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What determines hemodynamic stability in ventricular tachycardia ?

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , on October 3, 2008| Leave a Comment »

Ventricular tachycardia is considered as one of the most  dangerous  cardiac arrhythmia .Rather , it is the label  VT  that spreads more  fear than the arrhythmia itself. It is a fact many patients with VT walk into hospital , still  VT will always be a sinister arrhythmia as long as it carries a risk of degenerating into ventricular fibrillation.

What determines hemodynamic stability in VT ?

  • Origin and location of VT
  • The ventricular rate
  • Presence or absence of AV dissociation
  • Impact on mitral inflow pattern
  • Associated left ventricular dysfunction or valvular heart disease.
  • VT in the setting of acute coronary syndrome.(Ischemic VT)
  • Inappropriate drug selection

Origin and location

VTs originating high up in the ventricle( High septal VT,Proximal VTs) have more organised ventricular contraction  and they are more stable.Distal VT  originating  in the myocardium away from the conducting system has chaotic myocyte to myocyte conduction.These are very unstable.

The term fascicular VT is nothing but VTs originating  in the His bundle and it’s branches( Can also be termed Septal VT ).These VTs are also stable and some of them respond well to calcium blockers indicating that they are very close to the AV junction and carry the properties of junctional tachycardia. QRS width gives  a rough estimate about the location of VT. Narrower the VT higher it’s origin.( But remember even in VT ,  qrs can further widen on it’s way downhill !)

LV dysfunction.

This is probably the most important determinant of the outcome in VT. Patients with severe LV dysfunction (EF <30%) fare badly .Hence the land mark concepts from MADIT 1& 2 demanded ICDs in these patients.The most common clinical setting is  dilated cardiomyopathy.SomE of them have bundle branch re entry(BBR).This particular  VT can be stable for many  hours.

Ventricular rate.

Usually VT has a rate between 120-200.Higher the rate of VT more the chances of instability .This rule is also not always true as fascicular VT can be well tolerated at high rates.So location of VT focus  and LV dysfunction usually over rides the impact  of ventricular rate.

Mitral inflow pattern

Proper left ventricular filling is the key to hemodynamic stability in VT. In proximal, septal,fascicular, LVOT VTs doppler studies  suggest (ACC /AHA Type C evidence : Personal observations in CCU during VT) near normal preservation of  bi modal filling of mitral valve inflow.In ischemic myocardial VT  the mitral inflow profile is critically affected . There is no distinctive forward filling was observed .In fact  at rapid rates a short pulsatile MR jets are noted instead.

Associated valvular diseases

It is obvious,  aortic  and mitral valve disorders can aggravate the hemodyanmic instability.

Final message

The clinical behavior of  ventricular tachycardia is widely variable and dependent on multiple factors.

Associated LV dysfunction and  structural heart disease ultimately determine the outcome.

 

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How do you grade pulmonary arterial hypertension ?

Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , on October 3, 2008| 1 Comment »

                                  Even as cardiology community is preoccupied with systemic hypertension & CAD  ,  pulmonary arterial hypertension(PAH) is a much neglected , still  an important clinical cardiac problem encountered . The irony is self evident , there are half a dozen methods to grade systemic hypertension not even a single stadardised grading available for pulmonary arterial hypertension. The WHO  working group defined pulmonary hypertension  few decades ago and was not clinically graded .The only grading available is based on  the pulmonary vascular biopsy changes (Heath Edwards) 

                                   Currently PAH management has gone through revolutionary changes. There is an urgent  need for grading  this entity .This will facilitate to  diagnose , manage and assess the efficacy of the currently available treatment.

