ECG Flashcards

Question

What's the QRS? normal duration?

Answer 1

represents the electrical forces generated by ventricular depolarisation. >=0.12s (3 small squares)= delay in ventricular depolarisation (eg. BBB).

Answer 2

L) side of the septum depolarises first then the impulse spreads to the R).

Answer 3

lateral leads (I, aVL, V5 & V6) they are usually <2 small squares deep (ie. <0.2mV),

Answer 4

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.

Answer 5

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

Answer 6

Lead V3-V4 typically has equiphasic QRS complexes, is located over the "transition zone", shifts to the L) with increased age

Answer 7

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

Answer 8

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

Answer 9

interval between end of ventricular depolarisation & beginning of repolarisation

Answer 10

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.

Answer 11

benign earl repolarisation, which is common in young males, athletes, black.

Answer 12

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".

Answer 13

Leads V3 & V4

Answer 14

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.

Answer 15

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.

Answer 16

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

Answer 17

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.

Answer 18

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

Answer 19

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

Answer 20

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.

Answer 21

age idiopathic fibrosis ischaemia (incl MI) high vagal tone myocarditis digoxin toxicity

Answer 22

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.

Answer 23

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).

Answer 24

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.

Answer 25

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.

Answer 26

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

Answer 27

myocardial ischemia/infarction degeneration of His-Purkinje system infection (eg. Lyme disease, diphtheria) immunological disorders (eg. SLE) surgery congenital heart disorders

Answer 28

BoH divides into R) & L) BBs, then the L) divides to anterior & posterior hemivas cycle

Answer 29

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

Answer 30

primarily due to coronary artery disease, hypertensive heart disease, dilated cardiomyopathy. Unusual for L) BBB to exist in absence of organic disease.

Answer 31

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.

Answer 32

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)

Answer 33

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

Answer 34

R) axis deviation >90 degrees in absence of other cause of RAD

Answer 35

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.

Answer 36

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

Answer 37

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

Answer 38

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.

Answer 39

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

Answer 40

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

Answer 41

physiological: anxiety, pain, exertion pathological: fever, hypoxia, hypovolaemia, anaemia endocrine: thyrotoxicosis pharmacological: adrenaline (from phaeochromocytoma), caffeine, ETOH, salbutamol

Answer 42

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)

Answer 43

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

Answer 44

higher degree AV block or rate slowing medications

Answer 45

inferior leads & V1 due to a re-entry circuit in the RA with secondary activation of the LA

Answer 46

uncommonly

Answer 47

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

Answer 48

cardiomyopathy COPD IHD rheumatic heart disease sick sinus syndrome digoxin toxicity

Answer 49

AVNRT ("SVT")

Answer 50

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)

Answer 51

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.

Answer 52

generally mild (eg. palpitations), symptoms are commonest if rapid rates & pre-existing heart disease. Severe symptoms= dizziness, dyspnoea, polyuria.

Answer 53

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.

Answer 54

bundle of Kent

Answer 55

depends whether the accessory pathway or AVN is used for antegrade conduction

Answer 56

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.

Answer 57

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.

Answer 58

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.

Answer 59

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.

Answer 60

drugs blocking AVN conduction (eg. digoxin, verapamil, adenosine) should be avoided as they reduce the refractoriness & increase conductivity through accessory pathway, may precipitate VF,

Answer 61

if associated with ventricular pre-excitation or a BBB

Answer 62

The origin

Answer 63

3 or more ventricular extrasystoles in succession with a rate >120bpm the tachycardia is "sustained" if it lasts >30 seconds

Answer 64

ventricular rhythm with rate 100-120bpm

Answer 65

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

Answer 66

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

Answer 67

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.

Answer 68

usually regular & 120-300bpm If an irregular monomorphic broad-complex tachycardia, it's generally AF with with either aberrant conduction or pre-excitation.

Answer 69

ventricular tachycardia, eg. lead aVR usually has a -ve QRS, a +ve QRS in lead 3 indicates an extremely abnormal axis,

Answer 70

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.

Answer 71

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.

Answer 72

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.

Answer 73

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.

Answer 74

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.

Answer 75

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

Answer 76

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).

Answer 77

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).

Answer 78

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.

Answer 79

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.

Answer 80

most likely AF with aberrant conduction or pre-excitation.

Answer 81

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.

Answer 82

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.

Answer 83

ST elevation >1mm in 2 contiguous limb leads or >2mm in 2 contiguous chest leads posterior MI L) BBB

Answer 84

>2/52 up to 2/52 persist indefinitely

Answer 85

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

Answer 86

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

Answer 87

highly specific for disease of the LAD artery

Answer 88

disease of the R) coronary or distal circumflex

Answer 89

disease of the proximal circumflex

Answer 90

40% may also complicate some anterior infarcts

Answer 91

inferior infarct ass'd with STE in V1.

Answer 92

asap, lead V4R (on the right sided chest leads, it's an electrode over the R) 5th ICS MCL) should be recorded, since R)-sided chest leads are more sensitive for RV infarction & the STEs in RV infarction may be short-lived.

Answer 93

it's associated with hypotension which may be compounded by nitrates or diuretics. The pt may respond to a fluid challenge. *they're preload-sensitive. 40% of inf stemi's complicated by RV infarction ST elevations in V1-2, STE III>IISTE in V4R (along with the STE in II,III, aVF & reciprocal changes lat leads I, aVL, V6)

Answer 94

RCA proximal to the RV marginal branches, hence it's association with inferior infarct. Less commonly, it may be ass'd with occlusion of the R) circumflex if this vessel is dominant, in which case the inferolateral wall may also be infarcted.

Answer 95

reciprocal changes in anterior precordial leads (V1-3), important as expeditious thrombolysis may improve outcome. since ischemia of the anterior wall produces similar changes, diagnose posterior infarct with posterior leads V7-9 (would show STE if posterior infarction).

