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Posts Tagged ‘dyspnea’

Anginal equivalents are distinct  (often vague  ) symptoms that occur in response to myocardial Ischemia , instead of angina. Dyspnea or shortness of breath  is the commonest anginal equivalent . The incidence and exact mechanism  is not clear. Both angina and dyspnea are sensory  events . Both are  perceived  at the level of cortex. Angina occurs when ischemic  muscle  triggers pain signals from the   nerve  twigs engulfing the myocytes membranes  and the vasavasorum.

Dyspnea during myocardial  ischemia  is multi-factorial

  1. Signalling error .( Mismatch between respiratory /Cardiac  receptors  neural traffic)
  2. Cortical perception disorder.
  3. Autonomic neuropathy (Blocks pain signals  but still may carry  myocardial stretch response)
  4. Coronary sinus lactate –  Biochemical /Chemo receptor stimulation
  5. Isolated  Ischemic LV relaxation defects  , and resultant elevation of LVEDP
  6. Ischemic systolic stunning  and secondary  diastolic dysfunction  (elevated PCWP  pulmonary stretch receptors stimulation )
  7. Ischemic MR . Eccentric MR jets and regional and segmental elevation of pulmonary venous pressure has been reported. (Unilateral and segmental pulmonary edema)
  8. It is possible  ,  Ischemic wall motion defect per-se  can induce myocardial stretch and create a feeling of dyspnea.

Out of the above eight factors  which is  most important  ?

The most popular and easy to comprehend   mechanism   is number 5 : Ischemic diastolic dysfunction .

(Fellows will be appreciated if they  know this !   )

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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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It is a well known fact  ,   CABG and PCI  provides immediate relief  for patients with angina ,  which is refractory to medical therapy. Of course , this happens only if a critical occlusion of  at least one epicardial coronary artery is  opened . It need to be realised ,  angina  due to  microvascular  disease can not be cured by maintaining  epicardial  patency .

While angina  relief is prompt ,  dyspnea is not ! . If we  believe,  opening  up a  coronary artery  in a patient with LV dysfunction will  restore the LV function  ,  it  is grossly mistaken !

Why is it so ?

Angina  relief requires  simple  restoration  of  oxygen supply and correction of local ischemia .  This happens without any issue as the blood  seeps in to the ischemic cells and soothes the ischemic nerve fibres that trigger the pain signals   . While  ,  for LV function to improve , the blood flow has to be converted to mechanical activity in the form of myocyte actin/myosin interaction. For this,   there need to be an intact  cellular contractile mechanism . The myocyte architecture should be appropriate .In post MI ventricles we know there is  zig zag  orientation of myofibrils due to myocyte slippage that interfere with mechanical recruitment . Further , integrity of  extracellular matrix  namely the collagen frame work is also vital . Note ,  angina relief  is not concerned with any of the above .

And now ,  we also realise  dyspnea  in failing ventricles  is vitally  dependent on diastolic function ,  which is also very much  impaired in ischemic DCM .There is little proof for  PCI/CABG  to correct the  molecular   mysteries in  diastolic dysfunction !

Dysfunctional LV means what ? (read the link )

It is a collection of  variety of myocardial tissues . Viz : Fully  necrosed , partially necrosed ,  ischemic viable, non ischemic viable, ischemic non viable, non ischemic non viable , Apart from this patchy necrosis, patchy ischemic, areas are common. Finally , necrosed segments   may  also be perfused normally by  spontaneous reopening of an IRA.

One can imagine the complexity  of events in these segments  once we do the  PCI /CABG . The response  is highly variable and unpredictable. The major concept we  , the physicians  believe or ( to be precise made to believe !) is  the  sanctity  devoted to  the viable myocardium .For  many us ,  it is considered a  holy  exercise  to identify viable myocardium in patients following MI and then revascularise them if  found to have significant viable myocardium (Atleast 20% of infarcted area )

A full 2 decades were lost or (shall  we   say wasted on this futile exercise !) as   we have since  realised most of the cardiologists do not follow this rule .

Now , even a scarred myocardium is revascularised in the hope of recovery .As such , we have reached a stage where  there is no contradiction for not doing a PCI /CABG   with reference to LV dysfunction.

Now every  patient  with post MI  LV dysfunction  is considered to  have  some amount of viable myocardium that is  fit   enough  for revascularization

Are we justified in doing  this ?

Many clinical  trials  have revealed  , the  recovery of LV function  in these segments  has not been consistent at all .

The most surprising discovery is  a viable myocardium need not  be ischemic   .It might get adequate blood supply either  from invisible collaterals or trickle of antegrade flow .  Hence an adequately  perfused myocardial segment can  still be   non contractile . This shatters the myth  that  revascularisation must have a dramatic effect on the recovery of contractility in all viable segments.

The other major finding is  ,  even ischemic   viable   myocardium ( documented by metabolic activities PET etc)  need not regain it’s original contractility  after the ischemia is fully corrected .

*reference for  both the above statements are available from variety of sources including real life experiences .(Type C evidence )

Final message

  • Do a PCI/CABG promptly for patients with refractory angina.
  • Never  advocate PCI/CABG  for  a primary relief of dyspnea .  (Never is a harsh word,  let it be  “use it  with caution ” ! and  the  patient  should be  revealed  the whole facts  about  what we know and what we do not know regarding the complex  hemodyanmic events  in  revascularisation   )

Counter point

If  the above statements are really true ,   How does PCI/CABG   help  relieving  dyspnea  and functional class  what is your answer for thousands of patients  with CAD and ischemic DCM who have greatly benefited from CABG ?

