Skip to main content

Clinical review: New technologies – venturing out of the intensive care unit


The delivery of critical care is no longer limited to the intensive care unit. The information gained by utilization of new technologies has proven beneficial in some populations. Research into earlier and more widespread use of these modalities may prove to be of even greater benefit to critically ill patients.


Diagnostic and therapeutic interventions done outside the intensive care unit (ICU) are an integral part of the multidisciplinary continuum of critical care. Presented here is a brief review of hemodynamic monitoring, ancillary studies, and therapeutic modalities that are currently used or that have potential applications in the emergency department (ED).

Esophageal Doppler monitoring

In treating critically ill patients it is often desirable to have available an objective measure of cardiac function and response to therapy. Determinations of cardiac output (CO) have traditionally used a pulmonary artery catheter, employing the thermodilution technique in the operative suite or ICU [13]. The risks associated with central venous access, pulmonary arterial injury, embolization, infection, interpretation, and reproducibility were previously addressed and render this modality impractical for use in the ED [2, 4, 5]. The esophageal Doppler monitor (EDM) can be used to evaluate the velocity and time at which blood travels within the descending aorta using a Doppler signal. EDM-derived variables include peak velocity, flow time, and heart rate. From the EDM-derived variables, CO, stroke volume, and cardiac index can be computed [69]. Peak velocity is proportional to contractility and flow time correlates with preload.

Recent reviews in the literature [1014] support the use of EDM for fluid management in the critically ill both in the operative and ICU settings. Placement of the EDM is similar to insertion of a nasogastric tube, and once it is correctly positioned, with a good Doppler signal acquired, the EDM correlates well with the thermodilution technique and serial measurements can be obtained [15, 16]. Reliability of the EDM may be hindered during dysrhythmic states because of the fluctuating or irregular aortic pulse wave. It is clinically useful in distinguishing between a low versus high CO state and determining the response of CO to therapeutic interventions such as an intravenous fluid challenge. Gan and coworkers [10] demonstrated a reduction in length of stay after major surgery using EDM goal-directed fluid management. Case report data support its successful use in guiding therapy in a septic patient [17]. The ease of insertion and interpretation was illustrated in ED studies [18, 19], which provide some of the limited evidence for the superiority of EDM data over clinical hemodynamic assessment. EDM may be useful as a tool with which to assess trends in cardiac parameters and clinical response to a given therapy (Table 1). Although outcome data utilizing the EDM are lacking, practical applications in the ED include monitoring intubated patients receiving intravenous inotropic or vasoactive agents. Mechanically ventilated patients often require sedation as part of treatment, and similarly patients being monitored with an EDM may benefit from sedative medications, as delineated in clinical practice guidelines regarding the use of sedation in the ICU [20, 21].

Table 1 Normal values (See Appendix 1)

Thoracic bioimpedance

Thoracic bioimpedance was initially devised for the space program in the 1960s as a noninvasive means to monitor astronauts during space flight [22]. The science of bioimpedance utilizes differences in tissue impedance that occur in response to low levels of electrical current to derive hemodynamic variables. Early work by Nyober and Kubicek [22, 23] derived bioimpedance by means of applying a small current to the thorax and measuring the returning signal coupled to a calculation to derive stroke volume. The currently available technology differs by the choice of two formulae that are currently in use: the earlier mathematical model by Kubicek and the later modification by Sramek-Bernstein, which corrected for certain clinical assumptions made by Kubicek.

Impedance cardiography (ICG) combines bioimpedance over time with the electrocardiographic cycle. The instrument is connected to patients by applying adhesive pads on the neck and/or lateral chest wall areas [8, 24]. Patients do not feel the current when the instrument is applied. Studies have shown earlier versions of thoracic bioimpedance to have a correlation coefficient with pulmonary artery catheterization of approximately 0.83 [25]. From the measured values of heart rate, impedance, and electrocardiographic parameters, other hemodynamic parameters are derived, which include cardiac index, CO, stroke index, stroke volume, systemic vascular resistance, and thoracic fluid content. Additional derived data include the pre-ejection period and left ventricular ejection time [24]. The pre-ejection period : left ventricular ejection time ratio reflects contractility [24]. Clinically, ICG has been studied in the management of congestive heart failure [2628], sepsis [2931], and trauma [3235]. In an ED study of patients presenting with shortness of breath [36], application of ICG changed the admitting diagnosis in 5% of patients and accounted for a change in therapy in more than 20%. In applying this technology it should be recognized that its limitations are that data output is derived from calculations, and that continuous electrode contact must be maintained with the skin, which may prove difficult in unstable or diaphoretic patients.

ICG may have a growing role to play in ED management of the critically ill, with further studies delineating the benefit and optimal application of this technique. The use of this technology could be particularly helpful in patients with poor vascular access such as those with peripheral vascular disease and hemodialysis patients (Table 1).

End-tidal carbon dioxide monitoring

End-tidal carbon dioxide refers to the presence of carbon dioxide at the end of expiration (end-tidal carbon dioxide tension [PetCO2]). Capnometry is the measurement of carbon dioxide gas during ventilation. Capnography refers to the graphical representation of end-tidal carbon dioxide over a period time. The characteristic capnographic waveform is composed of a baseline (representing dead space carbon dioxide), expiratory upstroke, alveolar plateau, end-tidal carbon dioxide, and downstroke. At the peak of the upslope is the PetCO2 [37]. Depending on the hemodynamic state, the amount of PetCO2 detected usually correlates with the degree of pulmonary alveolar flow and ventilation [3739].

