(Circulation. 1995;92:854-861.)
© 1995 American Heart Association, Inc.
Articles |
Transesophageal Echocardiographic Assessment of Mitral Valve Position and Pulmonary Venous Flow During Cardiopulmonary Resuscitation in Humans
From the Departments of Emergency Medicine (M.H.M., S.M.W., G.T.H.) and Internal Medicine (J.J.H., L.P.L., K.G.S., Y.L.K., J.L.L., W.J.C., K.L.H., J.J.C., P.K., Y.Z.T., W.P.L.), National Taiwan University Hospital, Taipei, Taiwan, ROC.
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Abstract |
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Background The mechanisms of blood flow during closed-chest cardiopulmonary resuscitation (CPR) in humans have been debated since the technique was first described in 1960. Two competing models, the cardiac pump theory and the thoracic pump theory, have been proposed, and some investigators have used mitral valve position during the downstroke of chest compression to distinguish between them. Previous studies using either transthoracic or transesophageal echocardiography have yielded conflicting results, and there have been few, if any, hemodynamic or echocardiographic studies on pulmonary venous flow (PVF) during CPR.
Methods and Results In this study, transesophageal two-dimensional and pulsed Doppler echocardiography were used to study mitral valve position and flow, together with PVF, in 20 adult patients undergoing manual CPR. In the 17 patients who could be analyzed, the mitral valve closed in 5 patients (group 1) during chest compression but stayed open or opened further in the remaining 12 patients (group 2). Peak forward mitral flow occurred during the release phase in group 1 but during the compression phase in group 2. During chest compression, PVF occurred in the forward direction (from the pulmonary vein to the left atrium) in 8 of the group 2 patients (group 2a) and in the backward direction (from the left atrium to the pulmonary vein) in all group 1 patients and the remaining 4 patients in group 2 (group 2b). The downtime (time from collapse to CPR) was significantly shorter (P<.05) for those in group 1 (7.0±4.4 minutes) than in groups 2a (19.8±7.7 minutes) and 2b (17.8±6.8 minutes).
Conclusions Transesophageal echocardiography performed during manual CPR in humans disclosed three different patterns of mitral valve position and PVF during chest compression. The presence of an opened mitral valve with forward mitral flow and backward pulmonary venous flow during chest compression in a small number of subjects underscores this heterogeneity in blood flow and suggests the possible existence of a "left atrium pump" in addition to the currently known "left ventricle pump" and "chest pump" mechanisms.
Key Words: cardiac arrest • cardiopulmonary resuscitation • echocardiography • blood flow
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Introduction |
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Although it has enjoyed widespread use in clinical practice for more than 30 years, the mechanisms of blood flow during closed-chest cardiopulmonary resuscitation1 (CPR) remain controversial. Thus far, efforts to elucidate the physiological basis for blood flow during CPR have included hemodynamic,2 3 4 5 angiographic,6 radionuclide,7 and echocardiographic assessments.8 9 10 11 Many of these studies have been carried out in animal models,2 7 10 11 12 13 14 15 and the degree to which their results could be extrapolated to human beings is not always clear.
The information obtained to date has produced two competing theories to account for the pattern of blood flow observed during closed-chest CPR: According to the heart pump (cardiac compression) theory,1 direct cardiac compression (of the left ventricle) between the sternum and the vertebral column during CPR produces a ventriculoatrial pressure gradient that closes the mitral valve and propels the blood into the systemic circulation. An alternative hypothesis, the chest pump2 6 16 17 theory, provides a means of explaining successful CPR in clinical conditions in which direct cardiac compression is unlikely or does not occur at all.18 According to this theory, the increased intrathoracic pressure produced by chest compression propels the blood into the aorta, and regurgitation of the blood is prevented by venous valves located at thoracic inlets.6 19 Whether the mitral valve opens or closes during chest compression has long been thought to distinguish between these two mechanisms, especially in echocardiographic studies.8 9 10 11 12 A closed mitral valve during the compression phase and forward transmitral flow during the release phase have been held as evidence to support direct cardiac compression,11 12 and (1) an open mitral valve with forward transmitral flow during chest compression and (2) an unchanged left ventricular volume are cited as indicators of the chest pump mechanism.8 9 The introduction of transesophageal echocardiography (TEE) has improved the visualization of the left atrium, mitral valve, and left ventricle during CPR but has not produced uniform results.20 21 22 23 24 Using TEE, Higano et al20 noticed mitral valve closure during chest compression in two adult patients, and Redberg et al21 found similar valve closure during a study conducted on a much larger scale. In contrast, both Wright22 and Porter et al23 reported patients with open mitral valves throughout chest compression. Porter and coworkers also indicated that those patients whose mitral valves were open during chest compression exhibited a lower peak forward transmitral flow than did those patients whose mitral valves closed during chest compression.
