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Archive for the ‘Clinical cardiology’ Category

Essential Cath lab philosophy !

Posted in bio ethics, Cardiology quotes, Clinical cardiology, Venkat quotes, tagged , , , , , , on April 30, 2012| Leave a Comment »

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What does Amiodarone do to the ventricular rate in AF ?

Posted in cardiac drugs, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -Therapeutics, Cardiology-Arrhythmias, Clinical cardiology, tagged , , , , on April 23, 2012| 2 Comments »

Amiodarone acts  by

  1. Correcting the  rhythm  to sinus .
  2. Controls  ventricular rate  alone
  3. Does both ?

Answer is 3

How can it correct the rhythm alone ?  If  the rhythm is corrected ,  rate will automatically be controlled,  unless Amiodarone converts AF into Sinus tachycardia  which is very unlikely !

Of course  Amidarone  is not a  magic drug .The success rate of  Amiodarone  restoring  sinus rhythm is far . . . far less . . . than our expectations ! . It fails to  convert to sinus rhythm in a significant chunk *. Interestingly ,   it may still  control the  ventricular response  by its beta blocking action .

*Our estimate is , the failure rate Amiodarone  is  between  30-40%  or even higher ,  as   bulk of AF we witness   is due to Rheumatic heart disease.

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Jugular venous pulse in congenital heart disease

Posted in cardiology congenital heart disese, Clinical cardiology, dr s venkatesan -Personal, My presentations, Uncategorized, tagged , , , , , , , , on March 11, 2012| 1 Comment »

Click  to down  load a PDF  version

This was presented in the cardiology fellow training course in Chennai – March 2012

(Acknowledgement : Paul wood collection , J.K Perloff , Credit to Images from open source )

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Unusual arrhythmias during Excercise stress testing

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Clinical cardiology, tagged , , , on February 29, 2012| 4 Comments »

A young  man  fell  off the tread mill  soon  after complaining of chest pain in the immediate recovery  phase.

He had just completed 8 minutes of standard Bruce without any difficulty .

Even as the defibrillator was being  moved near him , he was  successfully   shocked with hands  of a hefty nurse !  ( 25 joules ? )   . He  got into this rhythm !

Note the ECG shows diffuse ST elevation .  The ECG soon settled and a diagnosis of  variant angina was  presumed.

He was shifted to CCU. There was no elevation of enzymes , though he showed a transient wall motion defect lasting up to 48 hours.

The subsequent elective  angiogram did not reveal any critical CAD favoring  Prinzmetal angina.

Provocative tests for vaso spasm is not practiced in our part of the world  (I wonder  whether it is still in vogue at all !)

* The classical  angina of prinzmetal is not related to exertion .  Can we call this as a variant of the variant angina ?

Final message

  • VTs are rare arrhythmias  during EST. However , there are important link between exertion ,  VPDs and VT .
  • Exercise induced RVOT  VTs are  supposed  to  more  common. However , ischemic VT during exercise has to be ruled out in every patient.
  • Non sustained VTs in patients who have baseline VPDs are usually benign .
  • Paradoxically VPDs disappear in many  during exertion indicating overdrive suppression by sinus rate .This again can be ignored.
  • Mono morphic VTs  would suggest structural defects.
  • Polymorphic VTs during exercise indicate either ischemia or electrolytic origin

Also read

Wrong concepts in coronary spasm

Acknowledgement

ECG Courtesy:  Dr G.Gnanvelu MD,DM  Professor of cardiology . Madras medical college

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How accurate is the TR jet derived Pulmonary artery systolic pressure ?

Posted in Clinical cardiology, echocardiography, tagged , , , on February 21, 2012| Leave a Comment »

Measuring TR peak velocity is the most popular  method to assess pulmonary arterial  pressure.It is  universally  believed  TR jet predicts the systolic PA pressure fairly accurately. By all means it is  a wrong perception.

At best ,  it has only 40% correlation with cath  derived PAP  . In other words cardiologist are fooled by TR jet more often than not ! Here is an  elegantly done study  from American  Journal of  Respiratoty and critical care medicine  in  patients  who had undergone lung transplantation . It compared  systolic PAP derived from  Doppler vs cardiac  cath.

