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Archive for the ‘Cardiology – Clinical’ Category

Heart is not like a rigid structure built with  bricks . . . . so , its too architectural mindset to describe cardiac chambers to be made up of walls. Rather , Its a four chambered muscle mass moulded together in a complex 3D interface with distinct surfaces rather than walls. It’s also important to realise, since the heart is positioned (rather hanging )delicately in the middle mediastinum resting on the diaphragm , its subjected to one more dynamism due to respiratory motion blurring the definition of surfaces as well. (Vertical vs Horizontal)

4415_21_26-heart-human-posteriorly

Posterior surface is now referred to as infero-posterior

The posterior aspect of heart contains essentially the venous channels and the atrium (LA in particular)pulmonary veins and coronary sinus.  This happens right from 8 week heart open stage when venous end of lower straight heart tube folds up and posteriorly .

cardaic-looping-posterior-wall

It should be recalled only a small portion of lower aspect of posterior wall is alloted to left ventrilce.Instead the Infero diaphragmatic surface is formed by two-thirds  the LV and one-third Right ventricle.

anatomy-of-heart-posterior-wall-mi-lcx-rca-grays-grants-anatomy-netter

Image courtesy : From the great Netter

Nomenclature  issue 

The term posterior wall is now abandoned in most Echocardiography texts its replaced by inferior .The implication is more for Electrophysiologists with reference to accessory pathway localization

What is true posterior wall MI ?

As discussed before ,posterior surface of heart is different from posterior aspect of left and and right ventricle.

What does leads V7 V8 V9 record ?

It actually records electrical signals arising from posterior  aspect  of heart.  Left atrium,  pulmonary vein along with insulatory  effect of lungs dampens the potential . This makes the sensitivity of ST elevation  in posterior MI is low.

Blood supply of posterior surface

It’s highly variable.Both RCA and LCX arteries contribute with its  posterior left ventricular branches (PLV)

It can be inferred , LCX has more territorial rights than RCA in this unique zone of heart as the artery covers more posterior areas.

Read a related article

Back pain from anterior MI : Is it possible ?

 

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Syncope and seizure are most dramatic symptoms that rarely fails to call the attention of the patient and family.Syncope is primarily evaluated at medical or cardiac units. However ,when syncope presents as convulsions (often It is ! ) the patient lands up in a Neuro unit as a case of epilepsy.Some how, many of them are prescribed anti convulsants without being evaluated for what triggered the seizure.

heart_and_mind

Cardiac seizure and Neural syncope : Require a balanced approach ! (Image courtesy http://3.bp.blogspot.com)

Real life experience now suggest, a bothering  number of patients in epilepsy clinic might harbor a primary cardiac disorder in the form of either brady or tachycardia which is often inherited due to defect in ion channels of cardiac cell.

The issue is two fold. 

  • Cardiac patients mis-diagnosed as seizure
  • Primary seizure patients suffer a cardiac death (as seizure induced arrhymias or acute pulmonary edema )

Incidence of sudden cardiac death in patients with seizure disorder though rare is being increasingly recognised. Mechanical problems like valvular Aortic stenosis can also result in syncope followed by seizure.

Final message

Cardiologists do have a major role these situations.It may be wise to advice basic cardiac work up in  every seizure disorder.  As we are beginning to understand the neurogenic triggers in sudden cardiac deaths , the need for Neuro-Cardiac units is real.(Some of big university hospitals do have such departments)

Reference 

1.Zaidi A1, Clough P, Cooper P, Misdiagnosis of epilepsy: many seizure-like attacks have a cardiovascular cause. J Am Coll Cardiol. 2000 Jul;36(1):181-4.

2.Leestma JE, Annegers JF, Brodie MJ, Brown S, Schraeder P, Siscovick D, et al. Sudden unexplained death in epilepsy: observations from a large clinical development program. Epilepsia. 1997 Jan. 38(1):47-55.

3.Kloster R, Engelskjøn T. Sudden unexpected death in epilepsy (SUDEP): a clinical perspective and a search for risk factors. J Neurol Neurosurg Psychiatry. 1999 Oct. 67(4):439-44

4.Leestma JE1, Walczak T, Hughes JR, K A prospective study on sudden unexpected death in epilepsy.Ann Neurol. 1989 Aug;26(2):195-203.

