No procedure is impossible in medicine . . . but it should be useful for the patient !

//
No procedure is impossible in medicine . . . but it should be useful for the patient !

//
Posted in Atrial fibrillation, Cardiology - Electrophysiology -Pacemaker, rheumatic heart disease | Tagged maangement of af, maze corridor surgery in af and rhd, ptmc plus rf ablation of atria, pulmonary vien isolation rheumatic af is useless, rf ablation in rhd, RF ablation in rheumatic mitral stenosis, surgical la ablaton for atria fibrillation, therapeutics in atrial fibrillation | Leave a Comment »
Normal left atrial (LA) volume is about 22ml/sq.meter body surfacearea at all ages.Maximum LA volume in physiology is about 46ml in females and 56 ml in males( Average 35 ml)
LV stroke volume for each beat is about 70 ml . . . so where does the remaining 35ml come from ?
Answer .
It is logical to assume about 35 ml of fresh blood from 4 pulmonary vein* rushes into LV with every diastolic cycle .It never stays in LA .It just uses LA as a transit route ,
*In diastole the four PVs,LA and LV all act like one single chamber .
Is this reasoning correct ?.
If we believe the continuity equation this explanation is correct . However still what we need to know the fate of residual LV volume (End systolic LV volume which is also about 35 ml that would be in queue for ejection into Aorta for the next beat !)
Further , we know the LV end systolic volume is not constant .During exertion it can reach negligible levels (<10 ml) .At times of vigorous contractions it can touch near zero as well . Then , It become vital for the pulmonary venous reservoir to be act as a major donor for LV blood volume for every ensuing beat.
If the hemodynamics of pulmonary vein LA interface is tricky even in physiology , one can imagine the complexities if the LV diastolic function and left atrial compliance is affected
Debit and credits of LV end -diastolic volume .
Let us assume LVEDV is about 1o5 ml .LA blood volume is roughly one third of LV volume .For every beat equal amounts of fresh blood from pulmonary vein . These two (LA+PV) adds to the residual blood in LV to make LVEDV 105 ml . From this 70 ml is ejected as stroke volume leaving behind 35 ml.

Image template from http://www.cvphysiology.com
Further questions
LA Chamber volume and blood volume need not be same .What I struggle to understand is , total anatomical LA volume measures 35ml , while the amount of blood it is supposed to hold is also about the same .Does it mean the LA is completely filled with blood . . . air tight !
Will the LA compliance make it accommodate twice or thrice the blood volume during exercise ?
What is quantum of residual end diastolic LA volume ?
Reference.(Normal LV and LA volumes )
Posted in cardiac cycle, cardiac physiology, cardiac volume, Cardiology -Hemodynamics, Cardiology -unresolved questions | Tagged cardiac cycle, componets of LV stroke volume, end systolic lv volume, la volume vs lv volume, relationship between la volume and lv volume | Leave a Comment »
Obesity is a major cardio vascular risk factor.We earnestly believe this by evidence from Framingham and other studies.However , epidemiological truths can be dissociated from individuals .
We now understand some of the obese patients fare better in CHF outcomes apparently because of the obesity ! Even patients who undergo PCI show some benefits.This concept is being proved in large data base of > 200,00 patients.
Possible mechanisms
The lay man’s logic may apply (Science hidden somewhere !) Obese persons have basically a large heart with better cardiac reserve and muscle mass .These hearts are pre-conditioned to extra burden of MVO2 in it’s life time . So it is able to tackle hypoxia better, takes more time to get fully exhausted .After all heart can consume fatty acids for it’s energy requirement.
Adipose tissue may also secrete favorable anti-inflammatory chemicals , though majority of adipocytokines are detrimental except adiponectin .Paradoxically the tumor necrosis factor TNF (Same as cachectin or Interleukin 6) is less in obese patients .
