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359
Determinants of Hemodynamic Compromise
With Severe Right Ventricular Infarction
James A. Goldstein, MD, Benico Barzilai, MD, Thomas L. Rosamond, MD,
Paul R. Eisenberg, MD, and Allan S. Jaffe, MD
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To elucidate determinants of hemodynamic compromise in patients with acute right ventricular
(RV) infarction, we studied 16 patients with hemodynamically severe RV infarction by right heart
catheterization and two-dimensional ultrasound. Severe RV systolic dysfunction, evident by
ultrasound in all patients as RV dilatation and depressed RV free wall motion, was associated
with a broad sluggish RV waveform, diminished peak RV systolic pressure (27.6±4.5 mm Hg),
and depressed RV stroke work (4.6±2.4 g m/m2). Paradoxical septal motion was consistently
noted. In some cases, the septum bulged into the right ventricle in a pistonlike fashion and
appeared to mediate systolic ventricular interaction through which left ventricular septal
contraction contributed to RV pressure generation. RV diastolic dysfunction was indicated by
elevated RV end-diastolic pressures (13.7±2.7 mm Hg), RV "dip and plateau," equalization of
diastolic filling pressures, and reversal of diastolic septal curvature toward the volume-deprived
left ventricle. A prominent right atrial (RA) X and blunted Y descent, indicative of impairment
of RV filling throughout diastole, were confirmed in all patients by their relation to RV systolic
events. Patients manifested one of two distinct RA waveform morphologies differentiated by A
wave amplitude and associated with disparate clinical courses. In eight patients, an RAW pattern
was evident, characterized by augmented A waves; eight others manifested an M pattern
constituted by depressed A waves. Compared with those with an M pattern, patients with a W
pattern had higher peak RV pressures (29.6±3.8 versus 25.5±4.3 mm Hg,p <0.05), better cardiac
output (3.4±0.3 versus 2.9±0.7 Ilmin,p< 0.05), more favorable response to volume and inotropes,
and less frequently required emergency revascularization for refractory shock (none versus five
for those with an M pattern). Patients with a W pattern were more severely compromised if
atrioventricular dyssynchrony developed and were more dramatically improved by restoration of
physiological rhythm. Angiography in patients with depressed A waves demonstrated more
proximal coronary obstruction leading to ischemic compromise of RA function, whereas in those
with augmented A waves, the culprit lesion was proximal to the RV but distal to the RA branches.
These results indicate that hemodynamic compromise in patients with RV infarction is
exacerbated by deceased preload reserve that is dependent on atrial systole. The amplitude of the
RA A wave, an indication of the status of RA function, is an important determinant of RV
performance and hemodynamic compromise. (Circulation 1990;82:359-368)
I nfarction of the right ventricle is common in
patients with transmural inferoposterior myocardial infarctionl-3 and may result in hemodynamic compromise despite adequate left ventricular
(LV) function.2-5 In experimental animals, ischemic
injury of the right ventricular (RV) free wall
depresses RV systolic performance, which in association with diastolic ventricular interaction induced by
From the Washington University School of Medicine, St. Louis, Mo.
Supported in part by National Institutes of Health SCOR in
Ischemic Heart Disease grant HL-17646, Bethesda, Md.
Address for correspondence: James A. Goldstein, MD, Cardiovascular Division, Washington University School of Medicine, 660
South Euclid Avenue, Box 8086, St. Louis, MO 63110.
Received September 7, 1989; revision accepted March 13, 1990.
acute RV dilatation and elevated intrapericardial
pressure leads to deprivation of LV end-diastolic
volume, resulting in reduced cardiac output and
hypotension.6-9 Although the severity of hemodynamic derangements in patients with RV infarction is
related to the extent of RV free wall dysfunction,2,5
some patients tolerate severe depression of RV contractility without hemodynamic compromise, whereas
others manifest life-threatening low cardiac output
despite similar extents of RV systolic impairment.2.3,5
Furthermore, the mechanisms by which RV pressure
and stroke volume are generated in the absence of
demonstrable RV free wall motion have not yet been
delineated. To clarify factors that determine RV
performance and the magnitude of hemodynamic
360
Circulation Vol 82, No 2, August 1990
impairment in patients with severe RV infarction, we
studied 16 consecutive patients with hemodynamically severe RV infarction by right heart catheterization and two-dimensional ultrasound.
