Cardio circulatory and respiratory monitoring of mechanically ventilated critically ill patients

Habib Md Reazaul Karim

Department of Anesthesiology and Critical Care. All India Institute of Medical Sciences, Raipur (India)

Habib Md Reazaul Karim, Department of Anaesthesiology and Critical Care. All India Institute of Medical Sciences, Raipur, (India); Mobile: +1 9612372585; E-mail: drhabibkarim@gmail.com ABSTRACT
Respiratory support in terms of mechanical ventilation is very common in critically ill patients. These patients are often hemodynamically unstable too. The mechano-physiology of mechanical ventilation also affects other organ system and needs assessment and management accordingly. The procedure is not devoid of complication. It also has potential to failure to achieve the treatment objective requiring frequent assessment and adjustment. There is a very close temporal relationship between patients monitoring and management decision in critically ill patients in critical care practice. Early and appropriate information from monitoring can lead to better outcome including reduced mortality. The present review is intended to briefly highlight the current opinions and strategies for cardio circulatory and respiratory monitoring in such patients in critical care unit.
Citation: Karim HMR. Cardio circulatory and respiratory monitoring of mechanically ventilated critically ill patients. Anaesth Pain & Intensive Care 2018;22 Suppl 1:S­­142-S149
Received: 4 Jun 2018, Reviewed: 6 Jun 2018; Accepted: 13 Sep 2018

 
CARDIO CIRCULATORY MONITORING
Mechanically ventilated patients are mostly critically ill and hemodynamic instability is very common in such patients. Weil MH defined hemodynamic instability as either simply one or more out-of range measurements but not necessarily pathological values, or a clinical condition of either perfusion failure clinically presented as circulatory shock and/or advanced heart failure.1 As circulation / pumping the blood is the function of the heart, it becomes essential to monitor the functional status or hemodynamics in such patients. Hemodynamics monitoring can be described under two headings, i.e. basic and advanced. Basic monitoring includes clinical assessment, assessment of global perfusion and preload and fluid responsiveness monitoring. The advanced monitoring includes cardiac contractility and output monitoring and tissue perfusion.2
Clinical examination still remains useful tool and an important initial step in the diagnosis and risk stratification of hemodynamically unstable patients. Parameters like high pulse rate and low volume, increased respiratory rate, cold and clammy periphery, low blood pressure, low urine output, increased capillary refilling time etc indicates poor compromised hemodynamics.3 Although tachycardia is a common feature of hypovolaemia and hemodynamic instability, bradycardia can also be associated with low cardiac output. Therefore all such patients should be monitored for electrocardiography (ECG), blood pressure (BP) and pulse oximetry (SpO2). Continuous ECG monitoring will help us in detecting both rate and rhythm disturbances. ST segment analysis in the continuous ECG can also detect myocardial ischemia early. Unless indicated blood pressure can be monitored by non-invasive techniques.

Serum lactate level is a marker of global perfusion and elevated levels may represent poor tissue perfusion. It has been even regarded as new emerging vital sign in septic shock patients.4 Both initial serum lactate level and lactate clearance at a discrete time point is an important prognostic factor in septic shock patients.5 Therefore, a baseline serum lactate measurements and then follow up can give us information on tissue perfusion, prognosis and indirectly changing hemodynamics.

