Understanding the pacemaker coding system is essential for accurately interpreting EKG strips and evaluating the performance of the device. Before determining if a pacemaker is functioning correctly, it is important to comprehend its intended operation. The pacing mode is typically represented by a four-letter code, which provides critical information about the pacemaker’s functions.
Pacing Chamber(s)
Indicates which chambers can be paced
• A: Atrial
• V: Ventricular
• D: Dual (both atrial and ventricular)
Sensing Chamber(s)
Indicates which chambers are sensed
• A: Atrial
• V: Ventricular
• D: Dual
Response to Sensed Event
Indicates what happens when the pacemaker senses depolarization.
I: Inhibited
An inhibited response means that the pacemaker will withhold its pacing impulse when it detects an intrinsic electrical signal from the heart.
For example, if a ventricular pacemaker detects a natural ventricular depolarization, it will not deliver a pacing spike. This prevents unnecessary competition between the pacemaker and the heart’s intrinsic rhythm, ensuring efficient cardiac function.
e.g., In a VVI pacemaker, the device is programmed to pace the ventricles and sense ventricular activity. If the pacemaker detects a QRS complex indicating that the ventricles have depolarized naturally, it will inhibit ventricular pacing, avoiding redundant or excessive stimulation.
T: Triggered
A triggered response means that the pacemaker delivers a pacing impulse in reaction to a sensed event. This setting is used in scenarios where an electrical stimulus is needed to ensure proper cardiac conduction following a specific sensed activity. Triggered pacing is less common but can be essential in certain clinical situations.
For instance, in an atrial-triggered mode, the pacemaker senses intrinsic atrial activity and responds by triggering a ventricular pacing impulse. This maintains proper timing between atrial and ventricular contractions, ensuring synchronized heart function.
D: Dual (can both inhibit and trigger)
A dual response incorporates both inhibited and triggered modes, allowing the pacemaker to respond dynamically to sensed events in both the atria and the ventricles. This is most often seen in dual-chamber pacemakers, such as the DDD mode, which paces and senses activity in both chambers.
Function:
• If the pacemaker senses intrinsic atrial activity, it inhibits atrial pacing and triggers a ventricular pacing impulse after a programmed atrioventricular (AV) interval. This mimics the natural sequence of atrial and ventricular contraction.
• If intrinsic ventricular activity occurs before the programmed AV interval ends, the ventricular pacing is inhibited to prevent over-pacing.
Clinical Relevance: The dual response capability is particularly useful in patients with intermittent conduction abnormalities. For example, it ensures that the pacemaker steps in to maintain rhythm only when the heart’s natural conduction system fails, while minimizing unnecessary pacing when normal function is present.
Rate Modulation
• R: Rate-responsive (adjusts pacing rate based on physiological needs).
• Absence of a letter indicates fixed-rate pacing
Rate-Responsive Pacing
Some pacemakers adjust the pacing rate based on the patient’s physiological needs, known as rate-responsive pacing.
Mechanism
Sensors: The pacemaker uses sensors (e.g., accelerometers, minute ventilation sensors) to detect physical activity.
Adjustment: The pacing rate increases during activity and decreases at rest.
Clinical Significance
Enhances quality of life by accommodating varying activity levels.
Important to recognize on EKGs, as the pacing rate may vary appropriately.
Examples of Pacemaker Types
VVI Pacemaker
• Paces: Ventricles
• Senses: Ventricles
• Response: Inhibits pacing if intrinsic ventricular activity is sensed
• Rate Modulation: Fixed-rate (no “R” in the code)
DDD Pacemaker
• Paces: Both atria and ventricles
• Senses: Both atria and ventricles
• Response: Inhibits atrial output if atrial activity is sensed; triggers ventricular output after a set atrioventricular (AV) interval unless inhibited by sensed ventricular activity
• Rate Modulation: Can be rate-responsive if an “R” is added (DDDR)
Analyzing Paced EKG Strips
When interpreting a paced EKG strip, consider the following key questions:
1. What is the Nature of Pacing?
• Identify if the pacing is atrial, ventricular, or dual-chamber.
• Look for pacing spikes before the P wave (atrial pacing), before the QRS complex (ventricular pacing), or both (dual-chamber pacing).
2. Is the Pacemaker Functioning Correctly?
Assess for appropriate sensing and pacing. Is there any evidence of:
over-sensing: Absence of pacing spikes when they are needed, leading to pauses or bradycardia.
under-sensing: Pacing spikes appear at inappropriate times, disregarding the heart’s intrinsic activity.
Check for the presence of pacing spikes and corresponding cardiac depolarizations. This would help detect failure to capture.
Interpreting Specific Pacemaker Functions on EKG
VVI Pacemaker Interpretation
Normal Function: Regular pacing spikes before wide QRS complexes. Also, consistent pacing rate if fixed-rate; variable if rate-responsive.
Over-sensing: Missing pacing spikes leading to bradycardia.
Failure to capture: There is a pacemaker spike but no QRS follows it.
DDD Pacemaker Interpretation
Normal Function: Pacing spikes before P waves and/or QRS complexes and it maintains AV synchrony (p-waves followed by a delay followed by a QRS complex), mimicking normal physiological conduction. So, if it does not sense atrial depolarization, it will pace the atria and wait for a bit. If no ventricular depolarization occurs, it then paces the ventricles.
Malfunctions:
Under-Sense Atrial Activity: Leads to inappropriate atrial pacing.
Over-Sense Atrial Activity: Leads to no atrial pacing when warranted.
Failure to capture at the atria: an atrial pacer spike does not lead to atrial depolarization (so no P-wave after the spike)
Under-Sense Ventricular Activity: Leads to inappropriate ventricular pacing.
Over-Sense Ventricular Activity: Leads to no ventricular pacing when warranted.
Failure to capture at the ventricles: a ventricular pacer spike does not lead to ventricular depolarization (so no QRS complex after the spike)
Troubleshooting Steps
When to suspect?
symptomatic patient (dizziness from bradycardia, palpitations from extra beats, etc.)
abnormal EKG
What to do?
Device Interrogation: Use a programmer to check settings and battery status.
Lead Evaluation: Imaging or testing to assess lead position and integrity.
Adjusting Sensitivity: Modify device settings to optimize sensing without over-sensing.
Two fundamental mechanisms that enable pacemakers to function effectively are sensing and capture. A thorough understanding of these mechanisms is essential for healthcare professionals to manage patients with pacemakers and accurately interpret EKGs. This article offers an analytical overview of sensing and capture in pacemakers, exploring their functions, underlying mechanisms, and clinical implications.
Sensing in Pacemakers
What does it mean when a pacemaker is sensing?
Sensing refers to a pacemaker’s ability to detect the heart’s intrinsic electrical activity. By monitoring electrical signals through its leads, the pacemaker determines whether it needs to deliver a pacing pulse.
Function of Sensing
The primary function of sensing is to ensure that the pacemaker provides electrical stimulation only when the heart’s natural rhythm is insufficient. If the pacemaker detects an intrinsic heartbeat, it inhibits its own output to prevent unnecessary pacing, thereby conserving battery life and maintaining physiological heart function.
Chambers Involved in Sensing
Sensing can occur in different heart chambers:
• Atrial Sensing: Detects electrical activity in the atria (upper chambers).
• Ventricular Sensing: Detects electrical activity in the ventricles (lower chambers).
• Dual-Chamber Sensing: Monitors both atria and ventricles.
The specific chambers where sensing occurs are indicated by the second letter in the pacemaker’s code. For example, “A” stands for atrial, “V” for ventricular, and “D” for dual.
Purpose of Sensing
Sensing allows the pacemaker to work in harmony with the heart’s natural activity, providing support only when needed. This synchronization helps maintain an appropriate heart rate without interfering unnecessarily with the heart’s own rhythm.
Abnormalities related to sensing
Undersensing
Undersensing happens when the pacemaker fails to detect intrinsic cardiac activity that is present. Consequently, it delivers unnecessary pacing pulses, potentially causing competition between the pacemaker and the heart’s natural rhythm.
Mechanisms of Undersensing
• Inadequate Sensitivity Settings: The pacemaker’s sensitivity may be set too low to detect smaller electrical signals.
• Electrode Dislodgment: The pacing lead may have shifted, reducing its ability to detect cardiac signals.
• Interference: External or internal electrical signals can mask the heart’s activity.
• Lead Damage: Fractured or damaged leads can impair signal detection.
Clinical Implications of Undersensing
Undersensing can lead to inappropriate pacing and arrhythmias. Recognizing undersensing on an EKG allows for timely interventions, such as reprogramming the pacemaker or correcting hardware issues.
Oversensing
Oversensing occurs when the pacemaker detects electrical signals that are not true cardiac activity, leading it to withhold necessary pacing pulses.
Mechanisms of Oversensing
• Electromagnetic Interference: External devices can emit signals that the pacemaker misinterprets.
• Muscle Potentials: Electrical activity from skeletal muscles can be sensed erroneously.
