Cognisnap

Smarter Medicine in a Snap

Author: Anil Potharaju

  • Sinoatrial (SA) Exit Blocks: Types, EKG Patterns, and Differentiation

    The sinoatrial (SA) node functions as the heart’s natural pacemaker, generating electrical impulses that travel through the atria and ventricles, facilitating synchronized heartbeats. A sinoatrial exit block occurs when these impulses are produced by the SA node but experience delays or fail to reach the atrial tissue, resulting in disruptions to the heart’s rhythm. Since it is the atrial depolarization that generates the P wave (not the depolarization of the sinus node), a sinoatrial exit block is indicated by the absence of a P wave. This article offers a thorough examination of the various types of SA exit blocks, their electrocardiogram (EKG) manifestations, and methods to differentiate them from conditions such as sinus pause.

    First-Degree Sinoatrial Exit Block

    In a first-degree SA exit block, there is a delay between the generation of an impulse in the SA node and its transmission to the atria. This delay occurs before atrial depolarization, which is represented by the P-wave on an EKG. Since the delay precedes the initiation of the P-wave, it cannot be directly observed on an EKG tracing. The atrial and ventricular rhythms remain normal, and the condition is typically asymptomatic and undetectable without invasive electrophysiological studies.

    Second-Degree Sinoatrial Exit Block

    Second-degree SA exit blocks are characterized by intermittent failures of SA node impulses to reach the atria. There are two types: Type I (Wenckebach) and Type II. Each type has distinct patterns and implications for cardiac function.

    Second-Degree SA Exit Block Type I (Wenckebach)

    Characteristics

    Type I SA exit block involves a gradual delay in the conduction of impulses from the SA node to the atria until an impulse is completely blocked. This results in a cyclic pattern where the intervals between P-waves (P-P intervals) progressively shorten until a P-wave is absent. After the missed beat, the cycle restarts.

    EKG Interpretation

    • Progressive Shortening of P-P Intervals: The time between successive P-waves decreases gradually.
    • Dropped P-Wave: Eventually, a P-wave fails to appear, indicating that the impulse did not reach the atria.
    • Pause Duration: The pause caused by the missing P-wave is less than twice the normal P-P interval, , signifying that one impulse has been blocked after a series of gradually shortening P-P intervals.

    This forms a pattern similar to the “Wenckebach” pattern observed in some AV blocks. However, it is essential to note that, in this case of SA exit block, the PR interval stays consistent.

    Analogy

    Imagine a runner who becomes increasingly fatigued with each lap, causing them to slow down slightly each time. Eventually, they are too exhausted to complete a lap, rest briefly, and then resume running at their original pace.

    Second-Degree SA Exit Block Type II

    Characteristics

    Type II SA exit block is marked by sudden, unexpected failures of SA node impulses to reach the atria without prior changes in conduction time. The P-P intervals are consistent until a P-wave is abruptly missing, resulting in a pause that is a multiple of the normal P-P interval.

    EKG Interpretation

    • Consistent P-P Intervals: The intervals between P-waves remain uniform.
    • Sudden Dropped P-Wave: A P-wave is unexpectedly absent.
    • Pause Duration: The pause equals two or more times the normal P-P interval, indicating that one or more impulses were blocked.

    Distinguishing Factors

    • The SA node continues to fire at regular intervals despite the block. So, the timing of subsequent P-waves aligns with the expected rhythm as if the block had not occurred.

    Third-Degree Sinoatrial Exit Block

    Characteristics

    In a third-degree SA exit block, none of the SA node’s impulses reach the atria. The SA node continues to generate impulses, but a complete conduction block prevents atrial depolarization. This results in an absence of P-waves on the EKG.

    EKG Interpretation

    • Absent P-Waves: No atrial activity is detected because impulses fail to exit the SA node.
    • Junctional or Ventricular Escape Rhythms: The heart may rely on subsidiary pacemakers, leading to slower heart rates and altered QRS complexes depending on the origin of the escape rhythm.
    • This is virtually indistinguishable from sinus arrest on an EKG. This is because P-waves, which depict atrial activity, don’t show the activity of the SA node directly. However, if the conduction resumes in a short time, the P-waves reappear in sync with the expected timing as if no pause occurred since the SA node function itself is unaffected.

  • Differentiating Ventricular rhythms from Supraventricular rhythms

    Accurate identification of ventricular rhythms on an EKG is crucial for effective diagnosis and management of cardiac arrhythmias. Ventricular rhythms originate from the ventricles and can be life-threatening, necessitating prompt recognition and treatment. However, certain factors can obscure EKG interpretation, making it challenging to differentiate ventricular rhythms from non-ventricular ones. This article explores these complicating factors and highlights distinguishing features that aid clinicians in accurately identifying ventricular rhythms.

    Factors Complicating Rhythm Interpretation

    Understanding the factors that can confuse rhythm interpretation is the first step toward accurate diagnosis:

    Rate-Dependent Bundle Branch Blocks

    Rate-dependent bundle branch blocks occur when the heart’s conduction system becomes refractory due to rapid heart rates, leading to intraventricular conduction defects. When the heart rate increases, a part of the conduction system may be refractory while another part allows the conduction to happen- this results in distorted QRS complexes on the EKG, which can mimic ventricular rhythms even when the underlying rhythm is supraventricular.

    Pre-Existing Conduction Abnormalities

    Individuals with existing conduction defects or bundle branch blocks may present with abnormal QRS complexes. These abnormalities can resemble ventricular arrhythmias, making it difficult to distinguish between ventricular and supraventricular rhythms based solely on QRS morphology.

    Distinguishing Features of Ventricular Rhythms

    Despite these challenges, several key features can help differentiate ventricular rhythms:

    Lack of Response to AV Node Slowing Maneuvers

    Ventricular rhythms typically do not respond to interventions aimed at slowing conduction through the atrioventricular (AV) node. Maneuvers such as carotid sinus massage, which stimulates the vagus nerve by applying pressure to the carotid artery, or administration of adenosine, have little to no effect on ventricular rhythms. If the rhythm persists unchanged despite these interventions, a ventricular origin is more likely.

    Presence of Cannon A Waves

    Cannon A waves are prominent pulsations observed in the jugular venous pulse. They occur when the right atrium contracts against a closed tricuspid valve, leading to a noticeable neck pulsation. The presence of cannon A waves indicates atrioventricular dissociation, a hallmark of ventricular rhythms where the atria and ventricles beat independently.

    Electrocardiogram Indicators

    Several EKG features are indicative of ventricular rhythms:

    Atrioventricular (AV) Dissociation

    AV dissociation is a key sign of ventricular rhythms. On the EKG, P waves representing atrial activity occur independently of the QRS complexes, indicating that the atria and ventricles are not synchronized. This lack of coordination suggests that the ventricular rhythm is originating from an ectopic focus within the ventricles.

    Fusion Beats

    Definition: Fusion beats occur when impulses from two different sources—the normal conduction system and an ectopic ventricular focus—simultaneously activate the ventricles.

