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Posts Tagged ‘hypotension in stemi’

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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Hypotension is one of the dreaded complication of acute STEMI.

  • It can be due to either a  mechanical complication or hypovolemia.
  • The hypotension in inferoposterior MI is  often related to enhanced vagal tone and easily correctable with atropine  and fluid  administration.
  • RVMI is the classical example of hypotension that may improve with fluid resuscitation
  • Hypotension,  if  not reversible within 12  hours  ,  is more likely to  represent a more sinister mechanism like pump failure, MR or ventricular  septal tear etc .

A new mechanism for persistent  hypotension is increasingly recognised.

This is due to the

1.Loss of LVOT dynamic activity.

2.Excessive  dynamism of LVOT.

LVOT contractile and ejectile falure

Even though LV  outflow tract  contain  less  contractile myocytes  , it has an important mechanical  job to do. We know , it’s  primary job is that of a  conduit  but  it also  has to  eject the blood into aorta with sufficient force.  In fact, it is thought much of the acceleration of blood velocity occur in LVOT . So, LVOT  plays a key role in maintaining the cardiac index.  An excessively dynamic LVOT will impede the forward blood flow as in HCOM.  Similarly  less dynamic contraction  of LVOT  results in  low velocity propulsion , that interferes with   proper delivery of blood from LV cavity into the aorta .

These factors get amplified in  acute MI , as it is a compromised situation with fluctuating HR and contractility. So a properly functioning  LVOT conduit is  absolutely mandatory.

STEMI due to a proximal LAD obstruction   located can involve the septal .If the first septal branch  happens to be a major one,  there will be  definite impact on the LVOT function.

Excessive dynamism  , LVOT   desynchrony  LVOT collapse .

LVOT has a medial border formed  by IVS , an  anterior surface and  a posterior surface .The lateral border is relatively boundary less , except it is guarded by  the anterior mitral leaflet.

But one should recall , the AML comes towards the LVOT only in diastole . When it comes in systole it becomes a pathological event  called  SAM  (Systolic anterior motion )

The LVOT wall desynchrony can occur in both anterior and posterior MI.In a mulivessel CAD  this can happen when there is disproportionate inferior to anterior wall motion defect.

Management.

  • There is no specific management strategies aimed at restoring LVOT function.
  • Emergency revascularisation will attenuate the mechanical dysfunction
  • Dosage of powerful inotropic agents should be moderated in dynamic LVOT obstruction.
  • Spontaneous recovery  may occur in few

http://circ.ahajournals.org/cgi/reprint/116/5/e110.pdf

Haley et all Mayoclinciproceedings 1999

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