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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3597_Библиотеки_им_академика_М_И_Перельмана
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https://t.me/med1917
200 mm Hg
Figure 4-28 Simultaneous hemodynamic tracings of aortic (Ao) and left
ventricular (LV) pressures in a patient with a pacemaker. Loss of atrial
contraction (paced beats between arrows) decreases ventricular filling with
loss of systemic pressure. Lef t arrow, Initiation of ventricular pacing with
loss of the atrial contribution to LV filling; right arrow, return of atrial synchrony and normal sinus rhy thm. Systemic pressures are increased markedly during normal sinus rhy thm. ECG, Electrocardiogram.
Hemodynamic Data
ECG
Ao
LV
0
ECG
40 mm Hg
#1 #2
V
1
v′
a
a′
0
Figure 4-29 Simultaneous pulmonary capillary wedge (PCW) and left ven-
tricular (LV) pressures in a patient who has loss of atrial activity (beat 2).
On beat 1, the a wave is evident on LV (a) and pulmonar y capillar y wedge
pressure (PCWP) (a′). The a wave is lost on beat 2, with no atrial activity.
The a′ wave is considerably higher because of its contraction against the
closed mitral valve. ECG, Electrocardiogram.
a′
gradually returns as atrial activity becomes more connected to
the QRS.
Large v Waves on Pulmonary Capillary
Wedge Tracing
LV and PCW pressures generally match well in diastole (Fig. 4-29). The
PCW a wave (a′
wave is large. There is no important diastolic PCW-LV gradient. On
beat 2, because of late atrial activity, loss of the LV a wave is shown
by the different initial upstroke of the LV pressures. The PCW has large
and late a and v waves. The v wave on a PCWP tracing may be associated with significant mitral regurgitation but is neither highly sensitive
nor specific for mitral regurgitation. Large v waves may also be present
with a ventricular septal defect or any condition in which the LA
volume (e.g., ventricular septal defect) or LA pressure relationship
(stiffness or compliance) is increased (e.g., rheumatic heart disease,
postcardiac surgery, and infiltrative heart diseases). Mitral valve
obstruction from any cause and congestive heart failure (CHF) in the
absence of mitral regurgitation are also associated with large v waves.
Giant v waves, also seen in Figure 4-30, may be large enough to be
) follows the LV a wave by 150 msec (beat 1). The v
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Hemodynamic Data 213
ECG
v
a
*
PCW
(0–40 mm Hg)
Figure 4-30 Giant v waves on the pulmonary capillary wedge (PCW) tracing
can be transmit ted to pulmonary artery (PA) pressure, producing a notch (*)
on the PA downslope. ECG, Electrocardiogram.
transmitted to the PA pressure, which causes a notch on the diastolic
downslope.
Aortic Stenosis
The effect of increasing LV filling by a premature ventricular contraction (PVC) on simultaneous LV and Ao pressure tracings in a patient
with minimal Ao stenosis can be seen with the higher LV pressure after
an extrasystolic beat, called postextrasystolic potentiation (Fig. 4-31).
