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Fifteen hundred simultaneous measurements of blood volume and CVP in a heterogenous cohort of 188 ICU patients demonstrating no association between these two variables ( r ϭ 0.27). The correlation between ⌬ CVP and change in blood volume was 0.1 ( r 2 ϭ 0.01). This study demonstrates that patients with a low CVP may have volume overload and likewise patients with a high CVP may be volume depleted. Reproduced with permission from Shippy et al. 11 

Fifteen hundred simultaneous measurements of blood volume and CVP in a heterogenous cohort of 188 ICU patients demonstrating no association between these two variables ( r ϭ 0.27). The correlation between ⌬ CVP and change in blood volume was 0.1 ( r 2 ϭ 0.01). This study demonstrates that patients with a low CVP may have volume overload and likewise patients with a high CVP may be volume depleted. Reproduced with permission from Shippy et al. 11 

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Central venous pressure (CVP) is used almost universally to guide fluid therapy in hospitalized patients. Both historical and recent data suggest that this approach may be flawed. A systematic review of the literature to determine the following: (1) the relationship between CVP and blood volume, (2) the ability of CVP to predict fluid responsivenes...

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Context 1
... venous pressure (CVP) is the pressure recorded from the right atrium or superior vena cava. CVP is measured (usually hourly) in almost all patients in ICUs throughout the world, in emergency department patients, well as in patients undergoing major surgery. CVP is frequently used to make decisions regarding the administration of fluids or diuretics. Indeed, internationally endorsed clinical guidelines 1 recommend using CVP as the end point of fluid resuscitation. The basis for using CVP to guide fluid management comes from the dogma that CVP reflects intravascular volume; specifically, it is widely believed that patients with a low CVP are volume depleted while patients with a high CVP are volume overloaded. This concept is taught to medical students as well as to residents and fellows across a wide range of medical and surgical disciplines. Indeed an authoritative textbook 2 of cardiovascular physiology states as a key concept that “[the] central venous pressure gives clinically relevant information about circulatory [and volume] status.” The chapter on cardiovascular monitoring in a standard anesthe- siology text 3 states that “the most important applica- tion of CVP monitoring is to provide an estimate of the adequacy of circulating blood volume”, and “[that] trends in CVP during anesthesia and surgery are also useful in estimating fluid or blood loss and guiding replacement therapy.” Over 25 years ago, the “5–2” rule for guiding fluid therapy was popularized. 4 According to this rule, the change in CVP following a fluid challenge is used to guide subse- quent fluid management decisions. This rule is still widely used today. Recently, the idea that the CVP reflects blood volume has been challenged. Since CVP plays such a central role in the fluid management strategy of hospitalized patients, the goal of this study was to systemically review the evidence that supports this practice. The initial search strategy generated 206 citations; of these, 189 were excluded due to trial design or failure to report an outcome variables of interest. An additional seven studies were identified from the bibliographies of the selected articles and review articles. Of the 24 studies included in this analysis, 5 studies compared CVP with the measured circulating blood volume while 19 studies determined the relationship between CVP and change in cardiac performance following a fluid challenge (generally defined as a Ͼ 10 to 15% increase in stroke index/ cardiac index). In all, 830 patients across a spectrum of medical and surgical disciplines were studied 10 –33 (Tables 1, 2). In three studies, 10,15,33 the correlation coefficients were not reported in the article but were calculated from the raw data. The pooled correlation coefficient between the CVP and measured blood volume was 0.16 (95% CI, 0.03 to 0.28; r 2 ϭ 0.02). Heterogeneity was present between studies. Figure 1 illustrates the relationship between CVP and measured blood volume from the study of Shippy et al. 11 Overall 56 Ϯ 16% (mean Ϯ SD) of the patients included in this review responded to a fluid challenge. The pooled correlation coefficient between baseline CVP and change in stroke index/ cardiac index (reported in 10 studies) was 0.18 (95% CI, 0.08 to 0.28). The pooled area under the ROC curve (reported in 10 studies) was 0.56 (95% CI, 0.51 to 0.61). The pooled correlation between ⌬ CVP and change in stroke index/cardiac index (reported in seven studies) was 0.11 (95% CI, 0.01 to 0.21). The baseline CVP (reported in 11 studies) was 8.7 Ϯ 2.3 mm Hg in the responders, as compared to 9.7 Ϯ 2.2 mm Hg in nonresponders (not signficant; p ϭ 0.3). The Q statistic was not significant for the pooled correlation and area under the curve statistic. The results of this systematic review are clear: (1) there is no association between CVP and circulating blood volume, and (2) CVP does not predict fluid responsiveness across a wide spectrum of clinical conditions. In none of the studies