ECG & Dysrhythmias Flashcards
ECG basics- pace maker physiology
Electrical pacemaker physiology
Pacemaker potential
- Primary pacemaker: SA node
- Latent pacemakers (recruited if dysfunction of SA): AV, bundle of his & Purkinje fibres
- No resting state
- Display automaticity, automatic generation of AP
Phase 0: -40mV
- L L-type Ca+ channels (long) influx of Ca2+
Phase 3: Repolarisation -65mV
- Ca2+ close, K+ open- efflux
Phase 4: Funny current
- Na+/K+ influx, depolarisation
- SNS (increased funny current, increased depolarisation, increase HR)
- PNS (increased K+ permeability- hyperpolarises, decrease HR)
Phase 0: -40mV- L L-type Ca+ channels (long) influx of Ca2+
Ventricular action potential
Phase 0: Depolarisation (peak 30mV)
- voltage gated Na+ channels open at threshold potential
Phase 1 : Partial repolarisation
- Na+ close, K+ efflux, drop in voltage
Phase 2: Plateau in voltage
- L-type Ca2+ channels open, slow influx if Ca2+
- maintains depolarisation/muscle contraction
Phase 3: Repolarisation
- outward K+ returns to normal/negative
Phase 4: RMP (-85mV)
- T-type Ca2+ channels open at ~50mV
- sympathetic stimulation increases depol rate (increase HR)
- parasympathetic increases K+ permeability (decreased HR)
Ventricular action potential
Phase 0: Depolarisation (peak 30mV)
- voltage gated Na+ channels open at threshold potential
Phase 1 : Partial repolarisation
- Na+ close, K+ efflux, drop in voltage
Phase 2: Plateau in voltage
- L-type Ca2+ channels open, slow influx if Ca2+
- maintains depolarisation/muscle contraction
Phase 3: Repolarisation
- outward K+ returns to normal/negative
Phase 4: RMP (-85mV)
Parasympathetics
- SA node- R) vagus nerve
- Continuous input- reduces rate 90-120 to 60-100bpm
- Minimal innervation in ventricale
- No direct effect on inotropy only chronotropy
Sympathetics
- Stimulate cardiac B1 receptors with noradrenaline and adrenaline
- Positive chronotropy SA node, inotropy ventricles, shortens AP (opens K+ channels)
- Increases AV conduction
ECG basics - interpretation
-
Heart rate
* *Tachycardia**
- >140 kids, >170 babies, <200 overall
- Fever, hypovolemia/shock, anemia, CCF, thyrotoxicosis, myocardial disease, anxiety
* *Bradycardia**
- <60 kids, <80 newborn
- Fitness, vagal stimulation, increased ICP, hypothermia, hypoxia, drugs, hypothyroidism -
Rhythm
* *Sinus:** P wave before QRS (depol from SA node), PR interval constant
* *Non-sinus**: inconsistent P wave, abnormal P axis- heart blocks, arrythmia -
Axis
- Normal: lead I, II & AVF positive
- LAD: lead II & AVF negative (HOCM, AVSD, single ventricle pathologies, tricuspid atresia )
- RAD: lead II & AVF positive (physiological or RVH)
- Extreme axis: All leads negative (Only 4x- ‘NATE’ Noonans, AVSD, Tricuspid atresia, Ebsteins) -
Morphology
* *P wave:** amplitude 3mm, <0.07/0.09ms duration
- P pulmonale = RA hypertrophy
- P mitrale = L atrial hypertrophy
- *QRS complex** 0.02-0.03sec
- Deep = increased R wave amplitude (V1, precordial)- ventricular hypertrophy/overload
- *R wave progression**
- Down to up
- Equivocal at V3-4
- *T waves**
- Upright in precordial leads for first 8 days, then inverted leads 1-3, up to 4
- Upright L→R with growth
-
Intervals
* *PR <0.16-0.18ms**
- Prolonged: 1st/2nd degree HB, digitalis, high potassium, AVSD, Ebsteins, myocarditis
- Shortened: WPW, DMD/ Freidrich’s ataxia, pheo
- *QRS: <0.120ms**
