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Hemodynamics of valvular disorders as measured by
cardiac catheterization
Author: Morton J Kern, MD, MSCAI, FAHA, FACC
Section Editors: Catherine M Otto, MD, Donald Cutlip, MD
Deputy Editor: Susan B Yeon, MD, JD, FACC
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2022. | This topic last updated: Mar 06, 2020.
INTRODUCTION
Pressure waveforms obtained during cardiac catheterization can be used to diagnose and
evaluate congenital or acquired valvular heart disease [1-3]. However, echocardiography
provides adequate diagnostic data in most patients.
In a minority of patients with valvular heart disease (<5 percent), further evaluation with
invasive intracardiac pressure measurements and/or angiography is needed because the
echocardiographic data are nondiagnostic or there is a discrepancy between the clinical
presentation and echocardiographic findings. Invasive hemodynamic measurements are also
used to monitor therapeutic percutaneous procedures such as transcatheter aortic valve
replacement, transcatheter mitral valve repair with a clip, and balloon valvotomy.
Coronary angiography is often needed before transcatheter valve implantation or surgery,
but hemodynamic measurements are not recommended if noninvasive data are diagnostic.
An overview of the hemodynamics of stenotic and regurgitant valvular lesions, as measured
by cardiac catheterization, will be provided here. The clinical characteristics of valvular heart
disease are discussed separately.
AORTIC STENOSIS
Regardless of etiology, stenosis of the aortic valve causes obstruction of blood flow from the
left ventricle (LV) to the aorta. As a result, there is a systolic pressure gradient across the
valve with a higher pressure in the LV than the aorta [4]. As discussed separately, valvular
®

aortic stenosis should be distinguished from subvalvular and supravalvular aortic stenosis.
(See "Clinical manifestations and diagnosis of aortic stenosis in adults".)
Echocardiography has largely supplanted cardiac catheterization in the evaluation and
monitoring of patients with aortic stenosis ( table 1). The 2014 American Heart
Association/American College of Cardiology (AHA/ACC) guidelines recommended cardiac
catheterization for assessment of aortic stenosis if noninvasive data are nondiagnostic or if
there is a discrepancy between clinical and echocardiographic evaluation [1]. (See "Clinical
manifestations and diagnosis of aortic stenosis in adults".)
There is some risk of cerebral embolization associated with crossing the aortic valve in
patients with severe calcific aortic stenosis; as a result, this approach should be avoided if not
required [5,6]. (See "Stroke after cardiac catheterization", section on 'Incidence'.)
The separate issue of coronary angiography at the time of aortic valve replacement to
identify patients who might also benefit from coronary artery bypass graft surgery is
discussed elsewhere. (See "Indications for valve replacement for high-gradient aortic
stenosis in adults", section on 'Concomitant coronary revascularization'.)
Aortic valve gradient — A precise assessment of the aortic valve gradient can be obtained
by the simultaneous measurement of the aortic and LV pressure assessed with a dual lumen
pigtail catheter measuring pressure above and below the aortic valve within the LV. For
research purposes, dual high fidelity transducer catheters are also available ( figure 1).
However, if the aortic pressure is estimated from peripheral arterial pressure, realignment of
the pressure tracing is necessary since the peripheral arterial pressure is delayed by wave
transmission to the extremity compared with the central aortic pressure ( waveform 1 and
waveform 2). (See "Aortic valve area in aortic stenosis in adults".)
Although the most common qualitative assessment of a transvalvular gradient in clinical
practice is the observation of pressure during LV catheter pull back from the LV to a level just
above the aortic valve, it is not useful for quantitative calculations.
The time-honored method of evaluating the severity of aortic stenosis is a calculation of
aortic valve area (AVA in cm ) based upon the formulations described by Gorlin and Gorlin
[7]:
AVA = (SV ÷ SEP) ÷ (44.3 x [sq rt ΔP])
where SV = stroke volume (mL per beat), SEP = systolic ejection period (sec per beat), and ΔP
= mean systolic pressure gradient between the LV and aorta (mmHg). (See "Aortic valve area
in aortic stenosis in adults", section on 'Gorlin equation for aortic valve area'.)
2

