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2019 SVT guidelines Part-II.pptx
1. Guideline directed
management of SVT (Part-I)
Presenter: Dr. Al-Amin
Phase B resident, BSMMU
Chairperson: Prof.Dr.SM Mustafa Zaman
UCC, BSMMU
2. Definition and classification
• The term 'SVT' literally indicates tachycardia(atrial rate >100 bpm)
that originates from the tissue of His bundle or above
• 'Narrow QRS tachycardia' indicates those with a QRS duration 120 ms
or less
• A wide QRS tachycardia refers to one with a QRS duration >120 ms
• SVT may present as narrow or wide QRS tachycardia,most of
which,although not invariably, manifestation as regular rhythm
16. Vagal manoeuvres
• Used to terminate the narrow complex SVT with success rate of 19-54% if performed
correctly
• Stimulates the receptors in the internal carotid arteries causing reflex
stimulation of the vagus nerve and release of acetylcholine, which slow the
electrical impulse through the AVN and slow the heart rate
• safe and internationally recommended first-line emergency
treatment,most effective in adults, and in AVRT rather than AVNRT
• Can be provided in bedside or office setting
17. Carotid sinus massage
• Performed with the patients neck in an extended position,with the
head turned away from the side to which pressure is applied
• Always performed unilaterally with monitoring
• Carotid bruit must be checked before the procedure
• Should not be done >10 secs at a time
• Avoided in patients with previous transient ischemic attack or stroke
or in the presence of carotid bruit
18. Adenosine
• Endogenous purine nucleoside acts through cardiac adenosnie A1 receptor
• Progressive dose-related prolongation of AV conduction resulting in transient AV block
• First drug of choice with >90% success rate
• Average dose is 6-18 mg,required mean dose is ~6mg to terminate SVT
• Given as rapid bolus injection with immediate saline flush
• Large, centrally located (e.g. antecubital) veins are likely to deliver more effective drug
concentration to the heart than smaller distal veins
• Dosing should be incremental, starting at 6 mg followed by 12 mg.An 18mg dose can be
considered taking into account of tolerability and side effects
19. • Very short plasma half-life due to enzymatic deamination with end-organ clinical effects within 20–30
sec
• So,repeat administration is safe within 1 min of the last dose
• Transient dyspnea due to bronchoconstriction, Facial flushing,increased skin temperature due to
vasodilation, chest pain
• AF may occur as a result of either direct pulmonary vein triggering or increasing heterogeneity of
repolarization and more commonly associated with AVRT than AVNRT
• Occasionally,causes pre-exited atrial arrhythmia
20. Calcium channel blockers
• IV Non-dihydropytidine CCB (verapamil,diltiazem) used to treat frequent atrial or
ventricular premature beat with success rate of 64-98%
• Verapamil ;0.075 − 0.15 mg/kg (average 5 − 10 mg) over 2 min
• Diltiazem ;0.25 mg/kg (average 20 mg) over 2 min has been shown to terminate SVT
but is associated with a risk of hypotension.
• Should be avoided in patients with haemodynamic instability
• HF with reduced LV ejection fraction (<40%),suspicion of VT,or pre-excited AF
• Intranasal short acting CCB (etripamil) can be used with conversion rate is 65-95%
21. Beta-blockers
• IV short acting Beta-blocker(Esmolol/metoprolol) also used to treat SVT
• IV esmolol ; 0.5 mg/kg bolus or 0.05 − 0.3 mg/kg/min infusions
• IV metoprolol ;2.5–15 mg given in 2.5 mg boluses), are more effective in reducing the tachycardia rate
than in terminating it
• Although,evidence for the effectiveness of Beta-blockers are limited,they have an excellent safety
profile in haemodynamically stable patient
• Cautiously used with concomitant use of iv CCB or Beta-blocker because of potentiation of hypotension
and bradycardic effect
• Contraindicated in patients with decompensated HF
22. Wide complex tachycardia
• Heamodynamically unstable
-can occur with any wide complex tachycardia regardless of cause
but more common in VT
-synchronized DC cardioversion is recommended for any persistent
wide complex tachycardia resulting in hypotension,features of acute HF
or shock
23. • Heamodynamically stable
-vagal manoeuveres can be applied that revert to sinus rythm or
provide clue to mechanisms of arrythmia
-if SVT with aberrancy is identified definitively,can be treated like
narrow complex SVT
-procainamide or amiodarone can be used to terminate arrythmia
• Adenosine may be helpful allowing diagnosis or interrupting adenosisne
sensitive VT
-must be avoided in presence of pre-exitation
24.
25.
26.
