Electrocardiogram – Indications, Contraindications

ECG is a non-invasive diagnostic modality that has a substantial clinical impact on investigating the severity of cardiovascular diseases.[rx] ECG is increasingly being used for monitoring of patients on antiarrhythmics and other drugs, as an integral part of preoperative assessment of patients undergoing non-cardiac surgery, and for screening individuals in high-risk occupations and those who are participating in sports. Also, EKG serves as a research tool for surveillance and experimental trials of drugs with recognized cardiac effects.[rx] Cardiovascular disease, as the number one cause of death, puts a great emphasis on healthcare providers to develop skills and knowledge in interpreting ECGs to provide the best care promptly. Many healthcare providers find the advanced interpretation of ECG findings a complicated task. Errors in the analysis can lead to misdiagnosis resulting in delaying the appropriate treatment. This activity seeks to provide a general understanding of the ECG mechanisms, interpretation techniques, and commonly encountered ECG findings.

Anatomy and Physiology

A basic understanding of cardiac anatomy and coronary distribution is essential to understand the electrocardiographic findings.

The heart is a vital organ of the body and occupies the space in the central chest between the lungs. Together with the blood vessels and blood, it constitutes the circulatory system of the body. The heart is a muscular organ comprised of four chambers that includes two atria (right and left) opening into right and left ventricles via tricuspid and mitral valves, respectively. A wall of muscle called the septum separates all four chambers. The heart receives deoxygenated blood from the whole body via superior and inferior vena cava, which first enters the right atrium. From here, it transits through the right ventricle and then passes into the lungs via the right and left pulmonary arteries, where it is oxygenated. The oxygenated blood from the lungs pours into the left atrium through the right and left pulmonary veins, and from here, it is pumped by the left ventricle into the aorta to the rest of the body. The heart derives its blood supply from the coronary arteries that branch off from the aorta. The right and left coronary arteries lie on the surface of the heart. With considerable heterogeneity among the general population, different regions of the heart receive vascular supply by the various branches of the coronary arteries. This anatomic distribution is significant because these cardiac regions are assessed by a 12-lead ECG to help localize and diagnose ischemic or infarcted areas. Written below are the following regions supplied by the different coronary arteries.

• Inferior Wall – Right coronary artery
• Anteroseptal – Left anterior descending artery
• Anteroapical – Left anterior descending artery (Distal)
• Anterolateral – Circumflex artery
• Posterior Wall – Right coronary artery

The heart is a mechanical pump whose activity is governed by the electrical conduction system. It is essential to have a good understanding of the physiology of the cardiac cells as this will help the reader appreciate how the heart works and the implications of findings on the ECG. The heart is made up of specialized cardiac muscle, which is striated and organized into sarcomeres. These muscle fibers contain a single central nucleus, numerous mitochondria, and myoglobin molecules. Extensive branching of the cardiac muscle fibers and their end-to-end connection with each other through intercalated discs make them contract in a wave-like fashion. This mechanical work of pumping blood to the whole body occurs in a synchronized manner and is under the control of the cardiac conduction system. It is comprised of two types of cells, pacemaker and non-pacemaker cells. Pacemaker cells are located primarily in the SA and AV node, and it is the SA node, which drives the rate and rhythm of the heart. The AV node gets suppressed by the more rapid pace of the SA node. [rx] The specialized function associated with the pacemaker cells is their spontaneous depolarization with no true resting potential. When spontaneous depolarization reaches the threshold voltage, it triggers a rapid depolarization followed by repolarization. The non-pacemaker cells mainly comprise the atrial and ventricular cardiac muscle cells and Purkinje fibers of the conduction system. They consist of true resting membrane potential, and upon initiation of an action potential, rapid depolarization is triggered, followed by a plateau phase and subsequent repolarization. Action potentials are generated by ion conductance via the opening and closing of the ion channels. Knowing which ECG leads corresponds to specific arteries helps in localizing the obstruction in acute ST-elevation MI or an age-indeterminate Q-wave infarction by observing predictable patterns on the ECG.[rx]

Indications of Electrocardiogram

The evolution of EKG from a string galvanometer to the modern-day advanced computerized machine has led to its use as a diagnostic and screening tool, making it the gold standard for diagnosing various cardiac diseases.

Owing to its widespread use in the field of medicine, the EKG has several indications listed below:

• Symptoms are the foremost indication in use for the EKG which includes palpitation, dizziness, cyanosis, chest pain, syncope, seizure, and poisoning
• Symptoms or signs associated with heart disease including tachycardia, bradycardia and clinical conditions including hypothermia, murmur, shock, hypotension, and hypertension
• To detect myocardial injury, ischemia, and the presence of prior infarction as well
• Rheumatic heart disease[rx]
• EKG changes in cases like drowning and electrocution are very valuable in the determination of necessary interventions[rx]
• Detecting pacemaker or defibrillator device malfunction, evaluate their programming and function, verify the analysis of arrhythmias and monitor for delivery of the appropriate electrical pacing in patients with defibrillators and pacemakers[rx]
• Evaluation of metabolic disorders
• Helpful for the assessment of blunt cardiac trauma[rx]
• Cardiopulmonary resuscitation
• Valuable aid in the study and differential diagnosis of congenital heart diseases[rx]
• Electrolyte imbalance and rhythm disorders[rx]
• To monitor the pharmacotherapeutic effects and adverse effects of drug therapy
• Perioperative anesthesia monitoring including preoperative assessment and intraoperative and postoperative monitoring
• Screening tool in a sports physical exam to rule out cardiomyopathy[rx]