Central venous oxygen saturation (ScvO2) monitoring have been proposed as a surrogate for venous oxygen saturation (SvO2) monitoring, which can give idea about oxygen supply/demand or oxygen consumption. As O2 supply to the tissues is the basic objective behind hemodynamic management and mechanical ventilation etc., critical care physicians are trying to find out an integrative monitoring parameter which will assess global hemodynamic status of critically ill patients more suitably. To reduce measurement error, it is advised to measure ScvO2 from the tip of a central venous catheter placed close to, or within, the right atrium.6 Although the ScvO2 reflects the balance between oxygen delivery and oxygen consumption directly, the use of this monitoring parameters has remained in controversy. It was suggested as even a parameters to be monitored in goal directed therapy for septic shock patients but Meta-analysis failed find the benefit of early goal directed therapy itself.7,8,9 However, the new guideline and Surviving Sepsis Campaign Bundle do not mention the use of it.10,11 Data also indicates that lactate clearance in sepsis is non-inferior to continuous ScVO2 monitoring.12
If a patient is hypotensive, then we should know whether the hypotension is because of low preload. It is also important to know whether the patient is fluid responsive or not. Traditionally central venous pressure (CVP) had been used for knowing the preload status and increasing CVP value indicates increasing preload. Although the extreme values can predict fluid status satisfactorily, a single value of CVP has very less implications and is having many limitations for using as guide for resuscitation. However, CVP values provide important information about the cardio circulatory status and should not be abandoned yet.13
At present both static and dynamic parameters are used for monitoring preload in critically ill patients. Static parameters monitored can be pressure related, i.e. CVP and pulmonary artery occlusion pressure and volume related i.e. global end-diastolic volume (GEDV) and left ventricular end diastolic volume (LVEDV). Whereas the dynamic parameters monitored are variations in the pressure like pulse pressure variation (PPV), systolic pressure variation (SPV); volume variations like stroke volume variation (SVV), collapsibility of inferior vena cava and superior vena cava. Positive pressure ventilation in a patient produces physiological effects on the right and left sides of the heart which in turn leads to changing preload. During inspiration, increased LV filling causes an increase in LV stroke volume (SV) and opposite happens during expiration. In hypovolemic patients, these changes in LV SV are most marked leading to changes in PPV, SVV, and SPV etc. A PPV of > 13% and SVV of > 10% are considered as fluid responsive. Static preload monitoring like CVP has shown to be ineffective in predicting fluid responsiveness,14 and dynamic parameters are better than static parameters to be used as predictor of preload responsiveness.15
The commonly employed rapid and easy way of assessing fluid responsiveness in the bed side is fluid challenge test. The most commonly practiced fluid challenge (FC) consists in infusing 500 mL of crystalloids or colloids in 20-30 minutes, and considered an increase in cardiac index ≥ 15% as a positive response. However, definite standards for FC administration and evaluation remain undefined.16 In this context, we should also remember that the proportion of responder decreases with long infusion time.17 Therefore, some intensivists / critical care physicians use 15 – 20 minutes to transfuse the volume for challenge test. A mini fluid challenge with 100 ml fluid over 1 minute leading to 3 – 4% decrease in PPV and SVV has shown to predict fluid responsiveness accurately in mechanically ventilated patients (tidal volume < 8ml/kg of ideal body weight) with circulatory failure.18
In the critical care unit (CCU), fluid responsiveness can be determined by an alternative technique to fluid challenge by performing passive leg raising (PLR) maneuver coupled with SV monitoring.19 PLR test has shown to be a good predictor of fluid responsiveness in both patients adapted to ventilator versus those with inspiratory efforts as well as between patients in sinus rhythm versus those with arrhythmias.20
IVC diameters <12 mm has shown to be predictive of fluid responsiveness while values >20 mm predicted non-responders; diameter of 12 – 20 mm were not predictive at all.21 IVC collapsibility > 25% has shown to be predictive of fluid responsiveness among spontaneously breathing critically-ill patients.22 The variations in IVC with respiration can predict fluid responsiveness even in mechanically ventilated patients.23 It is to be remembered that in a spontaneously breathing patient, the IVC collapses in inspiration, whereas in patients with mechanical ventilation the IVC dilates.

Echocardiography allows to measure different volumes and function of heart directly. Bedside echocardiography is a versatile and accurate hemodynamic monitoring tool that can be used for hemodynamic management and fluid resuscitation guide in critically ill patients.24 Although hand held echocardiography appears to have a narrower diagnostic field as compared with conventional transthoracic echocardiography, it can accurately identify diagnoses based on two-dimensional imaging in ventilated critically ill patients.25 Echocardiographic examinations using miniaturized trans-esophageal echocardiography (TEE) after brief bed-side training has shown to be feasible and of sufficient quality.26 The use of hemodynamic TEE for monitoring hemodynamic instability has been also reported.27 However further prospective randomized study will be required to know their specificity, sensitivity and efficacy to recommend the use.

