Archive for the ‘Cardiology -Clinical signs’ Category

Not every one feels the palpitation during tachycardia / Bradycardia /VPDs , Why ?

Palpitation is awareness of one’s own heart beat. It is a complex perception of sensation at cortical level (like dyspnea) . It can occur during physical and mental exertion.However , if it occurs without any physiological reasons , it becomes abnormal. It can mean an abnormality  in heart rate , rhythm or  raise in stroke volume. The first rule of palpitation is both tachycardia and bradycardia can cause it. Tachycardic palpitation is due to valve motion and bradycardic palpitation is due to both motion and increased stroke volume.

The most common mechanism proposed for palpitation is hyperactive anterior mitral leaflet

How and where  does the sensation of  palpitation felt ?

Does  it originate in  the chest wall ?  or Is it the vibrations spreading along  the flow of blood in great vessels ?  or Simply  represent  the vigorous valve motion  sensed by Intra cardiac receptors ? How it is  transmitted to spinal cord where it’s felt at cortical level  ? We are not clear yet. Paccinian corpuscles is thought to sense these vibrations and hand over as electrical signals  to spinal cord either directly from cardiac valves /walls or indirectly from chest wall.

Paccinian corpuscles are predominantly present in sensory nerve fibres located in the dermis of skin. It is also observed in nerve ending to joints, Chestwall, blood vessel and also heart .They act like pressure as well as vibratory receptors * The exact reference for Paccinian corpuscle to be present within the heart is not available to me. Readers may contribute,

Importance of age and gender and IQ

Palpitation is primarily a symptom of young age where the heart is supple and more dynamic. Women tend to perceive more for some unknown reason. Elderly people rarely complaint about palpitation .It could imply aging  with or with out autonomic dysfunction which suppresses transmission of palpitation signals to brain.Chest wall thickness also matters. My guess would be, Chest wall thickness, epicardial fat pad could absorb the vibratory  energy  and chest wall receptors fail to recognise it. One curious observation is,  palpitation is described in a succinct manner by certain patients only. Since , it essentially involves  higher cortical senses , we believe spatial intelligence of the patient  may also be important.

Why Irregularity in heart beat is well recognized?

For the given heart rate , irregular rhythms are felt  more often as palpitation than sinus tachycardia. This is the reason single ectopic beat is easily felt than  sustained tachycardia. A common sequence of  palpitation due to ectopic beat is , a suddenly  missed beat, subsequent pause and forceful post ectopic beat.

Valve morphology and impact on palpitation

Mitral stenosis patients can feel their loud first heat sound (S 1)  or varying  S1 during atrial fibrillation as palpitation; Mitral valve prolapse with redundant , hyper kinetic motion is probably most common cause of benign palpitation.

Sclerosed  and calcific  valves attenuates palpitation. Calcific mitral valve in mitral stenosis make both S 1 intensity and opening snap feeble .These patients are less likely to feel palpitation .

Individual valve pathology can generate palpitation as in Ebstein anomaly , which has a the large sail like septal leaflet that flutters to create palpitation(Apart form pre-excitation syndrome common in this condition) As a general rule ,It is possible semi lunar valves are less likely to cause palpitation than AV valves as the latter only exposed to direct contractile pressure of ventricle.

Right vs left heart origin and localised palpitation

I am not sure one can differentiate left heart from right palpitation. But.palpitation arising from right ventricular  volume overload and increased pulmonary flow like in ASD  are associated with direct local sensation over pericardium . Mitral valve motion can not be localized by  patients .However apical impulse can be felt.Neck pulsations invariably mean high flow states. Venous cannon waves due to high pressure tricuspid regurgitation can be felt with each heart beat (RV systole)

Exertional vs Non exertional palpitation 

Palpitation occurring during exertion often imply its due to excessive handling stroke volume or (Pathological regurgitant volumes) Stenotic lesions are less likely to cause palpitation during exertion it’s never an absolute rule. Exercise Induced arrhythmia always happen in any valve lesions.

Relation with LV function

A dysfunctional ventricle cannot  generate forceful contraction and hence palpitation is uncommon symptom. Cardiomyopathy presents with more of dyspnea rather than palpitation .Even,  an episode of AF do not cause palpitation in such patients .They simply feel breathless (Dyspnea ? Or is it a palpitation equivalent ?)

New age palpitation

With so many foreign bodies and accessories entering the heart  it’s not surprising for patients to feel amusing sounds and vibrations hitherto unknown in human body.

  • Prosthetic valve clicks (Sounds from mechanical valves can be  annoying .Tissue valves, TAVR are more quiet)
  • Abnormal electrical activity  from pacemakers and ICD coils.(Apart form pacemaker mediated muscle twitches)
  • Now, we have entire mechanical LV assist devices  working inside the heart with a 24/7 motors .(LVAD hum its called) Very soon heart is going to become a noisy place and patients would learn to ignore these abnormal sounds

Pleasant physiological palpitation

What brings the unpleasantness during palpitation? (applies to dyspnea as well). It is purely state of mind. While, palpitation due to extreme fear is unpleasant , palpitation due to pleasant emotional arousal (Often referred to as flying butterflies ! (Is it the wings of AML ? ) within the chest  as we hear from some of young  women & men ).Since they know the reason why they get it, cortical input welcomes it ,converts them to pleasant  beats .The Non-academic stuff  is intentionally made to understand how the limbic system and Hipocampus  areas of brain can modify the incoming signals of palpitation that comes from down under.

