Figure 22. Second degree AV block with Wenckebach phenomenon

(Mobitz I) (4:3conduction) (lead V1)

+

C21 Cardiology and Cardiac Surgery Toronto Notes 2023

Table 5. Types of Bradyarrhythmias

C.Second Degree AV Block:type II (Mobitz II)

• the PR interval is constant;there is an abrupt failureol conduction of a P

wave

• Often associated with distal conduction system disease (BBB)

• AV block Is usually distal to the AV node|i.c. bundle ol His); increased risk ol

high grade or third degree AV block Figure 23.Second degree AV block (Mobitz II)(3:2 conduction) (lead

V1)

D.Third Degree AV Block

• Complete failure of conduction of the supraventricular impulses to the

ventricles

• Ventricular depolarization initiated by an escape pacemaker distal to the

block

• Wide or narrow ORS. P P and R-R intervals are constant, variable PR intervals

• No relationship between P waves and ORS complexes|P waves “marching

through")

Management (see

(leclticol Pacing.C29)

:

Figure 24. Thirddegree AV block (complete heart block) (leadII)

Supraventricular Tachyarrhythmias

Presentation for SVT (and Pre-Excitation Syndromes)

• presentation can include: palpitations, dizziness, dyspnea, chest discomfort, presyncope/syncope

• may precipitate CHF, hypotension,or ischemia in patients with underlying cardiovascular disease

• untreated tachycardias of long duration (i.e.days) can cause tachycardia- induced cardiomyopathy

(rare, potentially reversible with treatment of SVTs)

• arrhythmias involving the AV node (i.e. AVNRT and AVRT) may terminate spontaneously, after vagal

stimulation, or after adenosine treatment

Supraventricular Tachyarrhythmias

• tachyarrhythmias that originate in the atria or involve the AV junction

• this term is used when a more specific diagnosis of mechanism and site of origin cannot be made

• characterized by narrow QRS unless there is pre-existing BBB or aberrant ventricular conduction

(abnormal conduction due to a change in cycle length)

1. Sinus Tachycardia

• sinus rhythm with rate >100 bpm

• causes:

anxiety, exercise

metabolic (e.g. thyrotoxicosis, pheochromocytoma)

systemic demand (e.g.pregnancy, anemia, exercise, pain,fever, hypotension, hypovolemia,

anemia,CHF,Ml,shock, PH)

pharmacologic (e.g. cocaine, caffeine, alcohol, (3-adrenergic agonists, anticholinergic drugs)

idiopathic (i.e.1STu

idiopathic/inappropriate sinus tachycardia”) or POTS ( postural orthostatic

tachycardia syndrome)

• treatment:

• treat underlying disease; consider P-blocker if symptomatic, CCB if (3-blockers contraindicated;

ivabradine may be considered as an alternative agent for inappropriate sinus tachycardia

2. Premature Beats

• premature atrial contraction

ectopic supraventricular beat originating in the atria

P wave morphology of the PAC usually differs from that of a normal sinus beat

• junctional premature beat

• ectopic supraventricular beat that originates in the vicinity of the AV node

P wave is usually absent or inverted,which may come before or closely follow the QRS complex

(referred to as a retrograde, or “traveling backward” P wave)

• treatment usually not required

3. Atrial Flutter

• rapid, regular atrial depolarization from a macro re-entry circuit within the atrium (most commonly

RA involving isthmus of tissue between tricuspid annulus and inferior vena cava (1VC))

• atrial rate 250-350 bpm, usually 300 bpm

• AV block usually occurs; it may be fixed (e.g. 2:1,3:1, 4:1, etc.) or variable

• etiology:HTN,cardiomyopathy in association with AFib

less often:CAD,thyrotoxicosis, mitral valve disease,cardiac surgery,COPD, PE, pericarditis, in

association with long term endurance sport/exercise

• ECG: “sawtooth" flutter waves (most common type of flutter, called “isthmus-dependent, typical

flutter") in inferior leads, 11, 111, aVF; narrow QRS (unless aberrancy); commonly seen as 2:1 block

with HR of ISO

'

TP ^ r-\

(

_ j

Figure 25. Atrial flutter with variable ~l~

block

C22 Cardiology'

and Cardiac Surgery Toronto Notes 2023

• in atrial flutter with 2:1 block,carotid sinus massage (after checking for bruits), Valsalva maneuver, or

adenosine may decrease AV conduction and allow flutter waves to be more easily seen