The atrial contraction is important in patients with Ao stenosis
(Fig. 4-32). Simultaneous Ao and LV pressure (trans-septal approach)
shows that atrial activity is absent on the first beat, a junctional beat
(*). Without the atrial contribution, Ao systolic pressure is 132 mm Hg,
and LV systolic pressure is 190 mm Hg. On the following beat, number
3 atrial activity (P wave) precedes the QRS, and the Ao pressure
increases to 160 mm Hg; LV pressure increases to 225 mm Hg, representing an approximately 25% increase in pressure augmentation. This
effect is crucial in patients with poor LV function. Two additional
features of this tracing are worthy of note. The a wave on the LV pressure tracing (see Fig. 4-31, A and B, arrow) can be seen on LV beat 2,
and Ao regurgitation may be present when a wide pulse pressure (Ao
systolic-diastolic pressure) of >
pressure has decreased to <50 mm Hg at the end of diastole. Recall
that the least accurate method to measure an LV-Ao gradient is with a
single catheter pull back (see Fig. 4-31, C)
50 to 60 mm Hg is observed. The Ao
PA
(0–100 mm Hg)
Left Ventricular Gradient Below the
Aortic Valve
Hypertrophic obstructive cardiomyopathy (HOCM) is a condition in
which thick heart muscle, especially inside the LV chamber, contracts
so hard that it obstructs flow out of the ventricle and produces a pressure gradient inside the LV with a normal Ao valve. Figure 4-33 depicts
simultaneous LV and Ao pressure showing a large Ao-LV gradient (LV
pressure, 220 mm Hg; Ao pressure, 120 mm Hg). On pull back of the
LV catheter (end-hole multipurpose) from the distal LV to a position
just beneath the Ao valve, the Ao-LV gradient disappears (see the LV
pressure matching with Ao pressure in Fig. 4-33, far right.)
A PVC in a patient with HOCM produces a longer LV filling period
after the PVC beat. This increases both LV volume and contractility
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ECG
200 mm Hg
A
Ao
Hemodynamic Data
1 sec
113/47 (68)
LV
1
32
MONITOR
BPM
Ao
LV
147/-8,
r
r
I
(50)
II
(50)
200
s
LV
LV
s
s
s
100
Ao
Ao
0
B
200
180
160
140
120
100
80
60
40
20
13
0
2
12:10:57 PM
C
Figure 4-31
d
d
e
BPM
91/49 31 9
139
31
P1:AO 1000 PM
138
13
1
139
100
3072
33
30
0
12:10:59 PM 12:11:01 PM 12:11:03 PM 12:11:05 PM
d
e
A, Postextrasystolic accentuation of lef t ventricular (LV) and
IPM
d
116
112
38
36
aortic (Ao) pressures (closed arrow) after a premature ventricular contraction
(PVC) (open arrow). This patient does not have Ao stenosis. The PVC does
not generate pressure sufficient to open the Ao valve and results in a
dropped beat when the peripheral pulse rate is counted. B, Postextrasystolic
potentiation hemodynamics in a patient with mild aortic stenosis (AS).
C, LV to aorta pressure pull back with a single catheter, demonstrating difficulty in assessing a transvalvular gradient. (A, From Kern MJ, Donohue T,
Bach R, et al: Interpretation of cardiac pathophysiology from pressure wave form analysis: cardiac arrhythmias. Cathet Cardiovasc Diagn 27:223–227,
1992.)
P
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Hemodynamic Data 215
ECG
200 mm Hg
Ao
LV
0
Figure 4-32 Simultaneous lef t ventricular (LV) (obtained with trans-septal
technique) and aortic (Ao) pressures from fluid-filled catheter systems. Note
the contribution of atrial contraction (arrow) to the change in LV and systemic
pressures on beat 2. *, Absence of P wave on this tracing; P, P wave. The
wide pulse pressure is also indicative of Ao insufficiency.
*
1
2
Figure 4 -33 Simultaneous left ventricular (LV) and aortic (Ao) pressures
in a patient with hypertrophic obstructive cardiomyopathy (HOCM) during
pull back of the catheter from the distal portion of the LV. The pressure
gradient between the aorta and LV is lost. LV systolic pressure matches Ao
pressure during catheter pull back before the catheter is pulled out of the
LV. There is no true Ao valve gradient. This LV-Ao gradient is located in the
mid-LV wall beneath the Ao valve. Matching of Ao and LV systolic pressures
in the proximal chamber (arrow indicates transition from distal LV to proximal
LV under the aortic valve). See text for details.
