A clinician's guide to predicting fluid responsiveness in critical illness: applied physiology and research methodology.
Intravenous fluid administration is often used in critical care with the goal of improving haemodynamics and consequently tissue perfusion and oxygen delivery. While inotropic and vasoactive drugs are often necessary to correct haemodynamic instability, resuscitation usually begins with fluid therapy. As fluid challenge can result in clinical deterioration, the ability to predict haemodynamic response is desirable In this way it might be possible to avoid unnecessary volume replacement in critically ill patients
Cardiac preload is a concept that accounts for the relationship between ventricular filling and stroke volume It has been challenging to apply this concept to clinical practice. For this reason, the study of fluid responsiveness is of increasing research and clinical interest.
The clinical application of predicting fluid responsiveness requires an understanding of relevant physiological principles Furthermore, an improved understanding of these principles should assist the clinician in appraising published data, which has been characterised by significant methodological differences This review aims to assist the clinician by detailing the physiological principles that underlie the prediction of fluid responsiveness in the critically ill. In addition, the potential importance of methodological differences in the current literature will be considered.
Key Words: fluid loading, cardiac, preload, haemodynamic response, critical illness
Predicting fluid responsiveness in critically ill patients is of both scientific and clinical interest. The medical literature on this topic is expanding and the proposed variables have been integrated into several commercial monitoring systems and devices. The principal benefit of predicting haemodynamic response to fluid challenge is avoiding ineffective and potentially deleterious fluid loading.
Intravenous fluid administration is frequently used to improve haemodynamics and consequently tissue perfusion and oxygen delivery. The importance of fluid therapy has recently been highlighted by the demonstration of improved survival of septic patients treated with early goal-directed therapy. (1) However, fluid administration may have adverse effects, including decreased cardiac output, and interstitial fluid accumulation which may worsen gas exchange, decrease myocardial compliance and limit oxygen diffusion to tissues (2-5). Fluid challenge in non-responsive patients may also delay institution of effective treatment, such as inotropes and vasopressors. Excess fluid administration has been associated with increased mortality in critically ill patients (6,7). Therefore, accurate evaluation is important to avoid unnecessary volume replacement.
The clinical application of measurements used to predict fluid responsiveness in the critically ill patient requires an understanding of relevant physiological principles. This review outlines these principles, considering first preload, then fluid responsiveness. The importance of methodological differences in the published data is also reviewed to assist the clinician in appraising the literature.
THE CONCEPT OF PRELOAD
In assessing the contractile properties of muscle, it is important to specify the degree of tension on the muscle when it begins to contract (13), this is referred to as 'preload'. Cardiac preload is a physiological concept that accounts for the relationship between ventricular filling and stroke volume. Validation of a variable as an indicator of cardiac preload requires demonstration that the variable increases with fluid loading and that this increase is associated with an increase in stroke volume that is not attributed to altered myocardial contractility or afterload (11).
The length-tension (Frank-Starling) relationship of cardiac muscle predicts that cardiac stroke volume and the pressure generated during systole will increase when end-diastolic volume increases because this increases the resting muscle length (14). In normal physiological conditions, both ventricles operate on the ascending portion of the Frank-Starling curve and cardiac function is regarded as being 'preload dependent (9). However, the relationship between preload and stroke volume is curvilinear as illustrated in Figure 1. When one or both ventricles operate on the plateau of the Frank-Starling curve, the heart is regarded as 'preload independent (9). Further volume loading will contribute to increased diastolic pressures without a significant increase in stroke volume (15). Under these conditions, only an increase in cardiac contractility, heart rate or a decrease in afterload will result in increased cardiac output (16).
Excess fluid administration can result in right ventricular dilation, which in turn can decrease left ventricular (IV) compliance and filling (17). Decreases in cardiac output have been attributed to this 'ventricular interdependence' caused by right ventricular overdistension (18).
[FIGURE 1 OMITTED]
CLINICAL APPLICATION OF PRELOAD
Preload is a physiological concept that can be difficult to use at the bedside. For clinical purposes, left ventricular preload is usually defined in terms of left ventricular end-diastolic volume. However, bedside assessment of ventricular volumes can be challenging in critically ill patients (19). As a result, pressure-based surrogates, such as central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP) have been measured clinically to assess volume status and response to fluid therapy (20).
