This case involves a 22 day old male neonate presented with lethargy, poor feeding, tachycardia and reduced urine output. On examination the heart rate was 336/min with absent P waves on ECG consistent with supraventricular tachycardia (SVT). Adenosine was ineffective in terminating the arrhythmia. Synchronized cardioversion was required to restore sinus rhythm. The SVT recurred and the baby deteriorated with hypotension and acidosis despite treatment. Amiodarone may have contributed to worsening condition due to benzyl alcohol toxicity. The etiology of SVT was unclear but WPW syndrome was suspected. The baby was transferred for higher level care.
This presentation is a simplified version of the various types of cardiac arrythmias seen in pediatric age groups. We have discussed supraventricular tachycarsias and prolonged QT syndrome in details here. Hope everyone finds it useful.
This presentation is a simplified version of the various types of cardiac arrythmias seen in pediatric age groups. We have discussed supraventricular tachycarsias and prolonged QT syndrome in details here. Hope everyone finds it useful.
Presentation on basic principles of pediatric ecg with important examples: BY Dr. Nivedita Mishra (PGY2 PEDIATRICS, TRIBHUVAN UNIVERSITY TEACHING HOSPITAL,KATHMANDU,NEPAL)
Presentation on basic principles of pediatric ecg with important examples: BY Dr. Nivedita Mishra (PGY2 PEDIATRICS, TRIBHUVAN UNIVERSITY TEACHING HOSPITAL,KATHMANDU,NEPAL)
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
1. CASE SCENARIO
• 22 day old male neonate was brought to the ER with c/o
lethargy
poor feeding
reduced urine output
palpitations as felt by mother
Since morning
2. C: irritable
B: Rapid breathing, retractions (+)
C: No cyanosis, pallor (+)
Airway: clear
Breathing: Rate: 74/min
SCR, ICR (+)
No added sounds
Spo2 : 94% on RA
3. • Circulation HR: 336/min
Rhythm: Tachycardia- Narrow
complex (QRS) on ECG monitor with
absent p waves
Pulses: ++/+++
CFT: <3 sec
BP: 84/46mmhg
5. • History: Uneventful antenatal and early neonatal period. 2nd
born by SVD in virudhachalam PVT hosp with birth wt of
2.5kg. Current weight 3.06kg.
• Breast feeding was established immediately, no feeding
issues since birth, no cyanosis since birth
• No h/o previous sibling death in family.
6. • Managed according to pals. Tachyarrhythmia confirmed to
be SVT by rhythm strip.
• As baby was hemodynamically stable, first dose adenosine
given 0.1mg/kg.
No response on ECG
Second dose 0.2mg/kg given
7. No response on ECG
Synchronized cardioversion given
with 0.5J/kg
No response on ECG
Synchronized cardioversion given
with 1J/kg
Sinus rhythm (+)
8.
9. Synchronized cardioversion
• Sync button on defibrillator machine
• Synchronizes with the cardiac cycle so that shock is
delivered at the R wave of the cycle
Defibrillation is unsynchronized shock- delivers any time of
cycle, used in VF
IF unsynchronized shock is given for VT with pulse or SVT,
shock may be delivered during T wave- cardiac repolarization-
precipitation of VF
10. • ECHO done in casualty showed small PFO with L to R
shunt, LV function- good
• Baby shifted to NICU for further management.
• In NICU after one hour of stabilization, recurrence of SVT (+),
pulses well felt.
• Adenosine 0.2mg/kg given IV in central line with saline flush
• Reverted to sinus rhythm with Synchronized cardioversion of
2J/kg
• Loading dose of amiodarone 5mg/kg given IV over 20
minutes.
• In view of recurrence and worsening sensorium, not
maintaining spo2 on RA, Baby was intubated and connected
to mechanical ventilator with minimal settings.