• T-Wave Oversensing: The pacemaker mistakes the T-wave for a QRS complex.
Clinical Implications of Oversensing
Oversensing can result in bradycardia or pauses in the heart rhythm, causing symptoms like dizziness or syncope. Identifying oversensing is crucial for adjusting the pacemaker’s sensitivity or addressing contributing factors.
Capture in Pacemakers
What does it mean for a pacemaker to capture?
Capture refers to the successful depolarization of cardiac tissue following a pacemaker’s electrical impulse, resulting in a heart contraction. On an EKG, capture is indicated by a pacemaker spike immediately followed by the appropriate waveform—a P-wave for atrial capture or a QRS complex for ventricular capture.
Types of Capture
• Atrial Capture: A pacing spike followed by a P-wave indicates the atria have “captured” the pacemaker spike resulting in atrial depolarization.
• Ventricular Capture: A pacing spike followed by a QRS complex indicates the ventricles have “captured” the pacemaker spike resulting in ventricular depolarization.
• Dual Capture: Spikes precede both the P-wave and the QRS complex in dual-chamber pacing.
Abnormalities related to capture
Loss of Capture
Loss of capture occurs when a pacemaker’s electrical impulse fails to depolarize cardiac tissue, evident as a pacing spike not followed by the expected waveform on an EKG.
Mechanisms of Loss of Capture
• Lead Dislodgment: The pacing lead may have moved, losing effective contact with the heart muscle.
• Battery Depletion: Low battery power can reduce the energy of pacing impulses.
• Increased Pacing Threshold: The heart muscle may require a higher energy to depolarize due to factors like ischemia.
• Lead Integrity Issues: Damage to the lead can impair impulse delivery.
Clinical Implications of Loss of Capture
Loss of capture can lead to inadequate heart rates and reduced cardiac output, causing symptoms like fatigue or syncope. It requires immediate evaluation to adjust pacemaker settings or address hardware problems.
Cardiac pacing is a pivotal intervention in cardiology that involves providing electrical impulses to prompt the heart’s activity when its natural electrical system is unable to sustain an adequate rate or rhythm. Pacemakers, the devices that fulfill this role, are indispensable for patients whose conditions hinder the heart’s capability to beat efficiently on its own. For healthcare professionals overseeing the care of these patients, a thorough understanding of pacing mechanisms and the ability to interpret EKG (electrocardiogram) changes are vital.
The Purpose of Cardiac Pacing
The main goal of cardiac pacing is to ensure the heart maintains a proper rate and rhythm to facilitate efficient blood circulation. When the heart’s natural electrical system is impaired due to issues like bradycardia (an abnormally slow heart rate), heart block, or other rhythm disorders, a pacemaker can step in to deliver the necessary electrical impulses. This intervention helps prevent symptoms associated with insufficient heart rates, such as dizziness, fatigue, and fainting, while also lowering the risk of more serious complications.
Mechanisms of Pacing and EKG Changes
Pacemakers function by delivering electrical impulses to specific chambers of the heart, initiating depolarization and subsequent contraction. The mechanism of pacing and its effect on the heart’s electrical activity depend on which chamber is being stimulated and the patient’s underlying cardiac condition. These interventions result in characteristic changes on an EKG, a tool that records the electrical activity of the heart.
When a pacemaker stimulates the heart, it can alter the normal conduction pathways. For instance, ventricular pacing often leads to a widened QRS complex on the EKG due to the delayed spread of the electrical impulse through the ventricular muscle. Understanding these changes is essential for interpreting EKGs in patients with pacemakers and for identifying any potential issues with the device or the heart itself.
Types of Cardiac Pacing
1. Atrial Pacing
Atrial pacing involves delivering electrical impulses to the atria, the heart’s upper chambers, when the natural atrial activity is insufficient. This type of pacing is beneficial for patients with sinoatrial node dysfunction, where the heart’s natural pacemaker fails to generate impulses at an adequate rate.
EKG Interpretation: On an EKG, atrial pacing is indicated by a pacing spike preceding the P-wave, which represents atrial depolarization. The presence of this spike followed by a P-wave shows that the atria have responded to the pacemaker’s stimulus. The subsequent conduction through the atrioventricular node and ventricles should be normal if the conduction system is intact.
2. Ventricular Pacing
Ventricular pacing is used when the ventricles, the heart’s lower chambers, require direct stimulation. This scenario often occurs in patients with atrioventricular block, where the electrical impulses from the atria do not reach the ventricles.
Mechanism and EKG Changes: In ventricular pacing, the pacemaker delivers impulses directly to the ventricles, typically via a lead in the right ventricle. This direct stimulation causes the ventricles to depolarize in a manner that does not follow the normal conduction pathways, resulting in a widened QRS complex on the EKG. The pacing spike appears just before the QRS complex. Because the impulse starts in the right ventricle, it spreads to the left ventricle in a way that mimics a left bundle branch block (LBBB) pattern.
Clinical Considerations: Diagnosing myocardial infarction (heart attack) in patients with ventricular pacing can be challenging due to these EKG changes. The modified Sgarbossa criteria are used to identify acute myocardial infarction in paced rhythms by assessing specific EKG patterns.
3. Dual Chamber Pacing
Dual chamber pacing involves pacing both the atria and the ventricles, allowing for coordinated contraction and maintaining the natural sequence of heartbeats. This type of pacing is particularly useful for patients who need support in both chambers to optimize cardiac output.
EKG Interpretation: In dual chamber pacing, pacing spikes may appear before both the P-wave and the QRS complex. The pacemaker can sense the heart’s intrinsic activity and only deliver impulses when necessary. If a normal P-wave is detected, the device may inhibit atrial pacing but still pace the ventricles if needed. This flexibility helps maintain a more natural heart rhythm and improves the efficiency of the heart’s pumping action.
4. Biventricular (BiV) Pacing
Biventricular pacing, also known as cardiac resynchronization therapy (CRT), involves simultaneous pacing of both the right and left ventricles. This approach is used in patients with severe heart failure and intraventricular conduction delays that cause the ventricles to contract out of sync, reducing the heart’s efficiency.
Mechanism and EKG Changes: By pacing both ventricles at the same time, biventricular pacing helps synchronize their contractions, improving cardiac output and alleviating heart failure symptoms. On the EKG, this type of pacing may show unique patterns, such as QS or QR complexes in lead I and R or rS patterns in lead V1. These changes reflect the altered depolarization pathways due to the simultaneous stimulation of both ventricles.
Understanding Pacing Spikes on the EKG
Pacing spikes are sharp, vertical lines on the EKG that represent the electrical impulses delivered by the pacemaker. The presence and location of these spikes provide valuable information about which chamber is being paced.
• Atrial Pacing Spike: Appears just before the P-wave, indicating atrial stimulation.
• Ventricular Pacing Spike: Occurs immediately before the QRS complex, indicating ventricular stimulation.
• Dual Chamber Pacing Spikes: Both atrial and ventricular spikes are present, each preceding their respective depolarization waves.
The morphology of the subsequent waves helps assess the effectiveness of the pacing and the heart’s response. Abnormalities in the spikes or the associated waves can signal issues such as lead displacement, battery depletion, or pacemaker malfunction.
Mechanisms of Changes on an EKG in Pacing
Understanding the mechanisms behind the changes seen on the EKG with different pacing modes is crucial for accurate interpretation and patient management.
• Altered Conduction Pathways: Paced electrical impulses may not follow the heart’s normal conduction pathways, leading to changes in the duration and shape of the EKG waves. For example, ventricular pacing causes the impulse to spread through the ventricular muscle rather than the specialized conduction fibers, resulting in a widened QRS complex.
• Bundle Branch Block Patterns: Ventricular pacing, especially from the right ventricle, often produces an EKG pattern similar to a left bundle branch block. Recognizing this pattern is important to avoid misdiagnosing conduction system diseases.
• Assessment of Ischemia: In paced rhythms, traditional criteria for detecting ischemia or infarction may not apply due to the altered EKG patterns. The modified Sgarbossa criteria help identify acute myocardial infarction in these patients by evaluating specific concordant and discordant changes in the ST segments relative to the QRS complexes.
• Pacemaker Malfunction Detection: Abnormalities such as failure to capture (the heart does not respond to the pacemaker’s impulse) or failure to sense (the pacemaker does not detect intrinsic heart activity) can be identified by analyzing the EKG. This analysis is essential for timely intervention and correction of any device-related issues.
Accurate EKG interpretations hinge on the correct placement of electrodes, or leads. Misplaced leads can produce tracings that mimic serious cardiac abnormalities, leading to misdiagnosis and inappropriate treatment. This comprehensive guide delves into the mechanisms of lead reversal, how to identify them, and steps to correct misplacements to ensure precise cardiac assessments.
