Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3590_Библиотеки_им_академика_М_И_Перельмана
.pdf
4—HEMODYNAMICS FOR THE STRUCTURAL INTERVENTIONALIST 45
52
https://t.me/medicina_free
atmospheric pressure, and so require calibration to the fluid-filled pressure tracing. Once properly
calibrated, the pressure wire can even be advanced beyond the end of the catheter to allow measurement of valvular or subvalvular pressure gradients through a single end-hole catheter.
Volumetric Flow
In addition to direct pressure measurements, cardiac catheterization allows calculation of the CO
and forward flow to the body through either the thermodilution or Fick method.
THERMODILUTION CARDIAC OUTPUT
The thermodilution method involves injecting saline through the proximal port of a Swan-Ganz
catheter, with measurement of the area under the curve of temperature change over time in the distal
catheter tip. In low-output states there is a larger area under the curve due to the longer time required
for the temperature curve to return to its baseline, and therefore the area under the curve is inversely
proportional to cardiac output. This can be inaccurate in the setting of (1) severe tricuspid regurgitation (due to back and forth flow underestimating cardiac output),
dissipates temperature to the surrounding cardiac structures, decreasing area under the curve and
thereby overestimating cardiac output), (3) atrial fibrillation (with irregular cycle lengths during repeated saline injections), or (4) left-to-right shunts (where the thermodilution output represents flow
through the right heart, including shunt fraction and not systemic cardiac output).
FICK CARDIAC OUTPUT
The Fick method relies on measuring body oxygen consumption (VO2) in mL/min, which can be
directly measured at the mouth using a metabolic cart. In addition, sampling of the arterial and
pulmonary artery oxygen saturations can be used to determine respective O
serum hemoglobin (Hb) is also known. Because each 1 g/dL of Hb can bind to 1.34 mL of O
100% saturated, O
four measurements (Hb, VO
The premise of the Fick principle relies on the fact that the difference between O
the body in mL/min (CO 3 arterial O
(CO 3 mixed venous O
These values are related as
content can then be calculated as 1.34 3 Hb 3 % saturation. From the above
2
, arterial and venous saturation), CO can ultimately be calculated.
2
content) and O2 efflux from the body after tissue extraction
content) should equal the body oxygen consumption.
2
2
1
(2) very low CO (where low flow
contents in mg/dL if
2
delivery to
2
if
2
VO (inmL/min) Odelivery(in mL/min)O
22
VO =(CO arterial O× content) (COmixed venous Ocontent)
22
which can be rearranged as
CO(L /min)VO/[arterialvenousO content
where 10 is the factor to convert dL to L.
The Fick method using measured VO
method to calculate CO when thermodilution values are prone to error (see earlier). For maximal
accuracy, VO
must be directly measured at the mouth using a metabolic cart (and therefore
2
patients must not be on inhaled oxygen during this assessment). Although nomograms are
available to provide estimates of VO
or deviate from normal physiologic states, such as the critically ill, anxious, or sedated patient, and
this estimated Fick CO is then inferior to thermodilution outputs.
efflux(inmL/min)
23
5522 ddifference] 1033
22
is valid in all disease states and should be the preferred
2
, this introduces error, particularly when patients are obese2
2
22
2
3
46 1—BUILDING BLOCKS OF STRUCTURAL INTERVENTION
https://t.me/medicina_free
Shunt Calculation
Understanding shunt calculation is critical for the structural interventionalist, who is often called
upon to evaluate for closure of shunts if hemodynamically significant. If a left-to-right shunt is
significant, there will be an increase in venous saturation (“step up”) by .7% to 8% from before
to after the level of shunting. If a right-to-left shunt is significant, there will be systemic desaturation that does not correct with 100% O
from V/Q mismatch as the cause of hypoxemia can be done either by the administration of 100%
O
, as noted earlier, or by contrast echocardiography, or direct measurement of saturations in the
2
pulmonary veins and left atrium. Quantifying hemodynamic significance relies on calculating a
shunt fraction from measured systemic and pulmonary flow.