Answer 96

LAD branch of the L) coronary & from the R) coronary

Answer 97

coronary artery disease, HTN, DCM

Answer 98

poor, high mortality however thrombolytic treatment reduces mortality greatly, particularly if treated early. AMI in the presence of a pre-existing or new L) BBB both carry worse prognosis than in a MI with normal ventricular conduction.

Answer 99

ST elevation where there's a +ve QRS or ST depression in leads V1-V3 (which have predominantly -ve QRS's).. this is "inappropriate concordance" Marked (>=5mm) STE in leads V1 & V2 also suggests acute ischaemia

Answer 100

may mask posterior MI

Answer 101

mutation on cardiac sodium channel gene, familial clustering & autosomal dominant inheritance has been demonstrated particularly occurs in young men, characterised by partial R) BBB & ST elevation in R) precordial leads (a RSR' pattern, "coved" STE >2mm in >1 of V1-3 w inversion terminal portion T wave ) MUST be accompanied by clinical criteria for Dx: -documented VF or polymorphic VT -FHx SCD <45yo -coved-type ECGs in family -syncope -nocturnal agonal respiration type 2 brugada has saddleback ST elevation brugada 3 has either saddleback or coved STE but the STE is <2mm high incidence of sudden death due to ventricular tachyarrhythmias Structurally normal hearts high incidence in SE asia Definitive Rx= ICD, quinidine has been proposed if ICD unavailable or inappropriate (eg. neonates) The ecg changes can be unmasked or augmented by: Drugs: -Na channel blockers (eg. flecainide, procainamide) -lithium, amitriptyline -bupivacaine, procaine -ergometrine -Ca channel blockers -alpha agonists 0B blockers -nitrates -cholinergic stimulation -cocaine, ETOH Fever Ischaemia hypo/hyperkalaemia hypothermia post DCCV preferred to avoid amiodarone, lignocaine, propranolol, verapamil, phenytoin, metoclopramide propofol has been used uneventfully- appropriate measures should be taken to minimise pro-arrhythmogenic potential

Answer 102

acute MI high take off (upsloping of the ST segments of R)-sided chest leads esp leads V2 & V3) benign early repolarisation (often present in young healthy adults- most commonly seen in precordial leads esp V4, there's elevation of J point, distinct notch @ the J point, high take-off of the ST segment, upward concavity of the ST segment, symmetrical upright T waves often of high amplitude) antecedent MI (particularly old anterior MI)- comparison with old ECGs useful, care when interpreting an ecg within 2/52 of an MI, persistent STEs should consider a ventricular aneurysm. L) BBB LVH (ST elevation in precordial leads is a feature of LVH, due to secondary repolarisation abnormalities) ventricular aneurysm coronary vasospasm/printzmetal's angina- in these cases the changes may be reversible if treated promptly. changes ass'd with cocaine use may be a combo of vasospasm & thrombosis. pericarditis brugada syndrome intracranial, particularly subarachnoid, haemorrhage (may be that altered autonomic tone affects the duration of ventricular repolarisation) may be ass'd w ST changes (elevation or depression)

Answer 103

in acute pericarditis the ST elevations are diffuse (present in all leads except V1 & aVR), often associated with upward concavity of the ST segment (vs the upward convexity seen with AMI) & may be associated with PR segment depression, absence of reciprocal changes or Q waves.

Answer 104

Normal tall biphasic inverted flat

Answer 105

Posterior LV wall ischaemia (mirror image of T wave inversion)

Answer 106

III, aVR, V1 (in ass'n with a predominantly -ve QRS)- can also occur in V2 but only in association with TWI in V1

Answer 107

about 1/8th the size of the R wave, <2/3 the size of the R wave, height <10mm arrowhead T wave suggestive of myocardial ischaemia

Answer 108

partial thickness ischaemia such as with unstable or crescendo angina

Answer 109

LVH, digoxin

Answer 110

The R waves are smaller. the degree of ST depression is related to the size of the R wave so ST depression is most obvious in V4-6 (where the R waves taller)

Answer 111

ventricular fibrillation

Answer 112

early access to electrical defibrillation- cardiac arrest from VF outside a hospital only has 10% long-term survival cf initial survival of 90% if the arrest occurs in coronary care unit.

Answer 113

in most people it's a branch of the R) coronary, less commonly it originates from the L) circumflex, so pts with proximal occlusion of the R) coronary, causing an inferior infarction, may have compromised AV node supply resulting in varying degrees of heart block.

Answer 114

normal QRS morphology & rate 40-60bpm vs wide QRS & 15-40bpm.

Answer 115

The most widely adopted protocol for exercise stress testing, it has 7 stages each lasting 3 mins, the first stage (10% incline, 2.7kph) is considered to be 4.8 METs. Incline & speed increases with each stage. A modified Bruce protocol is used within 1/52 of MI.

Answer 116

Discontinue B blocker the day before the test, discontinue Digoxin (may cause false +ve, ST abnormalities) 1/52 before the test.

Answer 117

horizontal or down-sloping ST depression, however the specificity of ST depression as the main indicator of myocardial ischaemia is limited- ST depression occurs in up to 20% of normal individuals on ambulatory ecg monitoring.

Answer 118

3.5mLO2/kg/minute (the O2 consumption of an average individual @ rest

Answer 119

To achieve HR max which is 220-age in males (210-age in females). 85% of HR max is usually considered satisfactory (with 9-12 mins of exercise), attainment of HR max is considered a good prognostic sign.

Answer 120

adenosine or dobutamine scintigraphy or angiography

Answer 121

P wave height increases R wave height decreases J point depressed with ST segment sloping sharply upwards Q-T shortens T wave height decreases

Answer 122

60-80ms after the J point

Answer 123

When the diagnostic criteria are reached or when signs & symptoms dictate; recording continues for up to 15 mins after cessation since ST changes or arrhythmias occurring during recovery have equal significance to those occurring with exercise.

Answer 124

substantial ST depression (horizontal or downscoping)@ low work rate + angina-like pain & BP drop. Deeper & more widespread ST depression generally indicates more severe or extensive disease.