Overview
The Critical Role of Proper Lead Placement
Each EKG lead provides a unique perspective of the heart’s electrical activity. Correct placement allows clinicians to assess the heart’s function accurately. Misplaced leads alter the electrical vectors, resulting in waveforms that may suggest pathological conditions such as myocardial infarction, arrhythmias, or axis deviations. Understanding lead reversal patterns is essential to differentiate true cardiac events from technical errors.
Lead reversal alters the recorded electrical activity by changing the orientation of the leads relative to the heart. Each limb lead records the difference in electrical potential between two points. Swapping leads changes this difference, leading to characteristic changes in the EKG tracing.
Identifying Lead Reversals
A systematic approach is vital for recognizing lead misplacements:
Compare with Previous EKGs: Discrepancies without clinical correlation may indicate lead issues.
Assess for Global Changes: Widespread inversions or unexpected axis deviations suggest misplacement.
Examine Individual Leads: Isolated abnormalities, such as a flat line or inversion in a single lead, can point to specific swaps.
The Mechanism
Electrodes
LA = left arm
RA = right arm
LL = left leg
RL/N = right leg (neutral electrode)
Electrodes for V1-V6
Leads
Bipolar leads: I, II, III
Augmented unipolar leads: aVL, aVF, aVR
Unipolar Leads: V1-V6 (precordial leads)
Wilson’s central terminus (WCT)
Whenever the electrodes are misplaced, the leads no longer measure what they are supposed to measure. For instance, lead I is generated by ensuring right arm is negative and the left arm is positive. However, if the connections are switched, i.e., if the right arm is positive and the left arm is negative, lead I records the opposite of what it was normally supposed to record!
Analysis of precordial lead reversal
Check for unusual patterns in precordial leads: For precordial lead reversal, you would see an unexplained decrease in R-wave amplitude in two consecutive leads followed by a return to the normal pattern. A couple of examples follow:
V1 and V2 Reversal
EKG Findings:
Reversed R-wave Progression: Unusual patterns in early precordial leads.
Possible Misdiagnosis: May mimic posterior myocardial infarction.
Explanation:
Swapping V1 and V2 alters the septal view, changing the expected progression of depolarization.
Swapping V3 and V4
EKG Findings:
Unexpected Decrease in R-wave Amplitude: Between swapped leads.
Abnormal Transition Zone: Disruption in normal R-wave progression.
Explanation:
The anatomical perspective is altered, affecting the ventricular depolarization pattern.
Detailed Analysis of Specific Limb Lead Reversals
Limb leads include the right arm (RA), left arm (LA), left leg (LL), and right leg (RL, which serves as a ground). The bolded text is usually a shortcut to suspecting lead reversals.
RA/LA Reversal
Inverted Lead I
Lead II becomes lead III
Lead III becomes lead II
aVR becomes aVL
aVL becomes aVR (so aVR is positive and there will be a right axis deviation)
aVF is unchanged
RA/LL Reversal
Leads I becomes inverted lead III
Lead II is inverted
Lead III becomes inverted lead I
aVR becomes aVF
aVF becomes aVR
aVL is unchanged.
So, leads I,II, III, aVF that are normally positive become negative and aVR that is normally negative becomes positive!
Changes in electrolyte levels, drug toxicity, and specific medical conditions can lead to characteristic alterations on an EKG. Recognizing these patterns is crucial for prompt diagnosis and effective management. This article explores the EKG changes associated with electrolyte abnormalities, digoxin toxicity, and other significant conditions, providing insights into the underlying mechanisms.
Electrolyte Abnormalities
Electrolytes such as potassium, calcium, and magnesium are vital for maintaining the electrical activity of the heart. Abnormal levels can disrupt cardiac conduction and repolarization, leading to distinctive EKG changes.
Potassium Abnormalities
Hypokalemia (Low Potassium Levels)
EKG Changes:
Prominent U Waves: Extra waves following the T wave.
ST Segment Depression: Downward displacement of the ST segment.
Flattened T Waves: Reduced amplitude of T waves.
Prolonged QTc Interval: Extended duration of ventricular repolarization.
Hyperkalemia (High Potassium Levels)
EKG Changes:
Tall, Peaked T Waves: Elevated and narrow T waves.
Shortened QTc Interval: Reduced duration of ventricular repolarization.
Widening of PR Interval and QRS Complex: Prolonged conduction times.
Disappearance of P Waves
Sine Wave Pattern: Merging of QRS complexes and T waves in severe cases.
Eventual Flattening of the Waveform: Indicates impending cardiac arrest.
Mechanism:
Hyperkalemia causes partial depolarization of cardiac cells, making them more excitable. Initially, this leads to tall, peaked T waves due to rapid repolarization. As potassium levels rise further, conduction slows, causing widening of the PR interval and QRS complex. The disappearance of P waves and the sine wave pattern reflect severe conduction abnormalities, potentially leading to ventricular fibrillation.
Calcium plays a crucial role in the plateau phase of the cardiac action potential. Hypocalcemia prolongs this phase, resulting in a prolonged QTc interval.
Hypercalcemia (High Calcium Levels)
EKG Changes:
Shortened QTc Interval: Reduced duration of ventricular repolarization.
Mechanism:
Hypercalcemia shortens the plateau phase of the action potential, leading to a shortened QTc interval.
Bidirectional Ventricular Tachycardia: Alternating QRS axis with each beat.
Conduction Block:
Second or Third-Degree Heart Block: Partial or complete interruption of AV conduction.
ST Segment Depression:
“Scooped” Appearance (Concave Upwards): Downsloping ST segment resembling a hockey stick.
Mechanism:
Digoxin increases intracellular calcium by inhibiting the Na⁺/K⁺ ATPase pump which indirectly leads to an increase in calcium influx and ultimately enhances cardiac contractility. However, it also increases automaticity and decreases AV nodal conduction. Elevated automaticity can trigger arrhythmias, while slowed conduction can lead to heart blocks. The characteristic ST segment depression reflects altered repolarization due to digoxin’s effect on myocardial cells.
Causes of Prolonged QTc Interval
A prolonged QTc interval is significant because it predisposes individuals to dangerous arrhythmias.
Common Causes:
Electrolyte Disturbances:
Hypocalcemia
Hypomagnesemia
Medications:
Anti-arrhythmics (Classes IA, IC, III): Drugs like quinidine, flecainide, and amiodarone.
Tricyclic Antidepressants: Such as amitriptyline.
Antipsychotics: Including haloperidol and ziprasidone.
Antibiotics: Fluoroquinolones (e.g., levofloxacin) and macrolides (e.g., erythromycin).
Methadone: Used in opioid dependence treatment.
Azole Antifungals: Fluconazole prolongs QTc (but isavuconazole may shorten it!).
Most Antiemetics: Serotonin antagonists such as ondansetron, dopamine antagonists such as metoclopramide and compazine, antihistamines such as promethazine and diphenhydramine, etc. NK1 antagonists (aprepitant, fosaprepitant), steroids, scopolamine, etc. do not prolong QTc.
Congenital Syndromes:
Romano-Ward Syndrome: Autosomal dominant, normal hearing.
Jervell and Lange-Nielsen Syndrome: Autosomal recessive, associated with deafness.
ST-T Changes in Right Precordial Leads: ST depression and T wave inversion.
Mechanism:
A pulmonary embolism increases resistance in the pulmonary arteries, causing acute right ventricular strain. This strain leads to changes such as RAD and RBBB. The S1Q3T3 pattern reflects right ventricular overload and is a classic but not highly sensitive finding in PE.
Pericardial Effusion
EKG Changes:
Low Voltage QRS Complexes: Reduced amplitude in all leads.
Fluid accumulation in the pericardial sac dampens the electrical signals from the heart, resulting in low voltage readings. Electrical alternans occur due to the heart swinging within the fluid-filled pericardial sac, causing beat-to-beat variations in the electrical axis.
6. Acute Pericarditis
EKG Changes:
Diffuse ST Elevation: Elevation in most leads except aVR.
ST Depression in Lead aVR: Opposing changes in this lead.
No Reciprocal Changes: These are seen in myocardial infarction.
Concave Upwards ST Elevations: Saddle-shaped appearance.
T Wave Changes: Flattening followed by inversion as the condition progresses.
Normalization: EKG eventually returns to normal.
Mechanism:
Inflammation of the pericardium affects the entire heart surface uniformly, leading to diffuse ST elevations. The lack of reciprocal changes helps distinguish pericarditis from myocardial infarction. The concave upwards ST elevation is characteristic of pericarditis.
Intracranial Hemorrhage
EKG Changes:
Large Upright or Inverted T Waves
Prolonged QTc Interval
Prominent U Waves
Mechanism:
Intracranial hemorrhage can cause autonomic dysregulation, affecting cardiac repolarization and conduction. The sympathetic surge leads to abnormal T waves and prolongation of the QTc interval.
Hypothermia
EKG Changes:
Osborne Waves (J Waves): Positive deflection at the junction of the QRS complex and ST segment.
Sinus Bradycardia: Slowed heart rate.
Arrhythmias: Increased risk of atrial fibrillation, ventricular tachycardia, and ventricular fibrillation.