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Methods
From January 1988 through January 1989, 16 consecutive patients admitted to the Cardiac Care Unit
at Barnes Hospital, Washington University Medical
Center, within 72 hours of onset of acute transmural
inferoposterior myocardial infarction with hemodynamic compromise consistent with RV infarction
were studied. Criteria for study included 1) electrocardiographic evidence of inferior ST elevation or Q
waves with 2) hypotension (systolic blood pressure,
<95 mm Hg), elevated neck veins (jugular venous
pressure, .10 cm H20), and clear lungs without
radiographic evidence of pulmonary venous congestion and 3) echocardiographic evidence of RV dilatation and RV free wall motion abnormalities.
The clinical indication for right heart catheterization was hypotension. Right atrial (RA), RV, pulmonary artery (PA), and pulmonary capillary wedge
(PCW) pressures were measured with fluid-filled
floatation catheters (American Edwards, Irvine, Calif.).
A double-lumen catheter, with a proximal (RA) lumen
(nominal frequency response, 35 Hz) and a distal
lumen (RV or RA pressure frequency response, 25
Hz), was used in nine patients. In seven other patients,
a triple-lumen catheter was used with a distal (PA)
lumen (nominal frequency response, of 17 Hz), an
RV lumen (frequency response, 26 Hz), and a
proximal (RA) lumen (frequency response, 20 Hz).
The manometer and interconnect tubing were optimized for critical damping. The band-pass filters for
the strip-chart recorder (Hewlett-Packard, Palo
Alto, Calif.) was set at 250 Hz, and the photographic recorder (Honeywell Instruments, Minneapolis, Minn.) was set at 500 Hz. The recording
system (manometer, interconnect tubing, catheter,
and strip-chart recorder) had a flat frequency
response out to 40 Hz. Pressures were recorded
simultaneously with the electrocardiogram at paper
speeds of 25 or 50 mm/sec. The RA pressure
waveform was recorded simultaneously with RV
pressure in 10 patients and with PA pressure in the
remaining six. In seven patients, simultaneous and
superimposed RA and RV pressures were recorded
(Honeywell Instruments). Cardiac output was calculated by thermodilution and repeated in triplicate, and the results were averaged. Hemodynamic
measurements were recorded immediately after
placement of the right heart catheter. Blood pressure was measured by sphygmomanometry (n = 8) or
through an arterial fluid-filled catheter (n = 8). Twodimensional ultrasound studies (Hewlett-Packard)
were performed within 2 hours of the right heart
hemodynamic measurements. Hospital charts were
analyzed to assess changes in hemodynamics over
time and in the clinical courses of patients. Cinean-
giograms were reviewed to obtain results of LV and
coronary angiography.
Measurement of Hemodynamic Parameters
Peak pressures and electrical mean pressure were
measured from strip-chart and photographic recordings. Peak and mean pressures, slopes of the RA
negative waves (X and Y), and areas of the A and V
waves were determined by planimetry from the stripchart and photographic recordings. The RA waveform components, timed by simultaneous electrocardiography and RV or PA recordings, were defined as
follows. The A wave was the initial positive wave
after the P wave of the electrocardiogram and just
before RV/PA systolic pressure generation, the X
descent was the first negative wave after the A wave,
the V wave was the last positive deflection before the
next A wave and coincident with peak systolic pressure, the Y descent was the negative wave after the V
wave and just before the subsequent A wave, and the
C wave, when present, was a positive wave after the
A wave and occurring simultaneous with early systolic pressure generation. The presence of a C wave
separated the X descent into an X component before
and an X' descent after the C wave.
Echocardiographic Analysis
Echocardiograms were recorded on 1/2-in. videotape and analyzed by two experienced echocardiographers (J.G. and B.B.). RV dilatation was designated as mild, moderate, or severe, and RV free wall
motion abnormalities as normal, hypokinetic, akinetic, or dyskinetic. LV size and regional wall motion
abnormalities were assessed similarly. The enddiastolic orientation of the interventricular septum
was assessed as normal, flattened, or frankly reversed
curved. The presence or absence of paradoxical
systolic motion of the septum anteriorly toward the
RV cavity was noted.
Statistics
Group hemodynamic measurements were reported
as mean+ SD. Differences in measurements between
groups were analyzed by unpaired t test. Significance
was defined at the 95% confidence level.
