, alcohol/stimulant exposure and potassium/magnesium. Rate control, rhythm control and stroke prevention are separate decisions. The patient may need a beta-blocker, diltiazem/verapamil or another specialist-selected drug when appropriate, but these can worsen shock, severe heart failure, asthma or pre-excited AF.

• If unstable, synchronized cardioversion is the emergency treatment.
• If stable, establish onset and stroke risk, correct triggers, and involve a clinician for rate or rhythm control and anticoagulation. AF of more than 24 hours or unknown duration requires particular caution before elective cardioversion; follow the current local/ESC pathway, transoesophageal echo and anticoagulation protocols.
• Teach the patient to return for breathlessness, syncope, chest pain, new neurological symptoms or persistent rapid pulse.

5.4 Wide-complex tachycardia

Assume ventricular tachycardia (VT) until proven otherwise, especially in a patient with infarction or structural heart disease. Do not give verapamil or diltiazem to an undifferentiated wide-complex tachycardia. If unstable, synchronize and shock; if pulseless, defibrillate and begin CPR. If stable, obtain expert assistance, a 12-lead ECG and a protocol-approved antiarrhythmic, while looking for ischaemia, potassium disturbance and drug toxicity.

5.5 Monomorphic VT with a pulse

Assess perfusion, chest pain, heart failure and level of consciousness. Maintain monitoring and pads, correct oxygenation and electrolytes, and prepare synchronized cardioversion for deterioration. Stable VT still requires urgent senior review because it may recur or progress to VF. A patient with a history of infarction, reduced ejection fraction or syncope should not be discharged simply because the rhythm stopped.

5.6 Polymorphic VT and torsades de pointes

Polymorphic VT with prolonged QT is torsades de pointes. If sustained or unstable, give an unsynchronized shock/defibrillation and CPR if pulseless. Stop QT-prolonging medicines, correct potassium toward the high-normal range, correct magnesium and treat bradycardia or pauses with expert-guided pacing/isoproterenol protocols. Intravenous magnesium is generally used for torsades even when the measured magnesium is normal; follow local dosing and monitoring guidance. Do not rely on repeated adenosine.

6. Bradyarrhythmias and heart block

Bradycardia may be physiological in athletes or sleep, but it is dangerous when associated with shock, syncope, chest pain, confusion, pulmonary oedema or ventricular pauses. Review medications, glucose, temperature, oxygenation, potassium, infarction and vagal events.

1. Monitor, attach pads, obtain IV/IO access, oxygenate when indicated and obtain a 12-lead ECG without delaying stabilisation.
2. For symptomatic bradycardia, give atropine according to the current AHA/local protocol unless high-grade block is strongly suspected or the patient is peri-arrest.
3. If atropine is ineffective or the patient has Mobitz II, complete heart block, prolonged pauses or severe instability, start transcutaneous pacing and provide analgesia/sedation when safe.
4. Arrange transvenous pacing and specialist care; a dopamine or epinephrine infusion may be used as a bridge under a monitored protocol.

Important bradycardia patterns

7. Cardiac arrest rhythms

VF and pulseless VT

Start high-quality CPR, attach the defibrillator, give an unsynchronized shock when indicated, resume compressions immediately for two-minute cycles, obtain vascular access and give resuscitation medicines according to the current algorithm. Minimise pauses, rotate compressors, confirm rhythm and pulse carefully, and search for reversible Hs and Ts.

PEA and asystole

These are non-shockable rhythms. Continue CPR, give protocol-directed epinephrine, confirm asystole in more than one lead when appropriate, and treat a reversible cause. PEA can represent tamponade, tension pneumothorax, pulmonary embolism, severe hypovolaemia, hypoxia or toxins; a focused ultrasound examination may assist a trained team without interrupting compressions.

After return of spontaneous circulation

• Reassess airway, breathing and circulation; titrate oxygen to an appropriate saturation and support ventilation.
• Maintain blood pressure and perfusion, obtain a 12-lead ECG, treat seizures and fever, check glucose/electrolytes and urgently evaluate coronary occlusion or pulmonary embolism where indicated.
• Communicate time of arrest, rhythm, shocks, medications, CPR quality, ROSC time and neurological status during transfer.