27. Irregular tachycardia
• If the rhythm is well tolerated with a narrow complex irregular
tachycardia,considered likely to be AF
• A wide QRS irregular tachycardia is usually a manifestation of AF
-Rarely,polymorphic VT and very rarely, monomorphic VT may also
present as wide complex irregular tachycardia
28. Specific type of Supraventricular tachycardia
Atrial arrhythmia
• Sinus tachycardia (sinus rate >100 b.p.m)
-physiological sinus tachycardia
-pathological sinus tachycardia
• Treatment primarily depends on the idetlntification and treatment of
the cause
29.
30. Inappropriate sinus tachycardia(IST)
• Fast sinus rhythm (>100 b.p.m) at rest or on minimal activity that is out of
proportion with the level of activity
• Usually transient but tends to be persistent,affects generally young female
• cause is poorly understood,likely to be multifactorial
(dysautonomia,neurohormonal dysregulation and intrinsic sinus node
hyperactivity),anti beta receptor antibody (IgG)
• Can cause palpitation,dizziness,light-headedness,pre-syncope or syncope
• sually benign and is not associated with tachycardia - induced cardiomyopathy
31. • Diagnised by exclusion of POTS,sinus re-entrant tachycardia or focal
atrial tachycardia
• 24h Holter monitoring shows mean heart rate >90 b.p.m with an
exaggerated heart rate response >100 b.p.m during walking
• Tolerance exercise testing can be considered and EPS is generally not
required
• Managed by treating the cause if present,with life style
intervention(exercise training,avoidance of cadiac stimulants)
• Beta-blockers,non-dihydropyridine CCB or selective blocker of
pacemaker current (ivabradine) can be used
32.
33.
34. Postural orthostatic tachycardia syndrome (POTS)
• Most common orthostatic intolerance in young female
• Increase heart rate >30 b.p.m when standing for >30sec in absece of
orthostatic hypotension
• Autonomic dysfunctional, peripheral Autonomic
denervation,hyperadrenergic stimulation,diabetic
neuropathy,hypovolumia
• Treated by withdrawal of offending drugs or secondary causes with
life style intervention
35. • Regular supervised exercise,increasing blood volume by fluid intake 2-
3 l/d
• Enhanced salt intake 10-12 g/d
• Non-selective Beta-blockers(propranolol),alpha adrenergic agonist
(midodrine),cholinesterase inhibitor(pyridostigmine),ivabradine can
be considered
• ~50% patients recover spontaneously
36.
37. Sinus node re-entrant tachycardia
• Arises from a re-entrant circuit involving sinus node
• Paroxysmal tachycardia followed by palpitations,dizziness,light-
headedness
• Polarity and configuration of P wave is similar to the sinus P wave
• Suspected on the ECG and Holter, confirmed by EP study
• Managed empericaly with Verapamil,amiodarone;shows variable
response
• Effectively and safely treated with catheter ablation with good long-term
outcome
38. Focal Atrial Tachycardia
• Focal AT is an organized atrial rhythm >100b.p.m
• initiated from a discrete origin and spreading over both atria in a centrifugal pattern
• The ventricular rate varies, depending on AV nodal conduction
• Symptoms may include palpitations, shortness of breath, chest pain, and rarely syncope
or presyncope
• May be transient, sustained or incessant,dynamic forms with recurrent interruption and
reinitiation
• PV related AT,focus is located within 1cm of ostium of vein rather than distally
39. ECG findings
• P wave identification from a 12 lead ECG recording during tachycardia is critical
• Depending on the AV conduction and AT rate , the P waves may be hidden in the
QRS or T waves
• A negative P wave in lead I and aVL suggests an LA origin.
• P in V1 is negative ,the arrhythmia source is in the lateral right atrium, while
septal right atrial and LA origins show biphasic or positive P waves
• Negative P waves in the inferior leads suggest a caudal origin, whereas positive P
waves in those leads favour a superior location.
44. Multifocal atrial tachycardia
• Rapid, irregular rhythm with at least three distinct morphologies of P waves
on the surface ECG
• Commonly associated with underlying conditions, including pulmonary
disease(PH,COPD), Coronary artery disease and valvular heart disease, as well
as hypokalemia,hypomagnesaemia and theophylline therapy
• Also seen in healthy infants under 1 year of age
• Carries good prognosis in the absence of underlying cardiac disease
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49. Guideline Directed
Management of SVT (Part-II)
Presenter: Dr. Al-Amin
Phase B resident, BSMMU
Chairperson: Prof.Dr.SM Mustafa Zaman
UCC, BSMMU
50.
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55.
56. Atrioventricular nodal re-entrant
tachycardia(AVNRT)
• Re-entry circuit inooves the AVN creating a functional circuit
• Narrow complex tachycardia, i.e. QRS duration <120 ms, unless there is aberrant
conduction, which is usually of the RBBB type
• Typical form of AVNRT (slow-fast AVNRT), retrograde P waves are constantly
related to the QRS and in the majority of cases very close to the QRS complex
• P waves are either masked by the QRS complex or occurs at the end of the QRS
complex as pseudo R'(V1,V2) or S wave (inferior leads)
• In most cases absent p wave and tachycardia
57.