One of the intentions behind the use of hemodynamic monitoring is to promptly identify the circulatory condition and start resuscitation. On the other hand, the ultimate objective of resuscitation is to restore effective tissue oxygenation and cellular metabolism, which needs perfusion to the cellular level. Information gained from global whole-body monitoring may not detect regional organ perfusion abnormalities until they are well advanced.28 Moreover, increased microcirculation during resuscitation has been shown to be associated with reduced multi organ failure at 24 hours.29 These facts necessitate the use of peripheral perfusion monitoring. Peripheral perfusion index (PI), tissue oxygen saturation, continuous transcutaneous oxygen measurement, oxygen challenge test (OCT) etc. can be used to monitor peripheral perfusion. In one study with septic patients, the PI and OCT have been shown to be predictive of mortality after resuscitation.30 However, their use as a monitor to guide for resuscitation cannot be recommended yet and needs further studies.31 Although regional variables are the best predictors of outcome after stabilization of the critically ill patient with shock, initial resuscitation does not require monitoring of regional variables.32
RESPIRATORY MONITORING
Oxygen Saturation:
Monitoring of oxygen saturation is essential and should be continuously monitored.33 Pulse oximetry can reliably and accurately reflect real arterial oxygen saturation with minimum limitation. Oxygen saturation monitoring using pulse oximetry is important to ensure that adequate oxygen is provided to the patient. It can also help in detecting short, prolonged and recurrent desaturations. The readings can be used as an early warning sign, and decreasing the need for blood gas measurements.34 In the absence of partial pressure of arterial oxygen (PaO2) or PaO2/FiO2 (FiO2 – fraction of oxygen); oxygen saturation (SpO2) and SpO2/FiO2 can be an accurate measure for initial oxygenation assessment.35 Risk stratification using SpO2/FiO2 has shown to be practical and can be used for even moderate to severe acute respiratory distress syndrome (ARDS) / hypoxemic patient on mechanical ventilator.36, 37 Analyzing the breath-by-breath variation of the photoplethysmographic signals and arterial impedance, pulse oximetry can even now monitor non-invasive, real time hemodynamics of the ventilated patients.38 However, the pulse oximetry tracings during non-invasive ventilation (NIV) have low specificity. Abnormalities in pulse oximetry tracings are non-specific and do not allow a distinction to be made between, for instance, ventilation perfusion (V/Q) mismatch versus alveolar hypoventilation.39
End Tidal Carbon Dioxide (EtCO2):
End tidal carbon dioxide (EtCO2) has a good relation with partial pressure of arterial carbon-di-oxide (PaCO2) and PaCO2 can be grossly calculated from EtCO2. As PaCO2 represents ventilator function, EtCO2 monitoring can supplement clinicians with information regarding ventilation, V/Q mismatch and decision making. The EtCO2 can be monitored by capnography and continuous monitoring in mechanically ventilated patients is advised.34 However, it cannot replace the PaCO2 measurement by blood gas completely as the gap between EtCO2 and PaCO2 widens in patients of ARDS.40 The morphology of the capnography also gives valuable information about airflow, response to treatment etc. in mechanically ventilated patients.41
Although capnography has shown to be an efficient tool for assessing nocturnal hypoventilation and predicting good compliance with subsequent NIV treatment of patients with amyotrophic lateral sclerosis, EtCO2 measurement using a dedicating naso-buccal sensor was found to be inaccurate to predict both PaCO2 and PaCO2 variations over time in adult patients suffering from acute hypercapnic respiratory failure.42,43 Transcutaneous CO2 has shown to reflect PaCO2 accurately in patients with chronic hypoventilation and can detect nocturnal hypoventilation in patients with normal nocturnal SpO2, and can differentiate nocturnal hypoventilation from other causes of nocturnal hypoxemia.44 However, it is yet to be widely available and not routinely recommended. As carbon-di-oxide level gives an idea of both hypo and hyperventilation, EtCO2 monitoring and its trend is likely to contribute to the management of the patients despite having its limitations.

