Rhythm Gallery

In depth

The one-page summary above is what the PDF prints. These sections go further.

Conduction system and the action potential

The AV node, the slowest tissue in the heart (about 0.05 m/s), holds each sinus impulse while the atria empty; the His bundle, bundle branches and Purkinje fibers (up to 4 m/s) then activate both ventricles within a QRS under 0.12 s. Intrinsic rates fall down the system: sinus node 60 to 100/min, junction 40 to 60, ventricles 20 to 40. The right coronary artery supplies the sinus node in about 60% of people and the AV node in about 90%.

The cell is absolutely refractory from phase 0 until midway through phase 3. Near the T-wave peak some cells have recovered and others have not, so a stimulus there (an R-on-T PVC, an undersensed pacing spike, an unsynchronized shock) can fragment the wavefront into VF; synchronizing cardioversion to the R wave avoids this vulnerable period.

Reading any strip, step by step

1. Patient and signal first: pulse, pressure, mentation, SpO₂ or arterial waveform. A rhythm that does not fit the patient is artifact until proved otherwise.
2. Rate: 300 ÷ large boxes or 1,500 ÷ small boxes between R waves; if irregular, QRS complexes in 6 s × 10. At 25 mm/s a small box is 0.04 s, a large box 0.20 s.
3. Regularity: regular, regularly irregular (grouped beats, bigeminy) or irregularly irregular.
4. P waves: upright in II, one per QRS, one shape? Count the atrial rate; check T waves for hidden P waves.
5. PR: 0.12–0.20 s and constant? Short with a delta wave: pre-excitation. Lengthening: Wenckebach. Unrelated to the QRS: dissociation.
6. QRS: under 0.12 s, conducted normally; 0.12 s or more, bundle branch block, pre-excitation, paced or ventricular.
7. QTc, ST segment, T and U waves; then name the rhythm and decide whether it explains the patient.

Bazett's QTc (QT ÷ √RR, in seconds) overcorrects at fast rates, where Fridericia (QT ÷ cube root of RR) is more accurate. A QTc over 450 ms in men or 460 ms in women is long (AHA/ACCF/HRS 2009; Drew 2010 uses 470 and 480); over 500 ms, or a rise of more than 60 ms, carries high torsades risk (Drew 2010). A wide QRS inflates the QT: trend one lead and method. V1 best separates VT from aberrancy and right from left bundle patterns, and II shows P waves best (Sandau 2017).

Sinus rhythms and sinus node dysfunction

Sinus rhythm is a P upright in I and II before every QRS with a constant PR. Sinus arrhythmia, faster on inspiration, is normal. Sinus tachycardia speeds up and slows gradually, unlike the abrupt start and stop of reentry, and answers pain, fever, hypovolemia, anemia, hypoxia, PE or sepsis: slowing it with a beta-blocker removes compensation.

Exams call under 60/min sinus bradycardia; the 2018 ACC/AHA/HRS guideline and AHA 2025 use under 50, and symptoms decide treatment. Bedside causes: vagal surges (suctioning, vomiting, straining), hypoxia, hypothermia, hypothyroidism, inferior MI, hyperkalemia, raised ICP and drugs (beta-blockers, diltiazem, digoxin, amiodarone, dexmedetomidine, propofol).

Sinus node dysfunction includes inappropriate bradycardia, pauses, chronotropic incompetence and tachy-brady syndrome, in which AF stops and the suppressed sinus node takes seconds to restart. A permanent pacemaker treats the bradycardia and makes rate-control drugs safe.

Atrial rhythms: PACs, MAT, flutter and AF

A PAC is an early, differently shaped P that resets the sinus node, so the pause is less than compensatory. Very early, it can meet a refractory AV node (blocked PAC: a notched T wave, then a pause) or a refractory bundle branch (an aberrant, usually right-bundle-shaped QRS). In AF, aberrancy after a long then short R–R (Ashman phenomenon) is often miscalled a PVC.

MAT shows three or more P-wave shapes, varying PR and R–R intervals and a rate over 100; the distinct P waves separate it from AF. It follows decompensated lung disease, hypoxemia, low K⁺ or Mg²⁺ and theophylline. Treat those: cardioversion fails, and IV metoprolol or verapamil is reasonable for rate (2015 ACC/AHA/HRS SVT guideline, 2a).

Typical flutter circles the tricuspid annulus through the cavotricuspid isthmus at about 300/min (250 to 350): negative sawtooth waves in II, III and aVF, positive in V1. Adenosine unmasks the waves without ending it. Class IC drugs (flecainide, propafenone) slow the circuit enough for 1:1 conduction, so an AV-nodal blocker goes with them. Anticoagulation follows AF rules; isthmus ablation is first-line for recurrent typical flutter (2015 SVT guideline).

