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Archive for the ‘Cardiology – Clinical’ Category

LA volume assessment : A critical parameter with a time trouble !

Posted in Cardiology Illustrations, cardiology physiology, Left atrial enlargement, Uncategorized, tagged , , , , , , , on February 8, 2023|

LA dimension and volume have become vital parameters in recent times, especially, with the entity of HFpEF is becoming so common. LA not only acts as a live barometer, reflecting all that happens in LV, but it is also a chronic marker of LV diastolic function. (Funnily referred to as HBA1c of diastolic dysfunction) 

What is normal LA dimension & volume ? 

  • Normal left atrial diameter < 4.1 cm in men or < 3.9 cm in women
  • Normal left atrial volume indexed for body surface area (BSA) is 34 ml/m2 for both women and men 

Which part of the cardiac cycle do we measure? 

Ever since Wiggers introduced the overwhelming concept of LV systole and diastole, most of us ignored the fact that atria do have a separate contraction relaxation cycle, independent of what happens in the ventricle. Of course, atria and ventricles act as a single chamber in diastole. In reality, atria lack true boundaries when it acts as a conduit. The LA dimension varies considerably during the atrial cardiac cycle. Look at the  LA pressure-volume loop, which can frighten anyone, with its horizontally lying figure of 8 pattern. During every cardiac cycle, the volume reaches atleast two troughs and one peak.

Don’t get frightened with this graph, spend some time, and you will get it right, Begin at  “3” o clock position with the onset of diastole with a downsloping green loop, that continues as the red line of atrial contraction to end up in systole. The entire black loop, that happens during ventricular systole depicts the true reservoir function. with MV closed. ,

 

As of now, we have a consensus, LA volume is measured typically in LV end-systolic frame. ( Rather, we measure it at maximum LA volume ) However, we have 4 different LA  volumetric components to assess, as this article excellently depicts. (Hoit BD. Left atrial size and function: role in prognosis. J Am Coll Cardiol. 2014 Feb 18;63(6):493-505.)

What could be the limitations of the traditional end-systolic measurement?

No single measurement will give an overall LA function assessment. But still, Somehow, we have measured the maximum LA  volume as a reference of true diastolic function. This happens in LV end-systolic point where atria reach the maximum size. But, here is a catch, we assess the left atrial function before its main physiological function of emptying takes place.

How about assessing  LA efficiency after it completes its job, ie end diastole? 

In LV function end-systolic dimension has pride of place as it is devoid of influence from loading condition. If applying the same logic, the “end atrial” systolic dimension(Which is the same as LV end-diastolic point/or post A ) should be perfect. It can also help measure the residual LA volume after its systole.

A potential advantage of LV end-diastolic dimension (The Heart & Soul study )

Maybe, this is less affected in the presence of MR systolic jet will spuriously elevate LA volume. In AF also this parameter is less likely to be influenced by LA preload.

Final message

Suddenly, we are debating a fundamental Issue, ie timing of LA measurement. While the end-systolic size/volume is the current standard, the LA dimension in the end diastole also provides useful info. There are at least 4 different LA volumes, at different parts of the LA cycle that need to be studied for a proper understanding of diastology (Unlike LV which has only two).

Now, we may need to ponder, if there is a mean LA volume, measured with the 3D volumetric analysis or MRI, that could be representative of the global LA function. 

Reference

Thadani SR, Shaw RE, Fang Q, Whooley MA, Schiller NB. Left Atrial End-Diastolic Volume Index as a Predictor of Cardiovascular Outcomes: The Heart and Soul Study. Circ Cardiovasc Imaging. 2020 Apr;13(4):e009746. doi: 10.1161/CIRCIMAGING.119.009746. Epub 2020 Apr 20. PMID: 32306763; PMCID: PMC8846436.

 

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How is RCA angina different from LAD angina ?

Posted in acute coroanry syndrome, angina, cardiac embryology, Cardiology - Clinical, Cardiology -Mechnisms of disease, Clinical cardiology on April 26, 2022| 1 Comment »

William Heberden first introduced the term angina to the medical community in 1772. His descriptions became immortal. Still, no one would ever know what was the angina-related artery, Heberden was alluding to.

