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Basic lessons in STEMI :Does dying myocytes release potassium into the circulation ?

February 10, 2012 by dr s venkatesan

Human life is a bundle of energy orchestrated by ions coming  in and  going out  of  every cell . Potassium is the life sustaining ion which  determines the  resting membrane potential  of our cells.

When the  heart  suffers a massive necrotic attack  what  would  happen to the potassium dynamics  inside the  myocytes ?

K  + is the dominant  intracellular cation  ,  when  about  100 million myocytes   die  suddenly ,  a chaos in the  potassium  metabolism  is expected  is it not ? .

When skeletal  muscles dies  it  releases  potassium  . We  know   this  from typical crush injuries and rabdomyolyis.

It is  more of a  common sense  to expect this   . . . from myocardium as well .


Which ion is responsible for the current of injury ?

We know a  strong and continuous  negative current that  emanates from the necrotic zone after STEMI  .  (It is so powerful it  shifts the baseline  itself  !), We do not know yet what exactly  is causing this current of injury .  It goes without saying sodium should sustain the depolarisation wave but  potassium will  also have a major role in the  propagation  of this injury current.

Do dying myocytes   excrete the potassium into the circulation   ?

Is    k+  a marker of extent of MI  ?

What is the mechanism of hyper acute tall T waves in  MI ?

Questions  galore  . . . Answers struggle !

When a  large  area of  cardiac muscle goes for necrosis  it  leads to  leaking   of   K +    . If it is true  , it  is expected to be a marker for extent of  infarct. In reality it is not . Why ?  This is because cardiac  potassium pool is much  small . A  leak from  an organ which weighs   400 grams   do not elevate the ECF  potassium .  Still , there is ample evidence  for   K + to accumulate  in the local  intracellular milieu. (Myocardial hyper-kalemia ) In fact ,  one of  the mechanisms  suggested  for tall T waves in  hyper-acute MI phase   potassium excess .

Image courtesey hqmeded-ecg.blogspot.in/2009/02/hyperacute-t-waves.html

http://hqmeded-ecg.blogspot.in/2009/02/hyperacute-t-waves.html

Potassium levels and incidence of  ventricular tachycardia.

Many of the primary ventricular arrhythmias  are  due to acute ischemia .  We  have conflicting evidence  for  the effect of ischemia on QT interval. How does ischemia trigger VT  ?
The answer to this question  remain as a missing link !  . Grossly simplifying ,  one could suggest it is  due to   ischemic cell membrane damage that alters the ion channel function  , resulting  in intracellular accumulation of calcium and triggered  activity  .

What is the effect of potassium  on cardiac contractility  ?

Myocardial paralysis.  (Please note  it is the  hypokalemia  that primarily  causes paralysis in skeletal muscles !)

It causes  myocardial  stunning  a manifestation of local potassium  leak ! A temporary myocardial paralysis.

What does the current guidelines of ACC/AHA state about potassium hemostasis  in STEMI ?

It suggests   a fairly aggressive  maintenance of potassium levels  to  upper normal levels. Traditionally we are worried more about hypokalemia than the hyper. It is  surprising   we had the facts wrong . . .  for so long !

What is new in the regulation of potassium level during STEMI ?

This landmark paper from JAMA seeks  to set right the misconceptions about potassium during STEMI. It suggests  K + levels  has a U shaped  morbidity curve in STEMI . One need to be cautious in  correcting borderline hypokalemia .  Serum   K +   is   absolutely useless  surrogate marker for myocardial K +   . We do not know how  K  +  behaves in the vicinity of MI  zone . So  extreme caution is required  when giving IV  K +  supplements in coronary care units .