- Prolonged in RBBB/LBBB, WPW, intraventricular blocks, arrythmias
- *QT**
- Prolonged: long QT syndromes, low calcium, myocarditis/myocardial disease, malnutrition, drugs- antibiotics, antipsychotics etc
- Shortened: digitalis, high calcium
Sick sinus syndrome
Arrhythmia due to SA node dysfunction
- Bradycardia, alternating bradytachyarrythmia
- Sinus pause/arrest (absent P wave for short duration)
- Holter required to document HR variation
Causes
- Cardiac surgery (involving atria)
- Structurally normal heart/idiopathic
- Infective/inflammatory- myocarditis, pericarditis, rheumatic heart disease
- CHD (Ebsteins, LA isomerism, ASD)
- Hypothyroid
Features: exercise intolerance, fatigue, dizziness, headaches, nausea, palpitations, chest pain, SOB, if bradytachy can lead to syncope, death
Treatment
- Bradycardia: IV atropine, external pacing, permanent pacemaker (atrial demand pacing, or dual chamber pacing if AV dysfunction)
- Tachycardia: propanolol, quinidine, digoxin can reduce AV conduction, catheter ablation
- Tachybradycardia: pacemaker
Atrial arrythmias
Abnormal P wave morphology/number
Normal QRS duration
Premature atrial contraction (PAC)
Premature QRS, abnormal P wave morphology.
- Shortened P-P interval
- Healthy children, cardiac surgery, nil intervention
Wandering pacemaker
Changes in shape of P wave, PR intervals
- Healthy children, nil intervention
Atrial ectopic tachycardia
Rapid P waves, narrow QRS
- Rhythm from ectopic atrial tissue → overrides SA
- 20% of SVT, ‘warming up’ gradual increase of HR on Holter
- Structural atrial changes- cardiomyopathy, dilatation, inflammation, surgery
- If chronic can cause CCF, tachycardia induced CM
- Difficult to treat as refractory to medical Rx/cardioversion
- Digoxin/B-blocker, IV amiodarone for rapid control, long term amiodarone/fleccainide
- 90% effectiveness of radiofrequency ablation (LA near pulmonary veins/appendage)
- *Multifocal atrial tachycardia**
- Multiple P wave morphologies
- PP-RR intervals variable
- Common in infants, myocarditis, birth asphyxia, Noonan’s, HOCM
- May lead to CCF/long term LV dysfunction
- *- Refractory to pacing, cardioversion, meds**
- Adenosine to terminate, digoxin/propanolol to slow AV conduction
- Long term amiodarone Rcx of choice
- *Atrial flutter**
- Tachycardia ~300bpm atrial rate
- Ventricle response with variable block
- Sawtooth pattern on ECG
- Causes: structural- atrial dilatation, thyrotoxicosis, surgery, structurally normal heart in most
- Complications: decreased CO/shock, clot formation, uncontrolled can lead to CCF
- Treatment: syncronised DC shock, IV amiodarone/procainamide
- Rate control: calcium channel blockers, propanolol, digoxin
- Rhythm control: class 1 (quinidine), class 3 (amiodarone)
- Pacing if refractory
Atrial fibrillation
Fast atrial rate with irregular ventricular response (absence of visible P wave)
Same as above
Treatment: Cox-Maze procedure (96% cure), radiofrequency ablation
AV arrythmias
Absent or inverted P wave, normal QRS
- *Junctional premature beats**
- Normal, premature QRS
- Idiopathic, post cardiac surgery
- No treatment if haemodynamically stable
- *Junctional escape beat**
- Impulse initialted by AV/His
- P wave absent, QRS may occur later
- Following surgery/healthy children
- Nil treatment
- *Junctional rhythm**
- AV node becomes main pacemaker