Thoughts to ponder 

Does post heart transplantation (De-nerved heart) patients experience palpitation ? Again, I am not sure .If palpitation is carried by cardiac nerves it should disappear. Of-course , 30 % of transplanted heart do get re-innervated. When you get a chance to meet a heart transplant patient you ask yourself and find the answer.

*Please be reminded Anginal pain almost vanishes  post transplant.In fact ,there have been instances of cardiac auto-transplant for refractory angina in the past.

Final message

Though all of us can list causes of palpitation without any difficulty , we rarely dwell into exact  the mechanism of genesis of this symptom and  its perception. As we enjoy flying in an exotic world of cardiac  interventions  . . .  the principles of  practice of medicine also expect us to take adequate efforts to understand fully the cardinal  symptoms of our patients . After all , they are the true teachers of Medicine. It is because of their pursuit for explanation for their symptom (Often vague though)  we make our professional progress.

Further  reading

John T.Shepard  The Heart as a Sensory Organ JACC Vol. 5, No.6  June 1985:83B-878

(The heart has variety of sensory nerve endings , still to be explored)

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Syncope is a classical feature of LVOT obstruction especially with valvular aortic stenosis.The mechanism of exertional syncope in Aortic stenosis is traditionally attributable to the fixed obstruction .This fixed obstruction is not able to cope up with increased cardiac output as demanded by the exercising muscles . But exercise  induced reflex as well as local vaso-dilatation mechanism is intact . The consequence is predictable. A critical fall in SVR amidst a obstructed LVOT precipitating a syncope.

However , If the above mechanism is the sole reason for syncope in Aortic stenosis , we have a problem to explain why syncope is  rare even in critical mitral stenosis which is also fixed LV inflow obstruction ?

Is there some thing unique in LVOT obstruction that causes syncope ?

No, it is nothing to do with LVOT .To generate a true pathological syncope, reduction in cardiac output per-se may not be enough . It appears there should be an inappropriate systemic vasodilatation as well to precipitate a syncope.This can happen only if the parasympathetic system gets activated by some means . The trigger is located in the mechano- receptors of left ventricle . Hypertophied left ventricle with high Intra cavitory pressure (Often above 200mmhg) generated due to LVOT obstruction activates the syncope circuit.The same rule may apply for RVOT as well .One could get syncope with critical valvular PS or severe pulmonary hypertension when RV mechanical receptors get a triggered.

What happens in mitral stenosis ?

In mitral stenosis , LV is under- filled ,  wall thickness is normal .There is little likely-hood of LV mechno-receptors to get stimulated as the LV wall stress is normal. This is the reason syncope is less common in mitral stenosis. However , this is not  absolute rule , syncope can still occur in severely narrowed orifice of mitral valve due to low flow state alone or a ball valve thrombus and paroxysms of arrhythmia .

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When a patient comes with angina at rest , it could mean two things .Either a  STEMI or an NSTEMI .This , we can diagnose only after seeing the ECG .

Can we differentiate these two by the  character of chest pain alone ?

Very  tough task isn’t  ? But there are some definite clues .

Infarct  pain

  • Is mostly sudden .
  • Likely to be crescendo , lasts more than 20-30 minutes .
  • Fails to get relived by rest or even  Nitrites.
  • Sweating due to sympathetic activation is more pronounced.

Unstable angina

  • Is rarely  sudden .Often has a pro-drome.
  • UA is  mostly precipitated by an increased demand situation or a stress.
  • It has  a typical waxing and waning  pattern . Rarely assume a true  crescendo character  as myocytes  does not necrose (Just threaten to die !)
  • The chest pain radiation   to  shoulder is less  conspicuous , instead it  tends to  reach  the  jaw area .(* An observation,Is it something to do with multi-vessel CAD in UA ?)

Mechanism of the difference : Epicardial vs Endocardial angina

The pain of UA is   due to subtotal occlusion and  endocardial ischemia , while STEMI is  sudden total occlusion  and the resultant  transmural  ischemia . In STEMI  epicardial  surface is always involved (Which lifts the ST segment in ECG .).We know epicardium  is same as  visceral layer of pericardium which is well innervated .Hence  pain  of STEMI   acquires  more of somatic character  than a  predominately visceral type pain  that occurs with  UA/NSTEMI where epicardial ischemia is absent.

Clinical importance

The demarcation between unstable angina and Infarct pain becomes vital when we calculate the time window for thrombolysing STEMI .Many of them have a phase of pre infarction angina which is a type of unstable angina. If we mistake it for Infarct pain then one may falsely calculate a prolonged time window and deny re-perfusion therapy.

Post -amble

It is tricky issue  to differentiate the  chest pain of  STEMI and NSTEMI  .A significant overlap can occur  in  real coronary care scenario . We know   chest pain  that occurs in both   pre and post infarct  phase  is considered  as unstable angina .(With infarct pain sandwiched between them!) Hence differentiating  them may even be termed as futile.

Still,clinical cardiology  can be  made  fascinating by indulging in such exercise !


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