with greater intraventricular muscular obstruction, resulting in three
characteristic changes in post-PVC pressure waveforms: (1) The LV-Ao
gradient is greater, (2) Ao pulse pressure is narrower, and (3) Ao
waveform if deformed shows a spike and dome pattern characteristic
of early LV outflow obstruction. In addition, the Ao pressure upslope
is very rapid and parallels the LV pressure upstroke. These post-PVC
changes occur due to the increase in contractility, which outweighs
the effects of the increase in preload and leads to worse outflow
tract obstruction. Post-PVC findings in AS include a larger LV-Ao gradient but, unlike HOCM, they also include an increase in Ao pulse
pressure, with preservation of the Ao waveform including the delayed
Ao upstroke (Fig. 4-34). Table 4-4 lists provocative maneuvers to
increase an outflow tract gradient in patients with hypertrophic cardiomyopathy (HCM).
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Hemodynamic Data
II
aV
L
LV (200)
ART (200)
ART
LV
Figure 4 -34 Comparison of post-premature ventricular contraction (PVC)
hemodynamics in patients with aortic stenosis (AS, lef t) and hypertrophic
obstructive cardiomyopathy (HOCM, right). Post- PVC in AS has a larger gradient, slow upstroke, larger pulse pressure, and preser ved aortic (Ao) wave form. In contrast, post-PVC HOCM tracings show a larger gradient, smaller
pulse pressure, vertical Ao pressure upstroke, and spike- and- dome pattern
of Ao pressure. LV, Lef t ventricle.
Table 4 -4
AS
400
HOCM
200
0
Provocative Tests for Hypertrophic Cardiomyopathy*
Drug or Maneuver Mechanism Increasing Ao -LV Gradient
Drugs
Dobutamine Increased myocardial contractility
Isoproterenol (not commonly
used today)
Amyl nitrite Decreased systemic arterial pressure
Nitroglycerin Decreased venous return, decreased
Maneuver s
Extrasystole (PVC)* Postextrasystolic increase in myocardial
Valsalva maneuver Decreased venous return, decreased LV
Ao, Aortic; CO, cardiac output; LV, left ventricular; LVOT, left ventricular outflow tract;
PVC, p rematur e ventricular cont raction.
*Stroke volume and systemic ar terial pulse pressure decrease in the
postex trasys tolic beat (t he Brockenbrough-Braunwald-Morrow ef fect).
Increased myocardial contractility,
decreased blood pressure
(peripheral vasodilatation), reflex
increasing sy mpathetic tone,
decreased venous return, and
increased myocardial contractility
CO, and increased narrowing of LVOT
contractilit y and decreased pulse
pressure
volume, and increased narrowing of
outflow tract
Aortic Regurgitation
The characteristic hemodynamic feature of Ao regurgitation is wide
pulse pressure, brisk Ao (femoral) pressure upstroke, and rapid filling
of LV diastolic pressure. Often there is marked overshoot of the FA
pressure. Figures 4-35, 4-36, and 4-37 illustrate simultaneous Ao and
LV pressures in several patients with different degrees of Ao regurgitation. In Figure 4-36 the large and prominent a wave shows the effect
of first-degree AV block (long P–R interval, arrows) on the LV pressure.
Figure 4-37 diagrams the physiology of the Ao-LV gradient in diastole.
No atrial contribution of LV pressure is present.
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200 mm Hg
ECG
Ao
LV
4 —
Hemodynamic Data 217
1 sec
Figure 4- 35
Hemodynamic tracing in a patient with aortic (Ao) insufficiency
(and minimal aortic stenosis [AS]), showing the Ao-lef t ventricular (LV) dia stolic gradient (arrows) that are important for coronary perfusion. (Note the
loss of the a wave due to paced rhythm.) ECG, Electrocardiogram.
ECG
200 mm Hg
Ao
LV
Figure 4 -36 Simultaneous aortic (Ao) and left ventricular (LV) pressures
in a patient with Ao insuf ficiency. Note the absence of a systolic pressure
gradient. The time delay in the Ao pressure upstroke indicates that femoral
sheath pressure is used. The presence of a large and early a wave (thick
bottom arrow) occurs with P–R interval prolongation (top thick arrow). ECG,
Electrocardiogram.
