ECG Flashcards
What’s the ecg paper speed? large square? small squares? height?
25mm/second
0.2s (5mm)
0.04s (1mm)
0.1cm=0.1mV (height); gain is 10mm/mV
Example scenarios likely to have high amplitude ECG waveform? and low?
ventricular hypertrophy (relatively high myocardial mass)
reduced amplitude if pericardial fluid, pulmonary emphysema, obesity (increased resistance to current flow)
Where are the leads placed for 12-lead ecg?
V1= RSE 4th ICS
V2= LSE 4th ICS
V4=mid clavicular line 5th ICS
V3= btwn V2 & V4
V5= ant ax line 5th ICS
V6= mid ax line 5th ICS
What views of the heart do the leads obtain?
II, III & aVF= inferior surface
I, V5, V6 & aVL= lateral
V1-4= anterior
V1 & aVR= look through the RA directly into the cavity of the LV
What rate= tachycardia & bradycardia?
Tachy is >100bpm
Brady is <60bpm (or <50 during sleep)
How to calculate rate on an ecg?
if regular, divide the number of large squares btwn 2 consecutive R waves into 300 or divide the number of small squares btwn 2 consecutive R waves into 1500
if irregular, count the qrs complexes on a 25cm strip & multiply by 6
Which strip is used for rhythm identification? why? what type of arrhythmia may young healthy ppl often display?
lead II, best view of p wave, sinus arrhythmia (variation in HR with inspiration & expiration- beat-to-beat variation in R-R interval (rate INCREASES with inspiration, a vagally-mediated response to the increased blood volume returning to the heart during inspiration)
What’s the normal range for cardiac axis? What axis lies beyond -30 degrees? and >90 degrees?
-30 to 90 degrees
LAD
RAD
What’s sinus rhythm?
P wave upright in leads I & II
each P followed by a QRS
HR 60-99bpm
What’s a U wave?
an additional wave following T wave, in same direction, may be due to late repolarisation of ventricles or repolarisation of the mid-myocardial cells (those btwn the endocardium & epicardium) & the His-Purkinje system.
Tends to become apparent @ HRs <65bpm, inversely proportional to rate (higher rate smaller U waves)
Generally upright except in aVR & most prominent in leads V2-V4.
usually about 0.5mm, max 1-2mm, they’re usually <25% of the voltage of the T wave; disproportionally large U waves are abnormal
What are some U wave abnormalities & their causes?
prominent U waves (>25% amplitude of t wave)
in bradycardia, severe hypokalaemia, hyper Ca, hypoMg, hypoThermia, raised ICP, LVH, HCM, digoxin
inverted U waves (in leads with upright T waves) are specific for the presence of heart disease (CAD, HTN, valvular or congenital heart disease, cardiomyopathy, hyperthyroidism)
In pts presenting with chest pain, inverted U waves are very specific for myocardial ischemia. They may be the earliest marker of UA & evolving MI, they predict >=75% stenosis of the LAD/LMCA & the presence of LV dysfunction
What are some normal ecg findings in healthy ppl?
tall R waves
prominent U waves
ST elevation (high take-off, benign early depolarisation)
exaggerated sinus arrhythmia
sinus bradycardia
wandering atrial pacemaker
wenckebach phenomenon
junctional rhythm
1st degree heart block
For which conditions is it helpful to know the axis?
conduction defects (eg. L) anterior hemiblock)
ventricular enlargement (eg. RVH)
broad complex tachycardia (eg. bizarre axis suggests ventricular origin)
congenital heart disease (eg. ASD)
pre-excited conduction (eg. WpW)
pulmonary embolus
By the method of inspecting leads I, II & III, what’s normal, L) & R) axis?
normal is +ve in 1 & 2 but may be either +ve or -ve in lead III
right axis is -ve in 1, +ve in 3 & may be +ve or -ve in II
left axis is +ve in 1, -ve in III & -ve in II
At what direction relative to the lead is current travelling in a lead with an equiphasic trace?
90 degrees to that lead
Aside from looking at leads I-III, what’s another way of determining axis?
find the limb lead closest to being equiphasic.
