Some journals do a great work silently .Impact factors are a non issue for them
It is the content that matters . Pediatric cardiology is one such journal !
Of course , they don’t publish papers that have greatest significance to mankind !
like Telmisartan is not inferior to Ramipril in the mangement of hypertension
and Fondapaurinox is as effective as regular Heparin . . . etc . ..etc
They dedicate themself in the decoding the mysteries of congenital and acquired heart disease of children .
Posted in Uncategorized | Tagged cardiology journals, congenital heart disease, pediatric cardiology | Leave a Comment »
What will be the pulse rate in a patient who has ventricular bigeminy in ECG with a heart rate of 90 ( 45 sinus beats 45 VPDS/minute ) ?
A.Exactly Same as HR , ie 90/mt
B.Exactly half of HR , ie 45/mt
C.Can be anything between 45 to 90/mt
D.Any of the above can be true
The answer is D .
I have noted ,this simple question in cardiology resident examinations cause great anxiety among students .
Why is it difficult to arrive at an easy answer to this question ?
Traditionally , ventricular ectopic beat were also called extrasystole , implying every ectopic beat shall produce a peripheral pulse .Since , we learnt this is not true , we started refering them as VPDs.(Simple ventricular depolarisation which may or may not have a mechanical activity ) So , in a patient whose alternate beat is a VPD , things become little complicated.
What determines a VPD to acquire mechanical energy or simply remain as an electrical event ?
If the VPD is too early or too late it can not have a mechanical activity . It should be optimally timed midway between two sinus beat to have a good mechnically active VPD. Some refer this as an interpolated VPD .Here, the VPD becomes a true extra systole for that individual. So , in patient with ventricualr bigeminy in ECG the pulse rate is usually half , can be same as HR when the coupling interval is optimal or it can be totally irregular as someof the VPDS gain a mechanical activity and some do not (as often occurs multifocal VPDs. )
* Among the above four factors timing of the VPDS is the most crucial as it can influence all the other three factors.
** Whatever be the timing or force of contraction aortic valve should be opened to generate a pulse wave. If for some reason this does not happen there can be intermittent mechanial activity what we refer to as pulse deficit .
Read a related phenomenon: Ventricular paired pacing
Posted in Cardiology - Clinical, cardiology -ECG, Infrequently asked questions in cardiology (iFAQs) | Tagged bigeminy, interpolated ventricular ectopics, paired pacing, pulse deficit during vpds, ventricular bigeminy, ventricular extra systole, ventricular premature contraction, ventricular premature depolarisation, vpc, VPD, vpd vs vpc, vpds | Leave a Comment »
Recently in a southern Indian state a big cleansing action against fake , spurious and expired drugs were carried out .There was much hue and cry over the issue . It was found , millions of such drugs where in circulation and The Govt has initiated a blanket ban on all these drugs .Intriguingly it was the mainstream pharma industry that was indirectly driving the whip against these fakes.
Unless the medical professionals know what is really fake our patients can never be protected against the fake ! At the outset , let us recall the definition of the word fake
Courtesy http://www.thefreedictionary.com/fake
Fake means
Applying the above definition , all the following will fulfill the criteria for a “Fake drug ”
*In simple terms , it is estimated the bottom half or ( at least one third) of any long prescription in an average Indian prescription is occupied by the fake drugs .
(A unnecessary Vitamin, a cardiotoner, a catalytic enzyme, a mitochondrial stimulator, a metabolic juice, a mood enhancer or depressor etc etc . . . )
Final message
In this era of glorious medical industry mankind is on a futile journey searching for the elusive kindness and truth from the industry . The easiest job in today’s world is , fooling around the public. The victims are not only the patients but also the medical professionals . The later often do a role of perpetuators as well .
