Introduction to Cardiac Hemodynamic Tracings
Cardiac cycle pressure tracings involve three primary waveforms: arterial, ventricular, and atrial pressures, each with distinct morphological features. For an in-depth understanding of the conduction system influencing these tracings, refer to the Comprehensive Guide to Heart Conduction and ECG Fundamentals.
Key Morphological Differences
- Atrial Pressure Trace: Characterized by a-wave, x-descent, v-wave, and y-descent. The a-wave follows the P wave with an electromechanical delay (~80 ms). Both atrial and ventricular pressures show an upsloping pattern during diastole.
- Arterial Pressure Trace: Differentiated by a dicrotic notch and displays a downsloping diastolic phase. Peaks occur during the ST segment. Understand the significance of different ECG leads in capturing these phases in the Comprehensive Guide to ECG Lead Systems and Their Clinical Importance.
- Ventricular Pressure Trace: Shows a plateau pattern coinciding with the ST segment, with upsloping diastole similar to the atrial trace.
Detailed Analysis of Atrial Pressure Waveform
- A-wave: Reflects atrial contraction, closely linked with ventricular compliance.
- X-descent: Comprises two parts, x1 (atrial relaxation) and x2 (annular descent during ventricular ejection).
- V-wave: Represents atrial filling during ventricular systole, heavily influenced by atrial compliance.
- Y-descent: Marks early ventricular filling post-valve opening.
Hemodynamic Correlations and Clinical Relevance
- Mean right atrial pressure aligns closely with right ventricular diastolic pressure.
- Right ventricular systolic pressure approximates aortic systolic pressure.
- Pulmonary capillary wedge pressure (PCWP) generally matches left ventricular end-diastolic pressure (LVEDP).
- Discrepancies in these values can indicate pathologies such as pulmonary arterial hypertension or left heart failure.
Pathologic Waveform Patterns
Deep X and Y Descents
- Associated with constrictive pericarditis, restrictive cardiomyopathy, or severe right ventricular dilation. For detailed pathological distinctions, see the Comprehensive ECG Guide to Chamber Enlargement and Hypertrophy Diagnosis.
- More pronounced during inspiration due to increased venous return.
- Accompanied by minimal variation in mean right atrial pressure during respiration.
Flat Y Descent
- Seen characteristically in cardiac tamponade.
- Absence of early diastolic filling results in suppressed y-descent.
Large V Wave
- Indicative of overwhelmed atrial compliance.
- Commonly found in severe tricuspid regurgitation and decompensated right ventricular failure.
- Often occurs with deep y descent and variable x descent.
Ventricularized Right Atrial Pressure
- Occurs in massive tricuspid regurgitation with nearly simultaneous right atrial and right ventricular systolic pressures.
- Clinically recognizable via jugular venous pulsations mimicking arterial pulse.
Differentiating Pressure Waveforms
- Atrial vs. Ventricular vs. Arterial: Timing relative to ECG, slope morphology (upslope/down slope), and presence of specific notches (e.g., dicrotic notch) aid identification.
- Pulmonary Capillary Wedge Pressure: Surrogate for left atrial pressure with slower upslope and sharper downslope compared to pulmonary artery waveform.
- Proper catheter wedging is crucial for accurate PCWP measurement; under-wedging may mimic pulmonary artery pressure.
Clinical Implications in Heart Failure
Understanding LVEDP
- LV end-diastolic pressure is best identified by the atrial contraction wave (a-wave) on the LV pressure tracing.
- Elevated LVEDP can diagnose systolic or diastolic dysfunction, often before changes appear in wedge pressure.
Frank-Starling Mechanism in Heart Failure
- In systolic dysfunction, stroke volume curve shifts downward and plateaus earlier, sometimes descending at high preload.
- Diuresis in heart failure patients with low blood pressure often improves cardiac output contrary to normal physiology.
- Mechanisms include improved mitral regurgitation dynamics, reduction of interventricular constraint, and afterload reduction.
Pressure-Volume Relationships
- Diastolic dysfunction features normal LV volume with elevated LV diastolic pressure, reflecting impaired compliance.
- Optimal clinical management targets wedge pressures around 10-12 mm Hg for maximum cardiac output in severe systolic failure.
Summary
Accurate interpretation of hemodynamic tracings is essential for diagnosing cardiac pathologies and guiding therapeutic decisions in heart failure. Recognizing waveform morphology, correlating pressures, and understanding pathophysiologic changes enable clinicians to differentiate normal and abnormal states effectively. For practical application, integrating findings from the Essential Cardiovascular Examination Skills in Emergency Settings can refine bedside evaluation skills. Continuous practice and correlation with clinical findings enhance diagnostic precision.
