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Archive for the ‘Infrequently asked questions in cardiology (iFAQs)’ Category

I know ,there is a VSD out there !  but I am  unable to  get the gradient across it.This situation can be quiet  common .The reasons could  be technical, anatomical or  hemodynamic.

As a rule ,  if we hear  a  pan-systolic murmur clinically ,   one must be able to catch  a good  Doppler spectrum somewhere by  echocardiography . However , If  the murmur is restricted to  early or mid to late  systole, VSD  jet is often attenuated in echocardiography .

In the  following situations ,  VSD  jets  may not  record a distinctive Doppler spectra. Invariably the velocity is low , spectrum is short,  less intense ,  lacks good shape and borders are hazy !

  • A closing  VSD
  • A Small muscular VSD
  • VSD with  Severe pulmonary hypertension
  • VSDs with muscle bundle criss crossing
  • Double chambered right ventricle (DCRV, where VSD usually drains to high pressure chamber.)
  • VSD  associated RVOT obsruction  (Note: classical TOF VSD will never generate a murmur)
  • VSD with sinus of valsalva aneurusms (  Doppler  jet  can be really  difficult to record )
  • Inlet VSDs are missed because  convectional  views of echo are perpendicular to these inlet jets.(Short axis better  )
  • Another common situation  is post STEMI VSR.Both a small apical VSD or multi tract  VSD associated with  infero posterior  STEMI   gradients are  difficult to obtain.

What is   inference ?

Doppler spectrum will help detect  small VSDs and color doppler will not miss even a tiny VSD.Doppler spectrum across VSD  is dependent many  factors other than the presence of VSD. However some large VSDs are detected better by 2D echo rather than doppler signals.

Final message

Presence of a Anatomical  VSD does not  imply it should generate a noise.The murmur as well as Doppler signals  are  primarily  determined by the pressure difference on either side of VSD. After all , one of the  largest VSD  that  we encounter

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qt interval animation short and long002

The stretch and strain experienced by the action potential’s left shoulder region is almost similar* in both long and short QT syndromes that trigger a VT.(* Hope this explanation makes some electrical sense !)

*Click  over the image for  high resolution

What is short QT interval ?
It is a range . Any thing less than 380 ms can be considered  short.Generally It becomes important only at < 320ms.
Relationship between QTc and risk of VT .
U curve of long and short qt syndrome

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Time is muscle. This quote  became  sort of ” cardiology sermon”  in the last  few decades .Cardiologist think  they stand  on a 100 meters sprint track once a patient with STEMI arrives .This is indeed true ,  if we  agree  time is  muscle and  our urge is to reduce the door to balloon time .Please  remember ,  this rush matters  much ,  only if the patient comes through very early  when the muscle is really getting damaged . (No issues  . . . even if the fire engine comes in  slow motion if the  house is burnt fully !)

Time is muscle agreed  . . .  but  muscles are  kept alive by  factors other than time  !  So muscles can  defy time if God  is willing !

Time is one of the important components of management of STEMI.  Other things matter too !  Age , baseline co-morbidity ,  underlying extent of CAD, collateral support of IRA territory , and finally  individual variation in hypoxic damage in myocyte is (Rarely  been studied in detail.)

Door  to balloon time for a patient  who lands up within  1 hour window need  to be  much  different from a patient who comes at 10 th hour .The issue is important  because  we use a procedure which requires delicate decision-making ,(IRA-Non IRA issues etc)  the results can be  sub optimal ,  and even be hazardous in low risk STEMI . So , door to balloon time  may be a less  important  component of  time window in a patient who comes after 6 hours .This is the reason  overall outcomes are not changing in a large cohort  of rapidly performed PCI.

The presumed  absolute  relationship  between  “Time  and  muscle”  concept is  always been a suspect . This  is proven by a flawless study from  NEJM .

nejm stemi most important article

http://www.nejm.org/doi/full/10.1056/NEJMoa1208200

This study should infuse more sense to  us ,  time and again, we are  hijacked and sedated by high dose of  pseudo scientific concoction .In fact ,  indiscriminate rapid PCI may not be in  the good interest of  all  patients with STEMI ,  if it is not properly done  .Without realising this fact many developing countries are indulging in extravagance of  costly STEMI programs wasting  the exchequer.