Quantitative PetCO2 is currently measured using a mainstream detector or a sidestream detector utilizing infrared technology. Mainstream detectors are connected to an endotracheal tube for real-time detection of changes in Pet CO2. Sidestream PetCO2 detectors sample expired gas noninvasively (e.g. in nonintubated patients).

PetCO2 detection is used as an adjunct to confirm correct endotracheal tube placement [40]. It has also been studied in cardiac arrest as a surrogate of CO and coronary perfusion pressure [4144]. For victims of cardiac arrest of duration greater than 20 min, capnography readings consistently below 10 mmHg indicate that the chance that there will be no return of spontaneous circulation is nearly 100% [45]. Pet CO2 is useful for managing hemodynamically stable, mechanically ventilated patients. After establishing a gradient between PetCO2 and arterial carbon dioxide tension (PaCO2), PetCO2 can approximate PaCO2 and serves as a rough guide to ventilatory status [40].

In diabetic ketoacidosis the compensatory response to the metabolic acidosis is an increase in respiratory rate with a concurrent decrease in PaCO2. Using the relationship between PaCO2 and PetCO2, a recent study [46] showed a linear relationship between PetCO2 and serum bicarbonate with a sensitivity of 0.83 and specificity of 1.0 in patients with diabetic ketoacidosis. PetCO2 is a helpful noninvasive adjunct for monitoring critically ill patients and for guiding therapy. It potentially can have a more expanded role by providing a quantitative assessment of patients' ventilatory and perfusion status when they present with respiratory failure, metabolic derangements, and post-cardiac arrest (Table 1).

Sublingual carbon dioxide

Recognition of organ-specific sensitivity to decreased flow arose from an understanding of the differences in regional blood flow that occur during systemic hypoperfusion and shock states. Early investigations conducted by Weil and coworkers [47, 48] in animals and humans demonstrated an increase in gastric mucosal carbon dioxide during periods of poor perfusion. This led to the concept of gastric tonometry, which is used to measure mucosal carbon dioxide to derive gastric mucosal pH via the Henderson–Hasselbach equation. Experience with this technique demonstrated that it is sensitive and correlates well with other hemodynamic parameters [49]. The time consuming and complex nature of calculating mucosal pH is not practical in the ED; however, it was later discovered that sublingual mucosal carbon dioxide correlates well with the gastric mucosal carbon dioxide [50]. Recent data indicate that the sublingual carbon dioxide–PaCO2 gradient correlates well with illness severity in septic patients in the ICU [51]. Larger studies evaluating the applicability and response to therapy within the ED setting are needed. Sublingual capnography may serve as a surrogate marker of hypoperfusion. Currently marketed devices for measurement of sublingual carbon dioxide are rapid and easily applied (see Appendix 1). These devices may be useful in screening for hypoperfused states in ED triage (Table 1).

Point-of-care testing

Point-of-care testing has found its way into the ED. As more rapid bedside analyzers make their way into the marketplace, health care systems must find the appropriate fit at their institutions. A recent review by Fermann and Suyama [52] addresses the potential applications and pitfalls of their use. A comprehensive review of point-of-care testing will not be revisited here, but rather a few potentially useful biomarkers are discussed.


Whole blood analyzers are currently available that allow for measurement of lactate [53]. Lactate is a useful biomarker, providing an indication of tissue hypoperfusion [5356]. Ability to obtain lactate levels in the ED has significant implications for patient care, and recognition of subclinical hypoperfusion using arterial and venous samples has been shown to correlate well (r = 0.94) [57]. Arterial sampling has advantages over venous sampling in hemodynamically compromised patients [58]. Several published studies [57, 5963] have demonstrated the ability of lactate to predict morbidity and mortality even better than base deficit in critically ill patients. Smith and coworkers [59] found that elevated admission blood lactate levels correlated with 24% mortality, and in those whose lactate levels did not normalize within 24 hours the mortality was 82%. The level at which lactate becomes clinically significant may be disputed. Rivers and coworkers [61] used a cutoff of 4 mmol/l to initiate early goal-directed therapy in septic patients. Blow and coworkers [64] aimed for lactate levels of less than 2.5 mmol/l and found that patients in whom this level could not be reached had increased morbidity and mortality (Table 1).

The rate of lactate clearance corresponds to clinical response [63, 65]. The goal of resuscitation should therefore be directed not only at normalizing lactate levels but also at doing so in a timely manner, preferably within 24 hours. Lactate measurement in patients with suspected subclinical hypoperfusion served as both an end-point of resuscitation and a means to stratify the severity of illness [62].