The axis is about 90 deg to the L) or R) of that.
inspect adjacent leads wrt the hex axial diagram; if the lead to the L) is +ve, the axis is 90 degrees to the equiphasic lead towards the L), vice versa if the lead to the R) side is +ve
What’s the usual height & duration of a p wave?
no >0.25mV & no >0.12s (3 small squares)
in which lead is the p wave usually inverted?
aVR
In which leads are the P waves most prominent?
II and V1
What are differentials for an inverted P wave in lead I?
incorrect electrode placement (transposition of the R) & L) arm electrodes), dextrocardia or abnormal atrial rhythms.
In which lead are p waves often biphasic?
V1
What does a large negative deflection in V1 suggest?
L) atrial enlargement
What do bifid p waves suggest?
normal p waves often have a slight notch, particularly in precordial leads, which are due to slight asynchrony btwn RA & LA depolarisation.
more pronounced notch with peak-to-peak interval >1mm (0.04s) is pathological & suggests a LA abnormality (eg. mitral stenosis)
What’s the PR interval? normal? what leads to abnormalities of the PR interval?
time from onset of atrial to onset of ventricular depolarisation. normally 0.12-0.2 seconds. abnormalities of the conducting system causing transmission delays may prolong the PR interval.
What’s the QRS? normal duration?
represents the electrical forces generated by ventricular depolarisation. >=0.12s (3 small squares)= delay in ventricular depolarisation (eg. BBB).
What’s the dire action of septal depolarisation?
L) side of the septum depolarises first then the impulse spreads to the R).
in which leads are “septal” q waves (negative deflection) usually seen? how can we tell they are normal?
lateral leads (I, aVL, V5 & V6)
they are usually <2 small squares deep (ie. <0.2mV),
Why is there normally a deep S in V1?
the forces generated by the free wall of the LV predominate so after the small +ve deflection (R wave) as the septum depolarises L) to R), the depolarisation force through the LV moves away from V1, a large -ve deflection is seen.
What & why is the normal R wave progression?
increasing amplitude of R wave as progress from V1 to V6 with corresponding decrease in S wave depth, culminating in a predominantly +ve complex in V6, as they align more with the direction of LV depolarisation
Which lead in the precordium typically is equiphasic?
Lead V3-V4 typically has equiphasic QRS complexes, is located over the “transition zone”, shifts to the L) with increased age
What happens to the height of the R wave as move across the precordial leads?
typically increases progressively, is usually <27mm in leads V5 & V6 but may be higher in V5 than V6 since the former is closer to the LV
Where is the S wave deepest?
in the R) precordial leads, decreases in amplitude across the precordium & may even be absent in V5 & V6. It shouldn’t be >30mm deeper usually
What’s the ST segment?
interval between end of ventricular depolarisation & beginning of repolarisation
Where is “high take-off” seen?
Leads V1-V3, where a rapidly ascending S wave merging directly with the T wave makes the j point indistinct & the ST segment difficult to identify.
In which condition is non-pathological ST elevation seen (aside from “high take off”)?
benign earl repolarisation, which is common in young males, athletes, black.
What is the t wave? in which leads is it usually inverted?
represents ventricular repolarisation. should be in the same orientation as qrs complex so is inverted in aVR & may be inverted in lead III. May also be inverted in lead V1 which is occasionally accompanied by T wave inversion in V2 but isolated T wave inversion in lead V2 is abnormal. T waves are usually asymmetrical; an inverted symmetrical T wave is highly suggestive of myocardial ischemia (asymmetrical inverted t waves are frequently a non-specific finding. T wave inversion in 2 or more of the right precordial leads= “persistent juvenile pattern”.
Where are the tallest T waves usually seen?
Leads V3 & V4
What conditions are associated with tall T waves?
acute myocardial ischemia, hyperkalaemia
T waves should be at least 1/8 but less than 2/3 of the corresponding R wave. Amplitude is rarely >10mm.
What’s the QT interval, what does it represent & what’s normal value?
From start of QRS complex to end of T wave, represents total time taken for ventricular depolarisation & repolarisation. It increases as HR slows so HR needs to be taken into account.
Normal QT interval is 0.35-0.45s & shouldn’t be >1/2 the duration of the R-R interval.
QT interval increases slightly with age & is longer in women than men.
Why & how calculate QTc?
QT lengthens as HR slows so must take rate into account.
Bazett’s correction is used to calculate QT corrected for HR: QTc= QT / [(root)(R-R)] seconds
Where should the QT interval be measured?
