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Posts Tagged ‘ECG’

Why ECG reported by a technician is a crime . . . while Echo is not ?

Posted in Uncategorized, tagged , , , on July 20, 2013| 1 Comment »

A Cardiologist will never accept  the diagnosis ,  if a technician reports   a  ECG as normal in a  patient with chest  pain   . . .

While , the same cardiologist  gleefully  accepts  an  echocardiogram   done by a technician  and  treats  the patient without  verifying the veracity of the finding !

Why ?

Some where along the cardiology training  , we have been made to believe Interpreting  Echo Images does not require serious medical knowledge . . . but we strongly believe  ECG  cannot be read by technicians however well they are trained .(In-spite of the fact , Echo images are highly dependent on the person who does it , while ECG wave forms are  totally independent of the person who record it ! )

ECG, still has a  prestigious place  in cardiologist’s mind ,  while Echo is often considered  an inferior  Investigation.  Many of us consider ECG interpretation  as a  brainy work while Echo image acquisition and  interpretation is perceived a dumb job* !

Lastly , probably most importantly ,  performing  Echo  is   a time intensive process for the  present day cardiologist  who’s hands are tied with  catheters and  guide-wires  .He has little time for  the meanly echo . .  . hence  ready to compromise on the quality .

* With due respects to all non invasive cardiologists (That includes the author !)

Final  message

I would think it is  fundamentally inappropriate  for technician  to  report Echocardiogram (Of-course they may record it  ) . Unfortunately , for some reason this practice is continued  in many  parts of world .

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What is the reference point to measure ST elevation in STEMI ?

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, Cardiology -unresolved questions, Cardiology-Coronary artery disese, Clinical cardiology, tagged , on May 31, 2013| 1 Comment »

ST segment elevation is the key parameter on which the fate of millions of infarct patients are recognised and managed. It is ironical we do not have standardised reference point for measuring the quantum of SR elevation .

This is especially difficult when ST segment blends with forward limb of T waves.

While we have reference point for measuring  ST depression  (Like during EST ). . . why we do not have one for ST elevation ?

Now we have adopted a rough criteria .Read below .

where will you measure st segment

How to measure ST elevation in ECG
How to measure ?
Measure The ST segment 40 ms from J point.
how to measure ST elevation in STEMI 2
                        I lost track the source of this Image .(STEMI hand book 2012 ?)
Final message
ST segment  elevation  is  the key parameter in ACS.  Quantifying  it becomes  important in  assessing  the efficacy of reperfusion strategies and risk stratification. Fresh ST elevation can represent pericarditis, reinfarction or an early dyskinetic  segment . Unless we have  proper reference point there is  a room  for  error in this simple parameter.

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“Inferior MI” by ECG . . . “Anterior MI” by echocardiography . How common is that ?

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Cardiology -unresolved questions, cardiology-Anatomy, Cardiology-Coronary artery disese, Clinical cardiology, echocardiography, tagged , , , , , , , , , , , , , on January 14, 2013| Leave a Comment »

Surprises are hall-marks of medical science . The cardiologists do  get  it ,   in enough doses   from  echo  labs  on a regular basis !   . One such thing is  the total ECG-ECHO myocardial  territorial  mismatch following  a STEMI .  Human myocardial segments are divided by cardiologists  by 17 segments by echocardiogram . Long before  echo came into vogue ,  electro-cardiologists  divided the  heart electrically into three zones to  localise MI . (Anterior , inferior and  the  poorly defined entity  lateral walls* ) .Inferior and posterior  segments are  almost used interchangeably. So , when we have 17  echo  segments to be fit into these three electrical category !   were  bound to have  some overlap . The issues of fitting in septal segments is really complex as septum  is a three dimensionally engulfs all three electrical surface of the heart .

* By the way , anatomists  never agreed about existence of walls in heart.They simply said  , heart has smooth  surfaces that blends with one another.  We cardiologist have  built imaginary walls and struggling to come out it !

We will   try to answer the question that’s been asked here .  “Inferior MI”  by ECG   . . . “Anterior MI”  by  echocardiography . How common is that ?