”

Source : http://ajrccm.atsjournals.org/content/167/5/735.full.pdf+html

Important observations about TR jet derived PAP

  • Over estimation is the key error.
  • Error of  under -estimation  less common .
  • Over estimation often occur in normal persons
  • Under estimation more frequent in patients with PAH.

(The above study documents  over estimation of 10mmhg  in systolic PAP in 50 out of  100 patients )

Final message

Nothing is perfect in science ,  especially in medical science.  In spite of the limitations  of  TR  jet  , it   will remain the corner stone in the hemodynamic evaluation of right heart pressures . (Forget for the moment . . . the umpteen variables  in  the modified Bernolui equation  , flow acceleration , viscous friction etc )

It is prudent ,  cardiologists  are expected to be aware of this harsh  fact  and  should be meticulous in tracing TR jet and  reduce the error.

One controversial  but logical  suggestion  would be  to drop the ritual of adding  empirical  RA pressure   5- 10mmhg  over the TR  jet  while  calculating PAP , as there is   60 %  error  of  over-estimation  that naturally occur with TR jet. 

Reference

http://www.registroep.org/documenti/IPERTENSIONE%20P.%20CRONICA%20TE/06_Sciomer%20ECO.pdf

 http://ajrccm.atsjournals.org/content/167/5/735.full.pdf+html

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What are the mechanisms of “Pulmonary Arterial Hypertension” in Dilated cardiomyopathy ?

Posted in cardaic physiology, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, myocardial disease, tagged , , , , , on February 18, 2012| 1 Comment »

Pulmonary  arterial hypertension (PAH ) is  an uncommon manifestation of dilated cardiomyopathy .While pulmonary venous hypertension of some degree is expected in most patients with DCM,  it is rare for these patients to go for severe arterial hypertension.

The reason for this may be the  natural history of DCM do not allow these patients to live that longer to manifest severe PAH.  Still ,  we encounter this problem  atleast in tertiary hospitals. Presence of moderate to severe PAH (> 50mm peak PAP) is a sinister sign in  DCM. They not only do badly , they also make  the transplant outcome dismal .

What causes this severe   PAH in DCM ?  The following observations are made in our institute .

Now we know , isolated  systolic dysfunction is  rarely associated with PAH  .It is the presence of  LV diastolic dysfunction (Often restrictive )  that raises the pulmonary pressures.  PAH of DCM is rarely progressive.

One important suggestion is the DCMs  which are associated with  severe  PAH may indeed represent  late stages of RCM , when the LV begin to dilate.

Associated mitral regurgitation   contributes  to PAH

Atrial fibrillation has a significant impact on elevating  pulmonary  venous and arterial  pressures in DCM.

Hypoxic PAH can occur in any medical situation  in susceptible population . DCM is no exception

For some reason  idiopathic DCM is more often result in PAH than ischemic DCM . (Is that possibel , some form of  idiopathic   PAH and DCM are etiologically  related ?)

Further , the positive inotropic agents when liberally used will worsen the diastolic  properties of LV.

Finally involvement of  right ventricle  in the cardiomyopathy  process can have an ameliorating effect on PAH.  A good RV function is essential to lift the PA systolic pressure. If RV failure is causing a low PAP , do not be happy .It simply means RV is going to  say  good bye  . . .  for the final  time !

How to manage PAH in DCM ?

There is no specific management strategy .

We do not know yet  whether Sildenafil ,  Bosentan, and Epoprostenol  have any role in this  form of  PAH. These are all basically vasodilators. It’s use in DCM is vested with a risk of  catastrophic hypotension . Of course ,  we do have a role for balanced vasodilators in cardiac failure .(As most of these patients would be already on adequate ACEI )

Presence of PAH should be considered as an independent indication for anticoagulants as in situ  pulmonary thrombus is common.

The effect of  cardiac resynchronisation therapy in reducing the PAH of DCM is not convincing.

Final message

PAH  in DCM is an unwelcome development. It makes the situation  tough .  The mechanisms are diverse  .Understanding the mechanism would help us deal  this problem better .  Conventional anti failure treatment may help  ,but  it is wiser to try  reserve drugs.

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Tough calls in cardiology : How will you manage ventricular tachycardia with a mobile LV clot ?

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, tagged , , , , on February 16, 2012| Leave a Comment »

Clinical cardiac  problems can be very demanding at  times. Here  is a  situation even the toughest will struggle.