Reference
Reference
The landmark Lancet article that first raised the question of obesity paradox
http://www.ncbi.nlm.nih.gov/pubmed/16920472
http://care.diabetesjournals.org/content/36/Supplement_2/S282.full.pdf+html
Counter to the concept
http://science.howstuffworks.com/life/human-biology/obesity-paradox.htm/printable
Obesity paradox applies in stroke too ! This study (TEMPIS) from Berlin Germany suggest controversially though
Posted in cardiac failure, cardiac physiology | Tagged adipoctokines, adiponectin, Gross obesity, lipids and heart, obesity and tumor necrois factor, obesity paradox, paradox in cardiology, smokers paradox | Leave a Comment »
Pacemaker lead implantation is basically a blind procedure .We are supposed to pace the RV apex . It is akin to anchor a ship in the sea bed. Screwing leads are preferred in permanent pacing ,but tined leads have few unique advantages as well .
Can we combine the advantage of both ?
It is believed displacements are more common with tined leads . May be yes . . . or is it really so ?
It is not the tines or screws that is going to determine the early displacement , rather , it is the expertise , commitment and the time spent during the implantation that matters . I have witnessed equal number of early lead dislodgement in both .
One issue often goes unreported is that , when screwing lead is used operator is subconsciously complacent.While cardiologists who implant tined lead is more cautious , make sure it is well trapped in RV.
Screwing leads.
Tined leads
What does experienced cardiologists say ?
Cardiologists before the era of EPs were using only tined leads without any major hitch . I know electrophysiologists rarely use tined leads now . In our institute , with a cumulative experience of over 3000 pacemakers over 30 years( 99% are with tined leads ) , we have no reason to believe they are vastly superior technique.
However there are few definite Indication for screwing lead
* Note all atrial based pacing are screw based as atria lack trabeculae.
A suggestion
Final message
I would believe ,there is no major difference in both short and long term outcome between these two system of leads.Each has it’s own advantage.
After thought
Why can’t we accrue the benefits of both ? I think we have good scientific reason to request the pacemaker industry to design a lead which can have both tines and screws to provide double safety .Simple isn’t ?
Posted in Cardiology - Electrophysiology -Pacemaker, Cardiology Innovations, Pace maker Tips and tricks | Tagged advantage of tine over screwing lead, anchoring a lead in rv apex, combined tine and screw leads, inter trabecualr screwing, pacemaker lead, rv apex and sea bed, rv pacing lead acute dislodgement, tine vs screw, tips and tricks in pacemaker lead, trabecular screwing of pace amker lead | 2 Comments »
Cardiologists are not single organ specialists . They are supposed to be sincere guardians of the the entire vascular system .Sexual dysfunction in males is almost synonymous with erectile dysfunction(ED) .The male sex organ is equally dynamic organ like the heart . It demands a sudden gush of blood to the tune of 500 ml during complete erection .This conveys an important message . The penile macro and micro vasculature is as important as coronary mIcrovascular bed. Atherosclerois of LAD can be as common as atherosclerosis of pudendal artery .It can precede or follow the coronary lesion. Penile insufficiency is a early marker of endothelial dysfunction. All patients with CAD should be screened for ED and vice versa.
This is not a sexual intrusion in academics , but I am sure , a sustained erection that completes a normal sexual act may very well rule out a proximal LAD lesion 99 % of times .
Do you know , > 7 Mets on a tread mill will rule out a significant left main disease with high degree of accuracy ! Sexual acts require more than that (One may do a study on this !)
There has been some interesting guidelines for managing issue of sexual dysfunction in CAD. .Princeton consensus conference is the famous one.
References
Posted in cardiology -Sexual health, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs) | Tagged erectile dysfunction in cad, princeton consenus conference 2 3, sexual dysfunction in cardiolgy | Leave a Comment »
While many of us are preoccupied with wires and balloons ,( coronary myopia ! ) , our radiology colleagues are making rapid strides . Let us spend some time to understand how the myocardial segments are inflicted the final insult . We need to realize , there is a pattern to this myocardial end game of scarring and fibrosis.
MRI is the gold standard to assess the myocardial architecture . It has a role in both assessing the anatomy , function , perfusion and viability .
Why is scar localisation and Quantification important ?
Apart from differentiating various cardiomyopathies it has few clinical implication .
Posted in Cardiac MRI, Cardiology -unresolved questions, myocardial disease | Tagged cardiac mri, demri, epicardial scars, how to differentiate ischemic from non ischemic dcm, late gadolinium enhancement, lge gadolinium, mid myocardial scar, myocardial scar Imaging, scar location within myocardium, subendocardial scars | Leave a Comment »
I know ,there is a VSD out there ! but I am unable to get the gradient across it.This situation can be quiet common .The reasons could be technical, anatomical or hemodynamic.