Watch out :  Beta blockers /ACEI   may worsen  hyperkalemia

Early introduction of ACEI and ARBs   is a strong risk factor for systemic as well as myocardial  hyperkalemia . This  is  especially true  in diabetic individuals  who have  low rennin  levels due to diabetic micro circulation defect in kidneys .(Hypo-reninic  hypo-aldosternosim )

Beta blockers are also known to raise potassium by two mechanism

1.Blocking rennin

2.Reduced uptake of K + in to  the cells.

http://medicineforresidents.blogspot.in/2010/09/hyperkalemia-with-beta-blockers.html

Final message

In the management of STEMI  ,   revascularization  of  the myocardium    is  considered as  the only  therapeutic aim . We  need to realise it   is  much more than that .  There are some subtle but important ways of resuscitating and  protecting  myocardium .  Over  indulgence in electrolytic management  in coronary care  is to be avoided.

Reference

Importance of sympathetic drive and  potassium levels

http://www.nejm.org/doi/full/10.1056/NEJM198002213020803

http://ccn.aacnjournals.org/content/23/6/14.full.pdf+html

Posted in cardaic physiology, cardiac physiology, cardiology -ECG, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Coronary artery disese | Tagged , , , , , , , , , | Leave a Comment »

Great men in medicine : Virchow is much . . . much greater than his “Lymph node and the Triad” he is known for !

February 8, 2012 by dr s venkatesan

Some scientists are  known for their discovery ,  few are known for their vision  few for their character .Here was a man who  had  all of them  can be termed as father of modern medicine .

Rudolf Virchow - German pathologist( 1821-1902)

Unfortunately the current generation knows him for his concept and theory of blood clotting  or  lymph  node in the neck .

Here is a  reviews about this man who single handedly   taught  the world

He  insisted  , caring  the sick and treating illness  is  more of a social science than medical one

We  have probably  not  learnt  a single lesson yet , from this master  teacher is a different story !

Avid listeners to Virchow in Berlin university

My  Virchowian thoughts

This man’s understanding of medicine was much . . .  much sharper than us –  100 years ago  , when  cardiology was practiced  with out  even an  ECG and   X-ray chest  . ( Is itn’t  true   today  we struggle with  loads of  3 dimensinal  gadolinium enhanced  cardiac MRI ! images )

Virchow’s  concepts  are most relevant in today’s world  , where the corporate and capitalist  culture  has  hijacked the  noble profession . Inhabitants of this planet are  threatened with eccentrically blown up  healthcare  system   where  the  development of   modern medical   modalities is completely out phase of with what  is required for the people .

We will pay a heavy penalty  if  this world  continues to witness   people die  for as  flimsy  reasons  like lack of oral re-hydration fluids   , while the other section of society is  marketing an exotic  mitochondrial DNA  slicers  for prolonging a  cancer victim  life by few months .

In a global society  where  social , economic  and environmental  responsibilities  and liabilities  are shared ,  it would be disastrous if  one country is simply not bothered about what is happening in other country.


WHO the world health organization came into being exactly for this reason .

We know  .  . . how it functions .  It is the  most abused united nation body . It has  neither the required  power nor the will to  tell the world  and insist them the  righteous  route for human health !

If the rich  are  not bothered about poor ,  it is certain  the rich will  also be eliminated  from the planet  for the same reasons  . . . it’s  just  a matter of time   !

Reference

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1305179/pdf/westjmed00323-0041.pdf

http://en.wikipedia.org/wiki/Rudolf_Virchow

Posted in general medicine, Great websites in cardiology, history of cardiology | Tagged , , | 1 Comment »

What is the mechanism of deep q waves in volume over-load of left ventricle ?

February 5, 2012 by dr s venkatesan

Here is an X -Ray and ECG  of a patient who came with  palpitation ,  which he  said  descriptively

“I  could feel  it   with  my hands over chest “

He also had class 3 dyspnea  and nocturnal chest pain . (Read here :  What is the mechanism of nocturnal angina in AR ? )

Clinically  it was classical  severe aortic regurgitation .

