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What is the mechanism of sinus tachycardia thyrotoxicosis ?

Posted Oct 21 2011 3:22am

The answer to this  seemingly innocuous  question is not  that simple at all.  We know ,sinus tachycardia is  a common expression of thyroid  excess while  sinus bradycardia is the  hall-mark of thyroid depletion. So  obviously ,  the first thing that would  strike us  is ,  there must be  something  cooking between thyroxine and the SA node .

We realised much later , there is no direct action of thyroid hormone on the SA node instead it has a crucial interaction with adrenergic system which   has the major influence on chronotropy.

Click on the image for flash Animation (Courtesy Mcgraw Hill )

How does thyroid interact with adrenergic system ?

Thyroxine (T4)  is an inactive molecule , it has to get converted to  T3 for its action. This conversion takes place inside target cells like myocytes, pacemaker cells  (of course  it has action  on virtually any metabolically active cell !  )

The most important point to remember is , unlike catecholamines the thyroid receptors are located  in the surface of  the nucleus  inside the cell , instead of cell membrane . Surprisingly T4 does not require any specialised transporter to enter the cell.It simply diffuses into the bi-lipid layer of cell membrane as T4 is immensely lipid soluble.  . After entering the cell in the cytoplasm it gets converted into  T 3.

This T 3 is attracted towards the nucleus. Once  it is attached to nucleus , it brings about  changes in the gene configuration and  through  messenger RNA results in new protein generation . These cellular  elements are vital for maintaining the  ionic channels and ports and anti-ports.Among these the most important is adrenergic receptor molecule , an its  signal system namely the GTP/Adenyl cyclase/Cyclic AMP units in the cell membrane .

Thyroxine is a physiological hormone  required to maintain these adrenergic  receptor complex on day-to-day basis. (It can be called as cell servicing hormone )

The circulating catecholamine’s  action is  heavily  influenced by the thyroid hormone status.   Sympathetic  nervous system is the live wire for human biological system.  So , when thyroid is in excess the entire metabolism of  cell is increased and vice versa happens.With the close interaction with adrenergic system  , one can understand how thyroid excess causes anxiety state and depletion causes  depression.

Coming back to heart ,

  • Thyroid hormone   up-regulates  beta receptors in cell membrane and augments the action of epinephrine and  result  sinus  tachycardia .It can have positive inotropic action as well (Hyperdynamic  state )
  • Aguments intracardiac  conduction.
  • The action of thyroid hormone on heart can well extend to the pathological phase, where in it can cause multiple ventricular ectopics and atrial fibrillation. (Note the striking similarities between  these arrhythmias   and   adrenergic  arrhythmias !)

What is time frame for  thyroid  hormone action ?

Obviously thyroid hormone can not  have a rapid onset action  since it invites the nuclear synthesis  (Like steroid hormones)  it may take few weeks time for thyroid hormone to express its effects.

How does beta blockers exert its action in thyrotoxicosis ?

This occurs in two ways.

  • The beta blockers occupy the adversely up-regulated dense  beta receptors of cell membrane and  prevents excess adrenergic  action.
  • There is some evidence beta blockers prevent conversion of T4  into T3 .This seems to be less important than its direct sympathetic blockade.

For effective control of thyrotoxicosis one need to administer beta blocker in combination with anti-thyroid drugs.

Will calcium blockers be effective in controlling the tachycardia of thyrotoxicosis ?

No it is not . It may  reduce the heart rate a little but never to the extent of beta blocker. This is another  indirect evidence for  the interaction between thyroxine and adrenergic system.

If thyroid hormone is able to potentate the circulating catecholamine action why not it be used as a

positive Inotropic in cardiac failure ?

A very valid question.  It was tried by many researchers especially in dilated cardiomyopathy. .For some reason it has not worked well , except in patients with  associated with hypothyroid  state.I personally believe thyroid hormone must have  a major role  in chronic heart failure in spite of the fact  we have  proposed sympathetic blockade as concept for regulating cardiac failure.


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