Answer 125

as per Baye's theorem of diagnostic probability, the predictive value of an abnormal test varies according to the probability of coronary artery disease in the population under study

Answer 126

early part of P wave Tall p waves in anterior & inferior leads (but duration of P wave not usually prolonged). A tall P wave (>=2.5mm) in leads II, III & aVF= P pulmonale (eg, seen transient with acute PE)

Answer 127

COPD pulmonary hypertension Congenital heart disease (eg. pulmonary stenosis & ToF) In practice most pts with R) atrial enlargement have RV hypertrophy RA enlargement without R hypertrophy can be seen in tricuspid stenosis

Answer 128

provided QRS duration is <0.12s: R) axis deviation >=110degrees Dominant R wave in V1 R wave in lead V1 >=7mm Supporting criteria: ST depression & TWI in leads V1-V4 Deep S waves in leads V5, V6, I & aVL, dominant S waves leads I-III (far RAD) p pulmonale (RA enlargement)

Answer 129

mitral stenosis, pulm HTN, less commonly congenital heart disease (eg. with pulmonary stenosis)

Answer 130

No, in mild cases the trace will be normal

Answer 131

RVH (the associated presence of R) axis deviation distinguishes this from the other causes of tall R wave in V1) posterior MI Type A WpW R) BBB *tall R wave in V1 is normal in children & young adults

Answer 132

RVH L) posterior hemiblock lateral MI acute R) heart strain * R) axis deviation is normal in infants & children

Answer 133

P pulmonale (can occur with or without clinical evidence of cor pulmonale) RV hypertrophy (indicating presence of cor pulmonale) there may be poor R wave progression & Deep S wave in the R) precordial leads (since the heart rotates clockwise along it's horizontal axis which shifts the transitional zone (progression of rS to qR) to the left), appearance simulates an anterior MI. QRS amplitude may be small as hyper-inflated lungs are poor electrical conductors. arrhythmias

Answer 134

depend on the size of the PE, pts underlying cardiopulmonary reserve & ecg timing small may have normal ecg or sinus tachycardia Massive PE associated with pulmonary artery obstruction & acute RV dilatation may have a deep S wave in lead I, a Q wave in lead III & TWI in lead III (this S1Q3T3 pattern only seen in 12% of pts with PE) RV dilation may lead to R)-sided conduction delays (incomplete or complete R) BBB), R)-axis deviation RA dilation may lead to prominent P waves in the inferior leads (II, III, aVF), atrial flutter or fibrillation TWI in the R) precordial leads may also occur

Answer 135

features of RV hypertrophy (R) axis deviation +110 deg or more, Tall R wave in V1, dominant S wave V5 or V6, QRS <120ms (ie. the changes aren't due to R) BBB, factors such as P pulmonale, RV strain w presence of an incomplete/complete RBBB suggest coexisting RVH)) ST depression & TWI particularly in leads V1 & V2 (also V3-4, II, III, aVF) May be seen in acute massive PE, pneumothorax or pleural effusion with acute RV dilation. May also be seen in RV hypertrophy with no apparent "strain" on the ventricle.

Answer 136

rheumatic heart disease appears as p pulmonale, generally occurs in association with mitral valve disease so the ecg often shows biatrial enlargement (large biphasic P wave in V1- initial +ve then -ve deflection)

Answer 137

no- the features are non-specific & related to the underlying disease. May see incomplete R) BBB & AF.

Answer 138

spectrum depending on severity- from normal to signs of RV/RA hypertrophy; R) axis, tall R) wave in V1, p pulmonale

Answer 139

middle & late portions of the P wave

Answer 140

while the P wave in V1 is often biphasic, a large negative deflection (>1 small square) of the 2nd part of the P wave may be seen, along with prolongation (>0.12s) of the P wave if depolarisation is delayed.

Answer 141

A minor notch probably is due to slight asynchrony btwn RA & LA depolarisation but if there's a >0.04s peak-to-peak interval this suggests LA enlargement

Answer 142

systemic HTN hypertrophic cardiomyopathy aortic stenosis mitral incompetence

Answer 143

lead II mitral valve disease, esp mitral stenosis

Answer 144

systemic HTN aortic stenosis coarctation of aorta

Answer 145

if using voltage criteria, inaccurate since young ppl often have large-amplitude QRS in absence of LV disease.

Answer 146

repolarisation changes of ST depression & T wave inversion in L) precordial leads along with reciprocal ST elevation in R) precordial leads poor R wave progression LA hypertrophy or prolonged atrial depolarisation & L) axis deviation

Answer 147

50% 20% have subtle changes, 30% have obvious features linear correlation btwn ecg changes & severity & duration of the HTN high amplitude QRS complexes seen first, then non-voltage criteria develop

Answer 148

tallest R in V5,6 + S wave depth in V1 is >35mm the voltage criteria must be accompanied by non-voltage criteria to be diagnostic of LVH: ST depression & TWI in L) precordial leads Delayed ventricular activation time (R wave peak time) >=0.05s in leads V5 or V6 (may also see.. not on the list but: LA hypertrophy & prolonged depolarisation, L) axis deviation, poor R wave progression) Other voltage criteria: Tallest R wave in V4-V6 is >26mm deepest S + tallest R in precordial leads sum >45mm for limb leads: R wave in lead 1 + S wave in lead 3 is >25mm R wave in aVL is >11mm R wave in lead aVF is >20mm S wave in lead aVR is >14mm

Answer 149

highly specific diagnostic tools, however their specificity is impacted by age & sex. Their poor sensitivity limits their use.

Answer 150

LVH may also see LA enlargement, L) axis deviation & L) BBB

Answer 151

hypertrophic (obstructed), dilated (congestive) & restrictive cardiomyopathy

Answer 152

IV septum & apex of the LV ecg evidence of LVH is found in 50% of pts. Abnormal Q waves in the anterolateral or inferior chest leads may occur, mimicking presence of MI (NARROW DAGGER Q WAVES) As the LV becomes increasingly less compliant, there's increasing resistance to atrial contraction & signs of LA abnormality (LA enlargement) are commonly seen. AF & SVTs are common, VT may occur (cause of sudden death in these pts). Bizarre QRS complexes masquerading, eg. as pre-excitation or BBB may be seen.