C-reactive protein and procalcitonin

Clinical decision making in the ED is often hampered in adult and pediatric patients with possible sepsis because of an inprecise history or a nonlocalizing physical examination. Newer bedside assays may suggest a greater likelihood of infection or severity of illness in the appropriate setting. C-reactive protein (CRP) and procalcitonin (PCT) are two biomarkers that are being investigated in the ED. CRP is a well known acute phase reactant and is a useful marker of inflammation. Its function is to activate complement, opsonize pathogens, and enhance phagocytosis [66]. The physiologic function of PCT is not known. Da Silva and coworkers [67] suggested that CRP might be a more sensitive indicator of sepsis than leukocyte indices alone. Lobo and colleagues [68] found that elevated CRP levels correlated with organ failure and death in an ICU population at admission and at 48 hours. Galetto-Lacour and coworkers [69] evaluated bedside PCT and CRP in a pediatric population and found the sensitivities for predicting a serious bacterial infection to be 93% and 79%, respectively. In a recent review by Gattas and Cook [70] they suggested that PCT may be useful in excluding sepsis if it is in the normal range (Table 1). Bedside PCT and CRP are currently not approved by the Food and Drug Administration in the USA, but they are on the horizon and may assist with clinical decision-making in the ED setting in patients with suspected sepsis or a serious bacterial infection [71].

Mixed/central venous oximetry and arterial–venous carbon dioxide gradient

Wo and coworkers [72] and Rady and colleagues [73] first described the unreliability of the traditional end-point of normal vital signs in the ED resuscitation of critically ill patients. Rady and coworkers [73] found a persistent deficit in tissue perfusion by demonstrating a decreased central venous oxygen saturation (ScvO2) despite normal vital signs after resuscitation. Increased capillary and venous oxygen extraction leads to a lower ScvO2, which is an indication of increased oxygen consumption or decreased oxygen delivery. Persistently decreased ScvO2 after resuscitation predicts poor prognosis and organ failure [73]. Rivers and coworkers [74] reviewed current evidence comparing mixed venous oxygen saturation and ScvO2; they found that, although a small difference in the absolute saturation value may exist, critically low central venous saturations may still be used to guide therapy. ScvO2 can be measured from blood obtained from a central line inserted into the subclavian or internal jugular vein. Alternatively, newer fiberoptic enabled catheters can provide a real-time display of ScvO2 after initial calibration [73] (Table 1).

Johnson and Weil [75] described the ischemic state seen in circulatory failure as a dual insult of decreased oxygenation and increased tissue carbon dioxide levels. Evidence of carbon dioxide excess was found in cardiac arrest studies demonstrating an elevated arteriovenous carbon dioxide difference [7678]. In a small observational study [78], derangements in the arteriovenous carbon dioxide gradient were found to exist in lesser degrees of circulatory failure and that this relation correlated inversely with CO. A relationship between mixed venous–arterial carbon dioxide gradient and cardiac index was also observed in a study of septic ICU patients [79]. By measuring ScvO2 or by calculating an arteriovenous carbon dioxide gradient, clinicians can detect subclinical hypopefusion and have a fair estimate of cardiac function when vital signs do not fully account for a clinical scenario [80]. These modalities can be employed in either an ED or an ICU setting (Table 1).


Early goal-directed therapy

The combination of early detection of subclinical hypoperfusion and goal-directed therapy in septic patients was advanced by the ED-based protocol devised by Rivers and coworkers [61]. With early implementation of ScvO2 monitoring to guide fluid, inotropic, and blood product administration, a significant mortality reduction was observed in patients with severe sepsis and septic shock. The absolute mortality benefit in the treatment group (30.5%) as compared with the control group (46.5%) was 16%. Benefits from early goal-directed intervention were seen as late as 60 days after admission. Efforts to disseminate and apply early goal-directed therapy are underway and multidisciplinary teams may be employed to continue the protocol started in the ED in the ICU. Early identification and treatment of patients at a critical juncture in early sepsis supports the application of this modality in emergency medicine and critical care.

Noninvasive positive pressure ventilation

Noninvasive positive pressure ventilation (NPPV) has been used for a number of years in the ICU and for patients with obstructive sleep apnea. Recently, NPPV has found an increasing role in the ED. Continuous positive airway pressure ventilation may assist patients by improving lung compliance and functional residual capacity [81]. In the ED patients with acute exacerbations of asthma, chronic obstructive pulmonary disease, and congestive heart failure resistant to medical therapy are often intubated for respiratory support. Previously studied indications for employing NPPV in the ED include hypoxic respiratory failure, exacerbation of chronic obstructive pulmonary disease, asthma, and pulmonary edema [81]. In a study into the use of NPPV for patients with congestive heart failure conducted by Nava and coworkers [82], overall outcomes were similar for patients who did not receive NPPV, although a greater improvement in arterial oxygen tension and partial carbon dioxide tension, and a decreased rate of intubations was observed in the NPPV group. In a controversial study of congestive heart failure pitting bilevel positive airway pressure against continuous positive airway pressure [83], a greater rate of myocardial infarction was seen in the bilevel group [83]. Asthma treatment in the ED utilizing bilevel positive airway pressure has yielded improved outcomes [8486]. The avoidance of endotracheal intubation in patients with reversible disease may have a significant impact on clinical care [83]. NPPV is a viable option for emergency physicians managing patients with COPD, asthma, and pulmonary edema to avoid intubations, and impact morbidity and hospital length of stay.


It has been increasingly recognized that the boundaries of critical illness are extending beyond the ICU. Increasing ED patient volumes compounded by limited ward and ICU bed availability introduce a higher percentage of critically ill patients awaiting ICU admission or transfer. Delays in ancillary testing and implementation of therapy must be avoided. Clinicians must be familiar with newer technologies as they arrive and employ those technologies that will most likely have an impact on clinical care. Earlier recognition and treatment of critical illness by physicians in multiple disciplines can potentially halt disease progression and have a positive impact on patient outcomes.