- 40-60bpm, absent/inverted P wave
- Can be accelerated if captures pacemaker function/ HR 60-120
- Structurally normal heart, post surgery, increased vagal tone, digitalis toxicity
- Atropine/pacing for symptomatic relief
Junctional ectopic tachycardia
- Ventricular rate 120-200bpm
- P waves absent or inverted, may ‘march through’ regardless of ventricular rhythm
- Similar appearance as SVT
- Congenital (rare, <6mo), post cardiac surgery
- Can lead to shock/decreased CO
- Post operative- endogenous catecholamines/administered inotropes- peripheral vasoconstriction, rise in core temp/worsening tachy
Treatment: atrial over pacing, maintian HR <170, hypothermia/cooling, IV amiodarone, ECMO
Congenital: amiodarone- effective in 85%
SVT
Most common dysrhythmia in children 90%
Rapid, regular, narrow complex tachycardia (220-320 younger children, 150-250 older)
P wave invisible or abnormal axis
Conduction occurs above ventricles
Early onset more likely to be accessory AVRT vs adolescence AVNRT
90% are re-entrant type
>95% of wide complex tachycardia’s are SVT + abberancy/BBB, accesory pathway (not VT)
50% have structurally normal heart
¼ congenital heart disease
¼ WPW
Other causes fever, drug exposure (stimulants)
- Re-entry: stable HR, begins & ends abruptly
- Automaticity (i.e junctional tachycardia)- less common
Re-entry tachycardias
- Two anatomic pathways SA→ AV node
- Slow (slow conduction, short refractory period)
- Fast (fast conduction, long refractory)
In re-entry SVT 2 pathways:
- Accessory pathway- via other bundle structure, will show WPW pre-excitation after conversion
- Nodal pathway - dual AV node pathway, more common than accessory pathways
AVRT (accessory atrioventricular re-entry tachycardia)
Subtypes (depending on direction of conduction)
- Orthodromic: PAC initiates, antegrade conduction from ventricle via AV node, narrow complex QRS
- Antidromic: PVC initiates, retrograde conduction through AV node (fast p’way → slow), wide QRS
AVNRT (nodal atrioventricular re-entry tachycardia)
Subtypes
- Orthodromic: antegrade conduction via slow → bundle of his, hidden P waves, narrow QRS
- Antidromic: (uncommon) via fast tract antegrade then slow transmits retrograde, normal QRS, short PR, inverted P wave
Clinical presentation
May be asymptomatic
Infants: pallor, SOB, poor feeding
Older children: palpitations, chest pain, pounding in neck
Hypotension
CCF
Nodal more triggered by exercise, stress, changes in position (SNS drive)
Associations: Ebstiens, HCM/DCM, single ventricle pathologies, L-TGA
Acute Treatment
1. Vagal manoeuvres- sinus massage, eyeball pressure, headstand, ice block on face in infants
- Adenosine: transient AV block to interrupt re-entry circuit
- 50mcg/kg then flush- 10 sec half life
- works for all SVT where AV forms part of circuit
- not effective in VT/AF/Aflutter
- SFx: bronchospasm, flushing, nausea
IV propranolol if WPW
- Cardioversion- if severe, haemodynamically unstable
Long term treatment
Without WPW pre excitation
- Valsalva (if infrequent/no haemodynamic compromise)
- Sotalol, fleccainide, verapamil
- Consider ablation
With WPW
- 40% will self resolve
- If intermittent/loss of WPW on excercise test likely low risk of SCD
- If high risk consider ablation (3-4% risk of heart block, structural damage, death)
Wolf-Parkinson White
Congenital accessory pathway + arrythmia
0.1-3 per 1000