Now, some jobless cardiologist is asking this question after 200 years. How is angina from the LAD system differ from the RCA  system? or let me put it another way, How does angina of anterior circulation (LAD) differ from posterior circulation (RCA/LCX)? Though there is distinct hemodynamic profiling of RCAvs LAD ACS, surprisingly, cardiology literature does not answer the chest pain aspect of it. One rare study, done  4 decades ago throws some light

Here is a curious little study, with a simple & crisp conclusion.

chest pain and IRA localisation angina LAD angian RCA

It concludes, that LAD angina rarely radiates to JAW or epigastrium. While RCA angina relay radiates to the left shoulder.

So, why does this happen?

What I could guess is the ubiquitous vagal fibers that travel in the posterior aspect of the heart, and carries pain signal directly up to the jaw whenever these areas become ischemia. LAD is less likely to irritate the vagus. Of course, there can be a definite overlap.

OMG, give me some time to keep in touch with  basic science 

Now, fellows of cardiology, please take a  pause from your regular aggressive cardiac cath lab workouts and get a break at least once in a while. How does the ischemia of myocardial tissue generate pain? Why it is severe in some, trivial in others, and even dead silent in some, 

The chest pain genesis is initiated by sensory electrical neural action potential, that captures the epicardial neural plexus first, switching over from somatic to the visceral pathway and trespassing the para ganglionic plexus and traveling further to the spinal cord. Where it may collide with other incoming sensory signals ascends in specific myelinated and non-myelinated neural cables, reaching the brainstem, interacting with local nuclei, and finally reflecting on subcortical and cortical pain matching centers.  We haven’t yet located the exact center for anginal pain. (Perithalmic and amygdala could be closer to real centers) 

So, it is a really complex sensory world yet to be understood fully. Mind you, I haven’t touched upon the neurophysics of referred pain, linked or clandestine angina.

  • What is the effect of cardiac denervation, autonomic neuropathy, or on the perception of chest pain(Does a quadriplegic feel angina ? or post-transplant heart immune to angina ? (Gallego Page JC,Rev Esp Cardiol. 2001) 
  • Is it biochemical or neural, can substance P in blood cause pain hitting the amygdala? 
  • Will hypoglycemia and anemia cause angina due to lack of glucose and oxygen?
  • Finally, how is Infarct pain is different from ischemic pain (Ischemic)

Where do get the answer to these questions?

This paper from Dr. Robert Formean(Ref 2) university of Oklahoma is just the best source I think, to explore and understand the topic. (Reading time 60 minutes: Let me tell you, it is worth more than a time spent on an insignificant angioplasty of painless PDA lesions)

Final message 

So, what have you learned from this post? Does this question about angina matter at all? Surely not. in this space-age cardiac care where we are right inside the coronary even before we listen to the patient’s complaint properly. We are always at liberty to do what we want( or love) to do. But, the urge to understand the foundations of clinical science is the last remaining hope, that will keep the specialty of cardiology enchanting. 

Reference
 
 
A comprehensive reference for the genesis and signal processing  of chest pain 
 
2.Foreman RD, Garrett KM, Blair RW. Mechanisms of cardiac pain. Compr Physiol. 2015 Apr;5(2):929-60. 
 

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Hypertrophic cardiomyopathy : Two posters that summarise everything essential

Posted in Cardiology Illistrations, Cardiology Illustrations, Cardiology teaching websites, Cardiology-Echocardiography, cardiomyopathy, hocm hcm, hypertrophic cardiomyopathy, Uncategorized, tagged , , , , , , on November 1, 2021|

Check out these two posters* for are a quick reference on HOCM with current updated evidence. The first one details about  Echo evaluation. The second one illustrates the genetic screening flow chart of the HOCM families.

Some of the queries, you will find the answers from these posters are,

1. How to recognize Intrinsic mitral valve defect by MR jet morphology?

2. How to cross-check the true LVOT gradient from MR jet?

3. When to do a provocative test to document the LVOT gradient?

4. What are the standard pre-myectomy measurements by Echo?

5. How to screen a family member of HCM?  Pros and cons of  Phenotypic vs Genotyping screening 

*Reference 

Download
 
The poster is created by: Karan Kapoor, MD; Allison G Hays, MD, FASE. Design and illustration by medmovie.com.

 

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What is the effect of Atrial fibrillation on blood pressure ?