Contraindications of Electrocardiogram

There are no absolute contraindications for EKG. The relative contraindications to its use include:

• Patient refusal
• Allergy to the adhesive used to affix the leads

Equipment

The American College of Cardiology (ACC), in conjunction with American Heart Association (AHA) and the Heart Rhythm Society (HRS), has formulated guidelines and also set technical standards for ECG equipment [rx]. With advancements, most of the EKG machines are digital and can autogenerate preliminary findings based on the morphology criteria.

The conventional ECG machine consists of 12 leads, which divide into two groups, i.e., limb leads and precordial leads. Limb leads are further categorized as standard bipolar limb leads I, II, and III, and augmented unipolar leads aVL, aVF, and aVR. The precordial leads include V1 to V6. The limb leads view the heart in a vertical plane, and the precordial leads record the electrical activity of the heart in the horizontal plane. The ECG represents a graphic recording of the electrical cardiac activity tracing on the electrocardiograph paper. The fundamental principle behind the recording of an ECG is an electromagnetic force, current, or vector that has both magnitude and direction. When a current of depolarization travels towards the electrode, it gets recorded as a positive deflection, and when it moves away from the electrode, it appears as a negative deflection.

• A current of repolarization traveling away from the positive electrode is seen as a positive deflection and towards a positive electrode as a negative deflection
• When the current is perpendicular to the electrode, it touches the baseline and produces a biphasic wave.

These concepts are easily applied to the heart while recording the ECG. There are several types of ECG monitoring equipment available, including continuous ECG monitoring, hardwire cardiac monitoring, telemetry, ambulatory electrocardiography, transtelephonic monitoring, and wireless mobile cardiac monitoring systems, etc. Furthermore, a duo of ECG and electronic stethoscopes have been designed into a portable, handheld device that can review ECG rhythms and intervals at the bedside for analysis. With the evolution of technology, there are electronic wristwatches that can also provide monitoring of the heart rate and rhythm and have proven to be of value in detecting atrial fibrillation.[rx] The accuracy of these devices, however, may be somewhat inferior when compared to a 12-lead ECG; and when prompted for abnormal findings, these require confirmation by standardized clinical testing available in the Cardiology office.

The equipment for performing a conventional 12-lead ECG includes:

• Electrodes (sensors)
• Gauze and skin preparation (alcohol rub) solution
• Razors or clippers or a roll of tape (for hair removal)
• Skin adhesive and/or antiperspirant
• ECG paper
• Cardiac monitor or electrocardiography machine

Personnel

The medical personnel that can perform the ECG procedure includes a doctor, nurse, or a qualified technician. Usually, it is performed by the technicians either in the clinics or hospitals and then interpreted by physicians. Often, these findings are confirmed by a cardiologist in a hospital-based setting.

Preparation

ECG merely requires special preparation. Before the procedure, a brief history regarding drugs and allergy to adhesive gel is necessary. The temperature of the room must be kept optimal to avoid shivering. The patient should be in a gown, and electrode sites identified. For good contact between the body surface and electrodes, it is advised to shave the chest hair and then apply the electrocardiographic adhesive gel for electrodes. Any metallic object like jewelry or a watch requires removal, if possible. Limb and precordial leads should be accurately placed to avoid vector misinterpretation. The patient must lie down and relax before recording the standard 10-second strip.

Technique

ECG machines are designed to record changes in electrical activity by drawing a trace on a moving electrocardiograph paper. The electrocardiograph moves at a speed of 25mm/sec. Time is plotted on the x-axis and voltage on the y-axis. In the x-axis, 1 second is divided into five large squares, each of which represents 0.2 sec. Each large square is further divided into five small squares of 0.04 sec each. The EKG machine is calibrated in such a way that an increase of voltage by one volt should move the stylus by 1 cm. The conventional 12-lead EKG consisting of six limbs and six precordial leads is organized into ten wires. The limb leads include I, II, III, aVL, aVR, and aVF and named as RA, LA, RL, and LL. The limb leads are color-coded to avoid misplacement (red- right arm, yellow- left arm, green- left leg, and black- right leg). The precordial leads V1 to V6 are attached to the surface of the chest.[rx]  For the correct location, the “Angle of Louis” method is an option, and the exact placement is as follows:

• V1 is placed to the right of the sternal border, and V2 is situated at the left of the sternal edge.
• V4 is placed at the level of the fifth intercostal space in the mid-clavicular line. V4 should be placed before V3. V3 is placed between V2 and V4.
• V5 is placed directly between V4 and V6.
• V6 is placed at the level of the fifth intercostal space in the mid-axillary line.
• V4 through V6 should line up horizontally along with the fifth intercostal space.