This landmark NEJM  paper convincingly underscores a fact  that  achieving  rapid door to balloon time  is not  going to be the game changer in  conquering  the Global   STEMI  championship  . We have to take the coronary care into the streets  or to their homes as well .This is where the pre-hospital thrombolysis will  emerge in a big way in the future .

A slow and steady thrombolysis beats a fast and furious primary PCI on any given day in all uncomplicated STEMI .This we have proven for over three decades in  one of the India’s largest coronary care unit .( Where is the data man ?  Genuine experience is data . Why  we require , the act of publication to convert an experience into evidence . Often times ,  I  would feel , data is the most unscientific word in medicine . Many Truths  lack evidence , false hoods come with plenty !  For all those  scientific  homo sapiens  , please recall  70 % of ACC/AHA class 1 recommendations are backed by level C evidence ie simple opinion from  perceived experts! )

Final message

A fast and furious primary PCI may not be  the answer in all STEMI population

Thrombolysis  can be  done  with near  zero time delay , it does not require special expertise where an ambulance driver can reperfuse   a myocardium without much fuss and glamor ! He does not have to  split his hair to identify which is the IRA in a complex multivessel STEMI as well ! The streptokinase and TPA will home in  to the target site  smoothly and swiftly .

If indeed ,  time is the major factor in STEMI , we have many other ways to tame  the time . If muscle is more important than time ,  pPCI is  rarely  the answer !

Some India specific  thoughts

Is it not a shame  , we talk about primary PCI  for all  our patients  who do not even get timely Aspirin* after a STEMI! .It is something akin to what we witness every day ,  as our country folks  wield touch screen  Androids  . . . conversing  in open air toilets !

* While the importance of  Aspirin is undermined , It is different story altogether , these patients  get sorbitarate promptly whenever they get chest pain  (mis-placed and  dangerous priority ! )  prescribed by the  roaring  GPs ,  who suffer from discontinuous medical education ,  propelled  by the deeply penetrated 1000 crore oral Nitrate market .

And STEMI workshops are conducted by self-proclaimed experts  every few months in posh  7 star hotels all over India .

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Anterior mitral leaflet  has a classical M  shaped motion. Infrequently , M mode echo will record a triphasic pattern .

Triphasic AML motion

The exact  answer is not known . I guess it is a normal variant.

Often  it is recorded  when there is a long  and redundant AML , especially if the M-mode cut is too close to  the tips.

Though it is not common , I have seen in few the triphasic gets converted into classical M shaped pattern if the cursor is moved slightly away from the tip of AML.

Relationship to Heart rate

Some times it appears in slow heart rate and tends to disappear with tachycardia .

Triphasic Doppler filling vs Triphasic M-Mode

We do not know yet ,  how  the  triphasic AML motion  correlate  with triphasic Doppler filling pattern which  is considered a fairly good evidence for  LV dysfunction.

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The pericarditis  of acute rheumatic fever is not a true infective pericarditis.It is more of inflammation .It is primarily  T cell mediated  reaction . Neutrophils rarely take part  in this inflammation and hence  no significant  exudation . Hence , there is less  sticky and adhesive molecules inside the pericardial space .The most inflamed layer is epicardium which a nothing but visceral  pericardium .This layer lacks the tensile strength to constrict the underlying myocardium.

why rheumatic pericarditis does not go for constrictionFor constriction to occur the fibrinous  ( thick ) layer of pericardium need to be involved . In rheumatic fever  even though it is  pancarditis ,  fibrous layer is not  involved. Further the inflammatory gradient is thought to spread from within  (Unlike tuberculosis )

Note :  In chronic tuberculous pericarditis,  diffuse inflammatory process  invade from the exterior surface . Very often ,  one can not differentiate  layers. In extreme cases even myocardium and pericardium can not be separated .

Summary

The peri-cardial effusion of acute rheumatic fever

  1. Is transient ,non infective and resolving (Unlike valvular inflammation !)
  2. Less of neutrophil activation  (Less adhesion)
  3. It does not involve the thick , tensile  fibrous layer of pericardium hence lacks the contractile force .

Other lingering  questions

1.How common is tamponade  in acute rheumatic fever ?

2.How important is the mass of the effusion (Viz  a Viz  Intra pericardial pressure !) in causing tamponade ?

//

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Human physiology can dramatically surprise us.Here is a situation regarding K+ ion and cardiac function.

