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 on August 19, 2010| 1 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 Uncategorized, tagged lbbb hv interval on August 18, 2010| Leave a Comment »
These simple questions were asked once upon a time when cardiologists were not known as interventionists.Now many of them have neither time nor interest to ask such questions .! An article which came in Circulation 1974 addresses this question lucidly.
It is known, HV interval represents infra hisian conduction . And LBBB is just that ! Then , why it is not prolonging it ?
The answer is , it does prolong the HV interval by 20 -40 ms , but , it is not manifested in surface ECG . A 20 ms increment in PR interval (Say 160 to 180 ms ) is not a big issue generally.
* Then the concept of incomplete and complete LBBB is always there to confront us !
Many believe , the intraventricular conduction delay in LBBB may simply represent the “unmaking effect” of LBBB which re-routes the conduction in the slightly delayed , circuitous right bundle highway . But it is only a assumption.Many things can happen in a ischemic , degenerative, dysfunctional heart.
When does the HV interval prolong pathologically in LBBB ?
Acute LBBB (Note Left bundle has two fascicles , technically equivalent to bifasicular block ) A 40ms increment in HV interval (Hence in PR interval also) can be a dangerous delay in LBBB .
Posted in Cardiology - Clinical, tagged head up tilt test, mechanism of syncope, neural circuit for neurocardiogenci syncope, neurocardiogencic syncope, syncope, vaso vagal syncope on August 17, 2010| Leave a 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 Uncategorized, tagged dialysis pericarditis, ecg changes in uremic pericarditis, uremia, uremic pericarditis on August 13, 2010| Leave a Comment »
Pericardium is a fine biological sensor. It makes noise when the kidney is in distress .
We call this as uremic pericardial rub . This is not a universal phenomenon in renal failure.
Occurs in about 10% of renal failure .
Mechanism
Two themes can occur .
The later is more common .
Is it a exudate or transudate ?
Usually a transudate. Protein accumulation may occur .
Hemorrhagic or non hemorrhagic effusion ?
Again both can occur. Platelet dysfunction is well known feature of renal failure .Bleeding into pericardial space even a few cc of blood is suffice , to color the entire effusion red .
ECG features of uremic pericarditis , how is it different ?
The uremic pericarditis less often results in classical ST elevation (concavity upwards) instead the hyperkalemia features dominate , if present.
The reason for less conspicuous ST elevation is due to the relative lack of epicardial electrical injury . Further , the pericardial fluid is enriched with oppositely charged uremic molecules which neutralise’s the
electrical gradient .
Relationship of pericarditis with acuteness of renal failure
Though it can occur in any form of uremia.It is more often observed in rapidly worsening renal failure
Relationship to dialysis
Complication
Tamponade is common .Usually tolerated well till late stages as LVH and mild PAH are common which resists fluid compression.
Constriction can rarely occur. Tuberculosis can co exist.
Management
Patients with pericardial rub should be dialysed heparin free .
Reference
Review article
http://emedicine.medscape.com/article/244810-overview
http://circ.ahajournals.org/cgi/content/short/53/5/896
Surgical management
Posted in Uncategorized, tagged classification of pericardial effusion, constrictive pericarditis, grading of pericardial effusion, horowitz classification, minimal pericardail effusion, pericardial effusion, pericardial thickening, systolic pericarail effusion, thickened pericardium on August 13, 2010| Leave a Comment »
Detection of pericardial effusion was the earliest clinical application of echocardiography. Diagnosing large effusions is a non issue .Assessing minimal effusions (Systolic vs diastolic echo free space) and associated thickened pericardium is tough even after 50 years of echocardiography.
Mainly , we are limited by the resolution power of echo. Further , lack of echocardiographic landmark for visceral layer of pericardium (It is same as epicardium !) makes diagnosis of thickened pericardium a real tough exercise.It is said , normal pericardium is less than 4mm .
Where to measure it ? how to measure is still not clear.
Why differentiating minimal pericardial effusion from thickened pericardium is important ?
Here is a link to Horowitz classification of mild pericardial effusion ...
http://circ.ahajournals.org/cgi/reprint/50/2/239
It could help us understand, How thickened pericardium presents in echo. Of course, CT and MRI now have increased sensitivity for diagnosing pericardial thickening.
Posted in Uncategorized, tagged anaesthesia in pregnancy, heart disease complicating pregnancy, hemodynamics of pregnancy, normal vaginal delivery vs ceserian, obstetrical anaesthesia, pregnancy and heart disease on August 12, 2010| Leave a Comment »
Cardiologists are often confronted with pregnant women in distress with heart disease. Obstetricians promptly refer them to cardiologists.
There is a tendency among cardiologists, to make fun of obstetricians who some times call them for frivolous cardiac problem at odd hours .(Say a VPD in the monitor or a systolic murmur of anemia etc)
Of course , this doesn’t mean in any way , cardiologists belong to a superior species ! The fact is , many cardiologists fare poorly in their knowledge about the hemodynamics of pregnancy (Let them prove this wrong !)
A small quiz . . . for all cardiologists
If a cardiologist is able to answer all these 5 questions correctly without guessing , probably they have the right to make fun of obstetricians or else they have to quietly buy this book and read !
Final message
Every responsible cardiologist must have good awareness about hemodynamic stress of pregnancy and the intricacies of obstetrical anesthesia
Posted in Uncategorized, tagged british heart journal, echo normal measurements, echocardiography, foale, normal rv dimension, normal rv inflow, normal rv size, normal rvot, rv body rv inflow view, rv enlargement, rv inflow vs outflow, rv out flow, rve, rvh, rvh by echo on August 12, 2010| Leave a Comment »
It sounds to be a simple question . But, cardiology literature is sparse on the subject.
RV mimics a three dimensional triangular chamber .The inflow, body and outflow align themselves in complex planes .This makes measurement difficult.
What are the measurements to be made ?
How to measure RV size ?
What is the normal range ?
RV Body
< 3 cm in parasternal long axis view
<8 cm Long axis ( RV apex to mid point of TV )
RV inflow(RVOT)
< 3- 4cm
RV outflow (RVOT)
1.8 to 3 cm
Note :
How common is the differential RV enlargement*?
The complex shape and architecture of RV make the direction , sequence and magnitude of RV enlargement less predictable .
* The fact that , RV can enlarge in focal and localised manner make it mandatory to measure RV dimension in multiple views and in all possible diameters.
At what pressure RV begins to enlarge ?
RV is believed to enlarge at > 60mmhg .Hypertrophy is usually precedes dilatation .
At what volume overload RV begins to enlarge ?
Our experience with ASD indicate when the pulmonary blood flow is twice that of systemic blood flow RV is distinctly enlarged. May be it begins to enlarge at> 1.5: 1 shunt
RV begins to enlarge horizontally or longitudinally ?
this aspect is not studied much. Generally volume overload causes more uniform enlargement.
How does acute RV enlargement differ from chronic RV enlargement ?
Dilatation is more conspicuous in acute RVE ( Pulmonary embolism, RV infarct ) associated wall motion defects and thinning favors acute RVE.
Normal or increased thickness is expected in chronic RV enlargement
Here is a five-star rated article on RV dimension
Published in 1986 , still considered a land mark paper . . .
