Feeds:
Posts
Comments

How to prevent contrast induced nephropathy in cath lab

July 10, 2009 by dr s venkatesan

Contrast induced  nephropathy (CIN)  is potentially a serious problem. The following precautions are useful in the prevention of CIN.Patients with  serum creatinine>1.5mg carry a  progressive  risk .Diabetics and elderly are more prone.Protienuria is a added risk.

  • Adequate pre procedure hydration is a must . Normal saline (.45%NaCl) infused over 6 hours on the day prior  to flush the kidneys  of protiennaceous  substances.
  • Low protein diet in the days prior to procedure could be useful.
  • Ionic contrast to be  avoided.
  • Among noninionic  low osmolar , monomeric Iohexol may be avoided . Use of isoosmolar , dimeric Iodixanal has some advantage.
  • Oral antioxidant N-acetyl cysteine  600mg twice a day pre and post procedure along with .45% NaCl infusion  is found to be  useful.
  • Sodium bicorbonate infusion . Three  ampuoles of normal saline .9%  in one  litre normal saline infused 3ml/kg per hour started i hour prior to procedure and continued at 1ml/kg for 6 hours post procedure has a renoprotective effect.
  • There could be a role for combination of N -acetyl cystiene and sodium bicorbonate

Apart from the above measures the following general rules are vital

  1. Use minimal amount of dye .<30ml. Dye volume  is more important than the type.(50 ml of isoosmolar dye is more likey to cause CIN than a 30ml of ordinary dye !)
  2. Minimal views to delineate anatomy.
  3. Whenever possible utilise biplane angiography.
  4. Do not  give in to the  temptation of injecting a renal shot.( Although you could miss a renal artery stenosis (RAS), which is likely in these patients .Some may argue  for it ,  as  it gives us an opportunity to cure the RAS )
  5. Stage the  procedure and post it on different day if intervention is required.
  6. PCI for discrete straightforward lesions may be attempted
  7. Avoid complex PCI in renally compromised
  8. Review all the drugs for the potential renal offenders.
  9. Manage the diabetes , cardiac failure meticulously
  10. Have nephrologist always on a  standby mode

Post procedure follow up .

Hydration to continue

Follow up biochemistry

How often we require dialysis   in these patients  ?

It can be avoided in most if we have taken sufficient precaution. In severely compromised renal  function peri procedural dialysis is often used.

Finally , before doing a CAG in renally compromised patient always ask this  question and answer it genuinly . Is the CAG/PCI is really indicated in the given patient ?   Does it going to make a difference for the patient ‘s life ? If the answer is  – No – please avoid it !

Posted in Uncategorized | Leave a Comment »

What are the usual & unusual causes for cardiac source of emboli ?

July 10, 2009 by dr s venkatesan

Common causes

  • Left atrial appendage clots
  • Left atrial  clots
  • LV mural thrombus (Post MI, DCM)
  • Mitral aortic valve infective vegetations

Conditions that could be commoner than we think!

  • Aortic valve  calcific debri
  • Aortic arch atheromas
  • Paradoxical embolism through foramen ovale.*

If we consider incidence of patent foramen  ovale in general  population is up to 20%  the problem of paradoxical embolism could be really significant.PFO is a potential  right  to left channel of more than 5 square cm .

Unusual causes

  • Mitral annular  and posterior leaflet  calcification
  • Tumor embolus (Myxoma etc)
  • Prosthetic valve thrombus.

Cause never known and identified.

There are times a cardiac source can never be identiifed.This can very well happen , as a transient arrhytmia can trigger a thrombus formation and subsequent examination are totally normal .The incidence of such group can never be known !

A brief  account on cardiac embolus

Cardiac  embolus constitute an important cause for stroke or TIA. There are number of important conditions that can result in cardiac embolism. The embolus could be a  thrombus(95% of times ) , Vegetation, tumor, calcific debri, cholesterol , atheromatic particles , rarely chordal and subchordal structures following it’s rupture.The size of the embolus could vary between <.5mm to 1-2cm in diameter.The average size is 1cm . The clinical presentation depends upon the size, content of the emboli(Thrombus vs non thrombus) )  site of trapping, freshness of thrombus, natural lytic process.