In critical illness cardiac filling pressures might not accurately reflect preload. This is because the relationship between end-diastolic pressure and volume can be confounded by a number of factors altering IV compliance (myocardial ischaemia and infarction, hypertrophy, cardiomyopathy) as well as positive end-expiratory pressure (21-23). Even when IV volumes can be measured, this may not be an optimal marker because the relationship between ventricular end-diastolic volume and stroke volume is also influenced by ventricular contractility (Figure 2). Furthermore, the relationship between ventricular end-diastolic volume and stroke volume can change with time, even in the same patient (23).
As illustrated in Figure 2, a given estimate of preload can be associated with preload dependence in one patient and preload independence in another. This result can be observed regardless of the method used to assess preload (24). This can be an important problem clinically because static estimates of preload do not necessarily provide information regarding optimal cardiac filling for a particular patient at a particular point in time.
[FIGURE 2 OMITTED]
Many of the problems associated with applying the concept of preload to critically ill patients are overcome by the concept of fluid responsiveness. It must be noted that the terms 'preload' and 'fluid responsiveness' are not interchangeable. The concept of fluid responsiveness will now be considered in more detail.
THE CONCEPT OF FLUID RESPONSIVENESS
The clinical decision to administer fluid is usually based upon a desire to improve patient haemodynamics. Restoration of ventricular filling should improve stroke volume and cardiac output, as well as correcting or contributing to correction of hypotension (19). The implicit goal is usually improved tissue oxygen delivery via improved tissue perfusion.
Stroke volume is a critical determinant of cardiac output and therefore oxygen delivery (25). Both stroke volume and cardiac output can be monitored at the bedside with commercially available equipment. These variables are clinically meaningful endpoints against which to define the clinical response to fluid challenge (fluid responsiveness). A variable is a predictor of fluid responsiveness if there is a relationship between the baseline value of that variable and changes in stroke volume or consequently, cardiac output after fluid loading (11,19).
A number of prerequisites must be met before a fluid load can result in a significant increase in stroke volume. First of all, the fluid challenge must result in increased cardiac preload. A fluid challenge will increase intravascular volume but not necessarily cardiac preload when venous capacitance is increased or ventricular compliance is decreased (26). In addition, both ventricles must operate on the ascending portion of the Frank-Starling curve (biventricular preload dependence) (9). In other words, the left ventricle is unable to demonstrate fluid responsiveness unless the right ventricle is also preload dependent.
Importantly, a fluid responsive state does not mean that fluid administration is indicated (27). Biventricular preload dependence is the normal physiologic state and does not necessarily imply the need for intravenous fluid challenge. The clinical relevance of predicting the haemodynamic response to fluid challenge lies in the avoidance of ineffective or deleterious fluid administration (28).
PREDICTION OF FLUID RESPONSIVENESS
Clinical examination is of limited value in predicting fluid responsiveness in critically ill patients (29). However, a number of potentially useful predictors have been described. Authors have divided these predictors into static and dynamic variables (28). Examples of static and dynamic variables are presented in Table 2. Static variables are estimates of ventricular preload at a point in time, usually end-expiration. These include variables such as CVP, PAOP and ventricular end-diastolic volume. Dynamic variables are characterised by measurement of variation in haemodynamic measurements in response to changes in cardiac loading conditions". Typically, dynamic variables refer to respiratory induced changes in variables such as right atrial pressure, arterial pressure and aortic blood velocity. In this review, changes in haemodynamic variables due to postural manoeuvres such as head-down tilt (Trendelenburg) or passive leg raising (PLR) will also be regarded as dynamic variables. In general terms, dynamic variables appear to be more robust predictors of fluid responsiveness than static variables (19,28).
Most data validating predictors of fluid responsiveness are derived from studies of deeply sedated mechanically ventilated patients in sinus rhythm (28). In order to best appreciate the physiologic basis of dynamic variables, the influence of mechanical ventilation and postural manoeuvres upon cardiovascular physiology will now be considered further.
CARDIOVASCULAR EFFECTS OF MECHANICAL VENTILATION
Ventilation conveniently provides a mechanism by which ventricular preload is altered (28). Assessing differences between inspiratory and expiratory haemodynamics allows comparison of cardiac function at different levels of cardiac preload without requiring fluid administration (9). This offers insight regarding an individual's cardiac performance in relation to preload dependence and fluid responsiveness.