included in this analysis was CVP able to predict either of these variables. Indeed, the pooled area under the ROC curve was 0.56. The ROC curve is a statistical tool that helps assess the likelihood of a result being a true positive vs a false positive. As can be seen from Figure 2, an ROC of 0.5 depicts the true-positive rate equal to the false-positive rate; graphically, this is represented by the straight line in Figure 1. The higher the AUC, the greater the diagnostic accuracy of a test. Ideally, the AUC should be between 0.9 to 1 (0.8 to 0.9 indicates adequate accuracy with 0.7 to 0.8 being fair, 0.6 to 0.7 being poor, and 0.5 to 0.6 indicating failure). In other words, our results suggest that at any CVP the likelihood that CVP can accurately predict fluid responsiveness is only 56% (no better than flipping a coin). Furthermore, an AUC of 0.56 suggests that there is no clear cutoff point that helps the physician to determine if the patient is “wet” or “dry.” It is important to emphasize that a patient is equally likely to be fluid responsive with a low or a high CVP (Fig 1). The results from this study therefore confirm that neither a high CVP, a normal CVP, a low CVP, nor the response of the CVP to fluid loading should be used in the fluid management strategy of any patient. The strength of our review includes the rigorous selection criteria used to identify relevant studies as well as the use of quantitative end points. 8,9,34 Furthermore, the studies are notable for the consistency (both in magnitude and direction) of their findings. This suggests that the findings are likely to be true. 8,9,34 The results of our study are most disturb- ing considering that 93% of intensivists report using CVP to guide fluid management. 35 It is likely that a similar percentage (or more) of anesthesiologists, nephrologists, cardiologists, and surgeons likewise use CVP to guide fluid therapy. It is important to note that none of the studies included in our analysis took the positive end-expiatory pressure levels or changes in intrathoracic pressure into account when recording CVP. This is important because right ventricular filling is dependent on the transmural right atrial pressure gradient rather than the CVP alone. 36 However, in the real world, transmural filling pressures are rarely if ever calculated. As demonstrated by this study, only about a half of patients administered a fluid bolus will demonstrate a positive hemodynamic response to the intervention. With an ROC of 0.56, the play of chance (or a dice) will be as helpful as CVP in predicting which patients will respond to a fluid challenge. If fluid resuscitation is guided by CVP, it is likely that patients will have volume overload and pulmonary edema. Indeed the practice parameters for hemodynamic support of sepsis in adult patients concludes that “fluid infusion should be titrated to a filling pressure” and that “pulmonary edema may occur as a complication of fluid resuscitation and necessitates monitoring of arterial oxygenation.” 37 Should volume overload and pulmonary edema be the end point of fluid resuscitation? 38 This is clinically important because a positive fluid balance in both ICU patients and those undergoing surgery has been associated with increased complications and a higher mortality. 39 – 41 It is however equally likely that resuscitation guided by CVP will results in inadequate volume replacement. Furthermore, the use of diuretics based on CVP may result in intravascular volume depletion leading to poor organ perfusion and ultimately renal failure and multiorgan failure because a “high” CVP does not necessarily reflect volume overload. Fundamentally the only reason to give a patient a fluid challenge is to increase the stroke volume. 6 This assumes that the patient is on the ascending portion of the Frank-Starling curve and has “recruitable” cardiac output. Once the left ventricle is functioning near the “flat” part of the Frank-Starling curve, fluid loading has little effect on cardiac output and only serves to increase tissue edema and to promote tissue dysoxia. It is therefore crucial during the resuscitation phase of all critically ill patients to determine whether the patient is fluid responsive or not; this determines the optimal strategy of increas- ing cardiac output and oxygen delivery. 42 The results from this article clearly demonstrate that CVP should not be used for this purpose. The notion that CVP does not reflect intravascular volume and is a misleading tool for guiding fluid therapy is not new. In an article published in 1971, Forrester and colleagues, 43 the pioneers of hemodynamic monitoring, concluded that “CVP monitoring in acute myocardial infarction is at best of limited value and at worst seriously misleading.” In their landmark article that was published in 1975, Baek and colleagues 10 convincingly established that “there was no correlation of blood volume with central venous pressure” and suggest that “inaccurate physiologic evaluation of critically ill patients is likely to jeopardize survival by inviting inappropriate and ineffectual therapy.” In 1977, Dr. Burch, 44 a well- respected cardiologist, noted that “to accept non- critically the level of central venous pressure as a quantitative index of blood volume can only lead to physiologic and/or therapeutic errors.” The observa- tions of Forrester et al, 43 Baek ...
