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Abstract

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

Congest Heart Fail. 2010;16(4)(suppl 1):S45–S51. ©2010 Wiley Periodicals, Inc.

Early in the management of acute illness, it is critically important that volume status is accurately estimated. If inappropriate therapy is given because of errors in volume assessment, acute mortality rates are increased. Unfortunately, as the gold standard of radioisotopic volume measurement is costly and time-consuming, in the acute care environment clinicians are forced to rely on less accurate measures. In this manuscript, the authors review the currently available techniques of volume assessment for patients presenting with acute illness. In addition to discussing the accuracy of the history, physical examination, and radiography, acoustic cardiography and bedside ultrasonography are presented.

In the acute care environment, patients present with wide-ranging symptoms indicative of volume abnormalities. Volume perturbations, either a deficit or an excess, occur as a result of many different pathologies, so a wide range of presentations are possible. Volume deficits may be caused by blood loss in hemorrhagic shock or a crystalloid deficit from gastrointestinal losses, diabetes insipidus, or poor intake. Volume excess can present as cardiac, renal, or hepatic failure or may be the result of excessive oral intake or iatrogenic error. Because the differential diagnosis is long and complicated, and the impact of therapeutic intervention critical, the accurate assessment of volume is mandatory.

When volume assessment inaccuracies lead to the implementation of inappropriate therapy, the consequence can be fatal, as shown in a number of studies. Wuerz and Meador1 reported outcomes from 8315 patients transferred by ambulance, 499 of whom were thought to have acute decompensated heart failure (ADHF). In this study, using a prospectively established protocol, patients with elevated blood pressure and determined to be volume-overloaded by clinical evaluation were treated with bolus furosemide, sublingual nitroglycerin, and intravenous morphine before ambulance transfer. The implementation of this intervention resulted in an increase in mean scene time of only 1.1 minutes; however, patients received therapy 36 minutes earlier than if treatment was delayed until hospital arrival. While this seems a short therapeutic delay, in patients with a high severity of illness (requiring emergency medical services transport suggests greater acuity of illness), earlier treatment was associated with decreased mortality. Of the 241 patients later confirmed to have ADHF and who received early treatment, the probability of survival increased by 248% (P<.01) compared with the 252 ADHF patients who did not receive prehospital therapy. It seems reasonable that in patients for whom the clinical impression is volume-overloaded ADHF, immediate furosemide, nitroglycerin, and morphine would be a reasonable course.

The clinical assessment of volume overload due to heart failure (HF) can be challenging, however, and in this analysis errors in volume assessment were costly. In patients receiving HF therapy but ultimately found to not have ADHF, mortality increased. In the non-HF cohort receiving bronchodilators, the death rate was 3.6%, which compared with a mortality of 13.6% in non-HF patients receiving HF therapy (a 358% mortality increase). In fact, it was actually better to receive no treatment than erroneous treatment, as the non-HF group that received no therapy had a mortality of only 8.2%.

As demonstrated in the above study, in the potentially acutely ill patient, accurate volume status assessment predicates appropriate therapy. When errors of volume assessment occur, the result can be the absence of necessary treatment or the administration of unneeded therapy. Both types of errors are associated with increased mortality in the critically ill. This same relationship is also true in chronic illnesses, where blood volume assessment can be even more challenging. In a report of 43 nonedematous apparently normovolemic ambulatory patients with a history of CHF, blood volume analysis found that 5%, 30%, and 65% were hypovolemic (mean deviation from normal values, −20%±6%), euvolemic (mean deviation from normal values, −1%±1%), and hypervolemic (mean deviation from normal values +30%±3%), respectively. Although examination findings of congestion were infrequent and not associated with blood volume status, increased blood volume was associated with increased pulmonary capillary wedge pressure (PCWP) (P=.01). More important, increased blood volume was also associated with increased risk of death or urgent cardiac transplant during a median follow-up of 719 days (1-year event rate, 39% vs 0% in the normovolemic cohort, P<.01). This analysis supports the contention that clinically unrecognized hypervolemia is common in nonedematous HF patients, is associated with increased cardiac filling pressures, and results in worse outcomes.2

Some physicians have promoted the early use of pulmonary artery catheter placement to assess volume in patients presenting with ADHF. The pulmonary artery catheter is a common hemodynamic monitoring tool, and it must be highlighted that it does not actually measure volume; rather it measures pressure and temperature changes from which blood flows and volumes are then calculated. While knowledge of these data may have clinical utility, some of these parameters have relatively poor correlation to overall volume status.3 This is supported by the examples of sepsis and HF, 2 conditions in which excess volume may exist. While septic patients may have markedly increased cardiac output and low filling pressures, HF patients will have low cardiac output and high filling pressures. Ultimately, this suggests that an objective measure of volume status would be clinically useful.

