EKG Rhythms Flashcards
Wolff Párkinson White (WPW)**
- Short PR Interval
- Delta Wave
- Widened QRS
Accessory conduction pathway which allows for re-entrant SVT, predisposing to cardiac symptoms and ventricular arrhythmia and SCD
Delta Wave**
Slurring of P wave into QRS complex, widening the QRS
Sinus Arrhythmia
Inspiration: HR increases
Expiration: HR decreases
Normal finding
Predictable irregularity in HR that occurs with respiration
Pronounced in adolescents
Measurement of cardiac health
Sinus Rhythm
Rhythm originates at SA Node
P wave present before every QRS complex
Normal P wave axis (0-90 degrees)
Sinus Bradycardia
SA Node & ECG complexes normal
HR lower than expected for normal age
ICP, Hypothermia, Hypoxia, Hypothyroidism, Hyperkalemia, Sedation, Sleep, Medications (Digoxin)
Treatment only if symptomatic (hemodynamic instability): Atropine, isoproterenol, cadiac pacing
Sinus Tachycardia
HR > than expected
ECG complex & intervals normal
Pain, anxiety, excitement, fever, sepsis, anemia, hypovolemia, shock, medications (albuterol, steroids)
Treatment: Underlying cause
Sinus Pause
Sinus node fails to initiate impulse
Pause is short –> No P wave or QRS recorded
Young people: common in sleep (< 2 secs only)
Hypoxia, increased vagal tone, digoxin toxicity
Treatment: Atropine, isoproterenol, cardiac pacing
Rhythms originating in Atrium
Originated outside SA node, but above Bundle of His
Atrial arrhythmias:
Unusually contoured P waves and/or
Abnormal # of P waves per QRS complex
Follow a QRS complex of NORMAL duration
Includes: Premature Atrial Contraction (PAC) Supraventricular Tachycardia (SVT) Atrial Flutter Atrial Fibrillation
Premature Atrial Contraction (PAC)
Atrial beat that occurs too early
Common in healthy children
Usually no clinical significance
CHD, digitalis toxicity, cardiac surgery,
Treatment: Only if due to digitalis toxicity
If PAC consecutive, incessant, or produce bradycardia –> abnormal electrolytes (K, Mg)
Supraventricular Tachycardia (SVT) **
Rapid HR with narrow QRS
- Infants: HR > 220 BPM
- Children: HR > 180 BPM
Includes any rapid rhythm occurring ABOVE the Bundle of His. Most common rhythm disturbance in pediatric patients
- Focal SVT
- Re-entrant SVT
Focal SVT**
Rapid firing of a single focus in atria
Focal is RARE
Ectopic Atrial Tachycardia (EAT)
- Most common chronic SVT in children
Leads to:
Arrhythmia - induced tachycardia (Tachycardia induced-cardiomyopahty)
Treatment:
Medication, ablation
Focal SVT resolves in predictable fashion once tachycardia is treated
Re-Entrant SVT **
2 Circuits: Normal conduction pathway (SA -> AV Node) & Accessory conduction pathway (BoH -> Purkinje Fibers)
Conduction travels down either circuit & up the other. More rapid conduction in accessory pathway
Anatomically separate accessory pathway:
WPW (delta wave)
Atrioventricular Reciprocating Tachycardia (AVRT)
or
Structurally separate accessory pathway:
Dual AV Node Pathway: Atrioventricular Nodal re-entrant tachycardia (AVNRT)
SVT Treatment**
Unstable/poor perfusion
- Synchronized Cardioversion (0.5 - 1 J/kg, up to 2 J/kg)
- Adenosine 0.1 mg/kg/dose (half life < 1.5 sec), CAUTION: bronchospasm in asthmatic
Stable
- ICE
- Valsalva maneuver
Chronic Management
- Digoxin, propanolol, nadolol, flecainide, propafenone, stoalol, amiodarone, radiofrequency cath ablation
Atrial Flutter**
Atrial Rate ~ 300 BPM
Ventricular Rate ~ 150 BPM
“sawtooth” ECG
Causes Cardiac surgery involving atria Structural Heart disease - Atrial dilation - Myocarditis - Digitalis toxicity
Atrial Flutter Treatment**
Rate control • Digoxin • Propranolol • Calcium channel blocks • AF is difficult to rate control**
Rhythm control
• Antiarrhythmic medication
Ablation
• Class I indication for recurrent/persistent AF
o Only if over 15 kg!!