Dextrocardia
EKG Changes:
Inverted Waves in Leads I and aVL: Negative P, QRS, and T waves.
Reversed R-Wave Progression: Abnormal transition of R wave amplitude across precordial leads.
Mechanism:
In dextrocardia, the heart is located on the right side of the chest. This anatomical reversal causes the standard EKG lead placements to record inverted electrical activity. Correct lead placement or a right-sided EKG can confirm dextrocardia.
Brugada Syndrome
EKG Changes in Leads V1-V3:
Type 1 Pattern:
ST Elevation (≥2 mm): Elevated ST segment with upward convexity.
Inverted T Wave: Following the ST elevation.
Type 2 Pattern:
“Saddle-Back” ST-T Wave: ST elevation that descends and then ascends, ending with an upright or biphasic T wave.
Mechanism:
Brugada Syndrome is a genetic disorder affecting sodium channels in the heart. The altered sodium channel function leads to abnormal repolarization in the right ventricular outflow tract, predisposing individuals to ventricular fibrillation and sudden cardiac death.
This guide delves into the mechanisms of EKG alterations in ischemia and infarction, providing a detailed analysis to enhance understanding and clinical application.
EKG Changes in Ischemia and Infarction
ST-Elevation Myocardial Infarction (STEMI)
STEMI is characterized by specific EKG changes that typically appear in at least two contiguous leads. These changes reflect acute transmural myocardial injury.
Hyperacute T-Waves
The earliest electrocardiogram (ECG) indicator of STEMI is the presence of hyperacute T-waves, which are characterized by their symmetric and peaked appearance.
ST Elevation Criteria
ST elevation is a hallmark of acute MI. Abnormal ST elevation is measured at the J point—the junction where the QRS complex meets the ST segment. The criteria for significant ST elevation are:
General Leads (excluding V2 and V3): Elevation of ≥0.1 mV (1 mm).
Leads V2 and V3:
Women: ≥0.15 mV.
Men ≥40 years: ≥0.2 mV.
Men <40 years: ≥0.25 mV.
Understanding these gender and age-specific thresholds is crucial for accurate diagnosis.
Differentiating ST Elevation Causes
Myocardial Infarction
In MI, the ST segment is typically convex upwards and may merge with the QRS complex, creating a “tombstone” appearance. This bowing upwards indicates significant myocardial injury.
J-Point Elevation (Early Repolarization)
J-point elevation is a benign variant often seen in healthy young adults. It features a slight elevation at the J point with a distinct ST segment and T-wave morphology. The ST segment is usually concave upwards, and there is no merging with the QRS complex.
Pericarditis
Pericarditis presents with diffuse ST elevation that is concave upwards and lacks reciprocal changes. A key distinguishing feature is PR segment depression in multiple leads except for lead aVR, where PR elevation may occur. The changes in pericarditis are more widespread compared to the localized patterns seen in MI.
Persistent ST Elevation and Ventricular Aneurysm
ST elevation usually resolves within a few hours in acute MI. If it persists beyond three weeks, consider the possibility of a ventricular aneurysm resulting from extensive myocardial damage.
Abnormal Q Waves
Q waves signify irreversible myocardial necrosis. Abnormal Q waves are defined as:
Leads V2 to V3: Any Q wave ≥20 milliseconds or a QS complex.
Other Leads (I, II, aVL, aVF, V4 to V6): Q wave ≥30 milliseconds and ≥0.1 mV deep in two contiguous leads or a QS complex.
The presence of Q waves without accompanying ST changes often indicates a previous infarct rather than an acute event.
Reciprocal Changes
Reciprocal changes enhance the diagnostic accuracy for MI. They occur in leads opposite the site of infarction and include:
Tall R-Waves: Reciprocal of Q waves.
ST Depression: Reciprocal of ST elevation.
T-Wave Inversions: Reciprocal of hyper acute T waves.
Recognizing reciprocal changes helps confirm the diagnosis and localize the infarct.
Localization of Infarcts on EKG
Inferior Infarcts
Inferior MI involves the diaphragmatic surface of the heart and affects:
Primary Changes: Leads II, III, and aVF.
Reciprocal Changes: Leads I and aVL.
Note: Changes in V1 – V3 may be reciprocal; however, be alert for a concurrent posterior myocardial infarction if such changes are observed. An EKG with posterior leads can help confirm the diagnosis.
Right Ventricular Infarcts
Right ventricular infarction should always be considered in any patient with an inferior myocardial infarction, particularly under the following conditions:
ST Elevation in Lead V1: V2 may show ST elevation or depression.
ST Elevation in Lead III > Lead II: Because lead III is more rightward-facing.
Right ventricular involvement can significantly impact management and prognosis. An EKG with right sided leads can help confirm the diagnosis.
Anterior and Lateral Infarcts
Anterior MI affects the anterior wall of the left ventricle, while lateral MI involves the lateral wall.
Anteroseptal MI
Leads Involved: V1 and V2.
Significance: Indicates septal wall infarction.
Anteroapical MI
Leads Involved: V3 and V4.
Significance: Reflects damage to the apical region.
Anterolateral MI
Leads Involved: I, aVL, V5, and V6.
Significance: Involvement of the lateral wall.
High Lateral MI
Leads Involved: I and aVL.
Significance: Indicates infarction in the high lateral wall.
Poor R-Wave Progression
Poor R-wave progression across the precordial leads may signify anterior MI. However, it can also be caused by:
Lung Disease: Alters electrical conduction.
Right Ventricular Hypertrophy (RVH): Changes ventricular depolarization patterns.
Wellens’ Syndrome
Wellens’ syndrome is characterized by:
EKG Findings: Symmetric T-wave inversions or biphasic T-waves in leads V2 and V3 without significant ST segment changes.
Cardiac Enzymes: Typically normal.
Clinical Significance: Indicates critical stenosis of the proximal left anterior descending (LAD) artery, posing a high risk for extensive anterior MI.
Posterior Infarcts
Posterior MI affects the posterior wall of the left ventricle. Needs to be suspected in all patients with inferior wall MI.
EKG Challenges
Standard 12-Lead EKG: Lacks posterior leads.
Reciprocal Changes in Leads V1 to V3:
Tall R-Waves: Reciprocal of Q waves.
ST Depression: Reciprocal of ST elevation.
Upright T-Waves: Reciprocal of T-wave inversions.
Diagnostic Approach
15-Lead EKG: Incorporates posterior leads (V7 to V9) to detect posterior MI.
Conditions Mimicking Posterior MI:
RVH
Right Bundle Branch Block (RBBB)
Wolff-Parkinson-White (WPW) Syndrome
These conditions can cause early R-wave progression, complicating the diagnosis.
Non-ST-Elevation Myocardial Infarction (NSTEMI) and Unstable Angina
EKG Changes
Both NSTEMI and unstable angina may present with:
ST Depression:
Horizontal or down-sloping ST segment depressed ≥0.5 mm below baseline.
Measured 0.08 seconds (2 mm) after the J point.
Present in at least two contiguous leads.
T-Wave Inversions:
Especially significant if inversion exceeds 1 mm.
Differentiating NSTEMI from Unstable Angina
NSTEMI
Persistent EKG Changes: ST depression and T-wave inversions persist for longer.
Troponin Elevation: Indicates myocardial injury.
Unstable Angina
Transient EKG Changes: Normalize as symptoms resolve.
Normal Troponin Levels: No myocardial necrosis.
ST Elevation in Lead aVR
Significance: ST elevation in lead aVR with widespread ST depression suggests:
Left Main Coronary Artery Disease
Severe Triple-Vessel Disease
Prinzmetal Angina
Pathophysiology
Cause: Coronary vasospasm leading to transient myocardial ischemia.
Occurrence: Often at rest and can be cyclical.
EKG Presentation
Transient ST Elevation or Depression: Mimics acute MI.
Resolution: EKG changes and symptoms resolve when the vasospasm subsides.
Occlusion Myocardial Infarction (OMI)
Electrocardiography (EKG) remains an indispensable tool in diagnosing and managing myocardial ischemia and infarction. Traditionally, the focus has been on identifying ST-Elevation Myocardial Infarction (STEMI) through specific EKG criteria to expedite reperfusion therapy. However, recent advancements advocate for a shift towards the Occlusion Myocardial Infarction (OMI) paradigm. This approach emphasizes the underlying pathophysiology—coronary artery occlusion—over strictly adhering to EKG criteria.
What Is OMI?
Occlusion Myocardial Infarction (OMI) refers to myocardial infarctions caused by a complete or near-complete blockage of a coronary artery, leading to significant myocardial ischemia and necrosis. Unlike the traditional STEMI classification, which relies heavily on EKG findings, OMI focuses on the presence of an occlusion, regardless of whether the classic EKG criteria for STEMI are met.
Why Shift from STEMI to OMI?
