Heart and kidney work in tandem and share a close functional relationship during health and disease.Progressive cardiac failure causes kidney function to deteriorate,what we call it as cardio -renal syndrome.Similarly, progressive renal disease inflicts either a reversible /irreversible LV dysfunction .The mechanism of LV dysfunction has not been fully decoded. It is primarily biochemical mediated but at later stages it can be irreversible and structural damage can occur.
We believe uremic micro molecules leaking from plasma into cardiac Interstitium (Myocardial proteinuria ?) are somehow responsible for the progressive LV dysfunction. Now , we have new evidence for albumin – carbon interaction possibly at myocardial level due to formation of carbamino albumin (C-alb) .
This paper from Kidney International (2015) 87, 1201–1208; highlights this new finding .
Elevated C-albumin is a new marker for this unique , still not fully understood entity “Uremic cardiomyopathy”.
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Radial coronary interventions has become a global norm .Even complex procedures are being accomplished with ease adding on to the patient comfort and low risk for access site complications.However !occasionally we need to have multiple access sites to know the detailed real time contra lateral coronary anatomy is desirable .This becomes vital in the retrograde approach for CTO.
Want to have a quick glimpse of RCA flow while one is attempting LAD PCI without additional puncture ?
How about doing a contra-lateral angiogram with the same guiding catheter and wire in-situ within the ipsilateral ostia ? Here is an Innovation.
Of course ,the same concept can be used in femoral angiogram as well.It could reduce procedural time, adds more efficiency of the hardware system handling. One can’t ignore the idea as well as the comment of the author, who says the trick is only for an advanced Interventional cardiologist.
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STEMI occurs due to acute occlusion of a coronary artery (ATO) which needs emergency opening at the earliest, ideally within 3 hours , or up to 12h . The opening shall be either by pharmacological / catheter means or both. After 24 hours opening a ATO has questionable benefit unless the patient is hemodynamically unstable or symptomatic.
What is a CTO ?
Traditionally we believe 3 months is the period to call a coronary occlusion as chronic.(Previously it was 6 months) This time frame was considered appropriate based on our understanding of the infarct process , that may take up to 3 -6months for complete healing of infarct .This 3 month period is arbitrary as the chronology of intra-coronary lesion organisation is different from myocardial infarct healing. Its worthwhile to note the chronicity of a coronary lesion and its morphology is nothing to do with the quantum of myocardial damage it inflicts .This is because in many patients with STEMI who present late , the ATO progresses to CTO silently without any clinical demarcation or progressive myocardial damage.
If 24 h is the cut off point for opening the ATOs to accrue any meaningful benefit , can we call all ATO’s beyond 24 h as physiological CTO equivalents ?It doesn’t make sense isn’t ? But , consider this , how do you call an occluded coronary artery between 24 h t0 say 2 weeks or 2 weeks to to 3 months ? Sub acute total occlusion (STO) ? .Some experts have argued to remove CTO as an entity from acute coronary setting .This can’t be done as chronicity has to set in for ACS lesion as well. Obviously , we have a nomenclature issue here. We require a new terminology to differentiate CTO related to ACS and CTO related to chronic coronary syndromes.
The moment we diagnose a true chronic total occlusion , not only the urgency of intervention but also the indication to open becomes questionable in an otherwise asymptomatic population.
An ironical situation often arises , when we can’t technically open a ATO in a one week old STEMI .However , the same lesion one may open after 3 months as it has acquired a new name by now as CTO , which is perceived a lesser guilty act of violating the sacred PCI guidelines !
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Posted in Clinical cardiology, Jugular venous pulse, pericardial disease, tagged bernhiem effect, effect of inspiration on jvp, kusmals sign, kusmaul sign, kussmal's sign, Kussmaul sign, pulsus paradoxus, Reverse bernheim effect, ventricular interdependence on May 10, 2015|
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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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Right ventricle,being a venous chamber has distinct anatomical and physiological features to carry out this function.RV has a complex shape, its triangular in long axis and crescent like in short axis , thin (<5mm) more distendable .Contraction of RV begins slightly early but ends later than LV (30ms )
RV receives blood from RA and ejects in to PA in a sequential manner .The inflow, body and outflow contract somewhat like intestinal peristalsis. This is facilitated by the incremental delay in the electrical depolarization of right ventricle.In physiological conditions, the later half of QRS is responsible for RV activity and RVOT is the last to contract. (This intrinsic electrical and mechanical delay in RV contraction is a physiological inter ventricular desynchrony . One should be aware of this when planning cardiac resynchronisation therapy in cardiac failure. )
Click over the image for an animation of RV contraction.
Image courtesey Oxford spcialist hand book in cardiology :Echocardiography Paul Leeson , Second edition ,.Oxford university press 2012 Multi media .
Note:LV is a fairly elliptical and strongly muscular pump and contracts in a single go with maximum force.(dp/dt).
Though both right and left ventricle originate from same straight heart tube , developmentally the right ventricle evolves for a different form and function . Now,we realise there are lots of sharing of parental muscle fibers that engulfs and bonds both chambers.(Mind you ,This is the fundamental mechanism of ventricular interdependence.Of course ,IVS is a common wall shared lifelong by both chambers without any (sibling related?) hemo-dynamic dispute !
3D echocardiography and MR imaging has helped us to understand the RV morphology better and exciting articles written by pioneers are available free for those who are interested.
1.Ho S.Y., Nihoyannopoulos P.; Anatomy, echocardiography, and normal right ventricular dimensions. Heart. 92 2006:i2-i13.
5.Guidelines for the Echocardiographic Assessment of the Right Heart in Adults: A Report from the American
Lawrence G. Rudski, Chair, Wyman W. Lai, Jonathan Afilalo, Lanqi Hua, , Mark D. Handschumacher, Krishnaswamy Chandrasekaran, Scott D. Solomon,, Eric K. Louie, and Nelson B. Schiller,,(J Am Soc Echocardiogr 2010;23:685-713.)
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These two quotes on practice of medicine are close to my heart , one from Voltaire , a non medical man (a French poet ) and the other from ,one of the greatest medical professional of our times, William Osler .
It is amazing ,how the thinking pattern of a philosopher and a true scientific professional living centuries apart are almost in sync with a great medical reality !
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