Assess ventricular (RR intervals) and atrial (PP intervals) rate and rhythm:
- Is ventricular rhythm regular? What is the ventricular rate (beats/min)?
- Is atrial rhythm regular? What is the atrial rate (beats/min)?
- P-waves should precede every QRS complex and the P-wave should be positive in lead II.
- Sinus rhythm (which is the normal rhythm) has the following characteristics: (1) heart rate 50–100 beats per minute; (2) P-wave precedes every QRS complex; (3) the P-wave is positive in lead II and (4) the PR interval is constant.
- Causes of bradycardia: sinus bradycardia, sinoatrial block, sinoatrial arrest/inhibition, second-degree AV block, third-degree AV block. Note that escape rhythms may arise during bradycardia. Also note that bradycardia due to dysfunction in the sinoatrial node is referred to as sinus node dysfunction (SND). If a person with ECG signs of SND is symptomatic, the condition is classified as sick sinus syndrome (SSS).
- Causes of tachycardia (tachyarrhythmia) with narrow QRS complexes (QRS duration <0,12 s): sinus tachycardia, inappropriate sinus tachycardia, sinoatrial re-entry tachycardia, atrial fibrillation, atrial flutter, atrial tachycardia, multifocal atrial tachycardia, AVNRT, AVRT (pre-excitation, WPW). Note that narrow complex tachyarrhythmia rarely cause circulatory compromise or collapse.
- Causes of tachycardia (tachyarrhythmia) with wide QRS complexes (QRS duration ≥0,12 s): ventricular tachycardia is the most common cause and it is potentially life-threatening. Note that 10% of wide complex tachycardias actually originate from the atria but the QRS complexes become wide due to abnormal ventricular depolarization (e.g sinus tachycardia with simultaneous left bundle branch block).
- P-wave always positive in lead II (actually always positive in leads II, III and aVF).
- P-wave duration should be <0,12 s (all leads).
- P-wave amplitude should be ≤2,5 mm (all leads).
- PR interval must be 0,12–0,22 s (all leads).
- P-wave must be positive in lead II, otherwise the rhythm cannot be sinus rhythm.
- P-wave may be biphasic (diphasic) in V1 (the negative deflection should be <1 mm). It may have a prominent second hump in the inferior limb leads (particularly lead II).
- P mitrale: increased P-wave duration, enhanced second hump in lead II and enhanced negative deflection in V1.
- P pulmonale: increased P-wave amplitudes in lead II and V1.
- If P-wave not clearly visible: look for retrograde (inverted) P-waves, which can be located anywhere between the J point and the terminal part of the T-wave.
- PR interval >0,22 s: first-degree AV block.
- PR interval <0,12 s: Pre-excitation (WPW syndrome).
- Second-degree AV-block Mobitz type I (Wenckebach block): repeated cycles of gradually increasing PR interval until an atrial impulse (P-wave) is blocked in the atrioventricular node and the QRS complex does not appear.
- Second-degree AV-block Mobitz type II: intermittently blocked atrial impulses (no QRS seen after P) but with constant PR interval.
- Third-degree AV-block: All atrial impulses (P-waves) are blocked by the atrioventricular node. An escape rhythm arises (cardiac arrest ensues otherwise), which may have narrow or wide QRS complexes, depending on its origin. There is no relation between P-waves and the escape rhythm’s QRS complexes, and atrial rhythm is typically faster than the escape rhythm (both rhythms are typically regular).
- QRS duration must be <0,12 s (normally 0,07-0,10 s).
- There must be at least one limb lead with R-wave amplitude >5 mm and at least one chest (precordial) lead with R-wave amplitude >10 mm; otherwise there is low voltage.
- High voltage exists if the amplitudes are too high, i.e if the following condition is satisfied: S-waveV1 or V2 + R-waveV5 >35 mm.
- Look for pathological Q-waves. Pathological Q-waves are ≥0,03 s and/or amplitude ≥25% of R-wave amplitude in same lead, in at least 2 anatomically contiguous leads.