Appendix 1

The following is a brief listing of manufacturers of various critical care technologies. This is not an endorsement of any of the listed products or manufacturers. The authors do not have any disclosures or financial interests in any of the listed manufacturers.

Esophageal Doppler monitors:

Mixed–central venous monitor

Impedance cardiography

End-tidal carbon dioxide:

Point-of-care testing:



cardiac output


C-reactive protein


emergency department


esophageal Doppler monitor


intensive care unit


impedence cardiography


noninvasive positive pressure ventilation


arterial carbon dioxide tension




end-tidal carbon dioxide tension


central venous oxygen saturation.


  1. 1.

    Anonymous: Pulmonary Artery Catheter Consensus Conference: consensus statement. Crit Care Med 1997, 25: 910-925.

    Article  Google Scholar 

  2. 2.

    Connors AF Jr, Speroff T, Dawson NV, Thomas C, Harrell FE Jr, Wagner D, Desbiens N, Goldman L, Wu AW, Califf RM, et al.: The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996, 276: 889-897. 10.1001/jama.276.11.889

    Article  PubMed  Google Scholar 

  3. 3.

    Sandham JD, Hull RD, Brant RF, Knox L, Pineo GF, Doig CJ, Laporta DP, Viner S, Passerini L, Devitt H, et al.: A randomized, controlled trial of the use of pulmonary-artery catheters in high-risk surgical patients. N Engl J Med 2003, 348: 5-14. 10.1056/NEJMoa021108

    Article  PubMed  Google Scholar 

  4. 4.

    Dalen JR: The pulmonary artery catheter: friend, foe, or accomplice? JAMA 2001, 286: 348-350. 10.1001/jama.286.3.348

    CAS  Article  PubMed  Google Scholar 

  5. 5.

    Bernard GR, Sopko G, Cerra F, Demling R, Edmunds H, Kaplan S, Kessler L, Masur H, Parsons P, Shure D, et al.: Pulmonary artery catheterization and clinical outcomes: National Heart, Lung, and Blood Institute and Food and Drug Administration Workshop Report. Consensus Statement. JAMA 2000, 283: 2568-2572. 10.1001/jama.283.19.2568

    CAS  Article  PubMed  Google Scholar 

  6. 6.

    Berton C, Cholley B: Equipment review: New techniques for cardiac output measurement – oesophageal Doppler, Fick principle using carbon dioxide, and pulse contour analysis. Crit Care 2002, 6: 216-221. 10.1186/cc1492

    PubMed Central  Article  PubMed  Google Scholar 

  7. 7.

    Boldt J: Clinical review: Hemodynamic monitoring in the intensive care unit. Crit Care 2002, 6: 52-59. 10.1186/cc1453

    PubMed Central  Article  PubMed  Google Scholar 

  8. 8.

    Bilkovski R: Noninvasive cardiac output monitoring. In In Emergency Procedures. 4th edition. Edited by: Roberts. McGraw-Hill; 2004:358-366.

    Google Scholar 

  9. 9.

    Chaney JC, Derdak S: Minimally invasive hemodynamic monitoring for the intensivist: Current and emerging technology. Crit Care Med 2002, 30: 2338-2345. 10.1097/00003246-200210000-00025

    Article  PubMed  Google Scholar 

  10. 10.

    Gan TJ, Soppitt A, Maroof M, el-Moalem H, Robertson KM, Moretti E, Dwane P, Glass PS: Goal-directed intraoperative fluid administration reduces length of hospital stay after major surgery. Anesthesiology 2002, 97: 820-826. 10.1097/00000542-200210000-00012

    Article  PubMed  Google Scholar 

  11. 11.

    Singer M, Bennett ED: Noninvasive optimization of left ventricular filling using esophageal Doppler. Crit Care Med 1991, 19: 1132-1137.

    CAS  Article  PubMed  Google Scholar 

  12. 12.

    Mark JB, Steinbrook RA, Gugino LD, Maddi R, Hartwell B, Shemin R, Disesa V, Rida WN: Continuous noninvasive monitoring of cardiac output with esophageal doppler ultrasound during cardiac surgery. Anesth Analg 1986, 65: 1013-1020.

    CAS  Article  PubMed  Google Scholar 

  13. 13.

    DiCorte CJ, Latham P, Greilich P, Cooley MV, Grayburn PA, Jessen ME: Esophageal doppler monitor determination of cardiac output and preload during cardiac operations. Ann Thorac Surg 2000, 69: 1782-1786. 10.1016/S0003-4975(00)01129-2

    CAS  Article  PubMed  Google Scholar 

  14. 14.

    Klotz KF, Klingsiek S, Singer M, Wenk H, Eleftheriadis S, Kuppe H, Schmucker P: Continuous measurement of cardiac output during aortic cross-clamping by the oesophageal Doppler monitor ODM 1. Br J Anaesth 1995, 74: 655-660.

    CAS  Article  PubMed  Google Scholar 

  15. 15.

    Penny JA, Anthony J, Shennan AH, deSwiet M, Singer M: A comparison of hemodynamic data derived by pulmonary artery flotation catheter and the esophageal Doppler monitor in pre-eclampsia. Am J Obstet Gynecol 2000, 183: 658-661. 10.1067/mob.2000.106579

    CAS  Article  PubMed  Google Scholar 

  16. 16.