Answer 153

LVH with LV strain pattern

Answer 154

L) atrial abnormality, AF & RVH

Answer 155

atrial fibrillation, L) atrial enlargement if the pt is in sinus, evidence of LVH may be seen

Answer 156

electrical holes (Q waves) arrhythmias conduction defects (bundle branch block & axis deviation)

Answer 157

While most have anatomical LVH, ecg findings of LVH are only seen in 1/3 of pts- signs of LVH may bee masked by a diffuse myocardial fibrosis reducing the voltage of the QRS complexes, and if there's also RVH, the rightward depolarisation forces may cancel out some of the leftward forces again masking signs of LVH. signs of LA enlargement are common & there's often biatrial enlargement. There may be abnormal q waves (esp in V1-4) although less common than in HCM. There may be L) BBB, LVH, arrhythmias (ventricular premature beats, VT, AF)

Answer 158

restrictive cardiomyopathy, associated with infiltrative disease eg. amyloidosis, sarcoidosis, haemochromatosis

Answer 159

low voltage QRS is most common, likely to do with the infiltration conduction disturbance arrhythmias; supraventricular & ventricular

Answer 160

5.5-6.5= tall peaked T waves (suspect hyper K if a T wave is >= the height of an R wave) 6.5-7.5= PR interval widens, p wave flattens & disappears 7-8= QRS widens 8-10= sine wave, ventricular arrhythmias/asystole (hyperK-induced asystole more likely in chronic hyperK) severe hyperkalemia: blocked, bradycardic & bizarre

Answer 161

ecg features are more reliably appear with severe hypoK (eg. below 2.7mmol/L) or if associated with hypoMg++ Broad, flat T waves ST segment depression QT prolongation (most presumed QT prolongation is actually the QU interval- pts with true QT prolongation & hypokalaemia generally also have hypoMg++ & are predisposed to ventricular arrhythmias eg. torsades de pointes). U wave (a prominent U wave associated with small T wave is considered classic ecg finding of hypokalaemia; prominent U waves & long "QU" interval, may descend to torsades (eg.if ectopic superimposed during the T/U wave repolarisation) ventricular arrhythmias (particularly if coexisting hypomagnesemia) supraventricular arrhythmias

Answer 162

Core temp < 35 degrees artefact due to shivering but the ability to shiver diminishes as body temp falls (uncommon below 32deg c core temp) as body temp falls, metabolic & cardiovascular processes slow- pacemaker (HR) & conduction velocity decline--> bradycardia, heart block, PR/QRS/QT prolongation occur below 32degC, regular organised atrial activation disappears & varying slow, disorganised, irregular activity occurs core temp below 28deg C, junctional bradycardia may be seen J (Osborn) waves (dome or numb elevation in the terminal portion of the QRS, best seen in L) chest leads) are the most specific ecg finding of hypothermia- their size often correlates with the severity of hypothermia <30 degrees, they're considered pathognomic of hypothermia but may be seen in hypercalcaemia, CNS disorders (eg. massive head injury, SAH) bradycardia, osborn J waves (notching @ J point, easiest seen in lateral leads), long Qt, shivering artefact

Answer 163

ventricular arrhythmias more common in rewarming as body temp rises through 28-32degC

Answer 164

sinus tachycardia, incr amplitude of all deflections (esp in younger pts) & AF (*atrial tachyarrhythmias particularly common a the atria sensitive to T2) In thyroid storm, paroxysmal SVT with rates >200bpm may be seen elderly pts may get ischaemic ST & T changes due to the tachycardias PVCs common

Answer 165

can be difficult as it may be refractory to cardioversion but most revert spontaneously to sinus when euthyroid

Answer 166

related to a general slowing of electrical conduction through the heart (along with slowing of metabolic rate & almost all bodily functions) most have a low-normal heart rate (50-70bpm), may have sinus bradycardia increased PR interval prolonged QT (may develop torsades VT in hypothyroidism, related to prolonged QT, electrolyte abnormalities due to hypothyroidism, hypothermia or hypoventilation) inverted or flat T waves (ST changes are rarely seen) low voltage QRS severe hypothyroidism esp if pre-existing heart disease may develop heart block or BBB (esp. R) BBB) ventricular extrasystoles conduction abnormalities ass'd with hypothyroidism resolve with thyroid hormone therapy uncommonly, pts with hypothyroidism may develop large pericardial effusions, giving rise to electrical alternates (beat- to- beat variation in QRS voltages)

Answer 167

myxoedema coma (other ecg abnormalities of severe hypothyroidism: bradycardia, low QRS voltage, widespread TWI, may get QT prol, 1st deg AV block, interventricular conduction delay)

Answer 168

hypercalcaemia associated with QT shortening but if severe, T wave will be prolonged, normalising the QT interval There's QT prolongation in hypocalcaemia, mainly due to ST prolongation. Hypocalcaemia may also have osborne waves. digoxin harmful in hypercalcaemia (may cause tachy or bradyarrhythmias) & it is also dangerous to give IV calcium to a pt on digoxin.

Answer 169

T wave flattening & QT prolongation

Answer 170

ST depression or elevation, T wave inversion, QT prolongation

Answer 171

ST depression or elevation, T wave inversion, QT prolongation

Answer 172

V3R or V4R to detect RV or atrial hypertrophy occasionally large QRS complexes may require the gain to be halved

Answer 173

1 month by 6/12 the ratio of RV to LV is similar to an adult

Answer 174

rate >100bpm (resting HR is approx 140bpm at birth & 120bpm at age 1 year, 100 @ 5 years & adult values by 10 years). QRS axis >90 degrees (R) axis deviation- at birth the QRS is +60=+160deg, by 1 year the axis changes to lie between +10 & +100deg) Large precordial R waves, T wave inversion in lead V1 occurs by 7 days & typically remains inverted until at least age 7. Upright precordial T waves are normal in the neonate (RV larger) but persistence of upright T waves in the R) precordial leads (V1-3) btwn 7 days & 7 yrs may indicate RVH. Short PR & QT intervals (the PR interval decreases up until 1 year then gradually increases- the P wave & QRS durations also increase with age) QT interval depends on HR & age; shortens with incr HR & increases with age. Q waves are usually seen in inferior & lateral leads.

