The heart’s ability to adapt to chronic stress often results in structural remodeling, most notably atrial enlargement and ventricular hypertrophy. These alterations, while initially compensatory, can lead to significant cardiac dysfunction if left unchecked. The 12-lead EKG serves as a valuable tool in detecting and characterizing these structural changes, offering clinicians important insights into a patient’s cardiac status. This chapter will explore the EKG manifestations of atrial enlargement and ventricular hypertrophy, providing a systematic approach to recognizing these conditions.

Pathophysiology of Atrial Enlargement

Atrial enlargement occurs as a result of chronic hemodynamic stress on the atrial chambers. This stress can be due to increased pressure or volume load, leading to structural and electrical remodeling of the atrial myocardium. In left atrial enlargement (LAE), common causes include mitral valve disease, left ventricular dysfunction, and hypertension, which increase left atrial pressure and impair its capabilities of emptying. Right atrial enlargement (RAE) often results from conditions that elevate right-sided pressures, such as pulmonary hypertension, tricuspid valve disease, or right ventricular dysfunction. The enlarged atria become more susceptible to thromboembolic events and arrhythmias, particularly atrial fibrillation, due to altered conduction properties and increased fibrosis. Over time, atrial enlargement can lead to further deterioration of cardiac function, contributing to a cycle of progressive cardiac remodeling and dysfunction.

Interpretation of Atrial Enlargement

The electrical signature of a growing heart chamber can be subtly revealed through careful examination of the EKG. When the atria grow beyond their normal dimensions, they leave telltale signs in the form of altered P wave characteristics, as the P wave represents atrial depolarization. These changes in the P wave morphology, duration, and amplitude can vary depending on whether the left or right atrium is affected. Generally, an enlarged atrium produces a larger, wider, or more notched P wave compared to normal. However, the specific criteria for LAE and RAE differ, and it is crucial to understand these distinctions for accurate interpretation. By focusing on the nuances of P wave appearances with a keen eye and a systematic approach across different leads, health professionals can uncover valuable information about the heart’s structure and function, which can then guide further diagnostic and therapeutic decisions.

1. Left Atrial Enlargement

The left atrium plays a crucial role in cardiac function, serving as a reservoir and channel for oxygenated blood returning to the heart from the lungs. When this chamber enlarges due to chronic stress or disease, it leaves distinctive signs on the EKG. Left atrial enlargement is also called “P mitrale” because of its characteristic appearance on the EKG, specifically in lead II. The P wave in LAE often appears broad and notched due to delayed left atrial innervation, resembling the letter “M”, which is reminiscent of the mitral valve shape, hence the term “P mitrale” (mitral P wave).

Figure 10.1  Illustration of the heart showing left atrial enlargement. The left atrium becomes enlarged often due to chronic increased pressure or volume overload. This enlargement can be caused by conditions such as mitral valve disease, chronic hypertension, or heart failure.^[1]

Figure 10.2  The characteristic EKG changes associated left atrial enlargement (LAE), including a widened and notched P wave in lead II, and a biphasic P wave in lead V₁ with a prominent negative component. These changes indicate an increase in left atrial size, often due to conditions like mitral valve disease or chronic hypertension.^[2]

Figure 10.3  EKG displaying left atrial enlargement (LAE) in lead V₁ with the characteristic biphasic P wave and prominent negative deflection, indicating an enlarged left atrium. Additionally, lead V₂ shows similar changes, supporting the diagnosis of LAE.^[3]

Characteristics of LAE

• Leads to assess:
  • Lead II: Examine the overall P wave shape and duration
  • Lead V₁: Look for a specific P wave pattern
    • The P wave in V₁ typically has two components, an initial positive deflection followed by a negative deflection
    • The negative deflection (or “dip”) at the end of the P wave is key for assessing LAE
• Criteria for interpretation, either:
  • Prolonged P wave duration (≥0.12 secs) in lead II
  • Notched P wave appearance in lead II with a gap >0.04 secs between the two peaks (P mitrale)
  • In lead V₁, look for a P wave with:
    • A positive initial deflection followed by a negative deflection (i.e., a biphasic wave)
    • The negative portion of the P wave being >0.04 secs in duration with a depth ≥1 mm below the isoelectric line