The common  sites  of trapping is middle cerebral artery.The average diameter of MCA is around 2 mm.So one can imagine almost most of the cardiac emboli can not traverse it, and hence a  dense stroke .But , micro thromboemboli , can safely cross cerebral circulation.they usually present as TIA or a chronic lacunar infarcts and many times vascular dementias. Cardiac thrombus rarely gets struck within the carotids.This is especially common if there is associated critical carotid stenosis.The situation is a dire emergency.(Inspite of the fact there is circle of willis for

How do you investigate ?

A complete physical examination with well documented clinical history

A meticulous echocardiography with possibly a TEE (Transesophagel echo)  may  done .

Underlying disorder to be tackled.

When a emboli is released from the heart , what determines  it’s entry into carotid ?

The aortic ejection force is such that whatever particle that exit from the heart , tend to hit on the carotid first.Only if it fails to accept it , it is pushed across the aortic arch into the descending aorta.This result in peripheral embolism .Some times a emboli gets struck within the carotid .This  especially happens  if there is associated with critical  carotid obstruction .This can result in massive stroke and sudden neurological death( The threat is real  inspite of the presence of circle of willis which supposed to come to rescue in cases of sudden unilateral carotid obstruction)

What is the relationship between atrial fibrillation and cardiac emboli ?

For long ,the two conditions were thought to closely linked entities.AF slows blood flow across the atria, predispose to left atrial clots and possibly increased stroke.So vigorous means to restore sinus rhythm were attempted. But to our surprise, the incidence of stroke was not greatly reduced between optimal anticoagualtion and sinus rhythn restoration. This indicated many of the cardiac source of embolism could be distal to left atrium aortic arch atheromas, carotid etc (AFFIRM study)

Restoration of AF into SR can possibly prevent thrombus  formation  only in one chamber , while systemic anticoagualtion can prevent thromboembolism virtually any where from the high risk zones across the LA, LV,  Valves, Aorta, arch, carotids etc. So , it defies scientifc logic , to attempt AF restoration by all means (The exotic pulmonary vein isolation etc !)  to  eliminate one of the cause of stroke.

Posted in Cardiology - Clinical, Uncategorized | Tagged | 2 Comments »

3 minutes crash course on ventricular ectopic beats (VPDs)

July 9, 2009 by dr s venkatesan

Ventricular ectopic beats are the most common cardiac electrical abnormality for which cardiologist’s consultation is sought.VPDs are one of most benign observations in ECG and  and almost every  heart experiences it. In 24 hour holter recordings it was reported up to 25% of healthy  individuals .

In spite of this ,  the fear of  noting a VPD in a given tracing of ECG is genuine both for the patient and his physician.This is because  VPDs  can be  a forerunner of dangerous ventricular arrhythmias.

  • VPDs are often graded according to the count and morphology and frequency.(Lown’s ,Bigger’s grading)
  • VPDs that occur in single are less fearsome.( It may not be so . . .)
  • VPDs in couplets and  triplets raise considerable anxiety.( Again it need not be . . .)
  • A series of VPD lasting for 30 seconds is called non sustained ventricular tachycardia(NSVT)
  • If it exceeds 30second it called sustained VT.
  • VT may remain as VT in many.
  • VT may degenerate into VF  ventricular fibrillation in minority( ie cardiac arrest)

The importance of VPDs do not lie  in the number ,  morphology or frequency  but most importantly  in  the underlying etiology. If it occurs in a structurally normal heart it is largely benign.

New onset VPDs should be investigated thoroughly. The commonest symptom is palpitation.

vpd ectopic

Friendly VPDs : Some of  situations where VPDs are  commonly observed and has little significance are.

  • Exercise induced VPDs
  • Pregnancy induced VPDs  (PIH /Peripartum DCM are  rare possibilities)
  • Thyroid associated VPDs
  • Alcohol /Smoke related

What are the VPDs that could be clinically  important ?