Because volume assessment is an important intervention for determining appropriate therapy, the available tools for evaluation should be reviewed. The current standard for determining blood volume is radioisotopic measurement.4,5 This technology calculates red cell mass by the dilution and temporal distribution of injected Cr-51 labeled autologous red cells, and plasma volume with I-125 labeled human serum albumin. Alternative techniques use an I-131 kit (Volumex; Daxor Corporation, New York, NY) for these measures. Although volume evaluation is difficult on strictly clinical grounds and accuracy early after presentation is critical, objective radioisotopic blood volume analysis cannot be performed in a rapid or inexpensive fashion. Although radioisotopic blood volume analysis is useful in both subacute and chronic presentations, no study describes its value in the emergency evaluation of patients suspected to have clinically significant volume abnormalities. Thus, in patients with acute HF, the very population in which the consequences of errors in volume assessment may be greatest, clinicians currently rely on a group of fairly inaccurate diagnostic testing procedures that will be reviewed below.

History

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

A number of reports examine the accuracy and reliability of routine history and physical examination for the determination of excess volume. In a meta-analysis of 18 studies using HF as a diagnostic model, Wang and colleagues6,7 evaluated the history and physical examination for assessing circulatory congestion (Table). Of historical parameters, having a prior HF diagnosis was predictive of volume overload. Risk factors helpful to assess the probability of volume overload included diabetes, hypertension, valvular heart disease, age, male sex, and obesity. Unfortunately, while risk factors are helpful to consider populations, they have limited utility for diagnosing an event resulting in an urgent presentation in a specific patient.8–11

Table Table.   Summary of Diagnostic Accuracy of History and Physical Findings for the Presence of Volume Overload in Emergency Department Patients Presenting With Dyspnea
FindingSensitivitySpecificityPositive LRNegative LR
  1. Abbreviations: LR, likelihood ratio; PND, paroxysmal nocturnal dyspnea; SBP, systolic blood pressure. From Wang and colleagues.6

Symptoms
 PND0.410.842.60.70
 Orthopnea0.500.772.20.65
 Edema0.510.762.10.64
 Dyspnea on exertion0.840.341.30.48
 Fatigue and weight gain0.310.701.00.99
 Cough0.360.610.931.0
Physical examination
 Third heart sound0.130.99110.88
 Abdominal jugular reflux0.240.966.40.79
 Jugular venous distention0.390.925.10.66
 Rales0.660.782.80.51
 Any murmur0.270.902.60.81
 Lower extremity edema0.500.782.30.64
 SBP <100 mm Hg0.060.972.00.97
 Fourth heart sound0.050.971.60.98
 SBP >150 mm Hg0.280.731.00.99
 Wheezing0.220.580.521.3
 Ascites0.010.970.331.0

In the same analysis evaluating symptoms at presentation, dyspnea on exertion had the highest sensitivity for circulatory congestion, and edema was also useful.6,7 Overall, the most specific symptoms were paroxysmal nocturnal dyspnea, orthopnea, and edema,6,7 with the presence of any one increasing the probability that volume overload was present. While Wang and colleagues6 reported that the overall clinical impression of the emergency physician had high sensitivity and specificity for volume overload due to HF, others have found the initial impression based solely on history and physical examination is inaccurate in approximately 50% of cases.12

Conversely, the possibility that a patient has hypovolemia must be considered when taking the history. In a study of 38 clinical dehydration indicators in elderly patients,13 the findings best related to the severity of volume deficit and, independent of age, included tongue dryness, longitudinal tongue furrows, dryness of the mouth mucous membranes, upper body muscle weakness, confusion, speech difficulty, and sunken eyes. All other indicators had only weak associations with dehydration severity or were age-related. Finally, although commonly believed to be true, a report of thirst was unrelated to dehydration severity.