The assumption that mitral valve closure during chest compression indicates direct cardiac compression has been challenged by Halperin and coworkers,13 who demonstrated in dogs that mitral closure can be produced by nonuniform increases in intrathoracic pressure in the absence of direct cardiac compression. Despite these results, however, mitral valve opening during chest compression is still generally viewed as a proof for the existence of the chest pump mechanism.
We have now taken a new approach to this controversial subject by using biplane TEE to examine pulmonary venous flow (PVF) as well as transmitral and aortic flow. Until now, most studies have concentrated on mitral and aortic flow, and there have been few, if any, hemodynamic or echocardiographic studies of PVF during CPR. We postulate that if the so-called chest pump does exist and the heart itself works as a conduit, then during chest compression, the PVF, which represents the inflow of this conduit, should also proceed in a forward direction (ie, from the pulmonary vein to the left atrium). To test whether such flow occurs in human beings during manual CPR, we used the higher imaging capacity of biplane TEE to delineate the sequence and direction of blood flow during CPR, paying special attention to mitral valve motion, transmitral flow, and PVF.
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Methods |
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Patient Selection
Twenty adult patients (>20 years old) who were admitted to the emergency department of National Taiwan University Hospital in cardiopulmonary arrest or who developed cardiac arrest in the emergency department were enrolled in the study. Patients whose cardiopulmonary arrest was due to trauma or terminal illness were excluded from the protocol. The time from onset of collapse until arrival at the emergency department and initiation of CPR was estimated by family members, by a bystander who witnessed the collapse, or by ambulance personnel. If the cardiac arrest occurred at the emergency department, the downtime was <1 minute.
Resuscitation Protocol
None of the patients had received
prehospital resuscitation.
Cardiopulmonary resuscitation was instituted as soon as
possible at the emergency department according to the American Heart
Association protocols and procedure algorithms.25 26
Manual chest compression with a 50% duty cycle was performed at the
lower sternum at a rate of 90 compressions per minute guided by a
metronome; 12 ventilations per minute with 100% oxygen were also
delivered through an endotracheal tube. Drug therapy and defibrillation
were given throughout the procedure when indicated. Epinephrine
1 mg IV was given every 5 minutes.
Transesophageal
Echocardiography
After successful endotracheal intubation, a 5-MHz
transesophageal probe was inserted into the distal
esophagus with the patient in a supine position. Biplane TEE was
carried out with an Aloka SSD-870 echocardiographic
machine according to the guidelines of the American Society of
Echocardiography.27
Echocardiographic views were first obtained in the
transverse plane, including (1) a basal short-axis view, (2) an apical
four-chamber view, (3) a transgastric short-axis view, and (4) a
posterior mediastinal view; these were followed by analogous
longitudinal views. The aortic valve and mitral valve motion during the
phases of chest compression were examined, and the contours of the
cardiac chambers were delineated. The direction and timing of the
transmitral flow were recorded by two-dimensional M-mode color flow
mapping and Doppler echocardiography, with the
sampling volume positioned at the tip of the mitral valve leaflets. The
peak transmitral flow velocity was also recorded. In addition, the
direction and timing of PVF during the various phases of CPR were
observed and detected with two-dimensional M-mode color flow mapping
and Doppler echocardiography with the sampling
volume at 0.5 cm from the orifice of the pulmonary
vein28 ; whenever possible, the data were obtained from the
left upper pulmonary vein in the longitudinal plane. All
echocardiographic examinations and metronome signals
were recorded continuously on super VHS videotapes. The tapes were
carefully reviewed by two cardiologists with extensive experience in
TEE who were blinded to the patients' clinical information. Timing of
the stages of chest compression, ie, compression versus release, was
determined independently of flow and mitral valve position and was
guided by metronome signals, echocardiographic
visualization of compression, and displacement noticed on
two-dimensional and color M-mode/pulsed Doppler strips and ECG
artifacts; these ECG artifacts, when present, could approximate the
chest compression as closely as by 20 to 30 milliseconds. The
development of spontaneous echo contrast, defined as a smokelike,
whirling echo pattern within the cardiac chambers,29 was
also monitored.