Posted in Cardiology - Clinical, tagged , , , on October 3, 2021| 1 Comment »

Atrial fibrillation has a direct effect on systemic blood pressure as stroke volume swings from beat to beat because of changing  RR Interval ( preload ). The variation in systolic pressure actually reflects not only the changing stroke volume but also the enhanced contractility of the ventricle to the preload( Frank-Starling principle ). The net effect is reflected in the pulse as an irregularly irregular pulse (Both rate and volume /Amplitude).* However, In dysfunctional ventricles or in acute AF* this variation in systolic  BP can be significant. Also realize, If the preload is changing every beat, there is a considerable dynamism in the afterload as well because of ventricular arterial coupling.

(*Acute effects on BP with the onset of AF : There can be transient hypotension with loss of atrial booster pump.This is not significant in otherwise healthy hearts. Inpatient with baseline LV or RV dysfunction, the onset of AF can be detrimental. The ventricular rate is also a determinant of blood pressure. At fast rates, there can be a fall in BP)

How to record BP during AF ? 

As you record the BP by cuff, the Phase 1 Korotkoff sound floats up and down with each beat. If the variation in RR interval is huge one may get a beat-to-beat variation even up to 40 mmHg.We also know, AF can cause pulse drop /deficit intermittently.

What happens to Korotkoff sound during pulse deficit?

Obviously, there will be a loss of these phase 1 sounds, though the other phases of sound may be heard, which are generated by the previous cardiac cycle. So, measuring blood pressure in AF is not a clinically pleasant task. That’s why we are asked to record 3 times and take an average.

Now, coming to diastolic BP in AF. It’s a real hemodynamic riddle. Traditional teaching is, systolic BP is determined by cardiac output and diastolic BP by peripheral vascular resistance. This is at best a gross understanding of circulatory physiology. Both systole and diastole are coupled together as blood flow across the system of varying resistance. In fact. The preceding systolic pressure head stores the elastic energy in large vessels that are thrown back as diastolic BP.

So what happens to BP during AF? What does the literature say? It doesn’t say much. So we decided to look for ourselves. Here is a tracing of femoral arterial pressure curves during atrial fibrillation. Note: the systolic BP shows considerable variations with changing RR interval with little change in diastolic blood pressure.

 

Final message

In Atrial fibrillation, the systolic blood pressure changes from beat to beat and it impacts the timing of the Korotkoff sounds. The diastolic blood pressure behaves the same, but it’s less in magnitude and difficult to detect by conventional sphygmo-manometry.

Further reading 

Clinical Implication for irregular BP of Atrial fibrillation  :https://drsvenkatesan.com/2021/05/04/cerebral-hemodynamics-in-af-irregularly-irregular-brain-perfusion-and-risk-of-dementia-cordis/

The effect of AF on pulmonary arterial pressure is an unexplored topic .Cardiology fellows please note.

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How to find which lesion is causing angina in multivessel CAD ?

Posted in Cardiology - Clinical, Cardiology -Definitions, cardiology- coronary care, Ethics in Medicine, Uncategorized, tagged , , , , , , , on August 20, 2021|

Yes, it is a triple vessel disease, with one tight lesion and at least two other significant lesions. One of them appears diffuse as well. 

Representative Image: Source courtesy DOI: 10.14740/cr548w LicenseCC BY-NC 4.0

“What to do next?. Is he symptomatic?  Yes. Definitely has significant angina” but LV function is normal.

“Ok then. If you are daring enough, ask this question”.

Which lesion is causing angina?

No easy answer at all. Try looking for some clues right from history, ECG, stress ECHO, meticulous assessment of individual lesions. Realize, even sophisticated imaging like SPECT, PET functional MR, may not help much either.

Oftentimes, we need to use the lean resources of collective common sense and clinical acumen. 

  • If it is post ACS status,  consider residual ischemia in the culprit artery is the cause for angina.
  • Second, consider the tightest lesion as angina-related.
  • Or the complex, eccentric, thrombotic lesion is responsible.
  • Next, consider LAD as default lesion as  angina related artery (Statistically right 75%, prognostically perfect decision) 
  • Watch for ECG changes during chest pain (ST depression usually don’t localize, but experience tell us V5 /V6 ST depression is more likely to be LAD ischemia )
  • Echo wall motion defect either during rest or (more usefully) in stress can really help. (It needs some effort to look for Wall motion mapping with coronary lesion subtending segment)
  • What about balloon inflation test during PTCA ? . Prompt angina when a lesion is occluded may give a direct clue.

Want to get more confused?

