While their cardiology colleagues are extravagantly indulging in coronary arteries ,It is heartening to note the pediatricians our country has silently come out with the first India specific criteria for Acute Rheumatic fever diagnosis and management.
It was long over due . . . three cheers to them !
*The most ironical, part of part of the story is , the guidelines which is is 4 years old ( came in 2008 ) . It is no wonder many of us are not even aware about the existence such guidelines , still every one wants to do PTMC at every given opportunity for a full blown mitral stenosis!
Highlights and Summary
- WHO criteria of 2001 is adopted
- ASO titre positivity alone has less value in the diagnosis .Hence the importance of which is down graded
- Steroids are mandatory in all carditis for 12 weeks
- Benzathine penicillin should be administered weight based and to be shortened every 15 days in children less than 27 kg
More high lights will be posted.
Secondary prophylaxis of for Rheumatic fever
Note the Important advice regarding weight based penicillin prophylaxis.
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What are the blind spots of aorta in Tans thoracic Echo ?
What are pseudo dissection flops in aortic arch ?
How to differentiate true from false lumen ?
Can TEE also miss any segments of Aorta ?
How is Aortic Intra mural hematoma differentiated form true dissection?
Spend a minimum of 30 minutes in this 14 page article. You will be able to answer all these and much more ! The knowledge gained , would easily beat a day long crash course on Echocardiogram !
Please thank the European society of cardiology for providing this article free of cost !
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Tachycardia – Bradycardia syndrome is the hall mark of sinus node dysfunction.
- The commonest tachycardia in sinus node dysfunction is Atrial fibrillation . Followed very closely by sinus tachycardia . In fact alteration between sinus tachycardia and sinus bradycardia without other pathological arrhythmia is rare . (Of course , we have a name for such an entity as inappropriate sinus tachycardia / bradycardia )
- Atrial tachycardia occurs a distant 3rd
- Ventricular tachycardia may be an exception (Please note , extreme bradycardias which lead to pause dependent VT is not directly related to sinus node disease )
The commonest bradycardia in SND is
- Sinus bradycardia (This fact is undisputed unlike the tachycardia component of SND !)
- Followed be sinus pause , SA blocks and sinus arrest .
- AF with slow ventricular response ( Bradycardic AF) We are not sure about the rhythm here (Is it truly junctional /or conducted atrial ? )
- Associated AV block can occur up to 20 % of patients .If AV block is present the true nature of SA node disease is masked and it’s function becomes almost irrelevant .
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Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Coronary artery disese, Clinical cardiology, tagged adrenergic wall motion defect, apical ballooning in stemi, remote ischemia, remote wall motion dfect, stress cardiomyopathy, takotsubo cardiomyopathy, unexplained wall motion defect in stemi, wall motion defect in stemi, what is remote wall motion defect on June 24, 2012 |
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Stress related wall motion defect is a well-known entity . It is referred to as Takotsubo cardiomyopathy .
These stress are often
- General systemic stress
The culprit seems to be pooling of adrenaline and nor adrenaline in myocardium .These remote neurogenic stress can cause significant wall motion defect due to adrenergic downpour
The image depicts the wide variation in the density of beta receptors in heart.The stress of MI can result in varying degrees of wall motion defect .It is important to realise the wall motion defect in STEMI has two components .One is related to ischemia and other is due to excess catecholamines. This explains many of the unexplained remote wall motion defects during STEMI .This may be referred to as Intrinsic Takosubo effect !
Then . . . the following questions arise
When systemic stress can have a profound effect on myocardium , what about local stress ?
Acute STEMI is a huge stress for the heart . . . isn’t . If so , can it alter the wall motion defect in adjacent or remote myocardial segments independent of ischemia ?
With the distribution of adrenergic receptors showing huge variation , we do not know how an acutely ischemic heart spills the adrenaline all over . Is there a pattern to it ? or it happens at random ? Further , the response to accumulated catecholamines is not going to be uniform. This will explain why certain patients go into ischemic LVF , very early in the course of STEMI even before the myocardium is necrosed. It will also explain the benefits that accrue in selected patients who receive early IV beta blockade ( Which is of course currently not popular after COMET study ! )
We have seen at least two patients with severe transient ballooning wall motion defect in LAD region (LV apex) with isolated RCA lesion and inferior Infarct .
The question raised is this
Can the stress of Inferior STEMI . . . result in apical Takatsubo like effect ?
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There was a big debate in one of my classes with cardiology fellows regarding the shunt quantification of ASD . We were talking about the significance of ASD shunting . We suddenly realised 2:1 left to right shunt is not a simple equation to comprehend . I was thinking 2:1 shunt would mean pulmonary flow would be twice the systemic flow . It was not to be !
Is ratio of shunting and Qp/Qs convey the same thing ?
No . Qp /Qs is the ratio of pulmonary to systemic blood flow flow . When we want to quantify shunt we express it in two different ways .
1. The amount of blood shunted form left side to right side of the heart .
2. The amount of pulmonary blood flow to systemic blood flow in absolute terms .
Though both are closely linked entities they do not denote the same meaning . When we say 2: 1 shunt we refer to the shunted blood across the defect but when we calculate pulmonary blood flow we take into account venous blood which does not take part in the shunting .