When patients present with more severe volume deficits, orthostatic symptoms and hypotension may suggest hypovolemia, although pump failure and excessive vasodilation may confound the differential diagnosis. Orthostatic symptoms may include dizziness upon standing, shortness of breath with exertion or at rest, weakness, malaise, and syncope if the deficit is severe. To qualify as orthostatic symptoms, the patient should relate that their complaints worsen when upright and improve or resolve if supine. Of importance, orthostatic symptoms can be confounded by neurologic events, although a careful examination can usually discern these presentations.

Physical Examination

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

Volume status can be assessed by physical examination. This includes evaluating lung sounds, the extent of peripheral edema, jugular venous distention (JVD), hepatojugular reflux (HJR), and the presence of extra heart sounds to determine whether fluid overload is present. Skin mottling, if a function of poor peripheral perfusion from pump failure, is ominous and has an odds ratio of 17.5 for acute in-hospital death.14

Unfortunately, there are limits to the physical examination in assessing for potential volume overload. JVD, rales, and lower extremity edema are commonly evaluated. Although JVD is reportedly associated with an elevated right atrial pressure,15–18 studies of the strength of the relationship with more objective invasive measures (eg, PCWP) have produced inconsistent results. Butman and colleagues19 reported that JVD was both specific and sensitive for an increased PCWP, while another study, defining volume overload as a PCWP >18 mm Hg, concluded that JVD and HJR had a predictive accuracy of only 81%. In the same study, rales had a positive predictive value of 100% for volume overload, but if absent had a negative predictive value of only 35%. Others, using clinical definitions of volume overload, have reported rales to have a sensitivity and specificity only in the 50% range. Finally, in terms of HJR, some have reported a sensitivity of 24% and a specificity of 94%.20

Stevenson and Perloff21 in a prospective evaluation of 50 chronic HF patients with low ejection fraction, compared physical examination findings and hemodynamics. They reported that rales, edema, and elevated JVD were absent in nearly 50% of those with increased PCWP. Chakko and colleagues,22 in a study of 52 patients with congestion, reported that while physical and radiographic findings were more common if an elevated PCWP was present, positive clinical findings had poor predictive power.

Contrary to volume overload, other examination findings suggest hypovolemia if vomiting, diarrhea, or decreased oral intake are reported at presentation. In one analysis of adults, dry axilla–supported hypovolemia (positive likelihood ratio, 2.8; 95% confidence interval [CI], 1.4–5.4), while moist mucous membranes and a tongue without furrows argued against it (negative likelihood ratio, 0.3; 95% CI, 0.1–0.6 for both findings).23 In the same analysis,23 capillary refill time and poor skin turgor had no diagnostic value, a finding supported by others. Finally, in a prospective study of blood donors giving 450 mL of blood,24 mean capillary refill time decreased from 1.4 to 1.1 seconds and had a sensitivity of 6% for blood loss. The authors concluded that the accuracy of capillary refill in a patient with a 50% prior probability of hypovolemia was only 64%.

Orthostatic Vital Signs

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

The performance of orthostatic vital signs refers to differences in pulse and blood pressure occurring as a result of postural change. Easily obtained, noninvasive, and rapidly performed, this technique is commonly used. To achieve the greatest accuracy, baseline heart rate and blood pressure are measured after the patient has been recumbent for at least 3 minutes. Afterward, the patient is kept in the standing position for 3 more minutes, and then vital signs assessed again. The conventional definition states that a significant change is a blood pressure drop >10 mm Hg or a heart rate increase >20 beats per minute

Although considered a hypovolemia indicator, the accuracy of orthostatic vitals is poor. In a prospective study of 132 euvolemic patients, statistically normal (mean±2 SD) orthostatic vital sign changes of heart rate ranged from −5 to +39 beats per minute and systolic blood pressure fluctuated from −20 to +26 mm Hg. In these normal patients, applying the standard definition of a significant orthostatic change would have defined 43% as hypovolemic.25 In another evaluation of 502 hospitalized geriatric patients with orthostatic vital signs obtained 3 times daily, 68% had significant changes at least once per day.26 Unfortunately, these reports define the inadequate specificity of orthostatic vital signs for diagnosing the presence of hypovolemia.