Aortic pressure — A reduced aortic pressure with delayed rise in the pressure upstroke and
the existence of a pressure gradient between the LV and the aorta are the principal findings
related to the aortic pressure among patients with aortic valvular stenosis ( figure 1). The
rise in aortic pressure is slow and delayed compared with the pressure rise in the LV.
Left ventricular pressure — In addition to an increased systolic pressure, abnormalities of
diastolic pressure may be observed because of LV hypertrophy with reduced compliance.
Although the mean LV diastolic pressure may be normal or elevated, the LV end-diastolic
pressure is most commonly elevated, a result of filling of the noncompliant LV after atrial
systole. Thus, there is usually a prominent "a" wave with increased amplitude ( figure 2 and
figure 3).
Left atrial or pulmonary capillary wedge pressure — The left atrial pressure tracing shows
large "a" waves because of the combination of a hypertrophied left atrium and a stiff or
noncompliant LV; this reflects the increased pressure generated during atrial contraction and
filling of the LV.
Low gradient valvular aortic stenosis — An important group of patients with aortic
stenosis consists of symptomatic patients who have low gradient aortic stenosis, defined as a
small transvalvular gradient (<30 mmHg), and a low cardiac output, with a calculated aortic
valve area of ≤0.7 cm [8]. In these patients, there is often doubt about whether the aortic
valve is sufficiently stenotic to account for the symptoms or the patient has only mild aortic
valvular disease and the symptoms are resulting from a significant reduction in LV function
due to a myopathic problem. (See "Clinical manifestations and diagnosis of low gradient
severe aortic stenosis".)
The concern about low gradient aortic stenosis is justified, since the Gorlin formula is flow-
dependent and tends to underestimate the valve area when the cardiac output is low, ie, <3
L/min [9,10]. Since cardiac output measured at the time of cardiac catheterization greatly
influences the clinical evaluation and subsequent management decisions, the use of valvular
resistance, which is a useful adjunct to the Gorlin formula in this clinical situation, and
recalculation of the aortic valve area after a pharmacologic stimulation of cardiac output
(such as with dobutamine) are often required for further evaluation to facilitate the decision
regarding surgery in these patients (see "Aortic valve area in aortic stenosis in adults",
section on 'Aortic valve resistance'). Maneuvers that increase cardiac output will almost
always increase calculated valve area, except in truly severe aortic stenosis. (See "Clinical
manifestations and diagnosis of low gradient severe aortic stenosis".)
Distinguishing aortic stenosis from hypertrophic cardiomyopathy — Certain
characteristics of the pressure gradient help distinguish HCM from aortic valvular disease. As
examples, the obstruction in HCM, unlike that due to aortic valvular disease, is associated
with the following features:
2

The hemodynamics of hypertrophic cardiomyopathy are discussed separately. (See
"Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".)
CHRONIC AORTIC REGURGITATION
Due to inadequate valvular closure, aortic regurgitation results in the backward flow of blood
from the aorta to the left ventricle (LV) during diastole. This may be due to a primary
abnormality of the valve leaflets, the wall of the aortic root, or both. (See "Clinical
manifestations and diagnosis of chronic aortic regurgitation in adults".)
Despite the absence of a fixed stenotic lesion in most patients with aortic regurgitation, the
large stroke volume crossing the aortic valve (which has a fairly fixed diameter) may
infrequently result in a small systolic gradient, which reflects "relative" stenosis due to high
flow during LV ejection.
In aortic regurgitation, the LV stroke volume (A) (measured angiographically) is greater than
the forward stroke volume (F) (determined by the Fick cardiac output); the difference is the
regurgitant fraction (RF) that leaks back into the LV during each cardiac cycle.
RF = [stroke volume (A) - stroke volume (F)]/stroke volume (A)
The 2014 American College of Cardiology/American Heart Association guidelines
recommended cardiac catheterization in patients with aortic regurgitation when noninvasive
tests are inconclusive or provide discrepant results from clinical findings [1]. Cardiac
catheterization should be performed with aortic root angiography and measurement of LV
pressure to assess the severity of the regurgitation, aortic root size, and LV function.
Aortic pressure — The aortic pressure tracing in aortic regurgitation reveals a rapid
upstroke (due to augmented LV contractility) and an increased systolic pressure (due to
increased stroke volume). However, a rapid fall in the aortic pressure results from the
It is within the LV (intraventricular) ( waveform 3).
●
It may be variable and labile. When obstructive, the aortic pressure has a characteristic
"spike and dome" configuration of early LV obstruction.
●
The timing and upstroke of the initial LV and the aortic pressure tracings are similar and
rapid in upstroke (as compared with slow upstroke in aortic stenosis).
●
A premature ventricular contraction can distinguish aortic stenosis from HCM.
Postextrasystolic potentiation produces an increase in LV contractility, which may result
in an increase in SAM and outflow obstruction, and a decreased aortic pulse pressure
(Brockenbrough-Braunwald-Morrow sign).
●

