Why hypotension is more common in infero posterior STEMI ?
Posted Apr 14 2010 11:06am
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 ?
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
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.