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Posts Tagged ‘atypical chest pain’

Chest pain as a symptom in  acute MI is vitally important as it only  brings the patient  to the ER. (Realise ,silent MIs  can never reach the hospital in time ! ). Heart is  located  few  centimeters beneath the chest wall and extend up to  15 cm posteriorly.The location heart within the chest wall  , make it a  three dimensional structure .Theoretically  pain can initiate in one focus and radiate to any direction. Traditionally , when we say  chest   pain , we mean the anterior chest wall on either side .Technically , chest contains a lateral  and a posterior wall .The posterior  surface of the chest is called back of chest , or some times simply the  back .

We know , chest pain can radiate to many sites , of course the  much hyped  (May not be common yet !) being  the radiation to left shoulder , and arm.

The ischemic chest pain , even though described  as classical angina over a century ago . It applies mainly to stable exertional  angina .In    STEMI  or  unstable angina  these rules are   can not be expected to be followed  strictly.

We often think the pain of MI comes only from the myocardium ,  but there are many potential sources

  • The adjacent pericardium
  • coronary artery dissection, plaque fissures
  • Neuralgic pain from the  ischemic  nerve terminals
  • Finally dermatomal  reference pain

What is the quantum of pain signals  arise from each of these  components ?   Obviously ,  myocardial pain should be the dominant one .Here again ,  there is a dichotomy .Whether   the infarct segment elicits more  pain or the surrounding  ischemic   segment is also not clear. The  is an important difference the character of pain infarct pain is a  severe continuous  dull  aching .Some believe in   a fully infarcted segment where the nerve terminals are dead can not carry  pain  signals and pain is absent, while partially dead muscle produce maximum pain.

The somatic nervous system , that mirrors the visceral pain  into the dermatomes that the patient  feels as if the pain is originating from these sites. Heart is a huge middle mediastinal structure , primarily reflects the pain to the anterior chest wall , but  no surprise if it deflects  the pain signals posteriorly  also. Of course , the spine and the thick posterior chest muscle walls tend to  block this transmission.

But , on many occasions  patient who are admitted with ACS in CCU complain pain in the   back of chest

the following things has been observed.

  • Severe back pain in  a patient with large STEMI invariably indicate a myocardial tear .
  • Mesentric and coeliac artery occlusion
  • Aortic dissection

Back pain only STEMI

Every cardiologists would have seen atleast   few cases of STEMI presenting only as back pain.The problem here is they land up in varied departments .We have on instance of  a STEMI landing to a ortho surgeon .He was good enough to suggest an ECG and that showed an extensive infero posterior MI and later shifted to coronary care unit.

Back pain as marker of impending rupture

Severe back pain in an established STEMI is a ominous  sign as it is often a  marker of impending rupture. Here the patient is in extreme distress, and may become violent and restless .(Hypoxia adds to woes!)

Does posterior  MI  more likely to produce back  pain or posterior chest pain ?

Not proven  but distinctly possible.  ( posterior MI -Posterior pericarditis- Back  pain .)We emphasize  posterior  chest leads  in  ECG V7  to V10 in inferoposterior MI .  We  expect  the injury current to  flow to  the back , is it not logical  some of the neural signals would  also  reach the back.

Final message

Never underestimate back pain. We are tuned to think chest  has only one surface that is anterior .This is a gross missense .After all , there is a huge area(> 30X 30 cm )  of chest wall located behind us .

Take an ECG in all patients with  acute  pain  in the back of the chest . Even though this may look a  funny advice   . . . it is  an  important clinical tip   for all those  budding physicians  of this world. If  one life   is  saved per 100 innocent back pain cases ,  this article  acheives it’s purpose !

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Pulmonary embolism is  one of the  important  causes of acute chest pain . It can mimic  acute coronary syndrome . In fact along with aortic dissection  , it forms  a  differential diagnosis for STEMI especailly if the ECG is not typical.

pulmonary embolism chest pain dvt d dimer ventilation perfusion

The Chest pain of acute pulmonary embolism can originate in one of the following structures  with different mechanism

  • Lung parenchyma ( Necrotic pain ?)
  • Pluritic pain in adjacent necrotic segment
  • Main Pulmonary artery and it’s branches
  • Right ventricular mechanical stretch
  • Right ventricular ischemia
  • Hypoxia induced LV ischemia with coexisting CAD.
  • Multiple contribution from any of  the above *

It should also be remembered , medicine never respects logic, as some times  an episode of pulmonary embolism can occur without any chest pain

Localisation of chest pain

One can imagine ,  how difficult for the  nervous system to zero in on the origin of this  pain as  the structures involved in acute pulmonary embolism are in different planes  and in different depths  within the chest cavity . Patients  often complain vaguely  the site of pain but  what is universal is severe resting pain deep within the chest . If the ischemic lung segment  transmit pain signals , the location and radiation depend on the  bronchpulmonary segment involved.This again adds on to the complexity in the  genesis of pain  .It can be virtually any where in the back or front of chest.