regurgitation. At the end of diastole, near equalization of the aortic and LV pressures occurs
because of the continuous leaking of blood back into the LV producing a rapid rise in LV
pressure across diastole. The pulse pressure, which is defined as the systolic minus the
diastolic pressure, is therefore widened, since the systolic and diastolic pressures are raised
and reduced, respectively ( figure 4).
Left ventricular pressure — The LV end-diastolic volume is increased; however, the LV end-
diastolic pressure is usually normal or only slightly elevated since LV compliance is also
increased as the LV compensates ( figure 4). The LV systolic pressure may be normal or
elevated, because of the increased diastolic volume and augmented LV contractility.
Left atrial pressure — With isolated aortic regurgitation, the left atrial pressures and
waveform are usually normal. However, if LV hypertrophy is present, there may be a
somewhat increased "a" wave, similar to that observed in aortic stenosis.
ACUTE AORTIC REGURGITATION
With acute aortic regurgitation, the usual adaptation of the left ventricle (LV) to chronically
large regurgitant volumes (eg, enhanced compliance) has not had time to develop. As a
result, the increased diastolic volume in the LV leads to a marked elevation in LV pressures.
(See "Acute aortic regurgitation in adults".)
The LV pressure tracing reveals a steep rise in diastolic pressure and a markedly elevated LV
end-diastolic pressure (which is equivalent to the aortic end-diastolic pressure). Since forward
stroke volume declines, aortic systolic pressure is reduced and the pulse pressure is
therefore smaller. In addition, the left atrial pressure is elevated. The pressure tracing shows
a small "a" and "v" wave, and the nadir of the "x" and "y" descents are less than normal.
CHRONIC MITRAL REGURGITATION
Regurgitation of the mitral valve produces a backflow of blood from the left ventricle (LV) to
the left atrium during systole. This disorder may be due to abnormalities of the mitral valve
leaflets, chordae tendineae, papillary muscles, or annulus ( figure 5), all of which result in
inadequate closure (also known as coaptation) of the two mitral leaflets. (See "Clinical
manifestations and diagnosis of chronic mitral regurgitation".)
The regurgitant flow produces a large left atrial pressure wave immediately with the onset of
ventricular systole ( waveform 4). During the initial part of diastole, the left atrium rapidly
decompresses with a large antegrade flow to the LV.

In mitral regurgitation, the LV stroke volume (A) (measured angiographically) is greater than
the forward stroke volume (F) (determined by the Fick cardiac output); the difference is the
regurgitant fraction (RF) that leaks back into the left atrium during each cardiac cycle:
RF = [stroke volume (A) - stroke volume (F)]/stroke volume (A)
Left atrial pressure — With chronic mitral regurgitation, the direct transseptal
measurement of the left atrial pressure demonstrates a marked pressure increase with the
very onset of systole, thereby producing a tall "v" wave. Since the "c" wave may not be
apparent, this has also been termed a "c-v" wave ( waveform 4 and waveform 5).
The height of the 'v' wave is a sensitive but not a specific marker for mitral regurgitation;
these waves are frequently associated with a ventricular septal defect and with disorders
associated with altered compliance and pressure-volume relationships within the atrial and
ventricular chambers.
With chronic mitral regurgitation, the LV and left atrium directly communicate during systole.
However, despite the large volume of blood in the left atrium, the mean left atrial pressure
may be normal or only slightly increased; this is largely due to a very compliant left atrium,
which dilates in response to the volume overload.
The amplitude of the tall "v" wave is therefore less than that of LV systole. By comparison,
the amplitude of the "a" wave is often reduced because of left atrial distension and
dysfunction. Left atrial pressure in diastole is normal and is similar to the LV diastolic
pressure ( waveform 5).
The pressure-volume curve produces different "v" waves depending upon volume and left
atrial compliance ( figure 6). With a left atrium of low compliance, increasing pressure is
obtained with increasing flow or volume in the left atrium; in this setting, a large "v" wave
can be associated with a small increase in pressure. By comparison, a higher compliance of
the left atrium would yield a much smaller "v" wave. The administration of vasodilators
frequently shifts the pressure-volume curve to a lower level.
Left ventricular pressure — In chronic mitral regurgitation, the LV is volume overloaded
due to the excess blood volume (generated during the prior systolic regurgitant beat) flowing
during diastole from the left atrium. However, since the compliancy of the LV increases, the
LV systolic and diastolic pressures are normal or only slightly increased. Although the LV
stroke volume is increased, the forward stroke volume is normal because a part of the stroke
volume regurgitates back into the left atrium. The LV pressure waveforms in systole and
diastole are therefore normal.
An assessment of the severity of mitral regurgitation uses the ratio of the area under the V
wave to the LV systolic area (Va/LVa) obtained during transseptal catheterization. In this first

