Tetrology of Fallot is the commonest cyanotic heart disease . In 1973 , working at Portland, Oregon , Bonchek and colleagues created this classic with intense clinical acumen , that defined the way how we understood TOF in infancy . Such studies have become extinct in this fast paced cardiology academia !
With due tributes , here is a slightly modified version of Bonchek classification of TOF in infancy .
Every cardiologist must read every line of this article which came 37 years ago !
Posted in cardiology -congenital heart disease | Tagged bonchek classification of tof, bonchek lawrence, classification of tetrology of fallot, classification of tof, how do you callsify tof, infantile tof, tetrology of fallot, TOF | Leave a Comment »
Cardiologist’s ultimate dream of monitoring their patients
Live ECG feed in your cell phone !
Thanks to the American “scientific pursuit” and the mankind will be the beneficiary !
Courtesy :
What’s next ?
Remote DC shock and pacing .
Watch out . . . it is going to happen in next 5-10 years !
Posted in cardiology -ECG, cardiology innovation, cardiology- coronary care | Tagged air strip technology, coroanry care unit, coronary care in mobile phone, ECG, ecg in iphone, ecg in mobile phone, remote ccu monitoring, tele cardiology, tele medicine | 1 Comment »
The commonest cause of syncope is the neuro-cardiogenic or vasovagal syncope .
The following is the possible neural circuit of this syncope . In fact . it is a “Neuro -vascular circuit”
The afferent* (Two components are present -Both trigger sympathetic signal )
* In some cases sensors and afferent can be same entities.
The centre – Medullary Nucleus ambiguous /Tractus solitarius
The efferent -Strong parasympathetic overshoot and sympathetic withdrawal
Parasympathetic excess lead to bradycardia primarily, while sympathetic withdrawal lead to
hypotension
Syncope recovery
As patient recumbent posture ; LV gets filled and LV mechanoreceptors are passified .
Final message
The exact pathophysiologic basis of this syncope still not elucidated.But one thing is clear , the syncope is due to sympatho- parasympatho signal mismatch( and sort of a rivalry reaction) !In this neural game , heart’s behavior is all the more funny , it initiates the reflex while the brain stem “Boomerangs” it back to heart and vascular system , with a vagal onslaught .
To call this simply as vasovagal is not proper , that is why neuro -cardiogenic syncope was used.
Ideal terminology would be to call it as cardio -neuro -cardiac syncope as the cardiac component form the afferent limb as well as the efferent (target organ )
Reference
Posted in Cardiology - Clinical | Tagged head up tilt test, mechanism of syncope, neural circuit for neurocardiogenci syncope, neurocardiogencic syncope, syncope, vaso vagal syncope | Leave a Comment »
Medicine is an art , evolving art to be precise .We need to use our sixth , if not , the seventh sense ! constantly to improve the quality of life our clients -The human beings.
If only we learn to think right . . . Always right . . . we can bring the heaven of health to the earth
This book fascinates .
Click for a preview in Google.com
Posted in Best books in cardiology, cardiology-ethics | Tagged ethics, ethics in medicine, health for all, hippocrates, how doctors think, kathryn montgomery, medicine is a science or art | Leave a Comment »
LVH is one of the commonest ECG abnormality . We know the hall mark of LVH is increased QRS voltage .We also know , ECG is not a fool proof method to detect LVH .It has very good specificity , but little sensitivity , meaning that increase in QRS voltage is fairly accurate in predicting LVH but absence of which cannot exclude LVH.
Why Increased QRS voltage does not occur in many with LVH ?
Even though we think myocardial mass is the sole determinant of QRS voltage , in reality it is determined by many other factors.
But ,what really matters is the fine balance of blood volume and myocardial mass that determine the incidence and magnitude of LVH pattern in ECG.
QRS voltage as a tool to differentiate pathological from physiological LVH
We know QRS current is generated from within the myocytes .If the myocytes are uniformly hypertrophy without altering the basic mechanical and electrical architecture QRS complex will be amplified in a sm0oth manner and result in classical high voltage QRS of LVH.