But , the central and retrosternal chest  pain are equally common as invariably the central pulmonary arteries go for a acute stretch which can be severely painful .In fact , current thinking is it could contribute maximum  for the intensity of chest pain. Similarly,  acute dilatation of RV result in mechanical pain. RV sub endocardial ischemia may   also contribute .An intact bronchial  circulation( From aorta)  can limit the  ischemic lung pain .

Final message

Analysing  the chest pain of acute pulmonary embolism can be an  interesting academic exercise . It could arise from multiple structures with different mechanisms. It may not be much significant with  reference to management . But it has a diagnostic role.  A pain which is severe , and  atypically located should raise the suspicion of acute PE especially  if the patient has associated dyspnea.

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Chest pain is one  of the commonest presenting symptom  in any  hospital both as  an emergency  or non emergency. Reaching an accurate diagnosis is very important. The main  purpose of evaluation of chest pain is to recognise it as cardiac or non cardiac origin . Cardiac chest pain almost always means ischemic chest pain . That is called angina. (Of course there are few important causes for non ischemic cardiac chest pain which Will be discussed later).

Standard features of typical angina.

Chest pain which falls short of typical features are called atypical chest pain . Some recommend at least three typical features to label it as angina.
After the clinical examination patients  should be categorised in one of the following .

  • Typical angina
  • Atypical chest pain
  • Non cardiac chest pain** Non cardiac chest pain is not a diagnosis. Any physician (or a specialist)  should take some effort to localise it. (Muscle, nerve , pleura , anxiety  etc) . But  generally once these patients are ruled out of cardiac pain  they become less special and are simply referred back to their  family physician, only to return back  with  another cardiac  pseudo-emergency  in a different hospital .

    Why we are diagnosing atypical chest pain liberally ?

    Currently   more number of  patients as well as  the physicians  are   aware of the looming epidemic of CAD. The other major reason is the  lack of application of mind during  foirst clinical appraisal  and examination. Many of the patients with non cardiac chest pain  (Muscle, nerve , pleura )  are termed as atypical chest pain. Though some of the popular texts use atypical  chest pain  and non cardiac chest pain interchangeably , it is not  correct to do so. For example don’t ever label a  patient with chest pain with chest wall tenderness as atypical chest pain and order a cardiac work up .It  is a poor model to  emulate , that consumes time and resources!.Instead they should be diagnosed a confident non cardiac chest pain and dealt properly.

Once a patient is diagnosed  atypical chest pain what’s next ?

They should get a  complete physical examination,ECG, and  undergo exercise stress test.   In the  screening of CAD , angina can be termed a hard sign,  atypical chest pain is a soft sign,  resting ECG is surprisingly  a soft sign again (unless you record it during chest pain). Exercise stress testing is  the ideal  investigation in evaluation of  chestpain.( 70-80% accuracy). This can be improved upon by Thallium, SPECT, stress echo etc. As of now coronary angiogram is considered the ultimate gold standard (Not pure gold !) to rule out  CAD.

It is also worthwhile to remember non anginal  chest pain can also be an emergency and life threatening

  • Pulmonary embolism
  • Pneumothorax
  • Thoracic tumors
  • Aortic aneurysm (Dissection and non dissection)  The list is not  exclusive

Final message

What do we really mean by  atypical chest pain ?

In reality we don’t mean any thing !

When a  cardiac  physician is confused or rather , unable to  rule out angina , at the same time he is not confident of calling it as non cardiac chest pain,  he has the luxury of using this terminology . It is obvious  this terminology  should  minimally  be used.  Once diagnosed  these patients  can’t carry on with this tag  for long. They should be reinvestigated , (Right from history  and clinical ex) .They should either enter the cardiac work up  protocol  or  a non cardiac source for pain should be fixed  immediately.

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Are we missing an entity called Primary cardiac neuralgia ?

Unexplained chestpain even after elaborate investigation is a very common clinical cardiac problem. Cardiac neural plexus has a complex network with mainly autonomic network ,with somatic projections. Neural dysfunction could occur in any organ which has rich neural network.Diabetes is the classical example of cardiac autonomic dysfunction and result in silent ischemia. The same disease can result in stimulation of type c nerve fibres that could result in cardiac neuralgic pain , which we may wrongly attribute to ischemia. One of the manifestation of this phenomenon occurs in syndrome X .

Future research is aimed at

Imaging cardiac neurons and sympathetic receptors will shed light on this . But clinical experience has taught us there should be many other sources of cardiac pain other than ischemia and neural pain definitely plays an important role.

It may take years to prove this by evidence !

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