In AF the atria fire at 350 to 600/min and the AV node passes an irregularly irregular response; the lost atrial kick (15 to 30% of stroke volume) matters most in a stiff ventricle. The 2023 ACC/AHA/ACCP/HRS guideline stages AF from 1 (at risk) and 2 (pre-AF) through 3A paroxysmal (ends within 7 days), 3B persistent and 3C long-standing persistent (over 12 months) to 4 permanent. ICU triggers are sepsis, surgery, catecholamines, hypoxia and low K⁺ or Mg²⁺.

AFFIRM (2002, 4,060 patients) found no survival gain from rhythm control (5-year mortality 23.8% vs 21.3%, P = 0.08); most strokes occurred off warfarin or below target INR. RACE II (2010) found lenient control (resting rate under 110) as good as strict (under 80), 12.9% vs 14.9% events at 3 years, and the 2023 guideline accepts a resting target under 100 to 110. EAST-AFNET 4 (2020, 2,789 patients) turned practice toward early rhythm control: started within a year of diagnosis, it reduced cardiovascular death, stroke and HF or ACS admissions (3.9 vs 5.0 per 100 person-years). Anticoagulate at an annual stroke risk of 2% or more, about CHA₂DS₂-VASc 2 or more in men and 3 or more in women (2023, Class 1); a DOAC is preferred except with a mechanical valve or moderate to severe mitral stenosis.

Junctional rhythms and SVT mechanisms

Junctional impulses travel up and down at once, so the P in II, III and aVF is inverted and falls just before the QRS (PR under 0.12 s), inside it or after it. Escape 40 to 60/min, accelerated junctional 60 to 100, junctional tachycardia over 100. Never suppress an escape; ask why the sinus node failed. Accelerated rhythms follow digoxin toxicity, inferior MI, myocarditis and cardiac surgery. AF that turns regular and slow is complete block with a junctional escape until proven otherwise: check digoxin and K⁺.

A WPW pattern (short PR, delta wave, QRS 0.12 s or more) appears in 0.1 to 0.3% of people (2015 SVT guideline); WPW syndrome adds tachycardia. A concealed pathway conducts only backward: a normal resting ECG, but orthodromic AVRT. In AF, a pathway with a short refractory period can conduct 250 to 300 impulses a minute and degenerate to VF; a shortest pre-excited R–R of 250 ms or less marks such a pathway.

For stable regular SVT, the modified Valsalva in REVERT (2015, 433 patients) restored sinus rhythm in 43% vs 17% with the standard strain: strain 15 s at 40 mm Hg, then lie flat with legs raised to 45° for 15 s. Adenosine goes through a large proximal vein with a rapid flush; its half-life is under 10 s, caffeine and theophylline blunt it, and dipyridamole and carbamazepine exaggerate it (label). Run a strip during every dose: the response names the rhythm.

Ventricular rhythms and wide-complex tachycardia

A PVC is early and wide (0.12 s or more), with no P wave, a T wave opposite the QRS and usually a full compensatory pause (none if interpolated). Patterns: unifocal or multiform, bigeminy, trigeminy, couplets, and three or more in a row over 100/min, which is VT (nonsustained under 30 s). A burden over 24% predicted PVC cardiomyopathy with 79% sensitivity and 78% specificity (Baman 2010, in Koester 2020).

Suppression does not save lives: in CAST (1989), encainide or flecainide after MI raised mortality to 7.7% from 3.0% on placebo. Treat the cause; beta-blockers for symptoms. Accelerated idioventricular rhythm (about 50 to 110/min) after reperfusion is benign, and suppressing it can leave no rhythm.

Most regular wide tachycardias are VT (62 of 84 in Baerman 1987, where prior MI, heart failure or recent angina each had a positive predictive value over 95%), and a normal blood pressure does not exclude it. AV dissociation proves VT, but its visible signs, fusion and capture beats, appeared in only 4 of 33 episodes in Wellens 1978; a QRS over 0.14 s and precordial concordance also favor VT.

Brugada reported 98.7% sensitivity and 96.5% specificity in 554 tachycardias, and Vereckei 91.5% accuracy against 85.5% for Brugada in 483. In an independent test of 260 tracings (Jastrzebski 2012) Brugada scored 77.5% and no newer method did better, so an unclear wide tachycardia is treated as VT. Verapamil or diltiazem given for presumed SVT can collapse a patient in VT. For stable VT, PROCAMIO (2017, 62 patients) found fewer major cardiac events within 40 min with procainamide than amiodarone (9% vs 41%) and more terminations (67% vs 38%).