dynamic tracing to look at three types of tracing you have the arterial
ventricular and atrial tracings and use that cardiac cycle here to understand the morphology and the
differences in morphology between each one of those three types of tracings
so as such you can see that this is the atrial pressure it has a x v y importantly it peaks
be after p wave and after st segment it does not peak during the st segment conversely the arterial and
ventricular tracing they peak during st segment another very important difference is that
both the atrial and ventricular pressure in diastole are upsloping versus the aortic or arterial
pa or aortic pressure tracing are down sloping diastole those are this is a very important feature
downsloping diastole for arterial up sloping for the other two okay timing outside st for
atrial and during sct for the other two another thing of course that you know the arterial pressure tracing has a
dicrotic notch evidently and does not have an airwave unlike the other two tracings which have
an a wave and evidently you know that crotic notch those features will become more helpful
as i go forward now i want to illustrate here the just i will go over multiple source
of tracings on the right and left side of the heart
uh basic and some pathologies so this is an atrial tracing um i hope most of you already know that the
eternal tracing has a ax v y so a wave corresponds to the atrial
contraction and follows the p wave it follows it by about 80 milliseconds there is always an
electromechanical delay the this is the airwave the x descent corresponds to two things it corresponds
to atrial relaxation as well as to the uh further annular descent
during uh ventricular systole so um and you can tell x descent without necessarily going into
all the details x descent is divided into x1 and x2 by c bound okay the x1 corresponds to
relaxation x2 corresponds to the further downward pull of the annulus during early ventricular ejection
and c corresponds to that closure of the material or tricuspid valve
in at the very beginning of systole this is the c bump x1 x2 then you have v wave which
corresponds to the atrial filling during ventricular system v wave is mostly a systolic
wave but it peaks at the very beginning of the asteroid just because before the material or
tricuspid valve opens and why descent is very early diastole
uh i will show you more of those as i go through keep in mind two things v wave
corresponds like i said to atrial filling in systole which means v wave is actually very much dictated by
the atrial compliance not the ventricular compliance the atrial compliance the
less the atrium is compliant the more that voa will shoot up as the atria
are as the atrom is filling during a ventricular system airwave on the other hand reflects
ventricular compliance so airwave is ventricular compliance the less the ventricle is compliant the more that
airwave will shoot up during atrial contraction v-wave corresponds to
atrial compliance keep those in mind okay normally in normal states
in the right on the left side the v wave is a little bit bigger than the a wave on the right side the a wave is a
little bit bigger than the v wave that's related to the difference in compliance the left atrium
is a less compliant than the right atron partly because it's thicker
so just keep those ideas in mind and here i illustrate what i explained a little
earlier about the differences in morphology between the three various types of um
hemodynamic tracings okay uh this is an illustration of how a cath
typically should look like how i write her cath i'm sure you probably know all that but
the right it and but be careful when you report a right heart cath and hemodynamic
report make sure you make the numbers match and make sure the numbers make sense as
such the mean right atrial pressure is typically
approximately equal to the rv and diastolic pressure the rv systolic pressure is typically equal to the
aortic systolic pressure and the aortic diastolic pressure is typically equal to the mean
uh capillary watch pressure pulmonary capillary watch pressure okay so those numbers typically has to
match i have to match another thing the mean pulmonary capillary watch pressure
typically match the lv edp so make sure all those match now of course there are disease states that
change that one of the common disease states is pulmonary arterial hypertension
where you have a gradient between the pa diastolic pressure and the wedge pressure over seven
millimeter of mercury but in pulmonary hypertension due to heart
to left heart failure this number would typically match the pie diastolic pressure
this should not be superior to pie diastolic pressure the wedge pressure should not be superior to the
pair of solid pressure so if you're reporting in your report if you write it and it looks superior
then you know something is wrong but make your report you know let your report make sense
okay so uh that's just an overview of those numbers and this is an example of how you report it you know make sure
those numbers make sense okay otherwise whatever reads it will be criticizing you okay
all right this is an example i'll start going through some pathologies um so this is a right atrial pressure
okay and what you can see this is a wave it follows the p wave this is a v wave here it follows the t wave okay v
wave follows the t wave now there are two prominent descents so we see a prominent
x descent and y descent so this is what we call deep x and d y descent
traditionally some of you may recognize that this has been you know overly described with constrictive
pericarditis but keep in mind that that's actually finding that can be seen in the
following pathologies deep x and y can be seen with constrictive pericarditis but very often
it can be seen with restrictive cardiopathy but also severe rv dilatation
basically deep x and d py correspond to anything that impairs atrial and ventricular
compliance in such a way that the pressure shoots up and shoots down
very easily that's what causes the deep x and d py and so that's the case here
there are two other interesting features of that tracing so again that reason could be either it it's definitely it
definitely not conclusive for constrictive pericarditis by any means and that particular patient has actually
severe rv failure there are two other features that you see in
all those illnesses including severe rv failure and constrictive pericarditis the wide descent becomes more pronounced
in inspiration and that's a very common finding and there is a third finding which is