Pertinent Considerations
The hemodynamic data reported in this study were
obtained from measurements recorded with fluidfilled catheters. Care was taken to ensure proper
catheter positioning by analysis of waveforms and
fluoroscopy. Catheters were flushed and balanced
before each recording. Catheter artifact from entrapment or excessive motion was unlikely because the
right heart chambers were markedly dilated and RV
contraction was depressed, conditions that tend to
lessen the likelihood of these types of artifact. Furthermore, the RA and RV waveforms in the present
study are morphologically similar in many respects to
those reported in previous clinical studies of severe
RV infarction10-13 and to those observed in experi-
Goldstein et al Hemodynamic Compromise With RV Infarction
1
FIGURE 1. Flow chart of hemodynamics and clinical courses of patients
according to morphology of right atrial
(RA) pressure waveform. Initial therapy included atropine, volume, and
short-term inotropic therapy (<2
hours). AV DYS, atrioventricular dyssynchrony; PTCA, percutaneous transluminal coronary angioplasty; CABG,
coronary artery bypass graft surgery;
L4BP, intra-aortic balloom pump.
4
PROLONGED
PTCA
CABG
INOTROPES
+/- IABP
A
AV PACER
(M)
4 (M)
2
361
o
(M),3(WM
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*p<O.OS.
RA Meon Pressure (mmHg)
RA Peak A Wove (mm Hg)
RA Peak A/Mean Pressure
RV Systolic Pressure Peok (mm Hg)
RV Stroke Work (9 /mIn2)
Cardiac Output (Liters/Min)
M PATTERN
W PATTERN
P<0.05
14.6 ± 4.7
12.8 ± 2.7
NS
16.3 4.5
1.1 ± 0.05
25.5 ± 4.3
2.9 ± 1.S
2.9 + 0.7
16.8 ± 3.9
1.3 0.09
29.6 3.8
NS
+
mental models of acute RV dysfunction using highfidelity micromanometer catheters.6-914 Waveform
analysis was facilitated by timing with mechanical
events by simultaneous RV or PA pressure as well as
with electrical events by electrocardiography. Due to
concern that fluid-filled catheters may not permit
quantitation, particularly of subtle abnormalities,
only clearly apparent qualitative distinctions have
been emphasized. The statistics reported have been
used only as descriptors of these qualitative observations. Furthermore, because our patient population
included only patients with predominant severe RV
infarction, caution must be used in extrapolating
these results to patients with less severe RV infarction or with associated severe LV infarction.
Results
Clinical Course
All patients in this study presented with RV infarction complicated by hypotension severe enough to
warrant hemodynamic evaluation with right heart
catheterization. The initial episode of hypotension
developed within the first 24 hours of infarction in 14
of 16 patients. Hypotension occurred initially in
association with sinus bradycardia in 15 of 16
patients. Subsequent progression to advanced atrioventricular (AV) block occurred in nine patients who
required temporary pacemakers. Ventricular
demand (VVI) pacing was adequate in five in whom
AV block was intermittent; however, in four other
6.2
±
*
±
*
±
1.8
*
3.4 0.3
±
patients, AV synchronous pacing was required. Six of
16 patients with hypotension and low cardiac output
responded to initial treatment with fluids, atropine,
and temporary pacing (Figure 1). Ten other patients
manifested hypotension and low cardiac output
refractory to these initial therapeutic measures; they
required support with positive inotropic drugs and
other interventions including intra-aortic balloon
pumping (n=3), emergency coronary artery bypass
graft surgery (n=4), or emergency percutaneous
transluminal coronary angioplasty (n=1). Although
all patients undergoing emergency surgical revascularization for cardiogenic shock had severe and protracted postoperative low cardiac output, all survived
and were ultimately hemodynamically improved.
Five of the 16 patients died; in each of the five
patients, volume expansion and cardiac stimulation
with drugs initially elicited apparent hemodynamic
stability. However, several days later, recurrent chest
pain associated with anterior or lateral ischemic
electrocardiographic changes heralded the onset of
refractory cardiogenic shock. All of the five patients
deteriorating in this fashion were elderly (71, 77, 80,
81, and 85 years old) and had contraindications to
more aggressive intervention or revascularization.