Possible causes for this wrong call

Technical errors  in  acquiring echo  imaging plane  or  it’s interpretation is the commonest . Many  times  ,  obliquely obtained long axis view  wrongly and strongly  suggests  a septal  MI  instead of   inferior posterior MI. This is  because  in  apical 4  chamber view  bulk of   septum  (Basal and mid third )  lies   in the  infero-posterior region .

wall motion defect

Perhaps ,  misunderstanding this  septal  geography is  the  commonest cause for  erroneously  calling inferior MI as anterior  in echocardiography . (A simple clue is the presence of MR . (It  fixes the infarct in infero-posterior zone with 90% accuracy )

Rotation  and  posture of heart

Alignment of the septum to the rest of the chambers  can influence  , how three inferior leads is going to look  at the septum (There can be  considerable errors  -Electrical myopia ? as these leads are located distantly )  . The plane of the septum is such that  in horizontal hearts  septal electrical activity  will be directed infero posteriorly inscribing a q waves in inferior leads rather than anterior leads . One can expect such ECG /Echo discrepancy in the following subset as well

  • Post CABG patients (Any pericardiotomy will make the septal motion  erratic )
  • Obese persons
  • COPD

There are three  more  situations  ,  which   mystified me   with  definite  ECG/ECHO  mismatch

  1. LVH and STEMI  is always an engima . Counter clockwise rotation when accopany  LVH  that masks anterior MI  electrically . It  however inscribes a   q wave in inferior leads.
  2.  In dominant LCX lesions  ( with at-least  one  major OM    )  and  left main bifurcation  STEMIs  ,  combination of  anterior and inferior  wall motion defects are  quiet common . When a such  a  MI evolves ( with or without  revascularization )   regeneration of R wave can be  time shifted . Septal R wave may appear  much earlier and inferior R may follow or vice versa . .Further,  anterior MI  may  evolve as  Non q MI  making it  ECG blind ,   still  echo may pick up the WMA . So there can be important  ECG-ECHO mismatch in myocardial segmental geography .
  3. Further , WMA  need not  always be an  infarct  .Any new episode of ischemia  can result in WMA . Hence a patient  with inferior Q waves  in ECG may experience anterior wall motion defect meagerly  due to fresh episode of   ischemia (This we should not attribute  to  old anterior  MI. It is also possible intra-myocardial conduction delays can elicit remote wall motion defects.

Final message

By general rule  , ECG  correlates  well  with  ECHO  for localising myocardial segments   . At times ,  it  can  really be tricky , and we  get into above situation  in echo labs.

While ,  it is common to observe  ECGs  to mimic  inferior MI  at the first look  and  subsequently echo  revealing  anterior  infarct ,  the reverse is also very much possible .

The  mechanisms are varied and technical  issues are for more frequent than true clinical discrepancy .The issue has important management implications.

Of course ,  coronary angiogram will pin point the   anatomy , still  it also has  strong limitations in localizing myocardial segments (to which it supplies ) especially with multi-vessel  CAD and  collateral dependent circulation .

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Why RR interval is irregular in Atrial fibrillation ?

Posted in cardiac physiology, cardiology -ECG, Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged , , , , on April 5, 2012| Leave a Comment »

RR interval in Atrial fibrillation is irregular because . . .

  1. The Atria  fires irregularly
  2. AV node conducts irregularly
  3. Atria confuses the AV node  with  its random firing  and varying penetration *
  4. The ventricle just reflects  irregular  response of atria .

The answer is all of the above. Response 3  explains  best.

*Please note , the AV nodal property is predominantly  responsible for the irregular RR interval in AF  . Atria confuses the AV node  with its random firing .The varying penetration into different depths of AV nodal structure and  the resultant concealed conduction make the   the AV nodal refractory period into continuous oscillation .This  random delays in AV node  is reflected in RR interval as irregularity   )

The response we get in ventricles  in AF  can be summed up as  “A filtered atrial rhythm”

Paradoxically,  amidst the chaos in atria  the rate  is fairly constant within the atria (Fibrillatory   wave firing  at up-to 600/mt )  Of course  , the FF interval in the atria will also be varying  .  At a rate of 450-600 this is difficult to quantitate  especially in fine AF.

When does RR interval becomes regular in AF ?

  • When the patient develops complete heart  block.
  • Digoxin toxicity
  • Associated Sinus node dysfunction

For advanced readers in EP : A mystery explanation for irregular  rhythm in AF  in the offing ?

AV node is a physiological and electrical sink .