As we realise , there are thousands of fakes masquerading as true drugs , let us pray the God to give us the strength to identify them , the courage to resist the temptation . (To prescribe)
Coming soon “The greatness of fake drugs “
Posted in bio ethics | Tagged drug, drug industry, fake drug, pharma industry, pharmacology, spurious drug | Leave a Comment »
Heart is one of the unique organs , that a physician can touch and feel before diagnosing a disease .The fact that , the heart is located superficially within the thoracic cavity makes tactile examination possible . The current generation cardiologists should realise cardiac palpation was a huge scientific specialty by itself centuries ago . Apical impulse demonstration in class rooms would go on for hours together in the days of Leannc and Dressler .
It is an irony , when we are able to see and feel many areas of the heart in the direct vision ( RV parasternal impulse, pulmonary arterial pulsation, contractility of LV ) we got addicted to imaging modalities now.
This article tries to extrapolate the morphology of apical impulse with that of ehocardiographic LV function . A normal apical impulse is a very subtle impulse often absent in a third of population.Some times it is called tapping impulse .The two common abnormalities of apical impulse are hyperdynamic and heaving .
Read the link for normal apical impulse
A hyperdynamic apical impulse
The hyperdynamic apical impulse is diffuse (Occupying at least two rib spaces > 3Sqcms) and very active with brisk motions visible to naked eye .This implies the leftventricle is dilated significantly and the wall is not much hypertrophied. This is eccentric LV enlargement . It also tells us the LV function is well-preserved as the term hyperdynamic infers very active LV .It is obvious , a dysfunctional LV can not be hyperactive. A hyperdynamic LV apex in a patients with AR or MR indicates they will do well after surgery for the simple reason their LV function is preserved. In the same logic a patient with hyperdynamic apex often complaints of palpitation as the apex hits the chestwall . Which is a good sign with reference to LV function .
Note :A patient with heaving apex rarely complaints of palpitation.
Hyperdynamism occur in systole or diastole ?
Logic would say apical impulse would be palpable only in systole .But in a hyperdynamic LV diastolic phase is also palpable (A palpable S3 is common associate of hyperdynamic apex)
Heaving apical impulse
The term heaving apex by definition indicate there is a brief localized sustained LV apex lasting at least 50% of systole.
The sustained lift may disappear with very severe LV dysfunction , apical impulse is barely perceptible in failing hearts . A sustained LV apex suggest reduced dp/dt of LV contractility .
Relationship between apical impulse character and LVH ?
Hyperdynamic LV apex is rare to be associated with LVH .Except probably in HOCM where the LV systole is interrupted very early in the ejection phase.
Heaving apex can be a marker of LVH .But, the onset of LV dysfunction can confound this finding.
Can a hyperdynamic and heaving characters occur together in apical impulse?
We have been taught cardiology with a black and white learning concept but unfortunately science more often exists in shades of grey An apical impulse can indeed have characters of both . A diffuse apical impulse with a heaving nature is common in regurgitating lesions with the onset of LV dysfunction Such situation can occur in LV apical aneurysm
Final message
Looking for apical impulse in current cardiology practice may be considered as the most foolish job a physician can indulge !
Ask the secretary to record the history , take an ECG, do an Echo , send both deserving (and of course many undeserving patients too !) to cath lab at the earliest . . . This is the modern-day cardiology mantra !
This article , does not vouch for the accuracy of what some may consider as a “medieval clinical sign” . But , it confers the patient a better rapport strightaway as the physician puts his or her hand on the patients heart . Some call this as a healing touch ! It work wonders in many !