Cardioversion
• Acute management if unstable
• Digoxin interaction Malignant Ventricular Arrhythmias ***
- Avoid cardioversion in patients receiving digoxin therapy, unless the arrhythmia is life-threatening
Rapid Atrial Esophageal Pacing
• If cardioversion is contraindicated!
Atrial Fibrillation **
Atrial HR 350 – 600 BPM (very rapid)
QRS duration normal
Irregular ventricular response (Lead V1)
Causes:
Structural heart disease
Myocardial dysfunction
Previous cardiac surgeries
SVT**
• AF can develop from rapid atrial activity of SVT in as many as 30% of children
• Elimination of SVT in patients with documented AF has been shown to prevent recurrence AF
A Fib Treatment **
Unstable (hemodynamically)
• Cardioversion
Stable
• Medical management
• Observation (Recurrence, rate control, rhythm control)
• Catheter ablation
Rate Control
• Digoxin
• Propranolol
• Verapamil
Rhythm control
• Sotalol
• Amiodarone
• Reduce risk of recurrence
Rhythms originating in the AV Node or Junction
AV node (Junctional Node) assumes role of main pacemaker due to SA node dysfunction
ECGs:
- Inverted P waves following QRS complex
- Absent P waves, normal QRS
Rhythms
- Junctional Rhythm
- Junctional Ectopic Tachycardia (JET)
Junctional Rhythm
HR 40 - 60 BPM
Structurally normal heart
Causes
- Cardiac surgical procedures involving atria
- conditions that raise vagal tone (sleep, increased ICP)
- Digoxin toxicity
Clinically significant only if patient is hemodynamically unstable *
Junctional Rhythm Treatment
Asymptomatic:
- Nothing
- Except if digoxin-toxic patient
Symptomatic (poor perfusion/CO)
- Atropine
- Temporary pacing
Junctional Ectopic Tachycardia (JET) *
ECG
- Ventricular Rate 150 - 300 BPM
- QRS narrow
- Ventricular Rate is FASTER than atrial rate**
- AV dissociation in ECG **
Type of SVT, but automatic tachycardia comes from AV Node
Most common arrhythmia occurring after cardiac surgery (< 2 years old) **
Risk Factors
- Younger patient age
- Longer CPB time
- Vasoactive agent use
- Catecholamine sensitive**
- Type of cardiac surgery
JET Treatment *
Restore AV synchrony - Atrial wires Slow ventricle rate - Sedation - Pain control - Electrolyte replacement (Mg) - Minimize vasoactive agent use - Hyperthermia avoidance - Induce Hypothermia (cooling blanket, fan, intubated, paralyzed)
Improve CO
Amiodarone
Procainamide
Precedex
- Highly selective alpha 2 adrenoreceptor agonist (slow HR & sedation)
Rhythms originating in Ventricle
Wide QRS complex
- Long in duration
QRS complex may be inconsistently related to P wave
T waves extending in opposite direction
PVC
Wide QRS complex
Not preceded by P wave
Bigeminy
- PVC every other beat, alternating with normal QRS
Trigeminy
- PVC every 3rd beat, separated by 2 normal QRS
Couplet
- 2 consecutive PVCs
Unifocal PVC
- From single focus in ventricle
- Consistent QRS pattern in same lead
Multifocal PVC
- Different foci in ventricle
- Varying configuration of QRS pattern in same lead
- OMNIOUS**
PVC
Cause & Treatment
Electrolyte imbalance Drug toxicity Cardiac Injury Tumor Cardiomyopathy Myocarditis Acidosis Hypoxia CHD Prolonged QT Mitral Valve Prolapse
Isolated, unifocal: No treatment
Frequent, multifocal:
- Correct underlying cause (Hypoxia, Electrolyte imbalance, Acidosis)
- Beta Blockers
- Procainamide
- Lidocaine
- Amiodarone
Ventricular Tachycardia (VT)**