    EKG Appearance: On the EKG, fusion beats appear as hybrid QRS complexes that are a blend of normal and ventricular beats. They do not resemble typical QRS complexes nor complete ventricular ectopic beats but are a combination of both.

    Clinical Significance: The presence of fusion beats indicates that while an ectopic ventricular focus is active, the normal conduction system occasionally penetrates the ventricles, suggesting ventricular tachycardia with intermittent normal conduction.

    Capture Beats

    Definition: Capture beats occur when a normal sinus impulse “captures” the ventricles amidst a run of ventricular beats, producing a normal QRS complex. Capture beats happen when the ventricles are “available” or free from the influence of the competing pacemaker. For instance, during a sequence of ventricular beats, if there’s a brief pause or delay in the ventricular rhythm, the sinus node (or another supraventricular source) might jump in and produce a normal beat. Like fusion beats, capture beats indicate the simultaneous existence of two different rhythms. They’re evidence that, even amidst an abnormal rhythm, the heart’s normal electrical pathways can still activate and produce a beat.

    EKG Appearance: On the EKG, a capture beat stands out as a normal QRS complex interrupting a sequence of wide, abnormal ventricular complexes.

    Clinical Significance: Capture beats confirm the presence of AV dissociation and indicate that the ventricles are temporarily responsive to normal sinus impulses, reinforcing the diagnosis of a ventricular rhythm. It stands out amidst abnormal rhythms, especially during a run of ventricular tachycardia, acting like a brief return to normalcy.

    Monomorphic vs. Polymorphic Rhythms

    • Monomorphic Ventricular Rhythms: These rhythms have QRS complexes that are consistent in shape and duration, indicating a uniform ventricular activation pattern from a single ectopic focus.
    • Polymorphic Ventricular Rhythms: These rhythms exhibit varying QRS morphologies and durations, suggesting multiple ventricular foci or changing conduction pathways within the ventricles.

    Changes in QRS Complex Morphology

    • Initial QRS Deflection: In ventricular rhythms, the initial deflection of the QRS complex often differs from that seen on a baseline EKG. The QRS complexes are typically wide (greater than 120 milliseconds) and have an abnormal morphology due to aberrant ventricular activation.
    • Comparison with Baseline EKG: Noting differences in QRS morphology compared to a patient’s baseline EKG can aid in identifying ventricular rhythms.
    • Precordial Lead Activity: In ventricular rhythms, the majority of deflections (movements) in the chest or precordial leads of the EKG are positive.

    Vereikei algorithm in aVR

    1. Initial dominant R-Wave in aVR
    2. Initial q- or r-wave in aVR ≥40 ms
    3. Notching on the initial Downstroke
    4. Vt≥Vi in aVR is suggestive of VT

    Conclusion

    Distinguishing ventricular rhythms from non-ventricular rhythms on an EKG is critical for appropriate clinical intervention. Recognizing factors that complicate EKG interpretation, such as rate-dependent bundle branch blocks and pre-existing conduction abnormalities, is essential. Key distinguishing features—lack of response to AV node slowing maneuvers, presence of cannon A waves, AV dissociation, fusion beats, capture beats, and changes in QRS morphology—provide valuable clues. By focusing on these indicators, clinicians can improve diagnostic accuracy.

  • Ventricular Rhythms

    Ventricular rhythms originate from the heart’s lower chambers—the ventricles. While these chambers are proficient at pumping blood throughout the body, they are not ideal pacemakers. When the ventricles initiate the heart’s rhythm, it often results in rapid and chaotic patterns. Recognizing these rhythms on an EKG is crucial, as they frequently indicate significant cardiac issues that can be life-threatening. The QRS is usually wide and distorted.

    Premature Ventricular Contractions (PVCs)

    PVCs are early heartbeats that start in the ventricles. They cause the QRS complex to appear prematurely and typically look wide and abnormal.

    • Retrograde P-Waves: Occasionally, a backward-moving (retrograde) P-wave follows the PVC, indicating that the impulse is moving back toward the atria.
    • Compensatory Pause: After a PVC, there is usually a compensatory pause. This means the interval between the beats surrounding the PVC is double the normal PP interval. This full compensatory pause helps distinguish PVCs from premature atrial contractions (PACs), which have an incomplete compensatory pause (the interval is less than double).
    • Patterns of PVCs:
      • Ventricular Bigeminy: A PVC occurs every other beat.
      • Ventricular Trigeminy: A PVC occurs every third beat.
    • R-on-T Phenomenon: Sometimes, a PVC occurs during the repolarization phase of the cardiac cycle, specifically on the T-wave. This is dangerous because it can lead to torsades de pointes, a form of ventricular tachycardia where the QRS complexes appear to twist around the baseline.

    Ventricular Parasystole

    Ventricular parasystole involves two independent rhythms occurring simultaneously: the normal sinus rhythm and an additional ventricular rhythm.

    • Independent Rhythms: Each rhythm is regular on its own, but together they create an irregular pattern on the EKG.
    • Consistent Intervals: The intervals between successive PVCs are consistent or directly related to the intrinsic rate of the ectopic ventricular focus.
    • Fusion Beats: Sometimes, the normal and ectopic impulses occur simultaneously, producing fusion beats that blend characteristics of both rhythms.

    Idioventricular Rhythms

    When the ventricles take over as the heart’s primary pacemaker due to failure of higher conduction systems, idioventricular rhythms occur. They consist of at least three consecutive ventricular beats with a rate of 100 beats per minute or less.

    • Types of Idioventricular Rhythms:
      • Idioventricular Rhythm: Heart rate is less than 50 beats per minute.
      • Accelerated Idioventricular Rhythm: Heart rate ranges from 50 to 100 beats per minute.
    • EKG Characteristics: Both types show wide, distorted QRS complexes. Retrograde P-waves may also be present due to the ventricles initiating the impulse.

    Thought for 19 seconds

    Understanding Ventricular Rhythms: A Comprehensive Guide to EKG Interpretation

    Introduction

    Ventricular rhythms originate from the heart’s lower chambers—the ventricles. While these chambers are proficient at pumping blood throughout the body, they are not ideal pacemakers. When the ventricles initiate the heart’s rhythm, it often results in rapid and chaotic patterns. Recognizing these rhythms on an EKG is crucial, as they frequently indicate significant cardiac issues that can be life-threatening.

    Characteristics of Ventricular Rhythms

    A key feature of ventricular rhythms on an EKG is a distorted QRS complex. This distortion occurs because the electrical impulse originates in the ventricles rather than following the normal conduction pathway from the atria.

    Premature Ventricular Contractions (PVCs)

    PVCs are early heartbeats that start in the ventricles. They cause the QRS complex to appear prematurely and typically look wide and abnormal.