It is evident that the non-invasive technologies and monitoring like pulse oximetry and capnography can contribute a lot in the monitoring, assessment and decision making in mechanically ventilated patients.

Arterial Blood Gas Analysis (ABG):
Continuous pulse oximetry and capnography monitoring can even reduce the need of arterial blood gas analysis (ABG) but it cannot substitute the need of blood gas analysis completely.45 The ABG in addition also gives the information on acid-base status. The ABG can guide clinicians by aiding in establishing diagnosis, guides treatment plan, ventilator and acid/base management.46
A prospective, multi-center, randomized, controlled clinical trial found that decreasing PaCO2 by at least 20% or to achieve PaCO2 values lower than 48.1 mm Hg at least 1 hour after the end of an NIV session in Global Initiative for Chronic Obstructive Lung Disease (GOLD) class IV stable chronic obstructive pulmonary disease (COPD) patients reduced the mortality.47 A univariate analysis has shown that pH, and base excess (BE) is associated with long term prognosis, whereas multivariate analysis identified a BE below 9 mmol/l was associated with better survival patients with COPD and chronic hypercapnic respiratory failure.48
Therefore it is regarded as a good practice to monitor pCO2, pH and their trend intermittently and BE can be monitored.33 An ABG should be measured after one hour of starting NIV and one hour after every further change in the settings. As a standard ABG should be taken and used to assist in the management plan at 4 hours or earlier in patients who are not clinically improving or judged clinically necessary and again at 12 hours unless the clinical improvement in the patient obviates the need for further ABG analysis.49
 

Venous Blood Gas Analyses:
Meta-analysis on the utility of peripheral venous blood gas analyses in exacerbations of COPD in the emergency department suggests that there is good agreement for pH and HCO3 values between arterial and peripheral venous blood (pVBG) results in patients with COPD, but not for PaO2 or PaCO2. [50] A systematic review and meta-analysis on comparison of peripheral venous and arterial blood gas analysis in adults found that pVBG analysis compares well with ABG analysis for pH estimations in adults but not to the PaCO2 or PaO2.51 Therefore pVBG analysis cannot completely replace the need of ABG.

Mechanical Ventilation:
Mechanical ventilation is often associated with positive end expiratory pressure which reduces venous return and preload. Therefore it has the ability to change hemodynamics. Mechanical ventilation is also not devoid of complications. Non-invasive ventilation, although non-invasive in nature and usually associated with minor complications; even potentially life threatening serious complications can happen.52 Modern mechanical ventilators have built-in software which records and stores data. These data can provide valuable information regarding daily use, leaks, obstruction, and patient ventilator synchronization which can be reviewed and utilized for decision making in patient management.53 Monitoring of the patients’ sensorium, respiratory muscle use can also provide us important clinical findings to aid in decision making.

What monitoring to be used and how frequently?

It is now very clear that continuous progression in the monitoring technology and practice has happened over the last two-three decades. The number of technologies and modalities are also increasing year after year. However, use of all the monitoring is not feasible due to multiple factors. Therefore it becomes an important question that what should be the minimum monitoring to be used and how frequently to be used. Unfortunately, we do not have such universally accepted guideline or standards. Moreover, the requirement of monitoring level in different mechanically ventilated patients are likely to be different based on the co-morbidities, severities of illness, organ failure status etc. The level or degree of monitoring even differs with the level of support required, for example, a patient requiring basic respiratory or cardiac support and a patient requiring advanced respiratory or cardiac support will need different levels of monitoring.

