Certificate No 7 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Certificate No 7 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Certified Cardiographic Technician

Cardiovascular Credentialing International

11 February 2016

Certificate No 6 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Certificate No 6 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Certified Rhythm Analysis Technician

Cardiovascular Credentialing International

31 December 2015

Certificate No 5 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Certificate No 5 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Registered Congenital Cardiac Sonographer

Cardiovascular Credentialing International

11 February 2016

Certificate No 4 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Certificate No 4 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Registered Cardiovascular Invasive Specialist

Cardiovascular Credentialing International

19 May 2015

Certificate No 3 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Certificate No 3 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Registered Cardiac Sonographer

Cardiovascular Credentialing International

18 May 2015

Certificate No 2 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Certificate No 2 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Registered Diagnostic Cardiac Sonographer

The American Registry For Diagnostic Medical Sonography

21 October 2014

Certificate No 1 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Certificate No 1 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt

Fellowship Society Of Invasive Cardiovascular Professionals

Society Of Invasive Cardiovascular Professionals

October 2016

Malaysia Northern Region First ECG Symposium 2019 Organised By NHAM-Malaysia Society Of Cardiovascular Technologist

Malaysia Northern Region First ECG Symposium 2019 Organised By NHAM-Malaysia Society Of Cardiovascular Technologist

Online Registration Officially Open

1st ECG Symposium 2019

Venue: Hospital Sultanah Bahiyah
Date: 20-21 March 2019

Register online 👇👇👇

https://goo.gl/forms/NHQwIl2HmOk03RMh1

or

QR CODE

MSCVT Member: RM 100
Student: RM 100
Paramedic/Nursing: RM 150
Doctor RM 250

Payment: 👇
NHAM-MSCVT RHB Bank: 2123 4900 0376 10

Reference:👇
ecgsympo

Detail:👇
(Your Name)(Last 4 Digit IC)

📞 Ms. Noraminah Aedrus (012 538 4781)
📞 Mr. Mohd Hafizudin Ishak (017 311 8772)

Register Online 👇👇👇

https://goo.gl/forms/NHQwIl2HmOk03RMh1

or

QR CODE

Collaboration between MSCVT & Unit Penyeliaan PPP Hospital Sutanah Bahiyah.

Jumpa disana!

Today ESC European Heart Rhythm Association EHRA Webinar - Ablation of Ventricular Tachycardias 18 December 2018

 Today Webinar - Ablation of Ventricular Tachycardias 

Learning Objectives

To discuss characteristics of arrhythmogenic substrate for ventricular arrhythmias in ischemic and non-ischemic cardiomyopathies To review the different approaches for catheter ablation of ventricular arrhythmias

Faculty

Professor Jozef Kautzner, FESC Institute For Clin And Exp Medicine Prague, Czech Republic Doctor Frederic Sacher Hopital Cardiologique Du Haut Leveque Bordeaux, France Doctor John Silberbauer Sussex, United Kingdom

Ablation of Ventricular Tachycardias (ischemic and non-ischemic) Tuesday 18 December 2018 from 18:00 to 19:00 Register Now

Grant To Attend European Heart Rhythm Association 2019 Congress. Thank You EHRA. See You In Lisbon, Portugal.

Grant To Attend European Heart Rhythm Association 2019 Congress

Dear Mr. Mohd Taufik We are happy to inform you that one of our Industry Partners has recently offered the funding for grants for a number of cardiologists to attend EHRA Congress 2019. Based on specific criteria, you have been selected for the unique opportunity to attend EHRA 2019 Congress which will take place in Lisbon from 17th to 19th March. What is included in the grant? One travel voucher (flight, economy class, non refundable and non changeable) based on EHRA Congress and hotel accommodation dates. One standard registration fee to be received directly from EHRA. One accommodation voucher - three nights stays (from Saturday 16 to Tuesday 19 March 2019) in one of EHRA appointed hotels.  To avail of this grant, please respond back by Monday 17th of December via your ESC Account here. Once your confirmation of interest is submitted, you will receive more information on further steps. We would like to draw your attention to the rules and processes for this grant programme. The EHRA Congress Team congratulates you on being selected for this grant and we all look forward to welcoming you to EHRA Congress 2019 in Lisbon. If you have any questions or issues, please contact us at ehra-congress@escardio.org With our best wishes, EHRA Congress Team

Introduction From The Blogger: Re-Activation Of The Blog

Introduction From The Blogger

I am a Former Senior Cardiovascular Technologist at Institut Jantung Negara (National Heart Institute of Malaysia) with almost 8 years qualified experience in various cardiovascular invasive and noninvasive procedure. As a graduate in Biomedical Science Degree from National University of Malaysia, Post Graduate Certificate of Cardiovascular and Thoracic Science from IJN College and Professional Certificate Of Cardiovascular Technology from Cardiology Department National Heart Institute Of Malaysia, I have acquainted myself with a range of skills that would allow me to blend with the organizational culture and propel the team to new height of success. Now i am a Staff Cardiac Technician at King Fahd Armed Forces Hospital, Jeddah, Kingdom Of Saudi Arabia starting November 2015 specialized in cardiac device & rhythm management and electrophysiology study.