Finally, in a systematic review23 evaluating suspected blood loss in adults, the most useful findings were postural dizziness to the extent that it inhibited measuring upright vital signs, or a postural heart rate increase >30 beats per minute. Unfortunately, the sensitivity of only 22% for moderate blood loss with either of these predictors limits their clinical value. Only when blood loss was >1 L did the sensitivity and specificity improve to 97% and 98%, respectively. These authors concluded that supine hypotension and tachycardia are commonly absent, even after >1 L of blood loss (sensitivity, 33%; 95% CI, 21%–47%, for supine hypotension) and stated that mild postural dizziness had no proven clinical value.

Auscultation as a Predictor of Volume Status

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

Cardiac sounds may evaluate the potential for volume overload. The presence of a third heart sound (S3), related to rapid filling of a noncompliant ventricle in the setting of increased filling pressure,16 suggests an unfavorable HF prognosis. Drazner15 reported that even after adjustments for other signs of severe HF, JVD and an S3 were independently associated with increased HF hospitalization, HF rehospitalization, and death from pump failure.

If present, the S3 is highly specific for ventricular dysfunction and elevated left ventricular filling pressures.6,15,27 In a report on the physical examination, an S3 had the highest positive likelihood ratio (11.0) for volume overload, but it was not valuable as a negative predictor (likelihood ratio, 0.88).6 The S3’s poor sensitivity is commonly attributed to the difficulty in hearing it in patients with confounding diseases (eg, chronic obstructive pulmonary disease and obesity) as auscultation can be challenging, especially in a noisy environments such as the emergency department, or when lung sounds obscure the heart sounds. Last, the interrater reliability of the S3 is at best low to moderate.28–31

Therefore, while history and physical examination are the earliest diagnostics available, both have accuracy limitations. In patients with the greatest severity of illness, where early therapeutic interventions are needed, clinical decisions are of necessity made before extensive evaluation. In addition, challenges exist when patients present with many simultaneous comorbidities and confounders (eg, coexistent heart failure and sepsis). In challenging cases, rapid objective measures of volume status are needed.

Objective Measures of Blood Volume

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

The gold standard for blood volume assessment is radioimmunoassay measurement. Although accurate, it requires radioisotope injection, time, and intermittent measures before a final evaluation is complete. Besides taking too long to be used in the emergency department, the requirement of transferring patients outside the acute care environment for imaging results in challenges in the critically ill. Ultimately, its significant expense has also resulted in few patients actually receiving this diagnostic test. Finally, there is a significant need for a rapid, objective, portable or bedside volume assessment technique that accurately determines volume status.

Acoustic Cardiography

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

Technologic advances now allow digital processing of heart sound data by using a recording microphone combined with electrocardiographic (ECG) leads. Early studies report that digital S3 detection may overcome the limitations associated with standard auscultation. Even in ideal settings, digital acoustic cardiography is superior to stethoscope auscultation for detecting the S3. Furthermore, it can be performed rapidly, within 10 minutes of emergency department presentation, concurrent with the initial ECG.28 This technology may provide early objective data for determining the presence of an S3 in patients presenting with undifferentiated dyspnea.17 However, trials further delineating its utility are needed. One study of undifferentiated dyspneic emergency department patients reported that while the digitally detected S3 was specific for ADHF and affected physician diagnostic confidence, it did not improve overall diagnostic accuracy, largely because of a low sensitivity.32

Chest Radiography

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

In patients requiring rapid evaluation of volume status, chest radiography is one of the earliest obtainable tests. Although not particularly helpful to rule in hypovolemia, it may still be helpful in determining the diagnosis leading to the patients symptoms. Additionally, they may be of value when hypervolemia is suspected. Radiographic findings can be highly specific and are associated with volume overload. When volume overload is present, chest radiographic findings occur in the following descending order of frequency: dilated upper lobe vessels, cardiomegaly, interstitial edema, enlarged pulmonary artery, pleural effusion, alveolar edema, prominent superior vena cava, and Kerley lines.33

It is important to note that radiographic abnormalities may lag the clinical appearance by hours, so that therapy is not to be withheld pending radiography. In patients with suspected volume overload, a lack of radiographic findings cannot exclude abnormal myocardial function, but it may define diagnoses responsible for the patient’s presentation (eg, pneumonia). Collins and colleagues34,35 reported that as many as 20% of patients ultimately receiving a diagnosis of HF had negative findings on initial chest radiography during their initial evaluation.