A point prevalence data on patient hemodynamics monitoring pattern from ICUs in Germany, Austria, and Switzerland shows that continuous ECG, pulse oximetry, and invasive or non-invasive blood pressure monitoring were used as basic in nearly all patients; majority of the patients also received invasive arterial and central venous catheterization. Extended hemodynamic monitoring for assessment of cardiac output was only performed in only one in eight patients. Mechanical ventilation, the need for catecholamine therapy, and treatment backed by protocols were the strongest independent predictors for the use of extended hemodynamic monitoring.54 The Task force of the European Society of Intensive Care Medicine recommends further / extended hemodynamic assessment if clinical and basic monitoring is ineffective in determining the type of shock. Non-invasive methods are the suggested initial and preferred choice; echocardiography can be used. Invasive cardiac output monitoring is not recommended as routine but should be used in those patients who are not responding to initial therapy for assessment to response to fluid and inotropes.55 Insertion of arterial and central venous catheter is recommended in shock not responsive to initial therapy and/or requiring infusion of vasopressors.55 For monitoring fluid responsiveness and therapy, dynamic parameters are to be used over static and it is recommended to use more than one variable to guide fluid resuscitation.55
In patients with respiratory failure, pulse oximetry and cardiac monitoring like ECG should be continuously monitored for the first 12 hours.49 Clinical parameters like respiratory rate, pulse, blood pressure and consciousness assessment for acutely ill patients is recommended every 15 minutes in the first hour; every 30 minutes in the 1-4 hour period and hourly in the 4-12 hour period. Patient – ventilator synchrony, mask interface, skin condition and degree of leak should be performed at the same time. Arterial blood gases should be taken as a minimum at 1, 4 and 12 hours after the initiation of NIV.49 Patient-ventilator synchrony, NIV compliance, and mask comfort should be checked regularly. Intensive monitoring is required for COPD patients with pH <7.26.49 Although no robust data to recommend capnography from intubation to extubation in mechanically ventilated patient, it appears reasonable to monitor it capnography as surrogate of PaCO2.56
To summarize, a critically ill mechanically ventilated patient will require continuous ECG, pulse oximetry and capnography, frequent blood pressure monitoring and intermittent ABG as basic. If the patient is also hemodynamically unstable, use of non-invasive monitoring like echocardiography, semi-invasive arterial and central venous catheter based hemodynamics parameters are indicated. Extended hemodynamics monitoring like CO, CI or lung fluid status like EVLW etc will be required in non-responders to initial therapy in level 3 ICUs who require advanced cardiovascular and /or respiratory support and management.57 Tissue oxygenation monitoring needs further validation and at present it is recommended for research purposes.55
CONCLUSION
Cardio circulatory and respiratory monitoring is very much essential in managing critically ill mechanically ventilated patients. As the severity of disease increases, extend of monitoring also increases. Clinical assessment and basic monitoring like continuous ECG, pulse oximetry is must. Although capnography has limitations, considering the fact that it is non-invasive, low cost device which can work as surrogate of PaCO2, continuous monitoring of capnography can be considered as best practice. Intermittent arterial blood gas monitoring can be considered as mandatory in level 2 and 3 ICUs dealing respiratory and cardio circulatory failure patients. Initial lactate as well as lactate clearance is an important monitoring in patients with shock. Basic invasive monitoring like arterial BP and CVP is frequently required in such patients. Present evidence suggests that the point of care ultrasound, echocardiography is also very essential monitoring to be used and probably can be used more frequently. Extended hemodynamic monitoring is not routine but to be reserved for failure to respond to initial therapy. Lastly, no machine or monitor can substitute the best monitor (i.e. intensivist him/herself) till now.