VPDs with chest pain(Ischemic etiology )

VPDs in patients with dyspnea.(CHF , COPD)

Drug induced VPDs(Digoxin etc)

Renal failure associated VPDs

VPDs due to hypoxia/Hypokalemia

In patients with pre existing heart disease.(Congenital, valvular, myocardial disease)

What prevents a non sustained VT from becoming sustained ?

No one really knows the answer.Most of the NSVT self terminates.A healthy heart some how gets the capacity to self terminate the arrhythmia.The normal  LV  fails to sustain the abnormal electrical circuit . A diseased heart may not be able to do so . Further if there is electrolyte abnormality (low potassium), or lack of oxygen it may maintain a VT.

What are the most dangerous forms of VPDs ?

  • VPDs that occur during  acute coronary syndrome.
  • VPDs associated with cardiomyopathy( Ischemic , nonischmic,)
  • Some forms of primary electrical disorders of heart( Brugada syndrome, ARVD , CMVT etc)

How do you investigate patients with VPDs?

General medical work up in all.

Echocardiogram is usually necessary in most.

Holter monitoring in occasionally.

Coroanry angiogram rarely

Electrophysiological study in high risk category

How do you manage  patients with VPDs?

  1. Generally do not require any specific drugs in vast majority of individuals .
  2. Reassurance is the key
  3. Ask them to avoid potential triggers like smoke, alcohol, coffee, tea and related bevarages.
  4. If palpitation is troublesome beta blockers( Propronolol, Atenolol, metoprolol can be used.)
  5. Anxiolytic may also be given.

*If the patient has  systemic disorder like hyperthyroidsm , anemia  or underlying heart disease he has to get the specific treatment.

Caution:It has become fashionable for the physicians  to use powerful antiarrhythmic drugs like amiodarone (Cordarone) liberally in patients with asymptomatic VPDs with structurally normal hearts.this practice must be absolutely avoided as amiodarone is one of most toxic  cardiac drugs known  with great pro arrhythmic activity.

When to refer a patient with VPD to a electrophysiologist ?

Physicians   can  treat   most of these patients. But the following will require EP consultations

  • Patients with syncope
  • Patient who have LV dysfunction(Low ejection fraction EF%)
  • Has had an episode of ventricular tachycardia
  • Cardiac arrest

What will the Electrophysiologist  do ?

These patients will be evaluated for inducibility of VT/VF and if the LV function is poor (EF<30%  MADIT 2 criteria ) many would receive implantable cardivertor defibrillator(ICD) or life long anti arrhythmic  drugs.

Some times radiofrequency (RF ablation)  waves are used to ablate the focus of VT.This is possible only if it occurs close to endocardium as  intracardiac catheters do not have access to epicardial  focus. Among  ICD and RF ablation later could be preferred whenever feasible as it eliminates the arrhythmia , while  the former only tackles it only after it occurs .( Hence ICDs  , even though a technological marvel can not be labelled as curative ! )

Final message

VPDs are the   most common cardiac arrhythmia .Most of them are benign. Few of them require extensive investigation.

Posted in Cardiology - Clinical, cardiology -Therapeutics | Tagged , | 5 Comments »

Non dilated cardiomyopthy : An under diagnosed entity !

July 9, 2009 by dr s venkatesan

How will you refer to a ventricle which is not dilated but still has severe global contractile dysfunction ?

Traditionally cardiomyopathy is classified as

  • Dilated (DCM)
  • Hypertrophic(HCM)
  • Restrictive (RCM)

But there is large group of pateints who do not show any of the above features and still have global hypokinesia  contractile dysfunction. this group has been largely ignored .It could constitute up to 25%of all cardiomyopathy.there can be some overlap between non dialted cardiomyopathy and RCM.

We report our experience here with

non dilated cardiomyopathy click to download PPT

non dilated cardiomyopathy

Posted in Cardiology - Clinical, My presentations | Tagged , , , , , , | Leave a Comment »

What is the mechanism of renal failure in infective endocarditis ?