As a rule , if we hear a pan-systolic murmur clinically , one must be able to catch a good Doppler spectrum somewhere by echocardiography . However , If the murmur is restricted to early or mid to late systole, VSD jet is often attenuated in echocardiography .
In the following situations , VSD jets may not record a distinctive Doppler spectra. Invariably the velocity is low , spectrum is short, less intense , lacks good shape and borders are hazy !
What is inference ?
Doppler spectrum will help detect small VSDs and color doppler will not miss even a tiny VSD.Doppler spectrum across VSD is dependent many factors other than the presence of VSD. However some large VSDs are detected better by 2D echo rather than doppler signals.
Final message
Presence of a Anatomical VSD does not imply it should generate a noise.The murmur as well as Doppler signals are primarily determined by the pressure difference on either side of VSD. After all , one of the largest VSD that we encounter
Posted in Clinical cardiology, Infrequently asked questions in cardiology (iFAQs) | Tagged doppler in vsd, doppler vsd jet morphology, inlet vsd jet in short axis long axis, late systolic murmur in vsd, mumur vs gradient in doppler vsd, short systolic murmur in vsd, vsd and pah murmur | Leave a Comment »
Syncope in CHB is due to unsafe escape rhythm, changing focus of VPDs, extreme bradycardia, (<20 /minute), pause induced VT, (Usually polymorphic and torsades is quite common .) ultimately may end with convulsions, ventricular fibrillation, and death.
Syncope in SND is due to extreme slowing of SA node . Sinus pauses or even arrest can happen resulting in ventricular standstill. Fortunately, a stable escape rhythm ensues more often than in CHB. (It may just be around 20 or 30/mt. still, ventricular arrhythmias are uncommon. ) This implies an important fact that stability is more important than slowness.Fatality is rare in SND.However, the mechanism of syncope in SND is influenced by the integrity of AV conduction also. If it is severely impaired it can trigger ventricular arrhythmias as well as the escape focus becomes unstable infra hisian location.
Paradoxically, in patients with SND, an episode of palpitation due to AF or sinus tachycardia precedes the episode of syncope. An intelligent patient may recognize this as a warning and can take lying posture after runs of palpitation.This is because of tachycardia-induced suppression of SA node prolong the sinus node recovery time still further.
How to differentiate cardiac syncope from simple vasovagal syncope?
Cardiac syncope is differentiated by common vaso-vagal syncope (VVS) as the latter occurs during erect posture . It may be entirely due to vascular component and hence it may simply represent hypotension without a true cardiac limb .(Vasodepressor syncope)
Hence the pulse rate and volume may take some time to recover in VVS, while Stokes Admas of CHB usually have a well-formed bounding pulse in the recovery phase, as the rate is low and systemic hypoxia is a consistent feature.
How is the respiration during Stokes – Adams syndrome ?
Intact. Oxygenation in the lungs goes on for time being. The pooled pulmonary blood gushes after the termination of syncope and causes the classical flushing. Since the hypoxia causes systemic vasodilatation the flushing is more obvious.(Unlike vasovagal syncope where they are often pale)
History of stokes Adam’s syndrome Morgagni is the one who gave credit to their discovery
Though Morgagni first described the clinical picture of this syndrome in 1761, It was published much later by Two Irish Physicians Stokes, Adams. Wish this entity is referred to as Morgagni-Stokes-Adam’s syndrome
Reference
2.W. Stokes. Observations on some cases of permanently slow pulse. Dublin Quarterly Journal of Medical Science, 1846, 2: 73–85
Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -Therapeutics, Cardiology -unresolved questions, Syncope | Tagged cardiac syncope, mechanism of syncope in chb, mechansim of stokes admas syndrome, sick sinus syndrome, sinus node dysfunction, stokes adams morgagni, stokes adams syndrome, stokes admas attack | Leave a Comment »

The stretch and strain experienced by the action potential’s left shoulder region is almost similar* in both long and short QT syndromes that trigger a VT.(* Hope this explanation makes some electrical sense !)