                                Developing countries like ours have a great number of PAH due to rampant rheumatic heart disease.  A simple study was done in  100 patients with PAH .Bulk of the study population had RHD .Few had primary pulmonary  hypertension .Systolic , diastolic, and mean pressure was assessed by doppler echocardiographic analysis of tricuspid regurgitation (TR) and pulmonary regurgitaion(PR) jets. TR jet provided the systolic PA pressure , PR jet provided mean as well as diastolic PA pressure .TR jet was available in all patients. PR jet was available only in 60 patients .Hence the diastolic andmean PA pressure data has been extrapolated in some  and  was plotted in a scatter diagram. Five equal quintiles were divided. Patients in first  and 2nd quintiles were graded 1   and third  and 4th  quintile were  graded 2 ,  5 th  was graded 3 respectively. From this cut off points for  various grades of PAH were identified .The top 3% of patients  with highest PAP were graded as grade 4 and all of them had supra systemic PAH. 

The following grading is suggested for PAH* 

 *This is a preliminary  attempt to grade PAH. This could be applicable mainly in rheumatic heart disese and primary pulmonary hypertension .Further refining of methodology is  required.PAH grading may be little different in congenital left to right shunts.

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Cardinal symptoms in cardiology : Palpitation , some observations

Posted in Cardiology - Clinical, Tutorial in clinical cardiology, tagged , , , , , , , , , , , on October 2, 2008| Leave a Comment »

                        Palpitation is one of the common symptoms for which cardiac patients are referred. Like dyspnea , palpitation can either be a physiological expression of normally beating heart or a  dangerous pathological state of the heart. This makes this symptom unique and warrants careful evaluation.                                                                                                                                                         By definition palpitation  is abnormal  awareness  of ones own heart beat. Heart is a mechanical organ with multiple mobile anatomical structures. There is  constant  blood  flow in multiple directions . Apart from this the heart   has  it’s unique translational, rotational movement . These intrinsic movements combined with proximity to chest wall  generate vibratory  motion  signals .These signals are generally dampened by the encircling pericardial space .The neural signals responsible for  perception  of palpitation is not clear. If the heart hits against the chest wall it is the  somatic nerves from the chest wall that carries the signal. Vibrations generated within the heart chambers, and  and the  valves  are  carried  by the  myocardial and intravascular  sensors.( Autonomic) 

What are causes of palpitation?

       Cardiac

  • All hyperdynamic circulatory states. It may be generated from either  right or left ventricle or both.
  • Regurgitant lesions ( Mainly Mitral and aortic regurgitation)
  • MVPS*
  • Congenital heart disese ( Mainly left to right shunts-ASD/VSD/etc)
  • Apart from this patients  with prosthetic heart valve, and pacemaker patients can feel their heart beats.
  •  Cardiac arrhythmia .Both tachycardia, and bradycardia . Ventricular ectopic beats are the very common cause .( It is often described as missed beat)

* Mitral valve prolapse, a very benign condition, over diagnosed in the last few decades raised considerable anxiety and palpitations for the patients (mainly after the diagnosis ! ).Now the cardiology community has sought to underplay this entity with strict diagnostic criteria.( Thickened mitral leaflet ,presence of MR both must be present to label a patient  as MVPS)

       Non cardiac

  • Physiological
  • Anxiety state
  • Anemia 

What is the relationship between ejection fraction and palpitation?

                                        Generally palpitation indicate a  hyper kinetic state of heart .The commonest cause of palpitation is  anxiety  state .This also happens in hyper dynamic circulations like anemia , fever, thyrotoxicosis, pregnancy etc . In all these situations palpitation indicate increased force of contraction which   generates high dp/dt(Rate of rise of ventricular pressure)  . So  the left ventricularejection fraction is normal or more than normal . So  presence of  palpitation could be an  indirect evidence  of reasonably good LV function.

    “Patients  with dilated cardiomyopathy or CHF rarely feel their heart beat during exertion , instead they have dyspnea  as the LV force of contraction is less”

What is the significance of palpitation that occur during rest ?

                              Palpitation occurring at rest indicate more often a  pathology.It is invariably due to an cardiac arrhytmia  either tachycardia or bradycardia. Intelligent patients can give accurate information about the  regularity of rhythm , any  extra beats or missed beats . Atrial fibrillation, VPDs  could be  diagnosed by history alone in them !