Right Atrial Pressure
Mean RA pressure increased in all patients (mean
RA pressure, 13.7±3.8 mm Hg), as did the mean
amplitude of the RA A wave (16.5±4.1 mm Hg)
362
Circulation Vol 82, No 2, August 1990
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TABLE 1. Hemodynamic Parameters in Right Ventricular Infarction
Initial rhythm/
RVEDP/
AoP
heart rate
CO
RA
Age (yr)/sex
RA A
X/Y
RVSP RVEDP RVDP
RVSW
PCW
Patients with RA Wpattem
90
80 F
2.8
12
SR/65
15
1.2
25
10
1.25
5.3
15
70
3.6
10
48 M
13
3.1
27
SB/45
9
1.8
8.2
10
70
61 M
3.6
18
20AV/62
24
2.2
36
16
1.23
7.2
17
1.2
95
3.4
10
13
30
12
81 M
8.5
Junct/60
1.2
19
14
1.3
26
3.3
11
13
2.17
52 M
85
5.5
SB/52
12
75
3.5
13
20
1.2
36 M
34
1.5
4.0
SB/45
18
12
95
3.7
13
46 M
16
2.7
29
16
1.14
SB/48
3.8
19
2.7
15
19
80
1.3
30
16
1.14
77 F
20AV/58
2.0
16
Patients with RA Mpattem
70
2.0
74 M
13
15
3.7
21
SB/52
13
1.08
1.0
14
3.1
11
71 M
75
12
1.4
27
30AV/54
13
1.0
2.5
13
30 AV/50
65
14
56 F
1.8
25
26
1.8
25
1.4
1.0
19
85
3.5
14
16
1.3
24
85 M
13
20/30 AV/45
1.0
2.3
13
90
3.2
14
15
2.1
35
52 M
SB/50
1.07
4.4
15
14
90
3.7
2.2
26
57 M
13
15
16
1.23
4.5
SB/48
14
80
3.3
10
12
1.3
22
55 M
9
1.29
2`AV/50
5.0
12
24
85
2.7
17
19
1.4
16
76 F
1.17
2.0
2°/30AV/40
16
81.3
3.2
13.7
1.8
27.6
Mean
51.5
16.5
13.7
1.27
4.6
14.8
±SD
(±6.9)
(±9.6) (±0.6) (±3.8) (±4.1) (±0.8) (±4.5) (±2.7)
(±0.32)
(±2.4) (±2.7)
AoP, aortic systolic pressure; CO, cardiac output (1/min); RA, mean right atrial pressure; RA A, peak RA A wave pressure; X/Y, ratio
of slope of X and Y descents; RVSP, peak right ventricular systolic pressure; RVEDP, right ventricular end-diastolic pressure;
RVEDP/RVDP, ratio of RVEDP to mean right ventricular diastolic pressure; RVSW, right ventricular stroke work (g. m/in2); PCW,
pulmonary capillary wedge pressure; SB, sinus bradycardia; Junct, junctional rhythm; AV, atrioventricular block. Values for pressures are
given in mm Hg.
(Table 1). The RA pressure was disproportionately
elevated in comparison to the mean PCW pressure
(14.8±2.7 mm Hg), and the ratio of the mean RA
pressure to the mean PCW pressure increased (RA/
PCW, 0.93±0.12; normal, <0.75). When the RA
waveform components were timed by the electrocardiogram, the most prominent RA descent coincided
with or followed the T wave in 13 of 16 cases and
occurred just before the T wave in three, in all cases
suggesting a diastolic Y descent (Figures 2-5). However, when the RA waveform components were
timed with RV mechanical events via simultaneous
RV or PA recordings, the most prominent negative
RA wave occurred during peak ventricular systole,
thereby confirming a prominent systolic X descent in
all patients (Figures 2-5). In each case, the Y
descent was comparatively blunted (ratio of X/Y
slopes, 1.8±0.8, p<0.05). In 12 of 16 patients, a C
wave separated the normally monophasic systolic
descent into initial X and subsequent X' components
(Figures 2-5).
In eight of 16 patients, the RA waveform manifested an M-shaped pattern characterized by a
diminutive A wave followed by a brisk systolic X
descent (or X' in presence of a C wave), a small V
wave, and a blunted Y descent (Figures 2 and 3). In
eight others, prominent A waves imparted a Wshaped pattern to the RA pressure tracing (Figures 4
and 5). The ratio of the peak A wave pressure to the
mean RA pressure was 20% greater in patients with
compared with those with an M pattern
(peak A pressure/mean RA pressure, 1.3 ±0.9 versus
l.l±O.O5, p<0.05; Figure 1).
In patients manifesting C waves, the most prominent negative wave was the X' descent. In patients
with a W pattern, the X component preceding the C
wave was also prominent, whereas in patients with an
M pattern, this X descent was comparatively blunted.
In one patient with a W pattern, C wave and 20 AV
a W pattern
block, atrial contraction was followed by an X
descent in all beats but an X' descent in conducted
beats only, suggesting that the X subcomponent
reflects atrial relaxation (Figure 5). This X descent
component was more exaggerated in patients with a
W pattern (Figures 4 and 5) than in those with an M
pattern (Figures 2 and 3).
