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Posts Tagged ‘vagal tone’

Human heart is a vital bundle of muscle  weighing  about 300-400 grams. The blood  supply of this muscle  mass  is highly variable . Some areas are abundantly  vascularised(  eg -IVS.) Some areas have a balanced blood supply with  twin blood supply (Often the  LCX and RCA in the  crux of the heart ). Certain areas have a precarious blood supply . They are  some time called as water shed areas or  vulnerable   Bermuda triangle of the heart – the  overlapping zone of   LV apex,  free wall and  the anterior surface.

When the blood supply is so  heterogeneous , it is  not surprising  to find  the neural innervation of the heart to have a  unique pattern as well .The cardiac  autonomic nervous system   is  mediated by the  cardiac plexus  . It  has a  dominant adrenergic  innervation in the anterior   aspect of the heart   that is  rich in catecholamines , while the infero posterior  aspect  of heart has a high density of  vagal fibres .

So , it becomes easy to understand , why  ischemia of inferoposterior regions often trigger  a vagal response and an adrenergic response  in  anterior ischemia  .Of course , overlap can occur especially in multivessel CAD with collateral dependent circulation.

The inferoposterior MI ,  generally  have  a better outcome as it imitates  naturally beta blocked heart . (Less heart  rate , less MVO2  more salvage ) Still  hypotension  can be  a worrisome complication in inferoposterior MI .

The following  factors contribute to hypotension in infero posterior STEMI

  • Heightened  vagal tone  due to Bezold  jarish reflex
  • Involvement of RV is known to occur up to 40% of all  inferoposterior MI. Loss of RV pumping action is the classical explanation of hypotension
  • Recently recognised  fact  : Infero posterior MI often have subclinical and subelectrical atrial involvement. This is a powerful trigger for  the atrial  naturetic peptide secretion. ANP  a water losing hormone explains much of hypotension in this situation. .It should also be noted atrial necrosis is not necessary for ANP release. Simple atrial stretch  or even RV stretch can be a stimulus for ANP .
  • Variable degree of LV involvement is  common in infero posterior  MI .This can have detrimental effect on LV pump function . It  can  be a independent  factor for  the hypotension.
  • Excess sedation with morphine may aggravate or precipitate hypotension.(Vagal  action of morphine )
  • Finally , and most importantly a common cause  is  hypovolemic  hypotension (Applicable for any STEMI – Severe sweating  and sometimes vomiting can  loose  up to  10 liters of body water )

How to manage ?

  • Correct hypovolemia
  • Water challenge in RVMI is a popular (Often abused) concept . Rule of thumb is , if 1000ml  of  rapid infusion  fails to correct the hypo it is  highly unlikely  it will  do it at 5 liters  ! Cases of fluid overload and dilutional hyponatremia have been reported.
  • Atropine (This is one of the rare situations  where vagal blockade increases the BP ) .Dopamine may be useful but logically we need to  reduce the high vagal tone  and bring autonomic parity  . (Increasing adrenergic tone to that of high vagal levels  for autonomic parity  is  a lesser logic !)
  • Temporary pacing may be needed if  blood pressure fail to raise because of  troublesome bradycardia.
  • And  of course  , rapid PCI and revascularisation  when Indicated

Final message

Hypotension in inferoposterior MI is often  considered innocuous. But , it can be dangerous in some , especially in the  elderly and comorbid individuals . It has  varied mechanisms  , that are distinctly different from anterior STEMI.  Recognising the underlying mechanism  hypotension  will aid us to correct it  rapidly.

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ECG of an athlete is many times difficult to interpret. The influence of autonomic tone in  athlete’s heart is an complex one.Contrary to our expectations the parasympathetic tone is higher in well trained athletes. The resting heart rate can be as low as 30/mt which is 99.9 times pathological in non athletes.This happens due to a concept called accentuated antagonism.The athletes who have episodic surge of high catecholamines keep stimulating the para sympathetic neurones in a constant fashion.

LVH is the most common feature.Here there is simple myocyte hypertrophy, without pathological fibrosis.This differentiates athlete’s, heart from HOCM .

Many ECG abnormalities are reported in athletes.

Excerpts from the ACC recommendation

1. Electrocardiographic findings that are common and training-related and that do not require additional evaluation are sinus bradycardia, 1° atrioventricular block (AVB), incomplete right bundle branch block (BBB), early repolarization, and isolated voltage criteria for left ventricular hypertrophy (LVH).

2. Uncommon and training unrelated electrocardiographic findings that mandate further evaluation include T-wave inversion, ST-segment depression, pathological Q waves, atrial enlargement, a hemiblock, right ventricular hypertrophy, a BBB, or a Brugada-pattern of ST-segment elevation.

3. Training-related electrocardiographic findings are more common in men than women, athletes of African descent, and high-endurance athletes such as cyclists.

4. Sinus rates <30 bpm and sinus pauses >2 seconds are common in highly trained athletes, particularly during sleep.

5. A normal chronotropic response to exertion and the absence of bradycardia-related symptoms distinguishes training-related sinus bradycardia from sinus node dysfunction.

6. 1° AVB and Mobitz I 2° AVB are common, but Mobitz II 2° AVB or 3° AVB should not be assumed to be training-related and require evaluation.

7. Early repolarization in Caucasian athletes most commonly consists of upwardly concave ST-segments and tall and peaked T waves; in black athletes, there often is convex ST-segment elevation and negative T waves, mimicking a Brugada pattern.

8. In the presence of voltage criteria for LVH, pathological hypertrophy should be suspected if there is left atrial enlargement, left-axis deviation, repolarization abnormalities, or pathological Q waves.

9. T-wave inversion ≥2 mm in ≥2 adjacent leads should prompt evaluation for structural heart disease.

10. Electrophysiological testing for risk stratification with possible catheter ablation is appropriate in athletes with ventricular pre-excitation.

Source :  Fred Morady, M.D., F.A.C.C.

http://www.ncbi.nlm.nih.gov/pubmed/19933514?dopt=Abstract

For an excellent article on the topic click here

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