Товар добавлен в заявку

Вход

Забыли пароль

Подписка

Резюме

Прикрепить файл

Файл слишком большой

Неподходящий тип файла

Регистрация

Ваш заказ принят!

Спасибо, менеджер свяжется с Вами в ближайшее время.

Алматы, Кунаева 21б, офис 73
+7 (727) 244 66 17
+7 (727) 244 67 17

Терапия недостаточности кровообращения и дыхания с использованием малоинвазивного функционального гемодинамического мониторинга.


1 Introduction/Technological considerations 

In patients instrumented with a central venous line and a thermodilution arterial catheter, the transpulmonary thermodilution technique – currently available on the “PiCCOplus” monitor (Pulsion Medical Systems, Munich, Germany) and on the “CCO” cardiac output module of Philips Medical Systems - allows the simultaneous assessment of valuable cardiovascular and dynamic heart-lung-interaction parameters. After injection of an ice-cold or room-tempered saline bolus central venously, a thermistor in the tip of the arterial catheter is used to measure the downstream temperature changes. The cardiac output is then calculated by the analysis of the thermodilution curve using a modified Stewart-Hamilton algorithm. The monitor also calculates the mean transit time and the exponential downslope time of the transpulmonary thermodilution curve. The product of cardiac output and mean transit time is the volume of distribution of the thermal indicator [1]. This volume of distribution, the so-called “intrathoracic thermal volume”, is made up of the intrathoracic blood volume and the extravascular lung water (fig. 1). The product of cardiac output and exponential downslope time is the “pulmonary thermal volume” [2], which is composed of the pulmonary blood volume and the extravascular lung water (fig. 1). Therefore, the volume of blood contained in the four heart chambers – called the global end-diastolic volume (GEDV) - is easily obtained as the difference between the intrathoracic thermal volume and the pulmonary thermal volume [3,4] (fig. 1). The intrathoracic blood volume has been shown to be quite consistently 25% greater than the GEDV [4]. Therefore, the intrathoracic blood volume is estimated as 1.25 x GEDV and the extravascular lung water (EVLW) as the difference between the intrathoracic thermal volume and the intrathoracic blood volume [4] (fig. 1).

Figure 1. Assessment of global end-diastolic volume (GEDV) and extravascular lung water by transpulmonary thermodilution. (CO = cardiac output, MTt = mean transit time, RA = right atrium, RV = right ventricle, PBV = pulmonary blood volume, LA = left atrium, LV = left ventricle, DSt = downslope time, ITBV = intrathoracic blood volume)

 

2 Transpulmonary thermodilution in shock states

2.1 Discrimination between high and low flow states

Acute circulatory failure is a clinical (cold extremities, low urine output, tachycardia ± systemic hypotension) and biological (renal or hepatic dysfunction, high lactate level…) syndrome that is usually due to a low blood pressure and/or a low cardiac output, since both pressure and flow are major determinants of organ function (fig. 2). A low cardiac output can be responsible of systemic hypotension, but a low blood pressure can also result from systemic vasodilation (fig. 2). Thus, in patients with acute circulatory failure, the measurement of cardiac output is useful to discriminate between high and low flow states, and hence to identify patients who may benefit from vasopressors (high cardiac output and low blood pressure) or volume therapy and/or inotropic drugs (low cardiac output).

Figure 2. Usefulness of transpulmonary thermodilution derived parameters to understand the pathophysiological mechanisms of acute circulatory failure and hence to choose the more appropriate therapeutic card (AP = arterial pressure, CO = cardiac output, SVR = systemic vascular resistance, GEDV = global end-diastolic volume, PPV = pulse pressure variation, SVV = stroke volume variation, GEF = global ejection fraction)

 

The measurement of cardiac output by transpulmonary thermodilution has been validated by many clinical studies as compared to pulmonary artery thermodilution [5-8] and the Fick method [9-11] both in children [8,9,11] and adult patients [5-7,10]. The reproducibility of cardiac output measured by this method is around 5% [5]. However, the measurement of cardiac output alone is generally insufficient to determine the correct therapeutic approach. In this regard, the major determinants of cardiac output, namely preload, contractility and afterload, have to be measured for gaining more insight into the pathophysiology of the circulatory failure.