• treatment of acute atrial flutter

if unstable (e.g. hypotension,CHF, angina): electrical cardioversion

if stable:

1. rate control:(5-blocker,diltiazem,verapamil, or digoxin

2. chemical cardioversion:sotalol, amiodarone, type 1 antiarrhythmics, or electrical

cardioversion

3. anticoagulation guidelines same asfor patients with AFib

• long-term treatment of atrial flutter to prevent recurrencesincludes antiarrhythmics and

radiofrequenq’

(RF) ablation (for isthmus dependent,typical flutter, treatment of choice is RF

ablation)

4. Multifocal Atrial Tachycardia (MAT)

• irregular rhythm caused by presence of 3or more atrial foci (may mimic AFib)

• atrial rate 100-200 bpm

3or more distinct P wave morphologies

PR intervals vary

• some P waves may not be conducted

• more common in patients with COPD or hypoxemia;less commonly in patients with hypokalemia,

hypomagnesemia,sepsis, theophylline use,or digitalis toxicity

• treatment:treat the underlying cause; calcium channel blockers may be used (e.g.diltiazem,

verapamil);(5-blockers may be contraindicated because ofsevere pulmonary disease

• no role for electrical cardioversion, antiarrhythmics, or ablation

5. Atrial Fibrillation

• see CCS Atrial Fibrillation Guidelines 2020 for details (free mobile app iCCS available on iOS and

Android)

• the most common sustained arrhythmia

• risk factorsinclude:older age,hypertension, heart failure, valvular disease (especially leading to

dilated LA),recent cardiac surgery,lung disease, excessive alcohol consumption,sepsis(particularly

pneumonia)

• symptoms:palpitations,exercise intolerance,fatigue, dyspnea, dizziness,syncope, may precipitate or

w'orsen HF

• classification

“lone”:generally occursin persons <65 yr and in whom no clinical or echocardiographic causes

are found

nonvalvular: not caused by valvular disease (usually MS), or prosthetic heart valves,or valve

repair

valvular disease is observed in patients/people with MS, prosthetic heart valves,or those who

have undergone valve repair

paroxysmal episodesthat terminate spontaneously

• persistent:AFib sustained for more than 7 d or Al'

ib that terminates only with cardioversion

permanent/chronic:continuous AFib that is unresponsive to cardioversion or in which clinical

judgement hasled to a decision not to pursue cardioversion

recu rrent:two or more episodes of A l ib

secondary: caused by a separate underlying condition or event (e.g. Ml,cardiac surgery,

pulmonary disease,hyperthyroidism)

• initiation

single circuit re-entry and/or ectopic foci,mostly arising from the pulmonary veins,act as

aberrant generators producing atrial tachycardia (350-600 bpm)

thisleadsto multiple re-entry circuitry (microre-entry)

impulses are conducted irregularly across the atrial myocardium to give rise to fibrillation

in most cases,ectopic foci have also been mapped to the pulmonary'vein ostia and can be ablated

• maintenance

the tachycardia causes atrialstructural and electrophysiological remodelling changes that further

promote AFib;the longer the patient isin AFib,the more difficult it isto restore normalsinus

rhythm

• consequences

the AV node irregularly filtersincoming atrial impulses producing an irregular ventricular

response (usually <200 bpm); tachycardia leads to suboptimal CO

fibrillatory conduction of the atria promotes blood stasisincreasing the risk of thrombus

formation

- AFib is an important risk factor forstroke or thromboembolic events (stroke risk can be

assessed by CHADS2 score in Alib;CHADS2-VASc if the former gives a score of 0 or I )

- all valvular Afib (those with mechanical valves or MS) need anticoagulation but CHADS

determines treatment for AS and MR

r T

i u I

+

C23Cardiology and Cardiac Surgery Toronto Notes 2023

Table 6. CHADS2 Risk Prediction for Non-Valvular AFib

Risk Factor Points CHADS2 Score Stroke Risk (%/Yr)

