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Posts Tagged ‘refractory hypotension’

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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micro circulation shockHuman circulatory system consists  of  the heart , the arterial  and the venous  systems . Together they constitute the  three important limbs of circulatory system namely , the  pumping, delivering and retrieval systems .In physiological conditions approximately 6 liters of  blood  has to traverse  the entire   circuit every minute . The  purpose of the  circulatory system is not simply circulating the blood within the body,  but  it has to perfuse different vital organs like brain, kidney, liver . Of course ,   the heart has to self perfuse the coronaries  by it’s own contraction.The organ perfusion is determined by local and systemic  regulatory mechanism. A gamut of intrinsic and extrinsic neuro humoral modulators take up this job. A functionally intact autonomic nervous system is an absolute necessity to maintain tissue perfusion.  The perfusion pressure is highly variable in different organs and different cells. Similarly the ability to with stand ischemia and hypoxia also varies. Shock  is a general term used to imply ,  circulation is seriously compromised.Here we will confine our self  to the intricacies of peripheral circulatory shock

Traditionally shock is  classified as

  1. Cardiogenic shock
  2. Hypovolemic shock
  3. Vasodilatory /Redistributive/Septic /Warm shock (Can be called  as  arterial shock )

The hemodynamics of the first two are straight forward and easily understood. In  cardiogenic shock , the pumping action of heart is primarily affected .In hypovolemic shock  there is no  structural defect in any of the   circulatory limbs but there is  a loading defect due to low blood  volume as in hemorhagic shock .

The term vasodilatory shock or redistributive shock is most poorly understood and most difficult to treat.

The  concept is further confounded as  combinations of   above three mechanism in a same a pateint can occur . ( More commoner than we believe !) . An example could be a septic patient  with an  internal bleed and myocardial  depression either due to preexisting LV dysfunction or circulating toxins.

Since  we have always perceived heart as  the  sole  vital  component of circulatory   system , our understanding of the role of the vascular tree which is primarily responsible for delivering the blood is largely undermined and neglected. We are always happy if the EF %  is normal.

Classical features of  circulatory failure ?

The cardiac contraction is good.This is documented by normally contracting LV by echocardiography. The pulmonary capillary wedge pressure is normal (<12mmhg).Still the patient is in  hypotension with  evidence for vital organ under perfusion like oliguria and reduced mentation.

What is vascular tone ? What sustains  the flow of blood into the tissues  ?

The entire  vascular tree could form a   few 100 kilometer length.(Capillary /arterioles /venules included). While , it is easy to  percieve heart as  a dynamic pumping organ ,  it is a less recognised fact the entire vascular tree is also  pulsating  to every beat. That is the rhythm of life. What makes the vascular tree to pulsate ? Apart from  contraction of the heart  , there is an  intrinsic tone for the large , small arteries and the arterioles and veins  .This tone is vital for pushing the bllood into various organs and return into venous circulation and subsequently back into the heart.

microcirculation shock cardiogenic septic

The  millions of perivascular cuffings and the artreriolar smooth muscles  can be considered as  small micro pumping stations situated along side every cell.

It is very important to emphasize here,   if  tone in these microcirculation is less than optimal , the patient’s circulatory  system can never complete the desired circuit  even if the heart has 75% EF . This exactly is happening in circulatory shock . The vascular tree fails to accept and return the pumped blood  in timely fashion.

What controls this tone ?

It is chiefly under the control of autonomic nervous system.The endogenous vasoconstrictors , the adrenergic nervous system, the endothelins , the angoitensins constrict the vascular smmoth muscles while endothelial relaxing factors ,( EDRF -nitric oxide relaxes it ). There is a delicate balance between these forces.

A cardiovascular health of a person is not simply having a healthy heart , he has to have a healthy vascular system with intact biological activity.The fact that , not every one with sepsis react with poor vascular tone indicate inherent capacity to neutralise toxic vasodilatory neuro transmitters.

Is there a invisible parameter called vascular ejection fraction  in circulatory  system?

Yes. It must be . We rarely discuss it . The vascular tree has an important role for pumping the blood into the tissues.  It needs micro manometers to assess the systolic and diastolic dimensions of small arteries and arterioles . But  what  we know is ,  it is grossly impaired in circulatory failure.The vessels especially the arteriolar smooth muscles which determine the perfusion pressure of cells go into state of permanent relaxation. The vascular smooth muscles lose control from autonomic innervation and become flabby. It is the   DCM equivalent for blood vessels. The arterioles no longer regulate blood flow and fluids get sequestrated in various viscera,( often called thrid spaces) and organ dysfucntion sets in. The resultant hypoxia aggarvates the tissue stagnation by producing still unnamed vasodialtory mediators.

What are the pharmocological approches to increase the vascular tone of a failing vascular tree ?