Statistical Analysis
Continuous variables were expressed as
mean±SD. For
continuous variables, ANOVA was used to compare the significance of
differences among groups. Significance was assumed if
P<.05. If any significant difference was detected among
groups, the Newman-Keuls multiple comparison test was used to identify
any significant differences between individual groups.
Ethical Considerations
The study protocol was approved by the
Ethical Committee on
Human Research of the Department of Emergency Medicine of National
Taiwan University Hospital. Although informed consent could not be
obtained from the patients involved in this CPR research, any family
members present were informed of the purpose of the TEE.
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Results |
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Patient Characteristics
In all 20 patients who were candidates for participation in this study, TEE was performed within 5 minutes of arrival at the emergency department. A satisfactory mitral valve image, mitral flow, and PVF were obtained in only 17 of these individuals. These 17 patients (13 men, 4 women) were used in further analysis (Table
). Their ages ranged from 38 to 72 years (mean,
59 years). None of these patients had received prehospital CPR by
bystanders or ambulance personnel. Only 3 patients survived the
resuscitation attempts, and none survived to be discharged. Medical
histories could be obtained in 11 of the patients: 3 had systemic
hypertension, 2 had known coronary artery disease, 3 had
diabetes mellitus, 1 had chronic obstructive pulmonary disease,
and 2 had had previous cerebral vascular accidents. The presenting
rhythm was ventricular tachycardia/fibrillation in
3 patients, pulseless electrical activity in 8, and asystole in 6. The
estimated time from collapse to CPR ("downtime") ranged from 1 to
30 minutes (mean, 13.1 minutes).
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Aortic and Mitral Valve Position
The aortic valve opened,
with forward aortic flow during chest
compression, in all 17 patients studied. The mitral valve opened during
the release phase in all patients (Figs 1a and
2a). During chest compression, the mitral valve closed
in 5 patients (group 1, Fig 1b) but remained open or opened
further in
the remaining 12 patients (group 2, Fig 2b).
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Transmitral Flow
In all group 1 patients, transmitral flow
exhibited a biphasic or
triphasic pattern, with initial mitral regurgitation
occurring during chest compression. Peak forward mitral flow occurred
later, during the release phase of chest compression (Fig 1c
).
In all group 2 patients, transmitral flow was forward during
chest compression (Fig 2c). No patients in group 2 exhibited
mitral
regurgitation during chest compression.
Pulmonary Venous Flow
Left upper PVF was recorded in 15
patients, and right upper
PVF was recorded in the remaining 2 individuals. In all group 1
patients, the PVF was backward (ie, from the left atrium to the
pulmonary vein) during chest compression and forward during the
release phase (Fig 1d). In group 2 patients, two patterns of
PVF were
noticed: In 8 patients (group 2a), the PVF was forward (ie, from the
pulmonary vein to the left atrium) during chest compression
(Fig 2d), and in the remaining 4 group 2 patients (group 2b),
the PVF
was backward during chest compression (Fig 2e).
Effect of Downtime
The mean estimated downtime was
7.0±4.4 minutes for group
1, 19.8±7.7 minutes for group 2a, and 17.8±6.8 minutes for group
2b.
ANOVA showed a significant difference among these three subsets of
patients (P=.01). Further analysis with the
Newman-Keuls multiple comparison test showed a significant difference
in downtime between group 1 and group 2a (P<.05) and
between group 1 and group 2b (P<.05). No significant
difference was detected between the values for group 2a and group 2b
patients.
Peak Mitral Flow Velocity
Peak forward mitral flow was
42.2±6.3 cm/s in group 1, 24.5±3.7
cm/s in group 2a, and 27.2±4.1 cm/s in group 2b. There was a
significant difference between group 1 and group 2a and between group 1
and group 2b (both P<.001). However, there was no
significant difference between the velocities for group 2a and group 2b
(P>.05).
Spontaneous Echo Contrast
Spontaneous echo contrast was
observed on initial resuscitation
after a lapse time as short as 4 minutes. It also appeared during
pauses in the resuscitation effort. This swirling echo usually
disappeared after initiation or resumption of chest compression, but in
some cases it persisted throughout a prolonged resuscitation
period.