With a working knowledge of the Fick principle, all shunts can be easily calculated using
some basic principles:
n
Pulmonary or systemic flow is calculated by the Fick method using the inflow and outflow
saturations that flow into and out of the lungs/body, respectively.
n
Pulmonary flow (Qp) using pulmonary artery and pulmonary vein saturation (which
equals arterial saturation if there is no right-to-left shunt)
n
Systemic flow (Qs) using arterial saturation and mixed venous saturation (which equals
pulmonary artery saturation if there is no left-to-right shunt)
n
If there is a left-to-right shunt, systemic flow should be calculated using the venous saturation
from before the level of the shunt.
n
Mixed venous saturation can be estimated by the Flamm formula as [3 3 SVC saturation
1 IVC saturation] / 4. This represents the hypothetical pulmonary artery saturation that
would exist if there were no left-to-right shunt
n
A Qp/Qs .1.5 represents a significant left-to-right shunt. Because flow is inversely
proportional to AVO
D (arteriovenous oxygenation difference) by the Fick principle,
2
Qp/Qs can also be calculated as the ratio of difference in saturation across the systemic
circulation to the difference in saturation across the pulmonary circulation.
n
Qp/Qs 5 [Systemic 2 mixed venous saturation] / [Systemic 2 pulmonary arterial
saturation]
n
The absolute pulmonary and systemic flows can be calculated using the VO2 and AVO2D
in order to more accurately represent the absolute volumetric loading to the ventricle
from shunting in mL/min. The Qp/Qs will be identical to the value calculated earlier
from the saturation differences.
n
Determining pulmonary vascular resistance is important to determine safety for shunt
closure, but importantly, the pulmonary flow must be used for the pulmonary vascular
resistance (PVR) calculation.
n
If there is a right-to-left or bidirectional shunt present, then the calculation of shunt fraction
requires understanding of the concept of effective flow (Q
thetical flow to the body that would exist if there was no shunting. It therefore incorporates
the earliest left-sided saturation before any right-to-left shunting (i.e., pulmonary vein
saturation) and the earliest right-sided saturation before any left-to-right shunting (i.e.,
Flamm-based mixed venous saturation). If there was no shunting, then the pulmonary vein
and Flamm-based mixed venous saturation would have represented the hypothetical arterial and pulmonary artery saturations, and therefore the hypothetical systemic and forward
flow that would have occurred (i.e., Q
n
The actual pulmonary flow (Qp) can be calculated from the inflow saturation (pulmonary
artery saturation) and outflow saturation (pulmonary vein saturation).
n
Similarly, the actual systemic flow (Qs) can be calculated from the inflow satura-
tion (arterial saturation) and outflow saturation (Flamm-based mixed venous
saturation).
administration. Differentiating right-to-left shunting
2
). This represents the hypo-
eff
).
eff
4—HEMODYNAMICS FOR THE STRUCTURAL INTERVENTIONALIST 47
–20
100
120
140
160
180
Mean LAWP 11 31
https://t.me/medicina_free
n
The discrepancy between the calculated Qp and Qs and Q
will therefore represent the
eff
left-to-right and right-to-left shunt volume, respectively.
n
The Q
n
The amount of right-to-left shunting will account for the difference between Qs and Q
n
If there is a bidirectional shunt, the amount of left-to-right shunting will account for
the difference between Qp and Q
will always be lower than the Qp or Qs in the presence of a shunt.
eff
.
eff
eff
Intracardiac Pressures to Diagnose Structural
Heart Disease
Measuring absolute pressures provides important diagnostic information in terms of localizing
the hemodynamic lesion contributing to symptoms in an individual patient. For patients with
valvular and SHD, precise localization of pathology is important because many potential contributors exist to cause symptoms ranging from postoperative constriction, residual valvular disease,
pulmonary vascular remodeling, and intrinsic myocardial systolic and diastolic function.
LEFT HEART “FILLING” PRESSURES
An elevated left ventricular end diastolic pressure (LVEDP) localizes pathology to the level of the
left ventricle and provides a measure of preload, but it is important to recognize that the LVEDP and
LA pressure provide complementary, but not interchangeable, information. It is the mean LA pressure and not the LVEDP that more accurately reflects pulmonary venous pressure that is reflected to
the pulmonary capillary bed and right ventricle, and therefore answers the question of whether the
left heart contributes to dyspnea in any given patient (Fig. 4.1).
sure (PAWP) provides a convenient method to estimate LA pressure without transseptal access, and
4
The pulmonary arterial wedge pres-
.
80
60
40
20
0
Patient 1
LVEDP 25 25
Mean LA 10 30
Fig. 4.1 Difference between LVEDP and mean left atrial pressure. Two patients with similar left ventricu-
lar end diastolic pressures (LVEDPs) but very different mean left atrial pressures. Patient 1 (left panel) has
compensated left ventricular diastolic dysfunction, with an elevated LVEDP (30 mmHg) but only mildly elevated mean left atrial pressure (22 mmHg). In contrast, patient 2 (right panel) has a similar LVEDP (30 mmHg)
but a severely elevated mean left atrial pressure (35 mmHg) and a large V-wave with no mitral regurgitation.