Small risk sudden cardiac death due to AF → VF
Short PR, delta wave (upslope to QRS), prolonged QRS, ST segment changes
Absent Q wave in V6 (absence of septal activation due to re-entrant pathway )
May be subtle/present intermittently
Ventricular arrythmias
Wide/bizarre QRS, T-waves pointing either direction, not related to P-waves
PVC
More common in older children
Bizarre, wide QRS followed by pause
Bigeminy - alternating 1x PVC to 1x normal
Trigeminy- 1x PVC, 2x normal
Couplets: 2x PVC in a row
Triplets: 3x PVC, if >3x then VT
Can be uniform or multiform, fixed coupling or variable
50-70% occur in healthy children
Also associated with CHD, inflammation, drugs, post cardiac surgery
More likely significant if underlying CHD, history of syncope, FHx SCD, multiform, worse with exercise, frequent/incessant episodes
Investigations: ECG, echo, Holter (if asymptomatic + multiform/couplets), exercise stress test/ EPS
Treatment: symptomatic/complex PVCs
- B-blockers
- AVOID Class 1a/class 1c, class 2
Accelerated ventricular rhythm
Wide QRS, short duration
Isolated, benign, no intervention
VT
HR 120-200
Wide, bizarre QRS
Sustained if >30sec, incessant
Moromorphic, polymorphic, bidirectional (change in QRS form)
Torsades
Causes: usually indicates significant myocardial pathology
Structural CHD, post op. infection- myocarditis, Chagas disease, Brugada, long QT, metabolic (acidosis, high/low K+, low Mg)
Can occur in healthy children
RVOT locus- inferior QRS axis, LBBB Rx B-blockers, RF curative
RBBB- Rx verapamil
Investigations ; ECH, Echo, holter, exercise stress test, MRI, EPS/biopsy
Management
if haemodynamically stable
- Amiodarone
- MgSO4
- Synchronised DC cardioversion
if haemodynamically unstable or pulseless VT
- Unsynchronised DC cardioversion
- Implantable defib/B-blockers if long QT
- Radiofrequency ablation
VF
Bizarre wide QRS
Fatal
Immediate CPR/unsynchronised cardioversion, ICD if survived
Long QT syndromes
Genetic disorder of ventricular repolarisation
- Prolonged QT interval, risk of ventricular arrhythmia leading to sudden cardiac death
QT interval >½ of cardiac cycle
- >440ms male
- >460ms female
- Rate dependant (QT interval decreases with increasing HR)
Bazzett: QTc = QTms/√RRsec (BPM)
1 small square = 40ms, large square 200ms
Pathophys/causes
- L type channel dysfunction: lets more Ca2+ in phase 2, early depolarisation and prolonged repolarisation
- Na+ channel dysfunction: early depolarisation
- K+ channel dysfunction: prolonged repolarisation/refractory period
- PVC → re-entrant tachycardia, associated with Torsades des Pointes (polymorphic VT) 150-250bpm, syncope
Congenital
- Present at birth, caused by gene mutations
- LQT1-LQT10
Autosomal dominant:
- KCNQ1 gene (LQTS1): K+ channel, 30-35% of cases, exercise emotion triggers
- KCNH2 (LQTS2) K+ channel 25-30% emotion, auditory stimuli, exercise, sleep
- SCN5A (LQTS3) Na+ channel 5-10%, sleep
- All have 6-8% chance SCD
Associated syndromes
- Jervell, Lange Neilssen (KCNQ1, K+ channel)- deafness/SNHL
- Roman-Ward
- Anderson-Tawil (KCNJ2): K+ rectifier channel -muscle weakness, dev delay
- Timothy (CACNAIC) L-type Ca2+- webbed digits, CHD, hypoglycemia, immunodeficiency, dev delay
- *Drug induced**
- A: antiArrythmics (amiodarone, sotolol, quinidine)
- B: antiBiotics (macrolide, bactrim, erythromycin)
- C: antipsyChotics (haloperidone, risperidone, CPZ)