Ike 2020CaiadiaiCartiorascalar Society/

Caaadiaa Heart tkyttnSociety Comprehensive

Cadetiaes fortke Management of Atrial

Fibrillation

Car J Cardiol 2020;36:1S47-T9-i8

Bate aid Btryttra Controt Long-tensrate

nataltterapy a Af0 patentsisreennnended

ta redace sjrptocs ant preient CV events- Based

oa tte parity of data informing HB targets,it is

recoamerded In state rate-controllingagents to

actme a resteg HB <100 bpm durng Af.-b.BSyttrm

coitroi at long-term antarrtydunicdrug tterapy

cgltsct coepletely suppressJFBrand Hassbcold

be fbcssed oo sysptw relief, improving functional

capacity.ard rerLting tealticare utilization,fibyttm

cottrnistrategies are rtcommended for patients

am esaPrsadAKb wbo remain symptomatic wntlr

rate cortro tberapy.nrin atom rate control tterapy

is unitety to controlsymptoms.In patents with

new y tagrosed AFib.as initialstrategy n!rbytbm

contol nas been assorted at

- redoced CV death

and redsced incidence of stroke.It isrecommended

to enrsder tatreter ablation of AFib as a reasonable

Menibve to pbaraacologc rate or rbytbm control.

Aatitbroabotk Tberapy io AFib: In patients win

AFd and coronary or artenal rascclar disease.Ibe

ctoce of antdtroabotc tberapy should be based on

a ba arced risk assessment of AFib-refafed stroke,

seberr c corosary everts.and doically relevant

Peed og.If as ora:antcoagnlant is indicated,nonVta-r lalegars!ora a-iicnagnlanis (NOACs) are

recommended orer warfare.

Congestive HF 0 1.9 (low)

2.8 (low-mod)

4.0-S.9 (mod), need anticoagulation

8.5-18.2 (high),need anticoagulation

1

HTN 1 1

Age >75

Diabetes

1 2-3

1 4- 6

Stroke/1IA (prior) 2

Can J Cardiol 2014:30:1114-30

• HCG findings

no organized P waves due to rapid atrial activity (350-600 bpm) causing a chaotic fibrillatorv

baseline

irregularly irregular ventricular response (typically 100-180 bpm), narrow QRS (unless aberrancy

or previous BBB)

wide QRS complexes due to aberrancy may occur following a long-short cycle sequence (“Ashman

phenomenon'

)

• loss of atrial contraction, thus no “A"wave seen in|VP, no S-t on auscultation

mmsm

Figure 26. AFib (lead II)

• management (adapted from CCS Atrial Fibrillation Guidelines 2020)

primary goal issymptom control

• stroke prevention is crucial,since patients who are not anticoagulated for AFib have, on average,a

4-5% annualstroke risk

all patientsshould be assessed forstroke risk and receive anticoagulation independent of the rate

or rhythm treatment

newly discovered AFib

if the episode isself-limited and not associated with severe symptoms, no need for

antiarrhythmic drugs

if AFib persists, consider one of the following:

1. rate control and anticoagulation (asindicated below)

2. cardioversion (asindicated below)

an initial rhythm control strategy for patients with newly diagnosed AFib (i.e. within past

year), is associated with reduced cardiovascular death and stroke rate

• recurrent or permanent AFib

if episodes are brief or minimally symptomatic, antiarrhythmic drugs may be avoided;rate

control and anticoagulation are appropriate

patients who have undergone at least one attempt to restore sinus rhythm may remain in AFib

after recurrence; permanent AFib may be accepted (with rate control and antithrombotics as

indicated by CHADS2 score) in certain clinical situations

» if symptoms are bothersome or episodes are prolonged, antiarrhythmic drugs should be used

• drug selection for rhythm control

no or minimal heart disease: tlecainide, propafenone once proven to have no underlying CAD

(may consider exercise stresstesting)

LV dysfunction:amiodarone

CAD: (3-blockers,amiodarone

if antiarrhythmic drugsfail or are not tolerated, can consider RF ablation for rhythm/

symptom control

treatment of AFib (RACE):all patients with AFib (paroxysmal, persistent, or permanent),should

be stratified using a predictive index for stroke risk and risk of bleeding, and most patientsshould

receive either an oral anticoagulant (OAC) or ASA

1. Rate control:(3-blockers,diltiazem, verapamil (in patients with H1-:digoxin, amiodarone)

- digoxin can be used to achieve rate control in patients whose response to|3-blockers

and/or CCB isinadequate, contraindicated,or not tolerated

2. Anticoagulation: use either warfarin or DOACs (e.g. apixaban, dabigatran, rivaroxaban,

edoxaban) to prevent thromboembolism

- DOAC use is preferred to warfarin

- for patients with non-valvular AFib (NVAF), OAC use is recommended for those >65

vr and/or with a CHADS2 >1. N VAF is defined as AF not due to mechanical valve or

moderate-severe mitral stenosis

- ASA 81 mg is recommended only for patients with none of the risks outlined in the