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Discussion |
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The major findings of the present study are as follows: (1) In most patients studied, the mitral valve opened during chest compression in manual CPR, and (2) among those patients with open mitral valves and forward transmitral flow during chest compression, two distinct patterns of PVF were noted, suggesting two different physiological mechanisms governing the generation of blood flow in this group of patients.
Most studies to date have concentrated on the flow pattern at the mitral or aortic level, and, to the best of our knowledge, no systematic study has been made of the PVF during CPR. Indeed, pulmonary circulation during CPR has been analyzed only by measurement of pulmonary artery pressure2 and by radionuclide angiography.7 Since the PVF constitutes the inflow of blood into the left atrium and the left ventricle, it should be considered along with mitral valve position and transmitral flow. If the chest pump model is correct and the left heart serves merely as a conduit, mitral valve opening should occur with forward PVF (from the pulmonary vein into the left atrium) during chest compression. Previous TEE studies have identified PVF in normal subjects to be composed of a monophasic or biphasic forward systolic flow, a monophasic forward diastolic flow, and a small reversal of flow during atrial contraction.30 31 In the present study, TEE provided an easy way to measure and analyze PVF in a real-time and beat-to-beat manner. This approach revealed two patterns of PVF during manual CPR: In one subset of patients, forward mitral flow and PVF were indeed observed during chest compression; however, in a second subset, an open mitral valve was accompanied by backward PVF during chest compression.
When we examined our observations concerning the position and timing of
both mitral flow and PVF during manual CPR, we identified three
different patterns of blood flow (Fig 3). During chest
compression, in group 1 patients we observed mitral valve closure with
mitral regurgitation and forward aortic flow. This
pattern is compatible with the traditional understanding of the heart
pump mechanism22 or, as we call it, the left ventricle
pump. The results of Halperin et al13 suggested that a
chest pump mechanism cannot be excluded in this group of patients, but
no observations analogous to theirs have been reported in humans. In
group 2a patients, during chest compression, we observed a
simultaneous forward flow at the pulmonary venous,
mitral, and aortic levels. This finding provides very strong evidence
for the existence of the chest pump because, in this situation, the
left heart does indeed work as a conduit. In group 2b patients, the
detection of an open mitral valve with forward mitral flow and backward
PVF suggests the possible existence of a left atrium pump as a third
possible mechanism for blood flow during CPR. In this model, the left
atrium, rather than left ventricle, would be the major target of
compression.
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Previous studies using transthoracic or transesophageal echocardiography have also identified phenomena that are consistent with a left atrium pump. Using transthoracic echocardiography, Rich et al9 studied four patients undergoing manual CPR in whom they observed an opened mitral valve, unchanged left ventricular volume, and severe compression of the right ventricle and left atrium during chest compression. In a TEE-based study of cardiac arrest patients in the operating room, Uenishi et al24 also noticed mitral valve opening and remarkable changes in the size of the left atrium during chest compression. They stated that the pressure gradient during chest compression is in the order left atrium>left ventricle>aorta and suggested that the left atrium is the main contributor to the flow generated in the early phase of compression. Nonetheless, in the absence of information about PVF, both Rich et al and Uenishi et al chose the chest pump model as a mechanism to account for their observations.
Having examined PVF as well as mitral and aortic flow, we would
like to propose a new algorithm for echocardiographic
study of the mechanism of blood flow during CPR, one that incorporates
both mitral valve position and PVF (Fig 4). We suggest
that an absence of information about PVF may cause patients with a
possible left atrium pump mechanism to be included among the group of
patients whose results are consistent with a chest pump
mechanism; such a situation would explain, to some extent, the
discrepancies that have been noted among previous studies. We
accordingly suggest that TEE be used and that information on PVF be
taken into consideration in all future
echocardiographic studies of CPR.
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In the present study, we identified downtime as a major determinant of the pump mechanisms considered. Shorter downtimes were associated with a heart pump mechanism, and longer downtimes were associated with a chest pump or left atrium pump mechanism. Since prehospital CPR is rather rare in our country, all of our patients received CPR only after arriving at the emergency department. Such a delay in the initiation of CPR may change the compliance of lungs and heart and thereby alter the mechanisms in effect during CPR.10 It is reasonable to suppose that the increased stiffness of the left ventricle that resulted from the longer lapse time in the group 2 patients made a chest pump or left atrium pump mechanism more likely. No significant difference in downtime was noted between patients with a chest pump mechanism and those with a left atrium pump mechanism; the sample numbers here may have been too small to allow us to detect any differences that might actually exist.