Complications

ECG is a safe, non-invasive, painless test with no major risks or complications. An allergic reaction or skin sensitivity to the adhesive gel can occur and usually resolves as soon as the electrode patches are removed, and in most cases, do not require any treatment. Artifacts and distortions pose serious diagnostic difficulties and may result in an inaccurate interpretation of the ECGs that may potentially result in an adverse therapeutic intervention.[rx][rx]

There can be a potential for misdiagnosis due to the inadvertent misplacement of ECG leads.[rx][tx]

Clinical Significance

Evaluation of Arrhythmia

In patients suspected of arrhythmias, an electrocardiogram (EKG) is the first step and will usually give the diagnosis. However, at times, the patient may suffer from paroxysmal arrhythmia. The following modalities can be used for diagnosing based on the frequency of the symptoms a patient has secondary to a suspected arrhythmia.

• Ambulatory EKG monitoring for patients with frequent symptoms
• The event recorder needs to be triggered by the patient to record and will not a viable choice for patients with syncope.
• Loop event recorder records up to 2 minutes before the trigger. It is good for patients with syncope.
• Implantable loop recorder for patients with less frequent symptoms.

Tachyarrhythmia

Tachyarrhythmia is defined as an abnormal rhythm with a ventricular heart rate of 100 beats per minute or more. It can be further classified based on the origin of the arrhythmia into:

Supraventricular Tachycardia (SVT): Arrhythmia originating from above the AV node (from atrial origin or AV junction origin).

• Atrial fibrillation (AFib)
• Atrial flutter
• Atrial tachycardia
• Atrial premature complex (PAC)
• Atrioventricular nodal reentrant tachycardia (AVNRT)
• Atrioventricular reentrant tachycardia (AVRT)
• AV junctional extrasystoles

Ventricular Tachycardia (VT): The origin of the arrhythmia is below the AV node.

• Ventricular fibrillation (V-fib)
• Ventricular premature beats (PVC)
• Ventricular tachycardia (sustained or non-sustained)

Tachyarrhythmias can also be classified based on the QRS complex duration into

Narrow QRS complex tachycardia when QRS is <120 milliseconds in duration:

• Sinus tachycardia
• Atrial tachycardia (AT)
• Atrial flutter
• Atrioventricular nodal reentrant tachycardia (AVNRT)
• Atrioventricular reentrant tachycardia (AVRT)
• Junctional ectopic tachycardia
• Sinoatrial nodal reentrant tachycardia (SANRT)
• Atrial fibrillation (irregular QRS complexes)

Wide QRS complex tachycardia (QRS ≥120 milliseconds in duration) is classified as monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, or ventricular fibrillation.

Supraventricular Tachycardia Syndromes

• These are usually narrow complex tachycardias with QRS width being less than 3 mm or 120 milliseconds on the EKG strip. Supraventricular tachycardia is further classified into atrioventricular reciprocating tachycardia, atrioventricular nodal reentrant tachycardia, and atrial tachycardia based on the mechanism of tachycardia. [rx][rx]

I. Atrioventricular reciprocating tachycardia (AVRT)

As found in Wolff-Parkinson-White syndrome (the presence of delta wave without arrhythmia doesn’t require investigation or treatment).

• Mechanism: Accessory pathway present outside of the AV node-Bundle of Kent. It can be further categorized into:
• • Antidromic: Conduction down the accessory pathway and up to AV node leading to the formation of a delta wave.
  • Orthodromic: Conduction down the AV node into an accessory pathway with no delta wave.
• Signs & Symptoms: Palpitation, shortness of breath, or syncope.
• EKG Findings: Slurred upstroke of the QRS, delta wave, may give an impression of the wide QRS complex.
• Management: Amiodarone or procainamide. If this fails, the next step is synchronized cardioversion.
• Definitive Therapy: Ablation of the accessory pathway.

 II. Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

• Mechanism: Slow & fast fibers present in AV node & peri-nodal tissue leading to re-entry. Signs & Symptoms: Sudden tachycardia, palpitation, shortness of breath, chest tightness, or syncope. EKG Findings: Narrow complex tachycardia with P waves hidden in T waves. Heart rate is in the range of 150-160 bpm.

Management

• Step 1: Carotid massage/Valsalva maneuver
• Step 2: Adenosine
• Step 3: Cardioversion
• Step 4: Ablation or chronic suppressive therapy with beta-blockers and calcium channel blockers such as diltiazem/verapamil.