His x – ray and ECG showed

  1. q  represents  LV end diastole  . The  maximum diastolic  stress  point.
  2. q  indicate septal forces . When  LV is dilated  q  also  reflect cavity potential . Both gets  summed up inscribing  a classical deep q
  3. In severe volume overload   LV  is not only  dilated , it’s  mass increases  and is brought near  the chest wall . Since the leas V 5 and V6 are the most proximal to LV  both  R and q  increase correspondingly (Shall we call as  reversed Brody effect ?  )

Other findings of volume overload of LV are

While deep q  is  very valuable in LV diastolic volume over load there are other useful ECG signs.

  • Increased  qrs  amplitude (May be equally important like deep q . Both always go together )
  • Absence of  typical ST/T changes (Systole is stress free !in pure AR/MR) . Still ,  ST/T changes  can occur if   there is associated  LV dysfunction.
  • Left axis deviation.
  • Left atrial enlargement (In case of MR/ Large L-R shunts / or late stages of AR )
  • Rarely  U waves are reported in LV volume overload*

Can we  dignose volume overload without q waves in V 5 , V 6 ?

Most times no, but if there is associated incomplete LBBB q wave disappears.

Which  is rare in pure volume over-load. In fact absence of q in isolated systolic overload of LV is attributed to the presence of incomplete  LBBB by the ECG legend  Shamroth !

Reference

* http://www.ccjm.org/content/78/8/505.full

Posted in Cardiology - Clinical, cardiology -ECG | Tagged , , , , , , , , , | Leave a Comment »

Importance of recognising type C RVH in clinical cardiology !

February 5, 2012 by dr s venkatesan

RVH is  traditionally  categorized into three types . With  the  advent of echocardiography  diagnosing  RVH by ECG would  appear  redundant. Still , it gives vital information about the electro-physiologcal basis  of RVH. Knowing different mechanisms of RVH helps us decode  regional variations in RVH.

Type A , Type B  are easy to diagnose as they fulfill the conventional criteria of tall R in lead V1

Type A  RVH occur in severe  pulmonary hypertension and critical valvular pulmonary stenosis.

Type B  RVH occur in  volume overload states like ASD and moderate  forms of mitral stenosis.

( Severe  MS may cause Type A pattern  if RV pressure exceed systemic pressure)

Type C  RVH    has  no classical signs of RVH. Here  RVH  is diagnosed by proxy . Look for RAE  and a  vertical QRS axis . ( For all practical purposes RAE will indicate  RVH  except in isolated tricuspid stenosis.

Type C RVH occurs classically in COPD and in some cases  of acute pulmonary embolism .In other- words type C  RVH  reflects  predominantly  RV dilatation rather than  hypertrophy.

Why Type C  RVH is important ?

It is important  for two  reasons

  • It  is  basically a  masked   RVH .
  • It mimics Anterior MI

Missing the first  one and erring  in  later  both  can have major  implications  in clinical cardiology  especially during emergencies.

What is  the mechanism of poor  R wave in precardial leads in  Type C RVH of COPD ?

The fact that  poor  R wave  in precardial  leads occur in  most  cases of  COPD  (whether or not RVH is present or not)   convey an important message.

The  lack of  R wave  progression   is probably  less to  do  with   rotation of  RV  than  the insulation effect  lung  . Further, the  elongated lungs   drags   the heart down , and  make it more vertical and in spite of RVH tall  R  is not picked up by v1 v2 .

Unlike primary PAH and critical MS where the RVH  can dominate the LV  ,  the  quantum of  RVH is never huge in pure COPD . However , presence of RBBB  could  alter  the R wave amplitude .

ECG in acute pulmonary embolism

This resembles the type  C  RVH . The  R  waves in V 1  and  V 2 can not gain the voltage acutely.

The S 1 . Q 3 , T 3  pattern if present indicate the  acute RV strain and  the resultant  RV wall motion defect.

.

Clinical scenario : Practical utility of  decoding    RVH   by ECG ?

A  middle aged female came  to our CCU  with acute  dyspnea with tachycardia .