that look at that mean pressure this patient is breathing he's not holding his breath
yet you see absolutely no change in the mean pressure very interesting see that too it's
another case this case has mainly pronounced y descent
uh again what's interesting here and that y descent is mainly pronouncing inspiration
and another feature is that you see absolutely no change in mean pressure which is
typically we see a lot of fluctuation with respiration and mean pressure but not in this
particular case and that's a feature of right heart failure you get that right atrial pressure that
doesn't change much also with constrictive pericarditis you get that right there pressure that
doesn't change much and you get those deep y sometimes deep x descent that become
more pronounced in inspiration the reason it's more pronounced in inspiration is that evidently you get
more venus return and inspiration and that creates more of a shoot up in pressure
during v and more of a shoot down in pressure during uh relaxation um
i mean during early diastole during ventricular feeling the passive phase so shoots up and shoots down it
actually shoots up but because of the negative direct negative uh intrathoracic pressure and
inspiration rather than it shooting up it will become
neutral and that's why you don't see any change in pressure it's a kind of counteraction of the direct negative
inspiratory pressure and increase in pressure with the venous return
they counteract and end up with neutral change in pressure so those are three features so i'll go back
to that second point deep x and apply those three things and along with them you typically see no
change in ra pressure immunore pressure and a deep ex especially deploy with inspiration
another uh finding here that you may see is this this is a patient who has v wave he has a flat y and he has deep
x so he has a flat y d x try i don't know if any fellow can recognize that i actually this they
asked that on board general cardiology board almost every year in one way or another
this is characteristic of temponary so temporary unlike right heart failure and unlike
constrictive pericarditis does not have a deep white descent it has a flat and y and deep x
this is because in order for you imagine in constrictive pericarditis the heart the right heart cannot fail
okay yet it can fail just in very very early diastole it will get that deep y
and it will shoot right up after the deep why it will feel it briefly in haridasa
in tamponade unlike in constricted pericarditis you have absolutely no diastolic feeling not
even in early diastole it's full prevention of diastolic expansion throughout the asteroid
that's why you get no white descent the only time uh the atria can the atrial pressure can dip and the
atria can create a negative suction pressure is actually
only after a throat contraction in very early okay so that's
so that's important to know they ask that on board and they sometimes they give you a jvp
description of a flat white ascent and remember all those right ether pressure waveform they correspond to jvp
pressure waveform or you know pressure description and in order to memorize it you can use
that in mnemonic um flat why i have it written somewhere but anyway
flat y temponade f y t flat y tamponade just at least beside understanding it
memorize it fyt because you will have it for sure uh here i have it actually okay good um
i want to show you another thing so another finding so i describe the deep x and d y d
x with a flat y another finding that you may see is what we call the large
v wave large v wave as i explained v-wave is a marker of overwhelmed atrial compliance and you see that in
the compensated right ventricular failure or in and or in severe tricuspid regurgitation
typically a large v wave is accompanied by a deep y i'll go to this here it's not very large
but imagine it the large viewer is typically accompanied by a deep y
which is the v descent typically it's accompanied by a flattened x because the big v will pull up the x
with it but not always the x can be pronounced depending on the atrial compliance okay
so just know those pathology um all right i will i will show you another very
interesting tracing here that i see very often actually so try to look at that and here i will
start wanting you to practice the difference between atrial ventricular and arterial waveform
so i'm going to tell you that this waveform is a right heart waveform okay and i want you to guess
is this right atrial pressure right ventricular pressure or pa pressure
and try to use the features that i discussed earlier so r a r v or p a
so i will explain them to you uh you know think first two seconds and i'll explain them to you
so one it is not arterial waveform it's definitely not pa for the simple fact that between
peaks the pressure is rising it's an up sloping pressure remember arterial pressure
here arterial pressure is descending in the assay that's the most constant feature of arterial pressure
so this is definitely not an arterial pressure okay so it is either ventricular
or atrial pressure so it's either rv or ra pressure so which one is it now one thing you can
look at the timing the timing of this remember if it is our a pressure it will be our a pressure
with a big v wave that's what's creating that big wave here
so but the v wave typically peaks after the t this is kind of peaking and plateauing
in a rectangular fashion throughout the tea as you would see with an rv pressure
it peaks and plateaus in a rectangular fashion during the st segment okay
so it looks like an rv pressure if i have to guess just by looking it seems like an rv
pressure okay between rna and rv output potentially rv pressure there are though some caveat if it is rb i mean
the pressure is 30 systolic and the end diastolic is close to 20 millimeter of mercury so it's really a very narrow
rv pulse pressure would suggest a very severe rv failure so the truth is that was not rv although
again it could have been rv pressure it was not rv and this is an entity i want you to recognize
this was what we call ventricularized r8 pressure it's an ra pressure that absolutely mimics an rv pressure and the
only way you can tell is by fluoro and by further advancing the catheter this is that patient so this is he's
actually our a pressure that was that i was just showing here on a different
scale so this is his our a pressure with a very pronounced and plateaued v
and d py descent and this is his rv pressure you kind of have the same morphology