Should measure QT interval @ a point where there aren’t prominent U waves as these may lead to overestimation of QT, so aVL is a good choice.
What are some physiological & pathological conditions associated with sinus bradycardia?
common during sleep or in those with high vagal tone (eg. athletes, young healthy adults)
acute myocardial infarction= the commonest pathological cause of sinus bradycardia, particularly an inferior MI since the SA & AV nodes + inferior myocardial wall are all usually supplied by R) CA.
Others:
hypothermia
hypothyroidism
sick sinus syndrome
raised ICP
drugs (B blockers, digoxin, amiodarone)
obstructive jaundice
What’s the commonest ecg feature of sick sinus syndrome?
inappropriate, persistent & often severe sinus bradycardia
other features include sinus arrest, SA block, junctional or ventricular escape rhythms, tachy-brady syndrome, paroxysmal atrial flutter & AF
CHARACTERISED BY EXTREMELY SLOW SINUS RATE, LONG SINUS PAUSES INTERSPERSED WITH RUNS OF TACHYCARDIA (may be atrial or junctional; junctional flurries are compensatory phenomena aiming to preserve CO; HR >100, p waves hidden, inverted, retrograde, short or upright); ie. the sick sinus syndrome can lead to tachy-brady
What’s sick sinus syndrome?
the result of dysfunction of the SA node, impaired ability to generate & conduct impulses, usually due to idiopathic fibrosis of the node but also ass’d with myocardial ischaemia, digoxin & cardiac surgery.
What are some conditions associated with SA node dysfunction?
age
idiopathic fibrosis
ischaemia (incl MI)
high vagal tone
myocarditis
digoxin toxicity
How does SA block differ to sinus arrest?
SA block is transient failure of impulse conduction to the atrial myocardium–> intermittent pauses btwn P waves which are the length of 2+ P-P intervals
sinus arrest= when there’s transient cessation of impulse formation @ the SA node, manifesting as a prolonged pause without P wave activity & the pause is unrelated to the length of the P-P cycle.
What are escape rhythms?
the result of spontaneous activity from a subsidiary pacemaker, located in atria, AV junction or ventricles. They take over when normal impulse formation or conduction fails & may be ass’d with profound bradycardia.
Junctional rhythms havenormal QRS complex & rate of 40-60bpm.
A ventricular escape rhythm has a broad QRS & is slow (15-40bpm).
What does 1st degree AV block look like & what’s it usually due to?
P precedes each QRS, PR interval is >0.2s, the PR interval remains constant, the delay in conduction of the atrial impulse to the ventricles is usually @ the level of the AV node.
What’s 2nd degree AV block & @ what level is the issue?
Intermittent failure of conduction between atria & ventricles. Some P waves aren’t followed by a QRS complex.
Mobitz 1 (wenckebach) is usually @ the level of the AV node, produces intermittent failure of transmission of atrial impulse to ventricles. Initial PR interval is normal but there’s progressive lengthening of the PR interval with each successive beat until AV transmission is blocked completely & a P wave isn’t followed by a QRS. PR interval then returns to normal & cycle repeats.
Mobitz II is less common, block usually @ the level of the bundle branches so the QRS is wider (a pacemaker in the BoH produces a narrow QRS complex) & more likely to produce symptoms, intermittent failure of conduction of P waves. PR interval is constant (may be normal or prolonged). 2:1. Higher degree may be 3, 4 or more : 1 block & it may progress to 3rd degree AV block.
3rd degree: complete failure of conduction btwn atria & ventricles, complete independence of atrial & ventricular contractions with the P waves bearing no relation to the QRS complexes (the p waves usually proceed @ a faster rate). A subsidiary pacemaker triggers ventricular contractions, occasionally no escape rhythm occurs & systolic arrest occurs. the rate & QRS morphology of the escape rhythm vary depending on the site of the pacemaker.
What’s tachy-brady syndrome?
it’s common in sick sinus syndrome
is characterised by bursts of atrial tacchyardia (or junctional) interspersed with bradycardia
paroxysmal atrial flutter or fibrillation may occur, cardioversion may be followed by severe bradycardia
What are causes of AV conduction block?
myocardial ischemia/infarction
degeneration of His-Purkinje system
infection (eg. Lyme disease, diphtheria)
immunological disorders (eg. SLE)
surgery
congenital heart disorders
What are the bundle branches?