Echo revealed a dilated  RA and RV . She had  mild TR and moderate to severe PAH (The TR jet measured 3.8m/sec)

The MPA showed a hazy shadow suspicious of thrombus . The patient  had no evidence for DVT .

The fellows  arrived at  a conclusion about a  severe  PAH  but , the etiology was debated.

One is chronic thrombo-embolic PAH . Other groups argued for acute massive pulmonary embolism and resultant PAH.

This raised an  important    therapeutic   issue  as one of them wanted to lyse the thrombus  ,  the  other argued for simple heparin .The  argument continued as the first fellow reminded ,  presence of RA, RV dilatation is a sign of acute RV strain  . The other countered the  same  as  it could be  a  chronic response  to pre existing PAH.

How do you know  in an emergency ,  whether the RA, RV dilatation is new onset  or a chronic one ?

In spite of  good   echocardiogram  we were confused .  Then it struck  to us ,  ECG would solve our problem . It indeed helped us. She had a tall  monophasic  R  in  V1  indicating   Type A RVH , which suggested chronic PAH   and  the thrombus in MPA  in all likely hood  was a sequel  to PAH  and  not vice versa . A type C RVH  would have voted  in favor of  acute pulmonary embolism.

Meanwhile a  CT pulmonary angiogram  report was available   . It showed a small  thrombus in MPA and LPA with no clearcut perfusion defects ruling out acute pulmoanry embolism . The thrombus was probably  de-nova in- situ thrombus due to PAH.

 

 

Final message

It may  appear  funny for the  present day cardiologists to waste so much time  to analyze  the  RVH  by surface ECG . But please remember ECG remain the only simple and cheap  investigation that transmit live data from the heart instantly  .Most importantly unlike other imaging  modalities  ECG data do not vary with person who records it !

Reference

A very good referen from   Basic and Bedside Electrocardiography   By Romulo F. Baltazar

Posted in Uncategorized | Tagged , , , , | 3 Comments »

What are the mechanisms of “Nocturnal” Angina ?

February 2, 2012 by dr s venkatesan

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

Posted in cardaic physiology, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, myocardial disease | Tagged , , , | Leave a Comment »

Why AV dissociation does not occur in all patients with ventricular tachycardia ?

January 31, 2012 by dr s venkatesan

AV dissociation is  the most specific diagnostic clue in VT.But this is not a constant finding. In fact one  would be  lucky to spot a fusion beat  which denotes AV dissociation . It occurs in less than 30% of patients with VT .

Technically ,  for AV dissociation to occur atria and ventricle should  not be related in either direction .

If there is  a retrograde VA association ante grade AV conduction   is not possible  and hence one can not get a  fusion beat or so.

What happens to p waves during VT ? How does atria depolarise during VT ?

Atrial chambers can not sit idle during  VT .It has to somehow get depolarized  and contract   but  the  timing    may not be appropriate .

P waves  during VT can either be antegrade or retrograde .

Theoretically both can be present   but most times  it is   the  retrograde  p waves we see.

The occurrence and timing of p waves  is related  to the VA conduction .

If there is  1 :1  VA conduction during VT there can not be AV dissociation  for the simple reason  we have VA association.In fact there is constant vigil to depolarise the ventricle  through the normal AV node and his purkinje  in spite of the VT .SA  node is aware of this fact ,  how difficult it is going to be  confront the upcoming  rapid ventricular impulse . Usually the ventricular impulse   prevails  over the atrial impulse and much part atria is controlled by the VT . In fact  the VT reaches  all the way to SA node and simply  overdrive it . At these fast heart rates  retrograde p waves are not visible. ( But surprisingly one may see a regular  cannon wave in the neck with 1: 1   VA conduction.

Mean while ,  the SA  is always under look out for a opportunity to sneak into the ventricles thorough AV node. This happens  when the VT focus slightly slows down or shifts to a new site . this sis the time  we are able to  witness the AV dissociation . When the atrial impulse capture fully or partially the ventricle fusion beats occur confirming  AV dissociation .