Conflict of interest: None

REFERENCES
  1. Weil MH. Defining hemodynamic instability. In: Pinsky MR, Payen D (editors) Functional Hemodynamic Monitoring: In: Vincent JL (editor) Update in Intensive Care and Emergency Medicine 42. Berlin:Springer Verlag; 2004:9-17.
  2. McCanny P, Colreavy F, Bakker J. Haemodynamic monitoring and management – Skills and Technique. European Society of Intensive Medicine [www.pact.esicm.org]. Brussels, Belgium; ESICM 2013.pp1-91. [Cited 2018 May 31]. Available from: http://pact.esicm.org/media/HaemMon%20and%20Mgt%208%20April%202013%20final.pdf
  3. Sevransky J. Clinical Assessment of Hemodynamically Unstable Patients. Curr Opin Crit Care 2009;15:234-8. [Free full text]
  4. Lee SM, An WS. New clinical criteria for septic shock: serum lactate level as new emerging vital sign. J Thorac Dis 2016;8:1388-90. [Free full text]
  5. Lee SM, Kim SE, Kim EB, Jeong HJ, Son YK, An WS. Lactate Clearance and Vasopressor Seem to Be Predictors for Mortality in Severe Sepsis Patients with Lactic Acidosis Supplementing Sodium Bicarbonate: A Retrospective Analysis. Lazzeri C, ed. PLoS ONE. 2015;10:e0145181. [Free full text]
  6. Walley KR. Use of central venous oxygen saturation to guide therapy. Am J Respir Crit Care Med 2011;184(5):514-20. [PubMed] [Free full text]
  7. Rowan KM, Angus DC, Bailey M, Barnato AE, Bellomo R, Canter RR, et al. Early, Goal-Directed therapy for septic shock - A PatientLevel Meta-Analysis. N Engl J Med 2017;376:2223–34. [Free full text]
  8. Yu H, Chi D, Wang S, Liu B. Effect of early goal-directed therapy on mortality in patients with severe sepsis or septic shock: a meta-analysis of randomised controlled trials. BMJ Open 2016;6:e008330 [PubMed] [Free full text]
  9. Society of Critical Care Medicine (SCCM). Updated Bundles in response to New evidence. Illinois:SCCM;2015.pp1-2. [last accessed 2018 June 1] Available from: http://www.survivingsepsis.org/SiteCollectionDocuments/SSC_Bundle.pdf
  10. Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, Kumar A, Sevransky JE, Sprung CL, Nunnally ME,et al. Surviving Sepsis campaign: international guidelines for management of Sepsis and Septic shock: 2016. Intensive Care Med 2017;43:304–77. [PubMed] [Free full text]
  11. Levy MM, Evans LE Rhodes A. The Surviving Sepsis Campaign Bundle: 2018 update. Crit Care Med 2018;46:997–1000. [PubMed] [Free full text]
  12. Jones AE, Shapiro NI, Trzeciak S, Arnold RC, Claremont HA, Kline JA; Emergency Medicine Shock Research Network (EMShockNet) Investigators. Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. JAMA 2010;303:739-46. [Free full text]
  13. De Backer D, Vincent J-L. Should we measure the central venous pressure to guide fluid management? Ten answers to 10 questions. Crit Care 2018;22:43. [PubMed] [Free full text]
  14. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008;134:172–8 [PubMed]
  15. Pinsky MR. Functional Hemodynamic Monitoring. Critical care clinics. 2015;31:89-111. [Free full text]
  16. Messina A, Longhini F, Coppo C, Pagni A, Lungu R, Ronco C, et al. Use of the Fluid Challenge in Critically Ill Adult Patients: A Systematic Review. Anesth Analg 2017;125:1532-43. [PubMed]
  17. Toscani L, Aya HD, Antonakaki D, Bastoni D, Watson X, Arulkumaran N, et al. What is the impact of the fluid challenge technique on diagnosis of fluid responsiveness? A systematic review and meta-analysis. Crit Care 2017;21:207. [Free full text]