Series of 3 or more PVCs + HR 120 – 200 BPM
• HR usually < 250 BPM
Sustained • > 10 seconds Non-sustained • < 10 seconds Unifocal Multifocal • Torsade de Pointes (Undulating QRS complexes, Appear to be spiraling along an axis)
VT
Causes/SS**
Cardiac surgery
• Right ventriculostomy (Early and late postoperative VT)
Torsade de Pointes causes • Drugs/chemicals that prolong QT interval o Antiarrhythmics o Phenothiazines o Tricyclic antidepressants o Antibiotics (Ampicillin) o Organophosphate insecticides
S/S
- Hemodynamic compromise
- VT can quickly deteriorate to VF ***
VT Treatment **
Reversible causes
Unstable (hemodynamically) or Unconscious • Synchronized Cardioversion o 0.5 – 1 J/Kg Pulseless VT • Immediate Defibrillation o 2 – 4 J/kg Uncontrollable VT • ECMO
Stable, conscious patient
• Amiodarone
• Sotalol
• Lidocaine
Torsade de Pointes
Treatment*
Shorten the QT Interval by increasing HR
• Cardiac Pacing
• Isoproterenol gtt
Unstable (hemodynamically)
• IV Magnesium
VT +CHD
Treatment **
Implantable cardioverter-defibrillator (ICD)
Ablation procedures
For patients with • Cardiomyopathy • LQTS • Life-threatening VT • Resuscitated patients following sudden cardiac death
Ventricular Fibrillation **
ECG
- Bizarre, wavy ventricular pattern with varying sizes and configurations of the QRS complex
Results from erratic firing of multiple foci within the ventricles
- Leads to infective circulation, pulselessness, death
Causes
- Hypoxia
- Hyperkalemia
- Digoxin toxicity
- Quinidine Toxicity
- MI
- Myocarditis
- Cardiothoracic surgery complications
Acute Management
- CPR
- Defibrillation following PALS guidelines
1st Degree Heart Block **
ECG
• NSR (P wave present before every QRS complex, QRS normal in duration and appearance)
• 1:1 Conduction (No dropped beats)
Prolonged PR Interval
• Due to abnormal delay in conduction through AV node
Can occur in healthy children
1st Degree Heart Block
Causes & Treatment **
Causes • Conduction disturbance • Rheumatic Fever Cardiomyopathies • Congenital Heart Defects o ASD o Ebsteins Anomaly o Endocardial Cushion Defect • Myocarditis • Digoxin Toxicity* o First degree AV block is a sing of digoxin toxicity o Most common cause in pediatric patients** • Lyme Disease* o PR Interval > 280 seconds**
Signs and Symptoms
• Increased Vagal Tone
• Usually asymptomatic & hemodynamically stable
Treatment
• None
• Unless digoxin toxicity
2nd Degree Heart Block**
ECG
• Some P waves are followed by QRS complex
o Dopped Beats
Mobitz Type I
Mobitz Type II
2nd Degree Heart Block**
Mobitz Type I
PR interval becomes progressively prolonged until 1 QRS complex is eventually dropped –> Missed beat
o Dysfunction of AV node, but does not progress to complete heart block
Causes o CHD o Myocarditis o MI o Cardiomyopathy o Drug Toxicity (Digoxin, BB, CCB, Quinidine) o Cardiac Surgery
Can occur in healthy children (11%)
o Sleep
Symptoms
o No hemodynamic compromise
Management
o Underlying cause (toxicity)
o Otherwise, treatment unnecessary
2nd Degree Heart Block**
Mobitz Type II
Characteristics can be one of the following
o 1. Normal AV conduction with normal PR Interval
o 2. Conduction is completely blocked - Ventricular rate depends solely on number of conducted atrial impulses, AV block at the level of Bundle of His
Causes
o Same as Mobitz Type I
Treatment
