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Estimation of right atrial pressure (Often referred to as  central venous pressure (CVP) is a common hemodynamic excercise both at the bed side and in echocardiographic lab. A venous catheter inside the right atrium is probably  the best way to measure it accurately .But, there are  practical issues  for  putting and maintaining a CVP catheter. ( & We also know , what happened to the concept of routine  swan  catheter in critically ill patients !).

A  rapid bed side echocardiography  can give us a fairly accurate estimation of RA pressure . We  don’t even need look into the heart , what you need is imaging the inferior vena cava , it’s size and it’s  behavior  with respiration  . You don’t require  a doppler probe either ! With these two parameters one can decode the mean RA pressure. This  modality is rarely used in the ICUs , it can be a simple aid to fluid management .

RA pressure echocardiography ivc collapse hepatic veins

ivc collapse ra pressure right atrial mean pressure

Shrewd clinicians would argue , we have a natural catheter inside the right atrium, ie the   internal jugular vein   This gives us a unique opportunity to study the moment to moment RV, RA pressure . And .  .  . yes ,  we know it but we rarely respect the neck veins !

Pulmonary embolism is  one of the  important  causes of acute chest pain . It can mimic  acute coronary syndrome . In fact along with aortic dissection  , it forms  a  differential diagnosis for STEMI especailly if the ECG is not typical.

pulmonary embolism chest pain dvt d dimer ventilation perfusion

The Chest pain of acute pulmonary embolism can originate in one of the following structures  with different mechanism

  • Lung parenchyma ( Necrotic pain ?)
  • Pluritic pain in adjacent necrotic segment
  • Main Pulmonary artery and it’s branches
  • Right ventricular mechanical stretch
  • Right ventricular ischemia
  • Hypoxia induced LV ischemia with coexisting CAD.
  • Multiple contribution from any of  the above *

It should also be remembered , medicine never respects logic, as some times  an episode of pulmonary embolism can occur without any chest pain

Localisation of chest pain

One can imagine ,  how difficult for the  nervous system to zero in on the origin of this  pain as  the structures involved in acute pulmonary embolism are in different planes  and in different depths  within the chest cavity . Patients  often complain vaguely  the site of pain but  what is universal is severe resting pain deep within the chest . If the ischemic lung segment  transmit pain signals , the location and radiation depend on the  bronchpulmonary segment involved.This again adds on to the complexity in the  genesis of pain  .It can be virtually any where in the back or front of chest.

But , the central and retrosternal chest  pain are equally common as invariably the central pulmonary arteries go for a acute stretch which can be severely painful .In fact , current thinking is it could contribute maximum  for the intensity of chest pain. Similarly,  acute dilatation of RV result in mechanical pain. RV sub endocardial ischemia may   also contribute .An intact bronchial  circulation( From aorta)  can limit the  ischemic lung pain .

Final message

Analysing  the chest pain of acute pulmonary embolism can be an  interesting academic exercise . It could arise from multiple structures with different mechanisms. It may not be much significant with  reference to management . But it has a diagnostic role.  A pain which is severe , and  atypically located should raise the suspicion of acute PE especially  if the patient has associated dyspnea.

Current data from TCT

TCTMD – The Source for Interventional Cardiovascular News and Education

Normal P waves

normal p wave ecg rae lae

What are the components of Pwave ?

RA component : The SA node depolarises the RA first  , so the initial part of  P wave represents  RA  current .After about 40msec  the wave front reaches LA and it begins it’s depolarisation .LA component :By the time LA is maximally depolarised the RA  already starts its repolarisation.So there is  overlap and also a short time lag between these two wave forms . This is very important to recognise as , even if the RA conduction is prolonged in pathology the RA component of P Wave still falls within the LA wave .Hence it is not shown in the ECG and P wave is not widened in RA enlargement. This is in contrast to LA enlargement , when the terminal half of P vector delayed it stretches the P wave wide beyond the normal 110ms .Hence LAE widens the Pwave.

Why P wave becomes taller in RA enlargement ?

In classical P pulmonale , the P waves are  tall >2.5mm. It is easy to explain why it not getting wide than  why it is getting taller ! The atrial vector has two components .The initial RA vector  is directed  anteriorly .The main reason for tall p with RAE is  due to the anatomical proximity of RA to the chest wall Further ,the  Initial atrial  electrical dp/dt is steep . Any RA voltage increase is easily picked up by the chest leads and P wave voltage increase and becomes tall. We need to realise LA is not only left of RA its equally posterior of RA. Hence LA enlargement rarely brings (Never ?)  it closer to chest wall ,and hence high voltage tall P is almost unheard of with LA . Note , deep negative late P wave activity is typical of LAE , consistent with its posterior location as well its late depolarisation compared to RA)

rae right atrial enlargement ecg tall p p pulmonale p tricuspidaleright and left atrial enlargement how to differentiate lae rae

Why LAE can not produce tall P wave ?