 III. Atrial fibrillation

It is the most common arrhythmia in the United States. It affects more than 20% of the general population at some time in their lives.[rx] There are five types based on their duration:[rx]

• • New-onset]
  • Paroxysmal: Self-terminating or intermittent
  • Persistent: Fails to self-terminate within 7 days and requires treatments (medical or electrical cardioversion)
  • Long-standing Persistent: Lasts for ≥ 1 year
  • Permanent: Persistent for ≥ 1 year despite treatment
• Mechanism: Multiple reentrant wavelets due to atrial ectopy from muscle fibers near the proximal part of the pulmonary vein.
• Signs & Symptoms: It can be asymptomatic or can cause symptoms like palpitation, shortness of breath, irregularly irregular pulse, or even hypotension.
• EKG Findings: Irregularly irregular narrow complex tachycardia with no discernable P-waves.
• Management: The management strategy for atrial fibrillation can be classified into rate control or rhythm control. The decision to use a rate control or a rhythm-control strategy depends on the hemodynamic stability, candidacy for ablation, and the presence of co-morbidities. Patients with atrial fibrillation are at increased risk of ischemic-embolic stroke, and anticoagulation recommendations are based on the CHA2DS2VaSc score.
• CHA2DS2VaSc score is determined by the presence of the following factors: Congestive heart failure (CHF) with ejection fraction (EF) less than 40%, hypertension, age > 65 years, diabetes mellitus, history of stroke (non-hemorrhagic) or transient ischemic attack (TIA), vascular disease (peripheral vascular disease – PVD), age > 75 years, female sex. Each factor adds a point to the score, except for a history of stroke/TIA, which adds 2 points.

• • If the score is 0: No anticoagulation or aspirin based on individual assessment
  • If the score is 1: Aspirin or anticoagulation based on individual assessment.
  • If the score is 2 or more: Anticoagulation is recommended if not at high risk of bleeding.
• Rate Control Strategy: The heart rate goal is < 110 bpm in patients with chronic atrial fibrillation. It can be achieved with either beta-blockers or calcium channel blockers. Digoxin is usually used as adjuvant therapy in a patient with difficulty controlling rate or in heart failure patients.
• Cardioversion Strategy: Cardioversion is preferred in hemodynamically unstable patients or if rate control fails. It is also preferred in a young patient with no other co-morbidities. Cardioversion can be performed within 36 hrs of the onset of atrial fibrillation, but if the presentation is delayed or is of unknown duration, the absence of thrombi needs to be confirmed with a transesophageal echocardiogram (TEE). If a thrombus is present on an echocardiogram, the patient will need anticoagulation for at least three weeks before cardioversion can be performed. The patient needs to be on anticoagulation for at least four weeks post cardioversion. Various modalities are available for cardioversion therapy and include synchronized electric cardioversion or chemical cardioversion with medications including flecainide, propafenone, amiodarone, or dronedarone. Maze procedure is usually reserved for the patient undergoing other cardiac surgery.

Atrial Flutter

• Mechanism: Reentrant circuit usually around the tricuspid annulus in the right atrium.[rx]
• Signs & Symptoms: Can be asymptomatic, or it can cause palpitation, shortness of breath, or hypotension.
• EKG Findings: Regular tachycardia with Saw-tooth appearance of P wave with a variable degree of AV block.
• Management: General goals include control of ventricular rate with AV blocking agents (beta-blockers or calcium channel blockers), but the restoration of sinus rhythm through cardioversion or ablation is preferred.

Multifocal Atrial Tachycardia (MAT)

• Mechanism: multiple automatic atrial foci due to increased sympathetic tone secondary to various causes, including hypoxemia (chronic obstructive pulmonary disease (COPD), or stimulant use.
• Signs & Symptoms: Usually asymptomatic. Patients will have symptoms of the underlying illness, such as dyspnea.
• EKG Findings: Three or more P wave morphologies with different PR intervals.
• Management: Oxygen therapy if hypoxemic and treatment of the underlying cause.
• Refractory cases: Rate Control with calcium channel blockers as the first choice in the setting of COPD followed by beta-blockers.

Junctional tachycardia

• Mechanism: Rhythm arising from the AV node.
• Risk Factors: Post cardiac surgery, myocardial ischemia (or during reperfusion), or digoxin toxicity.
• Signs & Symptoms: Usually well-tolerated and asymptomatic.[rx]
• EKG Findings: Inverted P Wave in the lead 2 with short PR or No P waves with a narrow complex.
• Management: Treat the underlying cause.

 IV. Ventricular Tachycardia

Origin is below the AV node. It is the major cause of sudden cardiac deaths in the United States.

a) Non-Sustained Ventricular Tachycardia:[rx] When the rapid ventricular rhythm terminates on its own within 30 seconds.