    Coelho JMC, Brauer L, Amaral ACKB, Taniguchi LU, Park M, Cruz LM: Is there a role for continuous esophageal Doppler in critically ill patients? Crit Care 2003, (Suppl 3):26. 10.1186/cc2222

  17. 17.

    Eachempati SR, Young C, Alexander J, Cirisano FD, Rodriguez GC, Reed RL II: The clinical use of an esophageal Doppler monitor for hemodynamic monitoring in sepsis. J Clin Monit 1999, 15: 223-225. 10.1023/A:1009963124127

    CAS  Article  Google Scholar 

  18. 18.

    Rodriguez RM, Berumen KA: Cardiac output measurement with an esophageal Doppler in critically ill emergency department patients. J Emerg Med 2000, 18: 159-164. 10.1016/S0736-4679(99)00187-0

    CAS  Article  PubMed  Google Scholar 

  19. 19.

    Urrunaga J, Rivers E, Mullen M, Nguyen B, Rittinger W, Karriem-Norwood V, Tomlanovich MC: Hemodynamic assessment of the critically ill: the clinician versus esophageal Doppler monitoring (EDM). Acad Emerg Med 2000, 7: 587-b.

    Google Scholar 

  20. 20.

    Nasraway SA Jr, Jacobi J, Murray MJ, Lumb PD: Task Force of the American College of Critical Care Medicine of the Society of Critical Care Medicine and the American Society of Health-System Pharmacists, American College of Chest Physicians. Sedation, analgesia, and neuromuscular blockade of the critically ill adult: revised clinical practice guidelines for 2002. Crit Care Med 2002, 30: 117-118. 10.1097/00003246-200201000-00019

    Article  PubMed  Google Scholar 

  21. 21.

    Jacobi J, Fraser GL, Coursin DB, Riker RR, Fontaine D, Wittbrodt ET, Chalfin DB, Masica MF, Bjerke HS, Coplin WM, et al.: Task Force of the American College of Critical Care Medicine (ACCM) of the Society of Critical Care Medicine (SCCM), American Society of Health-System Pharmacists (ASHP), American College of Chest Physicians. Clinical practice guidelines for the sustained use of sedatives and analgesics in the critically ill adult. Crit Care Med 2002, 30: 119-141. 10.1097/00003246-200201000-00020

    Article  PubMed  Google Scholar 

  22. 22.

    Kubicek WG, Karnegis JN, Patterson RP, Witsoe DA, Mattson RH: Development and evaluation of an impedance cardiac output system. Aerospace Med 1966, 37: 1208-1212.

    CAS  PubMed  Google Scholar 

  23. 23.

    Nyober J: Electrical Impedance Plethysmography. Springfield, IL: Charles C Thomas; 1959:243.

    Google Scholar 

  24. 24.

    Summers RL, Shoemaker WC, Peacock WF, Ander DS, Coleman TG: Bench to bedside: electrophysiologic and clinical principles of noninvasive hemodynamic monitoring using impedance cardiography. Acad Emerg Med 2003, 10: 669-680. 10.1197/aemj.10.6.669

    Article  PubMed  Google Scholar 

  25. 25.

    Appel PL, Kram HB, Mackabee J, Fleming AW, Shoemaker WC: Comparison of measurement of cardiac output by bioimpedance and thermodilution in severely ill surgical patients. Crit Care Med 1986, 14: 933-935.

    CAS  Article  PubMed  Google Scholar 

  26. 26.

    Vijayaraghavan K, Crum S, Hegelson Q, et al.: Impedance cardiography is a useful non-invasive modality in management of chronic decompensated heart failure. Chest 2002, 122: 170S-171S.

    Google Scholar 

  27. 27.

    Yancy C, Abraham WT: Noninvasive hemodynamic monitoring in heart failure: utilization of impedance cardiography. Congest Heart Fail 2003, 9: 241-250.

    Article  PubMed  Google Scholar 

  28. 28.

    Hail AN, Li J, Young JB: Equivalence of bioimpedance and thermodilution in measuring cardiac output and index in patients with advanced, decompensated chronic heart failure hospitalized in critical care. J Am Coll Cardiol 2003, (Suppl):211A.

  29. 29.

    Shoemaker WC, Wo CC, Yu S, Farjam F, Thangathurai D: Invasive and noninvasive hemodynamic monitoring of acutely ill sepsis and septic shock patients in the emergency department. Eur J Emerg Med 2000, 7: 169-175.

    CAS  Article  PubMed  Google Scholar 

  30. 30.

    Schwenk A, Ward LC, Elia M, Scott GM: Bioelectrical impedance analysis predicts outcome in patients with suspected bacteremia. Infection 1998, 26: 277-282.

    CAS  Article  PubMed  Google Scholar 

  31. 31.

    Young JD, McQuillan P: Comparison of thoracic electrical bioimpedance and thermodilution for the measurement of cardiac index in patients with severe sepsis. Br J Anesth 1993, 70: 58-62.

    CAS  Article  Google Scholar 

  32. 32.

    Bishop MH, Shoemaker WC, Shulesko J, et al.: Noninvasive cardiac index monitoring in gunshot wound victims. Acad Emerg Med 1996, 3: 682-688.