BoH divides into R) & L) BBs, then the L) divides to anterior & posterior hemivas cycle
What are the characteristics of R) BBB?
It’s usually a pathological cause.
LV depolarises in the normal way so the early part of the QRS is normal- the RV depolarisation is delayed & proceeds through non-specialised conducting tissue so the R) precordial leads have a prominent & late R wave & the L) precordial & limb leads have a wide slurred S wave. there are secondary repolarisation changes in the RV giving rise to ST-T changes in R) chest leads.
Overall:
QRS wide
Secondary R wave (R’) in V1 or V2
Wide slurred S wave in leads I, V5 & V6
associated ST depression & TWI in R) precordial leads
What are the primary causes of L) BBB?
primarily due to coronary artery disease, hypertensive heart disease, dilated cardiomyopathy. Unusual for L) BBB to exist in absence of organic disease.
What is the supply of the L) BB? implications?
anterior descending artery (branch of L) coronary) & the R) coronary, so pts with L) BBB generally have extensive disease.
See in 2-4% of pts with acute MI & is usually associated with anterior infarction.
What are the characteristics of L) BBB?
QRS >=0.12s
Broad monophonic R wave in I, V5 & V6
no Q waves in V5 or V6 (septum usually depolarises L) to R), producing Q waves in L) chest leads.. in L) BBB the direction of septal depolarisation is reversed, septal Q waves are lost & replaced with R waves.
associated features:
-ST-T changes in opposite direction to the dominant direction of the QRS (appropriate discordance- ie ST depression/TWI seen in leads with dominant R wave, ST elevation & +ve T waves seen in leads with a dominant S wave)
-poor R wave progression in the chest leads
-RS complex (rather than monophonic complex) in leads V5 & V6
-L) axis deviation (common but not invariable)
What’s L) anterior hemiblock?
L) axis deviation > -30 degrees in the absence of another cause (eg. inferior MI)
criteria= tall R waves I, aVL
deep S II, III, aVF
incr QRS voltage in limb leads
what’s the L) posterior hemiblock?
R) axis deviation >90 degrees in absence of other cause of RAD
What’s a bifascicular block?
R) BBB with L) (L) anterior hemiblock) or R) (L) posterior hemiblock) axis deviation
The most common bifascicular block is R) BBB with L) anterior hemiblock (the L) posterior fascicle is fairly stout & more resistant to damage so R) BBB with L) posterior hemiblock is rare.
What’s trifascicular block?
conduction delay in all 3 fascicles below the AV node (RBBB, LAFB, LPFB); on ecg, it manifests as 3rd degree AV block w RBBB & LAFB or 3rd degree AV block + R) BBB + LPFB
It’s NOT bifascicular block + 1st degree AV block (which has no difference in progression to CHB vs those w just bifascicular block)
Pts w true trifascicular block require pacemaker (if refractory to correction of reversible causes eg. medn/electrolyte/ischaemia causes.
symptomatic bifascicular block w syncope or presyncope should be admitted for monitoring likely PM insertion
asymptomatic bifascicular with or without 1st deg AV block isn’t an indication for pacing
causes incl IHD, strutural heart disease, congen HD, AV nodal blocking drugs, hyperkalemia (can correct!), infiltrative myocardial disease (amyloid, sarcoid, haemochromatosis), inflamm (myocarditis, lyme diseae) autoimmune (SLE, systemic sclerosis), AS, ant MI
How may vagal maneouvers help for a sinus tachycardia & for which supra ventricular tachycardias does it help?
slows AV conduction, help identify rhythm by slowing the ventricular rate allowing more accurate visualisation of atrial activity, doesn’t tend to stop the tachycardia unless it’s due to AVN or (rarely) SA node re-entry
Describe sinus tachycardia
usually physiological, may be precipitated by sympathomimetic drugs or endocrine disturbances.
Rate rarely >200bpm in adults.
Rate increases gradually & may show beat to beat variation.
Each p is followed by a qrs, the P wave height may increase & PR interval may shorten as rate increases, with fast tachycardia the p wave may be lost in the preceding t wave.
What are the supra ventricular tachycardias? how to analyse them?