When atria fires at 600/mt it absorbs about 60-70  % of the atrial response .Whether it releases the original impulse or initiate a new rhythm in the junction  is not clear.

There is some evidence to suggest the rhythm that control the ventricle in AF may not be  filtered original rhythm from the atria .Instead it could be a fast junctional  escape rhythm (Is that a junctional fibrillation ?)

 

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Please consult your cardiologist . . . you have a flat ST segment !

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -unresolved questions, tagged , , , , , , , , , , , on July 21, 2011| 7 Comments »

Often general practitioners refer  ECGs  with abnormal resting  ST/T wave patterns  to cardiologists .

Following are few of them

  • ST elevation
  • ST depression
  • T wave inversion
  • Tall T waves
  • A relatively uncommon  finding is  a flat ST segment  , which  is discussed here.

The commonest( benign) abnormality   is  T wave inversion  in women and tall ST /T waves   reflecting  early repolarisation  pattern in men. A flat ST segment is an occasional finding in general population.

ST segment is inscribed  during the most important  time  of  cardiac cycle.This is the period the ventricle is doing its prime function , namely ejecting the blood in systole .Hence it is subjected to maximum stress . During times of ischemia  ST segment  gets elevated or depressed depending upon the severity of ischemia. For the same reason , even  subtle changes in this segment is  frowned upon by cardiologists. Most of them would receive a EST.

It is ironical to note  , few normal people  show almost silent electrical activity during this  crucial  phase of   their  ECG .ST segment is often  a flat line  in them . This is a ECG of a women referred as CAD. She was asymptomatic . Echocardiogram  was normal . She was asked to do  a EST.

This asymptomatic women was refered for ECG opinion

The peculiar thing about T waves  are ,   a 10 mm upright  as well as  5 mm inverted T wave ,  both can be normal. So .  there is no element of surprise  to note absent  T waves  or a flat  T wave  to be called as normal .

The curious case of lost ST segment !

* T waves are recorded when K+ efflux occur rapidly out of cells . Hypokalemia  can be an important cause of flat T waves.

It is still a  mystery to me  why some people inscribe a tall T when  potassium comes out  of cell and  an equal number (Esp women)  record a down ward T wave  for the same event !  I wish  I get an answer  to this  lingering  question from  any of the readers !

Is a flat T wave represent  a T wave in  transition  to become inverted T wave  later ?

Possible .But we  are not sure ! A static T wave is safer than a dynamic T wave .

Final message

Flat ST segment and absent T waves  represent a same spectrum of ECG  findings  which  are  referred to as  non specific ST segment changes in  clinical practice .Generally , they have  little clinical significance.* In our experience we have found , female patients, Anemia  hypothyroidism  are  often associated with flat ST segments  . If CAD is suspected exercise stress test  should be done. Some believe a flat ST segment  is more likely to  result in EST positivity (Not necessarily true positive !)

* Non specific ST/T changes by itself is a  huge topic.  Ideally the term non specific ST /T changes should be avoided , as it  primarily came into vogue  to denote non ischemic ST segment (Still , other pathologies are very much  possible) It is estimated there are about  50 causes for non specific ST/T changes , right from a  benign situation  like deep   respirations , to significant  myocardial disorders. However , it still makes   good clinical sense for a  general practitioner  , to refer to a cardiologist , whenever ST  segment deviates  without any reason .

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Left bundle branch block : (iFAQs)infrequently asked questions

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Uncategorized, tagged , , , , , on August 23, 2010| Leave a Comment »

Why the qrs complex becomes wide and tall in LBBB ?

The qrs  complex is  wide , due to delayed conduction over non specialized fibres .The qrs  becomes are  tall due to temporal dissociation of RV  and  LV forces ,  which  leaves  the LV forces  unopposed , thus  a tall qrs  is inscribed  , without the neutralizing effect of RV forces.

Is muscle to muscle  conduction a hall mark of LBBB ?

No , it is not . Even though the left bundle is blocked , much of the conduction tend to occur in

specialized  conduction  system  . It depends upon the level of block of LBBB.

What is the mechanism and clinical significance of left axis deviation in isolated LBBB?

The mean qrs axis is surprisingly  not  altered greatly ,  in LBBB . If there is a significant left ward shift  it may imply associated organic LV pathology or involve ment of predominately  left anterior fascicle

What is  the impact of IVS contraction and timing in LBBB ?