2.2 Assessment of cardiac preload

In low flow states, assessment of cardiac preload may be useful to identify patients who may benefit from volume loading. Cardiac filling pressures (central venous, right atrial and wedge pressures), though still being widely used, are not accurate indicators of cardiac preload because of erroneous readings of pressure tracings [12], discrepancies between measured and transmural pressures (particularly in patients ventilated with high levels of PEEP or with dynamic hyperinflation) [13], and simply because the physiological relationship between ventricular end-diastolic pressure and volume depends on ventricular compliance [14]. Therefore, several volumetric (as opposed to pressure) parameters have been proposed to assess cardiac preload at the bedside (fig. 3). These include the right ventricular end-diastolic volume evaluated by fast response pulmonary artery catheters [15-17], the left ventricular end-diastolic area measured by echocardiography [18-21], the intrathoracic blood volume evaluated by the double indicator (thermo-dye) dilution technique [22-25], and more recently the GEDV that is evaluated by the easy to apply
single-indicator transpulmonary thermodilution [3,4,26-28] (fig. 3). The GEDV has been shown to behave as a true indicator of cardiac preload. It increases with fluid loading but not with dobutamine, and its increase following fluid loading is correlated with the increase in stroke volume (consistent with the physiological relationship between preload and stroke volume) [26-28].

Figure 3. Volumetric indicators of cardiac preload available at the bedside (RV = right ventricular, LV = left ventricular)

 

Furthermore, although cardiac output and GEDV are derived from the same thermodilution curve, a [31] (in contrast to the mesurement of right ventricular end-diastolic volume), and can be repeated as often as necessary (a single cold bolus, that can be done by a nurse, is sufficient) without being operator-dependent (in contrast to the echocardiographic measurement of left ventricular end-diastolic area).

2.3 Prediction of fluid responsiveness
The real clinical endpoint of fluid loading in low flow states, is not to “normalize” but to adjust preload with regard to the underlying pathology in order to achieve an increase in cardiac output using the volume pathway. Therefore, predictors of fluid responsiveness (i.e. of a significant increase in cardiac output in response to volume) are needed at the bedside. Because the slope of the relationship between ventricular preload and stroke volume depends on ventricular contractility, assessing ventricular preload alone is not sufficient to predict fluid responsiveness [32]. Even volumetric indicators of cardiac preload have been shown to be useful in predicting volume expansion efficacy only when they are low or high, but not for
intermediate values [32]. In this regard, dynamic parameters, mainly the changes in left ventricular stroke volume during mechanical ventilation, have been shown to predict the hemodynamic effects of fluid loading [33,34]. In deeply sedated mechanically ventilated patients, the respiratory changes in left ventricular stroke volume reflect the sensitivity of the heart to changes in preload induced by mechanical insufflation, and hence the sensitivity of the heart to a potential volume loading [34]. The response of the left ventricular stroke output to a mechanical breath can be estimated by the systolic pressure variation and its dDown component [20,35]. However, because the arterial pulse pressure (systolic minus diastolic pressure) is directly proportional to left ventricular stroke volume, the respiratory changes in pulse pressure have been shown to reflect even more closely those of left ventricular stroke volume, and hence to accurately predict fluid responsiveness [36] (fig. 4). The pulse pressure variation (PPV), defined as the percentage of variation of arterial pulse pressure over a floating period of 7.5 seconds, a parameter very close to the
respiratory changes in pulse pressure, is now automatically calculated and displayed on the PiCCOplus monitor.

Figure 4. The respiratory changes in arterial pulse pressure accurately predict fluid responsiveness (adapted from [36])

 

In addition, the PiCCOplus monitor also directly measures the left ventricular stroke volume by pulse contour analysis of arterial pressure. The algorithm used analyses the shape and the area under each stroke and uses mean stroke volume derived from transpulmonary thermodilution cardiac output to calculate the actual patient specific arterial compliance and impedance. Then compliance, impedance and the incremental changes of arterial pressure wave form yield continuous pulse contour stroke volume and cardiac output. Thus, the PiCCOplus monitor is able to provide a beat-to-beat measurement of stroke volume in real time, including the continuous calculation of the stroke volume variation (SVV). The SVV is defined as the percentage change in stroke volume over a floating period of 7.5 seconds. The continuously measured pulse contour cardiac output has been shown to be accurate in many studies [7,37-42]. Like changes in pulse pressure, the SVV has been shown to be an accurate predictor of fluid responsiveness in patients undergoing brain [43] and cardiac surgery [44,45].