Posted in Cardiology - Clinical | Tagged apical impulse, diastolic lv apex, diastolic vs systolic lv apex, heaving apical impulse, heaving vs hyperdynamic apex, hyperdynamic apical impulse, lv apex, lv apex and echocardiography, lv apex in hcm, lv apex in lv dysfuntion, sustained lv apex | 2 Comments »
Let ventricle is an elliptical or ovoid chamber .The pattern of LV enlargement can vary considerably in different pathologies. We know a dilated , globular heart is the typical feature of terminal congestive heart failure. But in the early stages of cadiac enlargement there are some distinct differences in the contour. (Aortic stenotic lesions retain the ellipitical shape till late in the course )
LV enlargement due to mitral regurgitation is somewhat different from aortic regurgitation. A globular configuration occurs more often in severe MR than AR. This is due to the fact, the long axis and short axis ratio of LV is maintained till late in the course of aortic valve disease . Cardiac long axis enlargement is more pronounced in aortic valve disease than in MR. The AR jet reaches LV at a higher pressure gradient (Diastolic pressure of aorta) than mitral inflow velocity . (Often mimic physiological flow with an S3)
For a given degree of regurgitant volume AR will cause more cardiac enlargement than MR. In the same note , one should realise the LA becomes huge in MR which receives high pressure regurgitant jet . Further ,mitral valve disease is more likely to result in early PAH and that results in right sided chamber enlargement giving the cardiac contour a more globular configuration
Is the cardiac contour different in rheumatic and degenerative(Myxamatous) mitral regurgitation ?
Yes , rheumatic MR results in less enlargement of the base of the heart as the fibrotic process restricts and restrains LV and prevents uncontrolled LV dilatation . In fact , giant LV are often reported in mitral regurgitation due to mitral valve prolapse than rheumatic MR.
Why the configuration of LV important in the management of cadiac failure ?
The globular configuration of LV implies , the papillary muscles are attached in a disadvantaged angle and keep the free wall stress high. Specialized procedures are required to restore the LV shape especially in secondary to mitral annular dilatation. Isolated aortic valve disease rarely require LV remodeling surgeries , even if AVR is done late stages.
What is the maximum dimension of LV reported in cardiac failure ?
The upper limit of normal for LV diastolic dimension is 5.6cms. In MR it often reaches 6-7 cms . The maximum of 10cm has been reported with AR. An LV beyond this level looses it’s elasticity and likely to be incompatible with survival unless LV reduction surgeries like Batista are performed.
Is secondary valvular cardiomyopathy an accepted entity ?
The term cardiomyopathy when originally defined decades ago , required exclusion of all known cases of cardiac enlargement. But now we have a more liberal working concept , if the LV enlarges disproportionate to the loading conditions of the valvular lesions , secondary cardiomyopathy is said to be present. If cadiomyopathy sets in, the cardiac shape invariably takes in a globular configuration irrespective of the valvular lesions. So, the simple parameter of shape of LV in X ray chest can give us a clue regarding the outcome in valvular heart disease.
Further reading
Also read sphericity index by echocardiography A spherical LV can be easily quantified by echocardiography
Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs) | Tagged aortic egurgitation, batisda, cardiomegaly, ct ratio, elliptical lv, lv configuration, lv enlargement, lv reduction surgery, mitral regurgitation, rv configuration | Leave a Comment »
Excercise physiology has been studied most extensively in the last century.The hemodynamic impact of excercise in various disorders of heart has been well established.
Dyspnea on exertion is the commonest symptom in clinical cardiology practice. It is well-known pulmonary stretch receptors located in pulmonary vasculature is one of the major mechanism of dyspnea.
Excercise increases the cardiac output manyfold.Transporting up to 10-12 litres of blood every minute across the lungs with a narrow pressure head (about 10 mmhg ) is not an easy job . It needs lot of lung discipline .
It is surprising to note, there is little data on excercise induced pulmonary hypertension in the evaluation of patients with unexplained dyspnea.
We know, excercise increases the systemic blood pressure ,we presume it should not raise the PAP (however severe the exertion is 1 )as pulmonary circulation is a high compliant low pressure system.
Is our presumption correct ?
Exercise induced PAH can occur in both health and disease
In patients with preexisting disease
Apparently healthy population
This is similar to hypertensive response to EST in systemic circulation.Existence of this entity , is controversial, But this may reflect reduced pulmonary vascular reserve or reduced pulmonary nitric oxide secretion.