Answer 175

rate >100bpm (resting HR is approx 140bpm at birth & 120bpm at age 1 year, 100 @ 5 years & adult values by 10 years). QRS axis >90 degrees (R) axis deviation- at birth the QRS is +60=+160deg, by 1 year the axis changes to lie between +10 & +100deg) Large precordial R waves, T wave inversion in lead V1 occurs by 7 days & typically remains inverted until at least age 7. Upright precordial T waves are normal in the neonate (RV larger) but persistence of upright T waves in the R) precordial leads (V1-3) btwn 7 days & 7 yrs may indicate RVH. Short PR & QT intervals (the PR interval decreases up until 1 year then gradually increases- the P wave & QRS durations also increase with age) QT interval depends on HR & age; shortens with incr HR & increases with age. Q waves are usually seen in inferior & lateral leads.

Answer 176

Lead II, V1 or V4R

Answer 177

multifocal atrial ectopic (or premature beats) rhythm- if tachycardia, multifocal atrial tachycardia (eg. in any pts with large atria such as COPD- these pts have higher risk of going into AF but the condition improves w Rx of COPD ), may also have evidence RVH (eg. dom R wave in V1, S in V6, RAD

Answer 178

details, calibration ps (look across (beat by beat/rhythm & up/down (comparing simultaneous leads))- sinus or not? block or not? rate rhythm axis qrs width bundle branch blocks? look at leads VI (most rightward), V6 (most leftward), I also useful (goes R) to L)).. where is the late part of the conduction delayed? if it's delayed to the L), it's L) BBB, if it's to the R), it's R) BBB.. if the late part of the QRS is positive in lead V6, it's L) BBB QRS&T all together in territories (lat, inf, anterior) any signs of hypertrophy

Answer 179

ventricular bigeminy

Answer 180

electrical interference shivering parkinsonian tremor

Answer 181

440ms males, 460ms females

Answer 182

wenchebach is AV node disease, often due to high vagal tone, asymptommatic/benign (responds to atropine). doesn't typically require pacemaker for proph vs CHB provided asymptomatic w normal BP, reversible causes (eg. drug toxicity B-block, digoxin, hyperkalaemia, myocardial ischaemia) have been excluded. very low progression to haem unstable AV block. mobitz II related to disease of distal conducting (HP) system, more likely a progressive disease- will need a pacemaker. Can't tell btwn wenckebach & 2:1 mobitz II block HOWEVER mobitz II typically a broader QRS. If the pt also has a bundle branch block, more likely mobitz II vs I. Could give atropine (unblock the AV node) to see if responds. Most useful to see a longer trace of the pts ecg- may reveal if it's wenckebach or mobitz II.

Answer 183

leads II, III, aVF (the impulse goes "up & down" in the RA)

Answer 184

no or hard to see or unusual P waves with the other SVTs (AVNRT is the most common type of SVT- where there are essentially dual AV nodal pathways, conducted to A & V simultaneously & can't see the P wave as it's buried in the QRS, they arrive simultaneously, congenital, on the ecg can't tell the difference between AVNRT & AVRT)

Answer 185

Block the AV node: valsalva, carotid sinus massage, adenosine

Answer 186

very bizarre- since there's conduction down both the AV node & accessory pathway, there'll be both wide & narrow QRS's, in these people you MUST NOT block the AV node otherwise there'll be unopposed conduction down the accessory pathway & risk VF Need to revert these pts to sinus (or somehow block the accessory pathway- amoidarone (both pathways), flecainide (accessory pathway)- ideally best to revert to sinus with a shock

Answer 187

Some.. a wide QRS tachycardia is almost always VT- if treat it as VT it'll also Rx SVT (eg. SVT with BBB or accessory pathway)- best to use DC shock early (GA required- often RSI with cricoid!)

Answer 188

Lateral MI, R) heart failure

Answer 189

evidence inferior wall MI (STE II, III, aVF) ST depression in V1 & V2 (place posterior leads to identify post STEMI)

Answer 190

evidence inferior wall MI (STE II, III, aVF) ST depression in V1 & V2 (place posterior leads to identify post STEMI)

Answer 191

Deep T-wave inversions in multiple precordial leads (eg. V1-4), may or may not have troponin elevations or ST elevations- due to high-grade LAD stenosis, unfavourable natural Hx; high risk reocclusion, need early angio/PCI/CABG 2 patterns of t-wave abnormality seen in Wellens: 1. type A (biphasic, initially +ve & terminally 0-ve)- in 25% 2. type B more common; deeply & symmetrically inverted (75% of cases)

Answer 192

characteristic of LAD occlusion, may be associated w other coronary lesions upsloping ST depression (which joins the asc limb of the T wave) in 2 or more of leads V2-6, along with relatively tall, symmetric "rocket-shaped" T waves & possible loss of precordial R-wave progression. ST depression & T wave height often maximal in V3. may have subtle aVR elevation anterior STEMI (LAD occlusion); urgent PCI & thrombolysis

Answer 193

mid-chest leads (V3-4), common in healthy pts esp males

Answer 194

dramatic downscoping ST depression in precordial, ST elevation in aVR which is > STE in lead V2

Answer 195

suggested by: in V1-3: -horizontal ST depression -tall, broad R waves (>30ms) -upright T waves -dominant R wave (R/S ratio >1) in V2 confirmed by STE & Q waves in V7-9 (simply move V4-6 electrodes to the back *look specifically @ V2 for combo of horizontal ST depression, Tall R wave (equivalent of posterior Q wave), upright T wave Should look for evidence posterior involvement in any pt w inferior or lateral STEMI

Answer 196

for example, in an irregularly irregular broad complex tachy, this may either be AF w aberrency or presence of an accessory pathway. the latter is suggested by extremely rapid ventricular rates (eg. up to 300 in some places, too fast to be conducted via the AV node) beat-to-beat variation in QRS morphology also suggests accessory pathway

Answer 197

Class 1 antiarrhythmic, targets the accessory pathway, PROLONGS action potential duration in atrial & ventricular myocardium. Does NOT block the AV node (therefore safe for ANTIDROMIC WpW, where blocking the AVN could allowexcessive vent rates, VT/fib. Effective in both reversion & slowing vent rate. For ORTHODROMIC WpW re-entry circuit, can take similar approach to AVNRT (vagal, then adenosine) however for antidromic, interrupting the AV node may interrupt the rapidly conducting re-entry circuit, Rx of choice is procainamide which slows conduction through AP, slowent vent rate & often causing reversion.