In isolated LBBB, it is expected an abnormal septal motion due to altered sequence of septal activation. This results in an abnormal appearance of  septal motion in Mode (Septal beak immediately following qrs complex) .In fact , this sharp downward movement indicate good LV  function  .Absence  of which  is a  good clue  for a pathological LBBB due to structural heart disease

Why does the abnormal  septal motion in LBBB  ,  do not  desynchronize  the normal LV ?

CRT is the much fancied  treatment in patients with LBBB and cardiac failure. In normal ventricles LBBB do not destabilize LV function in spite of septal /free wall desynchronisation  .This is still a mystery how IVS is cope up with the totally unexpected  insult of asking to work in head over heal situation !In spite of  this the ventricle gets used to the altered conduction pattern and the contractile pattern.(Nature’s  at it’s best !)

What are the mechanical disadvantage of LBBB

  • Septal contraction is  ill-timed
  • Mitral  regurgitation

Most isolated chronic LBBBs  do not  confer  any hemodynamic  disadvantage  to LV  – why ?

LBBBs are dangerous looking ECG , but in most patients it is benign , in the absence  0f structural heart disease like valvular , myocardial or ischemic  disease.

Can there be a small r wave in V1 and V2 in LBBB ?

Yes . Though we expect the  reversal of septal depolarization  extinguish  the initial r in v1 to v3 .It is  noted in many. Hence presence of small r in v1 to   v3 does not rule out LBBB. 

  1. The commonest explanation given is un-masking of RV free wall forces which is   normally  masked by early LV forces .
  2. Another possibility is the   orientation of septum  in pathological states.
  3. Third possibility is  “r” may  actually represent  the  septal q waves as in LVH or old AWMI  .(Counterpart of small  q in lateral leads )

How do we explain concordant  pattern  of QRS  v1 to v6  in LBBB ?

We expect the qrs to  transit from QS  complex  to RS ,  at-least by lead  v5/v6 .Some times even V6  shows a RS complex.This is usually due to faulty lead  position or a grossly enlarged  LV,  ie  if we  record V 7 or V8 we will be able to pick up the qs complex.

What will be the morphology of a VPD that is arising  from LV in the presence of  LBBB ?

A premature beat arising  from a  ventricle which is having  a bundle block  is  sort of  electrical blessing !The VPD often bye  passes the block and makes  the conduction near normal  and a normal  qrs may be  recorded. So , when a patient with LBBB suddenly develops a normal qrs beat or  normal qrs tachycardia  one  should consider a VT arising from the  Left ventricle .

And a studious electro physiology fellow  should  be able to answer the following !

What will be the morphology of  VPD if it arises from RV and septum in the presence of  LBBB ?

Kindwall has tried answer  this question

What is the effect of  LBBB on S1 and  S 2 ?

The classical  description in LBBB   is

  • Paradoxical split of S2
  • Wide split of S1

You are supposed to hear  4 components in complete LBBB  !  In reality this does not happen . At best you can hear the reversed  split of  S2 with difficulty .

One  more reason  for the  non manifestation of these splits is  confounding factors like LV dysfunction , MR , PR interval etc .(Each one tend to pull or push  S1 and S 2 in different directions )

Do  patients with LBBB  , are at increased risk for developing  complete heart block   when

beta blockers , calcium blockers etc  are administered ?

Common sense would say yes. Scientific  sense has  no answer .

We know, ventricles are innervated by two bundles  .When only one bundle  is  functional, it means the ventricles  are experiencing  50 % power shutdown .   In CAD  , single vessel blood supply due to a CTO  is considered  dangerous but in electrical  flow it is not so !  In spite of the fact  that  ventricle has numerous  cell cell electromotive conduction   it is  always better to exercise caution  when administering  beta blockers, calcium blockers and digoxin in patients with LBBB . If it is a must periodic  monitoring is advised .(HV interval in isolated LBBB is slightly prolonged ) Never administer beat blocker in a patient with recent onset LBBB and ACS

Also read the related article  in this blog  Incomplete LBBB

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Coronary care in your pocket !