July 8, 2009 by dr s venkatesan

Infective endocarditis (IE) continues to be a dreaded  medical problem. The clinical outcome has not improved much , in spite of  availability of powerful antibiotics. Early surgery in eligible patients  could provide the best possible results.

One of the major determinants of morbidity and mortality  in IE  is the renal involvement.

Kidney gets affected in almost all the patients  with IE.  As IE is a  a systemic illness and  immunological activation is  the  norm ,  some degree of renal involvement is universal. Microscopic hematuria confirms this. This is due to clogging and  globulin mediated  damage to glomerular membranes. There is a linear co relation between  the size of the vegetation and degree of renal involvement.

The following  mechanisms are attributed   for  rapid deterioration of renal function in patients with IE .

  1. Renal arterial emboli-occlusion-renal infarct
  2. Immune complex mediated  focal nephritis .
  3. Diffuse ,  rapidly progressive glomerulonephritis
  4. Drug induced renal dysfunction, especially with  aminoglycosides, vancomycin etc
  5. Finally &  most importantly , the underlying cardiac condition, which result in refractory cardiac failure  may either be primarily responsible for the renal compromise or aggravate the situation.
  6. Combination of each of the above can occur

How to manage renal failure and IE ?

This forms a deadly combination.  Aggressive  planning  & implementation  is  required. Cardiologists, cardiothoracic surgeons, nephrologists  should  discuss the strategies  together.  A microbiologist  is also welcome !

  • If it is purely a pre -renal failure due to CHF, there is no major worry.The  patient should  do well with cardiac failure management.
  • The role of CT surgeon is always vital, since 75% of times , IE patients require  valve replacement or vegetation/abscess  removal  in  an  emergency or semi emergency basis.
  • Pre operative and peri-operative dialysis will  improve the results.
  • Renal replacement therapy , combined with valve  replacement may be the ultimate therapy .It  could be the most heroic way to save a patient but carries near death mortality.

If ,  there is strong  evidence  to suggest  immune activation ,there could be a role for steroid administration. Literature  does not address this issue . Long term follow up of renal function is required in these patients .

Final message

Renal failure in IE is common and the underlying mechanisms are often complex.Early intervention is the key as there is  almost  “no  option” for   conservative management in this situation.

Posted in Cardiology - Clinical | Tagged | Leave a Comment »

What is the mechanism of LV dysfunction in severe longstanding aortic stenosis ?

July 7, 2009 by dr s venkatesan

Aortic stenosis is one of the commonest valvular heart disease.Degenerative, calcific aortic valve is the underlying pathology . Many of the degenerative aortic valve is thought to be  a sequel to bicuspid aortic valve .The exact incidence of BCAV  contributing to degenerative aortic  stenosis is difficult to determine as many of these leaflets  lose  it’s  identity  . Rheumatic aortic stenosis continues to be a problem in developing world.Though ,primary aortic stenosis  is the  dominant theme , some amount of aortic regurgitation is commonly observed in all these conditions.

Apart from the severity of aortic stenosis  there are two  other important factors that determine the long term outcome.

  • LV function
  • Associated CAD.
  • Timing of surgery

Left ventricular dysfunction is a common  companion in severe aortic stenosis .Once the LV dysfunction sets in , there is a rapid decline in the clinical outcome.Some  of these patients have very severe LV dysfunction (EF< 30%) .

LV dysfunction  ,  underestimates  the true gradient across LV .  Cardiologists are  often  preoccupied with assessment of  true severity  aortic stenosis  in the presence of LV dysfunction .Sophisticated dobutamine stress echo, is supposed to help us.

Unfortunately cardiology literature has  little to offer  regarding the mechanism of  LV dysfunction in critical aortic stenosis

Some of the possibilities are

  1. Sub endocardial  contractile dysfunction   due to long standing high wall stress.
  2. Diffuse myocardial fibrosis , scarring , apoptosis.
  3. Associated CAD and ischemic cardiomyopathy
  4. Finally it could be a “Pseudo LV dysfucntion”  ie , simple mechanical stunning due to high afterload.This is a distinct possibility as some of  these   patients with  worst   LV function  recover fully following AVR.
  5. Combination of the above mechanisms  can occur

How will you determine  whether , the LV dysfunction of aortic stenosis is reversible or irreversible ?  Is viability an issue in LV dysfunction associated with aortic stenosis ?