The Left atrial vector which  follows RA vector  is mainly directed posteriorly and hence inscribe a  descending  limb of   P wave . This causes the P terminal force .  So  the direction of vector forces  and the anatomical locality  make a  tall & positive P  deflection highly improbable in   LAE .

*Of  course  when LAE is   huge , where a antero -supero vector from  roof of LA may inscribe a positive wave .

What happens in bi atrial enlargement ?

It can have features of both . Tall & wide P waves .

Can RA generate a Q wave ?

Yes . When RA assumes a huge  size  , especially if the RV is also at high pressure as  in severe PHT or valvular PS   a  q wave is generated in the lead V1 .This q wave is nothing but the intra cavitary potential of the enlarged RA.

What is the difference between atrial enlargement, atrial dilatation, atrial hypertrophy, intra atrial block and inter atrial  block  ?

The p wave morphology has no  specificity to identify the various entities. In any pathology of atrium the first thing that happens is a conduction delay ! It is now realised the bulk of the changes we see in atrial enlargement especially in LAE is due to intra and inter atrial  blocks or more subtly conduction delay.

It is  obvious , a wide P wave can occur either  due to LAE or simple conduction delay .In elderly  hypertensive patients atrial fibrosis is more common , one can not confirm LAE  without echocardiogram .

A notched P wave  can be a very specific sign of   inter atrial block .Which is more common in severely diseased left atrium. A notch , slurred p wave is a good marker for impending AF or atrial flutter.

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The most popular criteria to differentiate VT from SVT aberrancy is  formulated by Brugada in 1991.

The greatness of  this  criteria is that  a single question asked  is able to confirm VT in vast majority of cases.

Is RS complex absent all  of the pericardial leads ? If  the answer is  yes  it is VT 100%

How is that,  we have been struggling for so long , a single question is able to solve the issue quite easily ?

wide qrs tachycardia vt svt aberrancy brugada

This is because , the term  “Absent RS complex ” actually means

Presence of  one of the  following three typical complexes Of VT.

  1. QS
  2. QR
  3. Monophasic R

Two of them  actually imply ,  q waves throughout   V 1-V6 .This  means a badly damaged ventricle and  with  little electrical activity coming towards the chest wall .This situation  almost always occur in VT.*

The third complex is Monophasic R .

A  monophasic , wide  QRS  complex  again indicate VT  as monophasic aberrancy is very rare as the supraventricular  impulse invariably conducts with  RSr’  (The right bundle  refractory period sees to that  at least a small r’ is inscribed however fast the SVT is !  )

So if there is no RS complex  it must be VT !

What  are the  difficulties  faced in applying this   first step of Brugada criteria ?

It is funny to note , in medicine criterias  often work perfectly in  text books only !

Is there a RS complex seems to be a very easy question ? There lies the catch !  .Even though this criteria may be 100% specific , differentiating RS from QS complex even by an experienced cardiologist may be difficult in a significant number of VT tracings.This  realistically ,  reduces    supposedly  100% specificity  of this criteria !

In fact we expect Brugada to develop an  another limb  to his now famous algorithm

Is there  absence  RS complex in precardial leads  ?  Yes / No / May be ,  not sure !

CHB and AV dissociation are often confused with one another . While CHB is an important cause for AVD , there are distinct differences  which have clinical implications. This table is an attempt to simpify the understanding of the two. Corections and suggestions welcome.

This is a high resolution image , to read better  right click on the table  copy image and open in any image viewer

complete-heart-block-chb-av-dissociation-avd-va-associationn-va-block-sinus-node-dysfunction-ecg-ep-study-interfernce-avd-aivr

orthopnea paroxysmal nocturnal dyspnea pnd www.drsvenkatesan.com

Some Infrequently asked questions in (iFAQ) in PND

What gives relief from PND?

The classical description is, the patient wakes up from sleep. sits up, often to stand up, and go to the nearest window and try to breathe fast and an episode of dyspnea settles down in a few minutes. The relief is completely in many unless the ongoing trigger and baseline cardiac defect overwhelms the reserve mechanism.

What is the hemodynamics behind relief?

Since symptoms are due to sudden unexpected congestion during sleep, assuming erect posture slows down the venous return of 400 ml instantly. It is equivalent to an IV diuretic push. Further standing up (even sitting up is sufficient)  brings the left atrium in its natural superior position, compared to LV. The gravitational forces emerge* and aid in LV filling and improve stroke volume and relieve the congestion backlog. Apart from this two more factors contribute. V/Q mismatch improves as more lungs get perfusion in an erect posture . Finally seeking the window is spontaneous, in search for better fractional oxygen content from the atmosphere. (One more related question. How do pillows give relief of dyspnea in acute LVF? Few of the above mechanism operates)

*Postural changes in LA mean pressure is a complex topic of physics involving lungs, pulmonary circulation, and LA mean pressure.