2.4 Assessment of cardiac contractility/function
In low flow states, assessment of cardiac contractility/function can be useful to identify patients who may benefit from the administration of inotropic agents. Accurate bedside assessment of cardiac contractility is very difficult since all hemodynamic parameters are more or less dependent on afterload and preload conditions [46]. Nevertheless, the ventricular ejection fraction, which is the ratio of stroke volume to ventricular end-diastolic volume, is commonly used to assess ventricular function [46] (fig. 5). Since the transpulmonary thermodilution provides the GEDV, which is the volume of blood contained in the four heart chambers, the ratio of stroke volume to a quarter of the GEDV represents the global ejection fraction (GEF) of the heart. This parameter, automaticaly calculated and displayed by the monitor, can be used to identify patients with right or/and left ventricular dysfunction (fig. 5).

 

Figure 5. Bedside available indicators of cardiac function (RV = right ventricular, RVEDV = RV end-diastolic volume, SV = stroke volume, LV = left ventricular, LVEDV = LV end-diastolic volume, GEDV = global end-diastolic volume).

 

3 Transpulmonary thermodilution in hypoxemic patients

3.1 Detection of patients with pulmonary edema
Chest X-ray, arterial blood gases and hence the current international definition of ALI/ARDS have been shown to be of little value in identifying patients with pulmonary edema [47-51]. Several techniques have been proposed to assess EVLW in humans [52-54]. Among these techniques, double indicator (thermodye) dilution has been used most frequently in ICU patients [55-61], since other techniques (CT scan, nuclear magnetic resonance imaging, positron emission tomography) are not available at the bedside. The double indicator dilution technique is, however, relatively time consuming, cumbersome and expensive, and therefore has not been widely incorporated into clinical practice. The assessment of EVLW by a single (cold) indicator has been recently validated against the double indicator (thermo-dye) dilution technique [3,4] and the reference gravimetric method [62]. Therefore, the transpulmonary thermodilution technique allows the reliable bedside assessment of EVLW in critically ill patients using a simple cold saline bolus. Since the maintenance of negative fluid balance has been shown to improve the outcome of patients with pulmonary edema [57], the assessment of EVLW is useful to identify and follow patients who may benefit from such a therapeutic strategy. In other words, the routine measurement of EVLW may settle the ongoing controversy between the “dry” and “wet” therapeutic approach of patients with ARDS [63]. Clinical studies are urgently needed to confirm this significant potential value of EVLW measurements. Finally, since the beneficial effects of fluid restriction/depletion in patients with pulmonary edema may be associated with worsening hemodynamics, the simultaneous assessment of cardiac preload (GEDV) and of the sensitivity of the heart to changes in preload (PPV and SVV) can be very helpful to deal with this issue.

3.2 Assessment of pulmonary vascular permeability
By definition, EVLW is increased in both permeability and hydrostatic pulmonary edema. In hydrostatic pulmonary edema, the increase in EVLW is due to an increase in pulmonary blood volume and pressure. Therefore, the ratio of EVLW to pulmonary blood volume is much higher in case of permeability than in case of hydrostatic pulmonary edema (fig. 6). The pulmonary blood volume is easily estimated by the PiCCOplus monitor as 25% of the GEDV [4]. Therefore, the ratio of EVLW to pulmonary blood volume – called the pulmonary vascular permeability index (PVPI) [60] - is automatically calculated and displayed by the PiCCOplus monitor. This parameter may be useful not only to discriminate between hydrostatic and permeability edema but also to assess the effects of various disease states and therapeutic interventions on pulmonary vascular permeability [60].