It is a very difficult problem even in this modern era of vascular medcine. Once set in ,  these patients invariably go downhill .The primary underlying problem  ,  often sepsis  need to be corrected. Usually these  patients need multi organ support.Vasoconstrictors like epinephrine,nor epinephrine , dopamine  can sustain vasoconstriction temporarily . As we know the vascualr smooth msucles can not be kept on this assited contrection mode for long.It is bound to fail .Patients native autonomic function has to recover fast to wean of this support.

What is normal circualtorty time .How is it altered in circualtory failure  ?

The normal circualtory time is 15-20 seconds.It is many times prolonged in circualtory failure inspite of the cardiac contraction being normal

What is effective circulatory volume ?

The body fluid compartment is divided into ICF,ECF & interstitial  spaces.At a given time , the fluid in the extracellular space  can only  take  part  in circulation. A good blood pressure does not always mean a good tissue perusion why ? This is very important to realise as blood pool has to dynamically exchange with intra cellullar compartment. At times of shock the blood can bye- pass the cells through the alternate circuits in the periphery of micro circulation. So what is circulating in the system may not be taking part in tissue perfusion .This is the concept of  effective circulatory volume.This is especially noted in hepatic shocks and in some terminally ill malignancy.

Is there a venous shock syndrome ?

Cardiologists  often show a  step motherly  attitude to venous disorders. In fact many  of the   cardiovascular  specialists   think their   job is  taking care of  heart ( Of course , a little bit of aorta and venacava !) .It is surprising  to know,  there is little  scientific data on determinants  venular and venous tone (Both small and large veins).

The power of venous system should not be under estimated  as it pumps  many litres of blood every minute  defying gravity ! For this to happen it needs a vigorous tone .Where do it get from ?  : The same  autonomic nervous system that controls the heart. Remember , in pathological states there is a  great chance for this to go out of control. So venous shock is a clinically distinct possibility. In fact inappropriate administration of nitrates which reduces the venous tone has resulted in many adverse events in RV shock.

In a patient with circulatory shock , we would  never know  how much is contributed by venous side and how much by arterial side .This is important as in circulatory shock we administer all vital drugs through veins.Now it is thought  systemic venous  dysfunction also contribute to shock state.

Clinical situations of circulatory failure or shock

Bacterial shocks

  • Gram negative sepsis
  • Staphylococcal shock

Viral shocks

Dengue/Swine flu etc

Others*

  • Dissiminated intravascular coagulation
  • ARDShypoxic shock
  • Elderly,Diabetic  autonomic neuropathy
  • Persistent post operative hypotension due to silent autonomic neuropathy.
  • Some cases of Spinal shock
  • Toxins – Scorpion etc(Intense vasoconstrictive shock )
  • Terminal shock in liver failure/Hepato pulmonary   syndrome

* Idiopathic unexplained persistent hypotension , with difficulty to wean off from vasoconstrictive agents is a commonly encountered problem in any intensive care unit.The exact mechanism is not known.When we are not clear about the mechanism  we  generally blame it on the  the autonomic nervous system !

How common is the mixed shock syndrome ?

This is more common than we realise .The classical description of multisystem failure is a direct consequence of this.

Can a cardiogenic shock transform into a peripheral circulatory shock ?

Such a scenario is  possible  .A  resuscitated cardiac arrest may end up with a recovered heart but a loss of vascular tone  possibly due to hypoxic vascular damage. .Many times cardiac patients are kept (Post PCI/CABG ) on large doses of  vasoconstrictors or IABP that can induce  tachyphylaxis. It may result in difficulty in weaning these drugs.

How can circulatory shock result compromised cardiac function ?

The common effect of any shock is  reduced organ perfusion.So even in peripheral shock , the coronary blood flow gets compromised especially if these patients have a silent coronary lesions which are otherwise not significant , becomes sites of hemodynamic hurdles during hypotension.This may result in global contractile dysfunction, or a coronary event.

What is vasoconstrictive shock ?

Epinephrine and nor epinephrine are  very potent  vasoconstrictors .If levels of these becomes excessively high , the blood vessels go in for sustained spastic state that can impair the micro circulation .Some times  this results  in a  good blood pressure in the major vessels but severely compromised tissue perfusion.This particular situation has been reported after scorpion envenomation , and in  rare cases of pheochromocytoma .

Final message

Primary circulatory failure or shock (With largely intact cardiac function without hypovolemia) is a common problem in critically ill.  The entire  macro and micro vascular tree goes for a  stunning reaction and  goes for  a sleep in a  semi dilated  state  . It can  be termed as  Arterial  or Arteriolar   shock. Contrary to  all those hi-tech   mechanical stuff for supporting a failing heart (LV assist, Impalla, Abiomed , ) the available options are very little here  . The response to vasoconstrictive agents are  also unpredictable. Correcting the multi organ failure  and targeting the primary cause  is the only hope.

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