With a Biomedical Sciences and Cardiovascular Technologist background, I have gained knowledge in health education and medical technology specifically in Cardiovascular and Thoracic Science.  From the courses, assignments and practical that I have completed, I have gained insight in marketing, promotional planning on product, conducting events, providing service on the health benefit, and quality management in health and medical area.

I am also a Registered Diagnostic Cardiac Sonographer (RDCS) from the American Registry for Diagnostic Medical Sonography (ARDMS), Registered Cardiac Sonographer (RCS) from Cardiovascular Credentialing International (CCI), Registered Cardiac Sonographer (RCS) from Cardiovascular Credentialing International (CCI), Registered Cardiac Invasive Specialist (RCIS) from Cardiovascular Credentialing International (CCI), Certified Cardiographic Technician (CCT) from Cardiovascular Credentialing International (CCI) and Certified Rhythm Analysis Technician (CRAT) from Cardiovascular Credentialing International (CCI). This credentialing was recognized by American National Standard Institute (ANSI) with certification of Malaysian Good Clinical Practice (GCP) personnel. I am accepted as Registered Conditional Clinical Physiologist from Clinical Physiologist Registration Board New Zealand. Recently I am accepted as Fellow Society of Invasive Cardiovascular Professional FSICP.

I am a proactive and progressive person involved in Cardiovascular Technology with a goal to improve skills, professionalism and experiences towards the development of new ideas, finding and technologies in Cardiovascular & Thoracic Sciences as well as medical field towards Personal Vision And Mission. Special interest in cardiac device & rhythm management, electrophysiology study, advanced echocardiography includes 2D echo strain imaging, tissue Doppler imaging, 3D echo strain imaging, 3D echocardiography, detail echocardiography for adult congenital heart disease, and ventricular assist device echocardiography assessment and also actively assisting cardiologist in various invasive cardiovascular lab diagnostic and interventional procedure.

Apart from being a proactive learner, I was actively involved in extra-curricular activities inside and outside of campus. I was an Exco of Student Representative Council National University of Malaysia as the representative for my faculty and also Malaysian Society Of Cardiovascular Technologist (MSCVT) committee member. I was the president of several organizations in National University of Malaysia. I have a good leadership and well organized person. I also have a good interest in community services.

My enthusiastic involvement in many activities outside of the academic circle has served me well in nurturing my leadership and communication skills, which are essential to succeed in the working world.

Yours sincerely,

Mohd Farid Bin Mohd Taufik,

Cardiovascular Technologist

King Fahd Armed Forces Hospital Jeddah

Kingdom Of Saudi Arabia

CVT Mohd Farid Bin Mohd Taufik Cardiac Rhythm Management Device Clinic Cardiac Cath Lab King Fahd Armed Forces Hospital Attended Cases Log Book Year 2016 Till August 2017 -New Experiences

CVT Mohd Farid Bin Mohd Taufik

Cardiac Rhythm Management Device Clinic

Cardiac Cath Lab

King Fahd Armed Forces Hospital

Jeddah KSA

Year 2016-August 2017

Attended Cases

Total Collected Cases Till Present

Total Cases 2016

Total Cases 2017 Till August 2017

(Click Image To See Detail)

Anyone interested to have Microsoft Excel format for this Log Book can email me at draser1@yahoo.com

As Promised Cardiac Rhythm Management Device Clinic Log Book Year 2016 Till August 2017
Pacemaker & Device Clinic Services King Fahd Armed Forces Hospital Jeddah

Basic ECG Part III-P Wave & PR Interval

Basic ECG Part III

P Wave & PR Interval

Credit To Dr Rayney Azmi Bin Ali

++Characteristics Of The Normal Sinus P Wave++

Morphology

Smooth contour

Monophasic in lead II

Biphasic in V1

Axis

Normal P wave axis is between 0° and +75°

P waves should be upright in leads I and II, inverted in aVR

Duration

*< 120 ms

Amplitude

*< 2.5 mm in the limb leads,

*< 1.5 mm in the precordial leads

Atrial abnormalities are most easily seen in the inferior leads (II, III and aVF) and lead V1, as the P waves are most prominent in these leads.