    CAS  Article  PubMed  Google Scholar 

  33. 33.

    Shoemaker WC, Wo CC, Bishop MH, Thangathurai D, Patil RS: Noninvasive hemodynamic monitoring of critical patients in the emergency department. Acad Emerg Med 1996, 3: 675-681.

    CAS  Article  PubMed  Google Scholar 

  34. 34.

    Shoemaker WC, Belzberg H, Wo CC, et al.: Multicenter study of noninvasive monitoring systems as alternatives to invasive monitoring of acutely ill emergency patients. Chest 1998, 3: 675-81.

    Google Scholar 

  35. 35.

    Velmahos GC, Wo CC, Demetriades D, Murray JA, Cornwell EE 3rd, Asensio JA, Belzberg H, Shoemaker WC: Invasive and non-invasive physiological monitoring of blunt trauma patients in the early period after emergency admission. Int Surg 1999, 84: 354-360.

    CAS  PubMed  Google Scholar 

  36. 36.

    Peacock WF, Summers R, Emerman C: Emergent Dyspnea IMPedance cardiography-aided Assessment Changes Therapy: The ED-IMPACT Trial. Ann Emerg Med 2003, 42: S82.

    Google Scholar 

  37. 37.

    Ward KR, Yealy DM: End-tidal carbon dioxide monitoring in emergency medicine, part 1: basic principles. Acad Emerg Med 1998, 5: 628-636.

    CAS  Article  PubMed  Google Scholar 

  38. 38.

    Fletcher R, Boris-Moller F: Can we improve the estimate of arterial PCO 2 from end-tidal PCO 2 ? Eur J Anaesthesiol 2000, 17: 306-310. 10.1046/j.1365-2346.2000.00660.x

    CAS  Article  PubMed  Google Scholar 

  39. 39.

    Shibutani K, Shirasaki S, Braatz T, et al.: Changes in cardiac output affect PETCO 2 , CO 2 transport, and O 2 uptake during unsteady state in humans. J Clin Monit 1992, 8: 175-176.

    Google Scholar 

  40. 40.

    Ward KR, Yealy DM: End-tidal carbon dioxide monitoring in emergency medicine, part 2: clinical applications. Acad Emerg Med 1998, 5: 637-646.

    CAS  Article  PubMed  Google Scholar 

  41. 41.

    Weil MH, Bisera J, Trevino RP, Rackow EC: Cardiac output and end-tidal carbon-dioxide. Crit Care Med 1985, 13: 907-909.

    CAS  Article  PubMed  Google Scholar 

  42. 42.

    Idris AH, Staples ED, O'Brien DJ, Melker RJ, Rush WJ, Del Duca KD, Falk JL: End-tidal carbon dioxide during extremely low cardiac output. Ann Emerg Med 1994, 23: 568-572.

    CAS  Article  PubMed  Google Scholar 

  43. 43.

    Sanders AB, Atlas M, Ewy GA, Kern KB, Bragg S: Expired PCO 2 as an index of coronary perfusion pressure. Am J Emerg Med 1985, 3: 147-149. 10.1016/0735-6757(85)90039-7

    CAS  Article  PubMed  Google Scholar 

  44. 44.

    Martin GB, Paradis NA, Rivers EP, et al.: End-tidal carbon dioxide and coronary perfusion pressure in human beings during standard CPR [abstract]. Ann Emerg Med 1990, 19: 457.

    Google Scholar 

  45. 45.

    Levine R, Wayne M, Miller C: End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med 1997, 337: 301-306. 10.1056/NEJM199707313370503

    CAS  Article  PubMed  Google Scholar 

  46. 46.

    Fearon DM, Steele DW: End-tidal carbon dioxide predicts the presence and severity of acidosis in children with diabetes. Acad Emerg Med 2002, 9: 1373-1378. 10.1197/aemj.9.12.1373

    Article  PubMed  Google Scholar 

  47. 47.

    Tang W, Weil MH, Sun S, Noc M, Gazmuri RJ, Bisera J: Gastric intramural PCO 2 as monitor of perfusion failure during hemorrhagic and anaphylactic shock. J Appl Physiol 1994, 76: 572-577.

    CAS  PubMed  Google Scholar 

  48. 48.

    Desai VS, Weil MH, Tang W, Yang G, Bisera J: Gastric intramural PCO 2 during peritonitis and shock. Chest 1993, 104: 1254-1258.

    CAS  Article  PubMed  Google Scholar 

  49. 49.

    Gutierrez G, Bismar H, Dantzker DR, Silva N: Comparison of gastric intramucosal pH with measures of oxygen transport and consumption in critically ill patients. Crit Care Med 1992, 20: 451-457.

    CAS  Article  PubMed  Google Scholar 

  50. 50.

    Weil MH, Nakagawa Y, Tang W, Sato Y, Ercoli F, Finegan R, Grayman G, Bisera J: Sublingual capnometry: a new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock. Crit Care Med 1999, 27: 1225-1229. 10.1097/00003246-199907000-00001

    CAS  Article  PubMed  Google Scholar 

  51. 51.

    Marik PE: Sublingual capnography: a clinical validation study. Chest 2001, 120: 923-927. 10.1378/chest.120.3.923

    CAS  Article  PubMed  Google Scholar 

  52. 52.