um minus some different degree of damping same morphology except the rv pressure
is higher in systole uh that's all so when do you see that this is pathognomonic for one
thing whenever you see ventricularized are a pressure this is always severe or massive
tricuspid regurgitation where the ra and the rv almost become one chamber so in early systole
that rv ejects fully into the right atrium and equalizes with the right atrium very
quickly so you end up with a ventricularized right atrial pressure that rises in
pressure nearly simultaneously to the rv and peaks
nearly simultaneously to the rv so this is pathognomatic pathognomatic mnemonic for very severe
massive tricaster regurgitation this can be recognized clinically too not just by cath
okay so recognize that entity and and that ventricularized our a waveform is actually just a big
v wave that is not just big it's also wide okay we call it cv wave sometimes
because the c and v are becoming together there is no more x2 okay there is no
more more no more x2 it's all pulled up by that
v wave and cv are fused this is an example you can recognize that clinically you
don't have to look at hemodynamic waveform this is a patient this is a jvp of a
patient i don't know if it shows up look at that jvp so whenever normally when you examine jvp you should see
a and v way you see two small notches boom boom boom boom av and if you if you match it
to the carotid pulse you will see two small waves for every carotid pulse in those patients you'll actually see
the jugular vein if you can see the external jugular you'll see that the standard external
jugular vein pulsating simultaneously to the carotid pulse and that is pathognomonic for a
ventricularized a pressure which is if you want to call it also it you know
it's speaking simultaneously to the arterial pressure so it's a ventricularized
r8 pressure just on physical exam you can be certain that this patient has severe
tract massive tricuspid regurgitation okay so recognize that they will ask you that
also as part of physical exam this is another case it's actually here from iowa i did it
uh last week with some other again it looks like rv but it's not rv look at this i mean this is speaking
throughout the stt segment in a rectangular fashion this was a patient with again massive
tricaster regurgitation same thing his jvp actually was like this patient i showed
it looked like a pulse all right i will mention uh some a little bit of doppler correlation for
some of you who are good with echo and doppler by the way do you hear me well
we can hear you okay good some echo correlation so this is an right atrial or left atrial pressure okay the
ax vy correlate those with the hepatic or pulmonary vein doppler hepatic vein on
the right for our a pulmonary vein doppler on the left for la
and i want you to know that the x descent corresponds to forward venous flow you
know when when the pressure dips in the atria it's sucking blood it's sucking venus
return the x descent is actually the s doppler velocity wave the y descent
is d doppler velocity weighs wave and the positive wave for the positive pressure wave form corresponds
to negative velocities so for example the positive a wave corresponds to what we
call a reversal v wave doesn't normally show up it's just uh
it really all that v wave is is the dip between s and d but the bigger the v wave
the more flat the s becomes and eventually the s may reverse as you see in severe mr or
severity r on the right so that big v wave flattens the s or reverse yes that's why
flat s on pulmonary vein doppler is a marker of the compensated left heart failure so
those are just some of the correlation for you in tamponade you will get that
question it's a flat y tampon so it's a flat d on um right atrial for example hepatic
vein doppler you will see flat d in tamponade okay so those are particularly marked in
expiration but still that's the the hallmark of it the flat d okay uh and the way to memorize it you
only memorize it s is x sex as is s is x that's how i memorize it so you can you know you can
have a reflex to think about it quickly d is why so this is another exercise in waveform
i hope it's not uh confusing all those waveforms but this is another exercise in practicing
waveforms analysis so this is a tracing here again i want you to guess is this rv
pa or wedge pressure so it's l a if you like not r a l a so is this r v
p a or a wedge pressure as a surrogate of l a pressure try to think for a minute for a few
seconds actually and so uh i'm going to tell you here so look at the segment
it's always easy to analyze the segment between peaks if that segment between peak it is not
down sloping it is horizontal or up sloping so look at it it's not downsloping like you see
with the artery so that eliminates an artery this is not an arterial waveform now there are other
features we look at as well when does it peak look it's peaking way past the t wave so that doesn't fit
with an arterial or a ventricular waveform okay it fits smaller than atrial
waveform there is another uh important feature here
the shape of it an artery here if you look at this an artery has usually sharp up slope
slow down slope okay conversely a v wave will have a slow up slope sharp down slope and this is what this
is suggestive of sorry okay this is a slower upslope uh this is actually here look at it this
is in the same patient so you can see is pa pressure sharp up slope
slow down slow compare it to this it's really very sluggish up slow probably more sluggish than the
downslope okay so this is actually a wedge pressure okay
pulmonary capillary wedge pressure and atrial waveform recognized by the horizontal
segment and by the fact that it's slow up slope sharp down slope by the fact that it
peaks after the t wave and you know by the fact that there is an a wave it's
a little hard to recognize a waves when you have such a big v wave but there is an airwave that
argues against uh arterial waveform okay compared to the pa you have it you have
again sharp up slopes slow down slope you have a nice dacrothic notch and it's down sloping in um diastole and
the timing is different this is much this is significantly later the v wave
than the pa okay so this is actually wedge pressure with a very big v wave and you will encounter that a lot so
wedge pressure with a big v wave will mimic the a pressure and you have to be able to
recognize those and this is just here some explanation another thing you can do is
when you deflate the balloon the wedge pressure the the the wedged catheter when you deflate the balloon of