Prior to considering the physiological effects of mechanical ventilation, it must be noted that even in intubated patients, the effects of spontaneous breathing differ from deeply sedated or paralysed patients because intrathoracic pressure is negative at initiation of or during inspiration, the respiratory rate is variable and intrathoracic pressure swings tend to be much lower (30).
Due to the predominance of data regarding the prediction of fluid responsiveness in the absence of spontaneous respiratory effort, the physiological effects of mandatory positive pressure ventilation upon the cardiovascular system (heart-lung interactions) are summarised in Table 3.
CARDIOVASCULAR EFFECTS OF POSTURAL MANOEUVRES
Changes in body position such as Trendelenburg position and PLR have been proposed as manoeuvres that potentially produce increased cardiac preload by a central translocation of peripheral venous blood". This potentially offers another mechanism by which changes in haemodynamics can be observed without fluid administration. The effect of postural manoeuvres upon stroke volume and cardiac output is transient and might be attenuated in patients with hypovolaemia (12,40).
Trendelenburg position can be associated with effects that might be undesirable in critically ill patients, such as decreased pulmonary compliance" and decreased cerebral blood flow (42). Also, there are scant data regarding the utility of Trendelenburg position in predicting response to fluid challenge. For these reasons, Trendelenburg position will not be discussed further.
The autotransfusion effect of PLR on stroke volume and cardiac output is small and transient". However, dynamic variables based upon PLR have demonstrated value as predictors of fluid responsiveness in critically ill patients (44,45). In contrast to those based upon heart-lung interactions, dynamic variables based upon PLR have demonstrated value in patients with cardiac arrhythmia and spontaneous breathing activity (45).
METHODOLOGICAL DIFFERENCES IN PUBLISHED DATA
There is an increasing quantity of published data regarding the prediction of fluid responsiveness in clinical settings. The significance of study methodology must be appreciated in order to interpret and apply research findings to clinical practice. To date, methodological differences between studies have prevented meta-analysis (28,30). These methodological differences broadly relate to clinical setting, fluid bolus characteristics and evaluation of haemodynamic response.
Patient selection: The clinical decision for a fluid challenge is often used as an eligibility criterion. This would tend to exclude patients who are maximally loaded and select patients more likely to respond to fluid challenge (46). In turn, this process of selection might favourably influence statistical calculations. Alternatively, research involving empiric fluid challenge might be difficult to justify in settings where fluid overload is expected and could be detrimental.
Exclusion criteria can also significantly influence study results. Pulse pressure variation has demonstrated high specificity (96%) in septic patients with acute circulatory failure (47). However, the exclusion of patients with severe hypoxaemia (ratio of arterial oxygen pressure to fraction of inspired oxygen [[P.sub.a][o.sub.2]/Fi[O.sub.2]] < 100 mmHg), might have excluded a number of patients with severe acute respiratory distress syndrome (ARDS) which is often associated with right ventricular dysfunction. For comparison, a similar study that included patients with acute lung injury (ALI) and ARDS reported the specificity of PPV as 87% (48). This was largely explained by a higher rate of false positives associated with right ventricular dysfunction.
Impact of intrathoracic pressures The magnitude of changes in pleural and pericardial pressures influences the value of dynamic variables based upon heart-lung interactions (49). Small changes in intrathoracic pressure throughout the respiratory cycle do not induce significant change in vena caval, pulmonary arterial or aortic flows, even during hypovolaemias (50). Factors affecting intrathoracic pressures during positive pressure ventilation include tidal volume, chest wall and pulmonary compliance (49,51). It has been demonstrated that increasing tidal volume or reducing chest compliance results in increased stroke volume and arterial pressure variations during mechanical ventilation (49,51,52).
In addition to influencing indices of fluid responsiveness, positive pressure ventilation possibly alters cardiac preload dependence (50). By decreasing venous return, increased pleural and pericardial pressures could move cardiac function from preload independence to dependence. Conversely, sternotomy (open chest conditions) increases cardiac preload, decreases stroke volume variation and probably decreases the sensitivity of the heart to fluid challenge. This is illustrated in a study by Reurter et al, in which opening of the thorax and pericardium was associated with an 18% increase in LV end-diastolic area index and a 40% decrease in stroke volume variation (53).