Identification of the pump mechanisms in effect during CPR may also have significant prognostic value. All 3 survivors of initial CPR in the present study belonged to group 1, and this group of patients also demonstrated higher peak transmitral flow velocities. This finding is similar to that of Porter and colleagues,23 who indicated that mitral valve closure during chest compression is associated with higher transmitral flow. Another animal study showed that a higher incidence of mitral valve closure is linked to an increase in systemic cerebral and diastolic myocardial perfusion pressure as well as in cardiac output.12 These observations seem to indicate that the left ventricle pump functions more effectively than the chest pump or the left atrium pump. Further studies involving hemodynamic or end-tidal CO2 measurements32 33 34 may help to establish this hypothesis.
Because of the limited time available to us during CPR, sampling of PVF could be done only from one pulmonary vein in each subject. In healthy subjects, Castello and colleagues30 indicated that a higher Doppler velocity, more laminar-appearing spectral signals, and a better identification of the biphasic systolic forward flow and atrial reversal are obtained when the sampling is done from the left pulmonary vein than from the right pulmonary vein. Others31 35 have suggested that it is important to sample all pulmonary veins when detection of systolic reversal is to be used to identify severe mitral regurgitation, especially if that regurgitation is eccentric. Whether the flow patterns from individual pulmonary venous orifices differ from one another during CPR remains to be determined, and such differences could have added to the variation in PVF patterns that we observed during CPR. In addition, although we noted left atrial compression in some of our patients, we did not measure left atrial volume in our study. A change in the left atrial shape (compression) could have occurred with no change in volume in this thin-walled chamber.
Our study differs from previous studies in several aspects: We systematically studied and analyzed PVF during CPR using biplane TEE, which offers better images of the pulmonary vein than can be obtained with single-plane TEE. On the basis of these observations, we were able to differentiate patients with open mitral valves into two groups, those indicating a chest pump and those indicating a possible left atrium pump mechanism, and we identified downtime as a possible major determinant of the various pump mechanisms. Finally, we showed that different pump mechanisms may have different prognostic meanings.
It is important to note that these three pump models may not be mutually exclusive. Variables other than the downtime, such as compression force and rate, body habitus, airway pressure, and presenting cardiac rhythm, may also influence the pump mechanism at work. Although the cross-sectional design of our present study did not allow us to identify time-related changes in pump mechanism, it would be very interesting to know whether different patterns of blood flow appear in different stages of CPR in the same patient.
Conclusions
This study has revealed that biplane TEE can
provide immediate
anatomic and functional information regarding the mechanism of blood
flow during CPR. On the basis of mitral valve position, transmitral
flow, and PVF during chest compression, we identified the left
ventricle pump, chest pump, and left atrium pump as three possible
mechanisms for generating forward flow during manual CPR. These three
different pump models were associated with downtime and may be related
to patient survival. Further studies that involve more
hemodynamic measurement are needed to determine whether
these pump models are interrelated.
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Acknowledgments |
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The authors would like to thank Dr Deborah Ann McClellan for critical reading and editing of the manuscript. Thanks go also to Mei-Huei Wu and Huei-Ming Kuo for preparing the manuscript and to Hang-Dai Liaw, Chia-Ling Chang, and Mei-Huei Feng for their assistance with transesophageal echocardiography.
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Footnotes |
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Reprint requests to Wen-Pin Lien, MD, Division of Cardiology, Department of Internal Medicine, No 7, Chung-Shan South Rd, Taipei, Taiwan, 100, Republic of China.
Received December 6, 1994; revision received February 1, 1995; accepted February 20, 1995.
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References |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
-
Kouwenhoven WB, Jude JR, Knickerbocker GG.
Closed-chest cardiac massage. JAMA. 1960;173:1064-1067.
-
Rudikoff M, Maughan W, Effron M, Freund P, Weisfeldt
M. Mechanisms of blood flow during cardiopulmonary
resuscitation. Circulation. 1980;61:345-352.
[Free Full Text]
-
Mackenzie GJ, Taylor SH, McDonald AK, Donald KW.
Hemodynamic effects of external cardiac
compression. Lancet. 1964;1:1342-1345. [Medline]
[Order article via Infotrieve]
-
Thomson J, Stenlund R, Rowe G. Intrathoracic
pressure during closed chest cardiac massage. JAMA. 1968;205:116-118. [Medline]
[Order article via Infotrieve]
-
Raessler KL, Kern KB, Sanders AB, Tacker WA, Ewy GA.