If palpitation  is associated with visible chest pulsation what is the likely diagnosis ?

    If  significant visible pulsation over chest wall  pulsations are seen   in young adults it could simply mean a hyper dynamic circulation and thin chest wall. Pulmonary arterial pulsations is not normally felt in left 2nd inter costal space.If felt one has to rule out shunt lesions like ASD or pulmonary hypertension.
                    “ASD is the commonest cause  of right ventricular  palpitation “  

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Forgotten concepts in cardiology : Amlodipine as an anti anginal drug

Posted in Cardiology - Clinical, cardiology -Therapeutics, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , on October 2, 2008| Leave a Comment »

                                                                

 

                         

                            Amlodipine , the most popular anti hypertensive drug  used world wide has an very important action on coronary blood flow.When nifedipine was introduced three decades ago it was  known for it’s powerful anti anginal properties. Subsequently  amlodipine was introduced with almost similar action. But over the years, amlodipine was projected primarily as anti hypertensive drug and gradually many of the physicians are made to believe it is a drug that  should be used only if the blood pressure is high.The fear of reflex tachycardia in few was exaggerated.

                      

                              In fact a cross section of  today’s general physicians were queried  about amlodipine  and none of them acknowledged  using this drug as an anti anginal drug. And few of them went to the extent of withdrawing amlodipine if it was used for the purpose of angina relief !

Why amlodipine’s  anti anginal action is in doldrums ?

The single word answer is unfortunate!   Marketing bias ,coupled with  the fact  that mainstream cardiology texts have ignored this aspect.

Final message

                                    Amlodipine , can still be used as a antianginal drug especially  in a patient who has angina with associated bradycardia  , significant LV dysfunction . Some reserve amlodipine and nifedipine exclusively for vasospastic angina where beta blockers alone are theoretically contraindicated .

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Why syncope is rarely fatal ?

Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged , , , , , , , , , , , , , , , , , , , on September 30, 2008| 1 Comment »

                                                    

                                                             Syncope by definition is a transient loss of consciousness due to cerebral hypo perfusion and loss of muscular tone, and the patient falls but  recovers fully and gets up either assisted or spontaneous.The cardiac and vascular counter response to syncope is most often intact .This makes syncope characteristically transient . If a patient does not recover from syncope it could either be a prolonged loss of consciousness( Stroke etc)  or if he never gets up he will be called a victim of cardiac arrest or  a SCD ! (Sudden cardiac death ) . So technically by defintion ,  all  patients  will  have to  survive  the  syncopal episode.

But the following questions need to be answered   

  1. How prolonged  a syncope can be ?
  2. Can syncope lead onto  sudden cardiac death ?(SCD)  
  3. What are  life  threatening syncope and non life threatening syncope ?                           

What is the link between, syncope and SCD in patients with ventricular arrhythmia’s ?

Some case of long QT syndromes could be life threatening especially in children as they inherit sudden death. A patient with a non sustained VT  may develop syncope  if  the  VT  becomes sustained especially  if there is underlying heart disease and LV dysfunction . Among this  few , may degenerate into ventricular fibrillation and patient may die.  

How common is syncope in acute myocardial infarction ? 
 Syncope is a very  rare presentation of acute myocardial infarction. 
 
Can syncope precipitate  or precede a  cerebro vascular accident  ?   

 

Prolonged syncope , TIA,  stroke in evolution and completed stroke   can be a continuous spectrum in patients with carotid and cerebrovascular  disese . But when a syncope evolves in to a stroke the   patient is not considered to be a victim of syncope but  they enter the stroke protocol.

There is a big list for the causes of syncope

But to put it simply

A.Cardiac

  •    Purely electrical ( Arrhythmic- Brady, Tachycardia)
  •    Mechanical( Valvular obstruction, and other structural heart disease etc)

B. Non cardiac

  • Vasovagal (Commonest 90% of all syncope)

C. Metabolic*

  •  Anemia
  • Hypoglycemia
  • Hypoxia
*Metabolic causes  coupled with simple  vaso vagal(Neuro cardiogenic)  constitute the bulk of causes of syncope .Siezure disorders are very  common and a close  mimicker of syncope and need to be ruled out.