• Mechanism: Channelopathies secondary to structural abnormality, electrolyte disturbances, metabolic imbalance, and the effect of pro-arrhythmic drugs.
• Risk Factors: Structural or ischemic heart disease.
• Signs & Symptoms: Asymptomatic or palpitations.
• EKG Findings: Monomorphic wide complex with more than three beats in a row but lasts less than three seconds.
• Management: Implantable cardioverter-defibrillator (ICD) and/or medical therapy.

b) Sustained Ventricular Tachycardia

• Mechanism: Presence of damaged fibers in ischemic heart disease leading to re-entry of current. Some patients do not have structural heart disease. Approximately 10% of the cases are idiopathic.
• Risk Factors: Structural heart disease and post-myocardial infarction.
• Signs & Symptoms: Palpitation, hypotension, or syncope.
• EKG Findings: Monomorphic wide complex tachycardia.
• Management: Intravenous lidocaine, amiodarone, or procainamide. Catheter ablation is an option too.

c) Ventricular Fibrillation

• Mechanism: Presence of damaged fibers in ischemic heart disease leading to re-entry of current leading to disorganized high-frequency excitation. Patients with Cardiomyopathies can have Ventricular fibrillation due to an increase in end-diastolic pressure, wall tension, or the presence of abnormal channels in ventricular fibers.
• Risk Factors: Structural heart disease and post-myocardial infarction.
• Signs & Symptoms: Syncope and death if not treated immediately.
• EKG Findings: Polymorphic fibrillatory waves.
• Management: Unsynchronized cardioversion followed by amiodarone.

d) Torsades De Pointes

• Mechanism: It is usually precipitated by premature ventricular contraction leading to “R on T phenomenon.”
• Risk Factors: Congenital long QTc with hypokalemia and hypomagnesemia.
• Signs & Symptoms: Syncope and death if not treated immediately.
• EKG Findings: Polymorphic wide-complex tachycardia with a heart rate > 300 bpm.
• Management: Intravenous magnesium or Isoproterenol, which increases heart rate and decreases QT-duration. Avoid hypokalemia and hypomagnesemia. Chronic therapy with beta-blockers in patients with long QT syndrome.

3. Bradyarrhythmias

Bradyarrhythmia is defined as a heart rate below 60 beats per minute (bpm) and comprises several rhythm disorders, including atrioventricular (A-V) blocks and sinus node disorders.[rx][rx]

Sinus Bradycardia

• Mechanism: Increased vagal tone. It can be physiological in athletes.
• Signs & Symptoms: Usually asymptomatic. It can lead to orthostasis or dizziness if pathological.
• EKG Findings: Sinus rhythm with an upright P wave in lead II and biphasic in V1.
• Management: No treatment is required unless pathological with an inadequate heart rate increase with leg raise test. Treat with isoproterenol or pacemaker if no relief.

Atrioventricular Blocks

• Mechanism: Atrial impulses are conducted with a delay or not at all when an electrical impulse reaches a tissue that not excitable or is in a refractory period.

a) First Degree AV Block: Caused by increased vagal tone or conduction impairment or due to medications.

• Signs & Symptoms: Generally asymptomatic but can cause dizziness.
• EKG Findings: PR interval is greater than 200 milliseconds.
• Management: Usually, no need to treat.

 b) Second Degree AV Block: Further classified into Mobitz I block, where there is a progressive prolongation of the PR interval followed by a skipped beat, and Mobitz II block, where there is a randomly dropped QRS complex on an EKG.

• Sign & Symptoms: Can be asymptomatic, dizziness, palpitations, weakness, syncope.
• EKG Findings: Mobitz type I shows progressive prolongation of the PR interval followed by a dropped QRS complex or dropped beat. Mobitz type II has randomly dropped QRS complexes.
• Management: Pacemaker is indicated in symptomatic Mobitz I and all of Mobitz II heart block.

c) Third Degree or complete AV Block

• Mechanism: Lack of conduction of atrial impulse to ventricle leading to independent contractions.
• Sign & Symptoms: Profound bradycardia, hypotension, and can lead to asystole and cardiac arrest.
• EKG Findings: Bradycardia, P waves occur independently of QRS and Wide QRS for ventricular rhythm.
• Management: Pacemaker placement.

Sinus Node Dysfunction

• Mechanism: Senescence of the SA node, an ischemic event involving SA node leading to impulse generation at a slower rate.

a) Sinus Pause: When the SA node has delayed impulse generation.

b) Sinus Arrest: Failure of impulse generation.

c) SA Nodal Exit Block: Failure of impulse transmission.

• Sign & Symptoms: Bradycardia, dizziness, palpitation, or syncope.
• EKG Findings: P wave not originating at a determined rate with regularity
• Management: Symptomatic patients require pacemaker placement.

The goal of the ECG interpretation is the ability to determine whether the ECG waves and intervals are normal or pathological. Electrical signal interpretation gives a good approximation of heart pathology. A standard 12 lead ECG is shown in. The best way to interpret an ECG is to read it systematically:

• RATE: For calculation of rate, the number of either small or large squares between an R-R interval should be first calculated. The rate can be calculated by either dividing 300 by the number of big squares or 1500 by the number of small squares between two R-waves. For an irregular rhythm, count the number of beats in a 10-second strip and multiply it by 6.[rx] Normal HR is 60 to 99 beats per minute. If it is less than 60, it’s called bradycardia and if greater than 100/min, it’s called tachycardia
• RHYTHM: The leads I, II, aVF, and V1 require inspection for an accurate interpretation of rhythm. It involves looking for five points: the presence or absence of regular P waves, duration of QRS complexes (narrow or wide), the correlation between P waves and QRS complexes, whether the rhythm is regular or irregular, and also importantly, the morphology of P-waves. A regular rhythm ECG has regular P waves, each preceding a QRS complex in a regular rhythm. Also, normal sinus rhythm demonstrates positive P-waves in leads I, II, and aVF, suggesting a downward propagation of atrial activation from the SA node. These features also help in identifying if the arrhythmia is originating in the atria or ventricles.[rx] Many disorders are related to rhythm abnormalities. For example, in atrial fibrillation, no real P waves can be seen due to the very fast atrial activity, and only a few impulses get delivered to ventricles making the rhythm irregularly irregular. The presence of ‘irregularly irregular’ narrow QRS complexes with no discrete P waves is the hallmark feature in the identification of atrial fibrillation.
• CARDIAC AXIS: It refers to the general direction of the heart’s depolarization wavefront in the frontal plane. The cardiac axis is related to the area of significant muscle bulk within the healthy conducting system. A typical cardiac axis is between -30 to +90 degrees. A quick way to estimate the axis is by looking at leads I and aVF. It can be defined as a normal axis when the QRS complex is positive in both leads I and aVF. A left axis deviation (between 0 and -90 degrees) is defined by the presence of positive QRS in the lead I and negative in lead aVF and right axis deviation(+90 and 180 degrees) by the presence of QRS negative in the lead I and positive in lead aVF. If both QRS complexes are negative in leads I and aVF, it is termed as extreme right axis deviation or indeterminate axis (-90 to 180 degrees).[rx] Other methods used for the determination of the cardiac axis include three lead analysis, isoelectric lead analysis, etc. There are several disorders in which the cardiac axis deviates.  Examples include conditions like old inferior MI, left ventricular hypertrophy, left bundle branch block where left axis deviation occurs while noting right axis deviation in conditions including right ventricular hypertrophy, pulmonary hypertension, hyperkalemia, and wolf-Parkinson-White syndrome, etc. The specific criteria on ECG for atrial and ventricular hypertrophy are devised from examining various leads and wave morphologies: for atrial abnormality (enlargement/ hypertrophy), leads II and V1 are usually assessed. Right atrial hypertrophy shows an increase in the amplitude in the first half of the P waves by 2.5 mm in inferior leads and a possible right axis deviation.[rx] It is often termed as P pulmonale because of its frequent association with chronic obstructive lung disease. Left atrial hypertrophy shows an increase in the amplitude of the terminal component and duration of the P wave, and it must descend at least 1 mm below the isoelectric line in lead V1 and must be at least 0.04 seconds (40 ms) in width. As the left atrium is electrically dominant, it shows no axis deviation.[rx]For the diagnosis of ventricular hypertrophy, it requires looking at several leads on the ECG. The right ventricular hypertrophy characteristically shows by right axis deviation along with the presence of a more significant R wave than S wave in lead V1, whereas in lead V6, a more significant S wave than R wave.[rx] Left ventricular hypertrophy is characterized by voltage criteria either by calculating the voltage of  R wave in V5 or V6 plus the S wave in V1 or V2 exceeding 35mm or by the voltage of R wave exceeding 13 mm in lead aVL. Infrequently, there is also the presence of secondary repolarization abnormalities, including asymmetric T wave inversion and downsloping  ST-segment depression, commonly also referred to as the strain pattern; the left axis deviation often accompanies this.[rx]
• P-WAVE: It represents atrial depolarization on the ECG. As atrial depolarization initiates by the SA node located in the right atrium, the right atrium gets depolarized first, followed by left atrial depolarization. So the first half of the P-wave represents right atrial depolarization and the second half left atrial depolarization. Its duration is three small squares wide and 2.5 small squares high. It is always positive in the lead I and II, and consistently negative in lead aVR in normal sinus rhythm. It is commonly biphasic in lead V1. An abnormal P-wave may indicate atrial enlargement.[rx]
• PR INTERVAL: It represents the time from the beginning of atrial depolarization to the start of ventricular depolarization and includes the delay that occurs at the AV node. The average interval is 3 to 5 small squares (120 to 200ms).[rx] Variations in the PR interval can lead to various disorders. Long PR interval may indicate first-degree AV block, and short interval may be present in conditions with accelerated AV conduction such as the presence of bypass tract or Wolf-Parkinson-White syndrome and Lown-Ganong-Levine syndrome.
• Heart Block: A conduction block can occur due to any obstruction in the normal pathway of the electrical conduction. Their anatomical location can be categorized as sinus node, atrioventricular node, or bundle branch blocks.