The Atrial Waveform-Relationship To The P Wave

*Atrial depolarisation proceeds sequentially from right to left, with the right atrium activated before the left atrium.

*The right and left atrial waveforms summate to form the P wave.

*The first 1/3 of the P wave corresponds to right atrial activation, the final 1/3 corresponds to left atrial activation; the middle 1/3 is a combination of the two.

*In most leads (e.g. lead II), the right and left atrial waveforms move in the same direction, forming a monophasic P wave.

*However, in lead V1 the right and left atrial waveforms move in opposite directions. This produces a biphasic P wave with the initial positive deflection corresponding to right atrial activation and the subsequent negative deflection denoting left atrial activation.

*This separation of right and left atrial electrical forces in lead V1 means that abnormalities affecting each individual atrial waveform can be discerned in this lead. Elsewhere, the overall shape of the P wave is used to infer the atrial abnormality.

First Degree AV Block Vs Second Degree Mobitz Type I (Wenckebach)

++First Degree AV Block++

*PR interval > 200ms (five small squares)
*‘Marked’ first degree block if PR interval > 300ms

Causes of First Degree AV Block

*Increased vagal tone

*Athletic training

*Inferior MI

*Mitral valve surgery

*Myocarditis (e.g. Lyme disease)

*Electrolyte disturbances (e.g. Hyperkalaemia)

*AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone)

*May be a normal variant

++Second Degree Mobitz Type I (Wenckebach)++

Definition Of Wenckebach Phenomenon:

*Progressive prolongation of the PR interval culminating in a non-conducted P wave.

*The PR interval is longest immediately before the dropped beat.

*The PR interval is shortest immediately after the dropped beat.

Other Features Of Second Degree Mobitz Type I

*The P-P interval remains relatively constant.

*The greatest increase in PR interval duration is typically between the first and second beats of the cycle.

*The R-R interval progressively shortens with each beat of the cycle.

*The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4.

Mechanism 

*Mobitz I is usually due to reversible conduction lock at the level of the AV node.

*Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct an impulse.

*This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly (i.e. producing a Mobitz II block).

Causes of Wenckebach Phenomenon

*Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone

*Increased vagal tone (e.g. athletes)

*Inferior MI

*Myocarditis

*Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)

Clinical Significance of AV Block: Second Degree, Mobitz I

*Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance and with low risk of progression to third degree heart block.

*Asymptomatic patients do not require treatment.

*Symptomatic patients usually respond to atropine.

*Permanent pacing is rarely required.

++Second Degree Mobitz Type II++

AV Block: 2nd degree, Mobitz II Overview

*Intermittent non-conducted P waves without progressive prolongation of the PR interval (compare this to Mobitz I).

*The PR interval in the conducted beats remains constant.

*The P waves ‘march through’ at a constant rate.

*The RR interval surrounding the dropped beats is an exact multiple of the preceding RR interval (e.g. double the preceding RR interval for a single dropped beat, treble for two dropped beats, etc)

Mechanism

*Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node).

*While Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs, reversible ischaemia), Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis).

*Patients typically have a pre-existing LBBB or bifascicular block, and the 2nd degree AV block is produced by intermittent failure of the remaining fascicle (“bilateral bundle-branch block”).

*In around 75% of cases, the conduction block is located distal to the Bundle of His, producing broad QRS complexes.

*In the remaining 25% of cases, the conduction block is located within the His Bundle itself, producing narrow QRS complexes.

*Unlike Mobitz I, which is produced by progressive fatigue of the AV nodal cells, Mobitz II is an “all or nothing” phenomenon whereby the His-Purkinje cells suddenly and unexpectedly fail to conduct a supraventricular impulse.

*There may be no pattern to the conduction blockade, or alternatively there may be a fixed relationship between the P waves and QRS complexes, e.g. 2:1 block, 3:1 block.

Causes of Mobitz II

*Anterior MI (due to septal infarction with necrosis of the bundle branches).

*Idiopathic fibrosis of the conducting system (Lenegre’s or Lev’s disease).

*Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair)

*Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease).

*Autoimmune (SLE, systemic sclerosis).

*Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis).

*Hyperkalaemia.

*Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.

Clinical Significance

*Mobitz II is much more likely than Mobitz I to be associated with haemodynamic compromise, severe bradycardia and progression to 3rd degree heart block.

*Onset of haemodynamic instability may be sudden and unexpected, causing syncope (Stokes-Adams attacks) or sudden cardiac death.

