Posts Tagged ‘hypertensive lvh’

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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