A 52 year old man comes with a wide qrs tachycardia  with a blood pressure of 90 /70 with class 4 dyspnea .He was restless , trying to sit up because of  orthopnea. The ECG showed  a definitive ventricular tachycardia  with LBBB morphology.The patient was   connected  the   oxygen line ,  cardiac monitor, oximetery, etc

The consultant  on call instructed   immediate DC shock   and  he  warned  about  impending ventricular fibrillation .He  casually told the fellow to  do a echocardiogram also and rule out any structural heart disease. Even as  the staff was  arranging the defibrillator , the fellow did   a  rapid bed side echocardiogram . He was  shocked to find a  large mobile LV clot   with a  dilated ,  severely dysfunctional left ventricle  having an  EF  of  25 % .

Now comes  the critical time . Should we shock this man with VT and LV clot?

What will be your option now ?

  1. I will not mind the LV clot  ,  will go ahead with DC  Shock . Let him dislodge his LV clot . If It is his fate  let it be !
  2. Defer the   DC shock . Fall back on medical cardioversion like  Bretyllium, Amiodarone or magnesium  . After all . . .  it is not a pulse less VT. He is not in cardiac arrest . He can afford to wait .We can’t risk a stroke .
  3. Give a low energy  shock  25 joules  with paddles  avoiding the LV apex.  .It may not dislodge the apical clot , still  VT may be terminated.
  4. Try overdrive  pacing instead of DC shock
  5. Refer the patient for emergency surgical removal of LV clot
  6.  Suck out the LV clot with a   LV suction catheter and plan elective DC version*
  7. Insert a temporary Aortic filter and shock the patient **

*  Such catheters are in preliminary stage of development . Is  that true ?  ( If  no I  should get the royalty for the idea  ! )

(Read the related article in my blog )

** A loud imagination . Such filters do not exist.( If  IVC  can be filtered   why not  Aorta ? )

What was finally done ?

After analysing each  of the above  , we decided   option one (  “Prey the  God  and shock the heart” ) After all if it is  a VF ,  this  issue becomes null and void !  . Luckily God was with us.  The  patient  was  reverted to sinus  rhythm with 50joules   and  had  no  untoward events . He was subsequently anti-coagulated .  He is being planned for CRT/ICD therapy

Final message

Critical care  medicine is all about risk taking .Many times , therapeutic maneuvers  confer a  significant   risk  to life  comparable  to the   index problem.  But that  should not be a deterrent .  A careful learned decision  is warranted.

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What are the mechanisms of “Nocturnal” Angina ?

Posted in cardaic physiology, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, myocardial disease, tagged , , , on February 2, 2012| Leave a Comment »

Angina occurring at night is relatively uncommon . It is  still  more rare  for angina to occur exclusively at night (With a possible exclusion of  syphilitic aortits with AR !) The underlying conditions and mechanism  of nocturnal angina  are largely unexplored. In most clinical situations nocturnal angina  is  associated with day time angina as well .

Various mechanisms are proposed

  • It is primarily due to  increased demand  (Holter monitoring has documented  brief bursts  of  HR acceleration  just before  nocturnal angina with  manifest  ST depression )
  • Increased demand  during  REM sleep .
  • Dreams  related adrenergic surge has been implicated.
  • Rarely it is due to supply side defect .
  • Coronary vaso-spasm ( Mostly  in a pre-exisiting lesion )
  • It could  simply  represent  paroxysmal nocturnal dyspnea (pnd)
  • Sleep apnea can precipitate angina  ( Ironically angina occur during   re-breathing  phase )
  • Altered hemo-rheology
  • Nocturnal gap in anti anginal medication *

* May be more  common than we realise.

Cardio vascular hemo-dynamics  at night

If we  believe , sleep is  the great relaxation , and the heart   would enjoy the   “night time”   we  are absolutely wrong . Even in sleep ,  heart has to pump the same 250 ml of blood every minute. Of course , the sleeping heart rate slows down considerably , still  it is interspersed with spikes of activity.  When the heart  rate  slows down  , diastole is prolonged , coronary blood flow  is expected to be copious  unless there is critical CAD.

                                      We  know , sleep is not a passive process  , even as the  autonomic nervous system takes complete control over the  somatic  system .The true colors of  our delicate autonomic system will come to light only during sleep.The muscle tone ,  the sympathetic drive fluctuates according  a pre-set degree . Dreams and REM sleep disturbance can have considerable impact on the sympathetic nerve terminals which ooze  catecholanines  .