How to work up  a patient with syncope ?

                   First ,  one need to confirm  it is indeed a syncope . If the initial examination is not clearcut   one  need to  go back to the  history and ask for  circumstances under which the syncope occured  and  details of prodromal symptoms  if any . Patient’s  family members who witnessed the event can give useful information . It  is the most  cost effective ( Comes free of cost infact !)  investigative tool available .Cardiac syncopes are usually sudden, vasovagal often have environmental or emotional factor. Apart from routine investigations , ECG, Echocardiography, holter are done generally, head up tilt test, Loop, event recorders may be reuired in few.

Final message

                                          Syncope is one of the common symptoms in cardiology and  general medical practice. Many times the diagnosis is easy . Common syncope is  never fatal but , ruling out dangerous  tachy and bradyarrhythmias is a key aim.  In a significant number (20-30%) identifying the cause could be really  difficult and  may never be made in spite  of the modern diagnostic tools. These syncope of unknown origin is grouped along with the neurocardiogenic category.

The one,  positive thing about syncope is (unlike chest pain) , it is rarely fatal in it’s first episode ,  gives the physicians to  investigate and correct the underlying problem.

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What is the mechanism of pericardial rub ?

Posted in Cardiology - Clinical, Tutorial in clinical cardiology, tagged , , , , , , , , , , , , , on September 28, 2008| 6 Comments »

Heart is externally covered by two layers of pericardium .  Pericardial space is formed between parietal and visceral layers of pericardium . It is a narrow space which is normally lubricated with pericardial fluid up to 25ml. When these two tissue surfaces  come into contact ,  pathological  rub takes place.It is heard  whenever the pericardium is inflammed . Pericardial rub is a distinctive but uncommon  clinical sign .

Common clinical conditions

  • Acute pericarditis
  • Uremic pericarditis.
  • Rheumatic pericarditis
  • Post myocardial infarction

Pericardium has two layers .

There are four  possibilities for pericardial rub to take place.

The rub can occur

1.Between the two layers of pericardium

2.Between the visceral pericardium and the epicardial layer of  heart*.

3.Between parietal pericardium and the  chest wall

4.Pericardium can rub with the adjacent pleura( Pleuro pericardial rub )

The second and third mechanisms are very rare.

An update

We have realized one more possibility . Diaphragm forms the floor of the heart on which the hanging heart  rests . Rubbing of pericardium over diaphragmatic surface is a beat to beat affair that lasts the entire life !. In inflammatory states of  diaphragm especially  the contagious  ones from abdomen  , can result in pericardio- diaphragmatic rubs .These rubs are almost impossible to hear clinically.

pericardial effusion rub plural pleuro pericadial

*The anatomic mystery : Is epicardium same as visceral layer of pericardium ?

Some anatomist feel that both are same entities. If that is the case myocardium can never split its relationship with visceral pericardium.But it is also a anatomical fact visceral pericardium engulfs the coronary artery and  are located sub epicardially.

How many components of pericardial rub are clincally heard ?

Pericardial rub  classically has three components. Systolic, mid diastolic, and pressytolic atrial components. Pericardial rubs are typically described as to and fro rub. Systolic component is most consistent. In atrial fibrillation mono component pericardial rub is heard.

Quality

Superficial , scratchy, high pitched ( Can also be low pitched)

Location

Left sternal border , left 2nd or 3rd space  .Best heard in  sitting , leaning forward in inspiration. Many times the rubs are transient and evanescent . Since it has multiple components it may be mistaken for added heart sound like S 3 or S 4.

What is the mechanism of pericardial rub in the immediate post MI phase ?