the wedge catheter you'll see that jump in mean pressure mean watch pressure is always lower than
mean pa and typically should be equal or lower than the
diastolic pa this interrupted line so that's another feature to look for to look to if the mean wedge ends up
being higher than the peri diastolic or equal to the mean
the fpa pressure then it's not the true wedge pressure so this is another case kind of
repetition just for for practice purposes again try to guess is this arterial
atrial or ventricular pressure it's not arterial look at the segment
between the two waves it's horizontal it's not arterial
look also at the morphology slow up slope sharpen down slope so it's not arterial
this is again another atrial pressure it's pulmonary capillary wedge pressure
with a very pronounced v wave like this one a pronounced v-wave okay
in that same patient again this is the pa pressure in that same patient kind of similar to the prior case
interestingly that same patient at one point earlier in the case we had the pa pressure
and we wedged the pa that's what we obtained so that's why it's important to
recognize those features because somebody else you know somebody without paying attention could have called this
sweat pressure but this is not a wedge pressure okay you look at the timing the timing
is similar to the pa pressure so this is not the wash pressure another thing is that
the mean of that is equal to the mean of the pa pressure so that's another reason why this is not
a true edge pressure this is what you call an under wedge pa catheter
this is the two edge pressure this is kind of the idea sorry the image is blurry but the idea
when you do wedge pressure so you advance your catheter in the pa and when you do edge pressure you
to basically totally occlude a pa branch you you make the catheter enter into pa
branch and you totally occlude it so that the tip of that catheter where you're measuring through which you're
getting the pressure waveform the tip of the catheter doesn't see anything upstream
it only sees the veins the pulmonary veins downstream okay so it only sees indirectly the left
atrial pressure so the tip of the catheter the pressure at the tip
is a direct transmission retrograde transmission of the left atrial pressure through the pulmonary vasculature okay
that's why the watch pressure is a surrogate of la pressure but you have to make sure it is truly a
surrogate you have to be properly wedged if you don't watch properly you're not going to get the proper waveform you're
going to get this that's why it's important to analyze those features to
to make sure you are getting a proper wedge okay uh
i want to show you another feature so another thing since that pa since the wedge pressure
is a retrograde transmission of the l a pressure uh it's usually a good surrogate of the
mean la pressure mean watch pressure is a good surrogate of the mean alien pressure
but since the la is being transmitted through the pulmonary vasculature the morphology of the lea pressure is a
bit different than the more foliage of the wet pressure because it gets attenuated it
gets damp as it's getting transmitted retrograde
especially in people with pulmonary hypertension if you have somebody with a lot of pulmonary
arterial constriction past that pulmonary va branch or pulmonary venous
constriction that l a pressure will be damped during its transmission and that will make
if the la pressure has sharp a and v waves okay this is the la pressure here the
red waveform if it has sharp a and v wave the wedge pressure will have less sharp a and v ray
is is this as if you take the two ends of the la pressure and you spread them out
and you flatten all the curves of the a pressure of the wedge pressure that varies by patient again that varies
according to pulmonary disease it's more pronounced in people with bigger wave if you have a bigger v
wave you're more likely to have attenuation of that v wave than if you have a smaller one
or the effect of that attenuation will be more pronounced okay so keep that so an a waveform
is sharper with sharper descents than the wedge pressure and of course l a waveform is earlier than the watch
pressure because it's a retrograde transmission the watch pressure is delayed
that's easy to to correct you can move the v you can move the watch pressure leftward
okay that's easy to account for but you cannot exchange the morphology unfortunately
the morphology is not something you can correct for you just need to be aware of it the
difference in morphology between the wedge pressure and the la pressure that's mainly relevant when you're
assessing for material stenosis when you're assessing where where the morphology and the dips of the la
pressure are meaningful to see the gradient between la and lv okay all right
and i think you know i want you to pay attention to i'll go to another in regard to the l a pressure versus uh
wedge pressures here the v wave when you're doing simultaneous tracing
the v wave of the la pressure is bisected by the lv descent okay that's how it typically is so when
you're moving when you're doing a wedge pressure simultaneous wedge lv
this is the wedge pressure the black one so in order to try to mimic la pressure and correct the first error of time
delay you move it until it intersects with the lv descent or just precedes it
okay all right um i guess that's another example you're probably sick of those it's
it's another example of the same thing you can guess it's again big v wave that mimics pa wave form this
is the big v wave this is the pa pressure of that patient okay again the timing of peak difference
this is speaking around t wave this is way later than t wave the morphology and
diastole down sloping in pa with dicrotic notch it's you know rather upsloping with
a wave in the kind of in the case of the wedge pressure note that the okay here this is an
important question i've talked a lot about big v-wave and i've showed you a lot of big v-wave
throughout this like here but how do you define big v wave what is a big v
wave and uh so i'll give you the answer uh interesting in the literature there are a lot of definitions
the classic definition that was used in the 70s and 80s is v wave that is over 10 millimeter larger
than the mean watch pressure so the mean watch pressure v wave is 10 millimeter of mercury
larger than it that's a classic definition for example here is 12 13
millimeter of mercury larger another definition of v wave uh that you can be that can apply
here is v wave that is larger than double the mean watch pressure and you