Answer 198

atrial or ventricular premature beat (or a shock) superimposed on the preceding T wave—> polymorphic VT, which risks degenerating into VF

Answer 199

think hyperK

Answer 200

camel hump t waves (P hidden).

Answer 201

camel hump t waves (P hidden).

Answer 202

Na channel blocker (eg. TCA) overdose QRS >100ms predicts seizures, QRS >160ms predicts cardiotoxicity (eg. broad-complex dysrhythmias, hypotension) also ass'd w long PR, long QT, brugada-like pattern in V1 (all signs sodium channel blockade) Signs of anticholinergic toxidrome (ed. dilated pupils, drowsiness): sinus tachy (p waves may be buried) needs bicarb & hyperventilation aggressive resus w: alkalinisation of serum sodibic intubate & hyperventilate aim alkaline arterial pH seizure management (BZD) BP Mx (fluid bolus pressors)

Answer 203

concurrent inf TWI (esp in leads facing RV, III), highly specific for differentiating pulm embolism from Wellen's, esp if ass'd w new RAD, new R) BBB & dominant R wave in Va, non-specific ST changes

Answer 204

concerning for L) MCA insufficiency, can also occur w severe TVD, after resus from cardiac arrest, sevre anaemia or hypoxaemia

Answer 205

suggest massive pericardial effusion

Answer 206

raised ICP hypokalemia (t waves typically down the up), Wellens (typically up then down if type A, type B deep symmetrical inversion) can cause widespread TWI but GIGANTIC "cerebral T waves" suggests raised ICP

Answer 207

Taller L) rabbit ear far northwest axis (ie. +ve QRS in aVR, -ve QRS in I & aVF) -ve QRS in V6 Age >35 structural heart disease FHx sudden cardiac death or arrhythmogenic conditons If it was VT with L) BBB pattern, VT is suggested by a broad (>30ms) initial R wave, notched/slurred S wave in V1 & the sR wave in V6 (as opposed to typical L) BBB where there's minimal initial R wave & in V6 the dominant R wave is often slurred also if it's VT, see av dissociation evidence (p waves occ distoriting the qrs, fusion & capture beats, it's more likely monomorphic w wide (>160ms) qrs

Answer 208

flutter w 2:1 block (elderly, IHD) *AVNRT ("SVT") *WpW w orthodromic conduction sinus tachycardia (usually should see P waves, they might be hidden in T waves if concurrent 1st degree AV block, there should be some HR variability *pseudo R' waves= retrograde P waves superimposed on terminal QRS, causes J-point peaking. differentiate btwn the 2 Dx w vagal maneouvers +/- adenosine- after a salvo of broad bizarre looking complexes (commen w chemical cardioversion w adenosine), if revert back to sinus w no delta waves, suggests the dx was AVNRT

Answer 209

RA on manubrium LA over 5th ICS R) sternal border LL on R) lower costal margin monitor lead 1 helps w detecting atrial activith wrt ventrical activith (eg. flutter waves), detecting P waves in wide coplex tachy (eg. AV dissociation)

Answer 210

R) axis; lung hyperinflation causes vertical orientation of the heart peaked P waves in inf leads (p pulmonate) rightward P axis (inverted in aVL) low voltage complexes in L)-sided leads (I, aVL, V5-6) lack of R waves in R) precordial leads (V1-3) “clockwise” rotation of heart, delayed R/S transition point (eg. V5)

Answer 211

sinus tachy (anticholinergic effect) prolonged QT interval (> half the RR interval) QT prog concern due to risk of TdP. QTc >500ms= a marker of incr risk TdP BUT tachycardia (which happens w anticholinergic effect) actually protective against TdP, so it’s rare w quetiapine tox.

Answer 212

correct QT-dependent electrolytes (K, Mg, Ca) to high-normal range, +ve chronotropy (eg. isoprenaline) to move pt below "at-risk of TdP" point of QTc 500

Answer 213

marked R) axis deviation (+180 degrees) aVR POSITIVE QRS complex (P & T waves upright) low voltage precordial leads lead 1: inversion of all complexes absent R wave progression in chest leads; dominant S throughout DDx= accidental reversal or LA & RA leads: -ve I RAD but normal precordial (eg. normal R wave progression); w LA-RA lead reversal, II & III switch places, aVL & aVR switch places, aVF unchanged; aVR often becomes positive & there may be marked RAD the difference= with dextrocardia absent R wave progression in precordials, this is present in RA LA reversal LA/LL reversal: lead III inverted, leads I & II switch places leads aVL & aVF switch places, aVR unchanged

Answer 214

fusion of ST-T waves may represent significant vessel occlusion, metabolic, toxicology

Answer 215

TC of >=450 (m) & >=460(f) considered prol

Answer 216

type 1 RSR’ pattern/partial RBBB “coved” STE in R) precordial leads (V1-3), >2mm, with inverse terminal portion T wave must be accompanied by clinical criteria type 2 saddleback STE, type 3 has morphology of T1 or T2 but STE <2mm

Answer 217

defib, resuscitate stop/remove/treat triggers (eg. fever, arrhythmogenic, electrolytes) Rx with isoprenaline 1-2microg bolus then infusion 0.15-2microg/kg/min or quinidine