11. • At 5 hours of admission, tachycardia settled, but perfusion
was poor. Peripheral pulses were absent and central pulses
were feeble. Hypotension (+)
• VBG showed acidosis :7.06 ph with bicarbonate of 10
• Hence baby started on ionotropes- Dobutamine 10mcg/kg/min
( suspected cardiogenic cause)
• As perfusion did not improve and poor femoral pulses with
unrecordable BP despite starting dobutamine, adrenaline
started suspecting myocardial dysfunction (0.2mcg/kg/min)
• Hemodynamic monitoring continued
12. • Case discussed with cardiology team:
Advised to discontinue amiodarone, and to consider on oral
propranolol
ECHO was repeated- showed Small PFO with L to R shunt
and Poor LV function
Adviced to continue adrenaline infusion
13. • Clinical dilemma:
- Whether amiodarone can be used for all forms of SVT
- Whether adenosine aborts all AV nodal pathway.
- In SVT refractory to adenosine, what drug to be followed
next apart from shock
- Amiodarone vs procainamide vs propanolol
14. • In between baby threw multiple episodes of seizures in the
form of posturing of all 4 limbs was loaded with
phenobarbitone
• After 7 hours of admission, baby’s perfusion only slightly
improved, sensorium worsened, tachypnoea (+) and
gasping (+)
• Possibilities :
- Severe metabolic acidosis
?Severe refractory cardiogenic hypotensive shock
? Amiodarone gasping syndrome
15. • In view of persisting acidosis on VBG , worsening PH- 6.9
with bicarbonate of 6, ‘Rescue Therapy’ bicarbonate
1meq/kg given as bolus and half correction initiated
• Usually not recommended for acidosis secondary to
hypoxia and shock. Here given since effect of acidosis on
cardiac contractility was uncertain and shock was refractory
to fluids and vasoactive agents.
16.
17. AMIODARONE GASPING SYNDROME
• Ampoules of amiodarone contain benzyl alcohol. Large
amounts of benzyl alcohol in neonates have been
associated with “gasping syndrome” particularly preterms.
• Potentially fatal condition characterised by metabolic
acidosis, respiratory distress, gasping respirations,
convulsions, intracranial haemorrhage, hypotension
and cardiovascular collapse.
18.
19. • Queries :
- Duration between amiodarone administration and
development of gasping episodes
- Whether this is dose dependant?
- Whether all the symptoms of hemodynamic compromise
was caused by amiodarone or underlying LV function
20. • By 12 hours of admission baby went into Ventricular
Tachycardia. Pulses well felt at that time
Possiblities:
- Ventricular tachycardia
- SVT with abberancy
• Reverted with synchronized cardioversion 2J/kg.
• Within 1 hour baby went into multiple episodes of VT. Pulses
felt throughout the episodes, all reverted with synchronized
cardioversion 2J/kg
• Adenosine not tried as previous 2 attempts were unsuccessful
21. • Ventricular Tachycardia
- Wide complex tachyarrhythmia generated within the
ventricle
• SVT with abberancy
- Occurs as a result of rate related BBB within the ventricle or
preexsiting BBB
- Impulse generated from atria to ventricle through accessory
pathway rather than AV node
22. • Difficult to differentiate SVT with abberancy from VT
- Both cause hemodynamic instability, similar heart rate and
both have wide QRS complex
- Sometimes can be differentiated with R-R interval and QRS
morphology
Clinician should assume the initial wide complex rhythmn is
VT unless proved to have pre existing abberancy
If RR interval is regular, with normal QRS morphology and
hemodynamically stable- may attempt one dose of adenosine-
SVT with abberancy will respond, VT will not. (PALS- 2010-11)
23.
24. • Although underlying hemodynamic compromise was (+) a/w
poor LV function,
Adrenaline could have triggered the VT, hence adrenaline was
stopped following which there was no VT episodes
Dobutamine was tapered and stopped within 2 hours.
• Discussed with cardiology: Told possible VT triggered by
adrenaline, still amiodarone role not clear
• Possibility of WPW syndrome discussed- only contradicting
evidence is response to adenosine
25. • Rationale behind amiodarone
- Used in all forms of SVT and atrial tachycardia
• Amiodarone 5mg/kg 2nd loading given over 20 minutes, and
infusion started at 5mg/kg/day ( 5mcg/kg/min)
26. • Dobutamine was stopped at 13 hours of life. Amiodarone
infusion was continued.
• Overall sensorium was poor
• VBG post bicarbonate correction improved.