report of this methodology, the Va/Lva was significantly lower in patients with 0-1+ MR
compared with =2+ MR (0.14 versus 0.23) [11].
ACUTE MITRAL REGURGITATION
With acute mitral regurgitation, the left ventricle (LV) and (more importantly) the left atrium
have not had time to adapt to the regurgitant volume overload, resulting in low compliance
chambers. As a result, with the onset of systole and the large volume of regurgitant blood
flow, the left atrial pressure rises abruptly, causing a very tall "v" wave. Because of this "v"
wave, the pressure gradient between the left atrium and LV declines by the end of systole;
the amplitude of the "v" wave and that of LV systole are nearly equivalent. The diastolic
pressure of the LV is increased because of an increase in the end-diastolic volume within an
undilated and noncompliant chamber.
MITRAL STENOSIS
In pure mitral stenosis, there is impairment of blood flow from the left atrium into the left
ventricle (LV), resulting in a pressure gradient between the two chambers during diastole.
(See "Clinical manifestations and diagnosis of rheumatic mitral stenosis".)
The 2014 American Heart Association/American College of Cardiology valve guidelines note
that adequate assessment of mitral stenosis is generally obtained by transthoracic
echocardiography, occasionally supplemented by transesophageal echocardiography [1].
Cardiac catheterization is indicated when noninvasive evaluation is nondiagnostic or if
clinical and echocardiographic findings are discordant.
Mitral valve gradient — In the cardiac catheterization laboratory, the severity of mitral
stenosis as reflected by the mean mitral valve gradient (MVG) is measured during diastole by
the simultaneous comparison of the LV pressure (obtained with an LV catheter positioned
retrogradely from the aorta), and the left atrial pressure (measured directly using a
transseptal catheter or indirectly with a pulmonary artery catheter in the wedged position
[PCWP]) ( waveform 6). The MVG is the difference between the mean left atrial pressure
(MLAP) and the mean LV pressure (MLVP) during diastole. In most cases a gradient is
present, although it decreases during diastole because of slow but continuous left atrial
emptying. With atrial systole, however, the gradient increases and is markedly higher than
the LV end-diastolic pressure.
Since the diastolic filling period is important in the assessment of mitral valve gradients, the
heart rate's effect upon the mitral valve gradient is important. The gradient is higher with a

faster heart rate since less time is available for left atrial emptying with a reduced diastolic
period. By comparison, the gradient is lower with a slower heart rate.
Among patients in atrial fibrillation, the severity of mitral stenosis as assessed via the PCWP
may differ from that obtained with the direct measurement of left atrial pressure. Patients
who are in atrial fibrillation require planimetry and the average of valve gradients over at
least 10 cardiac cycles ( figure 7) [12]. These factors are evident at cardiac catheterization
and should be considered in the computation of mitral valve stenosis [13].
A simplified method for estimating the mean mitral valve gradient (MVG) has been
developed in which mean LV diastolic pressure is estimated as LVEDP/2 [14], thus
MVG = MLAP - (LVEDP/2)
One potential limitation of this simplified method is that tachycardia may reduce the
accuracy of the LV diastolic pressure estimate with resultant overestimation of valve stenosis
severity. One advantage of the simplified method is that it does not require simultaneous
recording of LV and left atrial diastolic pressures.
The time-honored method of evaluating the severity of mitral stenosis is a calculation of
mitral valve area (MVA in cm ) based upon the formulations described by Gorlin and Gorlin
[7]:
MVA = (SV ÷ DFP) ÷ (37.7 x [sq rt ΔP])
where SV = stroke volume (mL per beat), DFP = diastolic filling period (sec per beat), and ΔP =
mean diastolic pressure gradient between the left atrium and LV (mmHg). The Gorlin formula
is best applied to patients in sinus rhythm without mitral regurgitation, normal LV function,
and no other concomitant valve lesions.
Left atrial pressure — As a result of the impairment to blood flow during diastole, the
volume of blood in the left atrium and the mean left atrial pressure are both increased
during this period. After mitral valve opening, the pressure only gradually decreases and the
"y" descent is gradual. The "a" wave, which is due to left atrial contraction, is markedly
increased because of the stenosis ( waveform 6).
Left ventricular pressure — Since the valve abnormality is proximal to the LV, the pressure
waveforms are normal except for a reduced amplitude of the "a" wave. The LV end-diastolic
pressure may be lower than normal because of the impaired filling of the LV from the left
atrium.
TRICUSPID REGURGITATION
2