Answer 218

less Na channels avail for conduction, limits their conduction reserve so, risk pro-arrhythmic risk of any drugs w Na blocking properties Propofol is listed as "avoid" however has been used uneventfully in Brugada, use caution to limit pro-arrhythmogenic potential -define the type of brugada; Type-1 has higher arrhythmic risk -if febrile, hypothermic, electrolyte abnormalities (esp hypokalaemia which may decr Na current), higher arrhythmogenic risk, manage. -if has an ICD, ensure checked, advice (if off, pads on) if documented SCN5A mutation, risk of drugs w Na blocking properties higher (these pts have use-dependent conduction phenotype, broad QRS complexes that further broaden (or PR broaden or ST increase) w higher rates, isoprenolol may worsen the conduction as it incr the HR). 2 loss-of function SCN5A mutations incr risk ++ -Communicate w pt, surgeon & team risks ass'd w anaesthesia, emphasise to surgeon that OT may need to be paused if an incr pro-arrhythmic conditions occur -prepare OT for recognition & Rx of vent arrhythmias (ext defibrillator ready & pads attached w pts anti-tachy therapy off the ICD but restarted @ end of procedure), continuous art line & ecg monitoring (esp of R) precordial ST segments V1,2,3), ALS cart, isoprenaline, consider quinidine if NGT. B-blockers if SCN5A mutation. continuous core temp monitoring & equip to manipulate temp. -intra-op, vigilant for any STE in R) precordial leads; if it occurs, try to work out why (stop OT, manage fever, administer isoprenaline) -Propofol may be used w caution. volatile & thiopentone no adverse events documented. -avoid SYSTEMIC lignocaine (ok if subcut w Adr), still caution & lowest possible dose) -postop ecg monitoring until all anaes eliminated (>=5 half lives)

Answer 219

Too fast? VT, TdP Too slow? conduction blocks, sinus brady/pauses Pump failure? myocardial ischaemia, PE syncope syndromes? WpW, long (>500ms) or short (<320ms) QT, Brugada RSR’ w STE V1-3, HOCM (LVH voltage criteria, precordial TWI, “dagger” Q waves), arrhythmogenic RV dysplasia (RV free wall fatty infiltration, predisposes to paroxysmal vent arrhythmias, SCD, biventricular failure; 2nd most common cause of young cardiac death (after HOCM). ecg findings include signs RVH (RAD, dominant R in V1, dominant S in V5 or 6, QRS <120ms (ie. not R) BBB), may also have RV strain: RA enlargement, ST/T changes V1-4 & inf, S1S2S3 pattern of dominant s waves leads I-III, deep S waves lateral leads), TWI in V1-3, epsilon wave (small +ve deflection buried @ end of QRS, pre-excitation of ventricle), prolonged S wave upstroke V1-3 w localised QRS widening, paroxysmal VT w L) BBB morphology, may have frequent PVCs) electrical probs: hyper/po kalmia, pacemaker failure

Answer 220

upright in lead II

Answer 221

high degree V block, frequent VEBs, atrial tachycardia dig tox causes dysrhythmias due to: -incr automaticity of A & V tissues (incr intracellular Ca++ via action on Na/K+ & Na/Ca exchangers; blocks NaKATPase which incr intracellular Na, promotes Na/Ca++ exch & Ca++ in) decr AV conduction (incr AVN vagal tone) -atrial automaticity: atrial tachy/ectopics/AF/flutter -ventricular automaticity: VEGs & bigeminy, polymorphic VT (eg. those alternating btwn L) & R) BB morphology) -AV blocks *contrast w digoxin effect which = "sagging' ST depression & TWI in pts on therapeutic digoxin ("reverse tick"). may also have mild PR prol, prominent U waves, J point depression in leads w tall R waves.

Answer 222

STE w subsequent Q waves in precordial leads (V1-5) +/- high lat leads, often preceded by hyperacute T waves. reciprocal ST depression inf leads (mainly III & aVF) from occlusion of LAD high mortality Wellen's & De Winter T waves are other high-risk presentations of ant ischaemia

Answer 223

septal infarct

Answer 224

w the former, the discordant ST depression & TWI has distinct inversion of whole T wave When there's superimposed STEMI, ST elevation causes appearance of inversion of only the terminal portion of the T wave. There's also Q wave formation.

Answer 225

ecg pattern w widespread STE, commonly seen in young healthy pts age <50yo, aka “high take-off” or “J-point elevation”, may mimic pericarditis or acute MI, the ST elevation is widely concave & mainly in mid-left precordial leads (V2-5), there may be notching or slurring at the J point, t waves concordant w QRS, ST:T wave ratio in V6 <0.25 suggests BER over pericarditis, no reciprocal ST depression (of occlusion MI) DDx: pericarditis; also has widespread concave ST elevation, also has PR depression, TP may downslope, there are no reciprocal STEMI changes, the ST/T wave ratio is >0.25 in V6 (distinguishing it from BER)

Answer 226

* the DDX for regular broad-complex tachy w no evidence atrial activity are VT, SVT w aberrency, due to BBB OR WpW absence of typical RBBB or LBBB morphology, capture beats (SA node transiently captures ventricles producing normal duration QRS), fusion beats (sinus & ventricular beat coincide, produce a hybrid complex), L)-sided rabbit ear taller if like R) bbb, extreme axis deviation (northwest), very broad complexes, positive concordance throughout the precordial leads or negative concordance also more likely to be VT if structural heart disease, age >35

Answer 227

when rate of ectopic ventricular pacemaker exceeds that of sinus node; may occur w incr vagal & decreases SNS tone (eg. athletes). the rhythm of the AIVR is regular, 3 or more ventricular complexes >120ms occur, there may be fusion & capture beats when simultaneous sinus & ventricular rhythms are present. Rates <50bpm consistent w ventricular escape rhythm, rates >110bpm VT.

