Posted in Brugada syndrome, Cardiology - Electrophysiology -Pacemaker, early repolarisation syndrome, tagged brugada syndrome, consensus conference brugada syndrome, how to follow up brugada pattern ecg, suspected brugada syndrome on April 26, 2015| Leave a Comment »
Have you felt like this query any time in your office ?
If “Yes” is your answer, then you are not alone .There was a unique conference that took place in 2010 to answer the same query in Rome , Italy on behalf of Italian cardiology society , where this entity is researched more than any other place.Its worth going through this.
Reference
Posted in Uncategorized on April 8, 2015| Leave a Comment »
During exercise stress test , systolic pressures should raise at least by 20-40mmhg.(Max 60 mm from baseline ) Diastolic BP will remain at baseline or show a marginal elevation or even a miniscule fall.This is primarily due to increased cardiac out-put , mediated by demand and dilatation of musculature in exercising muscle.
If the systolic BP falls or does not raise during exercise , it implies either poor LV function , vascular insufficiency or autonomic dysfunction.
If there is a fall of > 20mm , even in the first stage, accompanied by chest discomfort or giddiness with ECG changes ,it could be an ominous sign of serious left main or a tight proximal LAD disease and test should be terminated immediately.
Paradoxically , If BP raises more then 200 at any time we call it hypertensive response and may be a risk factor for future onset systemic HT or even a stroke. ( Stress test not only help us detect ischemia of heart ,it also can reveal how the vascular system would handle and adopt to increased cardiac output at time of hemodynamic demands)
Physical de-conditioning is an important cause for hypertensive response , as the entire vascular system lacks dynamism (Vascular tone ) , a precursor for hypertension, endothelial dysfunction and cardio vascular events..
Posted in Cardiology - Electrophysiology -Pacemaker, Pace maker Tips and tricks, tagged atrial lead issues in ddd pacing, best pacemaker tips and tricks, capture failure pacemaker, dc shock in pacing rhythm, ddd vs vvi pacing, intermittent pacemaker spikes, pacemaker syndrome, pacemaker trouble shooting best algorhythm, random pacemaker spikes, sensing and oversensing, sensing vs pacing failure on March 22, 2015| Leave a Comment »
We have been taught right from first year cardiology residency how to trouble shoot a pacemaker .It has been a real complex thing for us. Now looking back ,all the troubles we took to understand seems to be redundant.Here is a summary of my thought process on the issue. It can be approached with reference to time, symptoms and ECG features. With due respects to all those brainy hardworking EP experts , I have taken few academic liberties!
Timing
Symptoms
* Syncope can be unrelated to pacemaker but always consider them electrical unless proved otherwise . Few patients may continue to have significant symptoms in-spite of normal pacemaker parameters. This would mean , the original symptom for which pacemaker was put is not related to the Brady-arrhythmia .It could suggest alternative hemodynamic explanation like vaso-depressive component of vagal syncope ,autonomic dysfunction , orthostatic intolerance or a coexisting neurological /systemic condition.
**Never forget syncope is not an exclusive symptom of bradycardia .A new onset tachycardia , which is either a part of brady- tachy syndrome or separate arrhythmia can continue to provoke the symptom.
Gross ECG findings
Bradycardia /Often implies back to original rhythm – Indicates real trouble . Since ,in a paced patient HR cannot be less than programmed rate of 70.
Tachycardia -No spike.( Not to worry ?) A common situation if the original indication was sinus node dysfunction . Many of them are in own sinus rhythm or AF . Just ensure spikes reappear when the rate falls below 70 . If the rate never goes down , what to do ? Try a carotid massage or observe a nocturnal ECG or call analyst and increase the rate to document pacing . (In DDD mode we have a rare PM mediated re-entrant tachycardia , which is mainly used to grill cardiology fellows in their board exams with all those PVARP stuff !)
Simple pauses – Any pause more than the pacing interval is a definite concern .
Spikes more than QRS – Indicate capture failure.
