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Archive for the ‘Cardiology – Clinical’ Category

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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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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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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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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Localising  WPW syndrome is a favorite  time pass  for cardiologists in spite of  serious  limitations of surface ECG .Still , it is vital to generate a rough idea about the location of  these pathways ,  so that we can focus  our efforts  on  some sort of ablation procedure .

Arruda algorithm is probably a simple and fairly useful technique to remember. It asks us to climb 4 steps   and pause at each  step and look sideways   for the accessory  pathways !

Step 1 (Left free wall step )

Initially one need to look only two leads .

Look at lead 1  and  V1 for   delta wave and R/S ratio .After Identifying delta wave look for the polarity of delta wave (This can sometimes be really difficult ) .If there is iso-electric or negative delta it immediately  fixes the pathway  in left free wall . Similarly if V1 R >  S it also fixes in left free wall. To locate more precisely in left free wall  look  for  delta  wave polarity in  AVF  and proceed down*

If none of these finding are present then  Go to step 2 .

Step 2 (Coronary sinus step )

It is the most simple step . If negative delta  located in lead 2 (often mimic inferior MI)

Here the pathway is often located in coronary sinus /middle cardiac vein often as diverticulum.

After excluding left free wall and coronary sinus origin one has to look at possible septal  pathway  .

For this  go to step 3

Step 3  (Septal step ) And  again v1 lead  becomes important if v1 shows negative or iso-electric  go down  to septal  pathway decoding

After ruling out septal origin the scheme takes us to right free wall by default.

Step 4  (Right free wall step)  If the delta wave does not fit in  any   of the above three steps (Including  positive  delta in V 1 )  it  fixes  the right free wall  pathway

Arruda scheme summary

Arruda scheme  guides  us  to scan  systematically  for pathway from left free wall  to  septum and lastly  the right free  wall  (The key  to  locate  the APs is  to look at  delta waves in lead  1, 2  AVF and R/S ratio In V1 )

Here is a  simplified version for basic localization

Reference

  1. Arruda MS, McClelland JH and Wang X , et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. J Cardiovasc Electrophysiol 1998;9:2–12.

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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

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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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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 !

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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

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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

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