Even though it is logical to think  LV dysfunction of CAD and LV dysfunction of aortic stenosis  are similar it  may  not be so ! ( Unless the LV dysfuntion  due to obstructive coronary  disease coexists)

Following rules need to be applied in patients with AS and severe LV dysfunction.

  • Every patient with critical aortic stenosis should undergo CAG.
  • The question of reversible vs irreversible LV dysfunction generally need  not arise.
  • There is no better way to predict the recovery of LV function other than the trial of relieving the obstruction.
  • So ,all patients* irrespective of  any degree of LV dysfunction shall undergo AVR
  • If there is obstructive CAD they need to be taken for AVR with CABG

*AVR  is  probably contraindicated , in  systemically ill &  co morbid patients , with grossly  dilated  ventricles. Here balloon aortic valvotomy  and  possibly PVR(Percutaneous valve replacement)  could be an answer.

Final message .

LV dysfunction of aortic stenosis is a poorly understood phenomenon. Since it is very difficult  to predict whether it’s reversible or irreversible , real world clinical experience  would suggest there is no need to predict it at all !  and every one should have AVR  irrespective of their LV function.

Posted in Cardiology - Clinical | Tagged | Leave a Comment »

Why mitral valve replacement carries poorer outcome than aortic valve replacement ?

July 6, 2009 by dr s venkatesan

The valve replacement surgery is one of the great innovations in cardiac surgery. The common disorders that require mitral and aortic valve replacement are

  • Degenerative , calcific  aortic stenosis and regurgitation.
  • Rheumatic mitral, aortic valve disease.
  • Ischemic heart disease -Ischemic MR
  • Some cardiomyopathies

The mortality in valve replacement surgeries vary  between AVR, MVR, and DVR.

AVR – 2-5%

MVR 4-12%

DVR  6-15%

Source CTS.net

Determinants of outcome

General factors applicable for both valves

Elective vs Emergency

LV function

Associated CAD /CABG

Co morbid conditions

The following observations  can be  made  in valve replacement surgery

  • Mitral valve function is closely linked to LV function while Aortic valve  is not .
  • AVR  patients always do well than MVR in  the  immediate post operative period
  • Aortic stenosis patients do well than aortic regurgitation .
  • Mitral stenosis patient do well than mitral regurgitation
  • In   DVR  the excess mortality is due to  the addition of MV , not by  AVR .

Aortic valve replacement has better post operative outcome when compared to mitral valve replacement ,Why ?

Aortic valve has only two components namely a  annulus  and leaflets. The prosthetic  aortic valve  replaces both these natural components . Mitral valve has 6 components , prosthetic mitral valve has only two components . Hence  , any prosthetic mitral valve is far inferior to natural mitral valve . The  pap muscle, chordae, and LV muscle fail to assist the artificial  mitral valve.  So , between AVR and MVR   AVR is far perfect  prosthetic surgery and  the hemodynamics   mimic as closely to the natural valve.

Why aortic stenosis patients do better than aortic regurgitation ?

Aortic stenosis  results in severe  LV outflow obstruction .The LV struggles to pump across the obstruction.So , once it is relieved by a prosthetic valve , there is great relief for LV .We know the the aortic valve orifice becomes <1cm2 in critical AS . (Like a pin hole !) .Prosthetic aortic valve at least doubles or triples this orifice and the LV enjoys this sudden relief  and  becomes active or even hyperactive in immediate post operative phase , later  it    settles to a near normal LV function. It has been observed even very severe LV dysfunction associated with aortic stenosis recovers well .

What happens  in AVR done for  dominant or isolated  aortic regurgitation ?

Here the situation  is dramatically opposite.The purpose of  prosthetic aortic valve is  reduce the  aortic valve orifice .