From the atria or SA node: sinus tachycardia, AF, atrial flutter, atrial tachycardia
from the AVN: AV nodal re-entrant tachycardia, AV re-entrant tachycardia
look at the atrial rate & ventricular rate, regular/irregular, look for F or f waves & establish relation of p wave to ventricular complexes
Describe sinus, atrial tachycardias & atrial flutter/fibrillation
Sinus tachycardia: typically atrial & ventricular rate 100-200bpm, regular ventricular rhythm
each P followed by a QRS
p waves normal morphology
Atrial tachycardia:
abnormal p wave morphology
atrial rate 100-250bpm
ventricular rhythm usually regular
variable ventricular rate
Atrial flutter:
undulating saw-tooth baseline flutter waves
atrial rate 250-350bpm
regular ventricular rhythm, ventricular rate typically 150bpm (with 2:1 AV block, 4:1 also common but 1:1 and 3:1 rare)
Atrial fibrillation:
p waves absent, oscillating baseline fibrillation waves, atrial rate 350-600bpm, irregular ventricular rhythm, ventricular rate 100-180bpm
What are some causes of sinus tachycardia?
physiological: anxiety, pain, exertion
pathological: fever, hypoxia, hypovolaemia, anaemia
endocrine: thyrotoxicosis
pharmacological: adrenaline (from phaeochromocytoma), caffeine, ETOH, salbutamol
What are some causes of atrial fibrillation?
ischaemic heart disease, hypertensive heart disease, rheumatic heart disease, sick sinus syndrome
cardiomyopathy (dilated or hypertrophic)
post cardiac surgery
COPD
idiopathic
infection
thyrotoxicosis
ETOH misuse (acute or chronic)
What’s the most common sustained arrhythmia & what proportion of ppl does it affect? prognosis?
atrial fibrillation- overall prevalence 1-1.5%, increases w age (10% of ppl aged >70)
Prognosis depends on the ethology- excellent if idiopathic, relatively poor if due to ischaemic cardiomyopathy
In AF, what do rates of <100bpm suggest?
higher degree AV block or rate slowing medications
Where are the sawtooth atrial contractions (@ a rate of about 300/min) best seen? Whats A flutter due to?
inferior leads & V1
due to a re-entry circuit in the RA with secondary activation of the LA
Is atrial flutter ever idiopathic?
uncommonly
What are the 4 types of atrial tachycardia?
benign (common in elderly, paroxysmal, atrial rate 80-140bpm, abrupt onset & cessation & brief duration
incessant ectopic- rare chronic arrhythmia in children & young adults- rate 100-160bpm, difficult to distinguish from sinus tachycardia but is important to Dx as may lead to dilated CM if untreated
multifocal atrial tachycardia- occurs when multiple sites in the atria are discharging & is due to increased automaticity- p waves of varying morphologies, PR intervals of different lengths, irregular ventricular rate, it’s different from AF as there’s an isoelectric baseline btwn the P waves. Often ass’d with COPD or hypoxia or digoxin toxicity.
Atrial tachycardia with high-grade AV block often seen with digoxin toxicity. May end up with “regularised AF”; AF + CHB + accelerated junctional escape rhythm–> a paradoxically regular rhythm. Ventricular rhythm is regular but if the AV block is variable it may be irregular.
Dig tox may also get bidirectional VT (polymorphic w QRS complexes alternating btwn L)- & R)-axis deviation or L)BBB & R)BBB morphology
What are some conditions associated with atrial tachycardia?
cardiomyopathy
COPD
IHD
rheumatic heart disease
sick sinus syndrome
digoxin toxicity
What’s the most common cause of paroxysmal regular narrow complex tachycardia?
AVNRT (“SVT”)
What’s the pathophysiology of AVNRT?
there are 2 pathways in the AVN with different conduction velocities & refractory periods- one fast with long refractory period, one slow with short refractory period.
In sinus rhythm, the impulse travels down both but the impulse going down the slow pathway terminates as the final common pathway is refractory.
In 90% of ppl with AVNRT, it’s initiated as follows: If a premature beat occurs @ the critical point where the fast pathway is refractory, the impulse is conducted through the slow pathway then retrograde up the fast one & a re-entry through the circuit is created- AVNRT is initiated.