will almost get that here that's harder to fulfill so that's the second definition
larger than double the watch pres mean what the mean v larger than double the mean third
definition is if you have any v wave over 40 45 millimeter of mercury regardless of those comparisons
it's a big v wave okay and i have them summarized here so those are the three features
okay now what does big v wave imply i will tell you by personal experience
and by the old literature about v-wave in which pressure nla pressure the most common cause for v
wave the one that comes to mind is severe matter regurgitation but in truth the most common cause of v
wave is just decompensated left heart failure okay it's basically anything that
overwhelm remember v-wave is atrial compliance and how how much it's overwhelmed by venus
return you know it's a venus return that overwhelms
atrial compliance so you can imagine somebody with decompensated left heart failure they tend to have a
big v wave by definition and there is this 40 percent rule there was there was
one very nice old paper in the 80s 1983 that showed that around 40 percent of people with civilian
r have big v wave but remaining patients do not have a big v wave conversely about uh
uh 40 percent uh of patient with big v wave did not have severe mr
so you know that's kind of the 40 percent rule so know that there are other causes
of big v wave and know basically that mr frequently does not lead to big v wave if you have to guess when does mr
severe mr when does sivira mar cause big v wave it's really when it's when you have the
symptomatic decompensated mr if you take those what we call the chronic severe
asymptomatic mr by definition those patients do not have a big v wave their eternal compliance is
not overwhelmed okay so those page those are patient in whom
you will not have a big v wave despite severe mr conversely you have again big v wave and
the compensated lv failure you can have big v wave definitely in material stenosis you can
have big v big a at various stages of the disease a is initially bigger than v eventually
v becomes bigger than a as the left atrium becomes more and more fibrotic in mitral stenosis
but those are the most common tools the top two here keep in mind also that v-wave is very
sensitive to loading conditions meaning a patient on the table has a little bit of elevated wedge pressure
not elevated v wave you can just ask him to do hand grip or raise his legs or if he's sedated wake
him up and the v wave may dramatically rise sedation will drop
your v-wave okay because it improves loading condition it reduces preload and afterload i typically don't
like to give sedation if i can during right hard cath because sedation will it
you know you typically like to do right her cat in a stressful situation so you can elicit disease you give
sedation you attenuate a lot of the disease the a lot of the pathology but again you
can trigger it using some of those techniques okay we can do exercise
in the cath lab table using uh supine cycling so okay good this is a case from last
week okay this is the green is a left ventricle okay a little bit damp
very smooth so it's a damp left ventricle try to guess what the yellow is
i'll tell you it's easy when you have simultaneous recording it's even easy to guess what this
is it cannot be an arterial waveform or a ventricular waveform simply because an arterial or a ventricular waveform will
be plateauing simultaneous to the lv right by definition
they will plateau you don't even need to look at the ekg here they will plateau simultaneously to the lv
during st the fact that this is actually intersecting with the descent of the lv by definition
this is a v wave okay so imagine that v wave this is actually left atrial pressure
with a huge v wave look at that v wave it's over 60 millimeter of mercury okay so this is left atrial pressure
with a very big v wave in a patient with very severe mr the more pronounced v wave
the more it suggests mr as opposed to the other ones especially when v wave is over two
times the mean watch pressure which is the diff more difficult definition to fulfill
that tends to be more severely compensated mr okay all right good
uh this is the patient this was the case that sid did and they placed transcutaneous mitral valve
and this is the pressure the the left atrial pressure after mitral valve replacement look at
this dramatic improvement the v wave here was 60 and you could not see an air wave
partly because the pressure is damp uh but look at this here now you can actually see
the v wave has this is a different scale but the v wave is down to 25 from 60. this is a dramatic improvement
okay and uh you can see a wave in this part here you almost can see away because
everything is lifted up by the v there is no x a is kind of lifted up by this up slope
whereas now you can start seeing a distinct distinct a and you can see an x descent
which is no more not as much lifted by that v wave anymore okay evidently this patient has a very
impaired left atrial compliance so don't expect the v wave to normalize so quickly
but it already dramatically improved with time i expect that we have to further improve
as the left atrial compliance potentially improves so i hope you understood those things i
want to talk quickly about lvdp it seems simple but i just want to make sure everybody understands lvdp and
how to obtain it so this is this is the actually the hemodynamic measurement we obtained the
most in the cath lab so this is an lv tracing and this is the uh
so the lv edp there are two ways of looking at it one way the best way is to look for lv a wave
or rv if you're doing right ventricular pressure and the airwave typically most of our
patient will end up being a bump on the upslope of the pressure so you have this upslope
of pressure this bump on it this is the airwave the lva wave and lvdp is here
is at the end of that bump okay so this lvdp is very high here you know it's over 30 millimeter of mercury
be careful you know at one point when i was a first-year fellow i used to you know
maybe think this is this would be lvdp but that is what you call it pre-alv
pressure this patient has a normal pre-alv pressure but it abruptly rises with airway with
with atrial contraction i would imagine that patient is compensated at rest you know he's
probably you know his lv pressure is not elevated throughout the asteroid only elevates after a wave uh this is a
patient with normal pre-a very abnormal post alb pressure he probably is compensated at rest uh
but he has severe dysfunction diastolic dysfunction i'll kind of explain it a little more in a minute