Answer 228

In pts w L) BBB or ventricular paced rhythm, infarct Dx based on ecg can be difficult. Abnormal depolarisation should be followed by abnormal depolarisation (“appropriate discordance”), ST-T wave deviations that don’t necessarily indicate acute ischaemia the 3 criteria to Dx infarction in L) BBB: concordant STE >1mm in leads w +ve QRS concordant ST depression >1mm in V1-3 excessive discordant STE in leads w -ve QRS, w modified sgarbossa states it would be >=25% the depth of the preceding S wave

Answer 229

RVOT (RV outflow-tract tachycardia; a form of monomorphic VT originating from outflow tract of RV or occ from tricuspid annulus, so may have other general features of VT eg. AV dissociation, fusion/capture beats); either in pts w structurally normal hearts (70% idiopathic VD), or pts w arrhythmogenic RV cardiomyopathy. RVOT can be difficult to differentiate from SVT w L) BBB In stable pts, idiopathic RVOT can be terminated w vagal or adenosine, doesn't terminate w these measures if ARVD unstable, DCCV if unsure VT or SVT w a

Answer 230

if L) BBB morphology, indicates pacing electrode is in the RV. negative concordance (ie all precordial leads showing -ve complexes) can be a feature of VT but also paced rhythms, simply indicates depolarisation is spreading from ant to post ie. initiates in ant wall of RV)

Answer 231

may be pacemaker-mediated tachycardia (eg. re-entrant rhythm involving pacemaker circuit), sensor-induced tachycardia (eg. w resp impedance monitor or electrocautery), may be appropriate (eg. atrial tachycardia w sepsis, shock, exercise driving pacemaker to max rate if thought to be PMT (eg. triggered by ventricular impulses passing retrograde through AVN) or sensor-induced, terminate it by placing magnet or reprogramming pacemaker, have pads on & monitoring, urgent pacemaker check (if n/a, AVN blocking drugs eg. B block or verapamil, may terminate PMT)

Answer 232

high rates >100/min (newborn 110-150bpm, >6yo 60-100bpm) by 3-4yrs of age, paediatric ecg largely resembles adult (LV dominance) "juvenile T-wave pattern" of TWI V1-3 R) axis deviation dominant R wave & RSR' in V1 marked sinus arrhythmia short PR & QRS (smaller cardiac size) may have sl prol QTc (<=490ms if <=6/12)

Answer 233

both need rate control & anticoagulation, flutter will cardiovert w lower energy than AF (50J vs 100-200J)

Answer 234

V1-2, if more widespread it's likely tremor artefact

Answer 235

a form of VT, ass'd w rapid & profound haemodynamic compromise, usually short-lived & progresses to VF, rate usually >200/min

Answer 236

signs old anterolateral infarct: STE V1-3 w deep Q waves pathological Q waves in other relevant leads (I, aVL, V4) may also be seen, may also have inverted T waves in precordial/lateral leads

Answer 237

some degree of WPW

Answer 238

high voltage QRS, deep narrow Q waves in lateral leads, syncope

Answer 239

highly specific for L) MCA occlusion if ischaemia in other leads. if STE in aVR & V1, it's specific for proximal LAD or LMCA stensosis, if STE in aVR > that in V1, particularly likely to be LMCA look out for STE in aVR!

Answer 240

extremely short QT interval (<330ms or <360ms w convincing symptoms or FHx), markedly peaked T waves poor rate adaptation to the QT interval, absent ST segment it's ass'd w paroxysmal AF or VF genetically-inherited (heterogenous)cardiac channelopathy symptoms= cardiac arrest, syncope, FHx, SCD pts typically young & healthy, no structural heat disease, median age dx 30yo, presents w palpitations or syncope or cardiac arrest, cn be a cause of SIDS DDx short QT & peaked T waves of severe hyperK, short QT w severe hypercalcaemia Rx= ICD option is quinidine if not candidates for ICD (eg. very young)

Answer 241

severe alkalemia

Answer 242

fluid: pericardial effusion (tachycardia, electrical alternans; tamponade characterised by triad of bulging neck veins, low BP, HS distant/muffled), pleural effusion Fat: obesity infiltrative: myxoedema, restrictive CM (eg. sarcoid, amyloid, scleroderma) air: COPD, PTx loss of viable myocardium eg. prev massive MI, end-stage DCM

Answer 243

STE in III>II, isoelectric ST in V1 but depression V2

Answer 244

sinus dysfunction (SA node supplied by RCA in 60% of ppl), behold jarisch

Answer 245

inf STE & hyper acute T waves, ST depression V2-3 (which may have broad R wave; Q-wave equivalent, terminal portion of the T wave upright). Turning lead V2 upside down looks like classic STEMI. always look for post involvement in any pt w inf or lateral STEMI. confirm w leads 7-9.

Answer 246

L) axis deviation, LA abnormality, pathological Q waves, ST/T changes

Answer 247

>1mm wide >2mm deep (except III, aVR) >25% depth QRS if in V1-3 would indicate current or prev MI

Answer 248

dual p waves (native atrial cuff & transplanted atrium) R) BBB due to frequent endomyocardial biopsies atrial dysrhythmias (lack vagal tone, incr endogensou catecholamines)

Answer 249

RBBB + LAFB (which manifests as LAD) RBBB & LPFB manifests as RAD If no Hx advanced HB or symptoms, crack on as chronic bifascicular block in asymptom pts low risk of progression to high-degree AV block BUT new bifascicular block w AMI higher risk CHB. R) BBB more commonly seen in pts sans structural heart disease. LBBB often a marker of coronary heart disease, long-standing HTN, AV disease or cardiomyopathy.

Answer 250

LAD, qR in I,aVL, rS in II, III, aVF, QRS normal or very sl prolonged (80-110ms) LPFB: exclude RVH & other causes RAD see RAD & qR in Leads II, III and aVF are POSITIVE; rS Leads I and aVL are NEGATIVE

Answer 251

prolonged QR, QT atrial/ventricular ectopics predisposition to VT or torsades

Answer 252

prolonged PR, flat P

ECG Flashcards

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