If the hypertrophy occurs in a disorganised fashion, where in myocardial fibres slips out of plane with adjacent muscle bundles, the QRS voltage may not increase and even be slurred or notched as we see in many cases of LVH with non specific intravascular conduction defects
The classical disarray of myocardial fibers that occur in HCM causes pathological q waves.
* Other factors that determine LVH include bundle branch conduction delay or blocks which is not discussed here.(Ex: An incomplete LBBB can amplify the qrs without any LVH )
LVH with fibrosis
Fibrosis is not a standard feature of LVH. It occurs in few who are genetically predisposed , and mediated by heightened sensitivity to circulating growth factors.
Other conditions that attenuate LVH features in ECG
Final message
Diagnosis of LVH by ECG is a simple clinical exercise , but we realise now , the underlying mechanisms are too complex .
A simple question , ie Why every one with LVH do not increase their QRS voltage ? . . . exposes our ignorance on the subject!
But one thing is clear, physiological LVH (Meaning LVH , purely due to loading conditions including SHT/Aortic stenosis) more often result in high voltage , while in true pathological LVH(infested with fibrosis ) the increase in voltage is not consistent .
Posted in Cardiology - Clinical, cardiology -ECG | Tagged concentric lvh, eccentric lvh, hypertensive lvh, left ventricular hypertrophy, lvh, pathological lvh, physiological lvh | Leave a Comment »
Bifurcation lesions and ostial lesions continue to challenge the expertise of interventional cardiologists.
Variety of techniques have been described. Geo positioning of a ostial lesions , exactly on the rim of ostium is required . This is very difficult in many patients , as stent migration either into side branch or protrusion into the main branch is common. Both reduce optimal PCI outcome .
Here is a innovative technique described first by Szab0 in 2005 TCT conference .
Highlights of the technique
Technical hitch
The balloon and stent is to be manhandled prior to deployment. We are little awry to do it
Posted in Cardiology -Interventional -PCI, Cardiology-Coronary artery disese | Tagged bifurcation lesion, medina classification, ostial lad lesion, ostial lcx lesion, pci, szabo technique | Leave a Comment »
Japanese cardiovascular society publishes this journal called as “Circulation journal” It has some great articles in every Issue .The Impact factor is consistently rising.
Please do not get confused with AHA’s “Circulation”
Posted in cardiology journal club, cardiology journals | Tagged cadiology journal list, cardiology journals, circualtion, circualtion journal, japanese cadiovascualr society, japanese circualtion journal | Leave a Comment »
Learning (and of course unlearning! ) is a continuing process in the field of medicine. . We have exclusive medical universities for various specialties . The popularity of radial access for doing coronary interventions is progressing very fast and the femoral puncture technique is expected soon to become extinct !
Here comes a virtual on-line university for mastering radial artery interventions.
I wonder , they issue a Master’s degree on the subject !
Thanks to Terumo for initiating the concept .
Posted in Cardiology -Interventional -PCI | Tagged arrow radial kit, radial angiogram, radial aretery, radial artery spasm, radial force, radial pci, radial primary pci, radial vs femoral, radialptca, ulnar angiogram | Leave a Comment »
Digoxin is a wonder cardiology drug used for more than a century.We know the pioneering efforts of William withering in detecting the potential of the unknown herb Foxglove.
Mechanism of action
The beneficial effects of Digoxin is attributable to
Digoxin blocks the sodium potassium ATPase in the myocyte cell membrane .
This cause accumulation of NA + ions within the cells. The excess Na , then facilitates the Na -Ca exchange port .
This pumps in more calcium into the myocyte.
Increased calcium means more forceful contraction and that is positive inotropism* .
* This is a highly simplified version of Digoxin’s action . It should be remembered simple availability of excess calcium can not guarantee contractility, as it requires adequate number of receptors.
Digoxin is used in which type of cardiac failure ?
Digoxin is used for both for LV and biventricular failure .