    Fermann GJ, Suyama J: Point of care testing in the emergency department. J Emerg Med 2002, 22: 393-404. 10.1016/S0736-4679(02)00429-8

    Article  PubMed  Google Scholar 

  53. 53.

    Aduen J, Bernstein WK, Khastgir T, Miller J, Kerzner R, Bhatiani A, Lustgarten J, Bassin AS, Davison L, Chernow B: The use and clinical importance of a substrate-specific electrode for rapid determination of blood lactate concentrations. JAMA 1994, 272: 1678-1685. 10.1001/jama.272.21.1678

    CAS  Article  PubMed  Google Scholar 

  54. 54.

    Levere XM, Mustafa I: Lactate: a key metabolite in the intercellular metabolic interplay. Crit Care 2002, 6: 284-285. 10.1186/cc1509

    Article  Google Scholar 

  55. 55.

    Bakker J, Coffernils M, Leon M, Gris P, Vincent JL: Blood lactate levels are superior to oxygen-derived variables in predicting outcome in human septic shock. Chest 1991, 99: 956-962.

    CAS  Article  PubMed  Google Scholar 

  56. 56.

    Bakker J, de Lima AP: Increased blood lactate levels: an important warning signal in surgical practice. Crit Care 2004, 8: 96-98. 10.1186/cc2841

    PubMed Central  Article  PubMed  Google Scholar 

  57. 57.

    Gallagher EJ, Rodriguez K, Touger M: Agreement between peripheral venous and arterial lactate levels. Ann Emerg Med 1997, 29: 479-483.

    CAS  Article  PubMed  Google Scholar 

  58. 58.

    Markowitz DH, Irwin RS: Evaluating acid-base disorders: is venous blood gas testing sufficient? J Crit Illness 1999, 14: 403-406.

    Google Scholar 

  59. 59.

    Smith I, Kumar P, Molloy S, Rhodes A, Newman PJ, Grounds RM, Bennett ED: Base excess and lactate as prognostic indicators for patients admitted to intensive care. Intensive Care Med 2001, 27: 74-83. 10.1007/s001340051352

    CAS  Article  PubMed  Google Scholar 

  60. 60.

    Husain FA, Martin MJ, Mullenix PS, Steele SR, Elliott DC: Serum lactate and base deficit as predictors of mortality and morbidity. Am J Surg 2003, 185: 485-491. 10.1016/S0002-9610(03)00044-8

    Article  PubMed  Google Scholar 

  61. 61.

    Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M, Early Goal-Directed Therapy Collaborative Group: Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Eng J Med 2001, 345: 1368-1377. 10.1056/NEJMoa010307

    CAS  Article  Google Scholar 

  62. 62.

    Manikis P, Jankowski S, Zhang H, Kahn RJ, Vincent JL: Correlation of serial blood lactate levels to organ failure and mortality after trauma. Am J Emerg Med 1995, 13: 619-622. 10.1016/0735-6757(95)90043-8

    CAS  Article  PubMed  Google Scholar 

  63. 63.

    Rady MY, Rivers EP, Nowak RM: Resuscitation of the critically ill in the ED: responses of blood pressure, heart rate, shock index, central venous oxygen saturation and lactate. Am J Emerg Med 1996, 14: 218-225. 10.1016/S0735-6757(96)90136-9

    CAS  Article  PubMed  Google Scholar 

  64. 64.

    Blow O, Magliore L, Claridge JA, Butler K, Young JS: The golden hour and the silver day: detection and correction of occult hypoperfusion within 24 hours improves outcome from major trauma. J Trauma 1999, 47: 964-969.

    CAS  Article  PubMed  Google Scholar 

  65. 65.

    Nguyen HB, Rivers EP, Knoblich BP, Jacobsen G, Muzzin A, Ressler JA, Tomlanovich MC: Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med 2004, 32: 1637-1642. 10.1097/01.CCM.0000132904.35713.A7

    Article  PubMed  Google Scholar 

  66. 66.

    Povoa P: C-reactive protein: a valuable marker of sepsis. Intensive Care Med 2002, 28: 235-243. 10.1007/s00134-002-1209-6

    Article  PubMed  Google Scholar 

  67. 67.

    Da Silva O, Ohlsson A, Kenyon C: Accuracy of leukocyte indices and C-reactive protein for diagnosis of neonatal sepsis: a critical review. Pediatr Infect Dis J 1995, 14: 362-366.

    CAS  Article  PubMed  Google Scholar 

  68. 68.

    Lobo SM, Lobo FR, Bota DP, Lopes-Ferreira F, Soliman HM, Melot C, Vincent JL: C-reactive protein levels correlate with mortality and organ failure in critically ill patients. Chest 2003, 123: 2043-2049. 10.1378/chest.123.6.2043

    CAS  Article  PubMed  Google Scholar 

  69. 69.

    Galetto-Lacour A, Zamora SA, Gervaix A: Bedside procalcitonin and C-reactive protein tests in children with fever without localizing signs of infection seen in a referral center. Pediatrics 2003, 112: 1054-1060. 10.1542/peds.112.5.1054

    Article  PubMed  Google Scholar 

  70. 70.

