Archive for December, 2013
Posted in Cardiology - Clinical, tagged a2 os interval, a2-os interval after atrial fibrillation, atria fibrillation and pressytolic mumur cresendo accentuation criley concept, criley concept, cycle length and mdm, s3 in mitral stenosis, what happens to mdm after atrial fibrillation on December 31, 2013| 1 Comment »
Posted in bio ethics, Cardiology - Clinical, Cardiology -Pacemakers and ICD, cardiology -Therapeutics, Cardiology -unresolved questions, medical quotes, tagged ethics in cardiology, thromolysis vs priamry pci, vvi vs ddd pacemaker on December 29, 2013| Leave a Comment »
Following are revered facts . . . among the “Guardians of Cardiology” !
- Primary PCI is a greatest innovation in modern day cardiology .Without this modality most STEMI patients will buy Instant tickets to grave yard !
- A cardiologist who intends to thrombolyse a STEMI is considered as a low quality cardiologist .
- Streptokinase should have no place in the crash carts of modern coronary care units.
- There is nothing called “Time window” for rescue angioplasty.
- VVI pacemaker will convert an electrical problem of heart block into a mechanical one by depressing LV function .
- Digoxin is an obsolete drug even in well established cardiac failure with dilated heart.
- Beta blockers not only fail to control blood pressure smoothly , it often converts a hypertensive individual into a unhealthy one by it’s prohibitive side effects !
Posted in Atrial fibrillation, cardiac physiology, tagged atrial conduction physiology, electrophysiology of atrial conduction, inter nodal conduction, inter nodal pathway, sa node to av node connection, thorel bachman wenkeback pathways on December 24, 2013| Leave a Comment »
I am afraid the 4th response is closer to truth .Readers may share their thoughts. If there are three distinct pathways spreading widely connecting the two spacious chambers and converging again with precision at the compact AV node , it is a marvel .
Further , If these pathways are real , we must experience different types of inter nodal re-entrant tachycardias.Of-course ,we do come across few macro re-entrant tachycardia in the form of atypical atrial flutters They need a close watch .Tracking these arrhythmia may throw light on existence of these pathways.
However, the presence of nodal approaches with preferential inputs to AV node from different parts of atria would indeed suggest existence of such pathways !
What does sophisticated carto and other electro anatomic mapping say about these inter nodal pathways ?
Heterogeneous three-dimensional anatomical and electrophysiological model of human atria . Seemann G, Höper C, Sachse FB, et al. Institute of Biomedical Engineering, University Karlsruhe (TH), Kaiserstrasse 12, 76128 Karlsruhe, Germany. Transact A Math Phys Eng Sci 2006 Jun 15; 364(1843) :1465-81.
Posted in cardaic physiology, Cardiology - Clinical, Cardiology -guidelines, Cardiology -Mechnisms of disease, Cardiology -unresolved questions, Clinical cardiology, general medicine, Syncope, Tutorial in clinical cardiology, tagged clinical cardiology, event monitors in syncope, head up tilt test, holter monitoring, loop recorders, mechanism of syncope, syncope evaluation on December 19, 2013| Leave a Comment »
Recently , I came across a young women who underwent the following three tests for one episode of syncope after witnessing her pet dog bleeding with an Injury !
- Carotid doppler
- Holter monitoring and event monitors
- Brain MRI /MR angiogram
This was followed up by Head up tilt(HUT) in a premier hospital
After 1 week of investigation ,a diagnosis of Neurocardiogenic syncope was made and she was reassured and no drugs were prescribed.
(The collective yield of the above three investigation in fixing a specific diagnosis is less than 10 % of all known causes of syncope )
Syncope is a dramatic symptom.It is one of the commonest symptom in ER as well . Life time incidence of syncope is at least one episode in 50% all human life ! The definition of syncope until recently , was liberal .Any transient loss of consciousness with spontaneous recovery was termed syncope.
- Siezure disorders
- Structural neurogenic (Including , brain tumors , Dural hematomas etc )
- Panic attacks (psychogenic)
Cardiologists wanted to fix syncope as an exclusive disorder of circulatory insufficiency.By bringing in a modification in the definition , ie syncope is now defined as a transient loss of consciousness due to reduction in cerebral perfusion .
This definition helped cardiologists to exclude the above entities . Still many would include all in single basket as patient should be seen as a whole and we can’t expect them to land according to our convenience and classification.
Here is an incomplete* list about causes of syncope (* 99% complete ?)
- Vaso- vagal syncope in young ( Neuro-cardiogenic , Common , Benign)
- Autonomic dysfunction of elderly ( Including postural hypotension )
Arrhythmic ( Sinus node dysfunction /CHB/Idiopathic VT/Long QT syndromes)
Structural heart disease
- Valvular heart disease (LVOT/RVOT obstructions)
- Myocardial disease
- Rarely ischemic heart disease
- Severe pulmonary hypertension (Including PPH , pulmonary Embolism )
- Paradoxical embolism.
- Aortic arch disease -Takayasu related arteritis .
We have a sophisticated array of investigation for syncope .It can be a never ending exercise , ranging from spinal cord evoked potentials to diagnose Shy-drager syndrome , . . . to implanting long-term loop recorders to decode heart beat behavior.
However , evaluation of syncope is the ultimate wake-up call to all current generation cardiologists . . . Why clinical cardiology should never be allowed to die (and it will not ! )
Common sense begins with answering few simple questions . Is it really syncope ?