Final message

AV dissociation is present in  less than 30% of VT because in  70%  there is a VA  association.(Retrograde  VA conduction ) . When V is associated with A there can not be AV dissociation.

Posted in Uncategorized | Tagged , , | 1 Comment »

Do not undermine the Importance of “Poster presentations” in scientific conferences !

January 30, 2012 by dr s venkatesan

We do come  across ,  even  senior  cardiologists , who  tend to undermine  the importance  of  poster  presentations in scientific  conferences   (I know a  few ,  who  ridicule it as well  ? ) .

                      Is  it not a meanly  job   for  a  cardiologist  to paste a  poster  and stand  beside  it  for hours  , waiting for scientifically motivated audience !

But , what really matter is the thoughts ,  concepts  and often the hard work   that brings  these  posters to  big league  conferences .

Please remember   abstract posters  must cross the hurdle of  the conference peer review  committee’s scrutiny . Often times   the poster arenas   has  launched  some crazy ideas  ,  transform  them to  great  discoveries.

If   only  , Gruentzig had shied  away from the poster  he famously  pasted on lawns of   ACC  , Annual scientific sessions ,Florida

1975     .  .  .  the    revolutionary  concept  of  PTCA   would still be  in utero  !

Final message

I argue the young  fellows in cardiology to send as many  scientific  abstracts as  possible   in their  national or international  meets  . This is  where the  the future of cardiology lies ! Simply don’t  bother about the critics  .

Posted in Cardiology -Interventional -PCI, history of cardiology | Tagged , , , , , , , , , | 2 Comments »

When VPDs continuously bombard the ventricle . . . Mitral valve begins to leak !

January 24, 2012 by dr s venkatesan

There are many  organic causes of mitral regurgitation. ( Ischemic , degenerative , valvular , cardiomyopathy etc.) It is not  rare for  pure  electrical events to result in valvular regurgitation.   A 70year old  man  with SHT   presented  with palpitation  and exertional dyspnea  .He was  later referred  for  Echocardiography.  Echo revealed LVH with intermittent MR and moderate LV dysfunction.

His ECG looked like

Ventricular ectopic recorded in bi-geminal rhythm

His  echocardiogram showed

 

His echo showed randomly timed mitral regurgitation was detected .See the Doppler MR jets below.

We know ventricles are integral  part of mitral valve apparatus  .Hence  it  wouldn’t  be a surprise to note  abnormally timed ventricular contraction  can  have a major impact  on mitral valve function.

When ventricles  prematurely begin  to contract  ( As  during  VPDs) it  interferes with  opening of mitral valve. In other words every VPD  technically imparts a  sort of  diastolic dysfunction !

VPDs occur in which part of cardiac cycle ?

VPDs  occur  either in early   or mid  diastole . Thank fully VPDs can not occur in systole . (Refractory period )

What would be the status of mitral valve at times of  VPDs?

Though it depends upon the timing of VPD ,  generally it interrupts the rapid inflow period of diastole .

In fact ,  it converts the cardiac  cycle from diastole to a partial systole or  a combination( fusion ) of diastole   and systole ! *

More MR jets are visualised than LV filling waves . Note the some of the E waves are sandwiched between two MR jets. ECG gating should have made this image more interesting .Any way , we have good MR jets to time systole nicely

* Is that a funny  imagination  ?

During   diastole ,  if  LV suddenly  begins  to contract   instead of  receiving the blood  ,  what will happen ?

VPDs are such a common arrhythmia , we  rarely  wondered  ,  it can have a dramatic  consequence  in a any  given cardiac cycle .While   the cardiologists think too  technically  their  patients observe with  shrewd  sense and tell us clearly  what  they feel  is  actually a   missed beat !

