EKG Rhythms Flashcards

(45 cards)

1
Q

Wolff Párkinson White (WPW)**

A
  1. Short PR Interval
  2. Delta Wave
  3. Widened QRS

Accessory conduction pathway which allows for re-entrant SVT, predisposing to cardiac symptoms and ventricular arrhythmia and SCD

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2
Q

Delta Wave**

A

Slurring of P wave into QRS complex, widening the QRS

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3
Q

Sinus Arrhythmia

A

Inspiration: HR increases
Expiration: HR decreases

Normal finding
Predictable irregularity in HR that occurs with respiration
Pronounced in adolescents
Measurement of cardiac health

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4
Q

Sinus Rhythm

A

Rhythm originates at SA Node
P wave present before every QRS complex
Normal P wave axis (0-90 degrees)

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5
Q

Sinus Bradycardia

A

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

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6
Q

Sinus Tachycardia

A

HR > than expected
ECG complex & intervals normal

Pain, anxiety, excitement, fever, sepsis, anemia, hypovolemia, shock, medications (albuterol, steroids)

Treatment: Underlying cause

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7
Q

Sinus Pause

A

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

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8
Q

Rhythms originating in Atrium

A

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
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9
Q

Premature Atrial Contraction (PAC)

A

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)

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10
Q

Supraventricular Tachycardia (SVT) **

A

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

  1. Focal SVT
  2. Re-entrant SVT
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11
Q

Focal SVT**

A

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

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12
Q

Re-Entrant SVT **

A

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)

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13
Q

SVT Treatment**

A

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

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14
Q

Atrial Flutter**

A

Atrial Rate ~ 300 BPM
Ventricular Rate ~ 150 BPM

“sawtooth” ECG

Causes
Cardiac surgery involving atria 
Structural Heart disease 
- Atrial dilation 
- Myocarditis 
- Digitalis toxicity
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15
Q

Atrial Flutter Treatment**

A
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!

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16
Q

Atrial Fibrillation **

A

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

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17
Q

A Fib Treatment **

A

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

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18
Q

Rhythms originating in the AV Node or Junction

A

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)
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19
Q

Junctional Rhythm

A

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 *

20
Q

Junctional Rhythm Treatment

A

Asymptomatic:

  • Nothing
  • Except if digoxin-toxic patient

Symptomatic (poor perfusion/CO)

  • Atropine
  • Temporary pacing
21
Q

Junctional Ectopic Tachycardia (JET) *

A

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
22
Q

JET Treatment *

A
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)

23
Q

Rhythms originating in Ventricle

A

Wide QRS complex
- Long in duration

QRS complex may be inconsistently related to P wave

T waves extending in opposite direction

24
Q

PVC

A

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**
25
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
26
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) ```
27
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 ***
28
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
29
Torsade de Pointes | Treatment*
Shorten the QT Interval by increasing HR • Cardiac Pacing • Isoproterenol gtt Unstable (hemodynamically) • IV Magnesium
30
VT +CHD | Treatment **
Implantable cardioverter-defibrillator (ICD) Ablation procedures ``` For patients with • Cardiomyopathy • LQTS • Life-threatening VT • Resuscitated patients following sudden cardiac death ```
31
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
32
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
33
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
34
2nd Degree Heart Block**
ECG • Some P waves are followed by QRS complex o Dopped Beats Mobitz Type I Mobitz Type II
35
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
36
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
37
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
38
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) ```
39
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
40
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
41
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 ```
42
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 **
43
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 ```
44
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 ```
45
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