Context 2
... venous pressure (CVP) is the pressure recorded from the right atrium or superior vena cava. CVP is measured (usually hourly) in almost all patients in ICUs throughout the world, in emergency department patients, well as in patients undergoing major surgery. CVP is frequently used to make decisions regarding the administration of fluids or diuretics. Indeed, internationally endorsed clinical guidelines 1 recommend using CVP as the end point of fluid resuscitation. The basis for using CVP to guide fluid management comes from the dogma that CVP reflects intravascular volume; specifically, it is widely believed that patients with a low CVP are volume depleted while patients with a high CVP are volume overloaded. This concept is taught to medical students as well as to residents and fellows across a wide range of medical and surgical disciplines. Indeed an authoritative textbook 2 of cardiovascular physiology states as a key concept that “[the] central venous pressure gives clinically relevant information about circulatory [and volume] status.” The chapter on cardiovascular monitoring in a standard anesthe- siology text 3 states that “the most important applica- tion of CVP monitoring is to provide an estimate of the adequacy of circulating blood volume”, and “[that] trends in CVP during anesthesia and surgery are also useful in estimating fluid or blood loss and guiding replacement therapy.” Over 25 years ago, the “5–2” rule for guiding fluid therapy was popularized. 4 According to this rule, the change in CVP following a fluid challenge is used to guide subse- quent fluid management decisions. This rule is still widely used today. Recently, the idea that the CVP reflects blood volume has been challenged. Since CVP plays such a central role in the fluid management strategy of hospitalized patients, the goal of this study was to systemically review the evidence that supports this practice. The initial search strategy generated 206 citations; of these, 189 were excluded due to trial design or failure to report an outcome variables of interest. An additional seven studies were identified from the bibliographies of the selected articles and review articles. Of the 24 studies included in this analysis, 5 studies compared CVP with the measured circulating blood volume while 19 studies determined the relationship between CVP and change in cardiac performance following a fluid challenge (generally defined as a Ͼ 10 to 15% increase in stroke index/ cardiac index). In all, 830 patients across a spectrum of medical and surgical disciplines were studied 10 –33 (Tables 1, 2). In three studies, 10,15,33 the correlation coefficients were not reported in the article but were calculated from the raw data. The pooled correlation coefficient between the CVP and measured blood volume was 0.16 (95% CI, 0.03 to 0.28; r 2 ϭ 0.02). Heterogeneity was present between studies. Figure 1 illustrates the relationship between CVP and measured blood volume from the study of Shippy et al. 11 Overall 56 Ϯ 16% (mean Ϯ SD) of the patients included in this review responded to a fluid challenge. The pooled correlation coefficient between baseline CVP and change in stroke index/ cardiac index (reported in 10 studies) was 0.18 (95% CI, 0.08 to 0.28). The pooled area under the ROC curve (reported in 10 studies) was 0.56 (95% CI, 0.51 to 0.61). The pooled correlation between ⌬ CVP and change in stroke index/cardiac index (reported in seven studies) was 0.11 (95% CI, 0.01 to 0.21). The baseline CVP (reported in 11 studies) was 8.7 Ϯ 2.3 mm Hg in the responders, as compared to 9.7 Ϯ 2.2 mm Hg in nonresponders (not signficant; p ϭ 0.3). The Q statistic was not significant for the pooled correlation and area under the curve statistic. The results of this systematic review are clear: (1) there is no association between CVP and circulating blood volume, and (2) CVP does not predict fluid responsiveness across a wide spectrum of clinical conditions. In none of the studies included in this analysis was CVP able to predict either of these variables. Indeed, the pooled area under the ROC curve was 0.56. The ROC curve is a statistical tool that helps assess the likelihood of a result being a true positive vs a false positive. As can be seen from Figure 2, an ROC of 0.5 depicts the true-positive rate equal to the false-positive rate; graphically, this is represented by the straight line in Figure 1. The higher the AUC, the greater the diagnostic accuracy of a test. Ideally, the AUC should be between 0.9 to 1 (0.8 to 0.9 indicates adequate accuracy with 0.7 to 0.8 being fair, 0.6 to 0.7 being poor, and 0.5 to 0.6 indicating failure). In other words, our results suggest that at any CVP the likelihood that CVP can accurately predict fluid responsiveness is only 56% (no better than flipping a coin). Furthermore, an AUC of 0.56 suggests that there is no clear cutoff point that helps the physician to determine if the patient is “wet” or “dry.” It is important to emphasize that a patient is equally likely to be fluid responsive with a low or a high CVP (Fig 1). The results from this study therefore confirm that neither a high CVP, a normal CVP, a low CVP, nor the response of the CVP to fluid loading should be used in the fluid management strategy of any patient. The strength of our review includes the rigorous selection criteria used to identify relevant studies as well as the use of quantitative end points. 8,9,34 Furthermore, the studies are notable for the consistency (both in magnitude and direction) of their findings. This suggests that the findings are likely to be true. 8,9,34 The results of our study are most disturb- ing considering that 93% of intensivists report using CVP to guide fluid management. 35 It is likely that a similar percentage (or more) of anesthesiologists, nephrologists, cardiologists, and surgeons likewise use CVP to guide fluid therapy. It is important to note that none of the studies included in our analysis took the positive end-expiatory pressure levels or changes in intrathoracic pressure into account when recording CVP. This is important because right ventricular filling is dependent on the transmural right atrial pressure gradient rather than the CVP alone. 36 However, in the real world, transmural filling pressures are rarely if ever calculated. As demonstrated by this study, only about a half of patients administered a fluid bolus will demonstrate a positive hemodynamic response to the intervention. With an ROC of 0.56, the play of chance (or a dice) will be as helpful as CVP in predicting which patients will respond to a fluid challenge. If fluid resuscitation is guided by CVP, it is likely that patients will have volume overload and pulmonary edema. Indeed the practice parameters for hemodynamic support of sepsis in adult patients concludes that “fluid infusion should be titrated to a filling pressure” and that “pulmonary edema may occur as a complication of fluid resuscitation and necessitates monitoring of arterial oxygenation.” 37 Should volume overload and pulmonary edema be the end point of fluid resuscitation? 38 This is clinically important because a positive fluid balance in both ICU patients and those undergoing surgery has been associated with increased complications and a higher mortality. 39 – 41 It is however equally likely that resuscitation guided by CVP will results in inadequate volume replacement. Furthermore, the use of diuretics based on CVP may result in intravascular volume depletion leading to poor organ perfusion and ultimately renal failure and multiorgan failure because a “high” CVP does not necessarily reflect volume overload. Fundamentally the only reason to give a patient a fluid challenge is to increase the stroke volume. 6 This assumes that the patient is on the ascending portion of the Frank-Starling curve and has “recruitable” cardiac ...