Tricuspid regurgitation produces a backflow of blood from the right ventricle to the right
atrium during systole. Inadequate closure of the three tricuspid leaflets results because of
abnormalities of the tricuspid valve leaflets, chordae tendineae, papillary muscles, or annulus
(see "Etiology, clinical features, and evaluation of tricuspid regurgitation"). It may also occur
with certain arrhythmias.
Tricuspid regurgitant flow produces a distinct right atrial pressure waveform with the
transmission of the regurgitant wave into the right atrium, the vena cava, and ultimately the
jugular veins ( figure 8) [15-17]. The manifestations of tricuspid regurgitant flow are
therefore evident by inspection of the neck veins.
Right atrial pressure — The right atrial pressure waveform with tricuspid regurgitation is
similar to that observed in the left atrium with chronic mitral regurgitation. Direct
measurement of right atrial pressure demonstrates a marked increase in pressure with the
very onset of systole, thereby producing a tall "v" wave ( figure 8 and waveform 7). Since
the "c" wave may not be apparent, this has also been termed a "c-v" or an S wave; it is
proportional to the severity of regurgitation in most patients. As with left atrial or pulmonary
wedge pressures, "v" waves on the right side of the heart are determined by the pressure-
volume compliance characteristics of the chamber. As a result, severe angiographic
regurgitation may be present with minimal "v" waves.
During systole in tricuspid regurgitation, the right ventricle and right atrium are in direct
communication. However, despite the large volume of blood in the right atrium, the mean
right atrial pressure may be normal or only slightly increased; this is largely a result of a very
complaint right atrium. The amplitude of the tall "v" wave is therefore less than the
amplitude of that observed in right ventricular systole. In addition, the amplitude of the "a"
wave is frequently reduced because of right atrial distension and reduced contractility. The
right atrial diastolic pressure is normal and is similar to the left ventricular diastolic pressure.
The effects of tricuspid regurgitation on the right atrium and inferior vena cava can be
assessed by measuring two pressures simultaneously, one from each of the two lumens of a
balloon-tipped pulmonary artery catheter. The waveform of the inferior vena cava is slower
in upstroke and in downstroke and is associated with reduced velocity. The blunted
waveform is due, in part, to the considerably higher capacity and compliance of the vena
cava compared with that of the right atrium. In addition, the mean right atrial pressure is
lower than that in the vena cava, with a 2 to 4 mmHg pressure gradient required for
maintenance of normal blood flow. The pressure gradient between the inferior vena cava
and right atrium occurs predominantly during the end of atrial diastole ( figure 8). In most
cases, superior vena cava flow has a time course similar to inferior vena cava flow.
Jugular venous pulsation — The jugular venous pulsation closely reflects events in the
right atrium and the venae cavae [18,19]. However, the change in pressure within the right

atrium is reflected principally by a change in volume for the venous system. Tricuspid
insufficiency often produces a prominent "v" wave that begins early, tending to obliterate the
"x" descent. In severe tricuspid regurgitation, the "v" wave begins with the "c" wave and
shows a broad plateau, terminating in a steep "y" descent. This wave has been termed the
regurgitant or "s" wave. However, neither prominent "v" waves (>15 mmHg) or an elevated
mean right atrial pressure (>12 mmHg) can reliably predict the presence of moderate or
severe tricuspid regurgitation although their absence is predictive of its absence [20].
In the setting of atrial fibrillation, nearly complete obliteration of the "x" descent is required
before the diagnosis of tricuspid insufficiency may be made from a venous pulse wave. With
normal sinus rhythm, changes in the venous pulse may be only a slight decrease in the "x"
descent equal or above the level of the "y" trough. In some patients, a separate systolic wave
may appear on the "v" wave ascent and be a clue (albeit obscure) to the presence of tricuspid
regurgitation [16].
A normal jugular venous pulse cannot be used to exclude tricuspid disease, since
regurgitation may infrequently be associated with a relative normal venous pulse wave. In
this setting, although the characteristic pulse waves may be absent at rest, they may be
elicited by inspiratory maneuvers or an increasing heart rate [16].
TRICUSPID STENOSIS
As with the hemodynamic abnormalities observed in mitral stenosis, tricuspid stenosis
produces an obstruction of blood flow from the right atrium to the right ventricle, resulting
in a diastolic gradient between these two chambers.
Right atrial pressure — Because of the impairment to blood flow during diastole, the
volume of blood in the right atrium and the mean right atrial pressure is increased. After
tricuspid valve opening, the pressure slowly decreases and the "y" descent is gradual. The "a"
wave is markedly increased because of the stenosis.
Right ventricular pressure — Since the valve abnormality is proximal to the right ventricle,
the pressure waveforms are normal except for a reduced amplitude of the "a" wave. The
right ventricular end-diastolic pressure may be lower than normal because of the impaired
filling of the right ventricle from the right atrium.
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Cardiac valve
disease".)

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SUMMARY AND RECOMMENDATIONS
th th
th th
Basics topic (see "Patient education: Cardiac catheterization (The Basics)")
●
Echocardiography is the primary modality for diagnosis and evaluation of valvular
disease. In a small minority of patients, further evaluation with invasive intracardiac
pressure measurements and/or angiography is needed because the echocardiographic
data are nondiagnostic or discrepant with clinical findings. (See 'Introduction' above.)
●
Aortic valve disease
●
Cardiac catheterization is recommended for hemodynamic assessment of aortic
stenosis in older adults only in symptomatic patients in whom noninvasive tests are
inconclusive or provide discrepant results. There is some risk of cerebral
embolization associated with crossing a calcific stenotic aortic valve. (See 'Aortic
stenosis' above.)
•
A precise assessment of the aortic valve gradient can be obtained by the
simultaneous measurement of the aortic pressure (as assessed with a pigtail
catheter above the aortic valve), and the left ventricular (LV) pressure (measured
using the transseptal technique or using dual lumen fluid filled catheter or for
research dual high fidelity transducer catheter) ( figure 1). (See 'Aortic valve
gradient' above.)
•
The aortic pressure tracing in aortic regurgitation reveals a rapid upstroke (due to
augmented LV contractility) and an increased systolic pressure (due to increased
•