CCS algorithm (age <65 and noCHADS2 risk factors) who also have arterial disease

(coronary, aortic,or peripheral)

r -i

c j

+

C24 Cardiology and Cardiac Surgery Toronto Notes >023

3. Cardioversion (electrical)

- if AF'

ib <48 h, can usually cardiovert without anticoagulation (<12 h if high stroke risk)

- if AFib >48 h,anticoagulate 3 wk before and 4 wk after cardioversion due to risk of

unstable intra-atrial thrombus

- if patient is unstable (hypotensive,active angina due to tachycardia, uncontrolled HF),

cardiovert immediately

4. Etiology

- HTN, obesity'

,sleep apnea,CAD,heartfailure,valvular disease,pericarditis,

cardiomyopathy, myocarditis,ASD,postoperative, PE,COPD, thyrotoxicosis,sick sinus

syndrome, alcohol (“holiday heart”)

- may present in young patients without demonstrable disease (“lone AFib") and in the

elderly without underlying heart disease

- studies of patients with AF'

ib suggest that there is no difference in long-term survival

when treating patients with a rhythm-control vs. rate-controlstrategy (recent large

study suggests benefit of rhythm control for recent onset AF- see above)

- many patients with a significant underlying structural heart lesion (e.g. valve disease,

cardiomyopathy) will not tolerate AFib well (since may be dependent on atrial kick) and

these patients should be cardioverted (chemical or electrical) assoon as possible

•surgical management in AF'

ib ablation

sutured lesion

Cox-maze 111:definitive surgical treatment of chronic AF'

ib;indicated in patients who

have failed maximal medical therapy and have had embolic events or are symptomatically

compromised by AF'

ib; 90-95% postoperative freedom from AF'

ib;lesslikely to be successful

in patients with large left atria (>5 cm) or with longstanding AF'

ib (>5 yr)

modified maze and pulmonary vein isolation:more limited patient sets but takesless

time to perform than classical maze procedure;selected cases can be done off bypass with

concomitant OPCAB;60-75% postoperative freedom from AFib

• energy lesion

cryoablation: seeCatheter Ablation,C29

radiofrequency ablation:see Catheter Ablation, C

'

29

current experimental trialsinclude use of laser ablation, microwave ablation, and ultrasound

ablation

6. AV Nodal Re-Entrant Tachycardia

•re-entrant circuit using dual pathways (fast conducting (3-fibres and slow conducting a-fibres) within

or near the AV node;often found in the absence ofstructural heart disease

cause is commonly idiopathic, although familial AVNRT has been reported

•sudden onset and offset with patients often describing"

neck pounding” and “shirt flapping"

•fast regular rhythm of 150-250 bpm

•usually initiated by a supraventricular or ventricular premature beat

•AVNRT accountsfor 60-70% of all paroxysmal SVTs

•retrograde P waves may be seen but are usually lost in the QRS complex

•treatment

• acute;Valsalva maneuver or carotid sinus pressure technique, adenosine is first choice if

unresponsive to vagal maneuvers;if no response,try metoprolol,digoxin, diltiazem,electrical

cardioversion if patient hemodynamically unstable (hypotension, angina,or CHF)

long-term:1st line radiofrequency ablation (>98% cure rate and < < 1% complication rate),

(3-blocker, diltiazem,digoxin; 2nd line flecainide,propafenone

®Laura E.Smith »12 ^

Figure 27. AVNRT

N.B. Refer to ECG Made Simple for

further discussion and an animation of

the mechanism ( www.ecgmadesimple.

com)

+

AL GRAWANY

C25Cardiology and Cardiac Surgery Toronto Notes 2023

Bundle ol Kent

• Can exist in right

or left heart

Pathway A . , Pathway B

• Slow conduction APB • Fast conduction

• Short refractormessl , I. Long refractoriness

Della Wave

•

Pathway

Slow conduction

A

J2/L •Short refractoriness

Pathway B

Fast conduction

Long refractoriness 2.An atrial premature beat (APB) after a normal

depolarizing beat conductsthrough A (since

repolarized) but not B (still refractory-thus

producing unidirectional block)