  • Ask your colleagues for an opinion either online or offline.
  • Do FFR/QFR/IFR  and OCT and look for intracoronary pressure-flow data and plaque burden. We are entitled to get excited about fibrous cap thickness, and hunt for vulnerable lesions and decide thereupon.  

Finally some easy options. 

Which lesion is causing angina? Never entertain that troubling question at all. (Need not  squeeze your coronary intellect you know ) 

Consider every lesion as important 

  • Get ready to stent all three or more lesions.(Many times forbidden though !)
  • (or) More convenient, refer to CABG. (Surgeons will welcome for sure )

Final message

Which lesion is causing angina? is indeed an important query one should raise. This paves way for selective focussed PCI in deserving lesions alone. However, when dealing with complex lesions subsets. the most pragmatic way as of today is to educate the patient and include them in the decision-making process (Never forget to offer medical management as a permanent option, especially if there is no critical LAD disease, and say thanks to  ISCHEMIA/COURAGE/ BARI 2D.)

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MDM of mitral stenosis is a “mid diastolic misnomer”

Posted in Auscultation, Cardiology - Clinical, Clinical cardiology, Mitral stenosis, Uncategorized, tagged , , , , , , , , , on June 23, 2021|

Nearly a century ago, Carl Wiggers helped us understand the dynamics of cardiac cycle with a historical diagram depicting systole and diastole. We know diastole has 4 phases. They are  IVRT(nil)  early rapid filling,(70%) diastasis,(0-5%) atrial contraction(25%) (Percentage filling within the brackets)

What is mid diastole?

The easiest way to define mid diastole is to divide diastole into three parts with reference to time and call the mid-third as mid-diastole. (.5 seconds/ divided by 3). But, Physiologically we can’t do that. Even hemodynamically there is no distinct mid diastole as diastole is divided into 4 phases as described earlier. When there are 4 parts how can we slice out mid diastole without an overlap? 

So, what shall we do? Technically which is the best period to be referred to as mid diastole?

Maybe diastasis. In this period either little or no flow occurs. HR heavily influence the duration of diastasis. Cardiologists especially during auscultation created the concept of calling anything happening after mitral valve opening as mid diastole. ie after IVRT which equals* A2-MV opening interval (In the true sense,  it must be the early diastole that can begin with mitral valve opening for physiologists, but for cardiologists, it begins with aortic valve closure because we can hear only closing sounds)

What happens in mitral stenosis? 

Any significant obstruction of the mitral valve, the gradient builds up immediately after the mitral valve opens. The murmur gains momentum in the early rapid filling phase of diastole, gradient spills over to fill the diastasis, and finally accelerates in pre-systole to end up in loud S 1.

 Is there really an early diastolic murmur in mitral stenosis?

  (I can’t agree. We were never taught that way)

Yes for sure. In fact, it can be the dominant murmur in many, since the early rapid filling phase of diastole contributes 70% of filling. In mitral stenosis, the early diastolic gradient will always be present. So. mitral stenosis murmur indeed begins in early diastole and extends further depending upon the severity.

If there is really an EDM in mitral stenosis, why do we still keep calling it MDM?  

Just by tradition and for convenience. Auscultatory mid-diastole is different from hemodynamic mid diastole. This irony occurs because murmur descriptions are based not on time but on phases. So, by convention, a murmur that does not occupy the IVRT phase is labeled as MDM. This also helps us to differentiate MDM of mitral stenosis from aortic regurgitation which has the exclusive rights to be called an early diastolic murmur.(Since it occupies the IVRT phase) 

Final message

This is probably a too-long post to unmask a trivial nomenclature issue in the diastolic murmur of mitral stenosis. Still, it’s worthwhile to understand this. The word “mid in MDM” is arbitrarily used and doesn’t really reflect either the time or the true hemodynamics. In fact, the same reasoning is applicable for any flow murmur across the mitral valve that is inappropriately referred to as MDM. 

Caution  

*Let me not confuse the youngsters especially undergraduates. MDM of mitral stenosis will remain as MDM in exam halls. It will never become EDM as that of AR where the murmur starts in the IVRT phase. 

 

For advanced readers

What is the earliest murmur to appear in mitral stenosis?

The first noise comes in the early part of diastole or late presystolic when atria contracts. Never in true mid diastole and gets filled up the in mid part as the disease progresses. So, we can have mitral stenosis without murmur in mid diastole. The morphology of murmur can best be understood when we correlate with Doppler echo profiles.