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61.
62. AVRT
• Most common tachycardia associated with accessory pathway
• ECG features depend on the direction of conduction which may be
orthodromic or antidromic
• Orthodromic AVRT:common (>90%),anterograde conduction is via AV
node,producing a regular narrow complex rhythm (in absence of pre-
existing BBB or aberrance)
• P wave is usually visible at the beginning of The wave with a long RP
interval
• Rate is 200-300 bpm and rate related ischemia is common
63.
64. • Antidromic AVRT:occurs 3-8% of patents with WPW syndrome
• Anterograde conduction via AP and retrograde conduction via AVN or
another AP with longer refractoriness
• About 30-60% patients with spontaneous antidromic AVRT have multiple
AP on EPS
• Regular wide complex rhythm (fully pre-excited) ,rate is 200-300 bpm
• RP interval difficult to assess as the retrograde p wave is usually
inscribed within the ST-T segment
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68. Pre-excited AF
• Paroxysmal AF is found in about 50% of patients with WPW syndrome
• AF with fast ventricular rate often conduct through AP producing pre-
excited AF
• High rate AVRT often initiate AF
• Potentially life threatening arrythmia
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72. Chronic therapy in pre-excited AF
• Catheter ablation is the treatment of choice
• Class Ic anti-arrythmic drugs are recommended in patienrs with pre-
excited AF who don't have structural or ischemic heart disease if
cathter ablation is not feasible or desired
73. Asymptomatic pre-excitation
• Management depends on the risk stratification that can be assessed by-
-Invasive; Electrophysiology study
-Non-invasive;Exercise testing,pharmacological stress testing or ambulatory
monitoring of ECG
- Trans-oesophagial EPS
• High risk -
-Shortest pre-excited RR interval (SPERRI) <250ms
-AP mediated ERP <250ms
-Multiple accessory pathways
-Inducible AP mediated tachycardia
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79. SVT in Adult Congenital Heart Disease
• SVT is observed in 10 -20% of pattients with ACHD
• Most common form of SVT in ACHD is macro re-enrrant tachycardia
(atrial flutter) and 75% of which involves CTI
• Other forms of SVT in ACHD;Focal AT,AVNRT,AVRT
• Common ACHD associated with SVT are ASD, Ebstein anomaly,
TOF,TGA ,single- ventricle/fontan procedure
• Management depends on underlying cardiac anatomy and repairs
,haemodynamic sequelae and mechanism of SVT
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82. SVT in pregnancy
• SVT becomes more frequent during pregnancy
• May manifest for the first time in third trimester or peri-partum period
• Most common SVT is AF ,less common arrythmia are atrial
flutter,AVNRT,AVRT,VT
• Identification and trratment of underlying causes are the first priorities
• Although most of the exacarbation of svt in Pg are benign and can be treated
effectively with standard medical treatment
• Foetal well-being,effect on labour deliery lactation and haemodynamic
condition should be balanced while treated
83.
84.
85. Tachycardia induced cardiomyopathy(TCM)
• TCM is one of the few reversible causes of dilated cardiomyopathy
• Considered in any patients with new onset LV dysfunction in presence of
persistent or frequent tachycardia or frequent PVC
• Diagnsis is established by excluding of other causes of dilated
cardiomyopathy and an improvement of LV function within 3 months
after controlling of ventricular rate
• In TCM,LVEF <30%,LV end diastolic diameter <65mm and LV end systolic
diameter <50 mm
• Serial measurement of NT-proBNP is important to differentiate TCM
from idiopathic DCM
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87.
88. SVT in sports
• Sports activity is associated with inceased risk of AF
• Pre-excitation (WPW syndrome) is a rare cause of sudden cardiac death in
athletes
• Athletes with SVT should be assessed for structural heart disease,electrolytes
disturbance,thyroid dysfunction and use of stimulants
• Treatment of paroxysmal SVT with beta-blockers or sodium channel bloklckers are
discouraged because these drugs
- reduces the performance of sports
-can't prevent the recurrence of arrythmia during sports
91. Take home messages
• Vagal maneuvres and adenosine are the treatments of choice for the acute
therapy of SVT, and may also provide important diagnostic information
• Digoxin, beta-blockers, diltiazem, verapamil, and amiodarone are not
recommended and are potentially harmful in patients with pre-excited AF
• In all re-entrant and most focal arrhythmias, catheter ablation should be
offered as an initial choice
92. Take home messages
• Do not use sotalol in patients with SVT
• Do not use flecainide or propafenone in patients with ischaemic or structural
heart disease
• If a patient undergoes assessment with an EPS and is found to have an AP
with ‘high-risk’ characteristics, catheter ablation should be performed
• If possible, avoid all antiarrhythmic drugs during the first trimester of
pregnancy