Impact of vascular factors Many dynamic variables rely upon estimation of changes in LV stroke volume by analysis of the arterial pressure waveform (9,28). The relationship between LV stroke volume and blood pressure is influenced by vascular volume, vascular compliance (which is non-linear) and wave reflection (27,54). Furthermore, characteristics of the transduction system, especially damping and attenuation, will influence the relationship between the monitored arterial pressure waveform and stroke volumes (55). It is widely accepted that vascular compliance varies with age and disease; however, debate continues regarding the effect of height and heart rate and the cause of gender differences (54,56). Conditions of special relevance to intensive care that can affect the relationship between peripheral arterial pressure and stroke volume include sepsis, post-cardiopulmonary bypass systemic inflammatory response and vasoactive drug infusion (57-59).
Timing of intervention: Ventricular function influences response to fluid challenge and is not constant in critically ill patients. For instance, Breisblatt et al found that the mean left I V ejection fraction of coronary artery bypass graft patients was reduced from 58% preoperatively to 46% immediately postoperatively, reaching a nadir of 37% in the first few hours following surgery (60).
Fluid bolus characteristics
Volume and type of fluid: The haemodynamic effects of a hypertonic colloid infusion are expected to be more dramatic than those of an equal volume of isotonic crystalloid (28,61). Data resulting from the use of pump blood in cardiac surgery patients might be influenced by lack of consistency in haematocrit and viscosity due to inter-patient variation (62)
Rate of infusion: The speed of volume infusion should greatly influence haemodynamic response because of reflex changes in venous capacitance and equilibration between intra- and extra-vascular compartments. The presence of leaky systemic capillaries, as occurs in sepsis, might increase the impact of this effect (28,63). Thus, a more rapid infusion might result in a more appreciable increase in preload prior to equilibration with extra-cardiac compartments.
Evaluation of haemodynamic response
Definition of response to fluid challenge: Published data differ regarding definition of haemodynamic response in terms of assessing changes in either cardiac output or stroke volume (28). Stroke volume seems a more appropriate endpoint considering frequent reference to the Frank-Starling relationship of cardiac muscle; however, cardiac output is often accepted as a clinically meaningful target. It is measured more reliably than stroke volume by commonly used indicator dilution techniques, such as pulmonary artery or transpulmonary thermodilution. Comparability of future fluid responsiveness research might benefit from availability of individual data including documentation of change in heart rate when change in cardiac output is accepted as the primary endpoint.
Studies differ in the use of cut-offs to distinguish between responders and non-responder (28,30). Acceptance of arbitrary cut-offs allows data to be treated in a binary rather than scalar manner. This permits calculation of sensitivity, specificity and predictive values, as well as construction of ROC curves to compare different methods of predicting fluid responsiveness. However, the clinical relevance of such cut-offs is questionable. Small changes in haemodynamic measurements may represent test-retest variability rather than actual fluid responsiveness (64). Furthermore, these arbitrary cut-offs are often defined in terms of percent augmentation and may not appropriately regard significant increases from a higher baseline.
A number of studies present fluid responsiveness data in terms of correlation between baseline measurements of variables and subsequent haemodynamic response (65). Good discrimination between responders and non-responders provides evidence that such a correlation exists (66). However, explicit reporting of such correlation might offer a more robust way of comparing individual predictors of fluid responsiveness, particularly between studies.
Timing of assessment Although not always specified, many studies evaluate response to fluid challenge immediately following or soon after the completion of the fluid infusion (16,46,62,67-73). Timing of assessment should be important because haemodynamic responses can be transient in nature (12). A delay in assessment might result in underestimation of changes in stroke volume or cardiac output.
Method of assessment Many authors have defined fluid responsiveness in terms of pulmonary artery catheter bolus thermodilution (2,16,18,46,47,72-77) This thermodilution technique has become the de facto clinical standard because of its ease of implementation and long experience in a multitude of clinical settings (13). Reproducibility data suggest that when using commercial pulmonary artery thermodilution devices there must be a minimal difference of 12 to 15% between triplicate determinations of cardiac output to suggest clinical significance (64).
Taking measurements at a single point in the respiratory cycle provides more consistent measurements at the risk of introducing large systematic error in measurement accuracy (78,79). Despite demonstrating acceptable accuracy, continuous cardiac output measurement by pulmonary artery catheter has an inherent delay in responding to abrupt changes in cardiac output that could limit its usefulness in this research area (80,81).