Limitations of STEMI Criteria: Up to one-third of acute coronary occlusions may not exhibit the traditional EKG characteristics of STEMI, potentially resulting in missed diagnoses and delayed treatment. Notable EKG changes to monitor include the new onset of bifascicular blocks, new onset LBBB, and pseudonormalization patterns in the appropriate clinical context. Pseudonormalization on an EKG refers to a phenomenon where previously abnormal waves, such as inverted T waves, seem to revert to their normal position, creating a misleading impression of recovery or improvement. However, this “normalization” is deceptive as it often indicates a deterioration of the underlying cardiac condition, such as progressing myocardial ischemia.
Pathophysiological Focus: OMI emphasizes identifying and treating the underlying coronary occlusion promptly to prevent extensive myocardial damage.
Improved Patient Outcomes: Early recognition and intervention can significantly reduce morbidity and mortality associated with myocardial infarctions.
Clinical Implications
Diagnostic Approach: Clinicians are encouraged to consider the possibility of OMI even when EKG findings are subtle or non-specific.
Treatment Strategies: Prompt reperfusion therapy should be considered based on clinical suspicion of occlusion and acuity, not solely on EKG criteria.
Decision to Perform Emergency Intervention: Both American and European guidelines advise that any patient experiencing ongoing ischemic symptoms despite initial treatment should be promptly considered for an immediate angiography even if they do not have a STEMI.
Atrial Ischemia and Infarct
When to suspect
Atrial infarction should be considered in patients with ventricular myocardial infarction who present with any type of atrial arrhythmia.
Before we delve into the criteria, let’s first explore the concept of the PTa segment. On an electrocardiogram (ECG), the “PR segment” refers to the flat section between the end of the P wave and the start of the QRS complex, representing the electrical delay between atrial and ventricular depolarization. In contrast, the “PTa segment” (sometimes referred to as PTA) is a less commonly used term that describes the entire section from the end of the P wave to the end of the atrial repolarization wave. Essentially, this encompasses the PR segment and a portion of the “T wave” of the P wave itself. Since atrial repolarization is often lost in the QRS complex, PTa segment changes are evaluated by looking at the PR segment itself.
PR segment: A specific, short flat section between the P wave and QRS complex.
PTa segment: A broader section including the PR segment and the tail end of the P wave repolarization.
Now let’s explore the Liu’s criteria for atrial ischemia/ infarct:
Major Criteria
Elevation of the P-Ta segment of over 0.5 mm in V5 and V6, with reciprocal depression of the same segment in V1 and V2.
Elevation of the P-Ta segment exceeding 0.5 mm in lead I, with reciprocal depression of the same segment in leads II or III
Depression greater than 1.5 mm in the precordial leads and 1.2 mm in leads I, II, and III, particularly in the context of any atrial arrhythmia.
Note: Depression of the P-Ta segment of small amplitude without elevation of this segment in other leads cannot be regarded by itself as positive evidence of atrial infarction.
Minor Criteria
Abnormal P waves: M-shaped, W-shaped, irregular or notched
Importance
Often linked to a poor prognosis, these criteria can aid in diagnosing an ischemic event even when the ventricular criteria for ischemia or infarct are not fully met.
This guide delves into the EKG manifestations of right atrial abnormality, left atrial abnormality, right ventricular hypertrophy, left ventricular hypertrophy, and biventricular hypertrophy. We will explore the mechanisms behind these changes to enhance understanding and aid in accurate interpretation.
Right Atrial Abnormality
EKG Indicators:
P-Wave Amplitude in Lead II: Greater than 2.5 mm.
P-Wave Amplitude in Lead V1: Greater than 1.5 mm.
Prominent Negative P-Wave in V1: In extreme cases, the negative component of the P-wave may become pronounced.
Mechanism of Changes:
The right atrium is responsible for initiating the electrical impulse that triggers heartbeats. When the right atrium enlarges due to conditions like pulmonary hypertension or tricuspid valve disease, the increased muscle mass alters the electrical conduction. This results in P-wave changes in the EKG leads that reflect atrial activity, specifically Leads II and V1.
In Lead II, which aligns closely with the heart’s electrical axis, a P-wave amplitude exceeding 2.5 mm indicates right atrial abnormality.
Similarly, in Lead V1, which is positioned over the right side of the heart, a P-wave amplitude greater than 1.5 mm corroborates this finding.
Left Atrial Abnormality
EKG Indicators:
Negative Portion of P-Wave in V1: Greater than 1 mm in width or depth.
P-Wave in Lead II: Duration close to or exceeding 3 mm (more than 110 milliseconds), or a bifid P-wave with an interpeak interval greater than 1 mm.
Mechanism of Changes:
Left atrial enlargement often results from conditions like mitral valve stenosis or systemic hypertension. The increased size of the left atrium prolongs the electrical conduction time, leading to wider P-waves. In Lead V1, the negative portion of the P-wave becomes more pronounced due to the delayed activation of the enlarged left atrium, which extends the depolarization phase- This wave moves away from lead V1 causing the negative deflection.
In Lead II, a bifid or notched P-wave, often termed “P mitrale,” indicates that the atria are depolarizing at different times. The interpeak interval exceeding 1 mm reflects the prolonged conduction caused by the enlarged left atrium. A P-wave duration exceeding 110 milliseconds confirms this abnormality, signaling that the atrial depolarization is taking longer than normal.
Right Ventricular Hypertrophy
EKG Indicators:
R/S Ratio in V1 Greater Than 1: The R-wave amplitude exceeds that of the S-wave.
S/R Ratio in V6 Greater Than 1: The S-wave amplitude exceeds that of the R-wave.
Additional Findings:
Right Axis Deviation (RAD): The heart’s electrical axis shifts to the right.
ST Depression and T-Wave Inversions: Observed in right precordial and inferior leads.
Right Bundle Branch Block (RBBB): May be present.
Right Atrial Abnormality: Often accompanies RVH.
Mechanism of Changes:
Right ventricular hypertrophy (RVH) occurs when the right ventricle enlarges due to increased workload, often from pulmonary hypertension or congenital heart defects. The hypertrophied right ventricle generates stronger electrical impulses, especially evident in Lead V1, which lies over the right ventricle. An R/S ratio greater than 1 in V1 signifies that the R-wave (representing right ventricular depolarization) is larger than the S-wave.
In Lead V6, which is positioned over the left ventricle, an S/R ratio greater than 1 indicates that the electrical activity from the right ventricle is overshadowing that of the left ventricle. The right axis deviation arises because the enlarged right ventricle shifts the heart’s electrical axis toward the right. ST depression and T-wave inversions in right precordial leads reflect strain on the right ventricle. The presence of RBBB further indicates disrupted conduction pathways due to ventricular enlargement.
Left Ventricular Hypertrophy
EKG Indicators:
Sokolow-Lyon Criteria: Sum of S-wave in V1 and R-wave in V5 or V6 is equal to or greater than 35 mm.
Cornell Criteria:
Men: S-wave in V3 plus R-wave in aVL exceeds 28 mm.
Women: S-wave in V3 plus R-wave in aVL exceeds 20 mm.
R wave in V4, V5 or V6 > 26 mm
R-Wave in aVL Greater Than 11 mm without LAD or Greater than 18 mm if left axis deviation is present.
Additional Findings:
Left Axis Deviation (LAD): The heart’s electrical axis shifts to the left.
ST Depression and T-Wave Inversions: Observed in inferior leads.
Left Bundle Branch Block (LBBB): May be present, though its presence precludes the diagnosis of LVH on EKG.
Left Atrial Abnormality: May accompany LVH.
Mechanism of Changes:
Left ventricular hypertrophy (LVH) results from conditions that increase the workload on the left ventricle, such as systemic hypertension or aortic stenosis. The enlarged left ventricle amplifies electrical activity in the leads that overlie it. In Lead aVL, an R-wave exceeding 11 mm indicates increased left ventricular mass. The Sokolow-Lyon and Cornell criteria provide quantitative measures combining amplitudes from specific leads to improve diagnostic accuracy.
Left axis deviation occurs because the hypertrophied left ventricle shifts the heart’s electrical axis toward the left. ST depression and T-wave inversions in inferior leads are signs of left ventricular strain. The presence of LBBB complicates the EKG interpretation, as it alters normal conduction pathways, masking the typical signs of LVH. Therefore, if LBBB is present, LVH cannot be reliably diagnosed using EKG criteria alone. Left atrial abnormality may also be present due to increased pressure and volume overload transmitted backward from the left ventricle.
Biventricular Hypertrophy
EKG Indicators:
Large Biphasic QRS Complexes in V2-V5: Characterized by prominent R and S waves, known as the Katz-Wachtel phenomenon.
Mechanism of Changes:
Biventricular hypertrophy involves enlargement of both the right and left ventricles, often due to congenital heart diseases like ventricular septal defects. The simultaneous hypertrophy leads to exaggerated electrical activity in the precordial leads. The large biphasic QRS complexes in Leads V2 to V5 reflect the combined forces of both ventricles. The Katz-Wachtel phenomenon is indicative of significant ventricular enlargement, resulting in high-amplitude QRS complexes without the usual signs of bundle branch blocks.
