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Posts Tagged ‘physiological lvh’

  • LVH is classically diagnosed with high qrs voltage either in limb or chest leads or both.
  • High voltage is a specific ECG  sign,   presence  of  which  would strongly suggest LVH  ,   absence of which  is not  useful to rule out true LVH.
  • LVH with   flattish  or  down sloping   ST segment ,  with or without  T inversion  , can be a sole presentation of LVH . This should not be taken as sign of ischemia.  Here is  patient  with such an  ECG

Mechanism for LVH without high voltage

  • Intrinsic muscle  electrophysiological  property – Arrangement of muscle fibre orientation  will determine the voltage .(Parallel vs perpendicular, disarray etc)
  • Pathological LVH with fibrotic process and interstitial hypertrophy may not  record high voltage.
  • Presence of  high voltage LVH  would indicate a dominant physiological muscle mass that lacks interstitial reaction.
  • Finally , technical cause like thick chest wall in obese can dampen the LVH voltage.

Read a related  topic in this blog

https://drsvenkatesan.wordpress.com/2010/07/21/why-lvh-generates-high-voltage-qrs-in-some-and-low-voltage-qrs-or-even-q-waves-in-others/

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LVH is supposed to produce tall R waves . But , we know  often LVH is misdiagnosed as   myocardial infarction especially  anterior MI.  (With deep q waves*  in v1 to v3 and sometimes q in inferior leads as well)

Infarct tissue  is a  cluster of dead cells  , while  LVH is a bundle of live cells . How can the ECG produce similar changes  in both ?

One need to realise ,  ECG does not function  as  a tissue identifying  machine.  It’s job is to simply  tell which direction the current  is traveling with reference to the  recording electrode .

If it comes towards  the electrode ,  R  wave is recorded and  if it goes away Q is recorded.

In infarction it is obvious the dead cells  form a distinct electrically inert  window so that the  muscle  mass located in the opposite pole  (If viable ) will record  q waves.

In LVH  how the  direction of  current get reversed ?

We know,  cardiac muscle  is made  up of not only myocytes , it is enriched with, fibroblasts, interstitial cells, collagen and other extracellular matrix .These non contractile cells have little electrical energy to show off.  In physiological LVH there is  not much proliferation of interstitium . It simply  reflects hypertrophy of  individual contractile units. It robustly produce good quality electricity and the ECG inscribes a tall r waves

Causes of  physiological LVH include

  • Athletic heart
  • Many of the hypertensive patients
  • Early stages of Aortic stenosis
  • Any LVH due to increased loading conditions( In the initial stages )

Pathological LVH

Here  LVH  is predominately  due to  proliferation of fibroblasts  and interstitial cells  .This interferes with the alignment of sarcomeres of myocytes. When the  architecture of contractile units  are  altered ,  it finds difficult to generate good quality action potentials  . Since the ECG is the summation of action potentials  ,  it gets distorted  with local delay,   notch ,slur etc . Ultimately it many  cases q waves are inscribed .

Th  q waves ,  gets amplified by the fibrotic process which is  technically dead cells for the ECG machine at least !.

Note: Pathological LVH grows well with excellent nourishment from ACE gene dependent growth factors. In fact , who will develop pathological LVH  (and who will not  )  is  predetermined by our ancestral genes.  (Other wise called fate or destiny  !)

Conditions  causing pathological q waves

  • About 10% of  LVH due HT can manifest q waves
  • HOCM
  • Late stages of Aortic stenosis
  • Some cases of Diabetic HT combination
  • HT with CKD

* There is one more cause for q in LVH .This is technical .   As  the  heart rotates counterclockwise ,  septal activity instead of  recording a r wave  ,  merges  with the s wave mimicking q waves. In fact this could be very common cause for labeling LVH as MI.

Final message

Q waves are not sacred to diagnose MI.It can be generated  even by live myocytes  when it behaves like an  electrically dead ones.

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LVH is one of the commonest ECG abnormality . We know the hall mark  of LVH is increased QRS voltage .We also know , ECG is not a fool proof method to detect LVH .It has very good specificity , but little sensitivity , meaning that increase in  QRS voltage is  fairly accurate in predicting LVH  but absence of  which cannot exclude LVH.

Why Increased QRS voltage does not occur in many with LVH ?

Even though we think myocardial mass  is  the  sole determinant of QRS  voltage  , in reality  it   is determined by many other factors.

  • Distance between the ECG lead , and the myocardium is an important factor. In classical concentric LVH , the LV  cavity is not enlarged ,in fact it may shrink a little as the hypertrophy grow inwards and obliterate the LV cavity.(We do not know yet , how much of LVH grow out and how much  muscle grow in ! )
  • The blood volume within LV is a very good conductor of electricity.A good volumed LV may augment a QRS voltage.
  • This can be observed in some of the patients with DCM , where high voltage QRS  is recorded mimicking LVH.

But ,what really matters is the fine balance of blood volume and myocardial mass that determine the incidence and magnitude of LVH pattern in ECG.

QRS voltage as a tool to differentiate pathological from physiological  LVH

We know QRS current is generated from within the myocytes .If the myocytes  are  uniformly hypertrophy without altering the  basic mechanical and electrical architecture QRS complex will be amplified in a sm0oth manner and result in  classical high voltage  QRS  of LVH.

If the hypertrophy occurs in a disorganised fashion, where in myocardial fibres slips out of plane  with adjacent muscle bundles, the QRS  voltage may not increase and even be slurred or notched as we see in many cases of LVH with non specific intravascular conduction defects

The classical disarray of myocardial fibers that occur in HCM causes  pathological q waves.

* Other factors that determine LVH include bundle branch conduction delay or blocks which is not discussed here.(Ex: An incomplete LBBB can amplify the qrs without any LVH )

LVH with fibrosis

Fibrosis is not a standard feature of LVH. It occurs in few who are genetically predisposed , and  mediated by heightened sensitivity to circulating growth factors.

  • Fibrosis can have wide impact on the electrical as well as mechanical function of heart.
  • Fibrotic heart has a  potential to  blunt the  high voltage  QRS complex.
  • It  may even cause  pathological q waves .It predispose to ventricular arrhythmia
  • It prevents regression of LVH , even after the loading conditions corrected.

Other conditions that  attenuate LVH features in ECG

  • Diabetic hypertensive show less ECG voltage than isolated HT .
  • CKD patients often do not show ECG features of LVH inspite of LVH

Final message

Diagnosis  of  LVH by ECG is a  simple clinical exercise , but we realise now , the underlying mechanisms are too complex .

A simple question , ie  Why  every one  with LVH  do not increase  their  QRS voltage  ?  . . . exposes  our ignorance on the subject!

But one thing is clear, physiological LVH (Meaning LVH ,  purely due to loading conditions including SHT/Aortic stenosis)  more often result in high voltage , while  in true pathological LVH(infested with fibrosis ) the  increase in voltage is not consistent .

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