Recently, authors have chosen other means of assessing cardiac output, such as Doppler echocardiography (67,68,82) and transpulmonary thermodilution (83,84). Measurement of stroke volume from two-dimensional echocardiograms is particularly difficult--being limited not only by issues related to image quality but also by variations in image orientation from one scan to the next. Both Doppler evaluation of I V outflow velocity and measurement of I V outflow tract area may contribute to inaccuracy in assessment of stroke volume. However, provided that the angle of insonation remains constant through repeated assessments, its impact upon Doppler measurements should be less important in fluid responsiveness research because emphasis is placed upon changes in measurements, rather than absolute values. The assumption that aortic diameter does not change between repeated Doppler calculations of cardiac output is also potentially incorrect (85,86). While the practical implications of these considerations for fluid responsiveness research are unclear, the test-retest variability of the selected investigation is obviously critical.
Measurements of transpulmonary thermodilution cardiac output are consistent with, but slightly higher than, those obtained from pulmonary artery thermodilution and appear to be unaffected by respiratory phase (87).
Mathematical coupling Another consideration in the measurement of cardiac output is the possibility of mathematical coupling with the proposed predictor of fluid responsiveness. Mathematical coupling describes the potential for invalid correlations between measurements that share common determinants. The potential for mathematical coupling exists between thermodilution cardiac output and right ventricular end-diastolic volume (RVEDV) because RVEDV is derived from stroke volume which is calculated from thermodilution cardiac output (88). The possibility of mathematical coupling between respiratory variation in peak aortic blood flow velocity and changes in cardiac output, when both measured by Doppler techniques, is a topic of current debate (66,89).
The physiological concept of preload is of limited value in guiding fluid therapy in critical care. On the other hand, the prediction of fluid responsiveness potentially offers a useful clinical alternative. Escalating research and clinical interest in this topic has manifest in an increasing presence in the critical care literature and incorporation of new variables into haemodynamic monitoring systems.
However, appropriate use of these new technologies requires an understanding of relevant applied physiology and an appreciation of the impact of methodology upon research results.
This review has outlined many physiological principles that are necessary for the rational application of predicting fluid responsiveness in critical care. An overview of significant methodological differences and their potential impact on results is also presented.
The prediction of fluid responsiveness is an important consideration in attempting to avoid ineffective and potentially deleterious fluid loading in critically ill patients. In this regard, an important point is that prediction of fluid responsiveness does not mandate fluid administration.
A number of limitations characterise the current fluid responsiveness literature. One important consideration is the lack of patient outcome data relating to fluid therapy guided by predictors of fluid responsiveness. An important component of this is the lack of data regarding the potential development of pulmonary oedema.
Comparability of future clinical research is likely to benefit from more comprehensive reporting of results. Further research is required to define the potential benefits of predicting fluid responsiveness in terms of improved patient outcome. Moreover, additional research is warranted with regard to defining which patients need fluid challenge in terms of clinical benefit.
The literature review was conducted with the support of grants from the PA Foundation and the Australian and New Zealand College of Anaesthetists.
Address for reprints: Dr D. Sturgess, School of Medicine, University of Queensland, Princess Alexandra Hospital, Ipswich Road, Wolloongabba, Old. 4102.
Accepted for publication on May 22, 2007.
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D. J. STURGESS *, C. JOYCE ([dagger]), T H. MARWICK ([double dagger]), B. VENKATESH ([section]) School of Medicine University of Queensland and Department of Intensive Care Princess Alexandra Hospital, Brisbane Queensland, Australia
* M.B., B.S., F.R.A.C.G.P, Lecturer, School of Medicine, University of Queensland, Princess Alexandra Hospital and Intensive Care Fellow, Wesley Hospital.
([dagger]) M.B., Ch.B., Ph.D., F.A.N.Z.C.A., F.J.F.I.C.M., Associate Professor of Intensive Care, School of Medicine, University of Queensland, Princess Alexandra Hospital and Director of Intensive Care, Princess Alexandra Hospital.
([double dagger]) M.B., B.S., Ph.D., F.R.A.C.P, F.E.S.C., F.A.C.C., Professor of Medicine, School of Medicine, University of Queensland, Princess Alexandra Hospital and Director of Echocardiography, Princess Alexandra Hospital.
([section]) M.B., B.S., M.D., F.F.A.R.C.S.I., F.R.C.A., E.D.I.C.M., F.J.F.I.C.M., Professor of Intensive Care, School of Medicine, University of Queensland, Princess Alexandra Hospital, Deputy Director in Intensive Care, Wesley Hospital and Staff Specialist in Intensive Care, Princess Alexandra Hospital.