 

Figure 6. The pulmonary vascular permeability index (PVPI) is calculated as the ratio of extravascular lung water (EVLW) to pulmonary blood volume (PBV). The PVPI is greater in permeability than in hydrostatic pulmonary edema.

 

3.3 Mechanisms of arterial hypoxemia

The main mechanisms of arterial hypoxemia are ventilation/perfusion mismatch and intrapulmonary shunt. However, other mechanisms – mainly the “PvO2 effect” and a right-to-left intracardiac shunt - may also contribute to arterial hypoxemia

• “PvO2 effect”

In patients with increased intrapulmonary shunt, PvO2 is a major determinant of PaO2 [64]. By increasing peripheral oxygen extraction and hence decreasing PvO2, a decrease in cardiac output is able to worsen arterial hypoxemia. In this context, increasing cardiac output either by fluid loading or by inotropic agents may result in increased PvO2, which in turn may improve PaO2 [64]. Therefore, the measurement of cardiac output is important to rule out a low cardiac output and a possible “PvO2 effect” in the presence of arterial hypoxemia. Moreover, the assessment of cardiac preload (GEDV) and of dynamic markers of fluid responsiveness (PPV and SVV) is useful to choose the most appropriate therapy to improve cardiac
output.
• Right-to-left intracardiac shunt

Intracardiac shunt from the right to the left atrium through a patent foramen ovale may also cause hypoxemia. A patent foramen ovale is present at autopsy in 20 to 34% of the general population [65]. The unique nature of this membranous structure allows it to function as a unidirectional valve, opening from right-to-left. The prevalence of right-to-left intracardiac shunt is around 25% in patients with pulmonary hypertension [66] or during positive pressure ventilation [67] and is potentiated by positive end-expiratory pressure (PEEP) [68]. In patients with ALI/ARDS, the real prevalence of RL intracardiac shunt is unknown and may be clinically significant because of the usually associated pulmonary hypertension, mechanical ventilation, and PEEP. Color Doppler examination of interatrial septum and contrast echocardiography can diagnose right-to-left intracardiac shunt [67,68] but are not routinely performed in ALI/ARDS patients. A right-to-left intracardiac shunt is easily (a single cold saline bolus…) evidenced by the visual inspection of the transpulmonary indicator dilution curve [69] (fig. 7). Indeed, in case of right-to-left intracardiac
shunting, one part of the indicator passes through the interatrial septum and reaches rapidly the thermistor-tipped arterial catheter. As a result, the transpulmonary dilution curve appears prematurely and becomes biphasic [69] (fig. 7). Early recognition of such a shunt may have therapeutic implications such as nitric oxide inhalation [70] or PEEP decrease/removal [68]. The efficacy of these maneuvers can be immediately checked by the mere observation of the shape of the transpulmonary indicator dilution curve.

Figure 7. Detection of right-to-left intracardiac shunt by transpulmonary thermodilution: the curve (c = effective curve) appears prematurely and is biphasic.

 

3.4 Prediction of PEEP-induced hemodynamic instability

In ventilated patients with ALI/ARDS, PEEP may improve pulmonary gas exchange. However, it may also decrease cardiac output and thus offset the expected benefits in terms of oxygen delivery. The PEEP induced decrease in cardiac output is assumed to be mainly due to a decrease in systemic venous return secondary to the increased pleural pressure [71,72]. The adverse hemodynamic effects of PEEP are not predicted by conventional static hemodynamic parameters. In contrast, the respiratory changes in left ventricular stroke volume – assessed by arterial waveform analysis - have been shown to be closely related to the decrease in cardiac output in response to PEEP application [73,74], such that the higher the
respiratory changes in arterial pressure on ZEEP, the more marked the decrease in cardiac output after PEEP application [74]. Therefore, PPV and SVV can also be used to predict and hence to prevent the deleterious hemodynamic effects of PEEP.