The answer could  be  simple , The revascularization  piggybacks  over the   medical management (which , these patients pursue vigorously)     like  ACEI,  statins, salt restriction, betablockers  , optimal diuretics and tend to hijack the credits from the poor  drugs !

Read a related blog

Revascularisation for ischemic DCM

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orthopnea paroxysmal nocturnal dyspnea pnd www.drsvenkatesan.com

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Anginal pain is a type of visceral pain.It is carried by type  C  unmylinated  nerve fibres.The perception of angina is a complex process.It is a combination of visceral and cutaneous referral pain.

How often is angina silent in diabetes mellitus ?

Presence of  diabetes per se does not make an angina silent. In fact,  if  one takes 100 patients with diabetes  , if angina occur in them , it is more often  , manifest than silent. So , only few of  the  diabetic patients who develop diabetic autonomic neuropathy fail to have angina.The exact incidence is not known.It could be around 20%.

If angina can be silent in diabteics , can they have anginal equivalents ?

This again is not answered in literature. Among the anginal equivalents , the most common is  dyspnea , which  can occur in diabetics.But now , we know dyspnea also needs thoracic nerve signals  from the intercostal muscle spindle and colgi organs.This can also be impaired in diabetics.

Can silent and mainfest episodes occur in a same  patient  ?

Yes.

Once silent does not mean always silent, and similarly once angina is felt it  does not mean he is going to feel the next episode as well !

This  strongly reminds us medical science  is  much a complex  subject and what we know is very little in pain perception.

How is silent ischmia different from silent angina ?

There is considerable  overlap  between  silent ischemia and silent angina

The questions to be answered are 

Which is silent  ?  Is it the angina or is it the ischemia or both ?

Silent ischemia can occur in any individual ,  this is also called as silent CAD . When  ischemia occurs  but  fails  to generate pain it is silent ischemia .Undiagnosed  CAD in asymptomatic individuals is also called silent ischemia or CAD.In this population  Exercise stress testing detects  CAD which was otherwise silent and masked.These patients may develop angina during EST.

During exercise stress testing many times patient has significant ST depression  more than 2mm but still chest pain may not occur.These episodes may either be silent ischemia or  ngina. Many times the EST is terminated before angina is manifest .( Chest pain is the last to occur in the chain of events following ischemia- Concept of ischemic cascade )

What are the other situations where angina can be silent ?

  • Pain perception  and threshold  level is  high ,  so patient indeed has anginal  signals but fails to feel it .
  • Patients on  antianginal medication , fail to feel the angina.
  • Chronic betablocker therapy can exactly mimic  autonomic neuropathy

Is it a blessing for the patient  to have painless episodes of angina ? 

When their  ischemic colleagues , suffer a lot with chest pain it is tempting to think these diabetic patients  are blessed!

Scientifically , this could be true in at least in  some  especially in a patients  who’s coronary anatomy is known  and devoid of any critical proximal lesions. For example a small PDA  lesion can produce  severe angina  , but may be silent  in diabetic and be comfortable .This lesion is  insignificant other wise * !

It should  also be recalled , pain relief has been an important goal for treatment  of CAD .In olden days,  thoracic sympathectomy was done for angina . In fact ,  even in  CABG  , one of the the  mechanisms  for  angina  relief  is attributed  to cardiac denervation.

Caution: Even a small  episode of ischemia can trigger an electrical event .But it is rare.

 How common is silent infarct (STEMI) in diabetic patients ?

In a simple questionnaire we asked the diabetic patients in our CCU how they felt their pain during MI.Most felt it normally as do other non diabetic .  Diabetes  does not make  all anginal episodes  silent. Severe episodes of ischemia may be painful while less severe episodes may be painless. Diabetic autonomic neuropathy  is a  least recognized and  poorly understood complication of diabetes.Diabetes , involves  the vasanervorum of the autonomic nerves.

 The other mechanisms postulated in diabetic neuropathy are

  • Reduction in neurotrophic growth factors.
  • deficiency of essential fatty acids .
  • Reduced endoneurial blood flow and
  • Nerve hypoxia .

Is diabetic autonomic neuropathy treatable ?

Very difficult problem indeed.Controlling diabetes may partially correct  the neural dysfunction.Many add on neuro vitamins and aminoacids are having a good market !

If you successfully treat diabetic autonomic neuropathy will my patient  start feeling the  hitherto silent episodes of angina ?

We don’t know.Logic would answer ” YES”

What is the ultimate effect of cardiac autonomic neuropathy.

Cardiac denervation.  The manifestations  are

  • Tachycardia, exercise intolerance
  • Orthostatic hypotension

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Orthopnea is a classical sign of established CHF.

While paroxysmal nocturnal dyspnea is an early sign of cardiac failure,orthopnea is a late manifestation of cardiac failure .This symptom was mainly attributed to volume displacement from systemic venous to pulmonary circulation when the patient goes to recumbent posture.The exact mechanism of this has been speculative. Now with liberal usage of bedside echocardiography, we have found out there is postural variation in the diastolic function of the failing left venticle.

Many patients develop a restrictive ventricular filling pattern in recumbent posture (Grade 3 diastolic dysfunction). While sitting up some of them revert to normal or downgrade to grade 1 diastolic dysfunctionThis observation proves another fact that every patient with severe systolic dysfunction also has significant diastolic dysfunction at some point in their course of illness.

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