• No further arrhythmias were present. Amiodarone infusion
tapered to 2.5mg/kg/day
• Parents were requesting to go to higher centre for further
management, hence baby was referred at 36 hours of
admission to MMM chennai.
29. SINUS RHYTHM
• Normal rhythm of the heart
• Characterized by P waves followed by QRS complexes
• Normal PR interval for that age
REFRACTORY PERIOD
This is the time during which another stimulus given to the
muscle (no matter how strong) will not lead to a second action
potential
30. ARRHYTHMIA
• Abnormal electrical activity
• Too fast or too slow
• Regular or irregular
Sinus Arrhythmia:
Physiological variation of heart rate due to respiratory
influence on the autonomic nervous system.
32. NORMAL WAVEFORMS IN ECG
• P wave: Atrial depolarization
• Wave through AV node/ His bundle- isoelectric
• Q wave- Septal depolarization
• R/S wave: Ventricular depolarization
• T wave: Ventricular repolarization
• U wave: Mechanoelectric phenomenon
33. • Normal PR interval for age:
• Short PR interval: WPW preexcitation, Lown-Ganong-levine
Syndrome, Pheochromocytoma, DMD
• Long PR interval: Myocarditis, digitalis toxicity,
hyperkalemia
34. SUPRAVENTRICULAR TACHYCARDIA
• Commonest symptomatic arrhythmia in children and
infants.
• Tachycardia that originates proximal to the bundle of His (
above the ventricular level).
• Usually not a/w hemodynamic compromise- if (+)
- Congenital heart disease
- Cardiomyopathy
Underlying LV
function is impaired
35. EFFECT ON CARDIAC OUTPUT
• Increased HR leads to increased Output.
Further increase
Duration of diastole decreases
Reduction in stroke volume
Decreased Cardiac Output
Impaired coronary perfusion
Increased Oxygen demand
Myocardial dysfunction
CCF
36. • Often asymptomatic, episodic and paroxysmal in young
infants.
- Irritability
- Poor feeding, lethargty
- Breathlesness, palpitations felt by mother
37. ECG CHANGES
HEART RATE No beat to beat variability
Usually > 220/ min in infants
Usually >180/min in children
P WAVES Absent or Abnormal
P R INTERVAL Cannot be determined as P waves
are absent. Short PR in cases of
ectopic atrial tachycardia
R R INTERVAL Often constant
QRS COMPLEX Narrow
38. CHARACTERISTICS ST SVT
HISTORY Gradual Onset
H/O fever, pain,
hemorrhage,
dehydration
Abrupt onset,
cessation
Symptoms of CHF
PHYSICAL EXAM Signs of underlying
cause of ST
Signs of CHF
HEART RATE Usually < 220/ min Usually >220/min
MONITOR Variability in Heart
Rate
Minimally varying rate
with changes I activity
ECG P waves present/
Normal
P waves absent or
abnormal – inverted
in II, III, aVF
CHEST XRAY Usually normal heart
and lungs
Signs of CHF
39. TYPES OF SVT
• Mechanisms that produce SVT are classified as
Automaticity Re- Entry
JET-junctional
Ectopic Tachy
AET- atrial
Ectopic tachy
AVRT-
Atrioventricular
Reentry Tachy
AVNRT-
Atrioventricular
Nodal Reentry Tachy
40. AVRT- ATRIOVENTRICULAR REENTRY TACHY
• Most common type of SVT in children
*Paroxysmal Atrial Tachycardia (PAT)
• Two pathways are involved-
- Av node ( Slow )
- Accessory pathway ( Fast )
41. ORTHODROMIC REENTRANT TACHYCARDIA
• Commonest form of AVRT
• Impulse from atria goes through a close circuit formed by
an accessory pathway
• Direction is through the AV node- antegrade transmission,
and retrograde transmission from the ventricles through the
accessory pathway
42. Normal QRS complex- Antegrade conduction through a
normal AV node (slow)
Inverted P wave following a QRS- retrograde transmission
through the bypass tract
43. ANTEDROMIC REENTRANT TACHYCARDIA
• Less common
• Impulse goes through the faster bypass tract- antegrade
transmission
• Retrograde transmission through the slower AV nodal
pathway
44. Wide QRS complex- Due to antegrade transmission