*The risk of asystole is around 35% per year.

*Mobitz II mandates immediate admission for cardiac monitoring, backup temporary pacing and ultimately insertion of a permanent pacemaker.

Second Degree AV Block Vs SVT

++AV Block:Second Degree, “Fixed Ratio” Blocks++

Fixed Ratio AV blocks

*Second degree heart block with a fixed ratio of P waves: QRS complexes (e.g. 2:1, 3:1, 4:1).

*Fixed ratio blocks can be the result of either Mobitz I or Mobitz II conduction.

Mobitz I or II?

*It is not always possible to determine the type of conduction disturbance producing a fixed ratio block, although clues may be present.

*Mobitz I conduction is more likely to produce narrow QRS complexes, as the block is located at the level of the AV node. This type of fixed ratio block tends to improve with atropine and has an overall more benign prognosis.

*Mobitz II conduction typically produces broad QRS complexes, as it usually occurs in the context of pre-existing LBBB or bifascicular block. This type of fixed ratio block tends to worsen with atropine and is more likely to progress to 3rd degree heart block or asystole.

*However, this distinction is not infallible. In approximately 25% of cases of Mobitz II, the block is located in the Bundle of His, producing a narrow QRS complex. Furthermore, Mobitz I may occur in the presence of a pre-existing bundle branch block or interventricular conduction delay, producing a broad QRS complex.

*The only way to be certain is to observe the patient for a period of time (e.g. watch the cardiac monitor, print a long rhythm strip, take serial ECGs) and observe what happens to the PR intervals. Often, periods of 2:1 or 3:1 block will be interspersed with more characteristic Wenckebach sequences or runs of Mobitz II.

++High Grade AV Block++

High Grade AV Block Definition

*Second degree heart block with a P:QRS ratio of 3:1 or higher, producing an extremely slow ventricular rate.

*Unlike 3rd degree heart block there is still some relationship between the P waves and the QRS complexes.

*High-grade AV block may result from either Mobitz I or Mobitz II AV block.

++AV Block: Third Degree (Complete Heart Block)++

Complete Heart Block (CHB) Overview

*In complete heart block, there is complete absence of AV conduction – none of the supraventricular impulses are conducted to the ventricles.

*Perfusing rhythm is maintained by a junctional or ventricular escape rhythm. Alternatively, the patient may suffer ventricular standstill leading to syncope (if self-terminating) or sudden cardiac death (if prolonged).

*Typically the patient will have severe bradycardia with independent atrial and ventricular rates.

Mechanism

*Complete heart block is essentially the end point of either Mobitz I or Mobitz II AV block.

*It may be due to progressive fatigue of AV nodal cells as per Mobitz I (e.g. secondary to increased vagal tone in the acute phase of an inferior MI).

*Alternatively, it may be due to sudden onset of complete conduction failure throughout the His-Purkinje system, as per Mobitz II (e.g. secondary to septal infarction in acute anterior MI).

*The former is more likely to respond to atropine and has a better overall prognosis.

Causes Of Complete Heart Block

The causes are the same as for Mobitz I and Mobitz II second degree heart block. The most important aetiologies are:

*Inferior myocardial infarction

*AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-blockers, digoxin)

*Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s disease)

Clinical Significance

*Patients with third degree heart block are at high risk of ventricular standstill and sudden cardiac death.

*They require urgent admission for cardiac monitoring, backup temporary pacing and usually insertion of a permanent pacemaker.

Complete Heart Block Should Not Be Confused With

*High grade AV block: A type of severe second degree heart block with a very slow ventricular rate but still some evidence of occasional AV conduction.

*AV dissociation: This term indicates only the occurrence of independent atrial and ventricular contractions and may be caused by entities other than complete heart block (e.g. “interference-dissociation” due to the presence of a ventricular rhythm such as AIVR or VT).

PAC Vs Junctional Rhythm

Inverted P Wave

*P-wave inversion in the inferior leads indicates a non-sinus origin of the P waves.

*When the PR interval is < 120 ms, the origin is in the AV junction (e.g. accelerated junctional rhythm).

*When the PR interval is ≥ 120 ms, the origin is within the atria (e.g. ectopic atrial rhythm).

Multiple P Wave Morphologies

*The presence of multiple P wave morphologies indicates multiple ectopic pacemakers within the atria and/or AV junction.

*If ≥ 3 different P wave morphologies are seen, then multifocal atrial rhythm is diagnosed.

*If ≥ 3 different P wave morphologies are seen and the rate is ≥ 100, then multifocal atrial tachycardia (MAT) is diagnosed.