    • Retrograde P-Waves: Occasionally, a backward-moving (retrograde) P-wave follows the PVC, indicating that the impulse is moving back toward the atria.
    • Compensatory Pause: After a PVC, there is usually a compensatory pause. This means the interval between the beats surrounding the PVC is double the normal PP interval. This full compensatory pause helps distinguish PVCs from premature atrial contractions (PACs), which have an incomplete compensatory pause (the interval is less than double).
    • Patterns of PVCs:
      • Ventricular Bigeminy: A PVC occurs every other beat.
      • Ventricular Trigeminy: A PVC occurs every third beat.
    • R-on-T Phenomenon: Sometimes, a PVC occurs during the repolarization phase of the cardiac cycle, specifically on the T-wave. This is dangerous because it can lead to torsades de pointes, a form of ventricular tachycardia where the QRS complexes appear to twist around the baseline.

    Ventricular Parasystole

    Ventricular parasystole involves two independent rhythms occurring simultaneously: the normal sinus rhythm and an additional ventricular rhythm.

    • Independent Rhythms: Each rhythm is regular on its own, but together they create an irregular pattern on the EKG.
    • Consistent Intervals: The intervals between successive PVCs are consistent or directly related to the intrinsic rate of the ectopic ventricular focus.
    • Fusion Beats: Sometimes, the normal and ectopic impulses occur simultaneously, producing fusion beats that blend characteristics of both rhythms.

    Idioventricular Rhythms

    When the ventricles take over as the heart’s primary pacemaker due to failure of higher conduction systems, idioventricular rhythms occur. They consist of at least three consecutive ventricular beats with a rate of 100 beats per minute or less.

    • Types of Idioventricular Rhythms:
      • Idioventricular Rhythm: Heart rate is less than 50 beats per minute.
      • Accelerated Idioventricular Rhythm: Heart rate ranges from 50 to 100 beats per minute.
    • EKG Characteristics: Both types show wide, distorted QRS complexes. Retrograde P-waves may also be present due to the ventricles initiating the impulse.

    Ventricular Tachycardia (VT)

    Ventricular tachycardia is a rapid heart rhythm originating from the ventricles, characterized by three or more consecutive ventricular beats at a rate exceeding 100 beats per minute.

    • EKG Features: The QRS complexes are wide and distorted. Retrograde P-waves may appear if the atria are activated by impulses traveling backward from the ventricles.
    • Types of VT:
      • Monomorphic VT: The QRS complexes have a uniform shape and size, indicating a single focal origin.
      • Polymorphic VT: The QRS complexes vary in shape, size, and axis, indicating multiple focal origins.
    • Duration:
      • Non-Sustained VT: Lasts less than 30 seconds.
      • Sustained VT: Persists for more than 30 seconds and requires immediate medical intervention.
    • Causes of Polymorphic VT:
      • Torsades de Pointes: Associated with a prolonged QT interval. An R-on-T PVC can trigger this arrhythmia, leading to a characteristic twisting of the QRS complexes around the baseline.
      • Ischemia-Induced VT: Occurs with a normal QT interval. Ischemic cardiac tissue can lead to instability, and a PVC can trigger polymorphic VT via the R-on-T phenomenon.

    Ventricular Fibrillation (VFib)

    Ventricular fibrillation is a chaotic and life-threatening arrhythmia where the ventricles quiver instead of contracting effectively.

    • EKG Appearance: The EKG shows rapid, irregular waves without distinct QRS complexes. The pattern may appear as coarse or fine undulations.
    • Heart Rate: The ventricular rate exceeds 300 beats per minute.
    • Clinical Significance: VFib results in the absence of effective cardiac output, leading to immediate loss of consciousness and requiring prompt defibrillation.

    Conclusion

    Recognizing ventricular rhythms on an EKG is essential for diagnosing and managing potentially life-threatening cardiac conditions. Understanding the characteristics of PVCs, ventricular parasystole, idioventricular rhythms, ventricular tachycardia, and ventricular fibrillation enables healthcare professionals to initiate appropriate interventions promptly.

  • Supraventricular Rhythms

    Supraventricular rhythms are cardiac rhythms originating above the ventricles but not from the sinoatrial (SA) node. These rhythms can significantly alter the morphology of P-waves on an electrocardiogram (EKG), making their identification crucial for accurate diagnosis and management. This guide provides an analytical overview of various supraventricular rhythms, their EKG characteristics, and key differentiating features. Note that stating someone has SVT isn’t specific enough- stating the type of SVT is crucial in terms of best next steps.

    Premature Atrial Contractions (PACs)

    Premature Atrial Contractions occur when an ectopic focus within the atria initiates a heartbeat earlier than expected. On the EKG, PACs are identified by P-waves with different morphology and axis compared to normal P-waves. These P-waves appear sooner than anticipated in the cardiac cycle, disrupting the regular rhythm established by the SA node. Recognizing PACs is important as they can be precursors to more serious arrhythmias.

    Atrial Escape Beats

    Atrial escape beats arise when non-SA nodal atrial sites generate impulses later than expected, often due to a temporary failure of the SA node. These beats typically occur at a rate of 60–75 beats per minute. The EKG will show altered P-wave morphology and axis, distinguishing them from normal sinus beats. Atrial escape beats serve as a protective mechanism to maintain heart rhythm when the primary pacemaker fails.

    Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

    AVNRT is characterized by a regular rhythm with a rapid rate of 150–250 beats per minute. On the EKG, P-waves may be located before, during, or after the QRS complex, and they might be hidden within it. The P-wave morphology changes, appearing inverted in lead II and upright in lead aVR due to the retrograde conduction of impulses. Carotid massage can be effective in slowing down or terminating AVNRT by increasing vagal tone, which influences the AV node.

    Atrioventricular Reentrant Tachycardia (AVRT)

    Often associated with Wolff-Parkinson-White (WPW) syndrome, AVRT involves an accessory pathway that allows impulses to bypass the AV node. WPW is characterized by a short PR interval and a delta wave on the EKG. AVRT presents as a regular tachycardia with either broad or narrow QRS complexes.

    Atrial Flutter

    Atrial flutter features a regular atrial rate of approximately 300 beats per minute. The ventricular rate is usually slower due to a conduction block (e.g., 2:1 or 3:1 block) at the AV node. The EKG displays characteristic “sawtooth” flutter waves. If the conduction block varies, the ventricular rate may become irregular. Carotid massage can increase the degree of block, further slowing the ventricular rate. Atrial flutter can distort the baseline, potentially leading to pseudo-Q waves or ST-T changes on the EKG.

    Atrial Fibrillation

    In atrial fibrillation, the atrial rate exceeds 350 beats per minute, resulting in no distinct P-waves on the EKG. The baseline appears chaotic due to erratic electrical activity. The ventricular response is irregularly irregular, a hallmark of this arrhythmia. Coarse atrial fibrillation can distort the EKG baseline, causing pseudo-Q waves or ST-T changes. Effective management is crucial to prevent complications like stroke.

    Atrial Tachycardia

    Atrial tachycardia presents as a regular rhythm with a rate of 100–200 beats per minute. The P-wave morphology and axis differ from those of normal sinus rhythm, indicating an ectopic atrial focus.