No spikes (Can be so benign to ultimate danger )
* Anatomical issues like lead dislodgement , fracture , compression , perforation are to be ruled out in every pateitn with intermittent capture or failure .This is done by combinations of imaging as well physiological assessment.Dislodgement must be visualized .The term micro dislodgement may not exist.
Other Investigations
Pacemaker analysis
Management
The principle of management are simple. Few logical questions ,
Technical jargon like under sensing , over sensing or no sensing , fusion beats , micro dis-lodgement etc are important for academic reasons . We may talk any thing , realistically , what the ventricle want is a non stop heart beat every second or so !
Emergency
Bradycardia – Insert a temporary pacemaker /Call the analyst /Inform the electrophysiologist /Senior cardiologists /(Please realise , some fellows can be better than the personnel mentioned above in tackling emergencies !)
Tachycardia : Native or machine induced ?
Native – Mostly safe , Ignore or treat with drugs.
Machine induced :(very rare) Switch of the pacemaker . No off switch available as in a mobile phone ? *What to do ? if unclear about the whereabouts tachycardia origin . If hemodynamically unstable no harm in shocking .Nothing will happen .Call the EP guys on hot line and decide.
Elective symptom guided.
** While the above principles apply for both single and dual chamber pacemakers , the later doubles our thinking burden . While atrial tracking is a great technological advancement , what to do with those sensed event can be really tricky .The response of ventricles and the AV intervals can be tentative at times. Cross talks from unexpected atrial and ventricular arrhythmia can occur. Further , mechanical atrial lead issues are far more common . When confronted with recurrent atrial lead related problems , one simple solution is silently convert the mode to single chamber VVI mode.
Final message
Pacemaker trouble shooting appears complex at the first look .It’s all common sense.Thinking with simple state of mind and being clear about the intended goal is vital. Electrical intricacies are tough to understand but most situations do not require them. However ,If the initial indication was for complete heart block one has to be very alert.
Principles of medicine argue us to make an exact diagnosis before treating . But,realise this is rarely possible or even desirable in emergency .Curiously , most pacemaker troubles can be solved successfully without making a proper trouble shoot !
If we can summarize in one line , a prompt emergency back up temporary pacemaker insertion is key to management most of the serious pacemaker related problems.It ,not only tackles the emergency , buys time till we decode the real problem . . . if we wish to !
Related article.
Role of magnet application in pacemaker trouble shoot
Posted in Cardiology - Electrophysiology -Pacemaker, WPW syndrome, tagged wide qrs irregualr tachycardia, wide qrs regular vs irregular tachycardia on March 15, 2015| Leave a Comment »
We know , any wide QRS tachycardia would argue us to make a default diagnosis of VT.But, one has to be extremely cautious to apply this rule if wide QRS tachycardia shows significant irregularity in RR interval .
All classical VTs are fairly regular tachycardia (Note the key words , fair and regular) . Small cycle length variations are observed in VT, but they are usually not discernible in surface ECG.
There are no practical rules .A well appreciable irregularity in RR interval will seriously question the diagnosis of classical VT. To make an another statement, most of the irregular wide QRS tachycardias infact turns out to be atrial fibrillation with some form distal widening mechanism .(Preexisting blocks, or rate dependent or antidromic conduction through accessory pathways)
However , irregularity is still possible during VT .(May be less than 10% of times)
When can VT can be irregular ?
Final message
Statistically , as well as realistically , the commonest cause for any highly irregular tachycardia turns out to be AF , whether QRS is wide or narrow !
Posted in Cardiology - Electrophysiology -Pacemaker, ICD, tagged dual vs single chamber ICD, Indication for ICD, Which ICD to choose on March 7, 2015| Leave a Comment »
ICDs are primarily life saving devices.Whether single or dual chamber it does this function effectively.They will also take care of bradycardia by default back up pacing .For most indications single chamber ICDs are good enough.