Low potassium level is a well known cause for skeletal muscle  weakness and paralysis.While,in cardiac muscle usually the opposite happens.It is the high potassium levels that depresses and cause paralysis.(That’s why,it is used in cardioplegic solutions. )

But,the classical differences between skeletal and cardiac muscle need not apply in critically  low levels of K +

What happens when K + is critically low ?

We know, K + is the vital  ion that maintain not only the membrane potential ,(Recall Nernst potential ) but also keeps the action potential floating and dipping with every beat.

Imagine the intracellular chaos when these ion levels changes in dramatic fashion . (Of course,God has ensured very tight regulatory controls at various levels within each cell ! )

However , ECG changes are expected 100 % of time with falling K +  especially below 3meq.Surprisingly , low K + levels have little  mechanical impact.(Or is it our ignorance,considering the fact , cardiac electrical mechanical activities are tightly coupled?)We have to find answer from patients like this .

A  30 year old women came with breathlessness and fatigue and her ECG.

hypokalemia STEMI ECG changes

Can we afford to miss a diagnosis of STEMI ? With all our collective wisdom STEMI was diagnosed promptly . . . of course wrongly !

She was adviced  streptokinase.A shrewd fellow who reviewed  the old records spotted the past  history  hypokalemia , and Inj streptokinase was put on hold.(Lucky patient  . . . she was not shifted to cath lab )

Her  K + was 2.3 Meq. The LV function was significantly impaired with global hypokinesia, which  improved with correction of K+.

hypokalemia STEMI ECG changes 001

She was later referred for  nephrology work up , they had made a possible renal tubular disorder for the Hypokalemia.

Clinical Implication.

When potassium levels are critically low myocardial  function may deteriorate.Here is a patient with dramatic STEMI like ECG with extreme hypokalemia.

Our ignorance regarding electrolytes and myocardial function  remains unexposed .In critical care units  wide swinging metabolic and electrolytic  parameters are common.ECG is just a marker  for these .Similarly all LV dysfunctions are not primary myocardial disorders (Sepsis, Hypoxia, Extreme acidois , Uremia ,drugs,toxin  can lead to myocardial dysfunction.)

Experienced  physicians  do not form hurried opinion.Wait . . . allow things to settle down and assess again.After all ,there is long list of causes for ST elevation other than STEMI !

Reference

1.Chest. 1979 Feb;75(2):189-92.Cardiac dysfunction in a patient with familial hypokalemic periodic paralysis.Kramer LD, Cole JP, Messenger JC, Ellestad MH.
2.Acta Neurol Scand. 1978 Dec;58(6):374-8.Hypokalaemic periodic paralysis and cardiomyopathy.Schipperheyn JJ, Buruma OJ, Voogd PJ.

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Cannon waves occur when Atria contracts against a closing tricuspid valve of  right ventricle .( There  would be a equivalent left atrial cannon which  goes into pulmonary vein as well  , it is discussed elsewhere !)

Cannon waves  happen only when P waves fall within QT interval in ECG as QT represents the electro-mechanical systole of  ventricles.  (Since P wave represents atrial systole , it is simple to understand when it falls within QT both atria and ventricular contractions collide to produce a cannon wave into the neck or pulmonary veins.)

The following two images of cannon waves  taken from the legend  Dr Paul woods own tracing  .

irregular cannon waves in jvp  complete heart block

regular cannon waves in jvp  svt avnrt  11 va conduction  002

Regular cannon waves

Occur during SVT  with 1:1 VA conduction.*

1 : 1  VA conduction  can be considered as  absence of  AV dissociation  (Rather  disciplined  VA association with every beat ) This is essential to create a hemodynamic  milieu for regular cannon waves.

* In AVNRT , VA conduction in strict  sense  is a misnomer  .It is simply a retrograde conduction thorough  the AV node .

Irregular cannon waves 

  1. Complete heart block .
  2. Multiple random VPDs
  3. Some patients with VT.*(Who are those patients ?  Those with AV dissociation when retrograde “P” wave falls  within QT interval cannon occurs. As expected this occurs in random fashion  which makes  the cannon fire irregular.

Can we get regular cannon in VT ?

Yes , but rare . As explained earlier this can happen only if AV  association occur on a retrograde fashion.