(Yeh  . . .  how simple  they describe the complex  hemo-dynamics  of  missing  diastole !)  .They also tell  us ,  next systole is felt as big thump as palpitation . (Post VPD potentiation )

Just imagine ,  if a patient  has  multiple VPDs  with  different  coupling intervals   that fall in different location of diastole  also  interspersed with sinus beats ,   how chaotic  would be the  the  mitral   filling .

This is what  is recorded in the above patient with multiple random MR jets .

Why all VPDs do  not cause MR ?

The timing is critical .We know all VPDs do  not generate a powerful contraction to cause MR. Atrial fibrillation, Prolonged PR intervals , heart blocks , critically raised LVEDP all can influence the trans mitral gradient . In fact these situation can result in  an  entity called diastolic MR that would be discussed later.

Can  VPD induced MR be  referred to  as diastolic MR ?

When VPDs  occur  in  diastole  , it  interrupts the diastole  and a new systole begins. In any  particular point of time there will be  leak into the LA  if the mitral valve is open .This is technically a new systole but in true sense it is the diastole of  the  previous beat . I wonder , whether   VPD induced MR  may be referred  to as one  form of  diastolic MR.  Of course ,  this MR can spill over to true  systole as well .

This also  makes  sense (Non !) as many of the VPDs do not open the  aortic valve ,   hence technically we can’t call the phase reset  by  all  VPDS   as a true systole !

What is the effect of VPDs  on pulmonary venous flow ?

Left atrial  cannon waves can occur that can elevate PCWP .This is the prime reason for resting or  exertional  dyspnea in these patients. Some may get a paradoxical relief  during exertion   as  exercise  suppress VPDs which are frequent at rest.

If VPDs can seriously interfere with mitral valve function , why  they are  often  considered benign  ?

VPDs are well tolerated* as long as  the  LV function is intact.  If VPDs are associated with  LV dysfunction  it  can initiate a vicious cycle of   hemodynamic deterioration .  Multiple VPDs  if left untreated can lead to progressive LV dilatation  in a  significant population .  Hence patients with  recurrent VPDS need some sort of  follow up. It  makes good medical sense to suppress VPDs in the long run. (Of course the  available anti VPD  drugs  are not very safe  !  The search for non toxic ,  ideal drug should go on !)

*”Well tolerated VPDs”   in no way  means  normal physiology.  Read a related article in my site.  “3 minutes crash course on VPDs”

Final message

VPDs  though considered  largely benign , can lead to dramatic  alterations in the  functions  of mitral valve , especially in diseased hearts.

We  must  realise  when ventricular  ectopic beats occur frequently  , it  interfere with the  both opening and closing of mitral valve.

It is really surprising  ,  the literature is  devoid of  major studies  about the  impact of  VPDs on  mitral valve  physiology . . . rather pathology !

Posted in cardiac physiology, Cardiology - Clinical, cardiology -ECG, Cardiology-Arrhythmias, Hemodynamics, myocardial disease, Uncategorized | Tagged , , , , , | 3 Comments »

Iam sure . . . 9 out of 10 times , this ECG will mislead you !

January 23, 2012 by dr s venkatesan

This  is the ECG  of  a  45 year old man with  H/O hypertension  and  chest pain .The general practitioner who first saw him alerted this  patient about a possible  heart  attack  asked to meet a cardiologist immediately. The cardiologist who  saw  this ECG   tended to confirm  the diagnosis  and advised admission in  a coronary  care unit .

The patient   defied  both  and  somehow landed in my echo lab  .  Looking at the ECG   I also  expected  it to be a  STEMI  evolving into a  Non Q  MI .

I was surprised  to find  only LVH with absolutely no wall motion defect  . There was no evidence of ASH,  HOCM or apical cardiomyoapthy as one of my fellows initially  suspected . His  EF was 70 %.   Cardiac enzymes were sent by then. When  I spent few minutes  with him ,  listening the history , it was very clear  what  he had was  non cardiac pain . In the anxiety ,  no one  got it right  about the character of pain ,which  was localised , lasted  for few seconds and  least suggesed angina.