Context 3
... CVP is measured (usually hourly) in almost all patients in ICUs throughout the world, in emergency department patients, well as in patients undergoing major surgery. CVP is frequently used to make decisions regarding the administration of fluids or diuretics. Indeed, internationally endorsed clinical guidelines 1 recommend using CVP as the end point of fluid resuscitation. The basis for using CVP to guide fluid management comes from the dogma that CVP reflects intravascular volume; specifically, it is widely believed that patients with a low CVP are volume depleted while patients with a high CVP are volume overloaded. This concept is taught to medical students as well as to residents and fellows across a wide range of medical and surgical disciplines. Indeed an authoritative textbook 2 of cardiovascular physiology states as a key concept that “[the] central venous pressure gives clinically relevant information about circulatory [and volume] status.” The chapter on cardiovascular monitoring in a standard anesthe- siology text 3 states that “the most important applica- tion of CVP monitoring is to provide an estimate of the adequacy of circulating blood volume”, and “[that] trends in CVP during anesthesia and surgery are also useful in estimating fluid or blood loss and guiding replacement therapy.” Over 25 years ago, the “5–2” rule for guiding fluid therapy was popularized. 4 According to this rule, the change in CVP following a fluid challenge is used to guide subse- quent fluid management decisions. This rule is still widely used today. Recently, the idea that the CVP reflects blood volume has been challenged. Since CVP plays such a central role in the fluid management strategy of hospitalized patients, the goal of this study was to systemically review the evidence that supports this practice. The initial search strategy generated 206 citations; of these, 189 were excluded due to trial design or failure to report an outcome variables of interest. An additional seven studies were identified from the bibliographies of the selected articles and review articles. Of the 24 studies included in this analysis, 5 studies compared CVP with the measured circulating blood volume while 19 studies determined the relationship between CVP and change in cardiac performance following a fluid challenge (generally defined as a Ͼ 10 to 15% increase in stroke index/ cardiac index). In all, 830 patients across a spectrum of medical and surgical disciplines were studied 10 –33 (Tables 1, 2). In three studies, 10,15,33 the correlation coefficients were not reported in the article but were calculated from the raw data. The pooled correlation coefficient between the CVP and measured blood volume was 0.16 (95% CI, 0.03 to 0.28; r 2 ϭ 0.02). Heterogeneity was present between studies. Figure 1 illustrates the relationship between CVP and measured blood volume from the study of Shippy et al. 11 Overall 56 Ϯ 16% (mean Ϯ SD) of the patients included in this review responded to a fluid challenge. The pooled correlation coefficient between baseline CVP and change in stroke index/ cardiac index (reported in 10 studies) was 0.18 (95% CI, 0.08 to 0.28). The pooled area under the ROC curve (reported in 10 studies) was 0.56 (95% CI, 0.51 to 0.61). The pooled correlation between ⌬ CVP and change in stroke index/cardiac index (reported in seven studies) was 0.11 (95% CI, 0.01 to 0.21). The baseline CVP (reported in 11 studies) was 8.7 Ϯ 2.3 mm Hg in the responders, as compared to 9.7 Ϯ 2.2 mm Hg in nonresponders (not signficant; p ϭ 0.3). The Q statistic was not significant for the pooled correlation and area under the curve statistic. The results of this systematic review are clear: (1) there is no association between CVP and circulating blood volume, and (2) CVP does not predict fluid responsiveness across a wide spectrum of clinical conditions. In none of the studies included in this analysis was CVP able to predict either of these variables. Indeed, the pooled area under the ROC curve was 0.56. The ROC curve is a statistical tool that helps assess the likelihood of a result being a true positive vs a false positive. As can be seen from Figure 2, an ROC of 0.5 depicts the true-positive rate equal to the false-positive rate; graphically, this is represented by the straight line in Figure 1. The higher the AUC, the greater the diagnostic accuracy of a test. Ideally, the AUC should be between 0.9 to 1 (0.8 to 0.9 indicates adequate accuracy with 0.7 to 0.8 being fair, 0.6 to 0.7 being poor, and 0.5 to 0.6 indicating failure). In other words, our results suggest that at any CVP the likelihood that CVP can accurately predict fluid responsiveness is only 56% (no better than flipping a coin). Furthermore, an AUC of 0.56 suggests that there is no clear cutoff point that helps the physician to determine if the patient is “wet” or “dry.” It is important to emphasize that a patient is equally likely to be fluid responsive with a low or a high CVP (Fig 1). The results from this study therefore confirm that neither a high CVP, a normal CVP, a low CVP, nor the response of the CVP to fluid loading should be used in the fluid management strategy of any patient. The strength of our review includes the rigorous selection criteria used to identify relevant studies as well as the use of quantitative end points. 