Clinical Significance

• Indicator of chronic left atrial pressure or volume overload
• Associated with elevated risk of atrial fibrillation and thrombosis
• Predictor of adverse cardiovascular outcomes and mortality

Signs & Symptoms

• Often asymptomatic in early stages
• May present with symptoms of underlying cause (e.g., dyspnea in mitral valve disease)
• Palpitations or irregular heartbeat if atrial fibrillation develops

Treatment

• Address underlying cause (e.g., blood pressure control, valve repair)
• Anticoagulation may be considered if atrial fibrillation develops
• Regular monitoring and follow-up to assess progression

Causes

• Hypertension
• Mitral valve disease (stenosis or regurgitation)
• Left ventricular dysfunction or heart failure
• Aortic valve disease (stenosis or regurgitation)
• Chronic atrial fibrillation
• Congenital heart defects affecting the left heart

2. Right Atrial Enlargement

When the right atrium increases in size, it often occurs due to conditions that elevate right-sided cardiac pressure, altering the electrical signature of atrial depolarization with unique changes to the EKG. Recognizing these signs is crucial, as they can indicate underlying cardiac or pulmonary pathology. Right atrial enlargement is also called “P pulmonale” since it is commonly associated with pulmonary conditions, such as pulmonary hypertension, that increases chamber pressure of the right atrium. This results in a characteristic tall, peaked P wave on the EKG, particularly in the inferior leads, reflecting the strain on the right atrium due to pulmonary pathology.

Figure 10.4  Illustration of the heart showing right atrial enlargement (RAE). The right atrium enlarges often due to chronic increased pressure or volume overload as result from conditions such as chronic lung disease or pulmonary hypertension.^[4]

Figure 10.5  EKG displaying characteristic changes associated with right atrial enlargement (RAE), including tall, peaked P waves in leads II, III, and aVF, commonly referred to as “P pulmonale.” These changes indicate an increased right atrial size, often due to conditions such as chronic lung disease or pulmonary hypertension.^[5]

Characteristics of RAE

• Leads to assess:
  • Leads II, III, and aVF: Examine P wave amplitude
  • Lead V₁: Assess P wave shape and amplitude
• Criteria for interpretation, either:
  • Peaked, pointed P waves with amplitude ≥2.5 mm in leads II, III, or aVF (P pulmonale)
  • In lead V₁, initial positive deflection of P wave amplitude ≥1.5 mm
  • Width, or duration, of P wave does not change in any leads

Clinical Significance

• Indicator of right-sided cardiac pressure overload
• Associated with elevated risk of atrial arrhythmias
• May signal progression of underlying cardiopulmonary disease

Signs & Symptoms

• Often asymptomatic in early stages
• May present with symptoms of underlying cause (e.g., shortness of breath in pulmonary hypertension)
• Fatigue, peripheral edema, or right upper quadrant discomfort in advanced cases

Treatment

• Address underlying cause (e.g., treatment of pulmonary hypertension or tricuspid valve disease)
• Management of associated arrhythmias if present
• Regular monitoring and follow-up to assess progression

Causes

• Pulmonary hypertension
• Tricuspid valve disease (stenosis or regurgitation)
• Chronic lung disease (e.g., COPD, pulmonary fibrosis)
• Congenital heart defects affecting the right heart
• Right ventricular dysfunction or heart failure

Pathophysiology of Ventricular Hypertrophy

As we shift our focus from the atria to the ventricles, we encounter another form of cardiac adaptation to stress. The heart’s main pumping chambers respond to chronic pressure or volume overload by increasing muscle mass of the chamber walls. This process, triggered by conditions such as hypertension or valve disorders, initially serves as a compensatory mechanism to maintain cardiac function. However, this adaptation can eventually become counterproductive, leading to stiffened chambers and compromised function. The structural changes alter the heart’s electrical properties, manifesting as distinctive patterns in the QRS complex and ST-T segments on the EKG. These electrical changes serve as valuable clues, helping clinicians decipher the heart’s structural modifications and potential underlying issues.