Integrating EKG Findings for Accurate Diagnosis
Interpreting EKGs requires a holistic approach, considering all leads and findings in conjunction with clinical information. It’s essential to recognize that some conditions may mask or mimic others. For instance, the presence of bundle branch blocks can obscure the signs of ventricular hypertrophy. Moreover, atrial abnormalities often accompany ventricular hypertrophy due to the interconnected nature of cardiac physiology.
Understanding the mechanisms behind EKG changes enhances diagnostic accuracy. Recognizing that hypertrophy increases muscle mass, thereby amplifying electrical signals, helps explain the heightened amplitudes observed in EKG leads. Similarly, atrial enlargement prolongs conduction times, leading to wider or notched P-waves.
Bundle branch blocks (BBBs) are important findings on electrocardiograms (EKGs) that signify disruptions in the heart’s electrical conduction pathways. Recognizing and interpreting these blocks are crucial for diagnosing and managing various cardiac conditions. This comprehensive guide delves into the types of bundle branch blocks, their mechanisms, EKG manifestations, and clinical significance.
The Normal Cardiac Conduction System
Before exploring bundle branch blocks, it’s essential to understand the normal conduction pathway:
Sinoatrial (SA) Node: The heart’s natural pacemaker located in the right atrium initiates the electrical impulse.
Atrioventricular (AV) Node: The impulse travels to the AV node, where there’s a brief delay to allow ventricular filling.
Bundle of His: The impulse then moves into the bundle of His.
Bundle Branches:
Right Bundle Branch (RBB): Conducts impulses to the right ventricle.
Left Bundle Branch (LBB): Splits into three fascicles:
Septal Fascicle: Arises from the LBB or the LAF or the LPF. Depolarizes the interventricular septum from left to right.
Left Anterior Fascicle (LAF): Supplies the anterior and superior portions of the left ventricle.
Left Posterior Fascicle (LPF): Supplies the posterior and inferior portions of the left ventricle.
Purkinje Fibers: Distribute the impulse throughout the ventricles, leading to coordinated contraction.
Normal Ventricular Depolarization Sequence:
Septal Activation: Depolarization starts in the left side of the interventricular septum, moving from left to right. This is done by the septal fascicle.
Ventricular Activation: The impulse spreads down both the right and left bundle branches simultaneously, causing the ventricles to depolarize and contract together.
Free Wall Activation: Depolarization proceeds through the Purkinje fibers to the ventricular myocardium, from the endocardium to the epicardium.
Right Bundle Branch Block (RBBB)
In a complete bundle branch block (BBB), the QRS duration is typically greater than 120 milliseconds, while in an incomplete BBB, the QRS duration is between 100 and 120 milliseconds. This is true for both right and left bundle branches.
Mechanism of Conduction Alteration:
Site of Blockage: The RBB is impaired, slowing or preventing the conduction of electrical impulses to the right ventricle.
Altered Conduction Pathway:
The left ventricle depolarizes normally via the left bundle branch.
The right ventricle receives the impulse indirectly from the left ventricle through cell-to-cell transmission, which is slower.
Impact on Depolarization Sequence:
Initial Depolarization: The septum depolarizes normally from left to right, leading to a normal initial QRS vector.
Delayed Right Ventricular Depolarization: The right ventricle depolarizes after the left ventricle, causing secondary depolarization forces directed towards the right.
EKG Manifestations:
QRS Duration: Prolonged due to delayed right ventricular activation.
Leads V1 and V2 (Right Precordial Leads):
rsR′ or rSR′ Pattern: Characterized by an initial small r wave, an S wave, and a prominent secondary R′ wave due to delayed right ventricular depolarization.
Explanation: The initial r wave represents septal depolarization. The delayed R′ wave reflects the late activation of the right ventricle.
Leads V5, V6, I, and aVL (Left-Sided Leads):
Wide, Slurred S Waves: Result from the delayed right ventricular depolarization moving away from these leads.
ST-T Changes:
Secondary ST Depression and T Wave Inversion: May be seen in V1 and V2 due to the abnormal repolarization sequence.
The axis is generally normal. This is because the left ventricle is larger than the right ventricle and is the primary determinant of the QRS axis.
Clinical Significance:
Common Causes: Can be seen in normal individuals but also associated with conditions like pulmonary embolism, right ventricular hypertrophy, ischemic heart disease, or congenital heart defects.
Diagnostic Implications:
Difficulties in Diagnosing Right Ventricular Hypertrophy: RBBB obscures the typical EKG signs of RVH.
Ability to Diagnose Left-Sided Conditions: Left ventricular hypertrophy (LVH), left axis deviation (LAD), and Q-wave myocardial infarctions can still be diagnosed.
Left Bundle Branch Block (LBBB)
In a complete bundle branch block (BBB), the QRS duration is typically greater than 120 milliseconds, while in an incomplete BBB, the QRS duration is between 100 and 120 milliseconds. This is true for both right and left bundle branches.
Mechanism of Conduction Alteration:
Site of Blockage: The LBB is impaired, affecting the conduction to the left ventricle.
Altered Conduction Pathway:
The right ventricle depolarizes normally via the RBB.
The left ventricle receives the impulse indirectly from the right ventricle through slow cell-to-cell conduction.
Impact on Depolarization Sequence:
Altered Septal Activation: The normal left-to-right septal depolarization is reversed, occurring from right to left due to the impulse traveling from the right ventricle to the left.
Delayed Left Ventricular Depolarization: The left ventricle depolarizes after the right ventricle.
EKG Manifestations:
QRS Duration: prolonged due to delayed left ventricular activation.
Leads V5 and V6, I, and aVL (Left-Sided Leads):
Broad, sometimes Notched (‘M’-Shaped) R Waves: Reflect delayed left ventricular depolarization.
Absence of q Waves: Due to altered septal depolarization.
Leads V1 and V2 (Right Precordial Leads):
Deep, Broad S Waves: Result from the depolarization moving away from these leads.
ST-T Changes: These are usually discordant. They move in the opposite direction as the QRS complex vector.
ST Depression and T Wave Inversion: Common in leads with positive QRS complexes (e.g., V5 and V6) due to abnormal repolarization.
ST Elevation and Upright T Waves: May be seen in V1 and V2.
May cause Left Axis Deviation
Clinical Significance:
Common Causes: Often associated with underlying heart disease such as hypertension, coronary artery disease, cardiomyopathies, or valvular heart diseases.
Diagnostic Challenges:
Myocardial Infarction (MI): LBBB can mask or mimic the EKG signs of MI, making diagnosis challenging. Modified Sgarbossa Criteriahelp in diagnosing MI in the presence of LBBB by evaluating concordant and discordant ST-segment changes. The presence of any of these criteria in the appropriate clinical setting is concerning:
At least one lead with ≥1 mm of concordant ST elevation.
At least one lead of V1-V3 with ≥1 mm of concordant ST depression.
At least one lead anywhere with ≥1 mm of ST elevation and proportionally excessive discordant ST elevation (≥25% of the depth of the preceding S-wave).
Cannot diagnose LVH but most people with LBBB have LVH.
RBBB vs. LBBB
Feature
RBBB
LBBB
Site of Blockage
Right Bundle Branch
Left Bundle Branch
Affected Ventricle
Right Ventricle
Left Ventricle
Initial Depolarization
Normal septal depolarization
Altered septal depolarization (right to left)
QRS Duration
Prolonged
Prolonged
V1 and V2 Leads
rsR′ or rSR′ pattern (rabbit ears)
Deep, broad S waves
V5 and V6 Leads
Wide, slurred S waves
Broad, notched R waves (M-shaped)
ST-T Changes
T wave inversion in V1 and V2
ST depression and T wave inversion in V5 and V6
Cannot diagnose
Right ventricular hypertrophy (RVH)may be missed (though presence of RAD can suggest RVH), ischemia based on ST-T changes based on V1, V2 and V3.
LVH (but most people with LBBB have LVH), RVH, Q-wave MI (modified Sgarbossa criteria help), ST-T changes are harder to diagnose, axis deviation, WPW.
Can diagnose
pericarditis, left ventricular hypertrophy (LVH), left axis deviation (LAD), and Q-wave myocardial infarctions can still be diagnosed.
MI with Sgarbossa criteria.
Clinical Associations
Can be normal; pulmonary diseases
Often indicates underlying heart disease
Left Anterior Fascicular Block (LAFB)
Mechanism of Conduction Alteration
Blockage Site: LAFB occurs due to a conduction block in the left anterior fascicle of the left bundle branch.
Altered Conduction Pathway:
• Primary Pathway Blocked: The anterior and superior regions of the left ventricle are no longer depolarized via the usual pathway.
• Alternative Conduction: The impulse travels down the intact left posterior fascicle to the inferior and posterior regions first.
• Delayed Depolarization: Depolarization of the anterior and superior regions occurs later via cell-to-cell conduction from the posterior regions.