- D: antiDepressants (TCAs)
- E: Electrolytes (low Ca2+, Mg2+, K+)
- F: antiFungals (fluconazole)
- G: Genes
- H: antiHistamines
- Neurological, nutritional, cardiac
Symptoms
syncope 26%, seizures, arrest, palpitations
Diagnosis
- via Schwartz diagnostic criteria
ECG findings
QTc >480msec
3
QTc 460-470msec
2
QTc 450msec
1
Torsades de pointes
2
T wave alternans
1
Notched T waves in 3 leads
1
Bradycardia (for age)
0.5
Clinical history
Syncope (with stress)
2
Syncope (without stress)
1
Congenital deafness
0.5
Family history
Family member with definite LQTS
1
Unexplained sudden cardiac death <30y in immediate family member
0.5
>4 points = high probability
Genetic testing
Other investigations
Echo- structurally normal heart, exercise test may provoke QTP, Holter
Treatment
- Stop causative agent
- Exercise restriction if trigger
- Electrical pacing, medication to increase HR and decrease QT interval
- Acute: MgSO4+if Torsades or VT
Congenital
- B-blockers (reduces symptoms, syncope & risk of SCD 70-85%), compliance issue
- ICD most effective
- Cardiac sympathetic denervation
Brugada syndrome
- Autosomal Dominant
- SCN5A mutation (SE Asian males)
- Risk of SCD from VT
- Syncope ar rest
- ECG: concave ST elevation, J point elevation, RBBB, prolonged PR
- ICD standard treatment, quinidine alternative to prevent syncope
Antiarrythmic drugs
Vaughn- William’s Classification
Class 1
Inhibit sodium channels, decreases rate of depolarisation - slows conduction
- Can worsen arrhythmia
- *Class 1a:** quinidine, procainamide, disopyramide
- Block fast Na+, prolong repolarisation by blocking K+ channels
- VT, recurrent AF
- SFx: tinnitus, headaches
- *Class 1b:** lidocaine
- Block late phase Na+
- SFx: N&V, seizures/neurotoxicity
- *Class 1c:** flecainide
- Refractory VT
- SFx: dizziness, blurred vision, nausea
Class 2- B-blockers (propranolol, atenolol)
- Block B1 receptors, decrease HR & contractility, decrease SA automaticity, slows conduction
- Esmolol- rapid onset/half life- IV as rescue med
- Rate control in tachyarryythmias provoked by increased SNS activity
Class 3- Amiodarone, sotalol
- Block K+ channels for repolarisation, increased refractory period
- Amiodarone (also blocks Na+, B1)
- SFx: hepatotoxicity, fibrosis, blue eyes, thyroid, long half life
- Sotalol (Na+ channel and B1 blockade)
Class 4- CCBs - verapamil, diltiazem (non-dihydropyridine- cardiac selective)
- Block voltage sensitive Ca2+ channels in SA/AV node, reduce contractility
- Use in SVT, AF
Digoxin
- Inhibits Na+/K+ pump, increased Ca2+ intracellular, Na+ extracellular
- Increased PNS, Slows AV conduction, enhances contractility
- Useful in CCF and AF
Adenosine
- Stimulates A1 receptors in atrium SA/AV node
- Prolonged refractory period, decreased automaticity/conduction velocity
- Acute SVT
- Short half life- IV
- Non toxic- chest pain, flushing, hypotension
MgSO4+
- Na+, K+ transport, MOA unknown
- Treats VT/Torsades, digoxin induced arrythmias
Tachyarryhmia mechanism
- Abnormal automaticity
- Cell membrane abnormally permeable to Na+, lower threshold to generate AP - Triggered activity
- Abnormal leakage of positive ions into cell, increased positive charge = after-depolarisation, can trigger premature APs - Re-entry
- Accessory pathway between atria-ventricles, travels back to atria before SA node can re-trigger contraction
- I.e WPW, AVNRT/AVRT