*The main difference here is the PAH is more often an isolated systolic PAH. While LV dysfunction induced PAH is a combined diastolic and systolic PAH .
How to assess excercise induced PAH ?
It is not an easy job. Invasive catheter derived pressure measurements have been done ,but it is not practical .
The simplest way is to look for the TR /PR jet in echo in both pre and post excercise phase.
Final message
Excercise induced PAH is an inadequately studied entity in cardiology , in spite it’s great significance .
This phenomenon is observed in both diseased and normal heart.
The quantum of excercise induced PAH is widely variable depending upon the cardiac status especially LV function and the functional integrity of pulmonary microvasculature .
Posted in Cardiology - Clinical, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), Uncategorized | Tagged excercise induced pulmonary hypertension, exertional dyspnea, isolated pulmonary systolic pulmonary hypertension, pah, pulmonary, pulmonary hypertension, unexplained dyspnea | Leave a Comment »
Ventricular septal defect(VSD) is one the commonest congenital heart disease . Right from the days of Gasul , Abbot, and Keith we have analysed the natural history for nearly a century . VSD is an intriguing congenital heart disease where a child can develop a florid cardiac failure within weeks of birth in one end to a totally asymptomatic adult with a benign cardiac acoustics defect (Namely a systolic murmur in the left parasternal area.) But for this murmur , the patient would be labeled absolutely healthy.
In between these two spectra is the huge population of VSD that gets closed spontaneously. A rough estimate says 60 % of all small VSDs get closed by age 10 .
So ,what we are supposed to do once a child is diagnosed of VSD ?
Should we close or should we wait ?
The indication for closing a VSD is discussed elsewhere ( Read this link )
What are the factors that determine VSD closure ?
* Associated defects like PDA, RVOT obstruction are strong deerrants against spontaneous closure
General rules of VSD closure
Size
VSDs <5mm have great chance of closing Large VSD > 1cm is rarely get closed .
Supracristal VSDs located sub arterially are immune to spontaneous closure however small the size is .
Location & Site
VSDs that are located exclusively within the membranous septum rarely close . VSDs which are located in the perimembranous area (With at least 50% circumference is fenced by muscular or trabecular septum has the greatest potential to close by natural forces.)
Isolated muscular VSD if large can not get closed . Inlet VSD has anatomical difficulty to get closed.
Rim Morphology
Small muscular VSDs have a potential to close , but it is believed differential cellular lining of VSD rims (Eg : A combination of muscle, membrane , is more likely to close .)
Process of tissue growth As the child grows the it is expected the heart will outgrow the lesion . This is thought to be the commonest mode of VSD closure. As the IVS mass increases as he child grows it brings he rims together . But logic would suggest unless some degree of neocardiac proliferation occur a VSD may never get closed completely .
Some times even large VSDs try to close with the help of the neighboring structures like septal tricuspid valve leaflet . Indeed this can be the dominate mode of closure in many. This can induce a tricuspid regurgitation .
**Role of infection
Paradoxically an episode of infective endocaditis in the edges of VSD accelerate the process of approximation of tissue plane and healing .
Relation with Pulmonary arterial hypertension (PAH)
Once PAH sets in the VSD never gets closed spontaneously , This may be due to all VSDs that result in PAH has to be significantly large
Can a VSD get larger progressively?
In physics and hydraulics a hole under hemodynamic stress is destined to progress In human biology this is thought to be rare .Post MI VSRs can behave in an unpredictable manner as he edges of the defect a often softened and prone for tissue plane dissection and extension .
Why some VSDs never close ?
It is clear , size and location matters the most , but there are other issues some of them may be unique tissue properties .
Why is it important to know the biology of VSD closure ?
