Tachycardia DDx

The differential diagnosis of a regular narrow tachycardia in general includes 5 major mechanisms:

• Sinus tachycardia
• AVNRT
• Atrial tachycardia
• Orthodromic atrio-ventricular reentrant tachycardia (AVRT) involving retrograde conduction over a “concealed” bypass tract
• Atrial flutter with 2:1 block

Bradycardia DDx

Whenever you see a negative P wave and QRS complex in lead I the likely diagnosis is limb lead reversal.

Multifocal atrial rhythm

Differentiate from ectopic atrial rhythm. In ectopic atrial rhythm, the P-wave morphology remains consistent as the PACs originate from a single ectopic focus. In contrast, multifocal atrial rhythm shows varying P-wave morphologies from beat to beat, reflecting the random discharge of multiple ectopic atrial foci .

Early repolarization

on the LEFT, the T wave repolarization looks like a continuation of the S wave. This is not ST elevation and is seen often in young adults. It is called benign early repolarization. On the right, you clearly see the completion of the S wave and a clear ST Segment which allows you to do an accurate ST Elevation measurement.

Premature Atrial Complex (PAC)

A premature atrial complex (PAC) is a premature beat arising from ectopic pacemaking tissue within the atria. There is an abnormal P wave, usually followed by a normal QRS complex. AKA: Atrial ectopics, atrial extrasystoles, atrial premature beats, atrial premature depolarisations.

Tip

• Abnormal (non-sinus) P wave usually followed by a normal QRS complex (< 120 ms)
  • PACs arising close to the AV node (“low atrial” ectopics) cause retrograde activation of the atria, producing an inverted P wave with a relatively short PR interval ≥ 120 ms (PR interval < 120 ms is classified as a PJC)
  • The abnormal P wave may be hidden in the preceding T wave, producing a “peaked” or “camel hump” appearance
• Post-extrasystolic pauses may be present — PACs that reach the SA node may depolarise it, causing the SA node to be “reset”, with a longer-than-normal interval before the next sinus beat arrives
• PACs may also be conducted aberrantly (usually RBBB morphology), or not conducted at all. P waves will still be visible in both cases

Premature Ventricular Complex (PVC)

• Broad QRS complex (≥ 120 ms) with abnormal morphology
• Premature — i.e. occurs earlier than would be expected for the next sinus impulse
• Discordant ST segment and T wave changes.
  • ST segment and T wave are directed opposite to the main vector of the QRS complex
• Usually followed by a full compensatory pause
• Retrograde capture of the atria may or may not occur

Junctional Escape Rhythm

• Junctional rhythm with a rate of 40-60 bpm
• QRS complexes are typically narrow (< 120 ms)
• No relationship between the QRS complexes and any preceding atrial activity (e.g. P-waves, flutter waves, fibrillatory waves)

Mechanism

Pacemaker cells are found at various sites throughout the conducting system, with each site capable of independently sustaining the heart rhythm. The rate of spontaneous depolarization of pacemaker cells decreases down the conducting system:

• SA node (60-100 bpm)
• Atria (< 60 bpm)
• AV node (40-60 bpm)
• Ventricles (20-40 bpm) Under normal conditions, subsidiary pacemakers are suppressed by the more rapid impulses from above (i.e. sinus rhythm). Junctional and ventricular escape rhythms arise when the rate of supraventricular impulses arriving at the AV node or ventricle is less than the intrinsic rate of the ectopic pacemaker.