Interpretation of Ventricular Hypertrophy

As the myocardial walls thicken in response to chronic stress, distinct patterns on the EKG become apparent. These electrical signatures manifest primarily in the QRS complex and ST-T segments, reflecting the increased muscle mass and accompanying altered conduction patterns. Clinicians examining an EKG for ventricular hypertrophy look for several key features: amplified QRS voltages, widened QRS complexes, and specific repolarization abnormalities (i.e., ST segment, T wave changes). These changes can vary depending on whether the left or right ventricle is predominantly affected. By systematically evaluating these EKG patterns, healthcare providers can gain valuable insights into the heart’s structural adaptations, which often indicate underlying cardiovascular conditions requiring further investigation and management.

It is worth noting that while the following criteria are widely used, EKG changes are an insensitive means of detecting ventricular hypertrophy. Patients with clinically significant ventricular hypertrophy as assessed via echocardiography may still have a relatively normal EKG. Therefore, echocardiography is generally considered more reliable for diagnosing ventricular hypertrophy.

3. Left Ventricular Hypertrophy

When the left ventricle faces persistent challenges in pumping blood against increased resistance or volume, such as from hypertension or aortic stenosis, it undergoes hypertrophy, thickening its muscular walls and creating distinct changes to the EKG. This increased muscle mass means there are more myocardial cells contributing to the electrical activity during each heartbeat. As a result, the electrical signals generated are stronger, leading to increased QRS amplitude and duration. In other words, the larger the cardiac muscle, the larger the electrical signal it produces. When interpreting EKGs for left ventricular hypertrophy (LVH), we can focus on increased QRS amplitudes in left-sided leads (i.e., leads I, aVL, V₅, V₆) and deep S waves in right-sided leads (i.e., leads III, V₁, V₂), while also considering non-voltage criteria like ST-T changes and left axis deviation. In clinical practice, there are several criteria used to identify LVH on an EKG. However, it is important to note that there is no single, universally accepted method. Different criteria may be used in different settings, but for the purposes of this text, we will focus on one primary method for clarity and simplicity. Keep in mind that while specific criteria are essential, the clinical context is vital for an accurate diagnosis.

Figure 10.6  Illustration and EKG demonstrating left ventricular hypertrophy (LVH). The upper figure shows an anatomical representation of the heart with thickened left ventricular walls, indicative of hypertrophy. The lower figure displays an EKG with characteristic features of LVH, including tall R waves in leads V₅ and V₆, and deep S waves in leads V₁ and V₂.^[6]

Characteristics of LVH

• Axis deviation: Left axis deviation, but not always present in LVH
• Leads to assess:
  • Limb leads I, III, aVL, aVF
  • Precordial leads V₁, V₂, V₅, V₆
• Voltage criteria for interpretation:
  • Limb leads
    • Lead I R wave + Lead III S wave = >25 mm
    • Lead aVL R wave >11 mm
    • Lead aVF >20 mm
  • Precordial leads
    • Lead V₅ or V₆ R wave >26 mm
    • Lead V₅ or V₆ R wave + Lead V₁ or V₂ S wave >35 mm
    • Largest R wave + largest S wave in precordial leads >45 mm
• Non-voltage criteria for interpretation:
  • Increased R wave peak time >50 ms in leads V₅ or V₆
  • ST segment depression and T wave inversion in left-sided leads

Clinical Significance

• LVH is an independent risk factor for cardiovascular morbidity and mortality
• It is associated with an increased risk of arrhythmias and sudden cardiac death
• LVH indicates long-standing hypertension or other cardiac conditions

Signs & Symptoms

• Often asymptomatic in early stages
• May present with symptoms of underlying cause (e.g., shortness of breath, chest discomfort)
• Palpitations or irregular heartbeat if arrhythmias develop

Treatment

• Address underlying cause (e.g., blood pressure control, aortic valve replacement if stenosis is indicated)
• Medication to reduce cardiac workload (e.g., ACE inhibitors, beta-blockers)
• Regular monitoring and follow-up to assess progression and response to treatment

Causes

• Hypertension (most common cause)
• Aortic valve stenosis
• Hypertrophy cardiomyopathy
• Athletic heart syndrome (physiological adaptation in some athletes, see “The Athlete’s Heart” chapter)
• Obesity
• Chronic kidney disease

Other Criteria for LVH Interpretation

Again, several criteria for LVH interpretation exist. Below are the most common ones.