    Can be difficult to differentiate from other SVTs but the presence of the following suggest atrial tachycardia:

    • Rate: Atrial tachycardia has a slower atrial rate compared to atrial flutter.
    • Warm-Up Period: usually paroxysmal and may exhibit a “warm-up” period where the heart rate gradually increases.
    • Minimal response to carotid massage
    • Isoelectric Line: An isoelectric line is present between P-waves in atrial tachycardia, while atrial flutter lacks this due to continuous atrial activity.

    Wandering Atrial Pacemaker

    Wandering atrial pacemaker is characterized by an irregular rhythm with a heart rate below 100 beats per minute. The EKG shows at least three different P-wave morphologies and variable PR intervals, indicating multiple atrial pacemaker sites. This rhythm is generally benign and often seen in healthy individuals, particularly athletes or during sleep.

    Multifocal Atrial Tachycardia

    Similar to wandering atrial pacemaker but with a faster rate, multifocal atrial tachycardia has a heart rate of 100–200 beats per minute. The EKG reveals at least three different P-wave morphologies and varying PR intervals. This arrhythmia is commonly associated with pulmonary diseases and is significant in elderly patients with respiratory conditions. It is irregularly irregular and is often mistaken for atrial fibrillation on clinical exam as well as on EKGs.

    Junctional Rhythms

    Junctional rhythms originate near the atrioventricular (AV) node. On the EKG, P-waves may appear before, during, or after the QRS complex or may be hidden within it. The P-wave morphology changes, appearing inverted in lead II and upright in lead aVR due to retrograde atrial activation. Types of junctional rhythms include:

    Junctional Premature Complexes

    Occur earlier than expected due to premature impulses from the AV node.

    Junctional Escape Rhythm

    Occurs later than expected with a rate of 40–60 beats per minute, serving as a backup pacemaker.

    Accelerated Junctional Rhythm

    Similar to junctional escape rhythm but with a rate of 60–100 beats per minute.

    Junctional Ectopic Tachycardia

    A rapid rhythm exceeding 100 beats per minute. Differentiating it from AVNRT may require electrophysiological studies. Vagal maneuvers like carotid massage typically help in AVNRT but have minimal effect on junctional ectopic tachycardia.

    Conclusion

    Recognizing the differences in P-wave morphology, rhythm regularity, and response to interventions like carotid massage can aid in differentiating between the various supraventricular rhythms, leading to better patient outcomes.

  • Sinoatrial (SA) Node Rhythms

    The sinoatrial (SA) node, often called the heart’s natural pacemaker, initiates the electrical impulses that regulate heartbeats. Rhythms originating from the SA node are fundamental to cardiac function and EKG interpretation. This guide provides an in-depth analysis of these rhythms, including sinus rhythm, sinus arrhythmia, sinus bradycardia, sinus tachycardia, and sinus pause. Understanding these patterns is crucial for healthcare professionals to diagnose and manage cardiac conditions effectively.

    Sinus Rhythm

    Definition

    Sinus rhythm is the normal heartbeat rhythm originating from the SA node. It is characterized by:

    • Similar P Waves: Each P wave appears uniform and precedes every QRS complex.
    • Heart Rate: A steady rate between 60 and 100 beats per minute (bpm).
    • P Wave Axis: The P-wave axis is typically normal- P-waves are upright in I, II, and aVF- If inverted in any of these leads, an ectopic rhythm needs to be suspected even in the presence of P waves.

    EKG Characteristics

    • P Waves: Upright in leads I, II, and aVF.
    • QRS Complexes: Usually narrow unless there is a conduction defect.
    • PR Interval: Usually consistent duration, unless there is a heart block.

    Clinical Significance

    A normal sinus rhythm indicates proper functioning of the heart’s electrical conduction system. It serves as a baseline for identifying abnormalities and is essential for evaluating cardiac health.

    Sinus Arrhythmia

    Definition

    Sinus arrhythmia is a variation of normal sinus rhythm where there is a slight irregularity in the heartbeat timing. This irregularity is often related to the breathing cycle with the heart rate going up during inspiration and dropping during expiration.

    Mechanism

    The physiological mechanism involves interactions between the autonomic nervous system and cardiac pacemaker activity at the sinoatrial (SA) node:

    a) Respiratory Modulation of Vagal Tone

    • The primary driver of sinus arrhythmia is the respiratory-related changes in vagal (parasympathetic) tone:
      • Inspiration:
        • Increased input from stretch receptors in the lungs via the vagus nerve.
        • Reflex inhibition of vagal output to the SA node.
        • Heart rate increases due to reduced parasympathetic influence.
      • Expiration:
        • Reduced stretch receptor stimulation.
        • Enhanced vagal output.
        • Heart rate slows due to increased parasympathetic influence.

    b) Baroreceptor Reflex

    • The baroreceptor reflex helps stabilize blood pressure during respiration:
      • Inspiration decreases intrathoracic pressure, increasing venous return and cardiac output, momentarily lowering vagal tone and raising heart rate.
      • Expiration reverses this effect.

    c) Central Nervous System Regulation

    • Respiratory centers in the medulla oblongata influence both respiratory and cardiovascular rhythmicity, integrating signals to produce the sinus arrhythmia pattern.

    EKG Characteristics

    • P Waves: Normal appearance with consistent morphology.
    • P-to-QRS Ratio: Maintained at 1:1.
    • Heart Rate Variability (HRV): Slight changes in the R-R intervals corresponding to respiration—heart rate increases during inhalation and decreases during exhalation. The variability is typically between 0.12 and 0.2 seconds.
    • Rhythm: Regularly irregular due to predictable changes with breathing.

    Clinical Significance

    Sinus arrhythmia is common and typically benign, especially in young and healthy individuals. It reflects normal autonomic nervous system activity and does not usually require treatment. Impaired in old age, Parkinson’s disease (due to autonomic dysregulation), etc.

    Sinus Bradycardia

    Definition

    Sinus bradycardia occurs when the SA node generates impulses at a slower rate than normal, resulting in a heart rate of less than 60 bpm.

    EKG characteristics

    • Similar P Waves: Each P wave appears uniform and precedes every QRS complex.
    • Heart Rate: A steady rate below 60 beats per minute (bpm).
    • P Wave Axis: The P-wave axis is typically normal- P-waves are upright in I, II, and aVF- If inverted in any of these leads, an ectopic rhythm needs to be suspected even in the presence of P waves.
    • Note: Check for hidden P waves from premature atrial contractions (PACs) within the T waves in these cases to ensure it is infact sinus bradycardia and not a non-conducted PAC (resulting in a compensatory pause) followed by a normal sinus beat.

    Clinical Significance

    Symptomatic bradycardia typically warrants an intervention.

    Sinus Tachycardia

    Definition

    Sinus tachycardia is when the SA node fires impulses at a faster rate than normal, leading to a heart rate exceeding 100 bpm.