In the remainder of ppl with AVNRT, the circuit is initiated by a premature ventricular contraction with the impulse traveling retrogradely up the slow pathway- this is known as fast-slow AVNRT aka “long RP” tachycardia- an inverted P wave may follow the T, preceding the next QRS. (*this is similar to AVRT in orthodromic wPw; retrograde p waves occur later w long RP interval >70ms)
What are the ecg findings of AVNRT?
ECG is normal during sinus rhythm. During the tachycardia, the rhythm is regular, QRS complexes narrow & rate is 130-250bpm. atrial conduction proceeds retrograde producing inverted P waves in II, III & aVF but since atrial & ventricular depolarisation occur simultaneously the P waves are often buried in the QRS.
The P wave may be seen distorting the last part of the QRS complex giving rise to a “pseudo” S wave in the inferior leads & a “pseudo” R wave in V1.
Is AVNRT symptomatic?
generally mild (eg. palpitations), symptoms are commonest if rapid rates & pre-existing heart disease. Severe symptoms= dizziness, dyspnoea, polyuria.
What’s the ethology of AVRT?
an anatomically distinct atrioventricular connection, an accessory conduction pathway which allows the atrial impulse to bypass the AVN & excite the ventricles prematurely (ventricular pre-excitation), allowing a re-entry circuit to form & paroxysmal AVRT to occur.
What’s the accessory pathway in WpW called?
bundle of Kent
Does AVRT result in a narrow or broad complex tachycardia?
depends whether the accessory pathway or AVN is used for antegrade conduction
What are the ecg features of WpW?
in sinus rhythm, the atrial impulse is conducted via accessory pathway without AVN delay so the PR is short. the impulse enters non-specialised myocardium so ventricular depolarisation progresses slowly at first, distorting the early part of the R wave & producing the delta wave. This slow depolarisation is taken over by that propagated by the normal conducting system & the rest of the QRS complex appears relatively normal.
If the accessory pathway is concealed, ie. only capable of conducting retrograde, pre-excitation doesn’t occur & the ecg is normal.
There are 2 types of WPW:
Type A has a dominant R wave in V1 lead, which may be confused with R) BBB, RVH & posterior MI
Type B has a delta wave & QRS complex predominantly -ve in leads V1 & V2 but +ve in the other precordial leads (indicates R)-sided accessory pathway), may be confused with L) BBB or anterior MI.
What happens with orthodromic & antidromic (uncommon, only in about 10% of pts with WPW) AVRT in WpW?
for orthodromic, an impulse which has travelled via the AVN then travels retrograde via the accessory pathway & triggers a reentrant tachycardia, narrow complex, 140-250bpm, since the atrial depolarisation lags behind ventricular, the P waves follow the QRS. The delta waves can’t be seen & the QRS duration is normal.
For antidromic, the accessory pathway allows antegrade conduction- the QRS is broad & bizarre (conducted through non-specialised myocardium), the impulse then travels retrograde via the AVN back to the atria.
What happens with AF + WpW?
atrial impulses can be conducted via the accessory pathway, causes ventricular pre-excitation & producing completely irregular, broad qrs complexes with delta waves. occasionally impulses are conducted via the AVN & produce a normal QRS.
in some cases the accessory pathway allows conduction of very rapid ventricular rates (>300bpm) with risk deterioration into VF.
How does WpW present?
may be an incidental finding on ecg
often presents with tachyarrhythmias (tend to be more common in young people)
if there are rapid arrhythmias & AF, the pt may present w heart failure or hypotension.
What drugs can be dangerous in WpW? why?
drugs blocking AVN conduction (eg. digoxin, verapamil, adenosine) should be avoided as they reduce the refractoriness & increase conductivity through accessory pathway, may precipitate VF,
In which situation may a broad complex tachycardia be supra-ventricular in origin?
if associated with ventricular pre-excitation or a BBB
What’s an important determinant of the treatment of a broad complex tachycardia?
The origin
What’s a ventricular tachycardia?
3 or more ventricular extrasystoles in succession with a rate >120bpm
the tachycardia is “sustained” if it lasts >30 seconds
What’s an accelerated idioventricular rhythm?
ventricular rhythm with rate 100-120bpm
What are the types of broad complex tachycardia?