Posted in cardiology -ECG, cardiology innovation, cardiology- coronary care, tagged , , , , , , , , on August 19, 2010| 1 Comment »

Welcome to the new era of “medical avatar “

Cardiologist’s ultimate dream  of  monitoring  their patients

Live ECG feed in your cell phone  !

Thanks to the American “scientific  pursuit” and the mankind  will be  the beneficiary !

Courtesy :

Airstrip technologies

What’s next ?

Remote DC shock and pacing  .

Watch out  . . . it is going to happen in next 5-10 years !

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“Incomplete” left bundle branch block

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -unresolved questions, tagged , , , , , , , , on April 8, 2010| 1 Comment »

LBBB is probably the most important  conduction defect of the heart .When we say LBBB , we visualize a  strikingly  wide bizarre qrs complex .

Left bundle even though is considered  a discrete structure , the fascicles  make it a diffusely spread structure. Many varieties of LBBB with various degrees of involvement occur.

Talking about the basics of  LBBB  electrophysiology  is out of place for the current generation cardiologists,  who  have little spare time as  they sweat it out inside the cathlabs.

In early 1960s and 70s great articles came from pioneers regarding these defects. If we want get a good insight  read  this  articles from  Sodi palleres .Who  says LBBB is a dynamic process, where it can occur from mild functional  delay to a total block .

The conduction  properties of left bundle is very much influenced by heart rate.

Law of statistics would  suggest  for every complete LBBB  at least three to 4 times incidence of incomplete  LBBB

Then . . .

Why we are not diagnosing ILBBB often ?

  • We miss it
  • Mistake it with LVH
  • We know it  is there , but we do not  want  to diagnose it .

How to diagnose ILBBB?

See  Sodi palleres criteria*

What is the relationship between qrs width and completeness of LBBB ?

Surprisingly and contrary to the belief , the width of the qrs has no linear correlation between severity of LBBB. In fact incomplete  LBBB can occur with even 150ms qrs !

Then ,  what  exactly determine the completeness of LBBB ?

What  matters is , whether the down coming impulse gets blocked  and split in the  left side of the IVS or not ? This causes the  the septal vector to  change  it’s direction ( ie  right to left instead of the normal left to right) It  removes the initial small r wave in v1  and q in v6  in complete LBBB. In  incomplete LBBB these  r and q are  often retained .

What is the differential diagnosis of ILBBB ?

Type B WPW may mimic LBBB and vice versa.

LV hypertrophy .

Differences : See table in  the Barold’s article  linked above .

Unanswered questions

  1. How common is ILBBB in STEMI ?
  2. How often ILBBB progress to LBBB ?
  3. ILBBB in dilated cardiomyopathy : Is desynchrony an issue ? (Normal QRS CHF !)
  4. Is functional  rate dependent  LBBB in cornary care units  same as transient  ischemic LBBB ?
  5. Intermittent LBBB and Incomplete LBBB  aren’t they  synonymous ?

Final message

ILBBB is not that uncommon as one would  tend to perceive.

Reference

My humble tributes to  Barold, Sodi -palleres , and Leo  Schamroth . Probably  one of the best  article on ILBBB is linked below. Reviewed    in 1963 !  Not much data has been added  in the next 47 years as on 2010

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What is a cannon sound and what is a cannon wave ?

Posted in Cardiology - Clinical, cardiology -ECG, Clinical cardiology -JVP, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged , , , , , , , , , , , , , , , , , , on February 21, 2010| 1 Comment »

Cannon Sound

A loud first heart sound (S 1)   which is  heard intermittently in patients with complete heart block (CHB)  is  often referred to as  cannon sound .

What is the mechanism of loud S1 in CHB ?

We know , the intensity of S 1 is  mainly determined by the  relative position of mitral leaflet (To be precise, the  anterior mitral leaflet(AML) )   at the onset of systole.  We also know the  PR interval  has an intricate relationship to  mitral leaflet  position .

The shorter it is ,  wider the leaflet separation  and a longer PR interval makes a mitral leaflet assume a almost closed position   by the time the ventricle contracts.this happens because  a long drawn PR interval fills the ventricle more completely and LVEDV  reaches the maximal levels and LV blood column lifts up the mitral leaflets , and hence the LV  contraction  which follows does not close it with a  bang. In a short PR interval the opposite happens and hence a loud S1 .