PA WP, Pulmonary arterial wedge pressure. (Modified from Reddy YNV, El-Sabbagh A, Nishimura RA. Comparing pulmonary arterial wedge pressure and left ventricular end diastolic pressure for assessment of left-sided
filling pressures. JAMA Cardiol. 2018;3[6]:453-454.)
180
160
140
120
100
80
60
40
20
0
–20
Patient 2
48 1—BUILDING BLOCKS OF STRUCTURAL INTERVENTION
↑
↑↑↑ LA>>>↑
https://t.me/medicina_free
History and exam
echo
Doppler-derived
PA pressure
↑PAP
MV
Doppler
High E, low A
Cath
HFpEF
LA=↑ LVEDP
Fig. 4.2 Hemodynamic approach to dyspnea after atrial fibrillation (AF) ablation. (Reproduced from
Reddy YNV, El Sabbagh A, Packer D, Nishimura RA. Evaluation of shortness of breath after atrial fibrillation
ablation: Is there a stiff left atrium? Heart Rhythm. 2018;15[6]:930-935.)
Stiff LA
N PAP
Low E, high A
LVEDP
Exercise
PAH/
PE/
PV Sten
Severe
MR
LV gramDelayeda wave
cond delay
CT chest
Interatrial
the mean PAWP and LA pressure should be equal. However, we do not consider PAWP an adequate
surrogate for LA pressure.
5
Measurement of PAWP, LA, and LVEDP can help differentiate pulmonary vein stenosis, stiff LA syndrome, and heart failure with preserved ejection fraction (Fig. 4.2).
However, it is essential that when using the PAWP, this should be confirmed with a saturation from
the PAWP position of .95%. Without this confirmation, one can never be certain that the obtained
tracing is a PAWP tracing and not a damped pulmonary artery (PA) tracing. It is also important to
emphasize that the obtained PAWP saturation should be .95%, regardless of systemic arterial
saturation, as it is obtained directly from the pulmonary capillary bed.
LA WAVEFORMS
The waveforms in the LA/PAWP tracing provide valuable diagnostic information above and
beyond the absolute pressure values. The “a” wave represents atrial contraction, and the mid “a”
wave or “c” wave is closest in timing to end diastole and provides the best estimate of LVEDP
without entering the left ventricle. The “v” wave in contrast begins shortly after ventricular systole
and represents filling of the atrium, thereby reflecting left atrial operating compliance (Fig. 4.3).
A large v wave can reflect either poor operating compliance of the LA secondary to left ventricle
4—HEMODYNAMICS FOR THE STRUCTURAL INTERVENTIONALIST 49
Time
https://t.me/medicina_free
LAP, mmHgLAP, mmHg
LA volume
LA
RA
RV
Fig. 4.3 Mechanism of v wave. Mechanism of v wave is due to atrial filling during ventricular systole from
annular descent of the mitral annulus (suction) and right ventricle (RV) contraction (pushing). The operating
compliance of the atrium determines the height of the v wave. The upper-right figure is the left atrium (LA)
pressure volume relationship during atrial filling. The LA pressure increases exponentially as LA volume rises.
The bottom-right figure is the LA pressure curve over time, and the height of the v wave corresponds with
maximum LA volume during atrial filling. LAP, left atrial pressure; LV, left ventricle; RA, right atrium. (Reproduced from Reddy YNV, El Sabbagh A, Packer D, Nishimura RA. Evaluation of shortness of breath after atrial
fibrillation ablation: Is there a stiff left atrium? Heart Rhythm. 2018;15[6]:930-935.)
Annular descent
LV
v wave
(LV ) diastolic dysfunction, poor intrinsic compliance of the LA (stiff LA syndrome after atrial
fibrillation ablation), or mitral regurgitation (MR) increasing LA volume and worsening
operating LA compliance (Fig. 4.4). There is no reliable way to differentiate MR from the other
causes, and in the presence of a large v wave of unclear etiology, a left ventriculogram should be
performed to rule out severe MR. The x nadir reflects atrial relaxation and annular descent during
ventricular systole and is therefore blunted in restrictive cardiomyopathy. The y descent can be
prominent, with early rapid filling seen in constriction or restriction, but importantly is blunted
when ventricular early filling is compromised by cardiac tamponade (Fig. 4.5).