    EKG characteristics

    • Similar P Waves: Each P wave appears uniform and precedes every QRS complex.
    • Heart Rate: A steady rate above 100 beats per minute (bpm).
    • P Wave Axis: The P-wave axis is typically normal- P-waves are upright in I, II, and aVF- If inverted in any of these leads, an ectopic rhythm needs to be suspected even in the presence of P waves.

    Management

    Address the underlying cause is the usual treatment.

    Sinus Pause

    Definition

    A sinus pause is a temporary interruption of activity in the SA node, leading to a cessation of normal P waves or QRS complexes for at least two seconds. Typically, a regular rhythm is observed before and after the pause, which helps differentiate sinus arrest from other conditions like SA exit block. Unlike the predictable patterns observed in conditions such as second-degree SA exit block, sinus arrest lacks a discernible or consistent sequence.

    EKG Characteristics

    • Absence of P Waves: A flat line indicating no atrial activity.
    • Duration: The pause lasts for two seconds or more.
    • Escape Beats: If the pause is prolonged, other pacemaker cells (atrial, junctional, or ventricular) may initiate an impulse to compensate.
    • Rhythm: Irregular due to the unexpected pause.
    • Note: Check for hidden P waves from premature atrial contractions (PACs) within the T waves in these cases to ensure it is in fact a sinus pause and not a non-conducted PAC resulting in a compensatory pause followed by a normal sinus beat.

    Clinical Considerations

    • Symptoms: May include dizziness, lightheadedness, or syncope due to decreased cardiac output.
    • Causes: Increased vagal tone, medications (e.g., digitalis, beta-blockers), SA node disease, or ischemia.
    • Assessment: Look for hidden P waves within T waves from PACs to differentiate between sinus pause and blocked PACs.

    Management

    Treatment focuses on the underlying cause. Severe cases may require discontinuation of offending medications or implantation of a pacemaker to maintain heart rate and rhythm.

    Concern is warranted in the following conditions:

    1. Symptomatic patients:
      • exclude and remove any reversible causes
      • consider a pacemaker
    2. Asymptomatic patients:
      • While there is not a cut off as to when one might need to be concerned about a sinus pause in an asymptomatic individual, a pause> 3 seconds in sinus rhythm or >6 seconds in atrial fibrillation may warrant close monitoring as it may suggest underlying sick sinus syndrome.
    3. Pauses during sleep may suggest underlying sleep apnea.

  • A Step-by-Step Guide to reading an EKG

    Interpreting EKGs (Electrocardiograms) is an essential skill for healthcare professionals. As with any complex ability, mastering it necessitates the cultivation of robust habits and consistent practice.

    I fear not the man who has practiced 10,000 kicks once, but I fear the man who has practiced one kick 10,000 times.

    – Bruce Lee

    Bruce Lee’s wisdom extends to the interpretation of EKGs: the most proficient interpreters cultivate a systematic approach that they consistently apply until they attain mastery. Although the repetitive process may seem tedious and sluggish at first, with diligent practice, mastery is simply a matter of time.

    This guide aims to simplify EKG interpretation by outlining a systematic approach that covers all the essential aspects. By establishing the right habits and recognizing normal patterns, identifying abnormalities becomes straightforward. Let’s delve into the steps to enhance your EKG reading skills.

    Verifying the EKG

    Before interpreting an EKG, always verify:

    • Correct Patient Information: Ensure the EKG belongs to the right patient.
    • Quality of the EKG: Check for artifacts and confirm that the EKG was performed correctly.
    • Calibration: Confirm that the EKG is appropriately calibrated.
    • Clinical Context: Understand the patient’s clinical history and current presentation.
    • Comparison with Previous EKGs: If available, compare the current EKG with prior ones to identify new changes.

    Four Steps to Reading Every EKG

    Adopt these four essential steps when interpreting every EKG:

    Step 1: Calculate the Rate

    Determine the heart rate:

    • Normal Rate: 60–100 beats per minute (bpm)
    • Tachycardia: Heart rate > 100 bpm
    • Bradycardia: Heart rate < 60 bpm

    Step 2: Determine the Rhythm

    Assess the heart rhythm by examining:

    Regularity

    Is the rhythm regular, regularly irregular, or irregularly irregular?

    P-waves

    • Are normal P waves present?
    • Is the P wave morphology normal?

    P:QRS Ratio

    Is there a 1:1 ratio of P waves to QRS complexes?

    QRS Complexes

    • Are the QRS complexes narrow (< 100 ms) or wide (> 100 ms)?
    • A narrow QRS suggests a supraventricular origin.

    Step 3: Check the Axes

    Determine the electrical axis of the heart:

    P-wave axis

    • Normal: 0° and +75°.

    QRS axis

    • Normal Axis: Between -30° and +90°
    • Right Axis Deviation: Axis > +90°
    • Left Axis Deviation: Axis < -30°
    • Extreme Right Axis Deviation: -90° and +180°

    Step 4: Examine Intervals and Morphology

    Evaluate the intervals and waveform morphology:

    • P-wave morphology
    • PR Interval:
      • Normal: 120–200 ms (3–5 small squares)
      • Short PR Interval: May indicate pre-excitation syndromes.
      • Prolonged PR Interval: Suggests first-degree AV block.
    • PR Segment:
      • Elevated?
      • Depressed?
    • QRS Complex Morphology:
      • Check for normal morphology.
      • Assess for bundle branch blocks:
        • Right Bundle Branch Block (RBBB)
        • Left Bundle Branch Block (LBBB)
        • Left Anterior Fascicular Block (LAFB)
        • Left Posterior Fascicular Block (LPFB)
        • Non-Specific Intraventricular Conduction delay
    • ST Segment:
      • Elevated?
      • Depressed?
    • QT Interval: Use QTc and recognize that it’s use is limited if the heart rate is too high or too low or if there is a conduction defect.
      • Prolonged QTc: > 440 ms in men, > 460 ms in women.
      • Short QTc: < 350 ms.
      • Rule of Thumb: A normal QT interval is less than half the preceding RR interval.
    • T-wave abnormalities
      • Too tall?
      • Inverted?
    • U-waves
      • Are they prominent?

    Applying Occam’s Razor in EKG Interpretation

    When interpreting EKG findings, apply Occam’s Razor: choose the simplest diagnosis that accounts for all findings within the clinical context. If multiple abnormalities are present, consider whether they could be due to a single underlying cause rather than multiple unrelated issues.

  • Recognizing Normal Variations and Artifacts on an EKG

    While identifying pathological findings is essential, recognizing normal variations and artifacts is equally important to prevent misdiagnosis. This article explores several common normal variations and artifacts encountered during EKG interpretation, providing detailed insights to help clinicians distinguish between benign patterns and true abnormalities.

    Normal Variations in EKGs

    Early Repolarization

    Overview

    Early repolarization is usually a benign EKG pattern commonly seen in healthy young adults, especially athletes. The changes are typically seen in the precordial leads. However, in some individuals, it may be associated with an increased risk of sudden cardiac death, making accurate recognition vital.