8,9,34 Furthermore, the studies are notable for the consistency (both in magnitude and direction) of their findings. This suggests that the findings are likely to be true. 8,9,34 The results of our study are most disturb- ing considering that 93% of intensivists report using CVP to guide fluid management. 35 It is likely that a similar percentage (or more) of anesthesiologists, nephrologists, cardiologists, and surgeons likewise use CVP to guide fluid therapy. It is important to note that none of the studies included in our analysis took the positive end-expiatory pressure levels or changes in intrathoracic pressure into account when recording CVP. This is important because right ventricular filling is dependent on the transmural right atrial pressure gradient rather than the CVP alone. 36 However, in the real world, transmural filling pressures are rarely if ever calculated. As demonstrated by this study, only about a half of patients administered a fluid bolus will demonstrate a positive hemodynamic response to the intervention. With an ROC of 0.56, the play of chance (or a dice) will be as helpful as CVP in predicting which patients will respond to a fluid challenge. If fluid resuscitation is guided by CVP, it is likely that patients will have volume overload and pulmonary edema. Indeed the practice parameters for hemodynamic support of sepsis in adult patients concludes that “fluid infusion should be titrated to a filling pressure” and that “pulmonary edema may occur as a complication of fluid resuscitation and necessitates monitoring of arterial oxygenation.” 37 Should volume overload and pulmonary edema be the end point of fluid resuscitation? 38 This is clinically important because a positive fluid balance in both ICU patients and those undergoing surgery has been associated with increased complications and a higher mortality. 39 – 41 It is however equally likely that resuscitation guided by CVP will results in inadequate volume replacement. Furthermore, the use of diuretics based on CVP may result in intravascular volume depletion leading to poor organ perfusion and ultimately renal failure and multiorgan failure because a “high” CVP does not necessarily reflect volume overload. Fundamentally the only reason to give a patient a fluid challenge is to increase the stroke volume. 6 This assumes that the patient is on the ascending portion of the Frank-Starling curve and has “recruitable” cardiac output. Once the left ventricle is functioning near the “flat” part of the Frank-Starling curve, fluid loading has little effect on cardiac output and only serves to increase tissue edema and to promote tissue dysoxia. It is therefore crucial during the resuscitation phase of all critically ill patients to determine whether the patient is fluid responsive or not; this determines the optimal strategy of increas- ing cardiac output and oxygen delivery. 42 The results from this article clearly demonstrate that CVP should not be used for this purpose. The notion that CVP does not reflect intravascular volume and is a misleading tool for guiding fluid therapy is not new. In an article published in 1971, Forrester and colleagues, 43 the pioneers of hemodynamic monitoring, concluded that “CVP monitoring in acute myocardial infarction is at best of limited value and at worst seriously misleading.” In their landmark article that was published in 1975, Baek and colleagues 10 convincingly established that “there was no correlation of blood volume with central venous pressure” and suggest that “inaccurate physiologic evaluation of critically ill patients is likely to jeopardize survival by inviting inappropriate and ineffectual therapy.” In 1977, Dr. Burch, 44 a well- respected cardiologist, noted that “to accept non- critically the level of central venous pressure as a quantitative index of blood volume can only lead to physiologic and/or therapeutic errors.” The observa- tions of Forrester et al, 43 Baek and colleagues, 10 and Burch 44 have now been confirmed by 23 more recent studies. Indeed, limited data support using CVP to guide fluid therapy. The only study 45 we could find demonstrating the utility of CVP in predicting volume status was performed in seven standing, awake mares undergoing controlled hem- orrhage! In addition, Magder and colleagues 46 reported that the respiratory variation in CVP in spontaneously breathing patients was predictive of fluid responsiveness. Additional studies are required to support using the respiratory variation in CVP to guide fluid management. In addition, it should be noted that in the ARDSnet fluid management trial, ...

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... However, more than a decade ago we learned that CVP and blood volume correlate poorly with each other, although CVP had been used rather universally as one of the key guiding parameters for fluid therapy. 30 Echocardiographic parameters describing the geometry of the right ventricle may be more suitable to estimate the blood volume of a given patient and, therefore, perhaps also to identify patients at risk for VAE in the lounging position. However, this hypothesis has to be confirmed in further studies. ...