• Cornell criteria = Lead aVL R wave + Lead V₃ S wave = >28 mm in males; >20 mm in females
• Modified Cornell criteria = Lead aVL R wave = >12 mm
• Sokolow-Lyon criteria = Lead V₁ S wave + Lead V₅ or V₆ R wave = >35 mm
• Romhilt-Estes LVH Point Score System: If the total score equals 4 indicates probable LVH, whereas a score of 5 or greater indicates definite LVH.
  1. Largest R wave or S wave in limb leads = ≥20 mm = 3 points
  2. Lead V₁ or V₂ S wave = ≥30 mm = 3 points
  3. Lead V₅ or V₆ R wave = ≥30 mm = 3 points
  4. ST-segment and T wave changes opposite of QRS complex without digoxin = 3 points
  5. ST-segment and T wave changes opposite of QRS complex with digoxin = 1 point
  6. Left atrial enlargement = 3 points
  7. Left axis deviation = 2 points
  8. QRS duration >90 ms = 1 point
  9. Intrinsicoid deflection in lead V₅ or V₆ > 50 ms = 1 point

4. Right Ventricular Hypertrophy

Right-sided heart complications typically stem from conditions affecting pulmonary circulation. Right ventricular hypertrophy (RVH) occurs when the right ventricle thickens in response to increased pressure or volume overload, often attributed to pulmonary pathologies such as pulmonary hypertension and chronic lung diseases. As previously explained, a hypertrophied myocardium leads to stronger electrical conduction, or greater amplitudes, which are valuable signs to examine for on the EKG. These key EKG changes associated with RVH include taller R waves in V₁ and V₂, deeper S waves in V₅ and V₆, and right axis deviation. It is important to note that while these EKG criteria for interpreting RVH are specific, they have low sensitivity. In other words, false positives are not uncommon with these criteria. Thus, clinical context and other diagnostic tools should be considered alongside EKG findings for a comprehensive evaluation of suspected RVH.

Figure 10.7  Illustration and EKG tracing demonstrating right ventricular hypertrophy (RVH). The upper figure shows an anatomical representation of the heart with thickened right ventricular walls, indicating hypertrophy. The lower figure displays an EKG with features characteristics of RVH, such as right axis deviation, tall R waves in V₁ and V₂, and deep S waves in V₅ and V₆. These changes are often associated with conditions that increase the workload of the right ventricle, such as chronic lung diseases or pulmonary hypertension.^[7]

Characteristics of RVH

• Axis deviation: Right axis deviation of +100º or greater
• Leads to assess:
  • Precordial leads V₁, V₅, V₆
• Voltage criteria for interpretation:
  • Lead V₁ R wave ≥7 mm tall (or R wave/S wave ratio >1.0)
  • Lead V₅ or V₆ S wave ≥7 mm deep (or R wave/S wave ratio <1.0)
  • Lead V₁ R wave + Lead V₅ or V₆ S wave = >10.5 mm
  • QRS duration <0.12 secs (i.e., changes not attributed to right bundle branch block)
• Additional supporting criteria:
  • Right atrial enlargement
  • ST depression and T wave inversion in right precordial leads V₁–V₄ and inferior leads II, III, aVF (known as right ventricular strain pattern)
  • Deep S waves in lateral leads I, aVL, V₅, V₆

Clinical Significance

• RVH is an indicator of right-sided cardiac pressure or volume overload
• It is associated with conditions such as pulmonary hypertension and chronic lung disease (e.g., COPD, pulmonary embolism)
• RVH can lead to right-sided heart failure and arrhythmias

Signs & Symptoms

• Often asymptomatic in early stages
• May present with symptoms of underlying cause (e.g., shortness of breath, fatigue)
• Peripheral edema, abdominal edema, right-upper quadrant pain

Treatment

• Address underlying cause (e.g., management of pulmonary hypertension or chronic lung disease)
• Medication to reduce right ventricular workload (e.g., diuretics, pulmonary vasodilators)
• Regular monitoring and follow-up to assess progression and response to treatment

Causes

• Pulmonary hypertension (primary or secondary)
• Chronic lung diseases (e.g., COPD, interstitial lung disease)
• Congenital heart defects (e.g., tetralogy of Fallot, isolated pulmonary stenosis)
• Pulmonary embolism
• Regurgitation from tricuspid valve disease or pulmonary valve disease
• Right ventricular outflow tract obstruction