Posted in Uncategorized, tagged chest pain evaluation, triaging chestpain in emergency room, vancouver chest pain rule on September 30, 2012| 1 Comment »
For ruling out acute coronary syndrome in in men less than 40 years , here is 30 second protocol !
All you require is an ECG and some degree of common sense ! ( A flattish T wave is acceptable )
Please note cardiac enzymes are not required to R/O ACS in this group !
Vancouver chest pain rule is a glorified clinical sense !
http://emed.wustl.edu/images/journal_club/2006/September_2006/Vancouver_Chest_Pain_Rule.pdf
Posted in Uncategorized, tagged accessary av node, av nodal approaches, av nodal archipelagos, av node embryology, av node fragmnetation, conduction system development, duplication of av node, Electrical archipelagos, failuure of absorbtion of av node, fetal dispersion of av node, his bundle looping, non compacted av node, non compaction of left ventricle, pokkuri, remnats of av node, sudden death due to av nodal defects, wpw syndrome on September 30, 2012| 1 Comment »
AV nodal tissue is a not compact structure as we would be believe . But it is a fact , AV node do attempt to compact after birth.
It is never complete.
Note the islands of his bundle entrapped . Image source : M. Paz Sua´rez-Mier J Am Coll Cardiol 1998;32:1885–90 From the Section of Histopathology, Institute of Toxicology and †Department of Pathology, La Paz Hospital, Madrid, Spain.
All specialised cells should coalesce to form the compact zone .This fails to happen in many . Failure of AV nodal compaction results in islands of slow conducting cells in around AV node . Some of them can mutate , and acquire fast conducting properties as well . (Accessory pathway )
This failure of AV nodal compaction is termed as persistent fetal dispersion of AV node .
In the his bundle same phenomenon is called as his bundle de-fragmentation .These abnormalities are noted in pathological specimens of Pokkuri sudden death in Asians .
Unexplained sudden deaths and instant bradycardias and complete heart blocks are related to these dispersion of AV nodal cells downstream . This also explains some of patients with infra hisian escape show junctional characteristics.
Many cardiac pathologists have observed this . Still there is a missing link .
References
Kirschner RH, Eckner FAO, Baron RC. The cardiac pathology of sudden,unexplained nocturnal death in Southeast Asian refugees. JAMA 1986;256:2700–5.
Hudson REB. The conducting system: anatomy, histology and pathology in acquired heart disease. In: Silver MD, editor. Cardiovascular Pathology. New York: Churchill Livingstone, 1991:1367– 427.
James TN. Normal variations and pathologic changes in structure of the cardiac conduction system and their functional significance. J Am Coll Cardiol 1985;5:71B– 8B.
James TN, Marshall TK. De Subitaneis Mortibus XVIII. Persistent fetal dispersion of the atrioventricular node and His bundle within the central fibrous body. Circulation 1976;53:1026 –34.
Posted in cardiac physiology, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Infrequently asked questions in cardiology (iFAQs), tagged av junction, junctional tachycardia, va conduction on September 30, 2012| Leave a Comment »
Why Junctional rhythm has huge variation in P wave morphology ?
P waves in junctional rhythm can be
It depends upon the origin of junctional focus
Further ,the appearance and timing of P waves will be determined by the underlying structural heart disease also.
Final message
Medical students have grown up with the belief that AV junction is a single focused point .It is true in terms of electrical circuitry of normal AV conduction .However during pathological electrical disorders ( Which arise often because of structural disorder) it should be realised the AV junction is a huge plane . Arrhythmia can occur anywhere from this plane .The entire plane can become electrically active which may also acquire the ability to conduct bi-directionally .
Posted in Infrequently asked questions in cardiology (iFAQs), pericardial disease, Uncategorized, tagged albumin escape in hypothyroidism, edema in hypothyroidism mechanism, lymh edema in hypothyroidism, myxedema mechanism, pericardial effusion in hypothyroidism, what is the mechanism of pericardial effusion on September 30, 2012| Leave a Comment »
Hypothyroidism is a classical example of generalised edema formation . The mechanism of which is extensively studied .Still we are not clear about it .
Content of edema fluid
Mechanism
Why hypothyroid edema does not pit on pressure ?