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effect of inspiration on jvp and bp pulsus paradoxus bernhiem effect ventricular interdependence

Image  modified  from  http://www.anatomygallery.info

That’s  normal . . . what happens during pathological states ?

There are important diseases  that  restricts entry of blood into right heart chambers. They can occur either in an acute  (Tamponade) or in chronic  fashion like constrictive pericarditis  and restrictive cardiomyopathy.These entities  show distinctive impact on JVP and systemic pulse.

The two pathognomonic signs are Kussmaul sign and pulsus paradoxus* that go hand in hand in most  situations.Inappropriate elevation of JVP with inspiration is termed as Kussmaul sign , while exaggerated fall in systemic BP with inspiration is called Pulsus paradoxus.The later is the  arterial counter part of  Kussmaul sign in JVP .However, there can be dissociation between these two signs occasionally.

* Pulsus paradoxus is a term originally  used by Kussmaul when he noted heart sounds were  retained while pulse dissappeared  in  patients with cardiac  tamponade .Later we realised the loss of pulse was linked to inspiratory cycle  of respiration. To make  this sign objective  sphygmomanometery  criteria was formulated which measured the difference between inspiratory  and expiratory korotkoff’s  sounds .

Coming up next 

Why Kussmaul sign  is often absent in Tamponade while  its arterial counterpart pulsus  paradoxus may still be conspicuous ?

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We know aortic regurgitation causes  a deluge of   hugely popular peripheral signs of aortic run off  , which are taught  right from 2nd year medical school.

aortic runoof

When the aorta  leaks it reflects in the entire vascular tree .How is that a  leak in the remote aortic valve cause a quincke’s to and fro pulsations in the finger pulp ?

aortic-insufficiency

Is the blood in the finger  trying to follow  the regurgitant  jet  that  go back into left ventricle ? Does the to and fro murmur of  Duroziez over the  femoral artery imply  there is reversal of  blood flow in femoral artery ?

Things are  little complex than it appears

It is true the initiating event of collapsing pulse is the regurgitant jet , however the mechanism that amplifies and sustains it , lies in the altered peripheral hemodynamics.

The systemic arteriolar resistance is  dramatically low in chronic  severe AR  by a reflex phenomenon ,  as cardiac out put is increased and vascular tree adopt to it. So, with each  beat when blood is ejected two things happen in diastole .While a small fraction runs back into LV , the rest of  blood runs off , as if it goes in a free way  making all peripheral pulses dynamic , bounding and collapsible.

Hence as the name suggest all the peripheral signs of AR  are due to the peripheral mechanisms rather than primary event of aortic run off  into left ventricle.

Why carotid pulse does not show the collapsible nature of  pulse in AR  ?

If aortic leak into LV  is the dominant mechanism ,  carotid  artery should obviously manifest a collapse ,but it doesn’t  ,as carotid has no direct continuity with the  peripheral low resistance circuit

What is the hemo-dynamic  correlates of    descending  aortic flow reversal  in  severe AR ?

The central vascular tree  manifest  some  reversal till the regurgitant  velocity fades off . This can occur in severe AR, extending into certain length of aorta. This can be picked up by Doppler probe. Please realise  it is only  the wave form that get reversed  not the actual blood stream.( The momentum gained in systole  continues to push forward in-spite of the pulling back forces of regurgitation)

Why peripheral signs are  absent in acute AR ?

Acute AR even if it’s  significant does not cause a collapsing  pulse because it takes time for the peripheral vascular tree to go for vasodilatory mode.Further ,LV is also less compliant keeping the LVEDP high and regurgitant fraction low.

Summary

Answering  the title question ,the mechanism of  Aortic run off  in AR is both central and peripheral.  However  clinical  signs are largely due to high cardiac out put and the resultant   adaptive  response  of the  vascular tree due to low  systemic   vascular  resistance  triggered by  reflex  dilatation of small arterioles of the  peripheral vascular bed.

 

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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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This  query often  evokes  confusion  among fellows and General physicians .

              The answer is simple .Yes ,  you can.(With few conditions)

  • Thrombolysis  or PCI  is  done  with reference to  the  presence  or absence of ST elevation and chest pain.
  • If there is ongoing chest pain  and  significant new onset ST elevation  thrombolysis or PCI is indicated whether there is associated q  waves or not.