My professor used to tell us , dual lead means , dual expertise , dual cost , dual caution and dual set of complication . One should avoid it whenever possible. Make things as simple as it could be , without compromising the main goal (Here prevention of SCD) . The incidence of inappropriate shocks being lesser with dual chamber ICD has not been truly realised in real world scenario.
Recent studies tend to give credence to this perception .(Peterson JAMA 2013)
Dual Chamber ICDs may have an edge only in few situations .
Reference.
Posted in Cardiology - Electrophysiology -Pacemaker, RBBB/LBBB, tagged bundle branch reentry, eelctrophysiology, electrophysiology, ers pattern, moes theory, rentry mechanism, sloe conduction and reentry, theories on genesis of cardiac arrhythmias on February 12, 2015| Leave a Comment »
In the last few decades we have understood a major concept in the genesis of cardiac arrhythmia.Slowing in the propagation of cardiac impulse is a key trigger to precipitate a reentry circuit and initiate a tachy- arrhythmia.Still , many conditions like first degree AV block, chronic RBBB or even LBBB are benign entities as along as the heart is structurally normal .They seem never increase the incidence or life time risk of cardiac arrhythmia . Longevity is unaffected.( Or do we assume many things ?)
How is this possible ? or is the theory of slow conduction triggering reentry is flawed ?
Think again . . . if these patients who later on develop a structural heart disease , with an episode of ACS , myocardial or valvular disease, the original slow conduction substrates these people were harboring , will it become important ?
Surprisingly , we have no answers in literature.When Haissaguerre et al found preexisting ERS pattern could be a trigger for primary VF in case they develop ACS , he opened up a huge debate as it involved converting a vast number of normal population electrically anxious.
Now ,is it possible the so called benign blocks of heart like first degree AV blocks , RBBB , LAHBa , would be important at times of ACS and possibly make them prone for for primary ischemic arrhythmia .
Is bundle branch re-entry possible in structurally normal heart ?
We need answers. Some one , (Any EP fellow) somewhere could take up the issue and enlighten us !
Posted in Cardiology - Electrophysiology -Pacemaker, ICD -Tips and Tricks, ICD and Pacemakers, tagged aicd mirowski, boston scientific icd extedended life, el icd dynogen inogen, icd indication, life of icd, madit study icd on February 10, 2015| Leave a Comment »
ICDs are one of revolutionary devices , invented last century that can defy “death & fate” in high risk cardiac patients who are threatened with ventricular tachycardia or fibrillation .A decade long hard work by Mirowski and team from John Hopkins culminated in the dramatic the first AICD implant in 198o. ( In my opinion, this medical invention can be compared to an event of such significance as moon landing by Armstrong and team ! ) Ironically , in the last decade such a revolutionary device was sort of misused and thousands of devices were explanted for inappropriate indications.
Fortunately , better sense prevailed recently .The indications are getting refined. I am sure ICD will go a long way in prevention of both expected and unexpected sudden electrical deaths .We are into the 4th decade of its evolution.While the electrical circuitry has been mastered , power supply remains an issue as they require continuous power supply like a mobile phone. Current technology allows about 6-8 years of battery life.
Now , Boston scientific has come out with new technology which make its battery life extend by 100% to 12 years. It is a major break through , expected to evolve further until probably we have rechargeable batteries or biological power sources .Stretching a wild thought , the days couldn’t be far off when the smart phones which are omnipresent in every human-being , could not only power the ICD remotely and control it too !
Indications (ESC/AHA 2012)
CAD
Non ischemic structural disease ( Idiopathic DCM, ARVD etc)
Primary electrical disease
Reference
Link to Product manual form Boston scientific.
Posted in Uncategorized, tagged mechansim of systolic murmur in pulmonary arterial hypertension ?, pulmonary hypertension on February 6, 2015| 2 Comments »
A short systolic murmur over pulmonary area (ie Left second inter coastal space ) is listed among 6 other auscultatory feature of pulmonary arterial hypertension.Though it is an accepted sign many would question the existence of such a murmur or its relevance in PHT.