*Click over the image for high resolution
Posted in Cardiology - Electrophysiology -Pacemaker, Infrequently asked questions in cardiology (iFAQs), Long and Short QT syndromes | Tagged how short qt syndrome induce vt, long and short qt syndromes, Mechansim of VT in long and short QT syndrome, short qt syndrome | Leave a Comment »
Time is muscle. This quote became sort of ” cardiology sermon” in the last few decades .Cardiologist think they stand on a 100 meters sprint track once a patient with STEMI arrives .This is indeed true , if we agree time is muscle and our urge is to reduce the door to balloon time .Please remember , this rush matters much , only if the patient comes through very early when the muscle is really getting damaged . (No issues . . . even if the fire engine comes in slow motion if the house is burnt fully !)
Time is muscle agreed . . . but muscles are kept alive by factors other than time ! So muscles can defy time if God is willing !
Time is one of the important components of management of STEMI. Other things matter too ! Age , baseline co-morbidity , underlying extent of CAD, collateral support of IRA territory , and finally individual variation in hypoxic damage in myocyte is (Rarely been studied in detail.)Door to balloon time for a patient who lands up within 1 hour window need to be much different from a patient who comes at 10 th hour .The issue is important because we use a procedure which requires delicate decision-making ,(IRA-Non IRA issues etc) the results can be sub optimal , and even be hazardous in low risk STEMI . So , door to balloon time may be a less important component of time window in a patient who comes after 6 hours .This is the reason overall outcomes are not changing in a large cohort of rapidly performed PCI.
The presumed absolute relationship between “Time and muscle” concept is always been a suspect . This is proven by a flawless study from NEJM .
http://www.nejm.org/doi/full/10.1056/NEJMoa1208200
This study should infuse more sense to us , time and again, we are hijacked and sedated by high dose of pseudo scientific concoction .In fact , indiscriminate rapid PCI may not be in the good interest of all patients with STEMI , if it is not properly done .Without realising this fact many developing countries are indulging in extravagance of costly STEMI programs wasting the exchequer.
This landmark NEJM paper convincingly underscores a fact that achieving rapid door to balloon time is not going to be the game changer in conquering the Global STEMI championship . We have to take the coronary care into the streets or to their homes as well .This is where the pre-hospital thrombolysis will emerge in a big way in the future .
A slow and steady thrombolysis beats a fast and furious primary PCI on any given day in all uncomplicated STEMI .This we have proven for over three decades in one of the India’s largest coronary care unit .( Where is the data man ? Genuine experience is data . Why we require , the act of publication to convert an experience into evidence . Often times , I would feel , data is the most unscientific word in medicine . Many Truths lack evidence , false hoods come with plenty ! For all those scientific homo sapiens , please recall 70 % of ACC/AHA class 1 recommendations are backed by level C evidence ie simple opinion from perceived experts! )
Final message
A fast and furious primary PCI may not be the answer in all STEMI population
Thrombolysis can be done with near zero time delay , it does not require special expertise where an ambulance driver can reperfuse a myocardium without much fuss and glamor ! He does not have to split his hair to identify which is the IRA in a complex multivessel STEMI as well ! The streptokinase and TPA will home in to the target site smoothly and swiftly .
If indeed , time is the major factor in STEMI , we have many other ways to tame the time . If muscle is more important than time , pPCI is rarely the answer !
Some India specific thoughts
Is it not a shame , we talk about primary PCI for all our patients who do not even get timely Aspirin* after a STEMI! .It is something akin to what we witness every day , as our country folks wield touch screen Androids . . . conversing in open air toilets !
* While the importance of Aspirin is undermined , It is different story altogether , these patients get sorbitarate promptly whenever they get chest pain (mis-placed and dangerous priority ! ) prescribed by the roaring GPs , who suffer from discontinuous medical education , propelled by the deeply penetrated 1000 crore oral Nitrate market .
And STEMI workshops are conducted by self-proclaimed experts every few months in posh 7 star hotels all over India .
Posted in Cardiology -guidelines, Cardiology -Interventional -PCI, Cardiology -unresolved questions, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs), STEMI-Primary PCI, Two line sermons in cardiology | Tagged components of time window, door to balloon time, door to needle time, management issues in stemi, nejm time window, primary PCI vs thrombolysis, stream study stemi, streptokinase vs primary pci, symptom to door time, time windows in STEMI | Leave a Comment »