Terminology

• Junctional bradycardia = junctional rhythm at a rate of < 40 bpm
• Junctional escape rhythm = junctional rhythm at a rate of 40-60 bpm
• Accelerated junctional rhythm = junctional rhythm at 60-100 bpm
• Junctional tachycardia = junctional rhythm at > 100 bpm

Hyperkalemia

高钾血症：三低一高	低钾血症：三高一低
兴奋↑（↓）	兴奋↑
传导↓	传导↓
自律↓	自律↑
收缩↓	收缩↑（↓）

• Mild hyperkalemia: 5.5–6.4 mEq/L 
  • Tall, peaked T waves (膜对K⁺通透性增过，复极化3期加速，反映为3期复极T波狭窄而高耸)
• Moderate hyperkalemia: 6.5–8.0 mEq/L 
  • Lengthening of QRS interval
    • because of conduction delay
  • Widening and flattening of P wave, which eventually disappears 
• Severe hyperkalemia: > 8.0 mEq/L 
  • Absent P wave
  • Intraventricular conduction block
  • Unusual QRS morphology  
  • Sine wave pattern: a sinusoidal pattern with absent P waves and a wide QRS complex that merges with the T wave; a marker of impending V-Fib and asystole 
  • Cardiac arrhythmias (e.g., V-tach, V-fib), asystole

Hypokalemia

• Mild to moderate hypokalemia
  • T-wave flattening or inversion
  • ST depression
  • Prolonged PR interval
• Moderate to severe hypokalemia
  • Presence of U waves: small waveform following the T wave that is often absent but becomes more pronounced in hypokalemia or bradycardia
  • T and U wave fusion
  • QT prolongation [13]
• Dysrhythmias
  • Premature atrial and ventricular complexes
  • Sinus bradycardia
  • Paroxysmal atrial or junctional tachycardia
  • Ventricular dysrhythmias, e.g., Torsades de pointes
  • PEA/asystole

The push-pull effect

Mnemonic

To remember that low potassium may result in a flattened T wave, think of: “No pot, no tea (T)!”

Tip

Hypokalemia, hypocalcemia and hypomagnesemia all appear to prolong the QT interval, but they do so for different reasons:

• Hypokalemia prolongs the QU interval which can be mistaken for the QT interval
• Hypocalcemia prolongs the ST segment (resulting in a long QT with a normal T wave)
• Hypomagnesemia prolongs the T wave (resulting in a long QT with a long T wave)

Atrioventricular block

Bundle Branch Block

mnemonic: William Marrow In left bundle branch block

• The R wave in the lateral leads may be either “M-shaped”, notched, monophasic, or an RS complex In right bundle branch block, the right precordial leads will show ST-segment depression and T-wave inversion. Similarly, in left bundle branch block, ST-segment depression and T-wave inversion can be seen in the left lateral leads.

Mitral stenosis

Characteristic findings include:

• Left atrial enlargement/P mitrale (widened and biphasic P wave)
• Atrial flutter
• Right ventricular hypertrophy (e.g., right axis deviation, dominant R wave in lead V1)

Accelerated Idioventricular Rhythm

AIVR, also known as Accelerated Ventricular Rhythm, results when the rate of an ectopic ventricular pacemaker exceeds that of the sinus node. Often associated with increased vagal tone and decreased sympathetic tone.

Features

• Regular rhythm
• Rate typically 50-120 bpm
• Three or more ventricular complexes; QRS duration > 120ms
• Fusion and capture beats

Pathophysiology

• Proposed mechanism is enhanced automaticity of ventricular pacemaker, although triggered activity may play a role, particularly in ischemia and digoxin toxicity
• AIVR is classically seen in the reperfusion phase of an acute STEMI, e.g. post thrombolysis
• Usually a well-tolerated, benign, self-limiting arrhythmia

STEMI

Timeline of ECG changes in STEMI The sequence of ECG changes over several hours to days: hyperacute T wave → ST elevation → pathological Q wave → T-wave inversion → ST normalization → T-wave normalization

Pathological Q wave

Top: normal Q wave
Bottom: pathological Q wave with a duration ≥0.04 s and depth >¼ of R wave amplitude (red and green overlays)

Ventricular aneurysm

The pattern of persistent anterior ST elevation (> 2 weeks after STEMI) plus pathological Q waves has a sensitivity of 38% and a specificity of 84% for the diagnosis of ventricular aneurysm.