Torsades is polymorphic VT twisting around the baseline on a long QT, typically started by a short–long–short sequence. Risk rises with QTc over 500 ms, female sex, bradycardia, low K⁺ or Mg²⁺, heart failure and QT drugs (class IA and III antiarrhythmics, haloperidol, ondansetron, macrolides, fluoroquinolones, methadone). Sustained polymorphic VT gets an unsynchronized shock (AHA 2025 counts it as unstable). Preventing recurrence (Drew 2010): magnesium 2 g IV whatever the level, K⁺ 4.5–5.0 mmol/L, QT drugs stopped, pacing or isoproterenol to abolish pauses. Polymorphic VT with a normal QT suggests ischemia.

In refractory VF, DOSE-VF (2022, 405 patients) found survival to discharge of 30.4% with double sequential shocks and 21.7% with anterior-posterior pads vs 13.3% with standard shocks. AHA 2025 still grades both 2b.

AV blocks: level of block and management

Level of block predicts behavior. Nodal block is vagally sensitive, usually narrow-QRS with a junctional escape of 40 to 60/min, responds to atropine and often resolves. Infranodal block (His bundle or bundle branches) usually has a wide QRS and an escape of 20 to 40/min or none, ignores atropine and can progress to asystole without warning.

Typical Wenckebach groups beats: the largest PR increment comes after the first beat, so R–R intervals shorten before the drop. In 2:1 block, a long PR on conducted beats and a narrow QRS point to the node; a normal PR and a wide QRS point below it. Atropine or exercise speeds the sinus rate and improves nodal conduction but worsens infranodal block, which receives more impulses than it can carry; vagal maneuvers do the reverse.

Usually reversible: inferior MI (nodal), drugs, hyperkalemia, Lyme carditis, hypothyroidism, sleep apnea and vagal surges. Anterior MI blocks below the node through septal necrosis and carries a poor prognosis. New PR prolongation in aortic valve endocarditis suggests a root abscess. The 2018 ACC/AHA/HRS guideline gives a permanent pacemaker Class I for Mobitz II, high-grade or third-degree block without a reversible cause, symptoms or not, and for alternating bundle branch block.

Paced rhythms and pacemaker malfunction

A spike before a P is atrial pacing; a spike before a wide, left-bundle-shaped QRS is right ventricular pacing; a P followed by a ventricular spike after the programmed AV delay is tracking. A biventricular paced QRS is often narrower with a dominant R in V1; a broad left-bundle pattern suggests lost LV capture. CRT works only when nearly every beat is paced: survival was best above 98% (Hayes 2011, 36,935 patients), which fast AF or frequent PVCs prevent.

A magnet over a pacemaker gives asynchronous pacing at a maker-specific rate; over most ICDs it suspends shocks and anti-tachycardia pacing but leaves bradycardia pacing unchanged. Anti-tachycardia pacing shows as a short burst of fast paced beats that ends VT. Permanent devices need a programmer: request an interrogation.

Artifact, alarms and rhythm-specific nursing actions

Artifact mimics VT, VF, AF, flutter and asystole: tooth brushing, chest physiotherapy, shivering, seizures, tremor (4 to 6 Hz, which looks like flutter), 60 Hz electrical noise and loose or dry electrodes. Clues: native QRS complexes marching through at the old rate, an undisturbed arterial or SpO₂ waveform, the pattern in only some leads, and no pause or change after it stops. In Knight 1999, artifact read as VT led 12 patients to unnecessary procedures, including three catheterizations, a pacemaker and an ICD.

In Drew 2014 (461 ICU patients over 31 days), 88.8% of 12,671 annotated arrhythmia alarms were false. Prepare the skin, change electrodes daily (AACN alarm practice alert), place leads correctly, turn on pacer detection and set limits for the patient.

Exam pearls

• Regular narrow tachycardia at 150: flutter with 2:1 block until proven otherwise.
• Irregular, very fast and wide with changing QRS shapes: pre-excited AF; shock, procainamide or ibutilide, never nodal blockers.
• PR lengthens, then a beat drops: Mobitz I, nodal. Fixed PR, then a drop: Mobitz II, infranodal; pace.
• AF that becomes regular and slow: complete heart block; suspect digoxin.
• Wide regular tachycardia after MI: VT; AV dissociation, fusion and capture beats confirm it.
• Torsades: magnesium; sustained polymorphic VT needs an unsynchronized shock.
• QTc over 500 ms: hold QT-prolonging drugs, replace K⁺ and Mg²⁺.
• Brugada criteria sort wide tachycardias; Brugada syndrome is coved ST elevation in V1–V2, unmasked by fever.