4 Overview
Most of the hemodynamically unstable and/or severely hypoxemic patients are instrumented with a central venous line and an arterial line. Thus, advanced cardio-respiratory monitoring by the transpulmonary thermodilution method simply requires the use of a specific thermodilution arterial catheter, without any further invasive and costly instrumentation. In patients with circulatory failure, the transpulmonary thermodilution technique allows the simultaneous assessment of cardiac output, cardiac preload (GEDV), cardiac contractility/function (GEF) and the prediction of fluid responsiveness (PPV and SVV). Therefore, the transpulmonary thermodilution allows a better understanding of the pathophysiological mechanisms (vasoplegia, hypovolemia, heart failure) of acute circulatory failure and hence the choice of the most appropriate therapy (fig. 2). In contrast to echocardiography, transpulmonary thermodilution is a nonoperator dependent technique that can be used by all caregivers, in all ICUs, as often as is necessary, and that provides all hemodynamic parameters within few minutes. In hypoxemic patients, transpulmonary thermodilution enables the identification of patients with pulmonary edema (elevated EVLW) as well as the quantification of pulmonary edema and its response to therapeutic maneuvers (e.g. fluid restriction/depletion). In addition, it enables the assessment of pulmonary vascular permeability (PVPI), a better understanding of the pathophysiological mechanisms of hypoxemia (pulmonary edema, low cardiac output, right-to-left intracardiac shunt), and the prediction of the possible deleterious hemodynamic effects of PEEP. In conclusion, the transpulmonary thermodilution technique provides the caregiver a simple, reproducible and integrated approach of the heart and the lungs (cardio-respiratory monitoring) that cannot be considered separately in most critically ill patients.

References

1. Meier P, and Zierler KL (1954) On the theory of indicator-dilution method for measurement of blood flow and volume. J Appl Physiol 6:731-744
2. Newman EV, Merrel M, Genecin A, et al (1951) The dye dilution method for describing the central circulation. An analysis of factors shaping the time-concentration curves. Circulation 4:735-746
3. Neumann P (1999) Extravascular lung water and intrathoracic blood volume: double versus single indicator dilution technique. Intensive Care Med 25:216-219
4. Sakka SG, Rühl CC, Pfeiffer UJ, et al (2000) Assessment of cardiac preload and extravascular lung water by single transpulmonary thermodilution. Intensive Care Med 26:180-187
5. Gödje O, Peyerl M, Seebauer T, et al (1998) Reproducibility of double-indicator dilution measurements of intrathoracic blood volume compartments, extravascular lung water, and liver function. Chest 113:1070-1077
6. Sakka SG, Reinhart K, Meier-hellmann A (1999) Comparison of pulmonary artery and arterial thermodilution cardiac output in critically ill patients. Intensive Care Med 25:843-846
7. Goedje O, Hoeke K, Lichtwarck-Aschoff M, et al (1999) Continuous cardiac output by femoral arterial thermodilution calibrated pulse contour analysis: comparison with pulmonary arterial thermodilution. Crit Care Med 27:2407-2412
8. McLuckie A, Marsh M, Murdoch I, et al (1996) A comparison of pulmonary and femoral artery thermodilution cardiac indices in paediatric intensive care patients. Acta Paediatr 85:336-338
9. Tibby SM, Hatherill M, Marsh MJ, et al (1997) Clinical validation of cardiac output measurements using femoral artery thermodilution with direct Fick in ventilated children and infants. Intensive Care Med 23:987-991
10. Sakka SG, Reinhart K, Wegscheider K, et al (2000) Is the placement of a pulmonary artery catheter still justified solely for the measurement of cardiac output. J Cardiothorac Vasc Anesth 14:119-124
11. Pauli C, Fakler U, Genz T, et al (2002) Cardiac output determination in children: equivalence of the transpulmonary thermodilution method to the direct Fick principle. Intensive Care Med 28:947-952
12. Iberti TJ, Fischer EP, Leibowitz AB, et al (1990) A multicenter study of physician’s knowledge of the pulmonary artery catheter. JAMA 264:2928-2932
13. Teboul JL, Pinsky MR, Mercat A, et al (2000) Estimating cardiac filling pressure in mechanically ventilated patients with hyperinflation. Crit Care Med 28: 3631-3636
14. Calvin JE, Driedger AA, Sibbald WJ (1981) Does the pulmonary capillary wedge pressure predict left ventricular preload in critically ill patients ? Crit Care Med 9:437-443