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REFERENCES
stroke volume) and a rapid fall to a low diastolic pressure (yielding a widened pulse
pressure). (See 'Chronic aortic regurgitation' above.)
With acute aortic regurgitation, there is a steep rise in LV diastolic pressure and a
markedly elevated LV end-diastolic pressure (which is equivalent to the aortic end-
diastolic pressure). Since forward stroke volume declines, aortic systolic pressure is
reduced and the pulse pressure is therefore smaller. (See 'Acute aortic regurgitation'
above.)
•
Mitral valve disease
●
With chronic mitral regurgitation, the regurgitant flow produces a large left atrial
pressure wave immediately with the onset of ventricular systole ( waveform 4).
During the initial part of diastole, the left atrium rapidly decompresses with a large
antegrade flow to the LV. (See 'Chronic mitral regurgitation' above.)
•
With acute mitral regurgitation, the left atrial pressure rises abruptly with the onset
of systole, causing a very tall "v" wave. Because of this "v" wave, the pressure
gradient between the left atrium and LV declines by the end of systole; the
amplitude of the "v" wave and that of LV systole are nearly equivalent. (See 'Acute
mitral regurgitation' above.)
•
The severity of mitral stenosis as reflected by the mean mitral valve gradient (MVG)
is measured during diastole by the simultaneous comparison of the LV pressure
(obtained with an LV catheter positioned retrogradely from the aorta), and the left
atrial pressure (measured directly using a transseptal catheter or indirectly with a
pulmonary artery catheter in the wedged position [PCWP]) ( waveform 6). (See
'Mitral valve gradient' above.)
•
Tricuspid valve disease
●
Tricuspid regurgitant flow produces a distinct right atrial pressure waveform with
the transmission of the regurgitant wave into the right atrium, the vena cava, and
ultimately the jugular veins ( waveform 7). (See 'Tricuspid regurgitation' above.)
•
Tricuspid stenosis produces an obstruction of blood flow from the right atrium to
the right ventricle, resulting in a diastolic gradient between these two chambers.
(See 'Tricuspid stenosis' above.)
•

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17. Tavel ME. The jugular pulse tracing: Its clinical application. In: Clinical Phonocardiograph
y and External Pulse Recording, 2, Year Book Medical Publishers, Chicago 1972. p.207.

18. Morgan BC, Abel FL, Mullins GL, Guntheroth WG. Flow patterns in cavae, pulmonary
artery, pulmonary vein, and aorta in intact dogs. Am J Physiol 1966; 210:903.
19. BRECHER GA, HUBAY CA. Pulmonary blood flow and venous return during spontaneous
respiration. Circ Res 1955; 3:210.
20. Pitts WR, Lange RA, Cigarroa JE, Hillis LD. Predictive value of prominent right atrial V
waves in assessing the presence and severity of tricuspid regurgitation. Am J Cardiol
1999; 83:617.
Topic 8127 Version 18.0

GRAPHICS
Stages of valvular aortic stenosis
Stage Definition
Valve
anatomy
Valve
hemodynamics
Hemodynamic
consequences
Symptoms
A At risk of AS Bicuspid
aortic valve
(or other
congenital
valve
anomaly)
Aortic valve
sclerosis
Aortic V <2
m/s
None None
B Progressive AS Mild to
moderate
leaflet
calcification
of a bicuspid
or trileaflet
valve with
some
reduction in
systolic
motion or
Rheumatic
valve
changes
with
commissural
fusion
Mild AS: Aortic
V 2.0 to 2.9
m/s or mean ΔP
<20 mmHg
Moderate AS:
Aortic V 3.0 to
3.9 m/s or mean
ΔP 20 to 39
mmHg
Early LV
diastolic
dysfunction
may be
present
Normal LVEF
None
C: Asymptomatic severe AS
C1 Asymptomatic
severe AS
Severe
leaflet
calcification
or
congenital
stenosis
with
severely
reduced
leaflet
opening
Aortic V ≥4
m/s or mean ΔP
≥40 mmHg
AVA typically ≤1.0
cm (or AVAi ≤0.6
cm /m )
Very severe AS is
an aortic V ≥5
m/s or mean ΔP
≥60 mmHg
LV diastolic
dysfunction
Mild LV
hypertrophy
Normal LVEF
None:
Exercise
testing is
reasonable
to confirm
symptom
status
C2 Asymptomatic
severe AS with
Severe
leaflet
Aortic V ≥4
m/s or mean ΔP
LVEF <50% None
max
max
max
max
2
2 2
max
max