Impact on Depolarization Vectors
• Initial Vector: The initial depolarization vector is directed inferiorly and rightward due to the unopposed activation of the posterior-inferior left ventricle.
• Secondary Vector: The delayed activation of the anterior-superior left ventricle creates a vector that is superior and leftward.
• Resultant Mean QRS Axis: The overall QRS axis shifts markedly to the left, typically between -45° and -90°, resulting in left axis deviation (LAD).
EKG Manifestations
• QRS Duration: Usually normal (< 0.12 seconds) because the total ventricular depolarization time isn’t significantly prolonged.
• Axis Deviation: Pronounced LAD without other identifiable causes.
• Lead-Specific Changes:
• Leads I and aVL (High-Lateral Leads):
• qR Pattern: Small initial q waves followed by tall R waves.
• Explanation: The initial inferior-rightward vector produces small q waves.The delayed anterior-superior depolarization produces a strong leftward and superior vector, resulting in prominent R waves.
• Leads II, III, and aVF (Inferior Leads):
• rS Pattern: Small initial r waves followed by deep S waves.
• Explanation: The initial inferior-rightward vector produces small r waves, but the dominant leftward vector results in deep S waves.
• Other Features:
• Normal or Slightly Prolonged QRS: Due to asynchronous ventricular activation.
• No ST-T Changes: ST segments and T waves are generally normal unless other pathologies are present.
Clinical Significance
• Isolated LAFB: Can occur without apparent heart disease but often associated with conditions affecting the left side of the conduction system, such as hypertension, aortic valve disease, or coronary artery disease.
• Importance of LAD: Significant LAD in the absence of other causes (e.g., inferior myocardial infarction) strongly suggests LAFB.
Left Posterior Fascicular Block (LPFB)
Mechanism of Conduction Alteration
Blockage Site: LPFB occurs due to a conduction block in the left posterior fascicle of the left bundle branch.
Altered Conduction Pathway:
• Primary Pathway Blocked: The posterior and inferior regions of the left ventricle are no longer depolarized via the normal route.
• Alternative Conduction: The impulse travels down the intact left anterior fascicle to the anterior-superior regions first.
• Delayed Depolarization: Depolarization of the posterior-inferior regions occurs later via cell-to-cell conduction from the anterior regions.
Impact on Depolarization Vectors
• Initial Vector: The initial depolarization vector is directed superiorly and leftward due to the unopposed activation of the anterior-superior left ventricle.
• Secondary Vector: The delayed activation of the posterior-inferior left ventricle creates a vector that is inferior and rightward.
• Resultant Mean QRS Axis: The overall QRS axis shifts markedly to the right, typically between +90° and +180°, resulting in right axis deviation (RAD).
EKG Manifestations
• QRS Duration: Usually normal (< 0.12 seconds), similar to LAFB.
• Axis Deviation: Pronounced RAD without other identifiable causes.
• Lead-Specific Changes:
• Leads II, III, and aVF (Inferior Leads):
• qR Pattern: Small initial q waves followed by tall R waves.
• Explanation: The initial superior-leftward vector produces small q waves.The delayed posterior-inferior depolarization produces a strong inferior and rightward vector, resulting in prominent R waves.
• Leads I and aVL (High-Lateral Leads):
• rS Pattern: Small initial r waves followed by deep S waves.
• Explanation: The initial superior-leftward vector produces small r waves, but the dominant inferior-rightward vector results in deep S waves.
• Other Features:
• Normal or Slightly Prolonged QRS: Due to the altered sequence of ventricular activation.
• No ST-T Changes: ST segments and T waves are generally unaffected unless concomitant pathologies exist.
Clinical Significance
• Isolated LPFB: Less common than LAFB because the left posterior fascicle is shorter, thicker, and has a dual blood supply, making it more resistant to injury.
• Association with Heart Disease: Often associated with significant underlying heart disease, such as ischemic heart disease or cardiomyopathies.
• Importance of RAD: Significant RAD without other causes (e.g., right ventricular hypertrophy) suggests LPFB.
Comparative Summary of LAFB and LPFB
Feature
LAFB
LPFB
Initial Depolarization
Posterior-Inferior Left Ventricle
Anterior-Superior Left Ventricle
Secondary Depolarization
Anterior-Superior Left Ventricle
Posterior-Inferior Left Ventricle
Mean QRS Axis
Left Axis Deviation
Right Axis Deviation (+90° to +180°)
Lead I and aVL
qR Pattern
rS Pattern
Leads II, III, and aVF
rS Pattern
qR Pattern
QRS Duration
Normal (< 0.12 sec)
Normal (< 0.12 sec)
Commonality
More Common (thin and long- so more prone to damage)
Less Common (thick and short)
Associated Conditions
Hypertension, CAD (supplied by LAD), Aortic Valve Disease
Significant Heart Disease (supplied by LAD and Posterior Descending Artery (PDA))
_______________
Left Anterior Fascicular Block (LAFB)
LAFB involves blockage in the left anterior fascicle of the left bundle branch.
EKG Characteristics:
QRS Duration: Less than 0.12 seconds.
Axis Deviation: Left axis deviation without other causes.
High-Lateral Leads (I and aVL): Show a qR pattern.
Inferior Leads: Display an rS pattern.
Mechanism Explained: The blockage redirects the depolarization pathway to the left posterior fascicle first, altering the axis and the EKG patterns accordingly.
• The initial depolarization of the posterior-inferior regions creates a vector pointing down and right.
• The delayed activation of the anterior-superior regions creates a stronger vector pointing up and left.
• The overall mean axis is dominated by the delayed, unopposed anterior-superior depolarization.
Left Posterior Fascicular Block (LPFB)
LPFB is less common and affects the left posterior fascicle.
EKG Characteristics:
QRS Duration: Less than 0.12 seconds.
Axis Deviation: Right axis deviation without other causes.
Inferior Leads: Show a qR pattern.
High-Lateral Leads (I and aVL): Display an rS pattern.
Mechanism Explained: With the posterior fascicle blocked, depolarization occurs via the left anterior fascicle, causing a shift in the heart’s electrical axis.
Bifascicular and Trifascicular Blocks
Bifascicular Block
Occurs when two fascicles are blocked, commonly RBBB combined with either LAFB or LPFB.
EKG Characteristics: Features of RBBB along with either left or right axis deviation, depending on the fascicle involved.
Mechanism Explained: Simultaneous blockage in two pathways significantly delays ventricular depolarization, increasing the risk of progression to complete heart block.
Trifascicular Block
Involves blockage in all three fascicles, leading to a high risk of complete heart block.
EKG Characteristics: Alternating right and left bundle branch block patterns, possibly with prolonged PR intervals.
Mechanism Explained: The conduction system is severely compromised, with intermittent or complete failure of impulse transmission from the atria to the ventricles.
Aberrant Conduction and Rate-Related Blocks
Aberrant Conduction refers to temporary conduction abnormalities that often occur during tachycardia.
EKG Characteristics: Normal conduction at rest but showing RBBB patterns during increased heart rates.
Mechanism Explained: At higher rates, a specific conduction pathway (usually the right bundle branch as it has a longer refractory period) may not have sufficient time to repolarize, leading to transient blockages.
Wolff-Parkinson-White (WPW) Pattern
WPW is characterized by an accessory pathway (Bundle of Kent) that pre-excites the ventricles.
EKG Characteristics:
Short PR Interval: Due to early ventricular activation.
Delta Wave: Slurred upstroke in the QRS complex.
Wide QRS Complex: Resulting from the fusion of normal and accessory pathway conduction.
Mechanism Explained: The accessory pathway bypasses the AV node, allowing impulses to reach the ventricles prematurely, which alters the initial part of the EKG causing the delta wave. Eventually, the normal conduction pathway kicks in after delay at the AV node resulting in the rest of the QRS complex.
Diagnostic Limitations:
Ventricular Hypertrophy: Difficult to assess due to altered QRS morphology.
Myocardial Infarction: WPW can cause Q-waves and ST-T changes, mimicking infarction.
Axis Deviation and other conduction abnormalities: Hard to diagnose accurately in the presence of WPW.
Ventriculophasic Sinus Arrhythmia
Seen in second or third-degree atrioventricular block.
EKG Characteristics: Intermittent differences in PP intervals based on their relationship to the QRS complex. P waves surrounding a QRS complex have shorter intervals (i.e., they occur at a faster rate) compared to those without an intervening QRS.
Mechanism Explained: The variation in PP intervals is thought to be due to changes in autonomic tone or ventricular feedback affecting the sinus node timing.
Non-Specific Intraventricular Conduction Defect (NSIVCD) is a term used when there is abnormal ventricular conduction that does not fit the criteria for well-defined conduction blocks, such as Right Bundle Branch Block (RBBB), Left Bundle Branch Block (LBBB), or fascicular blocks like Left Anterior Fascicular Block (LAFB) and Left Posterior Fascicular Block (LPFB).