15. Reuse C, Vincent JL, Pinsky MR (1990) Measurements of right ventricular volumes during fluid challenge. Chest 98:1450-1454
16. Diebel LN, Wilson RF, Tagett MG, et al (1992) End-diastolic volume. A better indicator of preload in the critically ill. Arch Surg 127:817-822
17. Diebel L, Wilson RF, Heins J, et al (1994) End-diastolic volume versus pulmonary artery wedge pressure in evaluating cardiac preload in trauma patients. J Trauma 37:950-955
18. Thys DM, Hillel Z, Goldman ME, et al (1987) A comparison of hemodynamic indices derived by invasive monitoring and two-dimensional echocardiography. Anesthesiology 67:630-634
19. Cheung AT, Savino JS, Weiss SJ, et al (1994) Echocardiographic and hemodynamic indexes of left ventricular preload in patients with normal and abnormal ventricular function. Anesthesiology 81:376-387
20. Tavernier B, Makhotine O, Lebuffe G, et al (1998) Systolic pressure variation as a guide to fluid therapy in patients with sepsis-induced hypotension. Anesthesiology 89:1313-1321
21. Tousignant CP, Walsh F, Mazer CD (2000) The use of transesophageal echocardiography for preload assessment in critically ill patients. Anesth Analg 90:351-355
22. Lichtwarck-Aschoff M, Zeravik J, Pfeiffer UJ (1992) Intrathoracic blood volume accurately reflects circulatory volume status in critically ill patients with mechanical ventilation. Intensive Care Med 18:142-147
23. Preisman S, Pfeiffer U, Lieberman N, et al (1997) New monitors of intravascular volume: a comparison of arterial pressure waveform analysis and the intrathoracic blood volume. Intensive Care Med 23: 651-657
24. Sakka SG, Bredle DL, Reinhart K, et al (1999) Comparison between intrathoracic blood volume and cardiac filling pressures in the early phase of hemodynamic instability of patients with sepsis or septic shock. J Crit Care 14:78-83
25. Goedje O, Seebauer T, Peyerl M, et al (2000) Hemodynamic monitoring by double-indicator dilution technique in patients after orthotopic heart transplantation. Chest 118: 775-781
26. Wiesenack C, Prasser C, Keyl C, et al (2001) Assessment of intrathoracic blood volume as an indicator of cardiac preload: single transpulmonary thermodilution technique versus assessment of pressure preload parameters derived from a pulmonary artery catheter. J Cardiothorac Vasc Anesth
15:584:588
27. Reuter DA, Felbinger TW, Moerstedt K, et al (2002) Intrathoracic blood volume index measured by thermodilution for preload monitoring after cardiac surgery. J Cardiothorac Vasc Anesth 16:191-195
28. Michard F, Alaya S, Zarka V, et al (2002) Effects of volume loading and dobutamine on transpulmonary thermodilution global end-diastolic volume. Intensive Care Med 28:S53
29. McLuckie A, and Bihari D (2000) Investigating the relationship between intrathoracic blood volume index and cardiac index. Intensive Care Med 26:1376-1378
30. Buhre W, Kazmaier S, Sonntag H, et al (2001) Changes in cardiac output and intrathoracic blood volume: a mathematical coupling of data ? Acta Anesthesiol Scand 45:863-867
31. Schiffmann H, Erdlenbruch B, Singer D, et al (2002) Assessment of cardiac output, intravascular volume status, and extravascular lung water by transpulmonary indicator dilution in critically ill neonates and infants. J Cardiothorac Vasc Anesth 16:592-597
32. Michard F, and Teboul JL (2002) Predicting fluid responsiveness in ICU patients. A critical analysis of the evidence. Chest 121:2000-2008
33. Perel A (1998) Assessing fluid responsiveness by the systolic pressure variation in mechanically ventilated patientsAnesthesiology 89:1309-1310
34. Michard F, and Teboul JL (2000) Using heart-lung interactions to assess fluid responsiveness during mechanical ventilation. Crit Care 4:282-289
35. Perel A, Pizov R, Cotev S (1987) Systolic blood pressure variation is a sensitive indicator of hypovolemia in ventilated dogs subjected to graded hemorrhage. Anesthesiology 67:498-502