• Sinus node or sinoatrial exit block – occurs due to failed propagation of the impulses beyond SA node resulting in dropped P waves on the ECG. Common causes include sick sinus syndrome, increased vagal tone, inferior wall MI, vagal stimulation, myocarditis, drugs including digoxin, beta-blockers, etc.
• Atrioventricular or AV block – is a conduction block that can occur anywhere between the SA node and Purkinje fibers. There are three variants of AV blocks: first-degree, second-degree, and third-degree. Clinically significant points in diagnosing the AV blocks include careful measurement of the PR interval and examination of the relationship of the P waves to QRS complexes.
• First-degree heart block – is defined as prolongation of the PR interval by more than 200 milliseconds only. A single P wave precedes every QRS complex. It may be a normal finding in some individuals, but it can be an early sign of degenerative disease of the conduction system or a transient manifestation of myocarditis or drug toxicity, hypokalemia, acute rheumatic fever, etc. It usually does not require any treatment.[rx]
• Second-degree heart block – is of two types, i.e., Mobitz type I (also known as Wenkebach block) and Mobitz type II. In type I, the block across the AV node or bundle of His is variable and increases with each ensuing impulse, ultimately resulting in a drop of the impulse (usually every third or fourth impulse). On ECG, it shows as a progressive prolongation of the PR interval, and then suddenly, a P wave is not followed by the QRS complex. This sequence repeats itself in a regular manner. Most patients with Mobitz type I second-degree AV block are asymptomatic. Mobitz type I AV block may occur in the setting of acute myocardial ischemia or myocarditis and may also result in clinical deterioration if the resulting ventricular rate is inadequate to maintain cardiac output. Most patients with Mobitz type I second-degree AV block are asymptomatic and do not require any specific intervention. Rarely, patients with Mobitz type I block are symptomatic and demonstrate hemodynamic instability and may require treatment with either atropine (emergently) and eventually cardiac pacing. In type II  AV block, there is a dropped beat without the progressive lengthening of the PR interval. It follows the all-or-nothing phenomenon. It usually occurs below the AV node at the level of the bundle of His. It clinically signifies a severe underlying heart disease that can progress to third-degree heart block. When diagnosed, it usually requires prompt treatment with a permanent pacemaker.
• Third-degree heart block – is characterized by a complete electrical dissociation between the atria and ventricles, resulting in atria and the ventricles beat at their intrinsic rates. Degenerative disease of the conduction system is the leading cause of third-degree heart block. A complete heart block may present in acute myocardial infarction. Complete heart block may be reversible with prompt revascularization, especially in inferior MI. Lyme disease may be associated with a complete heart block and is potentially reversible with antibiotic therapy. In the case of irreversible or permanent complete heart block, a permanent pacemaker remains the mainstay of the treatment.
• Bundle branch block – results from the conduction block of either left or right bundle branches. It gets diagnosed by examining the width and configuration of the QRS complexes. The right bundle branch block is represented on the ECG by the presence of a widened QRS complex greater than 0.12 seconds along with an RSR pattern in V1 and V2. Also, there may be ST-segment depression and T wave inversions, and reciprocal changes in leads V5, V6, I, and aVL. Conduction system disorders can cause the right bundle branch block, but it may be present as a standard variant in specific individuals. The left bundle branch block is represented on the ECG by a widened QRS complex greater than 0.12 seconds, broad or notched R wave with prolonged upstroke in the leads V5, V6, I, and aVL, along with ST-segment depression and T wave inversion, and reciprocal changes in leads V1 and V2. Usually, a left axis deviation is also present. The left bundle branch usually signifies an underlying pathology, such as degenerative disease of the conduction system or ischemic heart disease.
• QRS COMPLEX: It represents ventricular depolarization as current passes down the AV node. A standard QRS complex has a duration of less than three small squares (under 120 ms, usually 60 to 100 ms). A prolonged QRS may indicate hyperkalemia or bundle branch block. A premature ventricular contraction or a ventricular rhythm can be associated with a wide QRS.
• SEPTAL Q-WAVE: Q-wave often appears as a tiny negative deflection in leads I, aVL, V5, and V6. It represents the depolarization of the interventricular septum. Its amplitude is not bigger than 0.1mV; that is why septal depolarization is not always visible on the EKG. Pathological Q-waves on EKG can signify an old infarct. A Q-wave duration of greater than 40 milliseconds (one small box), depth greater than 1 mm, or a size greater than 25% of the QRS complex amplitude is considered to be pathologic.[rx]
• R-WAVE: It is the tallest wave of the QRS complex, and it represents the electrical stimulus as it passes down the ventricles during depolarization. The R-wave progressively increases in amplitude moving right to the left in the precordial leads and is called R-wave progression. Lead V1 has the smallest R-wave, and lead V5 has the largest. A reduced R-wave progression has several causes, including prior anteroseptal MI, left ventricular hypertrophy or inaccurate lead placement, etc.[rx]