The impulse travels along A and reachesthe distal

end of B which has now repolarized, allowing

retrograde conduction to establish a re-entry circuit

©Young M.Kim 2011

Figure 29. Accessory pathway

conduction in WPW. Early ventricular

activation leads tothe appearance

of a delta wave (slurred upstroke of

the QRS) on the ECG before usual

conduction across the AV node

1.Setup for AVNRT:

Presence of fast and slow tractsin AV node

Figure 28. Mechanism for AVNRT

Pre-Excitation Syndromes

•refers to a subset ofSVTs mediated by an accessory pathway which can lead to ventricular preexcitation

AV Re-Entrant Tachycardia (AVRT)

•re-entrant loop in antegrade via normal conduction system and retrograde via accessory pathway

•usually'in patients with an antegradely conducting bypass tract (WPW);may also occur if there is an

exclusively retrogradely conducting (i.e. concealed) bypass tract-in these casesthe ECG is normal

and there are no delta waves

•initiated by a premature atrial or ventricular complex

•treatment

acute; treatment issimilar to AVNRT but avoid long-acting AV nodal blockers(e.g.digoxin and

verapamil)

• long-term;for recurrent arrhythmias, ablation of the bypass tract isrecommended

• drugssuch asflecainide and procainamide can be used

Wolff-Parkinson-White Syndrome

•congenital defect present in 1.5-2/1000 of the general population

•an accessory conduction tract (bundle of Kent; can be in R A or LA ) abnormally allows early electrical

activation of part of one ventricle

•impulses travel at a greater conduction velocity across the bundle of Kent thereby effectively

‘bypassing’AV node

since the ventricles are activated earlier,the ECG shows early ventricular depolarization in the

form of initialslurring of the QRS complex the so-called “delta wave"

•atrial impulsesthat conduct to the ventricles through both the bundle of Kent and the normal AV

node/His-Purkinje system generate a broad “fusion complex"

•ECG features of WPW

PR interval <120 msec

delta wave;slurred upstroke of the QRS (the leads with the delta wave vary with siteof bypass)

widening of the QRS complex due to premature activation

secondary'ST segment and T wave changes

tachyarrhythmias may occur most often AVRT and AEib

•orthodromic AVRT:the most common arrhythmia in WPW stimulusfrom a premature complex

travels up the bypass tract (ventricles to atria) and down the AV node (atria to ventricles) with narrow

QRS complex (no delta wave because stimulus travels through normal conduction system)

comprises 95% of the re-entrant tachycardias associated with WPW syndrome

•antidromic AVRT:more rarely, the stimulus goes up the AV node (ventricles to atria) and down the

bypass tract (atria to ventricles);wide and abnormal QRS as ventricular activation is only via bypass

tract

+

C26 Cardiology and CardiacSurgery Toronto Notes 2023

AFib in WPW Patients

• AFib is the index arrhythmia in up to 20% of patients with WPW syndrome

usually intermittent rather than persistent or permanent

• rapid atrial depolarizations in AFib are conducted antegradely through the bypass tract which is not

able to filter impulses like the AV node can and thus the ventricular rate becomes extremely rapid

(>200 bpm) and the QRS complex widens ( “pre-excited AFib” )

treatment: electrical cardioversion, IV procainamide,or IV amiodarone

do not use drugs that slow AV node conduction during pre-excited AFib (e.g. digoxin, p-blockers)

as this may cause preferential conduction through the bypass tract and increase the risk of VFib

note: even without drug administration, AFib with WPW can lead to VFib and would be an

indication for an urgent FPS and ablation (especially with very rapid ventricular rates during

AFib)

long-term:ablation of bypass tract

Accessory

Pathway

Ventricular Tachyarrhythmias 11

Premature Ventricular Contraction or Ventricular Premature Beat

• QRS width >120 msec, no preceding P wave, bizarre QRS morphology

• origin:LBBB morphology of VI'

= RV origin;RBBB morphology of VT = LV origin

• PVCs may be benign,but are usually significant in the following situations:

consecutive (S3 = VT) or multiform (varied origin)

PVC falling on the T wave of the previous beat (“R on T phenomenon"):may precipitate VT or

VFib

risk ofsustained arrhythmia depends on the clinicalsituation (i.e.Ml, HF), not the PVCs themselves