Sudden awakening  from  early sleep  is vested with a risk of dangerous   spikes of adrenaline release  .This becomes especially  important in compromised coronary circulation .In fact , this is commonest  sleep -awake  sequence  in patients with nocturnal angina.

Silent ischemia at night

It is curious to note 24 hour Holter  monitoring  reveals  most episodes of ST depression at night are silent. There must be a  specific pain threshold above which a patient awakens  with angina.   The  available  studies   do not  answer this issue   and are not perfect  . We have no way to find  true   silent ischemia  during  sleep.(PET scan in thalamus ?)

Nocturnal angina  in  Aortic regurgitation

Aortic regurgitation  has special relationship with dusk  .For angina to occur AR must be severe and usually isolated .

  • Prolonged diastole at night   -Regurgitation time is prolonged .
  • Dilated LV . Increased  LV mass .Increased demand.
  • Raised LVEDP due high wall stress.
  • Diastolic coronary stealing . Venturi  effect of AR jet

Nocturnal Angina : Is it stable or unstable ?

Most  consider it   as a type of stable angina .Now ,we have reasons to suspect  it could a  marker of unstable angina as it is an  expression of rest angina .

Nocturnal angina vs nocturnal STEMI

How often an episode of nocturnal angina end up in STEMI ?

STEMI is more  common in the early hours of the day and is more related to the hemo-rheological factors  . Please  note ,  STEMI is  a supply side defect  while most episodes of nocturnal angina is due to  demand ischemia . However  it is possible   nocturnal angina episode can precipitate STEMI if  vasospasm is  the underlying mechanism  and if  it is prolonged can trigger thrombosis.

We do not know the answer as yet.

Nocturnal  Angina : Can  it  be PND equivalent ?

Paroxysmal nocturnal dyspnea (PND)  is a classic manifestation of  episodic LVF.  We  know dyspnea can be an anginal  equivalent.  What prevents angina  to  become a  dyspnea  equivalent ! ( Especially the nocturnal ones ,   since the  mechanism  of generation of PND   are very similar  to the  genesis of  angina ). It is distinctly possible  one  may  be mistaken for the  other .  Both occur when  sudden hyper-adrenergic  state  is evoked  which demands   high MVO2 .  An  ischemic heart has every reason to  respond with  angina  .

It is well known  ischemia can result in transient diastolic dysfunction and  elevate the PCWP simultaneously  and PND  would be  the sequel .  When we analysed the  nocturnal calls (  Our fellows ,  do get lots of  such calls from   general wards  at night ),  many  patients with LV dysfunction  who complained  of  classic  chest pain  had  some degree of  dyspnea  and few crackles over lung base as well  .

Nocturnal angina and obstructive sleep apnea

The incidence of nocturnal angina is more common in obese population with obstructive sleep apnea.

The reason is two-fold

1 .Hypoxia mediated

2. Inappropriate tachycardia during recovery phase

Is there any  specific management strategies  to control nocturnal  angina ?

  • General  principles apply .
  • The timing of  anti anginal medication can be adjusted . Long acting preparations taken  in  morning hours to be avoided as they do not cover night time.
  • A calcium   channel blocker   (with optional  beta blocker )  at night may be the best bet to prevent nocturnal ischemia.
  • Dinner to sleep time to be widened.
  • Heavy diet at night to be avoided.
  • Sedatives role is not clear. (Can Diazepam suppress nocturnal angina ?  If so . . .  we  can call it as anti anginal drug  . . .  is isn’t )

References

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2884%2991693-3/abstract

http://www.ncbi.nlm.nih.gov/pubmed/8419815

http://www.nejm.org/doi/pdf/10.1056/NEJM199302043280502

  Obstructive Sleep apnea  and  Angina 1  : http://www.ncbi.nlm.nih.gov/pubmed/7715342

 Obstructive sleep apnea and Angina 2 http://content.onlinejacc.org/cgi/reprint/34/6/1744.pdf

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A dangerous suggestion : Is “Not taking” alcohol, a cardiac risk factor ?