P Pulmonale

Right Atrial Enlargement-Lead II

*In right atrial enlargement, right atrial depolarisation lasts longer than normal and its waveform extends to the end of left atrial depolarisation.

*Although the amplitude of the right atrial depolarisation current remains unchanged, its peak now falls on top of that of the left atrial depolarisation wave.

*The combination of these two waveforms produces a P waves that is taller than normal (> 2.5 mm), although the width remains unchanged (< 120 ms).

Right Atrial Enlargement-Lead V1

*Right atrial enlargement causes increased height (> 1.5mm) in V1 of the initial positive deflection of the P wave.

P Mitrale

Left Atrial Enlargement-Lead II

*In left atrial enlargement, left atrial depolarisation lasts longer than normal but its amplitude remains unchanged.

*Therefore, the height of the resultant P wave remains within normal limits but its duration is longer than 120 ms.

*A notch (broken line) near its peak may or may not be present (“P mitrale”).

Left Atrial Enlargement-Lead V1

Left atrial enlargement causes widening (> 40ms wide) and deepening (> 1mm deep) in V1 of the terminal negative portion of the P wave.

Biatrial Enlargement

*Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.

*The spectrum of P-wave changes in leads II and V1 with right, left and bi-atrial enlargement is summarised in the following diagram.

*Common P Wave Abnormalities.

Common P Wave Abnormalities

*P mitrale (bifid P waves), seen with left atrial enlargement.

*P pulmonale (peaked P waves), seen with right atrial enlargement.

*P wave inversion, seen with ectopic atrial and junctional rhythms.

*Variable P wave morphology, seen in multifocal atrial rhythms.

Wolff-Parkinson-White Syndrome Pre Excitation Atrial Fibrillation

Wolff-Parkinson-White Syndrome With Delta Wave

++PR Interval++

*The PR interval is the time from the onset of the P wave to the start of the QRS complex.

*It reflects conduction through the AV node.

*The normal PR interval is between 120 – 200 ms duration (three to five small squares).

*If the PR interval is > 200 ms, first degree heart block is said to be present.

*PR interval < 120 ms suggests pre-excitation (the presence of an accessory pathway between the atria and ventricles) or AV nodal (junctional) rhythm.

*Type Of AV Block has been describe above.

Short PR interval (<120ms)

A short PR interval is seen with:

*Preexcitation syndromes.

*AV nodal (junctional) rhythm.

Wolff-Parkinson-White (WPW) And Lown-Ganong-Levine (LGL) Syndromes.

*These involve the presence of an accessory pathway connecting the atria and ventricles.

*The accessory pathway conducts impulses faster than normal, producing a short PR interval.

*The accessory pathway also acts as an anatomical re-entry circuit, making patients susceptible to re-entry tachyarrhythmias.

*Patients present with episodes of paroxsymal supraventricular tachycardia (SVT), specifically atrioventricular re-entry tachycardia (AVRT), and characteristic features on the resting 12-lead ECG.

Wolff-Parkinson-White Syndrome

*The characteristic features of Wolff-Parkinson-White syndrome are a short PR interval, broad QRS and a slurred upstroke to the QRS complex, the delta wave.

*Short PR (<120ms), broad QRS and delta waves in WPW syndrome

Wolff -Parkinson- White Syndrome Cases Usually

*ECG pattern depends on where the accessory pathway inserts.

Classically:

*Short PR interval <120 msecs.

*QRS > 100msecs.

*Delta wave-slurred upstroke at beginning of QRS.

Different insertions:

*Normal QRS if pathway inserts into infranodal conduction tissue just below AV node

*Grossly wide and abnormal QRS if pathway inserts into non-conduction tissue.

Key Management Points For WPW

*A heart rate ≥ 200 should make you think of a pre-excitation syndrome.

*Narrow complex SVT is treated identically to non-WPW SVT.

*Don’t try and be clever with drugs in broad complex tachycardias and WPW.

*Using AV nodal blockers in WPW and AF can result in 1:1 conduction to the ventricles.

*This is also know as Ventricular Fibrillation.

*Just shut-up + DC cardiovert them.

Lown-Ganong-Levine Syndrome

*The features of LGL syndrome are a very short PR interval with normal P waves and QRS complexes and absent delta waves.

*Short PR interval with normal QRS complexes in LGL syndrome

AV Nodal (Junctional) Rhythm

*Junctional rhythms are narrow complex, regular rhythms arising from the AV node.

*P waves are either absent or abnormal (e.g. inverted) with a short PR interval (retrograde P waves).