Article
OBJECTIVE The overall benefit of employing a sitting/semisitting position for neurosurgical procedures remains under criticism due to concerns for additional risk, especially the risk of intraoperative venous air embolism (VAE). The aim of this single-center cohort study was to evaluate the frequency and severity of VAEs and associated complications in patients undergoing neurosurgery in the lounging position. METHODS From 2010 to 2020, 1000 patients, including 172 patients with a patent foramen ovale, underwent surgery in the lounging position for different neurosurgical pathologies. All patients were monitored intraoperatively using continuous transesophageal echocardiography (TEE). The anesthesia team documented any observed incidences of VAEs and scored their severity according to the Tuebingen classification system (TCS) for VAE (TCS-VAE). The patients’ clinical condition, radiological findings, and hospital course were subsequently analyzed to assess complications in a retrospective analysis of prospectively collected data. RESULTS In the cohort of 1000 patients, 5 underwent cervical spine surgery and 995 underwent suboccipital craniotomy. VAE was detected by TEE in 51.4% (95% CI 48.4%–54.5%) of patients, with synchronous changes in end-tidal CO 2 (grade 2–5 TCS-VAE) noted in 10.2% (95% CI 8.3%–12.3%). None of the patients presented with hemodynamic instability (grade 5 TCS-VAE). Patients with high-grade VAEs were significantly older (p = 0.02) and had lower BMIs (p = 0.001) than the respective mean value of the cohort. VAE grade was not associated with any of the outcome measures such as Karnofsky Performance Scale score, duration of ventilation, length of intensive care unit stay, and length of hospital stay. Postoperative acute respiratory distress syndrome (ARDS) was diagnosed in 0.3% (95% CI 0.0%–0.7%, n = 3) of all cases, and ARDS was associated with perioperative VAE grade (p = 0.001). No patient suffered a new permanent neurological deficit due to a paradoxical VAE. CONCLUSIONS In this large cohort, the risk of an intraoperative VAE during neurosurgery in the lounging position was assessed, and contrary to the general perception in the field, no permanent sequelae or fatal adverse events attributable to VAEs were observed. Furthermore, the overall incidence of ARDS was very low. This study clearly establishes that experienced interdisciplinary teams can safely use the lounging position for neurosurgical procedures.
... Future studies should investigate alternative targets for perioperative haemodynamic goals. Previous studies have highlighted that CVP and BP correlate poorly with blood volume, and thus, do not necessarily predict organ perfusion and fluid status [33,34]. Therefore, other measures of cardiac output such as transpulmonary thermodilution may provide a more accurate indication of haemodynamic stability [34] and ensure more appropriate administration of fluids and vasoactive agents in the perioperative period. ...
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Background Paediatric kidney transplantation has an increased risk of surgical and vascular complications, with intensive care monitoring required postoperatively. This study aimed to determine if perioperative management affects early graft function in living donor paediatric kidney transplantation. Methods Clinical data was extracted from the electronic medical record for living donor kidney transplants at two paediatric centres covering the state of New South Wales (NSW), Australia from 2009 to 2021. Estimated glomerular filtration rate (eGFR) of 7 days and 1-month post-transplant were calculated as measures of early graft function. Results Thirty-nine eligible patients (female n (%) 13 (33%)) with a median (IQR) age of 6 (3–9) years and pre-transplant eGFR of 7 (6–10) mL/min/1.73 m ² were analysed. Mean (SD) central venous pressure (CVP) after revascularisation was 11 (4) mmHg. Intraoperatively, mean volume of fluid administered was 84 (39) mL/kg, and 34 (87%) patients received vasoactive agents. Average systolic blood pressure (BP) in the first 24-h post-transplant was 117 (12) mmHg. Postoperatively, median volume of fluid administered in the first 24 h was 224 (159–313) mL/kg, and 17 (44%) patients received vasoactive agents. Median eGFR 7 days and 1-month post-transplant were 115 (79–148) and 103 (83–115) mL/min/1.73 m ² , respectively. Linear regression analyses demonstrated that after adjusting for age, the average CVP after revascularisation and average systolic BP in the first 24-h post-transplant were not associated with eGFR in the first month post-transplant. Conclusions Targeted intraoperative and postoperative fluid and haemodynamic characteristics were achieved but did not correlate with early graft function. Graphical Abstract
... The static nature of those latter variables limits any inference to vascular volume. This is often reported for CVP [39] but applies to P msa as well, while this acknowledgement should not be construed to dismiss their combined validity [33]. The VRdP around 3 mmHg in both groups was at the lower end of the normal range of 3-8 mmHg reported in humans [12,40,41], and corresponded to a cardiac output less than 4 L/min for most of the duration of the study. ...