o Asymptomatic - Prophylactic pacemaker therapy (Risk for complete heart block)
o Symptomatic - Pacemaker therapy
3rd Degree Heart Block**
ECG • P waves regular o Normal R-R interval o Slower rate than normal for age • Congenital o QRS duration & impulse normal appearing o Ventricular rate higher: 50 – 80 BPM • Acquired o QRS duration prolonged o Ventricular rate slower: 40 – 50 BPM o May appear as PVC
Complete Heart Block
• Complete failure of impulse conduction from Atria to Ventricles
• Atria and Ventricles beat independently from each other
3rd Degree HB **
Causes, Treatment
Causes - Congenital
o With or without structural heart disease
o Maternal Lupus
o L Transposition of the great arteries
Causes - Acquired
o Cardiac surgical complications (VSD, TOF)
o Rheumatic Fever
o Lyme Disease
Signs & Symptoms • Low CO o Fatigue o Dizziness o Syncope o Exercise intolerance • Infants o CHF
Treatment • CHB o Permanent pacemaker • Surgically induced post-op CHB o Temporary pacing o Permanent pacemaker (If CHB > 7 days)
LQTS**
ECG
Prolongation of QT Interval - Delayed ventricular repolarization
Corrected QT Interval (QTc) Measurements
• Normal QTc = < 440 ms
• Long QT Syndrome: QTc > 460 ms
T Wave
• Abnormal
• Notched, Biphasic
LQTS Diagnosis
Diagnosis requires ALL of the following:
ECG Findings
• May sometimes have normal QT interval*
Symptoms
Family history
• Positive family history for LQTS or premature, sudden death reported in 60% of patients*
Genetic testing (sometimes)
• All blood relatives of patients with congenital LQTS should have screening ECG in addition to genetic testing**
o Regardless of symptoms
LQTS Causes
Congenital • Jervell & Lange-Nielsen Syndrome o Congenital deafness (Autosomal recessive) • Romano-Ward Syndrome o No deafness (Autosomal dominant)
Acquired • Antibiotics • Antidepressants • Antipsychotics • Electrolyte disturbances • Hypokalemia • Hypocalcemia • Hypomagnesemia • Hypothyroidism • Anorexia nervosa • Head trauma
LQTS
S/S & Risks
Signs and Symptoms
- Syncope
- Palpitations
- Dizziness
- Cardiac arrest
- Most symptoms coincide with exercise, emotion, or sudden auditory stimuli** (doorbell, alarm)
Risk
-Ventricular Arrhythmias (High risk)
-Sinus bradycardia (Frequently associated with Long QT syndrome )
-Sudden Death
• QTc Interval > 500 msc = 5 – 8 x increased risk of cardiac event **
LQTS Treatment
Reduce sympathetic activity
Beta Blockers • Propanolol o 2 – 4 mg/kg/day • Atenolol o 0.5 mg/kg/day
Cardiac Pacemaker
ICD
• Only if high risk
• Previous cardiac arrest
• Failed medication therapy
Left cardiac sympathetic denervation surgery
LQTS + VT or Torsade de Pointes • IV Magnesium o 20 – 50 mg/kg o Max 2 g • Serum electrolytes • Toxicology screen
WPW
Causes/Diagnostics
Congenital Diseases accompanied with
- Ebstein’s Anomaly
- L-TGA (corrected transposition)
- Hypertrophic Cardiomyopathy
Diagnostic - ECHO - Evaluation if • Syncope with WPW - Risk Stratification • Exercise Treadmill Testing o Monitor loss of pre-excitation with increased heart rates • Electrophysiology study o Evaluate accessory pathway with potential ablation therapy
WPW Risks
At risk for
- Sudden death 48% children
- A Fib –> VF
- A Flutter –> VF
- Intermitted pre-excitation or SVT
Contraindications
- Digoxin
- Verapamil
- Both medications shorten refractory period of WPW accessory pathway
Restrictions
-Competitive Sports