Right Ventricular Hemodynamics
The RV systolic waveform was broad (mean RV
systole duration, 0.34+±0.5 seconds), with a narrow
pulse pressure (mean, 16.3 +4.5 mm Hg), a depressed
upstroke, and delayed relaxation (Figures 2, 4, and
5). Peak RV systolic pressure for the entire group
was 27.6+±4.5 mm Hg (Table 1). Peak RVSP was less
than 30 mm Hg in 11 patients and 25 mm Hg or less
in six. In 11 patients, the RV systolic waveform
exhibited a bifid morphology (Figures 2 and 5). RV
end-diastolic pressure was elevated in all patients
(mean, 13.7+2.7 mm Hg). A diastolic "dip and plateau" pattern in the RV waveform was present in 12
A
2-^tiECG
Goldstein et al Hemodynamic Compromise With RV Infarction
FIGURE 2. Tracings of Mpattem of right atrial (RA) pressure.
When timed by electrocardio-
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01
I I|
l Iigram
(panel A), most prominent negative deflection in right
atrium is coincident with T
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! ,ri
suggesting a diastolic Y
|iJ to right ventricular (RV) pressure
i,
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ECG
20r
. >1'
IVy A
'
A 7 ;1>1
comprises a depressed A wave, X
..prominent descent coincides
with peak RV systolic pressure
(RVSP), indicating a systolic X'
descent, whereas diastolic Y
|'' + 1|t*- |descent is blunted. M pattem
descent before a small C wave, a
prominentX' descent, a small V
4wave, and a blunted Ydescent.
RV systolic pressure
j.I t . t;Peak
.
(RVSP) is depressed and bifid
(arrow) with delayed relaxation
and an elevated end-diastolic
pressure (EDP). (All pressures
are measured in mm Hg.)
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ti
RA PRIESSURE
wall motion abnormalities were confined to the inferior wall in 13 patients (five hypokinetic and eight
akinetic) and the inferolateral wall in three (all
hypokinetic). Mild apical-septal wall motion abnormalities were present in two patients. Overall, qualitative global LV function appeared adequate in 14
patients and moderately depressed in two. Abnormal
diastolic orientation of the interventricular septum
was noted in all patients; septal flattening occurred in
10, and frank reversal of septal curvature was noted
in six others (Figure 6). Paradoxical systolic septal
B40
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I-:
11
.
f5 i:.:.::
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..
......*b ..,. a_ + _ ... _ .
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(panel B) demonstrates that this
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RA PRESSURE
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descent. In contrast, its relation
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patients (Figure 5), and an exaggerated RV enddiastolic pressure rise was evident in some patients
with augmented RA A waves (Figure 4). Equalization of the RV, RA, and PCW pressures occurred in
11 patients.
Echocardiographic Features
RV cavity enlargement and RV free wall dysfunction (Figure 6) were present in all patients. The RV
free wall was judged to be hypokinetic in three,
akinetic in 10, and dyskinetic in three patients. LV
A
363
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FIGURE 3. Tracings of simultaneous right atrial (RA) pressure and electrocardiogram
(ECG) (panel A) from a patient
with an M pattem demonstrate
most prominent negative deflection (X') coincident with T wave
suggesting a Ydescent. However,
timing of RA pressure with pulmonary artery systolic pressure
(PASP) (panel B) demonstrates
that this descent is coincident
with peak PASP and therefore a
systolic X' descent.
364
Circulation Vol 82, No 2, August 1990
A
B 40[
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RA
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FIGURE 4. Hemodynamic recordings from a patient with a W
pattem. Peaks of Ware formed byprominentA waves, and most
prominent right atrial (RA) descent occurs just before T wave of
electrocaFrdogram (ECG) (panel A). Simultaneous RA and
right ventricular (RV) pressures (panel B) demonstrate that this
prominent descent coincides with peak RV systolic pressure
(RVSP) and is therefore an X' systolic descent, followed by a
comparatively blunted Y descent. Peak RVSP is depressed, RV
relaxtion is prolonged, and there is a dip and rapid rise in RV
diastolic pressure. Prominent R4 A waves are reflected in the
right ventricle as an augmented end-diastolic pressure (EDP) rise
(arrows). These wave form relations are confirmed by simultaneous superimposed RA/RVpressure recordngs (panel C).
motion was present in 14 patients, whereas in two
cases, septal motion was difficult to assess due to
technical limitations. In eight patients, the septum
bulged dramatically into the akinetic right ventricle
in systole in a pistonlike fashion (Figure 6).
Results of Cardiac Catheterization
Eleven patients underwent cardiac catheterization.
