Atrial Rhythms

Atrial rhythms start in the atrial myocardium or the AV junction, above the bundle of His. Each one is supraventricular, and the site of origin shapes the QRS. An impulse from the atria that travels the normal His-Purkinje system gives you a narrow QRS. Wide QRS in a supraventricular rhythm? The conduction is abnormal. Think bundle branch block, rate-related aberrancy or conduction down an accessory pathway.

Atrial arrhythmias come from three mechanisms:

• Enhanced automaticity: A focus fires faster than the sinus node. Focal atrial tachycardia and MAT are examples.
• Triggered activity: Afterdepolarizations make the cell fire early. Digoxin toxicity and electrolyte shifts are the usual triggers.
• Re-entry: A circuit keeps conducting around its loop. Atrial flutter, AVNRT and AVRT all run on re-entry. The AV node or an accessory pathway may be part of the loop.

The conduction hierarchy sets the back-up rates. Sinus node fails? The AV junction takes over at about 40–60 bpm, and the ventricles at 20–40 bpm. AV nodal blockers slow the atrial rhythms that use the AV node. The ones that skip it, like ectopic atrial tachycardia and atrial flutter, often are not slowed.

Run the same six questions on every atrial rhythm. The table lists the core rhythms with their first-line action. Stability decides that first action. The table never replaces the bedside assessment.

1. Find the rate: Count the R waves over 6 seconds and multiply by 10, or use the R-R interval in a regular rhythm.
2. Check regularity: Regular, regularly irregular (PACs or blocks) or irregularly irregular (AF, MAT, or flutter with variable block).
3. Look for P waves: Use lead II and V1. Identify sinus, ectopic, flutter, fibrillatory or absent P waves.
4. Relate P to QRS: Determine the PR interval and the atrial-to-ventricular ratio. A 2:1 ratio at about 150 bpm suggests flutter.
5. Measure the QRS: Narrow means supraventricular unless aberrancy is proven. Wide means assume VT or pre-excited AF until proven otherwise.
6. Assess stability first: Hypotension, altered mentation, ischemic chest pain or acute heart failure means the patient is unstable and needs cardioversion.

Normal Conduction Values

That early beat from an ectopic atrial focus is a premature atrial complex. You will see PACs a lot. Run a prolonged monitor on healthy adults and they turn up. They are usually benign.

ECG Criteria

• P wave: Different from the sinus P wave; the shape depends on the focus.
• Timing: Earlier than the next expected sinus P wave.
• PR interval: May be shorter, normal or longer than the sinus PR, depending on how close the focus is to the AV node.
• QRS: Usually narrow and identical to sinus beats.
• Pause: Usually incomplete, because the PAC resets the sinus node.

Aberrant PACs

Land a PAC while part of the His-Purkinje system is still refractory, and the QRS goes wide. It can pass for a PVC or VT. The right bundle branch is the most common site, so the pattern is usually RBBB-like (rsR′ in V1).

• Ashman phenomenon: A short cycle after a long one is the classic setup for aberration.
• Clue to origin: Look for an ectopic P wave buried in the preceding T wave.

Blocked PACs

Too early for the AV node? A very early PAC can arrive while the node is still refractory. Then you get a P wave with no QRS. Blocked PACs look like pauses on telemetry. Always look for a premature P wave deforming the preceding T wave.

Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. Chaos replaces organized atrial contraction, with many re-entrant wavelets firing at once. The ventricles set their response through AV conduction. The atria have no say.

ECG Criteria

• Atrial activity: No discrete P waves. Fibrillatory waves vary in size and shape, at roughly 350–600 per minute.
• Ventricular response: Irregularly irregular R-R intervals.
• QRS: Narrow unless there is a bundle branch block, rate-related aberrancy or pre-excitation.
• Rate: Uncontrolled rates are often 100–180 bpm. AV nodal disease or drugs may slow them.

Classification

The 2023 ACC/AHA/ACCP/HRS guideline adds a 1–4 staging system (with 3A–3D) that describes how the disease progresses. At the bedside, the duration terms above still apply.

Pre-Excited AF

Put AF through an accessory pathway, as in WPW, and the QRS goes wide, very fast and irregular. The shape changes from one beat to the next. Ventricular rates can exceed 200 bpm.

Clinical Significance

• Stroke risk: Anticoagulation follows CHA₂DS₂-VASc scoring. The 2023 guideline covers this for AF and typical flutter.
• Duration before cardioversion: For AF of 48 hours or more, or of unknown duration, the 2023 guideline recommends 3 weeks of uninterrupted therapeutic anticoagulation or imaging to exclude thrombus before elective cardioversion (Class 1). Anticoagulation continues for at least 4 weeks afterward (Class 1).
• Anticoagulation after emergent cardioversion: Unstable patients get emergent cardioversion, and it does not wait for anticoagulation. Start anticoagulation as soon as possible afterward.
• Pre-excited AF: AV nodal blocking agents are harmful (Class 3: Harm), since they can precipitate VF or hemodynamic collapse. Treatment is in Bedside Management.