Is MDM of mitral stenosis crescendo or decresedo or both ?

Normally in diastole crescendo murmurs are uncommon as pressures are falling.( Ventricular contraction only can generate crescendo pressures.) Still, In mitral stenosis, there is minimal crescendo at the onset even when the  E velocity decelerates. However, there is a definite presystolic accentuation with atrial contraction which can also be referred to as late diastolic crescendo. 

*Is IVRT the same as the A2-OS interval? 

It is almost the same but not the same. Find out the difference.

 

Further reading

ongley1955

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What’s the relationship between JVP and PCWP/LVEDP?

Posted in Cardiology - Clinical, Jugular venous pulse, JVP -Jugualr venous pulse, tagged , , , , , , , , , , , , , on August 2, 2020|

We can consider Jugular veins of the neck as a naturally present right heart catheter. It faithfully reflects the live pressure and waveform data  from right atrium and ventricle .

Can JVP tell us anything about left heart pressures? Is there any relationship between JVP and PCWP or LVEDP ?

If you tell JVP reflects LV filling pressure in any graduate medical exams, you will be admonished. However in DM or post-doctoral exam, if you say there is no link between the two, you are likely to be chided.(It is unfortunate the answers vary depending upon the level of training , which I feel is not academically correct )

Though the JVP-PCWP link, apparently appears Illogical, it does  have a scientific basis. It is true, there is a huge (& multiple) anatomical barriers between the left heart and Jugular vein in the form of pulmonary arterial & venous circuits, the right ventricle and right atrium.Still ,the hemodynamic principles demand, whenever left heart filling pressure increases, the right heart pressure should increase correspondingly to drive the blood from RV across the pulmonary circuit.This raise should be in the mean pressure. (or diastolic pressure,) it’s rarely related to systolic pressures as RV systole normally generate more than twice or thrice the LVEDP.

 

This driving pressure across the lungs  is called the transpulmonary gradient. (PA mean minus LA mean) The normal being < 7mmHg. So if there is a sudden increase in LV filling pressure to 20mmhg, there has to be elevated right heart pressures.(20 +7) This will be reflected in JVP as well. So patients with acute diastolic heart failure as in HFpEF must show elevated JVP. This can be documented elegantly In patients with positive responses during diastolic stress testing.  (JACC: Cardiovascular Imaging  Volume 13, Issue 1 Part 2, January 2020)

There are important caveats in JVP-PCWP link

  • If the PH is long-standing and precapillary (Reactive PAH) has set in the right heart pressure will no longer reflect the PCWP.
  • If there is any organic Tricuspid valve disease (Both TR/TS) JVP can reflect PCWP.
  • Finally, any cause of RV dysfunction will immediately elevate the JVP so biventricular dysfunction makes correlation of JVP with PCWP meaningless.(Acute pulmonary embolism, and RV infarction)
  • Further confounding can occur if we contemplate RV diastolic dysfunction as seperate entity. (At what level of RV systolic dysfunction, does the RVEDP begin to raise ? I think we don’t have an answer for this . Researchers please note.)

Some more mechanisms of elevated JVP with left heart disease

  • Bernheim’s effect and ventricular interdependence can make JVP elevated spuriously without elevating PCWP.
  • Acute mitral regurgitation left atrial V waves can “tide-back” all the way to PA and the right heart to elevate the JVP
  • In ASD and Lutembachers syndrome  the RA pressure waveforms may reflect the LV filling pressure, though inconsistently.
  • Finally, and importantly in Fontan circuit JVP may exactly reflect the left heart pressure for the obvious reason, as SVC is connected to the pulmonary artery directly.

Final message

JVP will always tell what is happening to the right heart chambers only . It can, no way be taken as a direct marker of PCWP/LVEDP. However, there can be a correlation between JVP and PCWP/LVEDP in a certain subset of cardiac failure. (As in exclusive isolated left heart failure (typically HFpEF) the elevated JVP might just reflect the elevated LEDP provided there is normal RV function )

Reference

1.This study elegantly shows a correlation (or lack of it) in different subsets of heart failure. It tells us very clearly If JVP(RAP) is not correlating or disproportionate to PCWP, it implies RV dysfunction.

2. This paper suggests a really useful scheme to classify heart failure as concordant and discordant with reference to right and left heart.