• treatment

lifestyle changes (e.g. limiting or eliminating alcohol, caffeine, and stimulants) may be sufficient

in patients with mild symptoms

in patients with more severe symptoms or underlying structural disease, p-blockers, catheter

ablation, or antiarrhythmic therapy may be indicated

t

Orthodromic AVRT

Accelerated Idioventricular Rhythm

• ectopic ventricular rhythm with rate of 50-100 bpm

• more frequently occurs in the presence ofsinus bradycardia and is easily overdriven by a faster

supraventricular rhythm

• frequently

valvular h

Accessory

- at

'

i .'. ay

occurs in patients with acute Ml or other types of heart disease (i.e. cardiomyopathy, HTN,

eart disease) but it does not affect prognosis and does not usually require treatment

Ventricular Tachycardia

• 3or more consecutive ectopic ventricular complexes

rate >100 bpm (usually 140-200)

ventricular flutter: if rate approximately 300 bpm and monomorphic sinusoidal pattern

“sustained VT” if it lastslonger than 30 s or requires termination due to hemodynamic instability

FCG characteristics:wide regular QRS tachycardia (QRS usually >140 msec)

AV dissociation, bizarre QRS pattern

also favour diagnosis of VT:left axis or right axis deviation, nonspecific intraventricular block

pattern, monophasic orbiphasic QRS in VI with RBBB, QRS concordance in V1-V6

occasionally,during VT,supraventricular impulses may be conducted to the ventricles; these

impulses generate QRS complexes with normal/aberrant supraventricular morphology (I.e.

“ventricular capture") or summation pattern (i.e. “fusion complexes")

by itself, nonsustained VT (<30 s without hemodynamic collapse) independently increases

mortality and cardiovascular eventssuch as stroke; it can also indicate higher than usual risk of

subsequent sustained VT,especially with structural heart disease

• monomorphic VT

• identical complexes with uniform morphology

more common than polymorphic VT

can degenerate into polymorphic VT or VFib

typically result from intraventricular re-entry circuit, may be idiopathic without any structural

heart disease

potential causes:chronic infarct related scarring, cardiomyopathies, myocarditis,

arrhythmogenic right ventricular dysplasia, idiopathic, drugs (e.g. cocaine), electrolyte

disturbances

• polymorphic VT

complexes with constantly changing morphology, amplitude, and polarity

more frequently associated with hemodynamic instability due to faster rates (typically 200-250

bpm)

• potential causes: acute Ml,severe or silent ischemia, valvular heart disease, HCM, dilated

cardiomyopathies, myocarditis, congenital heart disease, WPW with anterograde accessory

pathway, electrolyte or acid-base disturbances, and predisposing factorsfor QT prolongation

Antidromic AVRT

Figure 30. Orthodromic vs.

antidromic AVRT

Premature Ventricular Contraction (PVC)

JU

Premature Atrial Contraction (PAC)

Note This diagram also shows invoited T waves

r t

L J

SCaitlin LaFlamme 2009

Figure 31. PVC (with bigeminy

pattern) and PAC. Note the difference

between the normal ORS/T wave and

the PVC-generated QRS/T wave +

C27Cardiology and Cardiac Surgeiy Toronto Notes 2023

• treatment

sustained VT (>30 s) is an emergency requiring immediate treatment

hemodynamic compromise:treat VT with electrical cardioversion and ACLS

no hemodynamic compromise: treat VT with electrical cardioversion,amiodarone,Type1A

agents (e.g.procainamide, quinidine)

• every patient with sustained VT/Vl'

ih and comorbid structural heart disease,in the absence of

reversible causes,should be considered for 1CD implantation to prevent SCD

A

s

jj;ij

Figure 32. VT (monomorphic)

Table 7. Wide Complex Tachycardia:Clues for Differentiating VT vs. SVT with Aberrancy* Arrhythmias that may present as a

Wide QRS Tachycardia

• VT (this is most common,especially

in older patients or those with

structural heart disease)

• SVT with aberrant conduction (rate

related)

• SVT with preexisting BBB or

nonspecific intraventricular

conduction defect

• AV conduction through a bypass

tract in WPW patients during an atrial

tachyarrhythmia (e.g. atrial fluttec

atrial tachycardia)

• Antidromic AVRT in WPW patients

(seePre-Exatotion Syndromes.C2S)

Clinical Clues ECG Clues

Presenting symptoms VT

History of CAD andpreviousHI VT

Physical exam

Cannon “a" waves

Variable S1

Carotid sinus massageadenosine SVT"

terminates arrhythmia

Not helpful AV dissociabon

Capture or fusion beats

ORS width»140 msec

Extreme axis deviation(leftor

right superior axis)