Presence of pericardial rub post MI indicate a transmural involvement or atleast significant epicardial involvement . Recognition of this is important as presence of pericardial rub increases the risk of rupture  and hemorrhagic effusion if anticoagulants are used.

What is the  relationship between  pericardial effusion and  pericardial rub ?

Generally it is said with the onset of effusion pericardial rub disappear.But this is not necessarily true.

Rubs after contusion chest and fracture ribs can be with the chest wall and may have  no relationship with effusion.

Is pericardial rub a painful condition ?

Pericardial  rub associated with acute inflammatory pathology is severely painful (like a pleuritis).But pericarditis associated with chronic inflammatory conditions are less often generate pain.The exact reason is not known.

What is pleuro pericardial rub ?

This  clinical entity is poorly defined , often taught by veteran professors  in clinical auscultation classes.It can be heard in the mid segment  or diaphragmatic pleuritis with or without pericardial effusion in patients with  atypical pneumonias.

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Why thrombolysis rarely fails in right coronary artery ?

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , , on September 22, 2008| 7 Comments »

Differential response of thrombolysis between left and right coronary system

  • Thrombolysis is the specific treatment for acute myocardial infarction. ( Privileged few , get primary PCI))
  • Failed thrombolysis occurs in significant number of patients ( 30-40%).
  • Persistent ST elevation  120 minutes after thrombolysis is best indicator of failed thrombolysis.
  • It has been a consistent observation  failed  thromolysis  is more frequent in anterior   or LAD myocardial infarction.

In a simple study we have documented  patients  with inferior MI  rarely had persistent ST elevation and thrombolysis  was   successful in vast majority  of  patients  ( Except in few patients associated lateral MI)

 

The mechanism of better thrombolysis in right coronary artery  is simple.The success of thrombolysis , apart from early time window , is directly correlated with pressure head  and the duration of contact between the thrombolytic agent and the thrombus. In right coronary circulation the  blood flow is continuous ,  occurs  both in systole and diastole that facilitates the maximum delivery of the thrombolytic agent . Further there is a favorable  pressure gradient  across RV myocardium  as the transmural occluding pressure across RV is considerably less then LV myocardium.

This paper was presented in the  “Annual cardiological society of India scientific sessions”

at Chennai, Tamil Nadu.India December 2000

Click to down load PPT full presentation

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In which tachycardias electrical cardioversion is ineffective or rather contraindicated ?

Posted in Cardiology - Clinical, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , on September 20, 2008| 4 Comments »

                              Cardioversion with DC shock  offers immediate cure in many of the dangerous ventricular and atrial tachycardias.  It is often  taught ,  any hemodynamically unstable tachycardia  refractory to  medical therapy respond to electrical cardioversion.  One should also  remember electricity is in fact be called  as a drug !  and it should be delivered in proper form and dose. Here it is the paddle size, paddle position and the axis of current flow all are important. Now we have bi phasic currents for better efficacy.

                             While it is true, most of cardiac arrhythmias respond to shock,  there are few which do not respond or respond very transiently.There are few arrhythmias  in which ,DC shock is not only ineffective but may precipitate a ventricular  fibrillation.

                            Generally arrhythmias of reentrant etiology respond well to DC shock were interuption of  electrical circuit by external current is easily possible. In arrhythmia’s of enhanced automaticity ,  and ectopic tachycardia  it is difficult  to extinguish  the tachycardia focus with DC shock .

Arrhythmias where DC shock is not going to work are

A. Mutifocal atrial tachycardia(MAT)

B. Digoxin induced arrhythmias.Patients who are on digoxin,  has  enhanced ventricular  automaticity.These patients if they  get a DC shock will unmask the  ectopic foci.

C. In elderly with atrial fibrillation and sinus node dysfunction it may be dangerous to shock them with out temporary pacing support as sinus node goes for prolonged sleep mode.