Patients with chronic HF may be a challenging cohort. This is because the radiographic signs of congestion in chronic HF have unreliable sensitivity, specificity, and predictive value for identifying individuals with high PCWP.22 In one report, radiographic evidence of pulmonary congestion was absent in 53% of patients with mild to moderately elevated PCWP (16–29 mm Hg) and in 39% of the group with a markedly elevated PCWP (>30 mm Hg).22

The identification of cardiomegaly may be a useful finding in the patient with suspected HF, and a cardiothoracic ratio >60% is associated with higher 5-year mortality.36 Unfortunately, chest radiography has limited sensitivity for detecting cardiomegaly. In a study of patients with echocardiographically proven cardiac enlargement, 22% had a cardiothoracic ratio <50%.37 The lack of radiographic detection of cardiomegaly was attributed to the presence of intrathoracic cardiac rotation.

The method by which radiography is performed and the clinical status of the patient affect the radiographic accuracy for volume overload detection. When radiography is performed portably, its sensitivity for volume overload is poor. In a study of patients with mild HF, only dilated upper lobe vessels occurred in >60%. However, there is a relationship between radiographic volume overload findings and illness severity. When HF was severe, radiography findings of volume overload were present in at least two-thirds of patients, except for Kerley lines (present in only 11%) and a prominent vena cava (present in only 44%).33 Last, pleural effusions can be missed, especially in intubated patients, when radiography is performed with the patient supine. The sensitivity, specificity, and accuracy of the supine chest radiography for detecting pleural effusions are 67%, 70%, and 67%, respectively.38

Thus, when a positive finding of volume overload or an alternative diagnosis is defined, chest radiography is clinically useful. Conversely, chest radiography is of less value in hypovolemia and is insensitive in chronic or mild acute volume overload presentations.

Natriuretic Peptides

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

Natriuretic peptides (NPs) are hemodynamically active neurohormones. Potentially elevated in volume overload, 3 NPs—brain natriuretic peptide (BNP), its synthetic byproduct N-terminal brain natriuretic peptide (NT-proBNP), and the mid-regional prohormone of ANP (MR-proANP)—have commercially available assays. These molecules behave similarly and are elevated in the setting of heart failure. However, because they can be elevated with any type of myocardial stress, independent of volume status (eg, myocardial infarction, pulmonary embolus), the cause of an elevated NP must be considered within the context of the clinical presentation. NP interpretation must be also considered in view of their confounders of obesity (lower NP levels than clinically predicted) and renal insufficiency/failure (associated with higher NPs). Last, in chronic HF, persistently elevated NP levels can occur despite the patient being at their baseline dry weight. Thus, knowledge of the patient’s baseline NP level may be needed to interpret the NP results.

While NP assays are available as a rapid bedside test to provide objective assessment in critically ill patients, their greatest utility is when levels are found to be in the normal range. This is because, except in obesity, a low NP accurately excludes an HF diagnosis. Conversely, an elevated NP may be nonspecific for identifying volume excess.

Bioimpedance

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

Although pulmonary artery catheterization provides useful information, because of the morbidity and mortality that can result from this invasive procedure, noninvasive techniques are now considered an appropriate alternative.39 One of the most studied of the noninvasive options is impedance cardiography (ICG). The use of ICG is based on the theory that the human thorax is an inhomogeneous electrical conductor.40,41 When a high-frequency electrical current is injected across the thorax, impedance measures can be obtained by pairs of electrodes placed at the edge of the chest. Thoracic voltage changes (ΔZ) result from changes that occur from blood volumetric and velocity alterations related to cardiac systole. By analyzing these changes and their relation with ECG-derived timing measures, hemodynamic parameters can be derived. Cardiac output measures using ICG have been compared with those obtained with thermodilution in a recent meta-analysis of more than 200 studies and report a correlation of 0.81 for ICG-determined stroke volume and cardiac output. Overall, ICG measures are less variable and more reproducible than many other strategies for volume assessment. Besides being noninvasive, other ICG advantages include that it can be used for continuous monitoring and trend identification.