In this era of interventional cardiology we are using mechanical devices to close VSDs and ASDs .It is fraught with many technical issues. If there is a biological glue or membrane that can be delivered by catheter to close small VSDs or ASDs .
So for no therapeutic approach to hasten the natural closure of these defects has been practiced .Further research is required to explore the cellular adhesiveness and help accelerate closure of these defects.
Posted in cardiology congenital heart disese, Uncategorized | Tagged ventricular septal defect | 2 Comments »
Chronic total occlusion is the cardiologist’s daymare .Here is an article that adds on to 1ooth technique to cross the chronic total occlusion within the coronary artery !
If only we succeed in this Arabin magic , in the cath lab we can open the doors of all CTOs .
This technique is based on the principle to push the hard plaque into the adjacent side branch like a sliding door, if the pateint has one !
The only isssue with this technique could be the “cave door” may close again immediately as it did for Alibaba !
Reference
http://www.ncbi.nlm.nih.gov/pubmed/20088015
http://www3.interscience.wiley.com/journal/122619470/abstract
Posted in Cardiology -Interventional -PCI, Uncategorized | Tagged cath lab, chronic total occlusion, cto, oen sesame technique in cath lab, open sesame | Leave a Comment »
Wide qrs tachycardia often evoke a OCD like reaction among many cardiologists (Obsessive compulsive disorder). Whenever we are given a strip of wide qrs tachycardia we are compelled to initiate a conscious or subconscious debate , whether it is VT or SVT . Tens of thousands of articles, seminars, CMEs , have been conducted for over 30 years for decoding wide qrs tachycardias . The fact that the confusion is still widely prevalent indicate only two things
The power of statistics and commonsense have never been applied in the management this vital cardiac entity .While a 75% sensitive exercise stress test (EST) has a huge following in clinical cardiology , a 99 % sensitive clinical criteria* for diagnosing VT is not respected .
*All wide QRS tachycardia in patients with with history of CAD/STEMI would be VT
If only we had applied our mind to this article published in 1988 we will never ever have the need to split our hairs for decades.(That too without success !)
In pursuit of knowledge , are we often chasing an imaginary issue ?
The cardinal principle of medicine says
“Diagnosis should precede treatment whenever possible ”
But there need to be a correction in the above statement . Time , effort , cost involved in arriving at a diagnosis should be meaningful .( Needless to say . . . it should a correct diagnosis too ) And if the power of statistics far exceeds the frivolous scientific data , street sense can be applied liberally even though current generation may call it un scientific .
The issue here is not being scientific or unscientific , but whether you are right or wrong . The article which is quoted here has a great insight about the philosophy of VT diagnosis.
The message form this article goes something like this . . .
In the diagnosis of wide qrs tachycardia , If we apply the so called scientific principles the chances for missing a real VT is extraordinarily high , while if you blindly apply common sense and logic you are going to be 90% right .
What a powerful statement this ! even though it appears absurd , it is absolutely true !
A young physician should realize the importance of this . Scientific decoding of arrhythmia may be an academic pursuit but in a given patient at bedside diagnosing by experience and common logic are far more productive and accurate. Miss diagnosis of VT was not common prior to 1980s . It has become a recent phenomenon .
Probably too much of electrophysiology haS made a simple diagnostic pathway a complex one. When we relied only on commonsense the errors were less . I have often observed fellows making mistakes quite frequently while nurses were too confident to call a wide qrs tachycardia as VT .
Final message
Medical decision making is an art , in fact it is a “fine art ” We keep saying this for centuries , still medicine as a science easily overtakes medicine as an art. Here comes the problem . Some times (or is it many times ! ) too much of inquisitiveness in the name of science make practice of medicine complicated and the victims are often the patients !
Let us simplify medicine . . . let us accept an occasional bad outcome . . . for not being 100 % scientific ! After all , a million mistakes happen every day in the pure scientific pathway .