Why does it occur ?
Acoustics principle tells us whenever velocity of blood flow exceeds a critical point(Raynolds number*) in a specific anatomical territory , a turbulent zone is created and a murmur could be generated .This is why many physiological situations like pregnancy, anemia, and some benign outflow murmurs occur.
In pulmonary hypertension , three things are thought to contribute for the murmur generation
Reference
* Reynolds number is a way to predict under ideal conditions when turbulence will occur. The equation for Reynolds number is:
(Where v = mean velocity, D = vessel diameter, ρ = blood density, and η = blood viscosity )
Posted in Uncategorized, tagged modern coronary hemodynamics on January 31, 2015| 1 Comment »
We know,management of STEMI is a race against time.It’s rather a group race run by the patient, his close relatives / associates , the ambulance driver, the ER physician, cath lab staff and finally the treating cardiologist .While the race is on , continuous monitoring and critical decisions are made.
Every minute gone could be a missed opportunity. While a patient is being moved to the hospital, a decision is to be taken whether its going to be primary PCI or lysis or combination of both.
Now,In India, as we embrace the quirky world of medical insurance and glamor based medicine , we have one more participant in this race of human life! The coronary flow dynamics in STEMI appears to be determined not only by thrombus load the residual plaque but also by the quantum, type and brand of insurance the patient is blessed with !
I wish , one could hear the silent howls made by the myocardium under distress even as their loved ones are anxiously waiting for insurance clearance from the myocardial reperfusion centers located in the far away back offices of urban metros !
Things won’t stop with that. Once the PCI is on,and the cardiac team is confronted with a multi-vessel CAD ,wondering which is true culprit ?, whether to consider multi-vessel stenting or early CABG . Meanwhile the cath lab liaison officer would desperately struggle to call the insurance guys again and upgrade the request to a newer therapeutic strategy !
Life was simple for every one till recently , when we would treat thousands of MI patients with conventional modality with a well proven reduction in mortality , comparable to the current bests .The concept of primary PCI has made things artificially complex without adding on to significant advantage except in some complicated subsets.
I still keep wondering , achieving a near TIMI -3 flow in a timely fashion by thrombolysis in CCU will far exceed the hype of documented TIMI 3 flow in cath lab in terms of absolute number and of course favorable outcome .Please realise acute myocardial salvage requires a minimum of TIMI 2 and not TIMI 3 flow !
Posted in Uncategorized on January 31, 2015| Leave a Comment »
Stent thrombosis is a dreaded complication as the number of PCIs are increasing in exponential fashion.The key issue is to take care of the stented segment till it gets fully endothleised. We have excellent , time tested dual anti-platelet protocol to take care of this . Still , they are not infallible . ARC has classified stent thrombosis with reference to the timing of implanting the stent .
The funny aspect of this classification is , it hides a fact , whenever a stent concludes suddenly it is acute for that patient and his myocardium . So in a given patient who presents with ACS every stent thrombosis is acute. Of course , chronic thrombotic process can occur in few and present as as CTOs within the stent . Generally stent thrombosis is considered resistant to lysis . This more on our perception than on sound scientific data. Every cardiologist would have experienced at least few cases of acute stent occlusion that had been successfully lysed.
Underlying mechanism of acute stent thrombosis.
The single important cause for stent thrombosis is not primarily hemo-rheological but related to the some technical insufficiency at the time of stent deployment (Apart from poor compliance of anti platelet agents )
FInal message
Though , it is risky to rely on lysis alone it is always worth a try . Lysis is easily available and can be instantly administered without a need of special expertise . Few lives can be saved while one ponders over shifting the patient to a bigger center. Pharmaco-invasive approach can be perfect for this situation.
And now , a provocative comment
Experience suggest , It may be wise , even if cath lab is available on site or in the vicinity , the option of thrombolysis is to be considered first for patients with suspected acute stent thrombosis , if the patient is otherwise stable .
References 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722500/
Dr.S.Venkatesan MD 