Further reading in this site

What-is-a-cannon-sound  , how is it related to cannon wave ?

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We do know about left main equivalent . Do we have a proximal LAD  equivalent ?

Proximal LAD lesions deserve a special attention and probably urgent intervention. Medical management is not an option in most  patients. (Proximal alone is not suffice , it should be critical as well )

But we have another issue on hand .What really is proximal LAD ? .

  1. First 5 Cm of LAD ? (LAD normally measure about  15cm so 1/3rd becomes proximal .How logical it looks  isn’t ?  )
  2. Before any  S1 or D1 ?
  3. Before any major S1 or D1 ?
  4. Septal branch is not considered at all  . A lesion is said to be proximal if it is before a major D1
  5. Some others may argue if there are  three major branch  distal to lesion it should be considered proximal.

Proximal LAD equivalents .

LAD first or second   bifurcation  lesions ( Medina1 1 1 , 1 1 0 , 1 0 1)

Mid LAD lesion with major D1 ostial  lesions

For  a super-dominant LAD  even  mid segment  lesion  can  be a   proximal equivalent (By area at jeopardy )

If LAD is giving collaterals  to LCX /OM  /  due to  associated  lesions ,   LAD lesion at any level  becomes  a left main equivalent .

Read the related article in this site

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cardiac auscultation murmurWe know clinical auscultation is an art . It is more of a  special sens rather ! It is a combination of natural and acquired ability of your brain to phase out a sound or series of sounds . Sound perception also has  two point discrimination  like touch .(Auditory cortex -Temporal lobe maturity)

It involves selective blanking  and noise cancellation techniques. Ambient noise  contamination is more in youngsters . Elderly men  often have otosclerois so they are benefited by  this handicap .Your chief maybe one of them .So simply do not bother.

Finally ,  clinical acoustics   require lot of imagination . Seniors professors  know what they are expected to hear in a given patient . They look for it rather than  they hear  it  .This is the secret of their  magic ears .

The famous quote  “What the mind do not  know  . . . the eyes do not see”   is very much  applicable  for the ears as well ! 

What your  temporal lobe  do not expect  . . . the ears do not hear!

Beware , even experienced cardiologists  mistake   systolic events   with that of  diastolic and vice versa !

Final message

With due courtesies  to great men like  Potain ,  Leatham , Austin flint,   and other pioneers of cardiac auscultation , I would modify  the  title  of this article .

The science of  cardiac auscultation  may appear more of an  auditory illusion to many  youngsters today  . Still , dedicated  auscultation , with a sound clinical knowledge in a quiet  room  with  a good stethoscope  would  make this illusion  into a  reality !

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The humble looking strip of ECG  recorded  in millions ,  every day across the globe  has a complex definition.

And this definition  is  the most apt I have found.

An electrocardiogram (ECG) is a curve showing the potential variations against time in the whole body stemming from the heart, which is an electrochemical generator suspended in a conductive medium.

Einthoven(Dutch)  is the the man who invented the ECG  ,  got a Nobel price for not only inventing the string galvanmeter to record ECG,  but also  making us understand   the rules  of the  electrical wave front  that emanates from the heart.( Not to forget the  original concept  of who demonstrated electrical activity from heart by by capillary electrometer.  by Waller.(British). In my opinion waller should have shared the Nobel prize. I am  sure ,even Einthoven would agree to it.

Of course , do not ask  which  comes first  ” Ionic  flow” or  “the current”  that  comes with it !

Credit goes to  the creators of this  wonderful book  on medical physiology and put that free on the net . Three cheers to  them .

The book is from  University of Copenhagen  , Pannum Institute of Medical Physiology.

physiology text book paulev Zubieta sweden

Reference
British physiologist Augustus D. Waller of St Mary’s Medical School, London publishes the first human electrocardiogram. It is recorded with a capilliary electrometer from Thomas Goswell, a technician in the laboratory. Waller AD. A demonstration on man of  electromotive changes accompanying the heart’s beat. J Physiol (London) 1887;8:229-234
Willem Einthoven introduces the term ‘electrocardiogram’ at a meeting of the Dutch Medical Association. (Later he claims that Waller was first to use the term). Einthoven W: Nieuwe methoden voor clinisch onderzoek [New methods for clinical investigation]. Ned T Geneesk 29 II: 263-286, 1893

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