Is basal rales mandatory during episodes of PND?

Yes. Most will have. But it should be emphasized in orthopnea patients, rales are rare since it takes some time for lung congestion take place. If rales appear immediately after lying down it may Indicate severely compromised LV function.

PND vs Orthopnea: Which is a reproducible symptom?

Obviously orthopnea. PND can never predict which day its going to come as there is CNS component to the circuit in triggering this. (REM sleep, Dreams etc)

How many episodes of PND can occur in one night?

Usually one. Because PND requires a time lag of at least few hours.Usually, these patients will not sleep thereafter or the usual wake-up time ensues.

Can episodes of PND be prevented?

Since its a volume-dependent pulmonary hemodynamic stress, a diuretic at dusk will prevent these episodes in many.

What is the sensitivity of PND for predicting heart disease?

It has low sensitivity( <30% ) but up to 75% specificity to diagnose heart disease.(Class 3 Non-Expert Evidence)

Is PND sign of advanced heart disease?

No.It has very low sensitivity to predict severity of heart disease.

Can PND and Orthopnea occur at same patient at same time a same day ?

Orthopnea has no time lag.It occurs immediately hence it is obviously more severe. Many of these patients, however, do get into sleep after some time as some sort of compensation or adaptation to neural signals of dyspnea take place.

These patients, later on, can get into the same cycle of PND . However, as heart disease (as in cardiomyopathy ) worsens the pulmonary interstitium shows some reactive fibrotic changes resist water logging in the lungs.

Since PND and orthopnea share a close relationship in terms of pathophysiology, we cluster it together in symptomatology. However, they are temporally separated in most patients in natural history.

PND : is it equivalent to acute heart failure?

Yes, it can be called so (If it is due to heart disease*) . It fulfills all criteria of cardiac failure. LV/LA filling pressure raised, forward output (Cardiac Index may still be normal ) .PND is a transient, acute, left-sided failure that results in acute oxygen debt for the body which is self-corrected usually.

* In volume overloaded, CKD patients PND can occur

What is the relationship between RV dysfunction to PND /Orthopnea?

There is a complex fluid regulatory mechanism in the failing heart. The lung can be congested if and only if the RV function is adequate enough to flood the lungs and at the same time LV function matches it with its inadequacy resulting in persistent congestion. In other words, a very high RVEDP is protective against pulmonary edema (However the patient will feel the dyspneic still due to hypoxia /VP VQ etc !)

Its prudent to give importance to PND/Orthopnea with reference to the balance of RV and LV function. One may recall why pericardial disease where right heart filling is impeded rarely lead to lung congestion.

Can PND be associated with Angina ?

Yes, it can but generally its not. Angina occurs due to nocturnal sub-endocardial Ischemia. This combination occurs in critical Aortic valve disease.(Both AS/AR)

Is PND a cardiac emergency?

Difficult question. Most times, no. Since its self-limiting especially if the patient knows he is going to settle with his past experience. But it can trigger dangerous events in severely compromised hearts.As expected, the first episode creates much panic and invariably elicits an emergency alert.

PND has sinister significance if is due to nocturnal ACS.Its a sign of ischemic LVF and requires immediate care.

Which is the most benign form of PND and Orthopnea ?

Students should know, medicine is a funny science. PND as a symptom is benign in some, while it denotes impending death in others.

Benign PND : Obese men, women, in pregnancy may experience terrifying dyspnea at night when they turn around or stretch. This is due to the upward movement of the diaphragm encroaching lung space.

If you record mitral inflow Doppler filling pattern during an episode of PND what will you find?

It’s quite simple logic. You do it yourself and find it as a learning exercise.(Please don’t make the patient suffer by doing echo at times of distress. One of your colleagues to attend to him as you simultaneously do an echo for academic purpose)

Try calculating LVEDP with various echo formulas.

AV dissociation is  common clinical situation that can occur  during both    bradyarrhythmias  and tachyarrhythmias .

Bradycardias

  • Complete heart block
  • During pacemaker rhythms

Tachycardias

  • Accelerated junctional  rhythm
  • Idioventricular  rhythm
  • Ventricular  tachycardia

AV dissociation is essentially an  ECG diagnosis. But it is associated with some  clinical  signs   ,which can be detected by an astute physician in the bedside. At rapid heart rates  it may be really difficult at times to recognise theses findings, but a  cardiology fellow should look for these whenever they encounter AV dissociation  in ECG.