ICG is not without limitations, the most common of which is the inability to obtain a signal. This may occur as a result of the following:

  •  Severe cutaneous abnormalities (large ulcers/wounds/eschars, crusting skin), excessive diaphoresis, inadequate skin cleaning, or excessive hair preventing adequate electrode adherence
  •  Erroneous electrode position, contact with an electrical ground (eg, metal bed frame), or electrical interference
  •  Excessive movement (dementia and severe psychiatric disease)
  •  Severe obesity
  •  ICG cannot distinguish compartmentalized volumes, so the clinical probabilities of pericardia or pleural effusions must be considered.

Thoracic Ultrasonography

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

Increasingly available, thoracic ultrasonography detects pulmonary water by the identification of the presence of sonographic artifacts, known as B-lines. When found, they suggest thickened interstitia or fluid-filled alveoli.42 B-lines occur most commonly in patients with congestive HF42–44 and are correlated with elevated PCWP and extravascular pulmonary water.45–47 Specifically studied in emergency department patients, B-lines demonstrate high sensitivity and specificity for alveolar interstitial syndrome. In a study of 94 patients evaluated for HF, the presence of B-lines had a positive likelihood ratio of 3.88 (99% CI, 1.55–9.73), and their absence was associated with a negative likelihood ratio of 0.5 (95% CI, 0.30–0.82).48

Although outside the scope of this review, echocardiography may have some utility in volume assessment. Certainly, information about left and right ventricular function can be rapidly obtained, which may be important regardless of the volume status. Additionally, visualization of the inferior vena cava on subcostal views, including size and respiratory dynamics, will provide considerable information on estimated right atrial pressure and indirect evidence of volume status. Echocardiography can also be helpful to suggest left atrial/pulmonary artery capillary wedge pressures, although these measures (even by direct assessment) do not correlate perfectly with volume status.

UIltrasonography can evaluate volume status by measuring the inferior vena cava diameter. In 31 volunteers undergoing a 450-cc phlebotomy, inferior vena cava diameter decreased by >5 mm, regardless of the respiratory cycle (P<.0001).49 Another study of hemodialysis patients, using radioisotopic blood volume assessment as the gold standard, Katzarski and colleagues50 reported that inferior vena cava diameter decreased during hemodialysis and increased in the 2 hours after (due to refilling of the intravascular space), indicating that inferior vena cava diameter changes are reflective in overall changes in blood volume.

Conclusions

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References

Rapid and accurate volume assessment is critically important in patients presenting with undiagnosed acute illness. Errors in volume assessment that result in inappropriate therapy may result in fatal outcomes. Unfortunately, the patient’s history, physical examination, and chest radiography each suffer from significant limitations. Although radioisotopic measurement is the gold standard for volume assessment, it is impractical in the acute care environment. New technologies including bedside ultrasonography offer the promise of both rapid and accurate bedside volume assessment.

Disclosures:  Dr. Peacock serves on Scientific Advisory Boards of Abbott Laboratories, Beckman-Coulter, Biosite, Inverness, and The Medicines Company. He has received research grants from Abbott Laboratories, BAS, Biosite, Brahms, Inverness, Nanospere, EKR, and The Medicines Company. He serves on the Speakers' Bureau for Abbott Laboratories, and Biosite and has ownership interests in Vital Sensors. He received an honorarium funded by an unrestricted educational grant from Abbott Laboratories and Otsuka America Pharmaceuticals for time and expertise spent in creating this article. Dr. Soto has no relevant financial relationships to disclose.

References

  1. Top of page
  2. Abstract
  3. History
  4. Physical Examination
  5. Orthostatic Vital Signs
  6. Auscultation as a Predictor of Volume Status
  7. Objective Measures of Blood Volume
  8. Acoustic Cardiography
  9. Chest Radiography
  10. Natriuretic Peptides
  11. Bioimpedance
  12. Thoracic Ultrasonography
  13. Conclusions
  14. References