36. Michard F, Boussat S, Chemla D, et al (2000) Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med 162:134-138
37. Godje O, Thiel C, Lamm P, et al (1999) Less invasive, continuous hemodynamic monitoring during minimally invasive coronary surgery. Ann Thorac Surg 68:1532-1536
38. Buhre W, Weyland A, Kazmaier S, et al (1999) Comparison of cardiac output assessed by pulse contour analysis and thermodilution in patients undergoing minimally invasive direct coronary artery bypass grafting. J Cardiothorac Vasc Anesth 13:437-440
39. Rodig G, Prasser C, Keyl C, et al (1999) Continuous cardiac output measurement: pulse contour analysis versus thermodilution technique in cardiac surgical patients. Br J Anaesth 82:525-530
40. Zollner C, Haller M, Weis M, et al (2000) Beat-to-beat measurement of cardiac output by intravascular pulse contour analysis: a prospective criterion standard study in patients after cardiac surgery. J Cardiothorac Vasc Anesth 14:125-129
41. Goedje O, Hoeke K, Goetz AE, et al (2002) Reliability of a new algorithm for continuous cardiac output determination by pulse-contour analysis during hemodynamic instability. Crit Care Med 30:52-58
42. Della Rocca G, Costa MG, Pompei L, et al (2002) Continuous and intermittent cardiac output measurement: pulmonary artery catheter versus aortic transpulmonary technique. Brit J Anaesth 88:350-356
43. Berkenstadt H, Margalit N, Hadani M, et al (2001) Stroke volume variation as a predictor of fluid responsiveness in patients undergoing brain surgery. Anesth Analg 92:984-989
44. Reuter DA, Kirchner A, Felbinger TW, et al (2002) Optimising fluid therapy in mechanically ventilated patients after cardiac surgery by on-line monitoring of left ventricular stroke volume variations: a comparison to aortic systolic pressure variations. Brit J Anesth 88:124-126
45. Reuter DA, Felbinger TW, Schmidt C, et al (2002) Stroke volume variations for assessment of cardiac responsiveness to volume loading in mechanically ventilated patients after cardiac surgery. Intensive Care Med 28:392-398
46. Robotham JL, Takata M, Berman M, et al (1991) Ejection fraction revisited. Anesthesiology 74:172- 183
47. Baudendistel L, Shields JB, Kaminski DL (1982) Comparison of double indicator thermodilution measurements of extravascular lung water (EVLW) with radiographic estimation of lung water in trauma patients. J Trauma 22:983-988
48. Halperin BD, Feeley TW, Mihm FG, et al (1985) Evaluation of the portable chest roentgenogram for quantitating extravascular lung water in critically ill adults. Chest 88:649-652
49. Eisenberg PR, Hansbrough JR, Anderson D, et al (1987) A prospective study of lung water measurements during patient management in an intensive care unit. Am Rev Respir Dis 136: 662-668
50. Takeda A, Okumura S, Miyamoto T, et al (1995) Comparison of extravascular lung water volume with radiographic findings in dogs with experimentally increased permeability pulmonary edema. J Vet Med Sci 57:481-485
51. Michard F, Zarka V, Alaya S, et al (2002) Extravascular lung water measurements in patients with ALI/ARDS. Intensive Care Med 28:S88
52. Pfeiffer U, Backus G, Blumel G, et al (1990) A fiberoptics based system for integrated monitoring of cardiac output, intrathoracic blood volume, extravascular lung water, O2 saturation, and a-v differences. In: Lewis F, Pfeiffer U, eds. Practical applications of fiberoptics in critical care monitoring. Berlin:SpringerVerlag, 114-125
53. Lewis FR, Elings VB, Christensen JM (1992) Extravascular lung water measurements. In: Artigas A, Lemaire F, Suter PM, Zapol WM, eds. Adult respiratory distress syndrome. Edinburgh: Churchill Livingstone, 215-225