8. Special high-risk rhythms

• Pre-excited AF/Wolff–Parkinson–White: irregular wide-complex tachycardia with very rapid rates. If unstable, cardiovert. Avoid AV-nodal blockers in suspected pre-excited AF unless a specialist protocol directs otherwise; obtain urgent cardiology help.
• Digoxin toxicity: nausea, visual disturbance, confusion, bradyarrhythmias, atrial tachycardia with block or ventricular arrhythmias. Stop digoxin, check level/electrolytes and arrange specialist digoxin-specific antibody fragments when indicated.
• Long-QT syndrome: ask about family sudden death, drugs and recurrent syncope. Avoid QT-prolonging medicines, correct potassium/magnesium and refer for specialist risk assessment.
• Brugada pattern: fever and sodium-channel-blocking drugs may precipitate VF. Treat fever, avoid triggering medicines and seek electrophysiology advice.
• Pregnancy: maternal oxygenation and perfusion are priorities. Defibrillation and cardioversion are not withheld when indicated; use pregnancy-adapted positioning, involve obstetrics and follow local protocols.
• Children: use paediatric weight-based algorithms, pads and doses; obtain a paediatric resuscitation team early.

9. Common medicines and procedures

10. Nursing and EMT care

• Place the patient in a monitored resuscitation area, attach appropriately sized pads and ensure a functioning defibrillator is immediately available.
• Record baseline rhythm strip, rate, blood pressure, SpO2, temperature, glucose, mental status, pain and symptoms. Repeat after every intervention.
• Check IV patency, flush medicines correctly, label lines, and watch for extravasation or rapid medication effects.
• Explain procedures calmly. Before cardioversion or pacing, check consent when possible, remove oxygen from the shock field, ensure adequate analgesia/sedation and maintain airway readiness.
• After shock or conversion, assess pulse, skin, blood pressure, consciousness, chest pain, burns and recurrence. Continue monitoring because relapse is common.
• Use aseptic technique for IV, IO and transvenous procedures. Secure pads, lines and oxygen tubing during transfer.
• Use closed-loop communication: repeat the rhythm, intervention, dose, time and response. Escalate a deteriorating patient immediately.
• Document onset, symptoms, ECG interpretation, contraindications, informed consent, medicines and doses, shocks, pacing current/rate, capture, complications and handover.
• Provide discharge teaching: medicine adherence, anticoagulation precautions, stimulant/alcohol reduction, pulse monitoring, warning symptoms and the exact follow-up plan.

11. Disposition and prevention

Admit or refer patients with instability, syncope, chest pain, heart failure, ventricular arrhythmia, high-grade block, prolonged QT, significant electrolyte disturbance, suspected ACS, drug toxicity or recurrent symptoms. A rhythm that self-terminates may still need observation, serial ECG/troponin testing, echocardiography, Holter monitoring or electrophysiology review. Review the medication list at every visit, correct potassium and magnesium, manage hypertension/diabetes/thyroid disease, treat sleep apnoea where suspected, and educate high-risk patients about CPR and AED access.

12. Clinical scenarios

13. Memory aid: RHYTHM-SAFE

14. Examination questions

1. What clinical findings make a tachycardia unstable, and why is synchronized cardioversion used?
2. Describe a systematic approach to a wide-complex tachycardia.
3. Compare Mobitz I, Mobitz II and complete heart block and state when pacing is urgent.
4. Outline the immediate management of torsades de pointes.
5. Why must the patient, rather than the monitor, guide emergency treatment?

Key takeaways

• Always establish pulse, perfusion and stability before naming the rhythm.
• Unstable tachycardia with a pulse needs prompt synchronized cardioversion; VF/pulseless VT needs defibrillation and CPR.
• Wide-complex tachycardia is VT until proven otherwise, and AV-nodal blockers can be dangerous in pre-excited AF.
• High-grade AV block, symptomatic bradycardia and torsades require early pacing/defibrillation preparation and senior support.
• Correct hypoxia, ischaemia, electrolytes, toxins and other reversible causes while continuing definitive rhythm treatment.

Educational note: This article supports study and supervised clinical learning. Emergency teams must use current local Uganda protocols, the approved drug formulary, device instructions and senior clinician guidance. Do not use it as a substitute for a bedside assessment.

Sources for further study

• American Heart Association 2025 CPR and ECC algorithms.
• AHA Adult Bradycardia With a Pulse Algorithm.
• European Society of Cardiology atrial fibrillation guideline.
• ACC summary of the 2024 ESC AF-CARE pathway.
• AHA Adult Advanced Life Support scientific statement.
• Current Uganda Ministry of Health emergency, ambulance, medicines and resuscitation protocols used by the supervising facility.