    Characteristics

    • J-Point Elevation: A subtle elevation of the J-point, which is the junction between the end of the QRS complex and the start of the ST segment.
    • Upwardly Concave ST-Segment Elevation: The ST segment shows a concave upward elevation.
    • Concordant T-Waves: Upright T-waves that are in the same direction as the QRS complex.
    • J-Point Notching: A small notch at the J-point may be present.

    Differentiation from Pericarditis

    Early repolarization can mimic pericarditis but can be distinguished by:

    • Absence of PR Segment Changes: Unlike pericarditis, early repolarization does not exhibit PR depression in most leads or PR elevation in aVR and V1.
    • Stable Pattern Over Time: Early repolarization patterns are usually consistent and do not evolve, whereas pericarditis shows dynamic changes.
    • Lack of Clinical Symptoms: Patients are typically asymptomatic, whereas pericarditis presents with chest pain.

    Non-Specific ST-T Changes

    Overview

    Non-specific ST-T changes are subtle alterations in the ST segment and T-waves that do not meet criteria for specific cardiac disorders.

    Characteristics

    • ST-Segment Deviations: Slight elevations or depressions that are not indicative of a particular condition.
    • T-Wave Changes: Relatively flat or minimally inverted T-waves.
    • Distribution: These changes can occur in one or multiple leads.

    Clinical Significance

    • Common Causes: Can result from electrolyte imbalances, medications, or be a normal variant.
    • Interpretation: Should be considered in the context of the patient’s clinical history and symptoms.

    Juvenile T-Waves

    Overview

    Juvenile T-waves refer to negative T-waves in the right precordial leads (V1-V3) seen in children and adolescents, sometimes persisting into young adulthood.

    Characteristics

    • Inverted T-Waves: Negative T-waves in leads V1 to V3.
    • Symmetry: Typically symmetrical and shallow.

    Differentiation from Pathological T-Wave Inversions

    • Age Consideration: Normal in younger individuals; persistence into adulthood is a benign variant.
    • Clinical Correlation: Absence of symptoms or risk factors for heart disease supports a benign interpretation.

    S1S2S3 Pattern

    Overview

    The S1S2S3 pattern is characterized by S waves in leads I, II, and III and is often a normal finding.

    Characteristics

    • Presence of S Waves: Prominent S waves in all three limb leads.
    • Normal Variant: Common in young, healthy adults.

    Clinical Significance

    • Differential Diagnosis: Must be distinguished from conditions like right ventricular hypertrophy or pulmonary embolism, which may present similarly but are associated with clinical symptoms.

    Changes Due to Hyperventilation

    • Effects on EKG: Can cause ST-segment depression and T-wave inversions.
    • Mechanism: Alterations in autonomic tone and electrolyte shifts during rapid breathing.
    • Clinical Relevance: temporary changes that may mimic more serious conditions.

    Changes Due to Hyperventilation or Large Carbohydrate Meals

    • Effects on EKG: May lead to transient ST-T changes.
    • Mechanism: Postprandial metabolic changes affecting cardiac repolarization.
    • Clinical Relevance: temporary changes that may mimic more serious conditions.

    Artifacts in EKG Interpretation

    Artifacts are extraneous markings on the EKG tracing that are not generated by the heart’s electrical activity. Recognizing artifacts is crucial to avoid misdiagnosis.

    Tremor Artifacts

    Causes

    • Muscle Tremors: Conditions like Parkinson’s disease can cause rhythmic muscle activity.
    • Shivering: Due to cold or fever.

    Appearance on EKG

    • Erratic Baseline: Wavy or fuzzy baseline mimicking arrhythmias like atrial flutter.
    • Identification: Normal P-waves and QRS complexes may be visible amidst the artifact.

    Differentiation

    • Consistency: True arrhythmias will have consistent patterns, whereas artifacts are irregular.
    • Patient Observation: Noting tremors or shivering during EKG recording.

    Artifacts from Patient Movement

    Causes

    • Physical Activity: Combing hair, brushing teeth, or other movements during EKG recording.

    Appearance on EKG

    • False Tachyarrhythmias: Rapid, irregular waves that may mimic ventricular tachycardia.
    • Identification: Presence of normal complexes within the artifact; correlation with patient activity.

    Skeletal Muscle Interference

    Causes

    • Voluntary Muscle Contractions: Tensing muscles can introduce noise.
    • Involuntary Movements: Such as spasms or twitches as in shivering.

    Appearance on EKG

    • Baseline Distortions: Irregular, high-frequency noise superimposed on the tracing.
    • Identification: Artifact is often localized to specific leads corresponding to the area of muscle activity.

    Equipment Issues

    Causes

    • Poor Electrode Contact: Due to dried gel, oily skin, or hair.
    • Faulty Leads: Damaged cables or connectors.
    • Machine Malfunction: Calibration errors or defective hardware.

    Appearance on EKG

    • Unstable Baseline: Wandering or drifting baseline making interpretation difficult.
    • Sudden Changes: Abrupt shifts or loss of signal in one or more leads.

    Resolution

    • Equipment Check: Ensuring all leads are properly connected and the machine is functioning.
    • Skin Preparation: Cleaning the skin and reapplying electrodes as needed.

    An interesting question: If you see a flat line, how do you know if it is because of sinus arrest or a third degree block or a disconnected lead?

    A flatline could be seen in one of the three conditions:

    • When a lead is connected to the chest, there is usually a “noise” even when it appears that the recording is a flat line- we would see some degree of activity because of reasons such as interference from other muscles, poor electrode contact from skin oil/ hair, etc. A perfectly flat line should prompt the consideration of a disconnected lead.
    • A flat line with small deflections may suggest a third degree heart block with asystole (the deflections being the p-waves) while a flat line would suggest sinus arrest.

    Unstable Baseline (Baseline Wander)

    Causes

    • Respiration: Deep breathing can cause the baseline to move up and down.
    • Movement: Shifting position or talking during the recording.

    Appearance on EKG

    • Slow Oscillations: The entire tracing appears to undulate over several seconds.
    • Identification: Baseline wander is typically synchronized with respiratory cycles.

    Management

    • Breath Holding: Asking the patient to hold their breath briefly can stabilize the baseline.
    • Comfortable Positioning: Ensuring the patient is relaxed and still.

    Understanding and recognizing normal variations and artifacts in EKGs are essential components of accurate interpretation. By being aware of these common patterns and their characteristics, clinicians can differentiate between benign findings and true abnormalities, thereby improving diagnostic accuracy and patient care.

  • The Basic Components of an EKG: Waves, Segments and Intervals

    An EKG tracing consists of repeating patterns that correspond to specific electrical events in the heart. The EKG captures the various waves, segments, and intervals that represent different stages of the cardiac cycle. But what do these terms mean?

    Waves

    Waves represent the electrical activity associated with the depolarization or repolarization of the heart chambers.