- Is the R-wave progression in the chest leads (V1–V6) normal?
- Is the electrical axis normal? Electrical axis is assessed in limb leads and should be between –30° to 90°.
- Wide QRS complex (QRS duration ≥0.12 s): Left bundle branch block. Right bundle branch block. Nonspecific intraventricular conduction disturbance. Hyperkalemia. Class I antiarrhythmic drugs. Tricyclic antidepressants. Ventricular rhythms and ventricular extrasystoles (premature complexes). Artificial pacemaker which stimulates in the ventricle. Aberrant conduction (abberancy). Pre-excitation (Wolff-Parkinson-White syndrome).
- Short QRS duration: no clinical relevance.
- High voltage: Hypertrophy (any lead). Left bundle branch block (leads V5, V6, I, aVL). Right bundle branch block (V1–V3). Normal variant in younger, well-trained and slender individuals.
- Low voltage: Normal variant. Misplaced leads. Cardiomyopathy. Chronic obstructive pulmonary disease. Perimyocarditis. Hypothyreosis (typically accompanied by bradycardia). Pneumothorax. Extensive myocardial infarction. Obesity. Pericardial effusion. Pleural effusion. Amyloidosis.
- Pathological Q-waves: Myocardial infarction. Left-sided pneumothorax. Dextrocadia. Perimyocarditis. Cardiomyopathy. Amyloidosis. Bundle branch blocks. Anterior fascicular block. Pre-excitation. Ventricular hypertrophy. Acute cor pulmonale. Myxoma.
- Fragmented QRS complexes indicates myocardial scarring (mostly due to infarction).
- Abnormal R-wave progression: Myocardial infarction. Right ventricular hypertrophy (reversed R-wave progression). Left ventricular hypertrophy (amplified R-wave progression). Cardiomyopathy. Chronic cor pulmonale. Left bundle branch block. Pre-excitation.
- Dominant R-wave in V1/V2: Misplaced chest electrodes. Normal variant. Situs inversus. Posterolateral infarction/ischemia (if patient experiences chest discomfort). Right ventricular hypertrophy. Hypertrophic cardiomyopathy. Right bundle branch block. Pre-excitation.
- Right axis deviation: Normal in newborns. Right ventricular hypertrophy. Acute cor pulmonale (pulmonary embolism). Chronic cor pulmonale (COPD, pulmonary hypertension, pulmonary valve stenosis). Lateral ventricular infarction. Pre-excitation. Switched arm electrodes (negative P and QRS-T in lead I). Situs inversus. Left posterior fascicular block is diagnosed when the axis is between 90° and 180° with rS complex in I and aVL as well as qR complex in III and aVF (with QRS duration <0.12 seconds), provided that other causes of right axis deviation have been excluded.
- Left axis deviation: Left bundle branch block. Left ventricular hypertrophy. Inferior infarction. Pre-excitation. Left anterior fascicular block is diagnosed if the axis is between -45° and 90° with qR-complex in aVL and QRS duration is 0,12 s, provided that other causes of left axis deviation have been excluded.
- Extreme axis deviation: Rarely seen. Probably misplaced electrodes. If the rhythm is wide QRS complex tachycardia, then the cause is probably ventricular tachycardia.
- The ST-segment should be flat and isoelectric (in level with the baseline). It may be slightly upsloping at the transition with the T-wave.
- ST segment deviation (elevation and depression) is measured in the J point.
- Benign ST segment elevation is very common in the population, particularly in the precordial leads (V2–V6). Up to 90% (in some age-ranges) of healthy men and women display concave ST-segment elevations in V2–V6 (this is called male/female pattern). ST-segment elevations which are not benign nor due to ischemia are rather common (listed below).
- ST-segment depression is uncommon among healthy individuals. ST-segment depression is particularly suspicious in the chest leads. Guidelines recommend that <0.5 mm ST-segment depression be accepted in all leads.