One-vessel disease was documented in four patients,
two-vessel disease in two, three-vessel disease in
four, and normal coronary arteries in one. The right
coronary artery was considered the infarct-related
artery in nine patients, a dominant circumflex with a
small hypoplastic right coronary artery was considered the infarct-related artery in one patient, and
normal coronary arteries were observed after thrombolysis in one patient. In the nine patients in whom
the right coronary artery was the culprit vessel, a
high-grade right coronary artery stenosis proximal to
the RV branches was present. The degree of right
coronary artery stenosis was estimated as 85% in one
ECG
FIGURE 5. Hemodynamic recordings from a patient with a
W pattem and severe low cardiac output precipitated by 2°
atrioventricular block (upper panel). Recording of right atrial
(RA) pressure and electrocardiogram (ECG) (upper panel)
demonstrates augmented A waves and prominent X' and
blunted Y descents, confirmed by simultaneous superimposed
RA and right ventricular (RV) pressure recordings (lower
panel). Presence of both X and X' descents, delineated in
conducted beats only (upper panel), demonstrates an additional problem with identification of components of RA
pressure waveform. RVsystolic pressure (RVSP) morphology is
bifid, and a diastolic dip and plateau pattem is evident. Slight
variation in timing of simultaneous superimposed RA/RV
pressure recordings may be due to differences in mamal
frequency response. RVEDP, RV end-diastolic pressure.
patient, more than 95% in two, 99% in two, and total
in four. Four patients had faint distal right coronary
artery collateral flow from the left circulation; in one
case, collateral filling of an RV branch was noted. LV
cineangiography revealed inferoposterior LV wall
motion abnormalities in all patients with lateral
extension in two cases and mild apical-septal hypokinesis in two others. Overall LV ejection fraction
ranged from 45% to 60% (mean, 52%).
Clinical-Hemodynamic Correlations
Patients manifested one of two distinct RA waveform morphologies differentiated by A wave amplitude and associated with disparate clinical courses
(Figure 1). Patients with depressed A waves (M
pattern) had more severe, protracted, and refractory
hemodynamic compromise than patients with augmented A waves (W pattern). Seven of eight patients
Goldstein et al Hemodynamic Compromise With RV Infarction
SHORT AXIS
.
TRANSESCPHAGEAL FOUR
CHAMBER
>\b
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.,a%,
with depressed A waves developed severe persistent
low cardiac outputs despite intact AV conduction
and treatment with inotropic agents. Patients with
diminutive A waves had more severe depression of
cardiac output (M pattern, 2.9±0.7 1/min; W pattern,
3.4+0.3 1/min, p<0.05), required higher dose and
more prolonged inotropic support, and more frequently required intra-aortic balloon pumping (M
pattern, three; W pattern, none) and emergency
revascularizaion for refractory shock (M pattern, five;
W pattern, none). Such patients also had more severe
depression of peak RV systolic pressure (25.5±4.3
compared with 29.6+±3.8 mm Hg, p<0.05) and RV
stroke work (2.9+± 1.5 compared with 6.2-t-1.8 g m/m2,
p<0.05). In contrast, only three of eight patients with
augmented A waves manifested refractory low cardiac output; in each, severe hemodynamic compromise was related to the development and persistence
of AV dyssynchrony. Six patients with augmented
RA A waves manifested a prominent rise in RV
end-diastolic pressure with atrial systole (Figure 4),
whereas patients with severely depressed RA A
waves (M pattern) had a less prominent increase
(Figure 2), as reflected in a lower ratio of RV
end-diastolic pressure to mean RV diastolic pressure
(W pattern 1.43 -+- 0.4; M pattern, 1.11 ± 0. 1, p < 0.05).
Angiographic correlates also were different
between these two groups of patients. Obstruction
365
FIGURE 6. Echocardiographic study
from a patient with a right atrial (RA) M
pattem, refractory shock, and gross evidence of RA infarction at surgery. Images
at end diastole (ED), end systole (ES),
and M-mode (MM) were obtained from
transthoracic short-axis and transesophageal four-chamber views. In short axis
at ED, right ventricle is markedly dilated,
' and septum is reversed curved (open
arrow). Four-chamber view demonstrates marked RA enlargement as well
as severe right ventricular (RV) dilatation and marked reversed septal (VS)
curvature (white arrows). At ES, septum
bulges paradoxically into right ventricle
in a pistonlike action in both short-axis
(open arrow) and four-chamber views
(white arrows). RVfree wall (FW, dark
arrows) was dyskinetic in four-chamber
view. Short-axis M-mode confirms that
septum (VS, white arrows) moves paradoxically in relation to RVcavity and LV
posterior wall (dark arrows). Transesophageal M-mode, oriented with RV
free wall (RVFW) posteriorly, reveals
marked reversed diastolic septal curvature (open arrows) toward left ventricle
(LV) and paradoxical systolic septal
motion (solid white arrows) toward dyskinetic RVFW (dark arrows).
was proximal to the major RA branches of the right
or circumflex coronary artery in all six patients who
had diminished A waves and were undergoing angiography. In contrast, the culprit stenosis was proximal to the RV branches but distal to the RA
branches in four of five patients with augmented A
waves (one patient had normal coronary arteries). In
two patients with depressed A waves who required
emergency surgical revascularization for refractory
shock, gross observation at thoracotomy documented
a dilated and akinetic right atrium consistent with
RA ischemia or infarction.