    • P Wave: Indicates atrial depolarization, which triggers the atria (upper chambers) to contract.

    • QRS Complex: Reflects ventricular depolarization, causing the ventricles (lower chambers) to contract.

    • T Wave: Represents ventricular repolarization, the process of the ventricles resetting electrically for the next heartbeat.

    Sequence: The heart’s electrical cycle follows this pattern—P wave, brief pause, QRS complex, short pause, T wave. This sequence repeats with each heartbeat.

    Segments

    Segments are the straight lines (normally isoelectric lines- i.e, they are relatively horizontal and correspond to the “baseline” of the EKG) between waves and represent periods without electrical activity.

    • PR Segment: The line from the end of the P wave to the beginning of the QRS complex. It reflects the delay at the atrioventricular (AV) node.

    • ST Segment: The line from the end of the QRS complex to the beginning of the T wave. It indicates when the ventricles are depolarized.

    While in a normal EKG, these segments should be at baseline, they may be elevated or depressed in certain pathologies. So, when trying to determine what the actual baseline of the EKG is when evaluating a pathology, the TP Segment should be used.

    • TP Segment: The line from the end of the T wave to the beginning of the P wave. This part of the EKG typically has no electrical activity even in most pathologies and so, is considered the baseline of an EKG.

    Intervals

    Intervals include one or more waves plus the connecting segments, representing the duration of specific electrical events.

    • PR Interval: Extends from the beginning of the P wave to the beginning of the QRS complex. It represents the time from the start of atrial depolarization to the start of ventricular depolarization.

    • QRS Interval: Measures the duration of the QRS complex alone, indicating how quickly the ventricles depolarize.

    • QT Interval: Spans from the beginning of the QRS complex to the end of the T wave. It reflects the total time for ventricular depolarization and repolarization.

    Electrical Activity vs. Mechanical Contraction

    While the EKG displays the heart’s electrical activity, it does not directly show the mechanical contraction (the actual pumping action).

    • Electrical Activity: Initiates muscle contractions through electrical impulses.

    • Mechanical Contraction: The physical response to electrical stimulation, pumping blood throughout the body—a process known as excitation-contraction coupling.

    Important: Normal electrical activity usually leads to effective mechanical contractions, but not always.

    Pulseless Electrical Activity (PEA)

    Sometimes, electrical signals occur without effective mechanical contractions. This condition is known as pulseless electrical activity (PEA).

    Characteristics of PEA:

    • The EKG may display normal or near-normal electrical patterns.

    • The heart fails to contract effectively.

    • There is no palpable pulse or blood circulation.

  • Normal EKG Rhythm, Axis, Intervals, and Waves

    Normal Sinus Rhythm

    Normal sinus rhythm is the typical rhythm of a healthy heart, distinguished by the following characteristics:

    1:1 Ratio of P-Waves to QRS Complexes: Each P-wave is succeeded by a QRS complex, demonstrating that every atrial depolarization triggers a corresponding ventricular depolarization.

    Regular Rhythm: The intervals between heartbeats are consistent, indicating a steady and uniform heart rate.

    Consistent P-Wave Morphology: P-waves exhibit uniform morphology, typically appearing upright (positive) in lead II and inverted (negative) in lead aVR.

    Intervals and Waves

    Grasping the different intervals and waves on an EKG is essential for accurate interpretation of cardiac function. Here is an overview of each component.

    P-Wave

    Represents Atrial Depolarization: The process of electrical activation in the atria.

    Components:

    • The first part reflects the right atrium.
    • The middle part reflects both atria.
    • The terminal part reflects the left atrium

    Depolarization Pathway:

    • Begins at the sinus node in the right atrium.
    • Spreads from right to left and slightly downward (angle of 0–75 degrees).

    Lead Deflections:

    • Leads facing the depolarization wave (I, II, aVL, aVF, V5, V6) show a positive deflection.
    • Leads facing away (e.g., aVR) show a negative deflection.
    • Lead V1, being perpendicular, records a biphasic P-wave (positive then negative).

    Normal P-Wave Characteristics:

    • Axis: 0–75 degrees.
    • Duration: Less than 0.12 seconds.
    • Amplitude:
      • Less than 2.5 mm in lead II (usually the tallest P-wave).
      • In V1:
        • Positive portion less than 1.5 mm.
        • Negative portion less than 1 mm in amplitude and duration.

    Note: The P-wave is smaller in amplitude compared to the QRS complex because the atria are smaller and less muscular than the ventricles.

    An interesting Exercise: What does a normal P wave look like in lead III, assuming the normal P wave vector is 0 to 75 degrees?

    If the P wave axis falls between 0 and 30 degrees, lead III records a primarily negative deflection. If it’s 30 degrees, it’s biphasic. If it’s between 30 and 75 degrees, it records a primarily positive deflection.

    PR Interval

    • Definition: The time from the start of atrial depolarization (beginning of the P-wave) to the start of ventricular depolarization (beginning of the QRS complex).
    • Reflects: primarily the delay in conduction at the AV node.
    • Duration: Typically 0.12 to 0.20 seconds (three to five small boxes on the EKG).

    PR Segment

    Straight line from the end of p-wave to the beginning of QRS- Should be isoelectric (at baseline). Elevations or depressions may indicate underlying pathology.

    QRS Complex

    • Represents Ventricular Depolarization.
    • Duration: Normally less than 0.10 seconds.
    • Depolarization Pathway:
      • After the AV node, the impulse travels through the bundle of His.
      • Depolarization starts in the inter-ventricular septum, usually from left to right, handled by the left bundle branch’s septal fascicle..

    Q-Wave: Normal vs. Abnormal.

    • Small Q-waves may be seen in leads I, aVL, V5, and V6 due to septal depolarization as it travels from left to right, away from these leads.
    • Concerning Q-Waves:
      • Any Q-wave in leads V2 to V3 ≥ 20 ms or a QS complex in these leads.
      • Q-wave ≥ 30 ms and ≥ 0.1 mV deep in two contiguous leads where a positive deflection is expected.
      • QS complex in leads I, II, aVL, aVF, V4 to V6 (leads where we expect a net positive deflection)
    • Note: Q-waves in aVR are not significant; can be normal in lead III.

    QRS axis

    The QRS complex amplitude is significantly greater than the P wave amplitude due to the ventricles’ much higher muscular mass compared to the atria. Furthermore, the left ventricle dominates what we see on the EKG due to its larger mass.

    Determining the Axis

    A good way to determine the axis is by looking at the net vector of the wave being analyzed in 3 leads:

    • I: since it is aligned at 0°, any vector between – 90° and +90° will be registered as a net positive deflection. Otherwise, it will be negative.
    • II: since it is aligned at 60°, any vector between – 30° and +120° will be registered as a net positive deflection. Otherwise, it will be negative.
    • aVF: since it is aligned at 90°, any vector between 0° and 180° will be registered as a net positive deflection. Otherwise, it will be negative.