• S-WAVE: It represents the final depolarization of the Purkinje fibers. It is any downward deflection after R-wave. It may not be present in all ECG leads. S-wave is most significant in V1 and progressively becomes smaller to no S-wave in the lead V6.
• T-WAVE: It represents ventricular repolarization. Its morphology is highly susceptible to cardiac and noncardiac influences like ( hormonal, neurological). In leads with tall R-waves, it is usually positive (upward deflection). The suggested criteria for the typical T wave include the size of one-eighth or less than two-thirds of the size of the R wave and a height less than 10 mm. Abnormalities in the T-wave morphology can include inverted, flat, biphasic, or tall tented T-waves. T waves can be helpful in a variety of pathologies, tall T waves in anterior chest lead III, aVR, and V1 with a negative QRS complex may suggest acute myocardial ischemia.[rx] Other causes of T wave abnormalities are caused by physiological factors (e.g. postprandial state), endocrine or electrolyte imbalance, myocarditis, pericarditis, cardiomyopathy, postcardiac surgery state, pulmonary embolism, fever, infection, anemia, acid-base disorders, drugs, endogenous catecholamines, metabolic changes, acute abdominal process, intracranial pathology, etc.[rx]
• ST SEGMENT: It depicts the end of ventricular depolarization and the beginning of ventricular repolarization. The average duration of ST segment is less than 2 to 3 small squares (80-120ms). ST-segment is an isoelectric line and lies at the same level as PR-interval. Elevation or depression of the ST segment by 1mm or more, measured at J point, is considered abnormal. A J point is a region between the QRS complex and the ST segment. ST-elevation is highly specific if present in two or more contiguous leads in the setting of acute myocardial infarction. If the vertical distance on the ECG trace and the baseline at a point 0.04 seconds after the J-point is at least 1 mm in a limb lead or 2 mm in a precordial lead is clinically significant for the diagnosis of acute myocardial infarction. Correct ST segment interpretation is crucial as there is a type of ST-segment elevation present in healthy individuals that occurs due to early repolarization and is termed as J-point elevation. It is distinguished by the fact that the T wave does not merge with the ST segment and remains an independent wave. Several other disorders are also associated with ST-elevation, i.e., Prinzmetal angina, acute pericarditis, acute myocarditis, hyperkalemia, blunt trauma, pulmonary embolism, subarachnoid hemorrhage, Brugada syndrome, ventricular aneurysm, and left bundle branch block.[rx][rx][rx] ST-elevations are diffuse in acute pericarditis and associated with PR-depression in reference to TP-segments (except for leads V1 and aVR).[rx][rx][rx][rx]. In myocardial infarction, the ST elevation tends to be localized (inferior, anterior, posterior, lateral), often, but not always with reciprocal ST depression.[rx] Second, the PR segment displacement, which is attributable to the subepicardial atrial injury. PR elevation can present in aVR, and PR depression is best seen in II, aVF, V4-V6. PR-depression and slight downsloping appearance of TP segments are often known as Spodick’s sign of pericarditis and help distinguish acute pericarditis from acute MI.[rx] ST depression greater than 1 mm is often a sign of myocardial ischemia or angina. It can appear as a downsloping, upsloping, or horizontal segment on the ECG. A horizontal or downsloping ST depression greater than 0.5 mm at the J-point in two or more contiguous leads indicates myocardial ischemia. An upsloping ST depression in the precordial leads with prominent De Winter T waves is highly indicative of MI caused by occlusion of the left anterior descending artery.[rx] ST depression can represent a reciprocal change with a morphology that resembles “upside-down” ST elevation and typically seen in leads electrically opposite to the site of infarction. For example, posterior wall MI manifests as horizontal ST depression in leads V1-3 and is associated with tall R waves and upright T waves. Likewise, inferior wall STEMI produces reciprocal ST depression in leads I and aVL, and there is often a reciprocal ST-depression in leads III and aVF in lateral wall MI.[rx] ST depressions are also associated with several non-ischemic causes, including digoxin toxicity, hypokalemia, hypothermia, and tachycardia.[rx]
• QT INTERVAL: It represents all start of depolarization to the end of repolarization of ventricles. The normal QT interval duration is somewhat controversial, and various normal durations have been previously suggested. In general, the normal QT interval is less than 400 to 440 milliseconds (ms), or 0.4 to 0.44 seconds. Women usually have a slightly longer QT interval than men. A QT interval has an inverse relation to the heart rate. A prolonged QT interval presents an imminent risk for serious ventricular arrhythmias, including Torsades de Pointes, ventricular tachycardia, and ventricular fibrillation. A common cause of QT prolongation includes medications, electrolyte abnormalities such as hypocalcemia and hypomagnesemia and congenital long QT syndrome.[rx]A short QT interval ( less than 360 milliseconds) may be present associated with hypercalcemia, acidosis, hyperkalemia, hyperthermia, or short QT syndrome.[rx]
• U WAVE:  It is a small wave that follows the T wave. It represents the delayed repolarization of the papillary muscles or Purkinje fibers. It is commonly associated with hypokalemia.
• J WAVE: also known as Osborn wave, is an abnormal EKG finding in hypothermia. It appears as an extra deflection on ECG at the junction of the QRS complex and ST-segment.[rx]
• EPSILON WAVE: It is a small positive deflection usually found buried at the end of the QRS complex as a characteristic finding in arrhythmogenic right ventricular dysplasia.[rx]