In CHB we have variety of PR intervals ranging between  very short to long   ( falling just before the qrs complex) It is not difficult to understand this , as P waves are totally dissociated with the QRS complex  in CHB.In fact p waves have a liberty to fall any where in the ECG tracing , some call this as marching through the qrs complex !.

Hence typically the S1 is variable in intensity , varying between loud to soft.  When  P wave falls just behind a QRS complex , it generates a very  loud S 1  that is called cannon sound .This happens intermittently.

Cannon wave

This is entirely different phenomenon except that it shares the word cannon . Cannon a wave is  a visual finding on the jugular venous pulse.(JVP) .It is a systolic event . It is also seen in CHB as like a cannon sound

This is a giant a wave  in  JVP  when the right atrium contracts against a closed tricuspid valve. In physiological situations atrium contracts with an open AV valves , so that ventricle gets  filled . So atrial contraction  does not does not cause any reflux of blood back into vena cava.

But, when the atrium  contracts and  finds , the AV valve closed  there is no other option   for the incoming blood  to reflux  back into  the neck veins. This is seen as giant a waves called as cannon ” a “waves

With reference to ECG  location ,  this cannon”  a” wave occurs   whenever p wave falls within the ventricular systole ie  the QT interval .The cannon waves also occur intermittently like the  cannon sounds.

What is the  peculiar relationship between cannon a wave and   sound ?

In fact , it is  a non- relationship.  Though  , both the sound and wave   can occur in a given  patient with CHB ,   they can not occur simultaneously .This is because ,  for cannon sounds   to occur  the  P  wave has to fall before  QRS  and for cannon waves to occur the  p   waves must fall after QRS  ie with QT interval .

Clinical significance  of  cannon wave

Complete heart block is the most common situation for cannon waves to occur.

Ironically ,the VVI pacemaker which is used  to treat CHB does not prevent the cannon waves , and atrial contractions continue to occur at random , causing various degrees of intermittent venous reflux into the veins .This may produce, worrisome venous palpitation in some (Usually settles down after few weeks !)

Some attribute , the so called pacemaker syndrome ie giddiness, dizziness to this abnormal venous waves triggering the carotid baroreceptors (Venous -artery spillover )

Will DDD pacemakers  eliminate venous cannon waves ?

We hoped so , it does in fact . But,  it really happens only if the A sense V pace mode . A pace V pace mode with programmed PR interval is not a realiable way to produce AV synchrony. It is  common ,  many of the DDD pacemakers fall back to VVI mode either intentionally or by mode switching  for various reasons.

//

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Can we diagnose unstable angina in a patient with normal ECG ?

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized, tagged on February 15, 2010| Leave a Comment »

It is said every clinical diagnosis needs to be substantiated with  documented objective  evidence .

Probably,  the commonest cardiac emergency , that can be  diagnosed purely by history is UA.

Yes , unstable angina is a symptom not a  disease entity !

By definition UA is

  • Any  new onset angina  of severe grade
  • Progressive crescendo angina
  • Angina with radiation to new site
  • Angina not controlled by nitroglycerine
  • Any angina after a PCI /CABG

If you read the definition again, you will realise ECG or enzymes never come into the  diagnostic picture .UA can be diagnosed even before one has a look at  the ECG ! So, it is too obvious one can diagnose UA irrespective of whatever is recorded in the ECG. Normal ECG is one such possibility.

When a patient is having severe  compromise  in the  blood supply to his / her heart  , how  on earth ,  it  is possible to have a normal ECG ?

It only tells us,  ECG is not a fool proof method to exclude ongoing ischemia . When we know , ECG can miss even a STEMI  it is not a big deal it misses a UA.

Apart from  the electrical blind spots of conventional 12 lead ECG, following are the other  explanations offered for a normal ECG in UA.We know UA occurs with ST depression(Classical ) , T inversion,  rarely ST eelvation

So UA can occur with

  • Pseudonormalised t waves
  • Pseudo normalised ST depression
  • Cancellation effect of two  opposing  subendocadrial ST segment vectors ( As in multiple active plaques PDA   and LAD lesion )
  • Even Ischemic cascade

Final message

Even though  UA  CAN  occur with normal ECG  , we are uncomfortable to   diagnose  UA without   documenting ECG changes . We should realise this fact , as missing a diagnosis of UA , just beause the ECG is normal  could have very costly consequence !

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