Discussion
Observations from the present study demonstrate
that hemodynamic compromise in patients with
severe RV infarction results from profound depression of RV free wall contraction and associated
severe RV diastolic dysfunction. When RV contraction is acutely depressed, RV systolic performance is
dependent, in part, on LV septal contraction. The
presence or absence of compensatory changes in RA
function and the integrity of AV synchrony are
important determinants of the hemodynamic impact
of RV systolic and diastolic dysfunction. Precise
quantitation of the magnitude of effect of each of
these abnormalities will require confirmatory data
from future studies.
366
Circulation Vol 82, No 2, August 1990
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Evidence for Diastolic Dysfunction
RV diastolic dysfunction was indicated by the
elevated RV filling pressures, an RV dip and plateau
pattern, and equalization of diastolic filling pressures
in the RA, RV, and PCW pressures, all reflecting the
effects of intrinsic RV myocardial stiffness and pericardial restraint.11,12 Judging from results of animal
studies of RV infarction, equalized filling pressures
result from diastolic ventricular interaction induced
by RV dilatation, mediated by the reversed curved
septum, and exacerbated by elevated intrapericardial
pressure.6-9 Mean RA pressures were elevated in all
patients. When RA waveform components were
identified by timing with RV mechanical correlates,
the RA waveform consistently demonstrated a prominent X but blunted Y descent, reflecting increased
resistance to RV filling throughout diastole. Previous
studies have characterized the Y descent as prominent
in patients with RV infarction10-'3 who are clinically
similar to those described in this report. Patients with
RV infarction manifest a spectrum of RA pressure
morphologies that may be affected not only by the
loading conditions and systolic and diastolic properties of the right heart chambers but also by arrhythmias and tricuspid incompetence. The RA waveforms
observed in the present study are morphologically
similar in appearance to those in patients with normal
sinus rhythm reported in prior studies.10-12 However,
by relating RA waveform components to mechanical
events rather than to electrocardiographic criteria, our
findings demonstrate that the predominant RA
descent is systolic and therefore an X descent,
whereas the diastolic Y descent is blunted. The distinction between X and Y descents may be confounded in some patients by AV dyssynchrony, the
presence of both X and X' descents when a C wave is
present, or significant tricuspid regurgitation, further
emphasizing the importance of timing waveform components to mechanical correlates.
The diastolic abnormality described should not be
unexpected. Ischemia and infarction increase intrinsic RV myocardial stiffness, the infarcted ventricle
dilates at end systole, and ischemia impairs ventricular recoil, relaxation, and early AV filling.15 Therefore, early in diastole there is increased resistance to
filling of the infarcted right ventricle, with progressive impedance to inflow as the right ventricle fills
and ascends a noncompliant diastolic pressurevolume curve. Acute RV dilatation results in elevated intrapericardial pressure,6,7 which further contributes to the pattern of diastolic dysfunction
reflected in the right atrium as a blunted Y descent
and in the RV wave forms as a sharp rise to a plateau.
These diastolic abnormalities contribute to a marked
reduction in RV preload reserve, which further compromises RV performance.
The abnormal diastolic orientation of the interventricular septum seen in our patients also reflects altered
RV diastolic properties. In all patients, the septum was
flattened or reversed curved from the dilated right
ventricle toward the left ventricle, indicative of abnormal RV compliance.1516 Because pressure or volume
overload of one ventricle can alter the compliance and
filling of the contralateral ventricle,15"17-19 the septum
may mediate as well as reflect diastolic dysfunction.
This occurs in experimental RV dysfunction where
similar diastolic interaction alters LV compliance and
contributes to low cardiac output.6-9"14
Role of Right Atrial Function in Severe Right
Ventricular Infarction
RA function was an important determinant of RV
performance and hemodynamic stability in patients
with severe RV infarction. RA pressure and the amplitude of the RA A wave are related to the interaction of
total blood volume, venous tone, atrial contractility,
tricuspid valve integrity, and RV compliance.20-24
Although the mechanisms determining RA A wave
amplitude were not specifically defined in this study,
two distinct RA waveform patterns were identified that
were differentiated by A wave amplitude and associated with disparate clinical courses.