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Background The European Resuscitation Council 2021 guidelines for haemodynamic monitoring and management during post-resuscitation care from cardiac arrest call for an individualised approach to therapeutic interventions. Combining the cardiac function and venous return curves with the inclusion of the mean systemic filling pressure enables a physiological illustration of intravascular volume, vasoconstriction and inotropy. An analogue mean systemic filling pressure ( P msa) may be calculated once cardiac output, mean arterial and central venous pressure are known. The NEUROPROTECT trial compared targeting a mean arterial pressure of 65 mmHg (standard) versus an early goal directed haemodynamic optimisation targeting 85 mmHg (high) in ICU for 36 h after cardiac arrest. The trial data were used in this study to calculate post hoc P msa and its expanded variables to comprehensively describe venous return physiology during post-cardiac arrest management. A general estimating equation model was used to analyse continuous variables split by standard and high mean arterial pressure groups. Results Data from 52 patients in each group were analysed. The driving pressure for venous return, and thus cardiac output, was higher in the high MAP group ( p < 0.001) along with a numerically increased estimated stressed intravascular volume (mean difference 0.27 [− 0.014–0.55] L, p = 0.06). The heart efficiency was comparable ( p = 0.43) in both the standard and high MAP target groups, suggesting that inotropy was similar despite increased arterial load in the high MAP group ( p = 0.01). The efficiency of fluid boluses to increase cardiac output was increased in the higher MAP compared to standard MAP group (mean difference 0.26 [0.08–0.43] fraction units, p = 0.01). Conclusions Calculation of the analogue mean systemic filling pressure and expanded variables using haemodynamic data from the NEUROPROTECT trial demonstrated an increased venous return, and thus cardiac output, as well as increased volume responsiveness associated with targeting a higher MAP. Further studies of the analogue mean systemic filling pressure and its derived variables are warranted to individualise post-resuscitation care and evaluate any clinical benefit associated with this monitoring approach.
... The central venous catheter facilitates the administration of vasoactive drugs and the monitoring of central venous pressure (CVP). However, it is important to note that CVP is not a reliable indicator of fluid status or fluid responsiveness [13]. ...
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Renal transplantation is a complex surgical procedure requiring meticulous anesthetic planning to ensure patient safety and optimal graft function. This review comprehensively examines the various aspects of anesthesia management during renal transplantation, including preoperative, intraoperative, and postoperative care. Key components of preoperative optimization include the management of anemia using erythropoiesis-stimulating agents and the identification of potential risks to reduce perioperative complications. Intraoperative management focuses on hemodynamic monitoring, volume maintenance, and the careful selection of anesthetic techniques, with particular emphasis on neuromuscular monitoring and maintaining mean arterial pressure within the range of 80-110 mmHg. Postoperative care highlights the importance of multimodal analgesia, prevention of delirium, and the implementation of enhanced recovery after surgery (ERAS) protocols to promote optimal recovery. The review underscores the importance of collaboration among surgical teams, anesthesiologists, and healthcare professionals in achieving successful renal transplantation outcomes.
... This means that it can be lethal very quickly. Hematocrit levels, biochemical markers, physical examination results, and other conventional measures are used to identify hypovolemia, but are not precise markers or trustworthy since they can be deemed normal when the body's compensatory mechanisms kick in, which could cause delays in the identification of volume loss [4]. ...
... As A central line is an invasive procedure with potential complications (venous thrombosis, infection, pneumothorax, arterial puncture) during or after the procedure [6] and poor predictive value [4], measurement of CVP is not practically used in hypovolemic patients admitted to the emergency department (ED). ...
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Introduction The assessment of hemodynamic status in polytrauma patients is an important principle of the primary survey of trauma patients, and screening for ongoing hemorrhage and assessing the efficacy of resuscitation is vital in avoiding preventable death and significant morbidity in these patients. Invasive procedures may lead to various complications and the IVC ultrasound measurements are increasingly recognized as a potential noninvasive replacement or a source of adjunct information. Aimof this study The study aimed to determine if repeated ultrasound assessment of the inferior vena cava (diameter, collapsibility (IVC- CI) in major trauma patients presenting with collapsible IVC before resuscitation and after the first hour of resuscitation will predict total intravenous fluid requirements at first 24 h. Patients & methods The current study was conducted on 120 patients presented to the emergency department with Major blunt trauma (having significant injury to two or more ISS body regions or an ISS greater than 15). The patients(cases) group (shocked group) (60) patients with signs of shock such as decreased blood pressure < 90/60 mmHg or a more than 30% decrease from the baseline systolic pressure, heart rate > 100 b/m, cold, clammy skin, capillary refill > 2 s and their shock index above0.9. The control group (non-shocked group) (60) patients with normal blood pressure and heart rate, no other signs of shock (normal