If you ask this question three times and with specific leads to the patient and the witness , truth will come out . 90% of times it may not be syncope at all (Near syncope, accidental fall, dizziness ,extreme blurred vision, drowsiness etc)
If it is syncope , Is there a non cardiac cause ?
It may related to the Hypoglycemia / Anemia /Panic attacks.Get a neurologist opinion , it would be terrible mistake if you miss a space occupying lesion within the brain. (Missing chronic silent sub dural hematomas is frequent in the evaluation of syncope of elderly !)
Ruling out cardiac syncope is relatively easy
In the remaining patients basic investigation like routine blood tests,ECG, ECHO will help us rule out most serious cardiac disorders.Similarly bulk of the electrical cardiac syncope can be diagnosed.(Holter , carotid study in selected few )
Need for neurologist -cardiologist interaction.
Syncope due to VBI, transient Ischemia attack , Senile vascular dementia is a grey zone . Many have complex neuronal -vascular mechanisms . What is Consciousness ? and What is LOC ? :Is it the lack of blood or severely depressed nerve signal in the reticular activating system? Lots of interaction between cardiologist and neurologist is required to clear our ignorance.(I have one such elderly patient who is intermittently awake ! I call this chronic syncope !) .
Undiagnosed syncope is not a crime
Realise the most important lesson in Medicine . If you have ruled out all serious causes of syncope you should have the courage to be satisfied with that !
Scientific pursuits has a limit. Searching for the mechanism of a psychogenic fainting attacks with intra cerebral electrodes is a clear case of physician acquiring a psychotic behavior !
Syncope is not only a dramatic symptom for the patient , it also unfolds a drama of costly investigations . . . many with dubious value.
Talk to the patient personally for 10 minutes in a quiet room, try to apply that elusive clinical sense . . . it would rarely let you down !
What is the true clinical value of * Head up tilt Test (HUT)?
Will be posted soon
Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), Primary PCI, STEMI-Primary PCI, tagged left main STEMI vs NSTEMI on December 15, 2013| Leave a Comment »
Last week there was a heated debate in our CCU regarding thrombolysis for a patient with severe rest angina and ST elevation in AVR and ST depression in V2-V5 as it implies Left main disease Few argued left main disease is an exception where one can thrombolyse even with unstable angina !
One of my fellows argued ACC guidelines vouched for lysis in UA involving left main .( I do not agree )
A logical attempt to differentiate Left main NSTEMI//UA and STEMI
(In the strict sense Left main NSTEMI is misnomer as AVR shows ST elevation isn’t ? )
Such patients with suspected LMD are to be rushed to cath lab . . . agreed . If it is not feasible , manage it as high risk unstable angina and do not thrombolyse .Let it be left main disease . Indications for lysis are clear. ST elevation in AVR alone can not be taken as an Indication for lysis.For thromolysis to be effective there should be high thrombus burden with total occlusion . ST elevation in single lead (AVR ) is not a good marker for left-main thrombus !
Posted in Cardiology -guidelines, Cardiology -Mechnisms of disease, Cardiology -Therapeutic dilemma, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Statistics, tagged dengue and coronary stent, des and dengue, falling platlets and coroanry stent thrombosis, how to manage fever, thromocytopenia and dengue on December 5, 2013| Leave a Comment »
Oral anticoagulant usage has been steadily increasing for variety of indications.Dengue fever is also appearing in different avatars with low platelet counts and bleeding being a primary risk.
I was recently contacted by a physician , regarding a therapeutic dilemma .A young lady with mitral prosthetic valve and a febrile illness diagnosed as dengue . She has a platelet count of 100,000 .She is on regular warfarin and aspirin .The physician wanted to know , should he stop the OAC and aspirin ?
What are the options ?
- Confirm if it is really dengue.
- Look for clinical bleeding.INR, platelet function tests are not helpful.
- Continue OAC.You can do that in most situations.
- Stop OAC only if there is clinical bleeding episode.
- Anti-platelet drug usage is more tricky .One may stop it if the trend of falling platelet is steep by at least two serial measurement.(or 50% fall from baseline)
- Fresh blood and platelet infusions should be ready .
- Finally and most importantly , Inform the patient and family about the difficult decision we are making.
*Is OAC safer than aspirin and clopidogrel in dengue ?
It is believed OAC has no major Impact on platelet function .It may not pose a threat of excess bleeding in the setting of falling platelet levels .(*Evidence base -nil )
Another potential situation : DES and dengue
The number of DES in developing countries are increasing where Dengue is endemic . It is not a surprising to expect both to occur together.
Anti-platelet agents can be problematic .It is better to withhold it during the active phase of dengue.(If the stent has recently been deployed you have no option !)
1. Prosthetic valve , Warfarin Dengue .
2. DES, Dual antiplatelet agents ,Dengue.
They extraordinary events throw a complex therapeutic task .There are only two options .Continue or discontinue ! Whichever way you do , you explain to your clients (patients!) the (un)reality games we play.
My personal option would be , with hold all hematological drugs during the active phase of dengue .
It is better to believe in the natural thrombus fighting force . Leave the job of anti-platelet action to the dengue virus for a week or two and give oral anticoagulants and dual anti-platelet agents a holiday
It may be foolish to rely on the dengue virus to guard against prosthetic valve and DES thrombus , In reality we have to do that !
No reference exists.It is a statistical mind game.Individual assessment should prevail. Either way, if something adverse happens court of law should protect us !