For pitting to occur tissue should be compressed and retain the elasticity .This means the fluid can escape into the cell when mechanically compressed and comes back when the elasticity of skin brings it back to its original status. For this to occur the skin and subcutaneous matrix should be normal in texture.
In cardiac failure and renal failure edema is primarily due to altered hydrostatic forces and skin is intrinsically normal .So some amount of pitting is retained . In hypothyroidsim and lymphedema where there is an intrinsic pathology of the skin pitting is rare.
Why constriction and cardiac tamponade are rare with hypothyroid pericardial effusion ?
Like the generalised slow response of hypothyroid individuals the effusion is also very slow forming and is rarely large so tamponade is rare .
The hypothyroid infiltrates which collects within the pericardial space it rarely infilitrates the fibrinous pericardium (The thick outer shell ) .Unless fibrinous pericardium is inflamed or infiltrated constriction is exceedingly rare .Simple epicardial infiltration may cause some restrictive physiology but not constriction .
Reference
Lancet. 1975 Mar 8;1(7906):564-6.Effusions into body cavities in hypothyroidism. http://www.ncbi.nlm.nih.gov/pubmed/47029
Posted in Uncategorized, tagged acute stent thrombosis, drug eluting stents on September 29, 2012| Leave a Comment »
Which is the “Numero uno” cause for acute stent thrombosis in real world Cath labs ?
Answer : 2 .(Indisputably correct )
It is estimated at-least 4 out of 10 stents we implant is sub-optimally deployed .Only a fraction of them go for complication .Coronary endothelium silently tolerates our aggression .
How to prevent this ?
Posted in cardaic physiology, cardiac physiology, Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology congenital heart disese, pulmonary hypertension, Uncategorized, tagged excercise induced pulmoanry hypertension, isolated pulmonary systolic hypertension, ispah, pulmonary hypertension, relationship between pulmonary artery pressure and rv function, rv dysfunction and pulmoanry arterial hypertension, total artifitial heart and pulmoanry hypertension on September 27, 2012| Leave a Comment »
The primary determinant of pulmonary artery systolic pressure is . . . ?
Answer : All of the above
But what is the relative contribution of each ?
I am 100 % sure , no one can answer this question correctly !
It is true , in some pathological situations one can be fairly certain about cause of elevated pulmonary arterial pressure .
When we confront a patient with left heart disease it is the transmission of mean venous pressure .
Whatever be our understanding ( Pre/Post capillary pulmonary hyper tension and the related stuff ! ), the one parameter that makes mystery contribution to PA pressure is RV contractility !
In physiology RV generates about 30mmhg systolic pressure that becomes the pulmonary systolic pressure .The diastolic pressure will be around 15 and mean around 20 . During exercise contractility of both RV and LV increase .There has been documented PASP up to 50 mmhg in normal healthy adults during exertion .
Here one can assume RV contractility is causing a entity called transient Isolated systolic pulmonary arterial hypertension.(ISPAH)
Consider a entirely different situation
A patient with COPD with raised PASP . The right ventricle pressure has to equilibrate with PASP during systole .For this to happen it has to generate the 60mmhg . If the RV fails to augment it’s contractility for some reason , will the ineffective RV contraction will lower the PASP ? This is the perplexing question !
While the popular understanding is , RV dysfunction will under- estimate the severity of pulmonary hypertension . . . still . . . we are not sure whether RV dysfunction will reduce the PASP per-se ( and subsequently PA diastolic pressure as well )
We often see a good example . A patient who develops tricuspid valve disease and RV dysfunction get symptomatic relief from lung congestion .
Final message
The relationship between RV function and pulmonary artery pressure is a real enigma. Though hyper functioning RV is expected to elevate PASP and hypo functioning RV would pull it down , the relationship is not that simple. If only we decode this mysteries we can try specific RV negative inotropic agents as a modality to treat pulmonary hypertension .
After thought
Total artificial hearts are going to come in a big way in the coming decades .It will specifically address this issue , as RV and LV contractility need to be individually tuned to avoid pulmonary congestion.
Coming soon
While RV function is critical for human survival , Fontan principle simply says entire RV is dispensable . How ?