through the fast bypass tract
Inverted P wave preceeding the QRS complex
45. Normally impulse
generated from the
SA node
Impulse reaches
the AV node
Impulse travels
through the septum
and reaches ventricle
46. In AVRT- acceossory
pathway is present
Impulse can travel
from atria through the
accessory pathway in
antegrade
Impulse can travel in
retrograde direction
Closed circuit-
tachyarrhythmia
47. WOLFF-PARKINSON-WHITE SYNDROME
Accessory pathway (+)
Impulse from SA node
reaches AV node
Impulse from SA node
also goes through the
accessory path-
Reaches ventricle faster
and causes
preexcitation
48. Impulse that travels
through slow pathway
reaches pre excited
ventricles
Gets masked by the
impulse from the
accesory path- so
travels in a retrograde
manner – in the
refractory period
Closed circuit for every
beat
49. ECG CHANGES
• Short PR interval – Preexcited ventricle
• Slow rising R wave due to prolonged ventricular
stimulation- delta wave
• Dominant R wave in V1 lead
50. MANAGEMENT
• Acute Treatment
- Vagal maneuvers
- Adenosine- Drug of choice
Administered as a rapid bolus with saline flush, very short half
life- <5 to 10 sec (needs to reach heart before that)
Transient AV block, slows ventricular rate
CI in AF, VT, Heart block
51.
52. SVT REFRACTORY TO ADENOSINE
• Amiodarone- prolongs the refractory period of AV node,
atria and ventricle
• Used in almost all Supraventricular tachyarrhythmias
• Adverse effects- hypotension, bradycardia
• IV dose- loading of 5mg/kg over 20 minutes followed by
continuous infusion of 5-20mg/kg/day
53. • Procainamide- Slows conduction within myocardium
• Potential adverse effects- hypotension, acute hemodynamic
compromise, prolongation of QT interval
• Hence avoided in young children, infants
• IV dose- 15mg/kg over 30 minutes , followed by continuous
infusion of 10-20mcg/kg/min
54. • Verapamil- Slows AV nodal conduction
• Used in older children
• Causes apnoea, hypotension and cardiovascular collapse
• CI in CCF and WPW
55. • Beta Blockers- In SVT which does not respond to
adenosine and the rhythm is well tolerated
• IV propranolol and IV esmolol are commonly used
• Dose- 0.5 to 1mg/kg/dose
• Esmolol- IV loading of 100 to 500 mcg/kg slow push
followed by 25 to 100mcg/kg/min
Digoxin- Not used routinely- Delay in achieving therapeutic
levels
56. PREVENTION OF RECURRENCE
• Infrequent episodes of SVT without hemodynamic
compromise- observation, taught vagal maneuvers- if not
effective beta or calcium channel blockers can be used
Rationale behind observation- children <5 years outgrow their
SVT and may not require chronic therapy
57. • Choice of drug in infancy
- Propranolol- oral 2to 4mg/kg/day divided in 4 doses
• Older children
- Longer acting atenolol 1 to 2mg/kg/day orally
Older children with adequate LV function- verapamil can be
tried
58. INTERVENTION
• SVT without symptoms and proven WPW
- Evaluated with HOLTER monitor
- Persistent preexcitation are at increased risk for sudden
death- offered Electrophysiological studies (EPS)
<5 Years- Do not need EPS routinely
59. • RFA- Radiofrequency Ablation
>5 years and >15kg
Performed as a part of electrophysiological study
Identification of the accessory pathway and termination
Complications:
- Perforation
- Pericardial effusion, emboli
- Brachial plexus injury
60. • Indications
- WPW syndrome after abortion of sudden cardiac death
- WPW at risk for sudden death
- Recurrent or chronic SVT a/w LV dysfunction
- SVT which doesn’t respond to oral therapy for more than 5
years
61. • Cryoablation
- Catheter based cryoablation
- Short term efficacy> RFA
- Recurrence rate higher
• Surgery
- Repeated failed attempts of RFA
- Underlying cardiac condition requires surgery