Posted in Cardiology -unresolved questions, Clinical cardiology, tagged , , , on January 3, 2012| Leave a Comment »

“It seems  certain . . . both  zero alcohol  intake and excessive alcohol  confers cardiac risk   “

I stumbled upon  the above   conclusion    from a respectable source*

*This  is from the  famous  INTERHEART  study published in Lancet.

Can it be true ?   What is the proof ?

Consuming  moderate   quantity of  alcohol  reduces  cardiac risk

  Does it make sense  to  skew   this   statement  like this

   . . . Not taking  alcohol   would   be a cardiac  risk  in other wise healthy individual .

Can we  profess  such a reasoning ?  My colleagues call it stupidity ?

If  it is true ,  are we justified  to use  alcohol as  a primary prevention drug ?

Which type  of alcohol we are  talking about ?

I am struggling to get specific answers .

After reading the INTERHEART study , my conviction is  the  “dangerous suggestion”   may indeed  have a significant  quantum of truth !  Readers may share their thinking .

In a country like India where alcohol is considered as a  killer chemical with a huge social stigma ,  it is  blasphemous to suggest  not taking it can be  cardiac  risk factor !

Reference

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2804%2917018-9/abstract#

A. DiCastelnuovo, S. Castanzo, V. Bagnardi, M.B. Donati, L. Iacoviello, G. de Gaetano. Alcohol dosing and total mortality in men and women. Arch Intern Med 166;2006: 2437-2445

R. Femia, A. Natali, A. L’Abbate, E. Ferrannini. Coronary atherosclerosis and alcohol consumption: angiographic and mortality data. Arterioscler Thromb Vasc Biol 26;2006: 1607-1612

D.L. Lucas, R.A. Brown, M. Wassef, T.D. Giles. Alcohol and the cardiovascular system. J Am Coll Cardiol 45;2005: 1916-1924

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Curious lessons in clinical cardiology : Auscultate your ejection fraction !

Posted in Cardiology - Clinical, Clinical cardiology, Uncategorized, tagged , , , on January 1, 2012| Leave a Comment »

How to rapidly  diagnose  significant LV dysfunction  at the bed side ?

Look for

  1. Tachycardia*
  2. Exertional LV  S3
  3. Muffled S1
  4. Weak carotids
  5. Often inconspicuous apical  impulse

If all these signs are present EF is likely to be less than 35 % with 90 % specificity . If this is accompanied by  true cardio-megaly in X-ray chest,  LV dysfunction can be diagnosed with a  precision  reaching almost  100% .

Note the sluggish motion of mitral leaflets and how closely the LV contractility is related to AML movement.This man had a soft S1 and his EF was 30 %

* Tachycardia may be  a non specific finding . Further ,base line tachycardia may  not be present  in all cases of LV dysfunction . When there is a  sudden surge in HR  even with minimal exertion , it  suggests   severe  LV dysfunction.

** The above clues  may not apply  in  valvular heart disease  , and isolated right heart disease  as multiple factors may impact S1 intensity .

*** LV failure must be distinguished from LV dysfunction (Vide infra)

Similarly , a  patient can not have significant  LV  dysfunction if  one  detects any of the following.

  • If the first heart sound is loud
  • If he feels chest thumping as palpitation.(A fluttering and audible   mitral  AML has 100 %  predictive value for normal LV function )
  • If you here an aortic ejection sound (Vascular clicks ) . Ejection clicks need significant force for it’s generation.

Final message

The most mobile structure of the heart is  anterior mitral leaflet . Fortunately it’s closure is  well heard as   S1 . Mind you, the most important determinant of  S1 intensity is  LV  contractility.  If your ear is sharp , and if you are able to  rule out other  reasons for soft S1  (Like obesity, pericardial effusion )  we are fairly  justified in suspecting significant Left ventricular dysfunction.

Further reading :

***What is the difference between LV dysfunction and  LV failure ?

Both these terms are  often  perceived  to convey the same meaning . But it  can  never be used synonymously .Cardiac failure is a clinical entity while LV dysfunction  is  a  derived  technical parameter  by and large an echocardiographic entity. Cardiac failure   is defined classically as a clinical syndrome .(elevated jvp, edema * S 3 rales etc)  Neuro hormonal activation  can occur with both.

A patient with   LV dysfunction    when destabilsed  develops   LV  failure and after stabilisation of   LV failure he is brought  back to  the baseline  LV dysfunction.

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