The confusion arises because we use both terms interchangeably.The following illustration will try to prove A 2: 1 shunt would actually correspond to a qp/qs of three (Pulmonary flow is 3 times the systemic flow !)
Let us begin with a hypothetical ASD patient who has systemic cardiac output of 4 liters.
He shunts 2 : 1 from left to right . ie he shunts 2 /3 of three parts into RA (66% ) .
A patient who delivers 4 liters from LA in the presence of 2;1 ASD shunt would mean he would receive 12 liters from the lung as pulmonary blood flow.
I am still not fully convinced about the above reasoning . It guess it is correct. I argue the fellows to give further insight into this equation. The complexities in Bi directional shunt and effective pulmonary blood flow in Eisenmneger syndrome is going beyond my heads !
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Essential qualification for becoming a great medical researcher is the “Fine art of mis-interpretating data “ Venkatesan sangareddi MD .Chennai .India
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Thrombolysis in acute stroke
- rtPA is indeed useful in acute Ischemic stroke
- Elderly need not be excluded (Even > 80y)
- Time window : It definitely works up to 4.5 hours and vary likely to be effective up t0 6 hours.
We are gradually widening the time window , which was 3 hours a decade ago .It may soon catch up with STEMI window of 12 hours ! ( Mitochondrially myocytes are not vastly different from cerebro-cytes ! )
So , the current role of of thrombolyis for stroke is best answered by the editorial accomplishing this article !
“The role of stroke and emergency physicians is now not to identify patients who will be given rt-PA, but to identify the few who will not.”
Reference : A Lancet Break through
- By the way , rTPA is prohibitively costly for common world citizens . Please tell us about streptokinase in stroke ? Does the poor cousin match the rich ?
- Do we have primary cerebral angioplasty ?
Please read the comment form Dr Anthony Andrew Bell it is a must read !
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Posted in Cardiology - Clinical, cardiology -Therapeutics, myocardial disease, pericardial disease, tagged constrictive pericarditis, deep y desend, differential diagnosis of constrictive pericarditis, pericardial knock, restrictive cardiomyopahty, square root sign on June 14, 2012 |
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A patient who presents with predominantly right heart failure is an interesting clinical challenge . Constrictive pericarditis (CP) remains a popular diagnosis in this setting. However in the bed side clinical examination (and in cardiology Board exams ) the following differential diagnoses are to be considered .( And ruled out one by one)
- Restrictive cardiomyopathy* especially Right sided .In India endo myocardial fibrosis tops the list
- Primary Tricuspid valve disease( Tricuspid stenosis / Carcinoid etc)
- Chronic cor-pulmonale in terminal RV failure
- Silent Mitral stenosis with right heart failure
- Ebstein anomaly
- Severe forms of valvular pulmonary stenosis with RV dysfunction
- SVC obstruction
- Cirrhosis of liver
- Porto pulmonary hypertension
( The list is not complete , readers may contribute )
Bed side clues
- Remember a deep “y” descent is the bed side counter part of Square root sign recorded by invasive RV pressure study
- Similarly , pericardial knock is the auditory equivalent (You hear the square root ! . . .yes )as the ventricle thuds the rigid thickened pericardial shell in very early diastole !)
- Pulsus paradoxus and kussmal sign can occur in both CP and RCM.
- If a good LV apex , is palpated it goes against CP .
- Please be reminded , even restrictive cardiomyopathy will ultimately dilate their chamber pre-terminal and clinical features may be confounded with that of DCM.
- Silent heart would suggest CP.
- AV valve regurgitation would favor RCM
- Features of Pulmonary hypertension will help confirm Mitral valve disease , Cor pulmonale,
- Deep “y”descents are against any form of Tricuspid stenosis.
- Opening snap of mitral valve is to be distinguished from pericardial knock.( Opening snap high pitched and occur later than pericardial knock in diastole , best heard in expiration )
- Cirrhosis liver with hypo- proteinimic fluid retention is a traditionally close mimicker .It may be ruled out by the careful history taking as exertional dyspnea is an exception , if at all , it is a very late event in cirrhosis.
- The issue gets further weird as chronic constriction can lead on to chronic congestive liver and cardiac cirrhosis .
- Severe forms of constriction can invade the myocardium and result in features of myocardial dysfunction .It is more common than we recognise.
How to confirm ?
Following should be performed in that order
- X -Ray
- CT scan
*Cath study is no longer done (Only for academic purpose )
Even in this era of sophisticated medical imaging , clinical examination remains the key . One should realise the importance of meticulous clinical history , sequential examination and interpretation .It will “rule out or rule in“ majority of cardiac disorders .
The hi tech imaging modalities should be used only to confirm , risk stratify and plan management . If you skip the clinical part , one may still arrive at a correct diagnosis but there is high chances of erring in management.
(Cardiac pearls lie in the bed side not in cath labs ! Here is one such pearl . Not every constriction require surgery !
Please note about 20 % of constrictive pericarditis are transient !)
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