what what i mean by that how do i know it's compensated basically that's another illustration of lvdp
again this is more subtle than the prior case always seek that bump don't call this here lvdp this is lvdp
it makes a big difference and lvdp is an important measure for us to assess
whether to make the diagnosis of heart failure specific especially the diastolic heart failure
which is more subtle than systolic heart failure at least by by from an echo standpoint
two it can help you decide how compensated that failure is so it's very important measurement
here's what i was talking about compensated versus the left ventricular dysfunction this is a
patient with compensated function look at his lv pressure okay it is fine or maybe this
one is easier so his lv pressure in diastole is fine all the way until atrial wave
until the eternal contraction it will shoot up because it's an impaired ventricle with impaired
compliance the pressure will shoot up with the atrial filling okay
this patient if you superimpose on it the left atrial pressure the left atrial pressure the mean left
atrial pressure is probably normal and that's why that patient is probably it is not symptomatic at
rest and may not be symptomatic with mild or moderate activity this mean which pressure is normal
now this patient is only anomaly will be in elevated lvdp the point i'm trying to
make here is that lvdp is even more sensitive than much pressure to make a diagnosis of
heart failure and i want to make a point that you can have even though i told you the very
beginning of the lecture that lbdp tends to match wedge pressure they tend to match each
other there are cases this particular case where lvdp
is higher than the mean watch pressure it's more sensitive to catch lv abnormality than
mean watch pressure or mean la pressure now when you're in the compensated heart failure
this is when the atrom left atrium is overwhelmed and you get that big v wave
and you get further rise of lvdp but at this point the whole segment the whole black
lv 3a pressure is rising not just post a so the whole lv diastole pressure is rising
and the v wave rise in this case mean watch pressure and lvdp are both elevated and they they may
match even sometimes the watch pressure may be higher than the ldp
okay so in the compensated failure you will get a rise in me wash pressure but in compensated failure the wedge may
be normal but the lvdp is elevated and this is what gives you here in compensated stages
s4 in decompensated stages that big v wave is what gives you s 3 okay those are just some correlation
here so you know most often lvdp is equal to mean much pressure grossly for your
assessments but those are the cases i explained well you may have some discrepancy between lvdp and
wedge pressure aside from the big one i will talk about in another session mitral stenosis evidently
but i'm excluding that that's self-evident in this case higher lvdp but even outside that you
can have discrepancy uh i think that's good i want to talk about one thing i'm switching gears if i
have five more minutes i just want so i finished talking about tracing for
the time being i'll go over more things in the future uh i want to show you just a couple of
uh since you wanted me to talk about a couple of things related to heart failure i want to
mention this i hope this is unrelated to the tracings portion this is just a little
bit of physiology here in heart failure i hope all of you know the frank stalin curve i hope all of you recognize that
this character output or stroke volume on the y and lv and a solid volume or pre-load on
the x be careful some places or textbook will say
lvdp that's terribly wrong it's not lvdp it's a preload volume it's not endostatic pressure it's
endosolic volume very important okay so this is a normal person
a cardiac output increases with the increase in pre-load up to a certain point
now the important thing in systolic heart failure is that one that curve is shifted down
two it becomes a flat much sooner and that may not be the best illustration here but it becomes a flat
much sooner so it's down it's flat much sooner and interestingly clinical data suggests it also has a
descending limb which you don't have in normal individuals so why is this important the reason it's
important is take somebody with and you see that very often take somebody with
a severe decompensated heart failure okay he's in pulmonary edema his blood pressure sbp is 90 millimeter
of mercury okay if you give him 200 milligram of iv lasik's bonus what will happen to his
blood pressure if you give me 200 milligram of iv lasix i'm here okay i'm here on that car
if you give me 200 milligram of iv lasix my alveoli volume will drop dramatically my cataract output will drop
i will pass out okay now the patient with systolic heart failure he's here
okay you give him lasiks nothing will happen his character is not going to drop actually there is a good
chance his character he might be here on the descending limb
most likely his current output will not drop his karat output may actually rise with diuretic so keep that in mind
giving you know diuresing and decongesting somebody with a low blood pressure does not
drop the blood pressure in fact it increases it and there are several explanation of for
why that that increase and there are this is a landmark paper in 1986 but there is
another paper in 2017 that that illustrate those points if you want to remember there are three reasons
why decongestion can actually improve your character but at the very least it doesn't worsen it
because again you're here you're not the normal person
one of you any of you in this uh you know listening will be somewhere here a heart failure patient is somewhere
here you can diagram as much as you want he's not going to become hypotensive now here's the thing a three explanation
for that i don't know if any of you know but one is
in that illustrated in that paper is severe mr functional mr you diuresem you shrink mr
and that will improve carrick output that that's why you get you increase correct output there the
second thing is um actually the rv lv interaction okay when
the uh when you severely overload it and i'll show you here a picture you probably all
of you know that but i'll still show it when you have severe uh volume overload the rv and lv become constrained that
pericardium stretches and cannot stretch anymore so the rv and lv start fighting each
other to expand in that one cavity okay so and you kind of start having what you