Continuous measurement of the left atrial pressure is important in guiding mitral valve
therapies. For example, during MitraClip therapy, decision-making regarding placement of one
or more MitraClips is aided through measurement of the absolute LA pressure and the changes
in LA pressure, as well as intraprocedural transesophageal echocardiography (TEE) (Fig. 4.6).
ASSESSING PULMONARY VASCULAR DISEASE
Determining the presence of pulmonary hypertension and intrinsic pulmonary vascular disease is
important for risk stratification of structural patients for surgical or percutaneous interventions.
This is most commonly performed by assessing the pulmonary vascular resistance, which reflects
steady-state resistance of the pulmonary circulation [(mean PA 2 PAWP) / CO]. In addition,
pulsatile load, as assessed by pulmonary arterial capacitance [stroke volume / PA pulse pressure],
provides complementary information on pulmonary vascular remodeling. In the presence of significant precapillary pulmonary hypertension, determining its reversibility with nitric oxide (if the
PAWP is normal) or nitroprusside (if the PAWP is elevated) is crucial to understand if a
structural intervention on the left heart is likely to improve symptoms or not.
50 1—BUILDING BLOCKS OF STRUCTURAL INTERVENTION
A
B
53
53
https://t.me/medicina_free
LA stiffness normal
v
LAP, mmHg
LAP, mmHg
Fig. 4.4 Left atrial pressure volume relationship. Left atrium (LA) pressure volume loop and correlation
with LA pressure tracing in (A) normal LA and (B) Stiff LA. LAP, left atrial pressure. (Reproduced from Reddy
YNV, El Sabbagh A, Packer D, Nishimura RA. Evaluation of shortness of breath after atrial fibrillation ablation:
Is there a stiff left atrium? Heart Rhythm. 2018;15[6]:930-935.)
a
x
LA volume
a
x
LA volume Time Time
y
↑LA stiffness
v
y
v wave, mmHg
v wave, mmHg
v
LAP, mmHg
Time Time
v
LAP, mmHg
v
a
x
a
x
y
v
y
RIGHT HEART PRESSURES
The right atrial (RA) pressure has similar waveforms to the LA, and prominent c-v waves that
begin early in systole often reflect severe tricuspid regurgitation (TR). In torrential TR, the RA
pressure tracing can appear ventricularized (Fig. 4.7). In addition, mean RA pressure most closely
approximates pericardial pressure and therefore can be used to estimate pericardial restraint. In
constrictive pericarditis, the RA pressure will equalize, with the LVEDP classically reflecting this
pericardial restraint, but this can also be seen to a lesser extent in other causes of significant cardiomegaly that stretches the pericardium with relative pericardial restraint, such as seen in severe
TR or advanced cardiomyopathy.
Pressure Gradients and Valve Areas
Cardiac catheterization remains the gold standard to assess the severity of an obstructive lesion.
By measuring the pressure gradient across an obstruction relative to flow, the severity of stenosis
can be assessed by the Gorlin valve area.
Aortic valveareaFlowrate/(44.3meangr
Mitral valveareaFlowrate/(37.5meangr
where flow rate 5 stroke volume / systolic or diastolic flow duration
The Hakki equation allows quick estimation of valve area using CO /
aadient )
aadient )
mean gr adient
4—HEMODYNAMICS FOR THE STRUCTURAL INTERVENTIONALIST 51
180
–10
https://t.me/medicina_free
160
140
120
100
80
60
40
20
0
–20
80
70
60
50
40
30
20
10
0
Fig. 4.5 Hemodynamic tracings in cardiac tamponade. This patient underwent evaluation for dyspnea on
exertion in the setting of suspected aortic prosthetic stenosis with transseptal heart catheterization to evaluate the aortic pressure gradient. The top panel shows aortic pressure, left ventricular (LV) pressure, and left
atrial pressure. During catheterization, hypotension developed abruptly, with systolic blood pressures declining from 140 to 50 mmHg along with ST elevation on the electrocardiogram leads. There was evidence of
pulsus paradoxus along with elevation of left atrial pressure and loss of the y descent consistent with pericardial tamponade. Echocardiogram confirmed a new pericardial effusion, which was emergently drained
with resolution of hypotension.
The contour of the pressure tracing can also be helpful, with a late-peaking aortic pressure
suggestive of severe aortic stenosis, a spike-and-dome pattern in the aortic pressure suggestive of
obstructive hypertrophic cardiomyopathy (Fig. 4.8), and a blunted y descent and end diastolic LA
and LV separation indicative of severe mitral stenosis (Fig. 4.9).