capillary refill, warm skin), and (shock index ≤ 0.9). Patients were evaluated at time 0 (baseline), 1 h after resucitation, and 24 h after 1st hour for:(blood pressure, pulse, RR, SO2, capillary refill time, MABP, IVCci, IVCmax, IVCmin). Results Among 120 Major blunt trauma patients, 98 males (81.7%) and 22 females (18.3%) were included in this analysis; hypovolemic shocked patients (60 patients) were divided into two main groups according to IVC diameter after the first hour of resuscitation; IVC repleted were 32 patients (53.3%) while 28 patients (46.7%) were IVC non-repleted. In our study population, there were statistically significant differences between repleted and non-repleted IVC cases regarding IVCD, DIVC min, IVCCI (on arrival) (after 1 h) (after 24 h of 1st hour of resuscitation) ( p-value < 0.05) and DIVC Max (on arrival) (after 1 h) (p-value < 0.001). There is no statistically significant difference (p-value = 0.075) between repleted and non-repleted cases regarding DIVC Max (after 24 h).In our study, we found that IVCci0 at a cut-off point > 38.5 has a sensitivity of 80.0% and Specificity of 85.71% with AUC 0.971 and a good 95% CI (0.938 – 1.0), which means that IVCci of 38.6% or more can indicate fluid responsiveness. We also found that IVCci 1 h (after fluid resuscitation) at cut-off point > 28.6 has a sensitivity of 80.0% and Specificity of 75% with AUC 0.886 and good 95% CI (0.803 – 0.968), which means that IVCci of 28.5% or less can indicate fluid unresponsiveness after 1st hour of resuscitation. We found no statistically significant difference between repleted and non-repleted cases regarding fluid requirement and amount of blood transfusion at 1st hour of resuscitation (p-value = 0.104). Conclusion Repeated bedside ultrasonography of IVCD, and IVCci before and after the first hour of resuscitation could be an excellent reliable invasive tool that can be used in estimating the First 24 h of fluid requirement in Major blunt trauma patients and assessment of fluid status.
... [2][3][4] The various hemodynamic parameters to identify fluid responders include central venous pressure (CVP), stroke volume variation (SVV), pulse pressure variation (PPV), perfusion index (PI), and positive pressure ventilation-induced changes in superior and inferior vena cava diameter. [5][6][7][8][9] All these parameters have their merits and demerits. The PLR maneuver-induced change in cardiac output, with peak hemodynamic effect around 60 seconds; is a reliable predictor of fluid responsiveness in mechanically ventilated patients and patients with spontaneous breathing efforts. ...
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Aim Acute circulatory failure is commonly encountered in critically ill patients, that requires fluid administration as the first line of treatment. However, only 50% of patients are fluid-responsive. Identification of fluid responders is essential to avoid the harmful effects of overzealous fluid therapy. Electrical cardiometry (EC) is a non-invasive bedside tool and has proven to be as good as transthoracic echocardiography (TTE) to track changes in cardiac output. We aimed to look for an agreement between EC and TTE for tracking changes in cardiac output in adult patients with acute circulatory failure before and after the passive leg-raising maneuver. Materials and methods Prospective comparative study, conducted at a Tertiary Care Teaching Hospital. Results We recruited 125 patients with acute circulatory failure and found 42.4% (53 out of 125) to be fluid-responsive. The Bland–Altman plot analysis showed a mean difference of 2.08 L/min between EC and TTE, with a precision of 3.8 L/min. The limits of agreement (defined as bias ± 1.96SD), were −1.7 L/min and 5.8 L/min, respectively. The percentage of error between EC and TTE was 56% with acceptable limits of 30%. Conclusion The percentage error beyond the acceptable limit suggests the non-interchangeability of the two techniques. More studies with larger sample sizes are required to establish the interchangeability of EC with TTE for tracking changes in cardiac output in critically ill patients with acute circulatory failure. How to cite this article Sharma S, Ramachandran R, Rewari V, Trikha A. Evaluation of Electrical Cardiometry to Assess Fluid Responsiveness in Patients with Acute Circulatory Failure: A Comparative Study with Transthoracic Echocardiography. Indian J Crit Care Med 2024;28(7):650–656.
... Classically, pulmonary artery catheter guided measurements were the gold standard for monitoring hemodynamic pressures and cardiac output. However studies have failed to demonstrate improvement in outcomes in critically ill [2]. Subsequently central venous catheters were considered as less invasive alternatives. ...
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Central venous pressure (CVP) serves as a direct approximation of right atrial pressure and is influenced by factors like total blood volume, venous compliance, cardiac output, and orthostasis. Normal CVP falls within 8-12 mmHg but varies with volume status and venous compliance. Monitoring and managing disturbances in CVP are vital in patients with circulatory shock or fluid disturbances. Elevated CVP can lead to fluid accumulation in the interstitial space, impairing venous return and reducing cardiac preload. While pulmonary artery catheterization and central venous catheter obtained measurements are considered to be more accurate, they carry risk of complications and their usage has not shown clinical improvement. Ultrasound-based assessment of the internal jugular vein (IJV) offers real-time, non-invasive measurement of static and dynamic parameters for estimating CVP. IJV parameters, including diameter and ratio, has demonstrated good correlation with CVP. Despite significant advancements in non-invasive CVP measurement, a reliable tool is yet to be found. Present methods can offer reasonable guidance in assessing CVP, provided their limitations are acknowledged.