In one half of the patients, the A wave was
markedly augmented, resulting in a W-shaped morphology in the RA pressure waveform, whereas
diminutive A waves imparted an M-shaped morphology in the other half. Increased RA contractility,
which would lead to augmented A waves, would be the
expected response to increases in RA preload and
afterload imposed by the stiff dilated right ventricle.
Judging from the markedly different hemodynamic
and clinical courses of patients according to the presence or absence of augmented A waves, this response
constitutes an important hemodynamic compensatory
mechanism. Augmented A waves, present when the
coronary obstruction leading to RV infarction spared
the RA blood supply, resulted in a greater rise in RV
end-diastole pressure and was associated with higher
peak RV systolic pressures, better cardiac outputs,
less severe hypotension, and a better therapeutic
response to volume and inotropes. Furthermore, such
patients less frequently required urgent revascularization for refractory shock. However, as might be
expected from loss of this atrial contribution,25-28
patients with augmented A waves were more severely
compromised by AV dyssynchrony.
Patients with diminutive A waves tended to have
lower peak RV systolic pressures, more severe low
cardiac output, hypotension necessitating higher
dose and more prolonged inotropic support, and
more frequent urgent revascularization for refractory
shock. Under the increased loading conditions
imposed by the infarcted right ventricle, the lack of
augmented RA A waves appears physiologically
inappropriate and was related to more proximal
infarct-related lesions compromising RA perfusion.
At thoracotomy in two such patients, gross RV
dilatation and akinesis were evident, indicative of RA
ischemia or infarction. These findings indicate that
enhanced RA contraction, reflected in augmented A
waves, improves RV filling and performance,
Goldstein et al Hemodynamic Compromise With RV Infarction
whereas ischemic compromise of RA contractility,
manifest as depressed A waves, contributes to low
cardiac output in severe RV infarction. These observations have not previously been reported.29
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Right Ventricular Systolic Dysfunction
Our data also provide new insights regarding RV
systolic dysfunction in patients with RV infarction.
Severe RV free wall contractile dysfunction on ultrasound was associated with a depressed and often
bifid peak RV systolic pressure, delayed RV upstroke
and relaxation, and severely depressed RV stroke
work. These changes are similar to those observed in
the left ventricle after acute ischemia.15,26 Under
conditions of normal RV function and in experimental animal preparations of RV free wall dysfunction,
left ventricular septal contraction contributes to RV
systolic performance through systolic ventricular
interaction mediated by the septum and reflected in
a bifid RV pressure trace'4 and bifid RV (+)dP/dt.30-34 Judging from these data, the bifid systolic
RV wave form observed may reflect the supportive
effects of ventricular interaction. Paradoxical systolic
septal motion, known to correlate with severe low
cardiac output in clinical RV infarction,2 was consistently present in our patients. In several cases, the
septum bulged into the akinetic right ventricle in
systole in a pistonlike fashion, similar to the septal
motion patterns observed in experimental RV
dysfunction.'434 This septal behavior likely contributes to RV systolic pressure generation and performance through mechanical displacement and primary right-sided septal contraction.
Conclusion
The findings in this study elucidate the importance
of RV diastolic dysfunction to hemodynamic compromise in patients with severe RV systolic dysfunction
due to RV infarction. Impaired RV filling throughout
diastole, reflected in the RA pressure waveform as a
blunted Y descent, decreases RV preload reserve
and renders the right ventricle more dependent on
atrial transport. In addition, RV diastolic dysfunction
alters LV compliance through diastolic ventricular
interaction. Under these conditions, RV systolic
pressure generation and performance are dependent,
in large part, on LV septal contractile contributions.
Enhanced RA function, manifest as augmented RA
A waves, is associated with improved RV performance, which contributes to hemodynamic stability.
The loss of this enhanced atrial transport function,
due to AV dyssynchrony or ischemic depression of
RA function, contributes to severe low cardiac output in patients with RV infarction.
Acknowledgments
The authors wish to express their appreciation to
Dr. Burton E. Sobel for review of the manuscript and
to Linda Gallo for secretarial support.
367
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KEY WORDs * right ventricular infarction * right atrial infarction
* diastolic ventricular interaction * systolic ventricular interaction
Determinants of hemodynamic compromise with severe right ventricular infarction.
J A Goldstein, B Barzilai, T L Rosamond, P R Eisenberg and A S Jaffe
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Circulation. 1990;82:359-368
doi: 10.1161/01.CIR.82.2.359
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1990 American Heart Association, Inc. All rights reserved.
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