LV
dysfunction
calcification
or
congenital
stenosis
with
severely
reduced
leaflet
opening
≥40 mmHg
cm (or AVAi ≤0.6
cm /m )
D: Symptomatic severe AS
D1 Symptomatic
severe high-
gradient AS
Severe
leaflet
calcification
or
congenital
stenosis
with
severely
reduced
leaflet
opening
Aortic V ≥4
m/s or mean ΔP
≥40 mmHg
cm (or AVAi ≤0.6
cm /m ) but may
be larger with
mixed AS/AR
LV diastolic
dysfunction
LV
hypertrophy
Pulmonary
hypertension
may be
present
Exertional
dyspnea o
decreased
exercise
tolerance
Exertional
angina
Exertional
syncope o
presyncop
D2 Symptomatic
severe low-
flow/low-
gradient AS
with reduced
LVEF
Severe
leaflet
calcification
with
severely
reduced
leaflet
motion
AVA ≤1.0 cm
with resting aortic
V <4 m/s or
mean ΔP <40
mmHg
Dobutamine
stress
echocardiography
shows AVA ≤1.0
cm with V
≥4 m/s at any
flow rate
LV diastolic
dysfunction
LV
hypertrophy
LVEF <50%
HF
Angina
Syncope o
presyncop
D3 Symptomatic
severe low-
gradient AS
with normal
LVEF or
paradoxical
low-flow
severe AS
Severe
leaflet
calcification
with
severely
reduced
leaflet
motion
AVA ≤1.0 cm
with aortic V
<4 m/s or mean
ΔP <40 mmHg
Indexed AVA ≤0.6
cm /m
Stroke volume
index <35 mL/m
Measured when
patient is
normotensive
(systolic BP <140
mmHg)
Increased LV
relative wall
thickness
Small LV
chamber with
low stroke
volume
Restrictive
diastolic filling
LVEF ≥50%
HF
Angina
Syncope o
presyncop
2
2 2
max
2
2 2
2
max
2
max
2
max
2 2
2

AS: aortic stenosis; V : maximum aortic velocity; ΔP: pressure gradient; LV: left ventricular; LVEF: left
ventricular ejection fraction; AVA: aortic valve area; AVAi: aortic valve area indexed to body surface
area; AR: aortic regurgitation; HF: heart failure; BP: blood pressure.
Reproduced from: Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC Guideline for the Management of
Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014; 63:e57. Table used with the permission
of Elsevier Inc. All rights reserved.
Information still current as of 2021, as found in: Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA
guideline for the management of patients with valvular heart disease: a report of the American College of
Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation
2021;143:e72.
Graphic 95630 Version 3.0
max

Pressures in aortic stenosis
Simultaneously recorded pressures from the left ventricle (LV) and
aorta (Ao) in a patient with aortic stenosis. There is a systolic
pressure gradient (shaded area) in which the LV systolic pressure is
greater than that in the aorta. The pressure gradient and systolic
ejection period (SEP, in sec/beat) are used in the Gorlin formula to
calculate the aortic valve area (aortic valve area = cardiac output ÷
[44.3 x SEP x HR x sq rt mean gradient]).
HR: heart rate.
Redrawn from Kern MJ (Ed). Cardiac Catheterization Handbook, 2nd ed.
Mosby-Year Book, St. Louis, 1995.

Central and peripheral aortic pressure tracings
Simultaneously recorded pressures from the aortic root (Ao) and femoral
artery (FA) demonstrate delayed transmission and a higher systolic
pressure in the femoral artery. There is smoothing of the waveform and
loss of the dicrotic notch.

LV and aortic pressure - high fidelity
LV and aortic pressures from dual high fidelity transducer catheter
during pullback across aortic valve. Note the matching of aortic
pressures between central locations.

Left ventricular pressure tracing in diastolic
dysfunction
The left ventricular pressure is initially recorded with a scale of 0 to
200 mmHg and then at 0 to 40 mmHg. Although the systolic and
diastolic pressures are normal, the pressure waveform in diastole is
abnormal; there is a continuing decline of pressure over the mid-
diastolic period (as opposed to the gradual rise seen in normal
subjects) with the pressure nadir occurring midway through the
diastolic period and there is a prominent "a" wave generated by left
atrial contraction.
Reproduced with permission from Kern MJ. ACC Current Journal Review,
1997.

LV and aortic pressures - two methods
LV and aortic pressures.
(A) Two high fidelity pressure transducers on single catheter across aortic
valve. Note normal LV diastolic waveform with early diastolic pressure as
lowest point with slow increase in pressure across diastole "a" wave after
atrial contraction.
(B) Fluid filled LV catheter and femoral sheath pressures. Note ringing
artifact of fluid filled systems. Note overshoot of femoral artery pressure
and delay in upstroke from central to peripheral location.
LV: left ventricular.