D.In electrical storm with VT ,  if more than three shocks are required within a minute,  the VT will most often going to be permanent and the  electrical therapy can be termed as a failure. These patients will require intensive pharmacological management( Including magnesium, bretyllium etc)

E. And finally , sinus tachycardia (whatever the rate)  is an absolute contraindication for DC shock.

 Verapmil is often effective in MAT  but correction of hypoxia and acidosis may be critical.For digoxin induced arrhythmias phenytoin may be tried.

What to do when the DC shock fails?

  • It will be a  tricky situation and one wonder what to do next when the so called  universal antidote for cardiac arrhythmia fails !
  • Cellular internal millieu  is altered  by hypoxia and acidosis .It may prevent the  effectiveness of cardioversion.So try to correct them .
  • Over dirve atrial  pacing  is one option for automatic tachycardia.
  • And now ablation of arrhythmic focus is possible with radio frequency waves  in some of these patients.( Diffiuclt as an emergency procedure)

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What will happen if you accidentally thromobolyse early repolarisation syndrome ?

Posted in cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , on September 19, 2008| 2 Comments »

                                  Indication for thrombolysis in ST elevation MI  is mainly determined by clinical and ECG features. ST elevation of more than 1mm in two consecutive leads with a clinical suspicion of acute coronary event demands immediate thrombolysis.

                                 Early repolarisation syndrome(ERS) is a  is typical mimicker of STEMI . In ERS , ST segment elevation occurs in many leads especially precardial .This entity is estimated to occur in nearly 3-5% of population where a genetic variation in the potassium channel activation is reported.

                              If they  land in ER with some sort of chest pain , chances are high for labelling  them as ACS . It is not uncommon for  CCU physicians  to  witness  an  ERS being lysed . Even in many of the land mark trials (ISIS ) there has been many inappropriate thrombolysis , recognised later on.

What can really happen if you thromolyse them inadvertently ?

Generally nothing happens . But they are exposed to the risk of thromolysis. The ECG changes persist. And troponin will be negative and  echocardiogram will not reveal any wall motion defect.

Are we legally liable if a patient  with ERS was thrombolysed and he ends up with a bleeding complication like stroke ?

                        While the physician may feel guilty , there is no reasons for him to feel so.The guidelines are kept little lineant  for  the indication for thromolysis. When we are promoting  a strategy of early  thrombolyis  on a population based approach  in STEMI ,  there is bound to have a overlap with normality .The benefits out of early thrombolysis for eligible  patients for outweigh the few inappropriate thromolysis.

When you want to catch  a   real criminal  it is unavoidable,  one gets hold of all suspected criminals before letting them free . Unfortunately  in this exercise , some of the innocent  might experience   intimidation or even a injury  at the hands of law enforcers.

                               Similarly if a patient with ERS develop a severe esophageal spasm and typical  angina like chest pain he is absolutely certain to receive thrombolysis. (Troponin, CPK come later , and the results never veto the clinical and ECG criteria ,except probably in LBBB) .Many times critical  time dependent decisions are prone for errors in CCU.   So it may be  unscientific to ask why an ERS was  thrombolysed !

 How can one prevent inadvertent thrombolysis in ERS ?

                            Always ask for the previously recorded ECGs .If it is available and  look exactly similar to the current ECG  chances are unlikely  for ACS. In ERS ST segment is generally concavity upwards . ACC/AHA  guideline for STEMI  ,is  aware of this fact , but still  advices thrombolysis for all ST elevation irrespective of the morphology of ST segment elevation. This is propably intentional,   not  to incorporate morphology cirteria of ST elevation  for thromolysis .It would potentially  make many true STEMIs  diagnosed falsely  as ERS and deny thrombolysis.

 

What is the latest news about ERS ?

                       Now data are coming up, ERS is not entirely benign condition.Some of them ( Even a fraction of ERS population could be a significant number) can have a overlap between Brugada syndrome and they  could be prone for dangerous ventricular arrhythmia when challanged with ischemic or other stress.

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What do we mean by atypical chest pain ?

Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , , , , on September 14, 2008| 4 Comments »

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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