ECG Motion Artefacts

Parkinsonian tremor:

• The irregular baseline in this ECG gives the appearance of atrial fibrillation
• The slow regular rhythm even suggests the possibility of atrial fibrillation with complete heart block and a junctional escape rhythm
• However, on closer inspection there are visible P waves in V3 (circled)
• This patient had sinus bradycardia and a resting tremor due to Parkinson’s disease

Miscellaneous

P wave

Time: < 0.12s = 3 small block Voltage: <0.25mV = 2.5 small block The P wave in V1 is often biphasic. Early right atrial forces are directed anteriorly, giving rise to an initial positive deflection; these are followed by left atrial forces travelling posteriorly, producing a later negative deflection. Thus,

• P mitrale (widened and biphasic P wave): Mitral stenosis, causing left atrium hypertrophy
• Peaked P wave: Pulmonary hypertension, causing right atrium hypertrophy In AVNRT, The retrograde P wave (or Atrial echo) shows up at the end of the QRS. Best observed in lead II or III. Also, Retrograde P wave (aka pseudo-R’ wave) is seen in V1.

ST segment

Time: 0.05-0.15s = 1-3 small block Elevation: ≥ 0.1 mV in a limb lead or ≥ 0.2 mV in a precordial lead. Depression: ≥ 0.05 mV (or 0.5 mm) in leads V2 and V3 or ≥ 0.1 mV in all other leads.

• Downsloping ST depression or horizontal ST depression: Subendocardial myocardial ischemia, i.e., NSTEMI
• Sagging type ST-segment depression: digoxin
• Secondary repolarization abnormalities: Ventricular hypertrophy, LBBB
• Nonspecific ST-segment depression: Hypokalemia

T wave

Pathophysiology of abnormalities

• Ventricular repolarization vector directed away from the electrode of the ECG lead
• Changes in myocardial cellular electrophysiology (e.g., during ischemia or infarction)
• Changes in the sequence of ventricular activation (e.g., in bundle branch blocks or cardiac hypertrophy)

Classifications

• Peaked T wave
  • Hyperkalemia
  • High vagal tone
  • Early stages of a STEMI
  • Prinzmetal angina
• T wave inversion (inverted T wave)
  • May be a normal finding in:
    • Leads III, aVR, or V1
    • Children
  • Coronary artery disease (myocardial ischemia)
  • Bundle branch blocks
  • Pulmonary embolism
  • Perimyocarditis
  • Ventricular hypertrophy
  • Digoxin
  • Intracranial hemorrhage
  • Persistent juvenile T-wave pattern
  • Wellens syndrome

QT interval

The QT interval includes the QRS complex, the ST segment, and the T wave.

• The two chief causes of a short QT are hypercalcemia and digoxin therapy (associated with characteristic “scooping” of the ST-T complex). A third and relatively rare cause is hereditary short QT (“channelopathy”-related) that may be associated with ventricular arrhythmia and sudden cardiac arrest.
  • Digoxin: The inhibition of the sodium/potassium atpase decreases the amount of intracellular potassium, which causes an increase in potassium influx during repolarization, shortening the qt interval
  • Digoxin increases parasympathetic tone, lengthening the pr interval
• Prolonged QT: Congenital Long QT syndromes, Drug side effects (e.g., antiarrhythmic agents, antidepressants, antipsychotics, phenothiazines, 1st-generation antihistamines, some antibiotics), Electrolyte disturbances (e.g., Hypocalcemia, hypokalemia, hypomagnesemia), Cardiac abnormalities (e.g., inflammatory heart diseases, bradycardia, myocardial ischemia), Arsenic poisoning

Rates

• Atrial flutter: 250-300/min — about 1 small block
• Atrial fibrillation: 350-400/min — less than 1 small block
• Atrial tachycardia, AVNRT: 130-240 — 1-2 small block
• Ventricular tachycardia: >100 — less than 3 small blocks