Invasive hemodynamic tracings of left ventricular and aortic pressures in hype
c cardiomyopathy and left ventricular outflow tract obstruction
Invasive hemodynamic tracings obtained during cardiac catheterization showing simultaneous left ventricu
(LV) and aortic pressures in a patient with hypertrophic cardiomyopathy (HCM) and left ventricular outflow t
(LVOT) obstruction. During the first five heart beats, with one catheter in the LV and another catheter in the
there is an 80 mmHg gradient across the left ventricular outflow tract. Following the fifth heart beat, the LV
catheter is pulled back into the aorta, where both catheters are now measuring aortic pressure, and no gra
is present.
Courtesy of Martin Maron, MD.

Aortic regurgitation hemodynamics
Aortic regurgitation. Note upsloping LV diastolic pressure and wide pulse
pressure.

Mitral valve structure

Pressure tracings in mitral regurgitation
Simultaneously recorded pressures from the left atrium (LA) and left
ventricle in a patient with mitral regurgitation. There is a tall "V"
wave in the LA occurring during ventricular systole, reflecting a
large regurgitant volume of blood ejected into the LA.
Redrawn from Kern MJ (Ed). Hemodynamic Rounds: Interpretation of
Cardiac Pathophysiology from Pressure Waveform Analysis. Wiley-Liss,
New York, 1993.

Left atrial and right atrial pressure in MR
A transseptal catheter is in the left atrium (LA) and the pressure
tracing shows large "v" waves as a result of mitral regurgitation
(MR). The "v" wave of 40 mmHg is twice the mean LA pressure which
is 20 mmHg. The asterisk shows where the catheter is pulled back to
the right atrium (RA); since the pressure tracing is continuous, it
accurately reflects the pressure gradient between the LA and RA.
The RA pressure is lower, and the a and v waves are diminutive
relative to the left side.
Redrawn from Kern MJ (Ed). Cardiac Catheterization Handbook, 2nd
Edition. Mosby-Year Book, Inc., St. Louis, 1995.

Left atrial pressure-volume relationship
The relationship between the volume within a chamber and the
resulting pressure defines chamber compliance or distensibility. The
top curve (red) is from a left atrium with low compliance; small
changes in volume result in marked changes in pressure. In this
situation large "v" waves due to mitral regurgitation will be seen.
The lower curve (blue) is from a left atrium that is very compliant;
changes in volume result in only small changes in pressure. In this
situation, the same degree of mitral regurgitation will cause small
"v" waves.

Mitral stenosis gradients
Mitral Stenosis. The LV and PCW (left side) is compared with LV and LA
pressures (transseptal) to demonstrate differences in mitral gradients.
LV: left ventricle; PCW: pulmonary capillary wedge; LA: left atrial

Effect of heart rate on mitral valve gradient
Simultaneously recorded pressures from the left atrium (LA) and left
ventricle (LV) in a patient with mitral stenosis who has a persistent
diastolic gradient (shaded areas) across the mitral valve. Top panel:
When the RR interval is shorter, the mean pressure gradient is
greater and the mitral valve area smaller. Bottom panel: A long RR
interval results in a gradual equilibration of the LA and LV pressures
and the mean gradient is smaller. There is no pressure gradient
present by the end of diastole.
Adapted from Kern, MJ (Ed). Hemodynamic Rounds: Interpretation of
New York, 1993.

Tricuspid regurgitation
Top panel: Right atrial (RA) and right ventricular (RV) pressure
tracings, obtained simultaneously, show elevated RA and RV
pressures. A large "V" wave is seen in the RA during ventricular
systole. Bottom panel: The venous pulse of the regurgitation can be
detected in the femoral vein. The femoral vein pressure is slightly
higher than that of the right atrium, a pressure gradient that
maintains normal blood flow.
New York, 1993.

Tricuspid regurgitation due to pulmonary
hypertension
Pressures, simultaneously recorded in the right atrium (RA) and
right ventricle (RV), are markedly elevated in tricuspid regurgitation
due to pulmonary hypertension, and there is a tall "V" wave in the
RA.
New York, 1993.

Contributor Disclosures
Morton J Kern, MD, MSCAI, FAHA, FACC Speaker's Bureau: Abbott [Coronary blood flow]; St Jude
Medical [Coronary blood flow]; Philips [Coronary blood flow]; Volcano Therapeutics [Coronary blood
flow]; Opsens [Coronary blood flow]; Acist Medical [Coronary blood flow]; Heartflow [Coronary blood
flow]; Boston Scientific Company [Coronary blood flow]. All of the relevant financial relationships listed
have been mitigated. Catherine M Otto, MD No relevant financial relationship(s) with ineligible
companies to disclose. Donald Cutlip, MD Consultant/Advisory Boards: CeloNova [Coronary artery
stent]; MedAlliance [Drug-eluting balloon]. All of the relevant financial relationships listed have been
mitigated. Susan B Yeon, MD, JD, FACC No relevant financial relationship(s) with ineligible companies
to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
Conflict of interest policy
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