    By looking at the wave in each of these leads and looking for an overlap, we can determine the axis of a wave.

    IIIaVFOverlapQRS Axis
    +++0° to 90°Normal
    ++–0° to -30°Normal
    +–+N/ANot possible
    +––-30° to -90°Left axis deviation
    –++90° to 150°Right Axis Deviation
    –+–N/ANot possible
    ––+150° to 180°Right Axis Deviation
    –––180° to -90°Extreme Right Axis Deviation

    Normal, early, and poor R-wave progression

    • R Wave Progression in Precordial Leads:
      • V1 and V2: Show deep S-waves due to right ventricle overlay.
      • V5 and V6: Show tall R-waves due to left ventricle overlay.
      • Transition Zone: R-wave becomes taller than the S-wave, usually in V3 or V4.
    • Early R-Wave Progression: Transition occurs in V1 or V2.
    • Late R-Wave Progression: Transition occurs in V5 or V6.

    Normal vs. Low voltage

    • Normal Voltage: R-wave height plus S-wave depth should be at least 5 mm in limb leads. Also, it needs to be at least 10 mm in precordial leads to avoid low voltage designation.

    J-Point

    • Definition: The point where the QRS complex transitions into the ST segment. The QRS complex represents the depolarization of the ventricles. The ST segment, on the other hand, represents the period when the ventricles are depolarized, but have not yet begun to repolarize.
    • Significance:
      • Used as a reference for assessing the ST segment.
      • Correct identification is crucial for detecting ST segment elevations or depressions, which can indicate myocardial infarction or ischemia.

    ST Segment

    • Definition: Extends from the end of the QRS complex to the beginning of the T-wave.
    • Represents: The period when the ventricles are depolarized but have not yet started repolarizing.
    • Normal Characteristics:
      • Usually horizontal or gently upsloping.
      • At the same level as the TP segment (isoelectric line).
    • Abnormal Elevations (Measured at the J-point):
      • Must be ≥ 0.1 mV in most leads.
      • In leads V2 to V3:
        • ≥ 0.15 mV in women.
        • ≥ 0.2 mV in men ≥ 40 years.
        • ≥ 0.25 mV in men < 40 years.
    • Abnormal Depressions: Horizontal or downsloping ST-segment depression ≥ 0.5 mm below baseline measured 0.08 seconds (2 small boxes) after the J-point in two contiguous leads.

    T-wave

    • Represents Ventricular Repolarization.
    • Normal Characteristics:
      • Positive in leads with a positive QRS complex.
      • Negative in leads with a negative QRS complex.
    • Amplitude: Usually 1/3 to 2/3 the height of the corresponding R-wave.
    • Shape: Typically asymmetric with a slow upstroke and rapid downstroke.
    • Abnormalities:
      • Peaked T-Waves: T-waves taller than 5 mm in limb leads or 10 mm in precordial leads may be concerning.
      • Inverted T-Waves: Symmetric inversion of more than 1 mm may indicate pathology.

    QT Interval

    • Definition: The time from the start of ventricular depolarization (beginning of QRS complex) to the end of ventricular repolarization (end of T-wave).
    • Measurement:
      • From the beginning of the QRS complex to where the T-wave returns to baseline.
      • Use a tangent line on the downslope of the T-wave if the end is not clear.
    • Duration:
      • Varies with heart rate; usually about 40% of the cardiac cycle.
      • Corrected QT (QTc): What is normal is dependent on the rate and QT is not very predictive of an adverse outcome at extremes of heart rate or in bundle branch blocks.
        • Adjusted for heart rate using the formula: QTc = QT / √RR.
        • Normal QTc Range: 0.35 to 0.46 seconds.
        • Quick Assessment: The QT interval should be less than half the preceding RR interval.

    U-Waves

    • Definition: A small wave that may follow the T-wave.
    • Origin: Not fully understood.
    • Characteristics: Typically a small upward deflection. Smaller than the T-wave and may be difficult to see.
    • Clinical Significance: Prominent U-waves (> 2 mm) may be seen in conditions like hypokalemia and bradycardia.

    TP Segment

    • Definition: The segment from the end of the T-wave to the beginning of the next P-wave.
    • Significance: Considered the true isoelectric line and used as a reference point to compare elevations or depressions in the PR and ST segments.

  • Estimating the Heart Rate on an Electrocardiogram

    This post will guide you through estimating the heart rate using the small and large squares on EKG paper, especially when the heart rhythm is regular.

    As we previously discussed, a standard EKG has several large squares measuring 5mm x 5mm that are divided into smaller squares measuring 1mm x 1mm. The standard EKG records at a rate of 25 mm/ second. Since each large square is 5mm wide, there are a total of 5 large squares per second. So one large square reflects 1sec/5 squares= 0.2 seconds. Since we have 5 small squares per large square, each small square is 0.2/5=0.04 seconds.

    Total Squares in One Minute

    Large Squares: 60 seconds / 0.20 seconds per large square = 300 large squares per minute.

    Small Squares: 60 seconds / 0.04 seconds per small square = 1500 small squares per minute.

    Calculating Heart Rate Using Large Squares

    Since we know that each large square is 0.2 seconds, if we had a QRS every large square, the rate would be 60 second

    Method: Divide 300 by the number of large squares between two consecutive heartbeats.

    • Formula: Heart Rate = 300 / Number of Large Squares between R-R intervals
    • Examples:
      • 1 Large Square: 300 / 1 = 300 bpm
      • 2 Large Squares: 300 / 2 = 150 bpm
      • 3 Large Squares: 300 / 3 = 100 bpm
      • 4 Large Squares: 300 / 4 = 75 bpm
      • 5 Large Squares: 300 / 5 = 60 bpm
      • 6 Large Squares: 300 / 6 = 50 bpm

    Calculating Heart Rate Using Small Squares

    Method: Divide 1500 by the number of small squares between two consecutive heartbeats (R-R intervals).

    • Formula: Heart Rate = 1500 / Number of Small Squares between R-R intervals
    • Example: If there are 25 small squares between beats, Heart Rate = 1500 / 25 = 60 beats per minute

    Estimating Heart Rate in Irregular Rhythms

    When the heart rhythm is irregular, the usual methods using small or large squares may not be accurate. Instead, use the 10-second rule.

    10-Second Rule Method

    • Step 1: Count the number of QRS complexes (heartbeats) in a 10-second EKG strip.
    • Step 2: Multiply that number by 6 to estimate the beats per minute.

    Why It Works

    • A standard EKG strip is 10 seconds long.
    • Multiplying by 6 extrapolates the 10-second count to a full minute (10 seconds x 6 = 60 seconds).

    Example

    • If there are 12 QRS complexes in a 10-second strip:
      • Heart Rate = 12 x 6 = 72 beats per minute

    Understanding Normal Heart Rates

    • Normal Range: 60 to 100 beats per minute for adults.
    • Below Normal (Bradycardia): Less than 60 beats per minute.
    • Above Normal (Tachycardia): More than 100 beats per minute.