Certain practical caveats in using the valve area formulae must also be considered:
n
When there is mixed aortic stenosis and regurgitation, the Gorlin valve area will be falsely
low, because the catheterization calculated CO represents the actual systemic perfusion,
which is only a fraction of the total LV stroke volume with every beat (due to aortic regurgitation). Using echocardiographic estimates of the total LV stroke volume or LV gram
calculation of total stroke volume allows a more accurate valve area calculation.
52 1—BUILDING BLOCKS OF STRUCTURAL INTERVENTION
Preprocedure Postprocedure
https://t.me/medicina_free
Fig. 4.6 Change in LA pressure after therapy for severe mitral regurgitation. Mitral perivalvular leak (PVL)
of a St. Jude mitral mechanical valve. After device deployment, 2D Doppler color flow did not demonstrate
significant improvement in the degree of paravalvular (top panels); however, the v-wave and mean left atrium
(LA) pressure both significantly reduced (middle panels). Pre-AVP II plug, the mean LA pressure was 16 mmHg
and v wave 28 mmHg. Post-AVP II plug, the mean LA pressure dropped to 7 mmHg with a v wave of 15 mmHg.
3D transesophageal echocardiography (TEE) (bottom panels) demonstrated the mechanism of this discrepancy:
the large PVL (arrow) had been successfully closed with a small residual high-velocity jet causing misleading 2D
appearances on color Doppler. (Reproduced with permission from Maor E, Raphael CE, Panaich SS, et al. Left
atrial pressure and predictors of survival after percutaneous mitral paravalvular leak closure. Catheter Cardiovasc
Interv. 2017;90:861-869.)
n
Similarly, with mixed mitral stenosis and regurgitation, the Gorlin valve area will also be
falsely low due to underestimation of the true flow across the mitral valve (forward stroke
volume 1 regurgitant volume).
n
When assessing mitral stenosis, the PAWP tracing will be damped and delayed compared with
the LA pressure and can therefore overestimate transmitral gradients (see Fig. 4.9). If the
severity of mitral stenosis is in question, a transseptal heart catheterization is often necessary.
4—HEMODYNAMICS FOR THE STRUCTURAL INTERVENTIONALIST 53
60
–10
https://t.me/medicina_free
50
40
30
20
10
0
Fig. 4.7 Severe tricuspid regurgitation. Right atrial pressure shows more prominent v wave and ventricu-
larization with inspiration from torrential tricuspid regurgitation.
Fig. 4.8 Aortic pressure tracing post–premature ventricular contraction (PVC) in aortic stenosis (left)
and hypertrophic cardiomyopathy (right). Aortic pressure tracing with late-peaking delayed upstroke post-
PVC in aortic stenosis (left) and spike and dome pattern with decrease in aortic pulse pressure in hypertrophic
cardiomyopathy (right). Ao, Ascending aorta; LA, left atrium; LV , left ventricle; RA, right atrium.
n
When there is a higher mean gradient by echocardiography that is found to be substantially
lower by catheterization, this likely represents clinical pressure recovery, which can occur in
smaller prostheses, small noncompliant aortas, or high-flow states.
n
A gradient that occurs immediately postoperatively that is confirmed by catheterization
represents patient–prosthesis mismatch. The tracing will peak early and occur in a smaller
prosthesis.
54 1—BUILDING BLOCKS OF STRUCTURAL INTERVENTION
https://t.me/medicina_free
Fig. 4.9 Difference between mitral stenosis gradient using wedge pressure and left atrial pressure.
Note the damped and delayed wedge pressure waveform, which overestimates mean gradient compared
with left atrium (LA) pressure–derived mean gradient.
n
Finally, because valve area calculations are dependent on flow and are based on multiple
assumptions, there can occasionally be discrepancy between the gradient and valve area. In
these situations, invasive valvular stress testing with dobutamine, nitroprusside, or exercise
can help differentiate pseudosevere from severe stenosis (Fig. 4.10).
Summary and Key Points
n
Understanding hemodynamics is essential for the practicing structural interventionalist.
n
Careful measurements, including accurate zeroing at the start of the case, is required for
accurate measurement.
n
Measurement of pressure and flow allows a better understanding of the patient’s underlying
pathophysiology and guides further therapy.
6
Соседние файлы в папке Библиотека им академика М.И. Перельмана