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Posts Tagged ‘venkatesan sangareddi’

How to become a good cardiologist in 7 minutes !

Posted in dr s venkatesan -Personal, general medicine, tagged , , , , , , , , , , on August 18, 2011| 11 Comments »

Here is a  video recipe  !

Please click here to  see more videos from my you tube site

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Aborted and abandoned primary PCI !

Posted in Cardiology -Interventional -PCI, My presentations, Uncategorized, tagged , , , , , , , , , , , on December 8, 2010| Leave a Comment »

It is well  recognised for STEMI  to get aborted   spontaneously or through intervention.

Can a glamorous procedure like  Primary PCI be redundant ?

Yes of course . This paper,  is about how a planned  Primary PCI  can go awry  . . . Presented in the Annual scientific sessions of cardiological society of India Kolkatta December 2010.

Down load full presentation  in PDF format (primary_pci_)

Summary of the presentation

ABORTED  AND     ABANDONED    PRIMARY PCI

S.Venkatesan  G.Gnanavelu.R.Subramanian .Geetha Subramaninan

Madras Medical College. Chennai

Primary PCI has become the  standard of care  for acute STEMI in all  those eligible patients. Apart from the individual & institutional expertise ,the  key  to success  lies in  expediting   the symptom to balloon time to less than an hour.

Even though  STEMI   is characterized  by  acute total obstruction , it  is also a fact during this critical time window , a less recognised   positive  phenomenon takes place within the  ill fated coronary artery. Intrinsic fibrinolytic activity gets activiated and begins to take on the thrombus head on .It should be recalled this is the  earliest intervention in STEMI by natural forces , with zero time window . The power of this natural lytic process has  never  been easy to predict and quantiate . But  we  have  often realised  such a phenomenon do occur often and  is referred  by  various  terminologies like spontaneuous  thrombolyis, aboted MI etc .The exact incidence  is not estimated .In this era of  primary PCI we have found a new opportunity to confirm  this concept.

It has been  observed during  primary PCI ,  an occasional patient  may  have  either  a totally  patent IRA  or a minimal &  insignificant lesion  like luminal irregularity .This has  subsequently led on to cancellation of the procedure .We report our experience with  two patients with  this particular situation .One patient with IWMI with a time window   of  6hours had a totally patent  RCA.  Even , the luminal irregularities were difficult to locate .The other patient had anterior MI with ongoing ischemic pain.He was taken up for primary PCI.The initial angiogram  showed a total mid LAD  obstruction . As soon as the  guidewire reached the thrombotic lesion the  artery opened up   wth a TIMI  3 flow .There was no residual lesion or thrombus  noted. Both of the above  patients  were  young , smokers . 2b 3a antagonists were not administered. We infered, both had thrombotic STEMI and   presumed  to  had either spontaneous reperfusion , or  reperfusion assisted by dye injection & guidewire manipulation. They were  shifted out of cath lab with a new code of aborted primary PCI and  were discharged with normal LV function .It need  to be  realised here, a   distinction must me made between  aborted PCI  and   abandoned or failed  primary PCI  as  the later  connote a negative outcome. The  causes for abandoning  primary PCI are due to complex  lesions like bifurcation /Trifurcation lesions , triple vessel disease  with difficulty in identifying culprit lesions.A  Primary PCI is  considered failed  when the  IRA patency  is not accomplished or  failure to  sustain myocardial flow inspite of  IRA patency (No-Reflow) . These patients may end up in CABG or occasionally fall back on  thrombolysis  which was considered a inferior modality just few hours earlier !

.                                         We conclude , in the management of STEMI ,  primary PCI once contemplated need not always reach it’s  logical conclusion. There are situations  it can  get  aborted or abandoned  at various levels . Aborted  primary PCI  due to spontaneous  lysis though uncommon ,  can be a therapeutically and financially rewarding concept for the patient  and  physician .

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What is the mechanism of pericardial rub ?

Posted in Cardiology - Clinical, Tutorial in clinical cardiology, tagged , , , , , , , , , , , , , on September 28, 2008| 6 Comments »

Heart is externally covered by two layers of pericardium .  Pericardial space is formed between parietal and visceral layers of pericardium . It is a narrow space which is normally lubricated with pericardial fluid up to 25ml. When these two tissue surfaces  come into contact ,  pathological  rub takes place.It is heard  whenever the pericardium is inflammed . Pericardial rub is a distinctive but uncommon  clinical sign .

Common clinical conditions

  • Acute pericarditis
  • Uremic pericarditis.
  • Rheumatic pericarditis
  • Post myocardial infarction

Pericardium has two layers .

There are four  possibilities for pericardial rub to take place.

The rub can occur

1.Between the two layers of pericardium

2.Between the visceral pericardium and the epicardial layer of  heart*.

3.Between parietal pericardium and the  chest wall

4.Pericardium can rub with the adjacent pleura( Pleuro pericardial rub )

The second and third mechanisms are very rare.

An update

We have realized one more possibility . Diaphragm forms the floor of the heart on which the hanging heart  rests . Rubbing of pericardium over diaphragmatic surface is a beat to beat affair that lasts the entire life !. In inflammatory states of  diaphragm especially  the contagious  ones from abdomen  , can result in pericardio- diaphragmatic rubs .These rubs are almost impossible to hear clinically.

pericardial effusion rub plural pleuro pericadial

*The anatomic mystery : Is epicardium same as visceral layer of pericardium ?

Some anatomist feel that both are same entities. If that is the case myocardium can never split its relationship with visceral pericardium.But it is also a anatomical fact visceral pericardium engulfs the coronary artery and  are located sub epicardially.

How many components of pericardial rub are clincally heard ?

Pericardial rub  classically has three components. Systolic, mid diastolic, and pressytolic atrial components. Pericardial rubs are typically described as to and fro rub. Systolic component is most consistent. In atrial fibrillation mono component pericardial rub is heard.

Quality

Superficial , scratchy, high pitched ( Can also be low pitched)

Location

Left sternal border , left 2nd or 3rd space  .Best heard in  sitting , leaning forward in inspiration. Many times the rubs are transient and evanescent . Since it has multiple components it may be mistaken for added heart sound like S 3 or S 4.

What is the mechanism of pericardial rub in the immediate post MI phase ?

Presence of pericardial rub post MI indicate a transmural involvement or atleast significant epicardial involvement . Recognition of this is important as presence of pericardial rub increases the risk of rupture  and hemorrhagic effusion if anticoagulants are used.

What is the  relationship between  pericardial effusion and  pericardial rub ?

Generally it is said with the onset of effusion pericardial rub disappear.But this is not necessarily true.

Rubs after contusion chest and fracture ribs can be with the chest wall and may have  no relationship with effusion.

Is pericardial rub a painful condition ?

Pericardial  rub associated with acute inflammatory pathology is severely painful (like a pleuritis).But pericarditis associated with chronic inflammatory conditions are less often generate pain.The exact reason is not known.

What is pleuro pericardial rub ?

This  clinical entity is poorly defined , often taught by veteran professors  in clinical auscultation classes.It can be heard in the mid segment  or diaphragmatic pleuritis with or without pericardial effusion in patients with  atypical pneumonias.

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