Atrial flutter is a macro-re-entrant circuit in the atria. The usual form, typical flutter, runs through the cavotricuspid isthmus. Unlike AF, the atrial activity is organized and repetitive.

ECG Criteria

• Flutter waves: A sawtooth pattern, best seen in II, III, aVF and V1.
• Atrial rate: 250–350 bpm, usually about 300.
• AV conduction: Usually 2:1, giving a ventricular rate of about 150 bpm. It can also be 3:1, 4:1, or variable.
• QRS: Narrow unless there is a pre-existing conduction abnormality.
• Regularity: Regular with fixed block. Irregular with variable block, which can mimic AF.

Typical vs. Atypical Flutter

• Typical, counterclockwise: The most common form. Negative sawtooth F waves in II, III and aVF, and positive in V1.
• Typical, clockwise: Less common. Positive F waves in II, III and aVF, and negative in V1.
• Atypical: Skips the cavotricuspid isthmus. Often involves the left atrium or an atrial scar. The F wave shape varies.

Clinical Significance

• Thromboembolic risk: Anticoagulation follows the same stroke-risk assessment as AF. The 2023 AF guideline covers typical flutter.
• Ablation: Ablating the cavotricuspid isthmus is a standard option for typical flutter.

Supraventricular tachycardia (SVT) is the umbrella term for paroxysmal re-entrant tachycardias. These run through the AV node or an accessory pathway. AVNRT and AVRT are the most common regular forms, and they start and stop abruptly.

AV Nodal Re-entrant Tachycardia (AVNRT)

• ECG criteria: Narrow QRS; very regular rate, usually 150–250 bpm.
• P waves: Usually buried in the QRS, or seen as a pseudo-r′ in V1 or a pseudo-S in II, III and aVF.
• Mechanism: The AV node is part of the circuit. That is why AV nodal blockers can terminate it.

AV Re-entrant Tachycardia (AVRT)

• Orthodromic AVRT: The signal goes down the AV node and comes back up the accessory pathway. The QRS stays narrow, and a retrograde P wave trails it.
• Antidromic AVRT: The signal goes down the accessory pathway and back up the AV node. The QRS is wide and passes for VT. It is rarer, and more dangerous.
• WPW pattern in sinus rhythm: Short PR (<120 ms), delta wave, and a wide QRS.

Distinguishing Features

• Abrupt onset and offset: AVNRT and AVRT start and stop like a switch. Ectopic atrial tachycardia usually warms up and cools down instead.
• Adenosine response: Stops abruptly with adenosine? Think an AV-node-dependent circuit. Slowing that unmasks flutter waves or AF points to an atrial mechanism.

Multifocal atrial tachycardia (MAT) is an irregular supraventricular rhythm. At least three atrial foci fire independently to produce it. You see it most often with severe lung disease, and it marks acute illness.

ECG Criteria

• P wave morphology: At least three distinct P wave shapes in the same lead.
• Rate: Above 100 bpm.
• Rhythm: Irregularly irregular, which is why it is confused with AF.
• PR and PP intervals: Variable, because each focus has its own conduction time.
• Baseline: Isoelectric between P waves, unlike the fibrillatory baseline of AF.

Causes

Clinical Significance

• Cardioversion does not work: The foci are not one re-entrant circuit. There is nothing to convert. Treat the underlying cause.
• Bedside priority: MAT means acute illness is in play. Treat oxygenation, the trigger and the electrolytes.

Wandering Atrial Pacemaker

A wandering atrial pacemaker meets the same criteria as MAT: at least three P wave shapes and variable PR and PP intervals. The rate is the difference, and it stays below 100 bpm. It is usually benign. You often see it in young, healthy people or with high vagal tone.

Focal atrial tachycardia comes from one atrial focus, driven by enhanced automaticity or triggered activity. Unlike MAT, the P wave keeps the same shape on every beat.

ECG Criteria

• Rate: Usually 100–250 bpm.
• P wave: Abnormal shape, the same on each beat, and different from sinus.
• Onset and offset: Gradual warm-up and cool-down, unlike the abrupt start and stop of AVNRT and AVRT.
• AV conduction: Variable. Some beats may be blocked, which can produce a pattern like 2:1 AV block.

Causes

• Digoxin toxicity, which drives triggered activity. Check the level and the potassium.
• Electrolyte shifts that change atrial automaticity.

Look-Alikes

• MAT: Irregular, with three or more P wave shapes. See Multifocal Atrial Tachycardia (MAT).
• AVNRT and AVRT: Abrupt onset and offset with a fixed relationship. See AVNRT and AVRT (SVT).

Adenosine may transiently slow focal atrial tachycardia or unmask its P waves. It often fails to terminate it. It can terminate some focal ATs, especially those from triggered activity. Termination therefore does not fully exclude an atrial source. Management is in Bedside Management.

Junctional rhythms start in the AV junction: the AV node or the bundle of His. They are supraventricular. They get their own category because the P wave timing is different.