Aortic and right atrial systolic pressures during
cardiopulmonary resuscitation: a potential indicator of the
mechanism of blood flow. Am Heart J. 1988;115:1021-1029. [Medline]
[Order article via Infotrieve]
-
Niemann JT, Rosborough JP, Hausknecht M, Gasner D,
Criley JM. Pressure-synchronized cineangiography during
experimental cardiopulmonary resuscitation.
Circulation. 1981;64:985-991.
[Free Full Text]
-
Cohen JM, Chandra N, Alderson PO, Van Aswegen A,
Tsitlik J, Weisfeldt ML. Timing of pulmonary and
systemic blood flow during intermittent high intrathoracic pressure
cardiopulmonary resuscitation in the dog. Am J
Cardiol. 1982;49:1883-1889. [Medline]
[Order article via Infotrieve]
-
Werner J, Greene H, Junko C, Cobb L.
Visualization of cardiac valve motion in man during external
chest compression using two-dimensional
echocardiography.
Circulation. 1981;63:1417-1421.
[Abstract/Free Full Text]
-
Rich S, Wix H, Shapiro E. Clinical assessment
of heart chamber size and valve motion during cardiopulmonary
resuscitation by two-dimensional
echocardiography. Am Heart J. 1981;102:368-373. [Medline]
[Order article via Infotrieve]
-
Deshmukh HG, Weil MH, Trevino RP, Bisera J.
Echocardiographic observations during CPR: a
preliminary report. Crit Care Med. 1985;13:904-906. [Medline]
[Order article via Infotrieve]
-
Deshmukh HG, Weil MH, Gudiputi CV, Trevino RP, Bisera
J, Rackow EC. Mechanisms of blood flow generated by
precordial compression during CPR, I: studies on closed chest
precordial compression. Chest. 1989;95:1092-1099.
[Abstract/Free Full Text]
-
Hackl W, Simon P, Mauritz W, Stenbereithner K.
Echocardiographic assessment of mitral valve
function during mechanical cardiopulmonary resuscitation in
pigs. Anesth Analg. 1990;70:350-356.
[Abstract/Free Full Text]
-
Halperin HR, Weiss JL, Guerci AD, Chandra N, Tsitlik
JE, Brower R, Beattie C, Wurmb E, Caden J, Weisfeldt ML. Cyclic
elevation of intrathoracic pressure can close the mitral valve during
cardiac arrest in dogs. Circulation. 1988;78:754-760.
[Abstract/Free Full Text]
-
Feneley MP, Maier GW, Gaynor JW, Gall SA, Kisslo JA,
Davis JW, Rankin JS. Sequence of mitral valve motion and
transmitral blood flow during cardiopulmonary resuscitation in
dogs. Circulation. 1987;76:353-375.
-
Barsan W, Levy R. Experimental design for study
of cardiopulmonary resuscitation in dogs. Ann
Emerg Med. 1981;10:135-137. [Medline]
[Order article via Infotrieve]
-
Chandra N, Rudikoff M, Weisfeldt M.
Simultaneous chest compression and ventilation at
high airway pressure during cardiopulmonary
resuscitation. Lancet. 1980;1:175-178. [Medline]
[Order article via Infotrieve]
-
Weisfeldt M, Chandra M. Physiology of
cardiopulmonary resuscitation. Annu Rev Med. 1981;32:435-442. [Medline]
[Order article via Infotrieve]
-
Criley JM, Blaufuss AH, Kissel GL. Cough-induced
cardiac compression: self-administered form of cardiopulmonary
resuscitation. JAMA. 1976;236:1246-1250.[Abstract]
-
Paradis NA, Martin GB, Goetting MG, Rosenberg JM,
Rivers EP, Appleton TJ, Nowak RM. Simultaneous
aortic, jugular bulb, and right atrial pressures during
cardiopulmonary resuscitation in humans: insights into
mechanisms. Circulation. 1989;80:361-368.
[Abstract/Free Full Text]
-
Higano ST, Oh JK, Ewy GA, Seward JB. The
mechanism of blood flow during closed chest cardiac massage in humans:
transesophageal echocardiographic
observations. Mayo Clin Proc. 1990;65:1432-1440. [Medline]
[Order article via Infotrieve]
-
Redberg RF, Tucker KJ, Cohen TJ, Dutton JP,
Callaham ML, Schiller NB. Physiology of blood flow during
cardiopulmonary resuscitation: a
transesophageal echocardiographic
study. Circulation. 1993;88:534-542.