Posted in Cardiology - Electrophysiology -Pacemaker, Cardiology-Arrhythmias, Uncategorized, tagged best review article in ventricular tacycardia, maasood akthar and ventricular tachycardia, mechanisms of ventricular tachycardia, ventricular tachycardia on September 5, 2012| Leave a Comment »
Ironically , in medicine we need to peep into the past for updating and scrutinizing current knowledge . Here is free ticket for a retro journey to the the Electro-physiology Laboratory of the University of Wisconsin-Milwaukee . This article , which was published in 1990 , still can explain many intriguing concepts of VT succinctly .
Thanks to circulation for sharing this article free !
Akhtar M . Clinical spectrum of ventricular tachycardia. Circulation 1990;82:1561-73.
Posted in cardiology-ethics, Cardiology-Land mark studies, cardiomyopathy, Echo library and gallery, Great websites in cardiology, Uncategorized, tagged pre discharge est, pre-discharge tmt est tredmill, primary pci est, status of pre discharge est, stress test following primary pci, sub maximal stress test on August 20, 2012| Leave a Comment »
The principles of pre-discharge EST
This concept came about 20 years ago (1980s) to risk stratify patients following ACS to triage early coronary angiogram and revascualrisation. Generally patients are discharged by 5-7 days after an MI (May be 3-5 days in some hospitals) . Doing an exercise stress test early within 2 weeks has not been very popular with many cardiologist even though it was recommended by many guidelines.The type of stress recommended here , is heart rate limited sub maximal 70% of THR (Usually around 140 /mt ) is performed . This is due fear of precipitation another ACS.
Still, there are definite advantages for pre-discharge EST .It help us identify high risk subsets of STEMI and reduce the intermediate term mortality .More importantly it gives us an opportunity to exclude inappropriate revascualriations even without an angiogram . (The well known coronary dogma ie if a post STEMI patient performs > 10 METS , his heart carries little risk for future events still holds good !)
With the advent of liberal usage of CAG and improved techniques of revascularistion , most patients directly undergo pre-discharge CAG rather than EST !
Further reading
Does any cardiologist have guts to do a pre- discharge EST after a successful primary PCI ?
Posted in Uncategorized, tagged renal transplantation in dilated cardiomyopathy, reverisble dcm, reverisble lv dysfunction, severe lv dysfunction in ckd, uremic lv dysfunction, uremic myocarditis on August 19, 2012| Leave a Comment »
Usually co -morbid conditions are relative contraindication for renal transplantation . LV Myocardial dysfunction is a fairly common association in CKD.
The uniqueness of this LV dsyfunction is , there is no primary myocardial failure . Further features observed are . . .
Mechanism of reversible LV dysfunction in CKD
Chronic pressure overload result in After load mismatch .
(Normally pre-load , after load , and contractility should be sequentially matching parameters . After load mismatch is an important concept where myocardial contractility is temporarily is depressed due to lack of adequate pre-load for a given level of after load )
Evidence for reversibility
Very often one can observe improvement of LV function significantly 24 hours after dialysis .The concept of uremic biochemical dysfunction is still valid .Though it can not be exactly quantified .
If significant coronary artery disease is excluded , these patients do well ( after transplantation ) from a cardiac point of view !
(64 slice MDCT may be a simple screening test to rule our significant CAD .)
Final message
How wise it is to do renal transplantation in DCM patients ? .
Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Cardiology -unresolved questions, Cardiology-Arrhythmias, Infrequently asked questions in cardiology (iFAQs), tagged antidromic vs orthodromic avrt, how common is orthodromic avrt in wpw syndrome, what are the wide qrs tachycardia in wpw syndrome, wpw syndrome on August 19, 2012| Leave a Comment »
AVRT is a second commonest cause of narrow qrs tachycardia. While , all narrow qrs tachycardia in AVRT must be ortho-dromic. wide qrs tachycardia in WPW can either be ortho-dromic or anti-dromic ,
The classical one is the much popular and fancied Antidromic AVRT . Please be reminded AVRT can conduct orthodromically through AV nodal tissue but still become aberrant , as it travel downwards thorough the bundles and result in a wide qrs tachycardia .
Among the two which is more common ?
My observation is ortho-dromic wide qrs AVRT is more prevalent . Do you agree ?
Final message
Not all wide qrs tachycardia in WPW is anti-dromic !
Dr.S.Venkatesan MD 