VENTRICULAR:
regular include monomorphic VT, fascicular tachycardia & RVOT tachycardia
irregular include torsades de pointes tachycardia & polymorphic VT
SUPRAVENTRICULAR:
BBB with aberrant conduction
atrial tachycardia with pre-excitation
What are some causes for VT?
re-entry or increased myocardial automaticity
the re-entry may be through a zone of ischaemia or fibrosis surrounding damaged myocardium
direct damage to the myocardium from ischemia, cardiomyopathy (congenital or acquired heart disease) the effects of myocarditis or drugs (eg. class 1 antiarrhythmics such as flecainide or quinidine)
monomorphic VT usually occurs after MI & is a sign of extensive myocardial damage; there’s a high in-hospital mortality
What’s are general rules re: the aetiology of a ventricular tachycardia?
the broader the QRS, the more likely the rhythm is to be ventricular in origin, esp if the complexes are >0.16s.
Broader complexes may be seen with electrolyte abnormalities, severe myocardial disease, antiarrhythmics (eg. flecainide).
If the tachycardia originates in the proximal part of the His-Purkinje system, the duration may be relatively short, eg, in a fascicular tachycardia the QRS is 0.11-0.14s
The complexes of tachycardias originating in the LV often have a R) BBB pattern while those originating in the RV often have a L) BBB pattern; those originating in the septum have L) BBB morphology.
What’s the usual rate & rhythm of a ventricular tachycardia?
usually regular & 120-300bpm
If an irregular monomorphic broad-complex tachycardia, it’s generally AF with with either aberrant conduction or pre-excitation.
What may a change in axis of more than 40 degrees to the L) or R) indicate?
ventricular tachycardia, eg. lead aVR usually has a -ve QRS, a +ve QRS in lead 3 indicates an extremely abnormal axis,
What happens with the atrial activity during a ventricular tachycardia? What are some other features suggestive of ventricular tachycardia vs SVT?
the sinus node continues to initiate activity completely independently of the ventricle. The P waves are generally +ve in lead I & II, however if there’s retrograde conduction of ventricular impulses to the atria, there may be inverted P waves after the QRS, usually with a constant RP interval.
Evidence of atrioventricular dissociation is diagnostic for VT however a lack of direct evidence of independent P wave activity doesn’t exclude VT.
Similarly, capture beats (occur relatively early, result in a narrow QRS) confirm a Dx of VT however these are uncommon & their absence doesn’t exclude the diagnosis.
Also, fusion beats (where an impulse conducted via the usual pathway fuses with one originating in the ventricles) support a Dx of VT but their absence doesn’t exclude the Dx.
Duration of QRS >0.14s generally ventricular origin, as is concordance through the chest leads.
A previous ECG may be useful- evidence of a prev MI increases the likelihood of a VT, if the mean frontal plane axis changes during the tachycardia (esp >40 deg to the L) or R)), this points to a ventricular origin.
If there’s an old ecg showing a BBB pattern during sinus rhythm that’s similar during the tachycardia, it may be a supra ventricular tachycardia with a BBB, however if the qrs morphology changes during the tachycardia it’s likely of ventricular origin.
What does positive concordance (where all the QRS complexes in the chest leads are predominantly +ve) suggest?
that the tachycardia has an origin in the posterior ventricular wall (concordance suggests that the tachycardia has ventricular origin, the direction of the wave of depolarisation will either be +ve or -ve depending on where in the ventricle it begins). Negative concordance correlates with a tachycardia originating in the anterior ventricular wall.
How does a fascicular tachycardia manifest?
it’s uncommon, not usually associated with structural heart disease.
originates from usually the posterior (rarely anterior) fascicle of the L) bundle branch, is partly propagated by the His-Purkinje network, it has a QRS 0.11-0.14s so is often misdiagnosed as SVT.
The QRS complexes have a R) BBB pattern often with a small Q wave vs primary R wave in lead V1 & a deep S wave in V6.
When the tachycardia originates in the posterior fascicle there’ll be L) axis deviation, when it originates from the anterior fascicle there’s R) axis deviation.
What’s RV outflow tract tachycardia?
originates from the RVOT & spreads inferiorly.
the ECG shows R) axis deviation with a L) BBB pattern.
May be provoked by catecholamine release, sudden changes in HR or exercise.
May be a brief & self-terminating tachycardia or a sustained one.