Positive OPS concordance

(P wave across chest leads)

Negative OPS concordance

(S wave across chest leads)

Axis Shift during arrhythmia

VT

VT

VI VI

VI

May suggest VI

VT (polymorphic)

•If patient >65yr and previous Ml or structural heart disease, then chance of VT >95*«

"May terminate VT in some patients with no structural heart disease

Torsades de Pointes

• a variant of polymorphic VT that occurs in patients with baseline QT prolongation “twisting of the

points”

• lookslike usual VT except QRS complexes “rotate around the baseline,” changing their axis and

amplitude

• usually startsfollowing a post extrasystolic pause ( “pause dependent” )

• ventricular rate >100 bpm, usually 150-300 bpm

usual onset after a post-PVC pause associated with “pause dependent"QT prolongation)

• etiology:occursin association with prolonged QT intervals

• congenital long QTsyndromes

• drugs:e.g.class 1A (quinidine), class 111 (sotalol), phenothiazines (TCAs), erythromycin,

quinolones, antihistamines

• electrolyte disturbances: hypokalemia, hypomagnesemia

• nutritional deficiencies causing above electrolyte abnormalities

• treatment:IV magnesium, temporary pacing (5 blocker, correct the underlying cause of prolonged QT

• electrical cardioversion and ACLS if hemodynamic compromise

Figure 33. Torsades de pointes

Ventricular Fibrillation

• chaotic ventricular arrhythmia, with very rapid irregular ventricular hbrillatory waves of varying

morphology without clear QRS complexes

• terminal event, unless advanced cardiac life-support (ACLS) procedures are promptly initiated to

maintain ventilation and CO, and electrical defibrillation is carried out

• most frequent cause of sudden death

• refer to ACLS algorithm for complete therapeutic guidelines

L J

VW\AA 55^

Figure 34. VFib +

C28Cardiology and CardiacSurgery Toronto Notes 2023

Sudden Cardiac Arrest

Definition

• cessation of cardiac electrical activity with circulatory collapse (loss of pulses) and gasping

respirations or lack ofspontaneous breathing

• patient becomes suddenly unresponsive

• presenting rhythms may be PEA, asystole, VFib (less commonly pulseless VT)

Etiology

• the likelihood of an underlying cardiac cause is proportional to age at time of arrest

• cardiac causes (especially CAD) are more likely in older adults

• non-cardiac causes are more likely in children and young adults(<35 yr)

Table 8. Etiology of Cardiac Arrest

Cardiac Causes Non-Cardiac Causes

SHMI

NS1EMI

Coronary spasm coronary

dissection

Anomalous coronary artery

myocardial Ischemia Vascular Pulmonary embolism

Aortic dissection

Aortic rupture

Stroke

Ischemic Cardiomyopathy HF Neurologic Sudden unexplained death in

epilepsy

Neurogenic

Subarachnoid

Intracranial

Gastrointestinal

Scar

Non-lschemic Cardiomyopathy Dilated CM

Hypertrophic CM

Infiltrative CM myocarditis

Arrhythmogenic RV CM

Hypertensive CM

VHD with IVfailure

Hemorrhagic

Valvular Heart Disease AS Infection Sepsis

MR Pneumonia

Heritable ion channel disorders long 01syndrome

Brugada syndrome

Respiratory Respiratory arrest

Tension pneumothorax

Substance overdose

Ketoacidosis

Trauma

Primary Arrhythmogenic Acquired 01prolongation

Idiopathic

Complete heart block

Other

WPW

Congenital Heart Disease Tetralogy olFallot

»1

Post-Surgical scar

Management

• acute: resuscitate according to ACLS guidelines (see Anesthesia, A32)

resuscitation can be grouped into those with and without shockable rhythms

• activation of emergency systems and high-quality chest compressions are essential for any

bystander

• investigate underlying causes using cardiac catheterization, electrophysiologic studies,

echocardiography

patients with ST -elevation require emergent coronary angiography and revascularization

sand therefore

See Urdu it Cardiac Inalsfor more information

on COACT. ninth dethilstte1-yr clinical outcomes ol

atgiogreplty timing on survival in resuscitated cardiac

arrest patients nrithourt SIEMI.