Digoxins is still often in isolated RV failure of any cause (Cor pumonale, PPH, Eisenmenger etc)
Digoxin and RV dysfunction
Digoxin has a tendency to hit the atrial muscles at random causing multiple short circuiting (Micro reentry ) forming a perfect nidus for complex atrial arrhythmias including MAT .The coexisting hypoxia (which is all the more common here ) aggravates the problem .
Inotropism of RV : Does it really exist ?
It is often quoted , RV is a passive pump. It does not mean inotrpism is an exclusive property of LV.
RV has to generate about 30mmhg to pump the blood into the lungs.
In cor-pulmonale the RV works against an afterload of around 50-70 mmhg , making RV inotropism much more important concept.
Rate control in atrial fibrillation Digoxin lowers the heart rate by vago mimetic action , primarily in AV node and to a certain extent in SA node .Ventricular rate reduction is the prime requirement in the management atrial fibrillation and this property is still the crowing glory of Digoxin.
Though beta blockers and verapamil can be used as rate controlling agent , lack of negative inotropism makes digoxin prevail over , especially in severely dysfunctional ventricle .
But , one disadvantage of Digoxin is , since it requires a vagal traffic to mediate it ‘ s rate controlling effect , it is less effective , when there is high sympathetic activity as during exercise.
What is the action of digoxin on interventricular septal contraction ?
Digoxin , simply does not know where it acts when administered in cor pulmonale ! We believe in cor-pulmonale the maximum action would be the area of maximum dysfunction .This is purely an assumption. In cor -pulmonale septum shifts it’s loyalty from LV to RV as the later is the distressed chamber.So , logic would be there is a theoretical compromise of LV function in patients with cor -pulmonale. These factors make the inter ventricular interaction and dependence a complex one.
Some believe the improvement of sub clinical LV dysfunction in cor pulmonale may be more important factor in giving relief to the patient’s symptom.
What are the other RV inotropes ?
Doubtamine has some RV inotropy .This again may be due to a spill over effect from LV rather than a primary RV inotropism .
As such , there is no great breakthrough in creating a powerful isolated RV isolated RV inotropic dug.
Probably the best way to give relief to RV is to reduce the pulmonary artery pressure as invariably sever PAH is the predominate accompaniment
(Nitric oxide , Epo prostenol etc)
Final message
Posted in Cardiology - Clinical, Cardiology-Arrhythmias, Infrequently asked questions in cardiology (iFAQs) | Tagged atrial fibrillation in copd, corpulmonale, dig trial, digoxin, digoxin in cardiac faiure, digoxin in cor pulmonale, lanoxin, mat, rate contrl in af, rv lv inter dependence, vagal action of digoxcin | Leave a Comment »
AV nodal reentrant tachycadia(AVNRT) is the commonest mechanism of SVT. It is divided into slow-fast, fast-slow, slow-slow , representing the two limbs of he circuit.
Slow -Slow circuit is the rarest type of AVNRT. It should be appreciated , the scientific validity of slow-slow circuit is applicable only in relative terms . A virtually similar antegrade and retrograde limbs with identical conduction velocity and refractory properties , can neither initiate nor sustain an AVNRT.
Caveat in the definition of slow -slow AVNRT.
Even though , we call it a slow-slow tachycardia , one of the limbs need to be faster than the other. So , every slow -Slow AVNRT in reality will have two types
Implication for electrophysiologists and points of contention for the ablationist !
It is not a smart practice to advocate wide area ablation as a routine protocol in all AVNRT
as it directly increase the rate of complication >
Final message
A hurriedly done slow pathway ablation which may temporarily terminate the AVNRT ,only to recur later as the retrograde slow pathway may again form a substrate .The area of slow conduction acts as a turnaround gateway and capture the retrograde fast pathway which could be available in plenty in the anterior aspects of AV node . (Note : The unablated slow pathway now form the antegrade circuit )
Posted in cardiac surgery, Cardiology - Clinical, cardiology -Therapeutics | Tagged avnrt, avrt, dual nodal physiology, electro physiology, fast pathway ablation, fast slow avnrt, RF ablation, slow -slow avnrt, slow fast avnrt, slow pathway ablation, svt | 1 Comment »
Dr.S.Venkatesan MD 