It usually responds to B blockers or CCBs.
What’s torsades de pointes?
a type of polymorphic VT where the cardiac axis rotates over 5-20 beats, changing direction- the QRS amplitude varies. The QT interval is prolonged & prominent U waves may be seen.
It’s not usually sustained but will recur unless the underlying cause corrected, it may deteriorate to VF.
It’s associated with conditions that prolong the QT, eg. drug or electrolyte disturbances.
What are some causes of torsades de pointes?
Drugs:
anti arrhythmic: class Ia eg. quinidine, class III (eg. amiodarone, sotalol)
antibacterials: erythromycin, fluoroquinolones, trimethoprim
other drugs: TCAs, haloperidol, phenothiazines, lithium
electrolyte disturbances: hypoK, hypoMg
IHD, myxoedema, Brady due to sick sinus or complete heart block, SAH
How does polymorphic VT vary cf torsades?
QT isn’t prolonged.
If sustained, polymorphic VT can lead to haemodynamic collapse, may deteriorate into ventricular fibrillation.
it must be differentiated from AF with pre-excitation (both have appearance of irregular broad-complex tachycardia with variable QRS morphology).
How does polymorphic VT vary cf torsades?
QT isn’t prolonged.
If sustained, polymorphic VT can lead to haemodynamic collapse, may deteriorate into ventricular fibrillation.
it must be differentiated from AF with pre-excitation (both have appearance of irregular broad-complex tachycardia with variable QRS morphology).
What ecg features help differentiate btwn a ventricular tachycardia & a SVT with BBB? How about clinical features?
If a R) BBB pattern, likely ventricular if the QRS is >0.14s, axis deviation, QS or predominantly -ve complex in V6, concordance of the QRS through chest leads (all +ve), if there’s a single R or biphasic (QR or RS) R wave in V1
If a L) BBB pattern, ventricular origin suggested if QRS >0.16s, axis deviation, QS or predominantly -ve complex in V6, concordance through chest leads (all deflections -ve), an rS complex in lead V1
A tachycardia in a pt aged >35yo is more likely to be ventricular- a Hx with IHD or CCF is 90% predictive of VT.
Clinical evidence of A-V dissociation includes “cannon” waves in the jugular venous pulse or variable intensity of the first heart sound- this indicates a Dx of VT but the absence doesn’t exclude the Dx.
What’s the danger of misdiagnosing a ventricular tachycardia as supra-ventricular?
may lead to wrong Rx- eg. giving verapamil to a pt with VT may cause hypoT, accelerate tachycardia- safest to Rx as ventricular unless strong evidence otherwise.
What’s the likely Dx of a broad-complex irregular tachycardia?
most likely AF with aberrant conduction or pre-excitation.
What are the early ecg findings in MI?
10% of pts with a proved AMI (on the basis of Hx & enzymes) don’t have ST elevation of depression.
in the early stages the ecg may be normal however ST elevation in 2 or more anatomically contiguous leads (the most frequent ECG criterion for identifying AMI) may evolve over serial ECGs.
The earliest change (5-30 mins following infarction) is hyper acute T waves, most prominent in the anterior chest leads.
ST segment changes are usually evident within hours of symptom onset.
What do pathological Q waves indicate?
myocardial necrosis under the recording electrode. They may develop within 1-2 hours of the onset of acute MI but they often take 12 hours & occasionally up to 24hrs to appear.
What are the ecg indicators for thrombolytic treatment?
ST elevation >1mm in 2 contiguous limb leads or >2mm in 2 contiguous chest leads
posterior MI
L) BBB
How long may the ST segment elevations take to resolve if anterior MI, inferior MI or LV aneurysm?
> 2/52
up to 2/52
persist indefinitely
In what proportion of inferior & anterior infarctions are reciprocal ST depressions seen?
70% of inferior & 30% of anterior infarctions
Reciprocal change has sensitivity & positive predictive value of >90% for acute infarction but it’s absence doesn’t rule out the Dx
In what proportion of inferior & anterior infarctions are reciprocal ST depressions seen?
70% of inferior & 30% of anterior infarctions
Reciprocal change has sensitivity & positive predictive value of >90% for acute infarction but it’s absence doesn’t rule out the Dx
What are anteroseptal infarcts due to?
highly specific for disease of the LAD artery