ECG Criteria

• P waves: Absent, retrograde (inverted in II, III, aVF), or buried in the QRS.
• QRS: Narrow unless there is a pre-existing bundle branch block.

Clinical Significance

A junctional rhythm can signal a failing sinus node or digoxin toxicity. When it shows up without a clear cause, check the digoxin level and the potassium. Bedside management is in the section below.

Irregularly irregular and fast rhythms cause the most errors. The table sets the three most-confused rhythms side by side.

Artifact & Lead Misplacement

• Shivering or tremor: Looks like AF or flutter. Look for a constant baseline alongside the QRS.
• Limb lead reversal: Can make P waves look inverted. Check that the pattern matches sinus rhythm in lead II.
• Transport vibration: Moving the monitor or the patient can fake a fibrillation-like baseline. Reassess once the vehicle stops.
• Electrode problems: A loose electrode gives you a wandering baseline. Reposition the lead before you treat.

Normal Variants

Sinus arrhythmia and PACs can make the rhythm look irregular with no true arrhythmia. Check the P wave before the QRS on each beat.

Start with stability. An unstable patient with a tachycardia needs synchronized cardioversion, not drugs. Stable patients can get drugs in the order below. Those doses track the 2025 AHA Guidelines, and the table marks where the FDA label disagrees.

Stability Approach

Rate Control in AF

• Target: Lenient is fine: a resting rate under 100 to 110 bpm is reasonable (2023 guideline, Class 2a). Relieve symptoms and check hemodynamics first.
• LVEF 40% or more, no decompensated HF, not hypotensive: diltiazem or verapamil (Therapy Table), or metoprolol.
• LVEF below 40% or decompensated HF: Avoid diltiazem and verapamil (2023 guideline: Class 3, Harm, for moderate or severe LV systolic dysfunction, and 2025 AHA Part 9: Class 3, Harm, C-EO, in decompensated HF or LV systolic dysfunction). Your options are IV amiodarone, which is Class 2a (B-NR) for rate control in critically ill adults without pre-excitation (2025 AHA Part 9), plus digoxin as an adjunct. Bring in expert or critical-care input.
• Unstable AF: Cardiovert now. Do not wait for anticoagulation (2025 AHA Part 9, COR 1, LOE C-LD). Start it as soon as possible afterward.

Therapy Table

Your scope of practice and local protocol decide which of these drugs you may give.

Pediatrics

• Heart rate: Normal sinus rates fall as kids get older. Compare them with the age-based values on pediatric vital signs.
• SVT rates: Infant SVT is usually above 220 bpm, and child SVT usually above 180 bpm. Pediatric SVT with a pulse and poor perfusion gets synchronized cardioversion, per PALS. Adenosine may go first, but only if IV or IO access is already in place and it will not delay cardioversion.
• Drug choices: Adenosine is the first-line drug for stable SVT. Verapamil is not routinely used in infants. Diltiazem and metoprolol are not established in children.
• Weight-based dosing: Use the weight-based dosing reference. Respect the maximum for every drug.

Other Populations

• Pregnancy: Vagal maneuvers, then adenosine, come first for regular SVT. Electrical cardioversion is used when needed at any gestational age, with fetal monitoring. Use left lateral tilt after about 20 weeks. Avoid amiodarone when alternatives exist. For AF with manifest pre-excitation, IV procainamide is an option (2023 AF guideline). Involve OB or MFM.
• Older adults: Give verapamil over at least 3 minutes. Plan on lower doses, and expect more bradycardia and hypotension.
• Heart transplant: The denervated heart responds poorly to atropine. Adenosine can cause prolonged asystole. Use the reduced dose and get expert input.
• Pacemaker or ICD: Check the device before you cardiovert. Device therapies may already have treated the rhythm.

1. Check the patient first: Note blood pressure, mental status, chest pain and heart failure signs. Unstable means cardiovert.
2. Measure the QRS in the widest lead: Narrow or wide determines the drug pathway.
3. Check regularity: Regular or irregularly irregular.
4. Find the P waves: Use lead II and V1. Classify them as sinus, ectopic, flutter, fibrillatory or absent.
5. Relate P to QRS: Note the PR and the atrial-to-ventricular ratio.
6. Choose the pathway: Narrow regular goes to vagal then adenosine. Irregular wide goes to procainamide or cardioversion. Regular wide is VT until proven otherwise: see Ventricular Rhythms. Irregular narrow with a rate problem goes to rate control.
7. Reassess after each step: Rate, BP and rhythm after every drug or shock.

Common Pitfalls

• Calling a wide, irregular rhythm AF. Check for pre-excitation first.
• Cardioverting MAT. It will not convert.
• Giving diltiazem or verapamil for an unidentified wide-complex tachycardia. Identify it first.
• Mistaking blocked PACs or flutter with variable block for a true pause or AF.
• Forgetting the anticoagulation requirement before elective cardioversion of AF of 48 hours or more.