NSIVCD reflects a delay in the transmission of electrical impulses through the ventricles, leading to a prolonged and abnormal QRS complex.
This condition is not a diagnosis in itself but rather an EKG finding that reflects an underlying conduction abnormality that does not fit a known, well-defined pattern.
The heart’s rhythm is a symphony orchestrated by electrical impulses that coordinate the contractions of the atria and ventricles. Two conditions that disrupt this harmony are atrioventricular (AV) dissociation and third-degree heart block. While they both involve independent beating of the atria and ventricles, their causes and clinical implications differ. This article delves into the distinctions between AV dissociation and third-degree heart block, providing a comprehensive understanding of their mechanisms, EKG features, and clinical significance.
What Is AV Dissociation?
AV dissociation occurs when the atria and ventricles contract independently, leading to a lack of coordination between their electrical activities. This condition is not always due to a block in the AV conduction pathway and can manifest in various cardiac scenarios. The key feature is the presence of P waves and QRS complexes that do not appear to be associated with each other; the atria and ventricles are “dissociated.”
Causes of AV Dissociation
Increased Ventricular Rate: An ectopic pacemaker in the ventricles may generate impulses faster than the sinus rhythm. When the ventricular rate surpasses the atrial rate, the ventricles become the primary pacemaker, resulting in AV dissociation. Ventricular parasystole is an example of such a condition.
Complete Heart Block: A complete interruption of the normal conduction pathway between the atria and ventricles can cause AV dissociation. In this case, the ventricles adopt an escape rhythm due to the absence of atrial impulses.
Ventricular Tachycardia: In conditions like ventricular tachycardia, the ventricles beat at a rapid rate independent of the atria, leading to AV dissociation without an underlying conduction block.
EKG Features of AV Dissociation
Direct Evidence of AV Dissociation
Independent P Waves and QRS Complexes: The P waves (atrial activity) and QRS complexes (ventricular activity) occur independently without a consistent relationship.
Variable PR Intervals: Since the atria and ventricles are not synchronized, the PR intervals vary, indicating a lack of conduction from the atria to the ventricles.
Indirect Evidence of AV Dissociation: Fusion and Capture Beats
AV dissociation can present with fusion and capture beats, providing clues to its presence on an EKG.
Capture Beats: These occur when an occasional atrial impulse successfully conducts to the ventricles amid dominant ventricular pacing. The result is a normal-looking QRS complex, representing a momentary return to coordinated atrioventricular activity.
Fusion Beats: Fusion beats arise when atrial and ventricular impulses simultaneously depolarize the ventricles. The resulting QRS complex has features of both normal and ectopic beats, appearing as a blend of the two impulses.
Clinical Significance of AV Dissociation
AV dissociation may be transient and asymptomatic or associated with symptoms like palpitations and dizziness, depending on the underlying cause. In cases related to ventricular tachycardia or complete heart block, it can signify a serious condition requiring medical attention.
What Is Third-Degree Heart Block?
Third-degree heart block, or complete heart block, is a severe conduction disorder where no electrical impulses pass from the atria to the ventricles. This results in the atria and ventricles beating independently at their intrinsic rates.
EKG Features of Third-Degree Heart Block
The EKG in third-degree heart block shows:
Regular P-P Intervals: The atria depolarize at a consistent rate determined by the sinoatrial (SA) node.
Regular R-R Intervals: The ventricles depolarize at a regular but typically slower rate due to an escape rhythm originating below the block.
No Association Between P Waves and QRS Complexes: There is a complete lack of conduction between the atria and ventricles, resulting in independent rhythms.
Clinical Implications of Third-Degree Heart Block
Third-degree heart block is often symptomatic and can be life-threatening due to inadequate cardiac output.
Comparing AV Dissociation and Third-Degree Heart Block
While third-degree heart block is a form of AV dissociation, not all instances of AV dissociation are due to third-degree heart block. Understanding their distinctions is essential for accurate diagnosis and management.
Underlying Mechanisms
AV Dissociation: Can occur without a conduction block. It may result from the ventricles pacing faster than the atria or from the presence of an ectopic ventricular rhythm overriding the sinus rhythm.
Third-Degree Heart Block: Always involves a complete block of conduction between the atria and ventricles, leading to independent rhythms due to the failure of atrial impulses to reach the ventricles.
EKG Differences
AV Dissociation in the absence of third degree heart block:
Variable PR intervals.
Presence of fusion and capture beats.
Atrial and ventricular rates may be similar or the ventricular rate may be faster.
Third-Degree Heart Blockwith no conduction whatsoever:
PR intervals that are variable due to the lack of conduction.
No fusion or capture beats.
Atrial rate is usually faster than the ventricular escape rate.
On an ECG, you will typically see P waves with a regular atrial rhythm and QRS complexes with a regular but unrelated ventricular rhythm. The P waves and QRS complexes are not synchronized, indicating no communication between the atria and ventricles.
Because of the block, the ventricles typically adopt a slower, escape rhythm to maintain pumping action, which is often insufficient for normal activity and can be life-threatening.
Clinical Presentation
AV Dissociation:
May be asymptomatic if the ventricular rate is neither too high nor too low.
Symptoms, if present, are often related to the underlying condition (e.g., palpitations in ventricular tachycardia).
Third-Degree Heart Block:
Symptoms are common due to bradycardia and decreased cardiac output.
Conclusion
AV dissociation is a broad term encompassing various scenarios, including situations where the ventricles pace faster than the atria without a conduction block. In contrast, third-degree heart block is a specific diagnosis characterized by a complete block in the AV conduction system, leading to a slow and potentially life-threatening ventricular escape rhythm.
The atrioventricular (AV) node acts as a critical gateway for electrical impulses traveling from the atria to the ventricles of the heart. When there’s a delay or blockage at this gateway, it can lead to various types of heart blocks, each with distinct patterns observable on an electrocardiogram (EKG). This article explores these heart block patterns in detail to aid in their recognition and understanding.
First-Degree Heart Block
A first-degree heart block represents a minor delay in the conduction of electrical impulses at the AV node, similar to a slight traffic slowdown on a highway. On an EKG, the hallmark of a first-degree heart block is a prolonged PR interval—the time it takes for the impulse to travel from the atria to the ventricles—that exceeds 0.2 seconds. Despite this delay, every atrial impulse still reaches the ventricles, so the heart rhythm remains regular.
Second-Degree Heart Block
Second-degree heart blocks are characterized by intermittent failures of electrical conduction from the atria to the ventricles. They are further classified into two types: Mobitz Type I (Wenckebach) and Mobitz Type II.
Mobitz Type I (Wenckebach)
In Mobitz Type I heart block, there is a progressive delay in AV node conduction until an impulse fails to conduct, resulting in a missed ventricular beat. This cycle then repeats.
On the EKG, this appears as progressively lengthening PR intervals with each beat until a QRS complex (which represents ventricular depolarization) is dropped. After the missed beat, the PR interval resets to a shorter duration, and the pattern starts over. Additionally, the R-R intervals (the time between ventricular contractions) typically shorten before the dropped beat.
A useful diagnostic tip is to compare the PR intervals just before and after the missing QRS complex; the PR interval following the dropped beat is shorter.
Mobitz Type II
Mobitz Type II heart block is more serious and can progress to a complete heart block. In this type, the AV node fails to conduct impulses intermittently without prior changes in the PR interval.
This means the PR intervals remain consistent, but some beats are suddenly dropped. On the EKG, there are more P waves (atrial depolarizations) than QRS complexes because some atrial impulses do not reach the ventricles. This irregularity can lead to bradycardia and symptoms such as dizziness or syncope.
2:1 Heart Block
A 2:1 heart block occurs when every alternate atrial impulse fails to conduct to the ventricles, resulting in one conducted beat followed by one blocked beat. This pattern makes it challenging to distinguish between Mobitz Type I and Mobitz Type II because only two beats are compared at a time. However, certain clues can aid differentiation:
Examination of Other EKG Leads: Observing for patterns indicative of Mobitz Type I or II in different parts of the EKG may provide hints.
Response to Physical Activity: If the heart rate does not increase appropriately with exercise—a condition known as chronotropic incompetence—it suggests Mobitz Type II.
Presence of Symptoms: Symptoms like fatigue, lightheadedness, or fainting are more commonly associated with Mobitz Type II due to its potential to cause significant bradycardia.
Third-Degree Heart Block (Complete Heart Block)
In a third-degree heart block, there is a complete dissociation between atrial and ventricular activity. The electrical impulses from the atria do not conduct to the ventricles at all. As a result, the atria and ventricles beat independently.
On the EKG, both the P-P intervals (atrial rate) and R-R intervals (ventricular rate) are regular, but there is no relationship between them—they are not synchronized. The atrial rate is usually faster than the ventricular rate. The ventricles often rely on an escape rhythm originating from a secondary pacemaker within the heart’s conduction system, such as a junctional or idioventricular rhythm, to maintain a heartbeat.