[Abstract/Free Full Text]
-
Wright RF. Transesophageal
echocardiography during cardiopulmonary
resuscitation in humans. Circulation.
1990;82(suppl III):III-483. Abstract.
-
Porter TR, Ornato JP, Guard CS, Roy VG, Burns CA, Nixon
JV. Transesophageal
echocardiography to assess mitral valve function
and flow during cardiopulmonary resuscitation. Am
J Cardiol. 1992;70:1050-1060.
-
Uenishi M, Sugimoto M, Sawada Y, Terai C.
Transesophageal
echocardiography during external chest compression
in humans. Anesthesiology. 1984;60:618-619. [Medline]
[Order article via Infotrieve]
-
Guidelines for cardiopulmonary resuscitation
and emergency cardiac care: Recommendations of the 1992 National
Conference. Emergency Cardiac Care Committee and
Subcommittees, American Heart Association. JAMA. 1992;268:2171-2302. Reprint No. 70-0014 (SA). [Medline]
[Order article via Infotrieve]
-
Report of the American Heart Association task force on
the future of cardiopulmonary resuscitation.
Cobb LA, Eliastam M, Kerber RE, Melker R, Moss AJ, Newell L,
Paraskos JA, Weaver WD, Weil M, Weisfelt ML.
Circulation. 1992;85:2346-2355.
Reprint No. 71-0015 (SA).
[Free Full Text]
-
Pearlman AS, Gardin JM, Martin RP, Parisi AF, Popp RL,
Quinones MA, Stevenson JF, Schiller NB, Seward JB, Stewart WJ.
Guidelines for physician training in
transesophageal echocardiography:
recommendations of the American Society of
Echocardiography Committee for Physician Training
in Echocardiography. J Am
Soc Echocardiogr. 1992;5:187-194. [Medline]
[Order article via Infotrieve]
-
Seward JB, Khandheria BK, Edwards WD, Oh JK, Freeman
WK, Tajik AJ. Biplanar transesophageal
echocardiography: anatomic correlations, image
orientation, and clinical applications. Mayo Clin
Proc. 1990;65:1193-1213. [Medline]
[Order article via Infotrieve]
-
Huang JJ, Kuan P, Chen JJ, Ko YL, Cheng JJ, Lin JL,
Tseng YZ, Lien WP. Significance of left atrial spontaneous echo
contrast in rheumatic mitral valve disease as a predictor of systemic
arterial embolization: a transesophageal
echocardiographic study. Am Heart J. 1994;127:880-885. [Medline]
[Order article via Infotrieve]
-
Castello R, Pearson AC, Lenzen P, Labovitz A.
Evaluation of pulmonary venous flow by
transesophageal echocardiography in
subjects with a normal heart: comparison with transthoracic
echocardiography. J Am Coll
Cardiol. 1991;18:65-71. [Abstract]
-
Klein AL, Tajik J. Doppler assessment of
pulmonary venous flow in healthy subjects and in patients with
heart disease. J Am Soc Echocardiogr. 1991;4:379-392. [Medline]
[Order article via Infotrieve]
-
Weil M, Bisera J, Trevino R, Rachow E. Cardiac
output and end-tidal carbon dioxide. Crit Care Med. 1985;13:907-909. [Medline]
[Order article via Infotrieve]
-
Sanders A, Kern K, Otto C, Milander M, Ewy G.
End-tidal carbon dioxide monitoring during
cardiopulmonary resuscitation: a prognostic indicator for
survival. JAMA. 1989;262:1347-1351. [Abstract]
-
Callaham M, Barton C. Prediction of outcome of
cardiopulmonary resuscitation from end-tidal carbon dioxide
concentration. Crit Care Med. 1990;18:358-362. [Medline]
[Order article via Infotrieve]
-
Lai LP, Shyu KG, Chen JJ, Ma HM, Hwang JJ, Li YH, Wang
TZ, Lin JM, Ko YL, Lin JL, Kuan PL, Lien WP. Usefulness of
pulmonary venous flow pattern and maximal mosaic jet area
detected by transesophageal
echocardiography in assessing the severity of
mitral regurgitation. Am J Cardiol. 1993;72:1310-1313.[Medline]
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