  1. Varying pulse volume
  2. Varying korotkoff  sounds during BP measurement.
  3. Cannon a waves in JVP
  4. Varying intensity of first heart sound on auscultation
  5. Mitral regurtitant murmur may be heard
  6. Hypotension in compromised hearts

What is the mechanism of clinical signs of AV dissociation ?

During AV dissociation , the atrial and ventricular contractions occur  out of phase  and the sequential contraction  is lost. So atrial contractions  might  occur with a closed AV valves .  This result in reflux of blood into the neck resulting in cannon waves . It may be visible only in few beats as the retrograde conduction VA conduction , is highly variable.

Further , only some atrial beats contribute for ventricular filling some do not.This results  in varying LV volumes and this  could result in changing pulse volume.Occasionally the ventricular and atrial   contraction occur simultaneously  .When this happens ,  some amount of blood  reguritates through the open tricuspid valve and mitral valve  which result in MR or TR .

Clinical utility

This could be important , in differentiating  the perennial  issue   of decoding the   wide qrs  VT from  SVT with  aberrancy .A rapid clinical assessment  here could  aid in the diagnosis  of VT  by  identifying  AV dissociation  . An experienced cardiologists will realise even in a given  ECG  with VT  identifying or ruling out  AV dissociation is not always a  pleasant excercise !

In this era of  high tech gadget  oriented cardiology is it not too much  to call for clinical   recognition of  this  entity ?

Definitely not , if  we know Wencke bach  recognised  the classical type 1 2nd degree  AV block in late 19th century even before the ECG machine was  invented ,

Simply by looking at the neck , by carefully observing progressive prolongation of  distance between a and c waves and subsequent dropping of c waves . Amazing isn’t it ?

This learning resource is  a must read for all cardiology fellows

Frank G. Yanowitz, M.D
Professor of Medicine
University of Utah School of Medicine
Medical Director, ECG Department
LDS Hospital Salt Lake City, Utah

Click the link to reach the master teacher

yanowitz great cardiology ecg website


Left ventricular  hypertrophy (LVH) is one of the most common  structural heart disease.Systemic hypertension, aortic valve disease are responsible for the bulk of the cases .Some  of the LVH occur due to cardiomyopathy (HCM/Non HCM variants).Athlete’s heart is a physiological response to exercise and  it  is largely a normal entity.

How many patients with SHT develop LVH ?

It is surprising to note , not every patient with SHT develop LVH .In fact estimates suggest only  about 30-40% of chronic  hypertensive individuals develop SHT .

What are the determinants of LVH in SHT ?

  • Magnitude of systolic pressure
  • Magnitude of diastolic pressure
  • Pulse pressure
  • Duration of SHT
  • Age
  • Gender
  • Body  weight/Obesity
  • Effect of treatment

While any of the above factors may operate in determining LVH

none of the above are important than this

“Genetic susceptibility ”

The myosin isoforms are determined by the genes .The re expression of   fetal isoforms in adults is responsible for LVH in many .This is determined by the genetic homogeneity

LVH  in  renal disease

Secondary hypertension due to renal dysfunction is a major determinant of LVH. This is espcially true if the pateints are dialysis dependent.The mechanism are not clear .

Diabetes and SHT :  LVH  friendly forces

When diabetes alone and SHT alone is less likely to result in LVH the combination of these two entities greatly increase the likely hood of LVH.DM induced microangitis amplifies the after load effect of HT and result in early LVH.Further this LVH is different from pure forms of hypertensive LVH  in that the interstitium goes for hypertrophy and in some cases neovascualrisation. In hypertensive LVH it is predominately myocyte hypertrophy  with little interstitial  proliferation. this has important therapeutic implication as any drug which reduce the blood pressure can regress pure myocytic hypertrophy, while in diabetic LVH  regression is difficult to achieve .

Lipid levels inversely related to LVH ?

There is no consistent relation between lipids and LVH .Occasional reports suggest a negative correlation.

Which LVH is associated with diastolic dysfunction ?

It is a well known fact , LVH has major effect on LV diastolic function.But it is also a fact only some forms of LVH develop this. Now it is clear only if the interstitial hypertrophy occur  diastolic dysfunction is manifested.  Even as the as the hypertrophied  myocyte  continue to  relax  the interstitium do not have molecular mechanisms to relax .Hence, as discussed earlier , diabetic hypertensive patient often  develop diastolic dysfunction .

Final message

LVH is not a simple expression of raised after load.It has major  non hemodynamic determinants which if identified , could have important therapeutic implication.

Coming soon . . .

Can  coronary artery  disease induce LVH in the absence of SHT or DM ?

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