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Posts Tagged ‘dyspnea vs angina’

Angina and dyspnea are the  two cardinal ( classic ) symptoms of cardiac disease . While dyspnea is a manifestation of raised LV filling pressure ,  angina  implies reduction in blood supply to heart .

In other words dyspnea is related to excess blood in the  lungs and angina is due to less  blood in  the coronaries  !

So , it is obvious  even though these  two  symptoms are closely knit entities , patho- physiologically  they are  distinctly different  in real time , when an actual  cardiac event unfolds in the bed side .

This also partially explains  , why simultaneous  presentation   of  angina and dyspnea is  relatively  uncommon in CCUs  , than one would expect .(In a given patient , one of them will be dominant)

Why and how our patients (and also  physicians !)  get confused  with dyspnea and angina ?

When William Heberden described  angina over a century ago ,  he was  so meticulous in his description and observation. In fact , it was,  as if  he felt the angina  himself  and wrote it .One can rarely  expect such a  description from any of our patients .  So , it is not at all a surprise  for mistaking  any mid sternal discomfort as dyspnea instead of  angina . (This error in describing angina  is the commonest cause  for dyspnea  playing this  dubious dual role !)

When to suspect  dyspnea  as an Anginal equivalent ?

Here  are some real situations ( and clues )  where  dyspnea  may be  considered as  anginal equivalent.

  • Diabetics
  • In elderly with autonomic dysfunction
  • Patients with chronic beta blocker and other anti anginal drugs.
  • Post PCI/CABG patients (Normal LV function but dyspnea : Denerved heart blocks pain  ?)
  • Exertional dyspnea that stops immediately could be anginal equivalent.
  • Dyspnea with palpitation is  rarely be anginal  equivalent as palpitation indicate good LV /mitral valve function.
  • Dyspnea on  isometric  exercise rather than isotonic exercise .

Mechanism of anginal equivalence

While the trigger for dyspnea is elevated LVEDP  which   stimulates the  stretch receptors in lung .For angina ,  it is the free nerve ending in myocytes that gets irritated and generate pain signals.

When ischemia  presents as dyspnea  two mechanisms are considered. One is myocardial , other is purely neurogenic.

  1. It is  believed critical   ischemia  of myocardium  ( Defective Ca ++ uptake  into sarcoplasmic reticulum) induce  “a wide area  diastolic dysfunction” of LV  that   raises  PCWP  to generate  dyspnea. Further , ischemia induced regional LV dysfunction  that  subtends the pap muscle could  result  in ischemic  MR and severe dyspnea. (Exertional Mitral regurgitation is getting major attention now  )
  2.  In many patients with diabetes or autonomic dysfunction the velocity of  pain signals  become sluggish  or  blocked  en-route  to brain stem . Often they change track to travel in the nerves  meant  for  carrying somatic siganls  ,  J receptors  , intercostal spindle etc . This spill over and cross talk  creates a  false sense of dyspnea , whenever ischemia  occurs. This is attributed to the  wide and complex  neural network of thoracic sympathetic ganglions.

Some of the known  associations with Angina equivalent .

  • Diastolic dysfunction
  • Ischemic MR
  • Small rigid  left atrium
  • Atrial fibrillation

How to  investigate a patient who is  suspected to have  angina equivalent dyspnea ?

  • ECG
  • X ray chest
  • Echocardiogram will settle the issue most times.

Nuclear scan and angiogram in deserving patients

When can  angina and   dyspnea occur together  ?

Angina and dyspnea  if   truely  occur together causes  grave concern for the physician.

This indicates two things .

  1. The myocardium is ischemic  and generates  pain (And possibly ongoing necrosis) .
  2. Simultaneously its  pumping or receiving function is also compromised resulting in  entry block from the lung resulting in acute dyspnea.

Both are ominous signals . This situation occurs  most often in  STEMI with LV failure .

If  dyspnea occur in NSTEMI/UA ,  it is a worst possible complication . GRACE  registry quotes  maximum  mortality for unstable angina with cardiac failure .The reason being the cardiac failure in UA is due to non necrotic global ischemic stunning of LV myocardium with or with out acute  mitral valve failure.(Flash pulmonary edema)

Why angina is rare  in  chronic congestive  cardiac failure ?

The main reason being  , a severely dysfunctional heart  contracts  poorly .In reality , it is never thirsty for blood  . Even if it  is  perfused  well  , there is no good muscle  mass  to burn the ATPs from it .A failed myocardium is  more or less a  sleeping  myocardium .It does not even have the  energy   to cry with pain at times of ischemia ! .However significant the ischemia  is ,   it can often  evoke only  a gasping sensation .

The other explanation  is more imaginative . In cardiac failure heart  dilates .The end diastolic and end systolic  volume is high. The cardiac chamber is always filled with  excess residual blood .This , some how tend to perfuse the myocardium directly and provide a good reserve .This may be  more important in  RV perfusion  .( Trans myocardial laser revascularization is based on this concept – direct myocardial perfusion from the chambers)

While angina is  rare in chronic cardiac failure,   it should also be realised ,dyspnea  is  rare in  uncomplicated acute coronary  syndromes. We know ACS  primarily present with angina.  Exceptions are always there.

In elderly, diabetic , with co morbid   patients ,    ACS  may  present without  angina . Instead  they present with vague dyspnea and shortness of breath . It is here ,  physicians  face a tough task to identify  dyspnea  behaving like   angina  equivalent.  Of course , the  good old  ECG bails us out most of the time.

Therapeutic importance of recognising anginal  equivalents ?

The revascularisation  procedures (CABG/PCI)  are too good  in  relieving  angina , but least effective in providing relief from dyspnea.So  real anginal equivalents if recognised properly can be subjected to early revascularisation .

Can we consider  exertional dyspnea as evidence for ongoing ischemia  in a post MI patient ?

This is tricky question . We do not have answers to it. Readers can try to  answer . The commonest cause of dyspnea following MI is due to physical deconditioning and associated LV dysfunction.

Final message

Coming back to the basic question  , Is  this dyspnea  . . .  an angina equivalent  doctor ?   No simple answer is available .

The first and foremost investigation to do  is ECG .This will settle the issue many times.  Next is the reassessment of  history  clinical  presentation and past history.  Every patient with unexplained dyspnea must undergo a minimum of three investigations (ECG,  X ray chest and Echocardiogram )  If any of these  suggest a cardiac compromise   further evaluation is   indicated.

So, the message here is ,  clinical findings  are insufficient  to rule out ischemic etiology for dyspnea.

References

Nil . Every thing is my random thoughts !

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