TABLE 1 Glossary of physiological terms Term Description Cardiac preload Describes the relationship between the length of cardiac muscle fibres at the onset of contraction (end-diastolic volume) and the resultant force of contraction (8). Length-tension The curvilinear relationship between cardiac relationship preload and stroke volume, as illustrated of cardiac muscle by the Frank-Starling curve (8). Preload dependence Describes the cardiac condition where increased preload is associated with a significant increase in stroke volume (the heart is operating on the ascending portion of the Frank- Starling curve) (9). Preload Describes the cardiac condition where independence increased preload is not associated with a significant increase in stroke volume (the heart is operating on the plateau portion of the Frank-Starling curve) (9). Ventricular Functional interaction between the cardiac interdependence ventricles that is dependent upon the location of the interventricular septum. Explains the observation that increased right ventricular filling is associated with decreased left ventricular compliance and filling. The effect is less pronounced in the absence of an intact pericardium (10). Fluid An individual is regarded as fluid responsive responsiveness if a fluid challenge results in a significant increase in stroke volume, or consequently cardiac output (11). Biventricular Describes the cardiac condition where both preload dependence cardiac ventricles simultaneously operate upon the ascending portions of their respective Frank-Starling curves. This is the normal physiological state (9). Heart-lung Cyclic changes in cardiac loading conditions interactions resulting from the influence of pressure changes during the respiratory cycle (9). Postural Changes in body position such as Trendelenberg manoeuvres (head down tilt) position and passive leg raising that potentially produce increased cardiac preload by a central translocation of peripheral venous blood (12). TABLE 2 Variables described as indices of cardiac preload or fluid responsiveness in critically ill patients. Variables have been divided into static and dynamic categories Static variables are estimates of ventricular preload at a point in time, usually end-expiration. Dynamic variables are characterised by measurement of variation in haemodynamic measurements in response to changes in cardiac loading conditions Static Dynamic Intracardiac pressures Spontaneous Respiratory Effort Central venous pressure (CVP) Inspiratory decrease in / right atrial pressure (RAP) right atrial pressure ([Delta]RAP) Pulmonary artery occlusion pressure (PAOP) Mandatory Mechanical Ventilation Cardiovascular volumes Systolic pressure variation (SPV) Thermodilution right ventricular Decrease in systolic end-diastolic volume (RVEDV) pressure ([Delta]down) Echocardiographic RVEDV Pulse pressure variation (PPV) Echocardiographic left Pulse contour analysis ventricular end-diastolic stroke volume variation area (LVEDA) / volume (LVEDV) (SVV) Transpulmonary thermodilution Respiratory variation global end-diastolic volume in peak aortic blood (GEDV) velocity ([Delta]Vpeak) Respiratory change in the pre-ejection period ([Delta]PEP) Respiratory systolic variation test (RSVT) Doppler Duration of the aortic Passive Leg Raising velocity signal corrected for heart rate (FTc) Change in aortic blood flow Change in pulse pressure Reprinted from Sturgess DJ, Morgan TJ. Haemodynamic Monitoring. In: Bersten A, Soni N, eds. Oh's Intensive Care Manual. 6th Ed. Sydney: Butterworth Heinemann; 2008. in press, with permission from Elsevier. TABLE 3 The influence of positive pressure ventilation upon cardiac loading conditions (heart-lung interactions) * Decreased preload (decreased venous return) and increased afterload (pulmonary capillary compression) of the right ventricle (31,32). This results in decreased right ventricular stroke volume which is minimal at end-inspiration (33,34). * After a lag of two to three heart beats due to pulmonary blood transit time, this manifests as decreased left ventricular preload (35). Left ventricular stroke volume reaches its lowest level during expiration (32). * Left ventricular stroke volume can actually increase during inspiration as a result of: --Increased pulmonary venous return (36,37) --Increased left ventricular compliance due to decreased right ventricular volume (38) --Decreased left ventricular afterload via external augmentation of the pressure gradient between the left ventricle and extra-thoracic aorta (39).
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|Author:||Sturgess, D.J.; Joyce, C.; Marwick, T.H.; Venkatesh, B.|
|Publication:||Anaesthesia and Intensive Care|
|Article Type:||Clinical report|
|Date:||Oct 1, 2007|
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