Reference
http://www.amjmed.com/article/0002-9343(88)90008-3/abstract
Also read Knowledge disease
Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology-ethics, Uncategorized | Tagged brugada criteria, clinical diagnosis of vt, decoding vt, vt vs svt, wide qrs tacycardia | Leave a Comment »
Like in neurological disease, one can locate the site of block in bundle branch blocks. Though it has never been thought , to be clinically important to localise a BBB . (Unlike coronary lesions)
Generally , RBBB can be proximal or distal peripheral type.The commonest site could be the distal type.
It should be realised , for over 100 years in electrocardiology , we have been using some inaccurate terminologies just because it is easy to understand or being traditional .It is difficult to assimilate a fact , even today that “An electrical delay in conduction and block are one and the same ”
In fact, bulk of the RBBB is nothing but delayed conduction over this bundle. So whenever we say RBBB , we imply an incomplete block ie conduction still occurring over the so called blocked bundle.(This dogma applies for LBBB and AV blocks also to a lesser extent)
Examples of delayed RV /RVOT conduction
What is the benign rSr’ pattern in V1 ?
This is nothing but a relatively late depolarisation of RV outflow or conus that produce a terminal RV activity .
Many of the ostium secundum ASD may show just this rSr’ pattern confirming there is no organic damage to RBB in ASD .
Calling rSr’ pattern as incomplete RBBB is not advisable (As many ECG books may suggest ) .This is because , even full blown RBBB pattern may actually be an incomplete one .Further , the degree of terminal r’ in V1 or s in lead 1 does not always determine the completeness of RBBB.
Is there a totally blocked right bundle branch block ?
Yes , it is not common .
It can be an working rule , complete RBBBs locate the lesion proximally and incomplete ones distally .
What is the other evidence for RBBB in ASD is only a simple delay in conduction ?
After ASD closure in many of the patients the RBBB pattern may disappear.This indicate RVOT regression .
Can you clinically differentiate the proximal from distal RBBB ?
Ironically ,what is difficult in ECG may some times be possible clinically.The classical description of wide splitting S2 occur often in peripheral RBBB.
It represents a delay in the closure of pulmonary valve due to delayed electrical activation or increased hangout interval as in ASD .Logically S1 should also be split in RBBB. But this is not often discussed.
This is because , the split in S1 is lesser in magnitude and is not influenced by the hangout interval .(Hang out interval is the time taken for the blood ejected from RV to fill the pulmonary circulation. Due to the low impedence of pulmonary circulation the the blood that is ejected into the MPA continue to run off for about 100milli seconds even after the RV/PA pressure crossover .)
S1(T 1) occurs immediately with the onset of RV contraction . Similarly M1 occur with LV contraction.It should be recalled it requires hardly 5mmhg of RV pressure to close the tricuspid valve and about 10mmhg for LV to close the mitral valve.
If for some reason if there is a delay in RV contraction , as in very proximal RBBB the T1 is delayed and hence S 1 split.
Note in most of the peripheral or distal RBBB the bulk of the RV free wall contraction is not interfered with . So , in distal RBBB it is highly unlikely the S1 will be delayed or split while S2 will be delayed.
What happens to S2 in proximal RBBB ?
Logic would dictate both S1 and S2 should be wide split.
Final message
There is a simple way (Some would call this an futile academic excercise !)to differntiate proximal from distal RBBB.If the first heart sound is split wide , it fixes the lesion proximally. This may indicate a more adverse outcome than a simple peripheral delay in conduction.
Posted in Cardiology - Clinical, cardiology -ECG, Uncategorized | Tagged asd, central rbbb, distal rbbb, ebstein anomaly, fixed split s2, incomplete rbbb, peripheral rbbb, proximal rbbb, proximal vs dital rbbb, rsr' in v1, si vs s2, split s1 in rbbb, split s2, t1 vs m1, wide spilt of s1, wide splitting of s2 | 1 Comment »
Dr.S.Venkatesan MD 