Introduction
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 Abnormalities
Hypocalcemia (Low Calcium Levels)
EKG Changes:
- Prolonged QTc Interval: Extended ventricular repolarization time.
Mechanism:
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.
Magnesium Abnormalities
Hypomagnesemia (Low Magnesium Levels)
EKG Changes:
- Prolonged QTc Interval: Extended ventricular repolarization time.
Hypermagnesemia (High Magnesium Levels)
EKG Changes:
- Prolonged PR Interval: Delayed atrioventricular (AV) nodal conduction.
- Wide QRS Complexes: Slowed intraventricular conduction.
Digoxin Toxicity
EKG Changes:
- Increased Automaticity Leading to Arrhythmias:
- Paroxysmal Atrial Tachycardia (PAT)
- Atrial Fibrillation (A. fib)
- 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.
Acute Pulmonary Embolism (PE) / Acute Cor Pulmonale
EKG Changes:
- Tachycardia: Elevated heart rate.
- S1Q3T3 Pattern:
- Deep S Wave in Lead I
- Q Wave in Lead III
- Inverted T Wave in Lead III
- Right Bundle Branch Block (RBBB)
- Right Axis Deviation (RAD)
- 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.
- Electrical Alternans: Alternating QRS complex amplitudes.
Mechanism:
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.