The moral of the story is   listen to the patient  however dramatic the ECG may look !

What is special in this ECG ?

It is common for LVH with ST depression to be  mistaken for  ACS/NSTEMI

Here , there were  other  observations that  added  more  complexity .

  • Presence  of  ST/T changes in inferior leads(ST elevation in lead 3)
  • Bi-phasic  T wave in v1 to v3
  • ST elevation  in precardial leads

In LVH  it is usual  to note  ST depresion , how do you explain ST elevation in LVH ?

ST elevation in LVH   may occur in  leads  v1 to v3   . It is very rare  for LVH to inscribe  ST  elevation in   v4 v5 v6  .   Why certain  leads elevate the ST segment while others depress  in LVH  is not clear. It may represent  incomplete LBBB pattern where the ST segment deviates opposite to the  dominant QRS  complex. Septal  hypertrophy often elevate  while free  wall  hypertrophy depress the ST segment . Since V5,V6 leads are free wall oriented , these leads  record  classical  ST depression .

Importance of Bi-Phasic T waves

Please remember  Bi phasic T waves are notorious for it’s  unpredictability. An  innocuous looking bi-phasic T waves  (especially  with dynamic behavior )   is a  harbinger of proximal  LAD or even left main disease.

Finally , what will be ECG  changes if a patient with classical  LVH  who  develops a  real  STEMI ?

  • LV strain  pattern normalises ?
  • Further ST depression  occurs ?
  • No great changes . ECG  Looks near normal ?

Answer : ?

What is the significance  of   Bi-phasic T  waves : A  link to  a related post

Posted in Cardiology - Clinical, cardiology -ECG, cardiology- coronary care, Cardiology-Coronary artery disese, critical care ccu | Tagged , , , , , , | 1 Comment »

What is the mechanism of Amlodipine induced edema legs ?

January 23, 2012 by dr s venkatesan

The mechanism of pedal edema in Amlodipine

Note : I lost track , the source of this Image .I thank with courtesy whoever has created this Image .

It is primarily a  local phenomenon . The calcium channels  are primarily  arteriolar dilators . Since the  venules  lack much muscle they  are not much affected by the Amlodipine   .  This  facilitates flooding of  venules and leaks into the peri venular interstitial space. It may be apt to call Amlodipine induced edema  as a form of   local venous edema .

This results in near permanent  collection of fluid  especially  near  the ankle . Systemic fluid retention has no major role . However few patients may  show an  augmented   RASS  response due to sudden arteriolar dilatation  .  In these patients   addition of ACEI or ARB may help relieve  edema legs .The Amlodipine  induced edema is  dose  and  time dependent .(Cumulative)  . It is mostly benign in nature ,  rarely warrants withdrawal of the drug.  The edema can  occasionally be generalised   and weight  gain is  possible .

Other factors that increase the chance of edema is age , women  , obesity. They have loose  interstitial  tissues.Many especailly women complain tingling feeling in the edematous zone.

The calcium blocker induced edema is  an  exclusive feature of dihydrpyridine group  .(For some reason  , Verapamil and Diltiazem do not  share  this side effect  as  theya balanced Arteriolar and venous dilator . )

Can we use diuretics to treat Amlodipine induced edema legs ?

Hydrochorthiazide  is rarely useful as the primary problem is not in the renal  retention.

How to  treat Amlodipine induced edema ?

Unfortunately the popular combination with diuretics do not work . Angiotensin  inhibitors which has some veno dilatation is shown to reduce this edema  . ( COACH study . Olmesartan / Telmisartan combination  is an option ) .It defies logic ,  to  add  another anti HT drug for the sole  purpose of reducing  the side effect of the initial  anti HT drug . Ideally if  your patient is not tolerating  Amlodipine due to edema ,  switch to  an another group of  anti HT drugs.

Reference

http://www.isdbweb.org/documents/file/1664_2.pdf

Posted in cardiac drugs, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions |

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