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 cardiac physiology, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, echocardiography, valvular heart disease, tagged after load mismatch, afterload mismatch in acute lvf, afterload mismatch preload reserve, afterload preload mismatch, contractile reserve, hypertensive lvf and afterlaod mismatch, what is afterload mismatch ? on September 30, 2012| 1 Comment »
Under physiological condition , pre-load , after load , and cardiac contractility should be a sequentially matching parameters . After load mismatch is an important concept , where myocardial contractility is temporarily depressed due to lack of adequate pre-load for a given level of after load .
This is also referred to as descending limb LV function paradox .
The three common clinical situation AL mismatch occurs
If it happens acutely the myocardium becomes dyfunctional due to mechanical non ischemic stunning .Once the after load comes down the contractility improves .
What is the chronic adoptive response to after load mismatch ?
LVH is the major chronic adoptive response to AL mismatch.
LVH reduces the wall stress which will reduce the after load indirectly .
So LVH neutralises the high after load .Laplace law at work . (Wall stress is equal to 2 times the radius divided by thickness of the wall )
Here is the Link to the great lecture by John Ross Jr in LA Jolla , California in one of the annual scientific session of AHA more than 25 years ago . http://www.ncbi.nlm.nih.gov/pubmed/966366 .The concept is alive and kicking even today .I am sorry to note this important physiological concept never received the attention it deserves . I would vouch , it can be as important as Frank starling principle .
Reference :
https://content.onlinejacc.org/data/Journals/JAC/22702/04186.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 Cardiology -Interventional -PCI, carotid interventions, cath lab tips and tricks, tagged catheter retrival of infective vegetation on September 30, 2012| 1 Comment »
Intra cardiac foreign bodies are frequent occurrences in clinical cardiology practice. The common ones are intra chamber clots , vegetations and rarely tumors. Some of these masses are very mobile are precariously attached to the cardiac strutures . It becomes a cardiac emergency as a major embolic event is imminent .
While surgery remains the mainstay approach in such situations , now it seems possible to trap these mobile masses with help of catheter and retrieval devices safely.
The only issue is , while retrieving these masses it should not be let into the circulation and result in embolisation . For this we can develop a porous net (Fishing net like ) that can be blown in the distal chamber or Aorta .
Devices can be structured in way that a single catheter can be used with different ports to capture and filter and retrieve the mass . ( vacuum enabled suction catheters can be additional option ) .The whole procedure can be accomplished with fluroscoy and fluroscopic guidance . Intra cardiac echocardiography might also contribute .
This innovation will be a great value addition to the interventional cardiology armamentarium ,would be be appreciated by clinical cardiologists . We in our tertiary teaching hospital have felt the need for a such a device quiet often .Currently many patients land up in surgical tables for the sole purpose of removing these clots and vegetations .Similarly left atrial clots becomes a contraindication for percutaneous mitral commissurotomy(PTMC) . Such capture devices can be very useful.
Posted in echocardiography, Top ten in cardiology, tagged best web site for echocadiography, echocardiography on September 30, 2012| Leave a Comment »
Learning and sharing of knowledge is one of essential qualities of that make the man kind unique.
But not everyone is ready to do that . A cardiologist from Paraguay shows the way . . .
Probably a model web site for all academicians .It exemplifies , how a medical web site is to be created and presented .This one is for learning echocardiography .
Though the author calls , it as basics it has fairly advanced contents , so it should be useful at levels .
With due courtesy to Dr Derliz Mereles I am linking his web site in my blog .
Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology-Coronary artery disese, cardiology-ethics, tagged acc aha guidelines, follow up after pci, medical ethics on September 30, 2012| 1 Comment »
Here is the two versions of a discussion by a cardiologist to his patient , on the day of his discharge from a state of the art trans national heart health service in southern India.
An alluring cardiologist .
A Bitter cardiologist
Final message
So , the art of medicine is to hide some of the unpleasant outcomes from the patient and project only positive aspects to our patients *
* This is often a controversial issue . Scientifically advanced health care system do not agree with this . But I would believe , that is one of the major reasons they are suffering from huge health care crisis !
I do not agree with the concept of empowering patients with bitter truths . This need not be vigorously practiced. Disclosure of all potential complication to our patients , by itself a trigger such events by meager anxiety .
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 Cardiology -Interventional -PCI, cardiology -Therapeutics, tagged aortic puncture, cardiac tamponade, free wall rupture, ias puncture, inoue balloon, pericardial space, ptmc, stitch phenomenon on September 29, 2012| Leave a Comment »
What are the structures that can get punctured and result in cardiac tamponade during PTMC ?
Traditionally cardiologist’s major fear is confined to accidental aortic puncture . With growing experience & inexperience we now know PTMC is vested with other risks for cardiac puncture other than Aorta .
Reference
http://interventions.onlinejacc.org/data/Journals/JCIN/22697/04019.pdf
Joseph G, Chandy ST, Krishnaswami S, et al. Mechanisms of cardiac perforation leading to tamponade in balloon mitral valvuloplasty.
Cathet Cardiovasc Diagn 1997;42:138–46.
Dr.S.Venkatesan MD 