call functional constriction pericarditis if you want so diuresis
will improve that will improve that pericardial constriction and will allow those ventricles to
expand outward rather than rather than at the expense of each other third reason is that uh lv and diastolic
volume is preload but it also correlates to some degree with afterload which is lv
and systolic which is lv systolic volume after all it's not just pressure systolic pressure it's also systolic
volume so the bigger your volume the bigger your volume after load you shrink that
after load you increase the correct output so those are three reasons i want you to
know very well for that thermodynamic uh i don't know if i have time i love this
picture i i it may be too much for you but i love this is the most important picture and heart failure for me
maybe i'll go over it another time but the idea here this is the starting curve it's correct
output to volume there is another curve that everybody talks about it's the pressure
volume loop or pressure volume relationship that's very different from starling okay it's a very different
curve it's the compliance curve you will see sometimes a loop
illustrated okay and this is part of that loop this is just the diastolic portion of what we call pressure volume
loop for me to illustrate the compliance the ventricular compliance
when you have the severe systolic dysfunction you're far off on the stalling curve on the
uh on the after on the sorry the preload and that creates a high wedge pressure but the interesting thing
thing you can keep dropping that pre-load volume you can keep dropping it all the way to here and actually it's
been shown so you can really dramatically drop that watch pressure and it has been shown that actually a
wedge pressure in that paper 10 to 12 millimeter of mercury provides you the optimum correct output in
patient with severe systolic heart failure okay that's not the case in diastolic heart
failure because the pressure volume relationship is more steep so in diastolic heart failure by
definition the solid cafe the ultimate hemodynamic definition is you have normal diastolic volume
normal lv diastolic volume yet high lv diastolic pressure that's the ultimate definition of
diastolic heart failure everything else we do tries to be a surrogate of that simple
fact okay so this is the pressure so those are cases where it's hard
so diastolic dysfunction is harder to diaries because their wedge pressure is high
at the normal volume that is necessary to produce a normal carriage output so they are more difficult to diagnose less
likely to to tolerate diuresis and loading changes that's not the case on systolic heart
failure where you can you know you can tolerate a dramatic
drop in volume and an even more dramatic drop in which pressure okay i will stop here i
i hope i didn't give too much or too confusing information any questions
that was really good dr hannah any questions from anyone wasn't confusing i hope uh it's a lot of
information but uh i don't know if you can see the chat but you know
i i think people really liked it i personally loved it so oh good good i will uh hopefully give
you more uh as we go as as i discuss with dr rossen
um we will see you know i'll give you some hemodynamic discussions tracings more
tracing so for those especially first year who feel overwhelmed with the info
you know we will get time to practice whether in the lab or through other sessions
all right good good thank you so much all right thank you thank you everybody and
welcome thank you
Atrial pressure tracings feature a-wave, x-descent, v-wave, and y-descent with an upsloping diastolic pattern following the P wave by about 80 ms. Ventricular pressures show a plateau during the ST segment and a similar diastolic upslope. Arterial pressure tracings have a dicrotic notch and a downsloping diastolic phase with peaks aligning to the ST segment. These distinctions help clinicians identify each waveform and understand cardiac cycle phases.
Specific waveform abnormalities correlate with distinct conditions; for example, deep x and y descents suggest constrictive pericarditis or restrictive cardiomyopathy, especially pronounced during inspiration. A flat y descent indicates cardiac tamponade due to suppressed early ventricular filling. Large v waves signal overwhelmed atrial compliance as seen in severe tricuspid regurgitation and right ventricular failure. Recognizing these patterns aids in precise diagnosis.
PCWP serves as a surrogate for left atrial pressure and closely approximates left ventricular end-diastolic pressure (LVEDP), reflecting left heart filling pressures. Accurate catheter wedging is essential because improper placement (under-wedging) can result in misleading measurements mimicking pulmonary artery pressures. Monitoring PCWP helps assess left heart function and guide treatment in heart failure.
The a-wave in ventricular pressure tracing corresponds to atrial contraction and effectively marks LVEDP. Elevated a-wave amplitude suggests increased LV filling pressure, which is an early indication of systolic or diastolic dysfunction before wedge pressure changes appear. Thus, tracking the a-wave provides clinicians with a sensitive measure of left ventricular compliance and function.
In systolic heart failure, the Frank-Starling curve shifts downward and plateaus earlier, sometimes even declining at high preload levels, indicating limited stroke volume response to increased filling. Contrary to normal hearts, diuresis in low blood pressure heart failure patients may improve cardiac output by reducing mitral regurgitation, interventricular constraint, and afterload. This understanding supports tailored volume management and afterload reduction strategies.
Clinicians differentiate waveforms by analyzing their timing relative to ECG events, waveform morphology including slopes (upsloping diastole for atrial/ventricular, downsloping for arterial), and distinctive features like the arterial dicrotic notch. Recognizing these nuances ensures accurate interpretation of cardiac pressures and guides appropriate clinical interventions.
Ventricularized right atrial pressure, characterized by nearly simultaneous right atrial and right ventricular systolic pressures, typically occurs in massive tricuspid regurgitation. It results in jugular venous pulsations that resemble arterial pulse. Recognizing this waveform abnormality helps diagnose severe valve disease and right heart failure, informing surgical or medical management options.
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