ECG
200 mm Hg
Ao
LV
0
1 2 3 4 5 6 1 2 1 23 4 5 6
Figure 4 -37 Severe aortic (Ao) regurgitation shown by rapidly increasing
left ventricular (LV) diastolic pressure (lowest closed arrow) and end-diastolic
equilibration of Ao and LV pressure (three small arrows). Peripheral ar terial
pressure overshoot or amplification is caused by forceful LV ejection and
compliant arterial system. (In this case, Ao pressure was matched with
femoral ar terial [FA] sheath pressure.) ECG, Electrocardiogram. (From Kern
MJ, Aguirre FV: Interpretation of cardiac pathophysiology from pressure
waveform analysis: aor tic regurgitation. Cathet Cardiovasc Diagn 26:232–
240, 1992.)
200 200
100
0 0
100
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200 mm Hg
Hemodynamic Data
ECG
Ao
0
Figure 4- 38 Hemodynamic tracings in a patient with mitral regurgitation,
characterized by a giant v wave in left atrial (LA) pressure. This v wave corresponds to marked increase in flow and volume into the L A. Ao, Aortic
pressure; ECG, electrocardiogram; LV, left ventricular pressure.
′V′
LV
LA
Hemodynamically severe Ao regurgitation is indicated by rapidly
increasing LV diastolic pressure and wide Ao pressure with near equilibration of Ao and LV pressure at end diastole (Figs. 4-36 and 4-37).
Mitral Regurgitation
In mitral regurgitation (Fig. 4-38), large v waves in the PCW tracing
represent LV volume transmitted backward through an incompetent mitral valve. The LA v wave occurs on the downstroke of LV
pressure.
Figure 4-39 shows large v waves with a persistent LV-PCW gradient
in patients with mixed mitral regurgitation and stenosis. Left ventriculography confirms significant mitral regurgitation. The slope of the v
waves in mitral regurgitation and stenosis is flatter than that in which
large v waves are associated with isolated mitral regurgitant flow
alone.
Mitral Stenosis
In mitral stenosis (see Fig. 4-39), LV and PCW pressures show the
diastolic pressure gradient, indicating the severity of LA outflow
obstruction. The a wave on beat 1 is associated with a normal v wave.
On the following beat, atrial activity is delayed and follows the QRS,
contributing to a giant v wave (36 mm Hg). The augmented filling
increases the mitral valve gradient, which is influenced by HR. When
the rhythm is irregular (as in AF), calculations of gradients should be
made from the average of 10 beats. Figure 4-40 illustrates the effect of
R–R cycle length on the mitral stenosis gradient. In some patients with
mitral stenosis, balloon catheter valvuloplasty may be used to open a
narrowed mitral orifice.
Constrictive Pericarditis
Constrictive pericarditis limits filling of the heart by the confining
pericardium. The RV fills at the expense of the LV, with the septum
pushing into the LV during RV filling (e.g., inspiration). Typical hemodynamic findings include Kussmaul sign (an inspiratory increase in
RA pressure), an elevated RA pressure with an M or W configuration,
and a dip and plateau pattern of early rapid diastolic filling, with
abrupt cessation of further caused by pericardial constraint (Fig. 4-41).
Discordance of LV/RV systolic pressures during respiration is the most
specific hemodynamic finding, establishing a diagnosis of constrictive
pericarditis.
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LV
LA
grad
4 —
Hemodynamic Data 219
A
v
a
e
d
v
a
e
d
v
a
e
d
v
a
e
d
B
Figure 4-39 A, Simultaneous lef t ventricular (LV) and left atrial (LA) pres-
sures (0- to 40-mm Hg scale) show distinct a and v waves with a large
diastolic gradient of mitral stenosis. B, LV and LA pressures with large v
waves demonstrate mixed mitral stenosis and regurgitation.