Clinical situations 

 Ischemic  q waves: Q wave can occur  with transmural ischemia which result in electrical stunning and loss of R waves . (Many of them  regenerate this R within few days after STEMI ,  indicating the q  waves can be  ischemic  in origin)

Reinfarction : Patients with  old  MI can develop fresh ST elevation  in q leads due to tachycardia and dyskinetic infarct segment .This group  of patients  should be carefully evaluated before labeling them as  re-infarction

* q RBBB in early hours of  anterior STEMI is fairly common which  may revert later. qRBBB is not a contraindication for re-perfusion .

Final  message

Presence of q waves does not  imply one should not  entertain  thrombolysis or PCI .The decision  to reperfuse  , rather  goes with  presence of  chest pain , ST elevation and  of course  within the  acceptable   time window!

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The right ventricle  is considered as a docile cardiac chamber with passive filling and  emptying  properties .

This belief  was reinforced when Fontan  in early 1970s suggested a principle in the management of  cyanotic heart disease  when  the right side of the heart is underdeveloped. He  proved  RV can be by-passed safely , with  great veins  (IVC/SVC)  by  themselves  take care of filling the pulmonary circulation  without the need of RV pumping function.

While it is true for few complex cyanotic heart disease, largely this a misleading  concept. In clinical cardiology practice  ,sudden or non sudden  RV deaths happen every day in the form of . . .

  • RV Infarction
  • Acute RV dysfunction in massive pulmonary embolism
  • COPD with RV dysfunction
  • Most cases dilated cardiomypathy  the terminal event is due to RV  failure.

So , RV function can never be dispensable in day to day cardiac hemodynamics.

RV has some unique properties in terms of shape , size and  hemodynamics . We are getting more insights from  modern blood pool imaging by MRI , about  how the RV handles the blood volume .

We know RV has a unique shape  triangular ( partially  pyramidal ) . It can be inferred the RV cavity is formed by fusion of  many  eccentric spacial planes. We have always believed  RV handles the blood it receives from right atrium in a unique way .Now we are beginning to understand it .It is now documented the RV segregates the blood it receives into 4 components.

 

right ventricle physiology anatomy hemodynamics

It is curious  to know  RV inflow is connected to the outflow by an invisible   physiologic Bridge . About 44% of  blood traverse the RV in this fashion.

 

RVOT blood flow right ventricle

Note : RV blood flow preferentially enters the RVOT with out transiting RV body and apex.Image courtesy http://ajpheart.physiology.org/

 

Which is the most important part in RV ? (Among Inflow, Body, Apex, Out flow)

After reading this article it seems to me , the mechanical  function of RVOT could be most  vital. If it fails to handle the first increment  which  comes directly from  RV inflow, stasis  is likely in RV body and apex , elevating RVEDP and later promoting stasis leading to clinical events.

Clinical implication of this study

  • Differential dilatation RV chambers to pressure or volume  overload is observed .
  • We need to analyse why RV dilates in some   but   goes for hypertrophy in others when confronted with pressure overload (VPS vs PAH)
  • RV apical clot in restrictive cardiomyopathy  is a direct consequence of stasis  of blood  in RV apical zone .
  • RVOT pacing  may have a hemodynamic advantage  over RV apical pacing  . However , for anatomical reasons RV apical pacing  is  far safer than RVOT pacing where the lead  is subjected to constant life long strain due to this busy RV inflow to outflow express  high way !

Final message

Traditionally we have labeled  RV  as a  passive venous chamber .It is clearly a misnomer.It  has to handle both the venous and pumping function beat to beat with precision  without  back log .Obviously ,  RV has to think and work  more than it’s  big brother !

Reference

I wonder , if  there is  any other site other than APS . . . to  find crucial  answers in cardiac physiology  !

 

Right ventricle physiology blood flow  3d 4d analysisAfter thought

  • There is huge gap between physiologists  who work in research labs and the physicians at bed side .
  • I appeal all young cardiologists  to visit  APS  once in a while ,between your busy cath lab schedule and help narrow this gap.
  • Without understanding the physiology properly how are we going to intervene the pathology ?

 

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