54. Schuster DP (1998) The evaluation of pulmonary edema by measuring lung water. In: Tobin MJ, ed. Principles and practice of intensive care monitoring. New York: McGraw-Hill, 693-705
55. Zeravik J, Pfeiffer UJ (1989) Efficacy of high frequency ventilation combined with volume controlled ventilation in dependency of extravascular lung water. Acta Anaesthesiol Scand 33:568-574
56. Zevarik J, Borg U, Pfeiffer UJ (1990) Efficacy of pressure support ventilation dependent on extravascular lung water. Chest 97:1412-1419
57. Mitchell JP, Schuller D, Calandrino FS, et al (1992) Improved outcome based on fluid management in critically ill patients requiring pulmonary artery catheterization. Am Rev Respir Dis 145:990-998
58. Bindels AJ, vander Hoeven JG, Meinders AE (1999) Pulmonary artery wedge pressure and extravascular lung water in patients with acute cardiogenic pulmonary edema requiring mechanical ventilation. Am J Cardiol 84:1158-1163
59. von Spiegel T, Giannaris S, Wietasch GJK, et al (2002) Effects of dexamethasone on intravascular and extravascular fluid balance in patients undergoing coronary bypass surgery with cardiopulmonary bypass. Anesthesiology 96:827-834
60. Holm C, Tegeler J, Mayr M, et al (2002) Effect of crystalloid resuscitation and inhalation injury on extravascular lung water. Chest 121:1956-1962
61. Boussat S, Jacques T, Levy B, et al (2002) Intravascular volume monitoring and extravascular lung water in septic patients with pulmonary edema. Intensive Care Med 28:712-718
62. Katzenelson R, Preisman S, Berkenstadt H, et al (2001) Extravascular lung water measured by a single indicator technique in dogs. Correlation with gravimetric measurements. Crit Care Med 29:A155
63. Schuster DP (1995) Fluid management in ARDS : « keep them dry » or does it matter ? Intensive Care Med 21 :101-103
64. Dantzker DR and Gutierrez G (1989) Effects of circulatory failure on pulmonary and tissue gas exchange. In: Scharf SM, Cassidy SS, eds. Heart-lung interactions in health and disease. New York: Marcel dekker, 983-1019
65. Hagen PT, Scholz DG, Edwards WD (1984) Incidence and size of patent foramen ovale during the first ten decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 59: 17-20
66. Nootens MT, Berarducci LA, Kaufmann E, et al (1993) The prevalence and significance of a patent foramen ovale in pulmonary hypertension. Chest 104: 1673-5
67. Konstadt SN, Louie EK, Black S, et al (1991) Intraoperative detection of patent foramen ovale by transesophageal echocardiography. Anesthesiology 74: 212-6
68. Cujec B, Polasek P, Mayers I, et al (1993) Positive end-expiratory pressure increases the right-to-left shunt in mechanically ventilated patients with patent foramen ovale. Ann Intern Med 1993; 119: 887-94
69. Swan HJC, Zapata-Diaz J, Wood EH (1953) Dye dilution curves in cyanotic congenital heart disease. Circulation 8: 70-81
70. Fellahi JL, Mourgeon E, Goarin JP, et al (1995) Inhaled nitric oxide-induced closure of a patent foramen ovale in a patient with acute respiratory distress syndrome and life-threatening hypoxemia. Anesthesiology 83:635-638
71. Viquerat CE, Righetti A, Suter PM (1983) Biventricular volumes and function in patients with adult respiratory distress syndrome ventilated with PEEP. Chest 83:509-514
72. Potkin RT, Hudson LD, Weaver LJ, et al (1987) Effect of positive end-expiratory pressure on right and left ventricular function in patients with the adult respiratory distress syndrome. Am Rev Respir Dis 135:307-311
73. Pizov R, Cohen M, Weiss Y, et al (1996) Positive end-expiratory pressure-induced hemodynamic changes are reflected in the arterial pressure waveform. Crit Care Med 24:1381-1387
74. Michard F, Chemla D, Richard C, et al (1999) Clinical use of respiratory changes in arterial pulse pressure to monitor the hemodynamic effects of PEEP. Am J Respir Crit Care Med 159:935-939

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Полезная информация