In AR ,  the  left ventricle  is  used to eject  the blood  with ease  across LVOT   without  much  resistance  ,  only to find part of the blood returning  back into the chamber . In  the next beat it does the same and  the cycle   continues for ever .This in due course , dilates the LV  and increases  wall stress and afterload.  LV dysfunction follows .This  takes long time to set in.That’s why chronic asymptomatic AR patients  do so well and they do not require surgery until after the onset of LV dysfunction .(End systolic LV >55mm)

After the aortic valve replacement , the LV suddenly finds  the newly introduced prosthetic valve  a hindrance !. As all artificial  valves  have  less than the natural orifice. LV   takes some time to adapt to the new environment . The EF initially may slightly fall and recovers later.

If pre- operative LV dysfunction was significant the immediate post operative period can be critical.As even a slight fall in EF can result in prolonged hypotension.Many of these   pateint may  require  prolonged inotropic  support.

What are the differences between MVR done for mitral stenosis and MVR done for mitral regurgitation ?

Here again ,  the same principles apply.The Mitral stenosis patients do well following MVR than MR patients.This is because of two reasons .  MR patients  have dilated LV  and may also have associated impaired LV function .A chronic MR is  some   what  a stress reliever  for the LV  ,  as  with every contraction it can decompress a little   bit  . It is an important hemodynamic  fact  ie  ,  presence of   even a  trivial  MR helps the LV to tackle the  it,s  afterload  easily by increasing the dp/dt and also the EF.

So when we introduce a a fully competent prosthetic mitral valve all of a sudden the LV again struggles for some time.

Final message

MVR  patients has less favorable  clinical outcome than AVR .

Coming  soon

How  different is the anticoagulation  protocol difference between AVR  and  MVR ?

Posted in Uncategorized | Tagged , | Leave a Comment »

The “not so” benign chiary network

July 5, 2009 by dr s venkatesan

It is the  embryological remnant within right atrium  often observed as , mobile strands within RA extending fromIVC orifice to IAS. Some  times  it is difficult  to differentiate from eustachian valve  of IVC.The network is formed by collagenous material  and mimic valvular tissue

chiary network echo

Incidence

2% of general population . ( Means 10 crore persons  in our world ! )

What is considered  a benign echocardiographic observation for long  ,  may not be innocuous  . It  can predispose to certain clinical events , although rare.

  1. Mistaken for right atrial mass
  2. May produce  innocent murmur
  3. Catheter entrapment within RA
  4. Infective endocarditis of the network , and tricuspid valve
  5. Abnormal P waves and trigger for  atrial tachycardia
  6. Disrupted chiary network  prolapsing into RV
  7. Associated  foramen ovale  may induce  streaming  .This maintains  an embryonic right atrial flow pattern into adult life and directing the blood from the inferior vena  cava preferentially toward the interatrial septum

Reference

http://content.onlinejacc.org/cgi/content/abstract/26/1/203

http://ats.ctsnetjournals.org/cgi/content/abstract/76/4/1303

http://content.karger.com/ProdukteDB/produkte.asp?doi=10.1159/000096780

Posted in cardiac surgery, Cardiology - Clinical | Tagged , , , , , , , , | Leave a Comment »

Why we look lead V1 to diagnose RVH but look at V4R , to diagnose RV infarction ?

July 2, 2009 by dr s venkatesan

The right ventricle  is a unique  chamber of the heart . It is the anterior most chamber and  triangular in shape.  Even though  the walls of RV are  not  clearly demarcated ,   it does  have  anterior ,  posterior, and lateral free surfaces   . Anatomically it has a inflow  body, apex and outflow portions . The apex of right ventricle , blends with the lower IVS at an acute angle.

How does RVH occur anatomically ?

The anatomy of RV is such that  it does not allow  it  a concentric  RVH ( like LVH ) . In fact , there is a  disproportionate free wall , anterior  wall   hypertrophy  many  situations  like  PHT/Pulmonary stenosis. The  infero posterior aspect of RV rarely show hypertrophy.

Since RV is the anterior most chamber, located just beneath the left border of sternum   RVH brings the RV  further closer to chest wall .This makes the V1 lead to show  tall R in V1.