patients without ST-elevation can still have clinically relevant coronary lesion

benefit from coronary angiography on a non-emergent basis

• initiate targeted temperature management to optimize neurologic recovery regardless of presenting

rhythm

• treat underlying cause

• antiarrhythmic drug therapy:amiodarone, lidocaine, p blockers

• 1CD forsecondary prevention

Electrophysiologic Studies

• invasive test for the investigation and treatment of cardiac rhythm disorders using intracardiac

catheters

• provide detailed analysis of the arrhythmia mechanism and precise site of origin when ECG data are

nondiagnostic or unobtainable

• bradyarrhythmias:define the mechanisms of SA node dysfunction and localize site of AV conduction

block (rarely performed)

• tachyarrhythmias: map for possible ablation, assess indudbility of VT prior to ICD implant

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C29Cardiology and Cardiac Surgery Toronto Notes 2023

Electrical Pacing

•the decision to implant a pacemaker usually is based on symptoms of a bradvarrhy thmia or

tachyarrhythmia with intermittent bradycardia precluding rate limiting medications

Pacemaker Indications

•SA node dysfunction (most common):symptomatic bradycardia ± hemodynamic instability

•common manifestations include:syncope, presyncope,or severe fatigue

•SA node dysfunction is commonly caused by:intrinsic disease within the SA node (e.g.idiopathic

degeneration, librosis, ischemia, orsurgical trauma), abnormalities in autonomic nervoussystem

function, and drug effects

•AV nodal- infranodal block: Mobitz II, complete heart block

Pacemaker Complications

•complications related to surgical implantation include venous access (pneumothorax, hemothorax,

air embolism), pacemaker leads(perforation, malposition), packet hematomas, and infection; rarer

complications include venousstenosis or thrombosis, and tricuspid regurgitation

•complicationsspecific to the pacemaker include a failure to pace,failure to sense, pulse generator

failure, pacemakersyndrome, lead fractures, and pacemaker-mediated tachycardia

Pacing Techniques

•temporary: transvenous (jugular,subclavian,femoral) or external (transcutaneous) pacing

•permanent:transvenous into RA, apex of RV, or both

•single or dual chamber:can sense and pace atrium, ventricle,or both

•rate responsive, able to respond to physiologic demand

•biventricular pacing (cardiac resynchronization therapy):leads are guided to RV and LV to stimulate

both ventricles

Implantable Cardioverter Defibrillators

• SCI) usually resultsfrom Vl-ib,sometimes preceded by monomorphic or polymorphic VT

• ICDs detect ventricular tachyarrhythmias and are highly effective in terminating VT/VFib and in

aborting SCD

• mortality benefit vs.antiarrhythmics in secondary prevention and selected patientsfor primary

prevention

• CRT'

-D may be of benefit in patients with LBBB, prolonged QRS, and LVEF

• see Heart l

-

'

ailure,C40 for current treatment recommendations

<35%

Catheter Ablation

Modalities

• radiofrequency (RF) ablation: a low-voltage high-frequency form of electrical energy (similar to

cautery); RF ablation producessmall, homogeneous, necrotic lesions approximately 5-7 mm in

diameter and 3-5 mm in depth

• cryoablation:technology which uses a probe with a tip that decreases in temperature to -20‘C and

-70"C;small necrotic lesions are produced in a similar fashion to RF ablation; when brought to -20‘C,

the catheter tip reversibly freezes the area;when brought to -70°C for 5 min,it permanently scarsthe

tissue

advantage:can “test"

areas before committing to an ablation

disadvantage:takes much longer than RF (5 min per cryoablation vs. 1 min per RF ablation)

cryoablation is most commonly used for AFib

Indications

• paroxysmal SVT

AVNRT:accounts for more than half of all cases;slow AV nodal pathway is targeted for ablation

in these cases

• accessory pathway (orthodromic reciprocating tachycardia): 30% of SVT

re-entrant rhythm with an accessory AV connection as one of the limbs

corrected by targeting the accessory pathway

• atrial flutter:re-entry circuit in RA

• AFib:primarily isolation of pulmonary vein triggers, usually with additional ablation in the atrial

chambers

• idiopathic VT:focus arisesfrom the right ventricular outflow tract or left ventricular outflow tract and

less commonly originatesin the inferoseptal LV near the apex

scar mediated VT most commonly due to scarring from previous Ml or other cardiomyopathies;

ablation less often successful and not first line therapy

significant benefit wasseen with catheter ablation vs. antiarrhythmic drug escalation among

patient with amiodarone-resistant VT, in contrast to non-amiodarone resistant VT

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