It throws some interesting facts. I guess it will help us guide diuretic management and prognosticate chronic heart failure.

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Pericardial effusion associated with Infective Endocarditis : Incidence , mechansim and clinical Implication.

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), pericardial disease, pericardial effusion, Pericardium, tagged , , on January 28, 2020|

Pericardial effusion is often detected in patients with Infective endocarditis. Incidence can be as high as 25% . Most often it is mild, can be moderate in few.

Mechanism

  1. Sympathetic effusion in response to endocardial infection. It’s never more than minimal. (Evidence ? it’s only an assumption)
  2. IE related cardiac failure (Raised systemic venous pressure to which pericardial veins drain)
  3. Local sepsis, Abcess formation tracks to pericardial space through transmural lymphatics
  4. Fungal , granulomatous , Tuberculous IE (Rare) Here IE and PE  share the same pathology
  5. Part of systemic sepsis activated Immune mechanism (Polyseroists)
  6. Renal Involvement of IE-Renal failure
  7. Postoperative pericardial effusion in Prosthetic valve IE (Common, often loculated)

Clinical Implication

  • If the pericardial effusion is more than mild, it often denotes worse outcome. This implies more extensive infection or a marker of extracardiac causes of effusion like renal dysfunction.
  • Effusion may predispose to local dissemination of infection and ends up as peri-annular abscess is whether it is a cause or effect of effusion remains to be understood.It is often exudate as one would expect, but transudative  effusions also occur and would indicate more benign course.
  • The sterility of pericardial fluid has not been proven. Culture studies are rarely done from effusions associated with IE.
  • Pericardial effusions appear more often seen in IE of right heart valves. They turn out to be  IV drug abusers.
  • Contained rupture of an abscess needs to be differentiated from effusion

Can we give steroids for PE associated with IE?

Steroids can rapidly plug the inflammatory pores in the from the pericardial surface.It may also prevent future constriction. Currently, routine steroid therapy is not advised in infective pathology . If the infection is confirmed and is being taken care of by antimicrobial therapy there could be a role for steroids with user discretion.

Final message

During the echocardiographic evaluation of IE, the presence of pericardial effusion should be specifically looked for. These patients should be flagged and will require monitoring as the prognosis of PE complicating IE is a concern unless proved benign.

Reference

Two studies one from Spain and other from Egypt looked into this issue specifically.

1.Regueiro A, Falces C, Cervera C Risk factors for pericardial effusion in native valve infective endocarditis and its influence on outcome. R Am J Cardiol. 2013 Nov 15;112(10):1646-51. 

 

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Does elevated RVEDP cause dyspnea ?

Posted in Cardiology - Clinical, Clinical cardiology, Uncategorized, tagged , , on December 18, 2019|

Exertional dyspnea disproportional to the effort is the most common (cardinal)symptom of heart disease. Whenever we discuss the mechanism of cardiac dyspnea , we primarily attribute it to left heart disease, elevated LVEDP and the resultant pulmonary congestion.Conventional teaching in the past (may be in the present too !) doesn’t implicate raised RVEDP in the genesis of dyspnea.

It’s good to recall , the sensation of dyspnea is felt at the peri -Amygdala nuclear zone after complex processing with various cortical and sub-cortical level .It is subjected to as many afferent triggers other than J receptors in pulmonary micro circulation. (Eg Exercising skeletal muscle). It is believed, mechanical stretch receptors exist within the walls of heart along  the sub-endocardial aspects of chamber.

(Muscle spindles which are the sensors of muscle tension are extensively noted in skeletal muscle that contribute to the origin of dyspnea .We are not yet accruing enough evidence  whether cardiac muscle do have the same muscle spindle or it’s equivalents to cause dyspnea when stretched. However, we clearly witness in the practice of clinical cardiology , isolated elevation of RVEDP ( also RVSP ) to cause significant dyspnea in specific clinical situations.