- Causes of ST-segment elevation: Ischemia. ST segment elevation myocardial infarction (STEMI/STE-AKS). Prinzmetal’s angina (coronary vasospasm). Male/female pattern. Early repolarization. Perimyocarditis. Left bundle branch block. Nonspecific intraventricular conduction disturbance. Left ventricular hypertrophy. Brugada syndrome. Takotsubo cardiomyopathy. Hyperkalemia. Post cardioversion. Pulmonary embolism. Pre-excitation. Aortic dissection engaging the coronary arteries. Left ventricular aneurysm.
- Causes of ST-segment depression: Ischemia. Non-ST segment elevation myocadial infarction (NSTEMI/NSTE-AKS). Physiological ST-segment depression. Hyperventilation. Hypokalemia. High sympathethic tone. Digoxin. Left bundle branch block. Right bundle branch block. Pre-excitation. Left ventricular hypertrophy. Right ventricular hypertrophy. Heart failure. Tachycardia.
- Causes of waves/deflections in the J point (J wave syndromes): Brugada syndrome. Early repolarization.
- Should be concordant with the QRS complex. Should be positive in most leads.
- T-wave progression should be normal in chest leads.
- In limb leads the amplitude is highest in lead II, and in the chest leads the amplitude is highest in V2–V3.
- Normal variants: An isolated (single) T-wave inversion is accepted in lead V1 and lead III. In some instances the T-wave inversions from childhood may persist in V1–V3(V4), which is called persistent juvenile T-wave pattern. Rarely, all T-waves remain inverted, which is called global idiopathic T-wave inversion (V1–V6).
- T-wave inversion without simultaneous ST-segment deviation: This is not a sign of ongoing ischemia, but may be post-ischemic. One type of post-ischemic T-wave inversion is especially acute, namely Wellen’s syndrome (characterized by deep T-wave inversions in V1–V6 in patient with recent episodes of chest pain). Cerebrovascular insult (bleeding). Pulmonary embolism. Perimyocarditis (after normalization of the ST-segment elevation, T-waves become inverted in perimyocarditis). Cardiomyopathy.
- T-wave inversion with simultaneous ST-segment deviation: acute (ongoing) myocardial ischaemia.
- High T-waves: Normal variant. Early repolarization. Hyperkalemia. Left ventricular hypertrophy. Left bundle branch block. Occasionally perimyocarditis. High (hyperacute) T-waves may be seen in the very early phase of STEMI.
- QTc duration men ≤0,45 s.
- QTc duration women ≤0,46 s.
- Prolonged QTc duration may cause malignant arrhythmias (torsade de pointes, which is a type of ventricular tachycardia).
- Shortened QTc duration (≤0.32 s) is rare, but may also cause malignant ventricular arrhythmias.
- The U-wave is seen occasionally, especially in well-trained individuals, and during low heart rate. It is largest in V3–V4. Amplitude is one fourth of T-wave amplitude.
- Acquired QT prolongation: anti arrhythmic drugs (procainamide, disopyramide, amiodarone, sotalol), psychiatric medications (tricyclic antidepressants, SSRI, lithium etc); antibiotics (macrolides, kinolones, atovaquone, klorokine, amantadin, foscarnet, atazanavir); hypokalemia, hypocalcemia, hypomagnesemia; cerebrovascular insult (bleeding); myocardial ischemia; cardiomyopathy; bradycardia; hypothyroidism; hypothermia. A complete list of drugs causing QT prolongation can be found here.
- Congenital QT prolongation: genetic disease of which there are approximately 15 variants.
- Short QTc syndrome (≤ 0,32 s): caused by hyperkalcemia and digoxin treatment. May cause malignant ventricular arrhythmia.
- Negative U-wave: high specificity for heart disease (including ischemia).
Compare with earlier ECG
It is fundamental to compare the current ECG with previous recordings. All changes are of interest and may indicate pathology.