What happens in RVMI ?

Unfortunately, when we  refer to RVMI , we generally do not make any efforts to locate or estimate it’s  size.  Since RV has , anterior , lateral and posterior surface  , the site  and  the  extent of the  mI will have a major impact  on the  ECG  features .

Most often  the RVMI occur as a  part of infero posterior MI  .Hence ,  it is uncommon for the anterior surface of RV to get involved.  But ,  it can be involved if  RCA gives of a   large RV branch  that reach the anterior surface of RV.

Anterior RVMI can occur as a part  of LAD MI  , if a large conal branch cross the RV surface.

What prevents the lead V1 from showing the  ST elevation of RVMI ?

  • Most of the RVMI do not involve the anterior surface of the RV so , less chances for ST elevation
  • Further , if a true posterior wall  MI  occur as a part of  RVMI (Which is often the case !)  V1 can never  show ST elevation  as the  posterior MI  tend to have a ST depressing effect in the V1, V2 leads.
  • Extensive IWMI , can have reciprocal ST depression in V1-V2.This again , prevents V1 lead to show the ST elevation

So many times , even though V1 lead is just sitting over the chamber RV it fails  to  pick  the  ST elevation forces of RVMI

Advantage of V4 R ?

V4R records remote RV forces , as these  signals are not contaminated by the inferio posterior ST forces. Hence  a  1mm ST elevation in right sided chest leads have good sensitivity  and specificity to diagnose RVMI .

When can V1 show ST elevation in RVMI ?

If the RV anterior wall is predominantly involved (Ie Anterior RVMI ) ST elevation can occur in V 1 like a anteroseptal MI.

rvmi ecg

Rarely a q RBB can occur in V1 in isolated RVMI.

Final message

V1 lead , though anatomically proximal to RV has less value in diagnosing RVMI since this lead picks up  Infero posterior  negative ST forces  and  the anterior  forces of RVMI get neutralised . So relying on lead V1 to diagnose RVMI is not adviced , except when  the anterior surface of RV is predominatly  involved.

Posted in Cardiology - Clinical | Tagged , , , , , , , , | 1 Comment »

Primary PCI is great for STEMI but “Primary CABG ” is not why ?

June 28, 2009 by dr s venkatesan

No one can deny ,  there is a huge revascularisation  dilemma  between CABG and PCI  in patients with CAD. This is especially  prevalent in multivessel disease in chronic coronary syndromes.

In acute STEMI , CABG is never considered as a primary revascularisation  procedure.There should be strong reason for this !  Few studies , suggested a role for CABG in acute MI if it is done within3- 6 hours .But it became very clear , by and large CABG for acute STEMI is contraindicated . This especially applicable when q waves are formed.

Reasons.

Performing a complex surgery  on a   blood vessel subtending a  dead  , irritable ,myocardium is dangerous. Even a graft for non IRA vessel has no great benefit in the acute setting. The mortality of CABG in the first 48hours of MI  can be up to 15%.  Primary PCI  opens up the IRA without the hazards of major surgery

Issues  for  CABG in STEMI

Failed thrombolysis :  Rescue PCI  could be useful provided it is also performed within the same time window . In most situations  there is nothing called  “rescue CABG ” 

Some would believe Left main and critical TVD is an  indication for an emergency  CABG. Yes , CABG may be indicated  in this setting , but even here it may be delayed for a week if there is no ongoing ischemia , angina or hemodynamic instability.

Still  , there is a  definite role for CABG in STEMI in the following situations.

  • Mechanical complication- VSR/MR/Free wall rupture
  • Cardiogenic shock
  • Failed  and complicated primary PCI.( Note : Simple failure to open a IRA is not an indication for CABG , there need to be a life threatening situation ! )

 Coming soon

Routine  CABG  is  generally  dangerous and contraindicated   for STEMI ,  while it  is  a great ,  life saving surgery  in  most of  the  refractory  NSTEMI : How ?

Posted in Uncategorized | Leave a Comment »

« Newer Posts - Older Posts »