Potential causes for Isolated Right ventricular dyspnea

  • Pulmonary hypertension  (COPD included* where in it could be a combination of lung and cardiac dyspnea)
  • Acute pulmonary embolism
  • RV Infarction
  • Acute rupture of sinus of Valsalva aneurysm (RSOV) Here RVEDP is often > LVEDP and dyspnea is due to the acute stretch of RV
  • Isolated normal pressure TR(RVEDP is low still cause dyspnea  due to volume related RV triggers)
  • Any RVOT obstruction (Classically valvular pulmonary stenosis)
  • Does RV dilatation without elevated RVEDP cause dyspnea ?  Though right ventricle is developmentally and hemo-dynamically better suited to handle volume , still, it  struggles to manage sudden increase in volume .(Another clinical example is seen in patients who are on dialysis)

*RV diastolic dysfunction is still a Infantile hemo-dynamic concept .Whether it can raise RVEDP significantly during exercise and Independently contribute to dyspnea is at best a hypo-science.

Role of muscle spindle and mechno-receptors

 

Muscle spindle

structure of skeletal muscle spindle. Though we don’t have a highly developed spindles in smooth muscle and cardiac muscle we have evidence to suggest cardiac neural ending do have mechano-receptors with afferent connection through visceral neural plexus that can trigger both heart rate and respiratory centers Further reading : Neuroscience. 2nd edition. Show details Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Sunderland (MA): Sinauer Associates; 2001.

Bain-Bridge reflex: The hidden link in right heart dyspnea

Bain-Bridge reflex is a 100 year old concept. still helping us to understand the basics of right heart hemodynamics and how adjustments with acute volume loading take place.He proposed that  veno-atrial stretch receptors are located  primarily in great veins as it enter ,right atrium (RV as well).

This gets activated through vagus and stimulates  in brain-stem sympathetic system and increase the heart rate to handle the excess blood reaching the heart. How often we feel the symptom of palpitation  whether due to this reflex ( when it is operating) is not really tested. But, what we can infer is , the surge in sympathetic tone perceived can be perceived as  dyspnea.

*Clinical Relevance of the Bezold–Jarisch Reflex and its possible interactions with Bain Bridge reflex is a different topic.

It is interesting to note many of these reflexes cause hypo-tension, bradycardia and hypopnea (Even near Apnea.) The word dyspnea is surprisingly not used .It is highly plausible many of the unexplained dyspnea we see in otherwise healthy population is attributed to acute or chronic volume overloading or under-loading of right heart.

Role of PFO in right heart dyspnea

PFO is a natural decompressing orifice in the IAS guarded by a flip-flap safety valve which is a remnant of septum primum .Though it can flow either way , since the flap of the valve is larger in LA side,  it gets closed when  LA pressure raises but opens up , if RA pressure raises making it more often a right to left shunt at times of elevated RA mean pressure. In isolated right heat pathology , this communication shunts  right to left and  adds a new dimension to cardiac dyspnea (Now, It becomes a hypoxic /biochemical dyspnea over and above the right heart stretch related dyspnea )

Other mechanisms in right heart dyspnea

Pulmonary arterial stretch and altered QP : Role of ventilation perfusion mismatch should also be considered as a cause for dyspnea in isolated RV pathology. The term V/Q mismatch is a poorly understood term fro me. My Inference is, since RV contraction  provides the Q in the equation V/Q .Whenever Q falls V has to fall to maintain neutrality causing net hypoxia and dyspnea.

Final message

Dear fellows, never hesitate to attribute the origin of dyspnea,  to elevated RA mean pressure /RVEDP. It is due to RA/RV stretch secondary to volume and pressure overloading with a perfectly normal pulmonary capillary wedge pressure or LVEDP. As in the left heart ,this occurs both in pathological as well as perfectly exaggerated physiological times.

Reference 

1.Bainbridge FA. The influence of venous filling upon the rate of the heart. J Physiol. 1915 Dec 24;50(2):65–84. [PMC free article] [PubMed] []

2..A J Crisp, R Hainsworth, and S M Tutt  The absence of cardiovascular and respiratory responses to changes in right ventricular pressure in anaesthetized dogs. J Physiol. 1988 Dec; 407: 1–13(This paper actually undermines the importance of RV receptors. It is still perplexing to note both the inflow into RV (ie RA  and the out flow  pulmonary artery circuit has richly innervated by receptors , its difficult to accept why we  have failed to get much evidence for RV stretch receptors) Its potentially great area of research for cardiac physiologists. That will be a tribute to the greats like  Bain Bridge and Bazolds Jarich.)

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Some thoughts about Origin , Genesis and Mechanism of palpitation !

Posted in cardinal symptom in cardiology, Cardiology - Clinical, Cardiology -Clinical signs, Clinical cardiology, Palpation, tagged , , on February 24, 2019| Leave a Comment »

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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