    Gattas DJ, Cook DJ: Procalcitonin as a diagnostic test for sepsis: health technology assessment in the ICU. J Crit Care 2003, 18: 52-58. 10.1053/jcrc.2003.YJCRC11

    Article  PubMed  Google Scholar 

  71. 71.

    Chan YL, Tseng CP, Tsay PK, Chang SS, Chiu TF, Chen JC: Procalcitonin as a marker of bacterial infection in the emergency department: an observational study. Crit Care 2004, 8: R12-R20. 10.1186/cc2396

    PubMed Central  Article  PubMed  Google Scholar 

  72. 72.

    Wo CC, Shoemaker WC, Appel PL, Bishop MH, Kram HB, Hardin E: Unreliability of blood pressure and heart rate to evaluate cardiac output in emergency resuscitation and critical illness. Crit Care Med 1993, 21: 218-223.

    CAS  Article  PubMed  Google Scholar 

  73. 73.

    Rady MY, Rivers EP, Martin GB, Smithline H, Appelton T, Nowak RM: Continuous central venous oximetry and shock index in the emergency department: use in the evaluation of clinical shock. Am J Emerg Med 1992, 10: 538-541. 10.1016/0735-6757(92)90178-Z

    CAS  Article  PubMed  Google Scholar 

  74. 74.

    Rivers EP, Ander DS, Powell D: Central venous oxygen saturation monitoring in the critically ill patient. Curr Opin Crit Care 2001, 7: 204-211. 10.1097/00075198-200106000-00011

    CAS  Article  PubMed  Google Scholar 

  75. 75.

    Johnson BA, Weil MH: Redefining ischemia due to circulatory failure as dual defects of oxygen deficits and carbon dioxide excesses. Crit Care Med 1991, 19: 1432-1438.

    CAS  Article  PubMed  Google Scholar 

  76. 76.

    Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL, Griffel MI: Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med 1986, 315: 153-156.

    CAS  Article  PubMed  Google Scholar 

  77. 77.

    Rivers EP, Rady MY, Martin GB, Fenn NM, Smithline HA, Alexander ME, Nowak RM: Venous hyperoxia after cardiac arrest. Characterization of a defect in systemic oxygen utilization. Chest 1992, 102: 1787-1793.

    CAS  Article  PubMed  Google Scholar 

  78. 78.

    Durkin R, Gergits MA, Reed JF: The relationship between the arteriovenous carbon dioxide gradient and cardiac index. J Crit Care 1993, 8: 217-221. 10.1016/0883-9441(93)90005-6

    CAS  Article  PubMed  Google Scholar 

  79. 79.

    Bakker J, Vincent JL, Gris P, Leon M, Coffernils M, Kahn RJ: Veno-arterial carbon dioxide gradient in human septic shock. Chest 1992, 101: 509-515.

    CAS  Article  PubMed  Google Scholar 

  80. 80.

    Cuschieri J, Hays G, Rivers EP: Arterial-venous carbon dioxide gradients as an indicator of cardiac index: a comparison between the mixed and central circulation. Crit Care Med 1998, 26: A56.

    Article  Google Scholar 

  81. 81.

    Meduri GU: Noninvasive positive-pressure ventilation in patients with acute respiratory failure. Clin Chest Med 1996, 17: 513-553.

    CAS  Article  PubMed  Google Scholar 

  82. 82.

    Nava S, Carbone G, DiBattista N, Bellone A, Baiardi P, Cosentini R, Marenco M, Giostra F, Borasi G, Groff P: Noninvasive ventilation in cardiogenic pulmonary edema: a multicenter randomized trial. Am J Respir Crit Care Med 2003, 168: 1432-1437. 10.1164/rccm.200211-1270OC

    Article  PubMed  Google Scholar 

  83. 83.

    Mehta S, Jay GD, Woolard RH, Hipona RA, Connolly EM, Cimini DM, Drinkwine JH, Hill NS: Randomized prospective trial of bi-level was continuous positive airway pressure in acute pulmonary edema. Crit Care Med 1997, 25: 620-628. 10.1097/00003246-199704000-00011

    CAS  Article  PubMed  Google Scholar 

  84. 84.

    Pollack CV, Fleisch KB, Dowsey K: Treatment of acute bronchospasm with beta-adrenergic agonist aerosols delivered by a nasal bi-level positive airway pressure circuit. Ann Emerg Med 1995, 26: 552-557.

    Article  PubMed  Google Scholar 

  85. 85.

    Pollack CV, Torres MT, Alexander L: Feasibility study of the use of bi-level positive airway pressure for respiratory support in the emergency department. Ann Emerg Med 1996, 27: 189-192.

    Article  PubMed  Google Scholar 

  86. 86.

    Girou E, Brun-Buisson C, Taille S, Lemaire F, Brochard L: Secular trends in nosocomial infections and mortality associated with noninvasive ventilation in patients with exacerbation of COPD and pulmonary edema. JAMA 2003, 290: 2985-2991. 10.1001/jama.290.22.2985

    CAS  Article  PubMed  Google Scholar 

Download references

Author information



Corresponding author

Correspondence to Ronny Otero.

Additional information

Competing interests

The author(s) declare that they have no competing interests.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Otero, R., Garcia, A.J. Clinical review: New technologies – venturing out of the intensive care unit. Crit Care 9, 296 (2004).

Download citation


  • emergency medicine
  • monitoring
  • non-invasive
  • point-of-care testing
  • technologies