In Figure 4-42, matching of elevated diastolic pressures with an
early dip followed by a plateau during diastole (on the first beat) is the
characteristic pattern. Often, the classic dip-and-plateau configuration
appears only during slow HRs. Tachycardia and respiratory effort
obscure the pattern, but matching of RV and LV pressures during
diastole is consistent. The most specific and sensitive sign that can
differentiate constrictive from restrictive physiology is the dynamic
respiratory variations in RV and LV systolic pressures. RV/LV systolic
pressures that increase and decrease in a concordant manner are
findings of restrictive cardiomyopathy, whereas discordant responses
during respiration of the RV/LV systolic pressures are the hallmark of
constrictive physiology (Fig. 4-43). RA pressure shown in Figure 4-44
demonstrates the characteristic pattern of prominent “y” descent with
a classic M or W configuration of constrictive physiology. These waveforms are the altered x and y troughs resulting from impaired ventricular filling. Myocardial restrictive heart disease or heart failure also
shows this pattern occasionally.
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40 mm Hg
Hemodynamic Data
1 sec
ECG
LA
LV
A
1 sec
ECG
40 mm Hg
LA
LV
B
Figure 4-40 Influence of heart rate (HR; diastolic period) on mitral valve
gradient. The mitral stenosis gradient changes with heart rate (R–R inter val).
A, A short R–R interval is associated with a gradient (shaded area) of
22 mm Hg. B, A long R–R inter val has a mean gradient of 29 mm Hg. When
computing mean valve area in atrial fibrillation (AF), average is 10 beats.
ECG, Electrocardiogram; LA, left atrial pressure; LV, left ventricular pressure.
(From Kern MJ, Aguirre F: Interpretation of cardiac pathophysiology from
pressure waveform analysis: mitral valve gradients: Par t I. Cathet Cardiovasc Diagn 26:308–315, 1992.)
1 sec
ECG
40 mm Hg
0
Figure 4- 41 Right atrial (RA) pressure showing pattern of constrictive
physiology with large “y” descent and smaller “x” descent. Mean RA pressure is 20 mm Hg. ECG, Electrocardiogram.
x
y
Hemodynamics of Tamponade
In contrast to constrictive physiology waveforms, observe the RA pressure in a patient with cardiac tamponade (Fig. 4-45). High pericardial
pressure blunts all diastolic filling waveforms. Tamponade physiology has an elevated RA pressure with blunted “y” descents, reflecting
impairment in early diastolic filling and the life-threatening nature
of this disorder. The arterial pressure shows pulsus paradoxus (an
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ECG
LV
4 —
Hemodynamic Data 221
50
25
RV
0
Figure 4-42
pressure tracing in a patient with constrictive pericarditis. Matching of diastolic pressures is one of the hallmarks of this condition. However, dynamic
respiratory variation of systolic pressures is diagnostic in differentiating
constriction from restrictive cardiomyopathy. ECG, Electrocardiogram.
Simultaneous left ventricular (LV) and right ventricular (RV)
50
25
0
RV vs. LV
Figure 4- 43 Dynamic respirator y variation in constrictive and restrictive
physiology. Normal respiratory activity results in a parallel decrease in
right ventricular (RV)/left ventricular (LV) systolic pressures. Left, RV/LV
systolic pressures move together with respiration in a concordant manner,
a finding highly consistent with restrictive cardiomyopathy. Right, RV/LV
systolic pressures move discordantly during respiration, a finding highly
specific for constrictive physiology and constrictive pericardial disease.
ECG
40 mm Hg
Paced
RA
Figure 4-44 Right atrial (RA) pressure in a patient with constrictive peri-
carditis showing abnormally elevated pressure with a classic M configuration. The elevated pressure with exaggerated “y” descent is also seen in
cardiomyopathy. ECG, Electrocardiogram.
a V
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