  18. Mallat J, Meddour M, Durville E, Lemyze M, Pepy F, Temime J, et al. Decrease in pulse pressure and stroke volume variations after mini-fluid challenge accurately predicts fluid responsiveness. Br J Anaesth 2015;115:449-56. [PubMed] [Free full text]
  19. Marik PE, Monnet X, Teboul J-L. Hemodynamic parameters to guide fluid therapy. Ann Crit Care 2011; 1: 1 [PubMed] [Free full text]
  20. Cavallaro F, Sandroni C, Marano C, La Torre G, Mannocci A, De Waure C, et al. Diagnostic accuracy of passive leg raising for prediction of fluid responsiveness in adults: systematic review and meta-analysis of clinical studies. Intensive Care Med 2010;36:1475-83. [PubMed]
  21. Sant'Ana AJ, Otsuki DA, Noel-Morgan J, Leite VF, Fantoni DT, Abrahao Hajjar L, et al. Use of pulse pressure variation to estimate changes in preload during experimental acute normovolemic hemodilution. Minerva Anestesiol 2012;78:426-33. [PubMed] [Free full text]
  22. Corl KA, George NR, Romanoff J, Levinson AT, Chheng DB, Merchant RC, et al. Inferior vena cava collapsibility detects fluid responsiveness among spontaneously breathing critically-ill patients. J Crit Care 2017;41:130-137. [PubMed]
  23. De Backer D, Fagnoul D. Intensive care ultrasound: VI. Fluid responsiveness and shock assessment. Ann Am Thorac Soc 2014;11:129-36. [PubMed] [Free full text]
  24. Au SM, Vieillard-Baron A. J Clin Monit Comput (2012) 26: 355. Miller A, Mandeville J. Predicting and measuring fluid responsiveness with echocardiography. Echo Res Pract 2016;3(2):G1-G12. [PubMed] [Free full text]
  25. Vignon P, Chastagner C, François B, Martaillé J-F, Normand S, Bonnivard M, et al. Diagnostic ability of hand-held echocardiography in ventilated critically ill patients. Crit Care 2003;7(5): R84–R91 [Free full text]
  26. Cioccari L, Baur H-R, Berger D, Wiegand J, Takala J, Merz TM. Hemodynamic assessment of critically ill patients using a miniaturized transesophageal echocardiography probe. Crit Care 2013;17(3):R121. [Free full text]
  27. National Institute of Health and Care Excellence. The hTEE system for transoesophageal echocardiographic monitoring of haemodynamic instability. London:NICE; 2014.pp1-29 [cited 2018 June 2] Available from: https://www.nice.org.uk/advice/mib7/resources/the-htee-system-for-transoesophageal-echocardiographic-monitoring-of-haemodynamic-instability-pdf-1763870532037
  28. Ekbal NJ, Dyson A, Black C, Singer M. Monitoring tissue perfusion, oxygenation, and metabolism in critically ill patients. Chest 2013;143:1799-1808. [PubMed]
  29. Trzeciak S, McCoy JV, Dellinger RP, Arnold RC, Rizzuto M, Abate NL, et al.; Microcirculatory Alterations in Resuscitation Shock (MARS) investigators. Early Increases in Microcirculatory Perfusion During Protocol-Directed Resuscitation are Associated with Reduced Multi-Organ Failure at 24 hours in Patients with Sepsis. Intensive Care Med 2008;34:2210-7. [PubMed] [Free full text]
  30. He HW, Liu DW, Long Y, Wang XT. The peripheral perfusion index and transcutaneous oxygen challenge test are predictive of mortality in septic patients after resuscitation. Crit Care 2013;17(3):R116. [PubMed] [Free full text]
  31. Hasanin A, Mukhtar A, Nassar H. Perfusion indices revisited. J Intensive Care 2017;5:24. [PubMed] [Free full text]
  32. Poeze M, Solberg BC, Greve JW, Ramsay G. Monitoring global volume-related hemodynamic or regional variables after initial resuscitation: What is a better predictor of outcome in critically ill septic patients? Crit Care Med 2005;33:2494-500. [PubMed]
  33. Davidson AC, Banham S, Elliott M, Kennedy D, Gelder C, Glossop A, et. Al.; BTS Standards of Care Committee Member, British Thoracic Society/Intensive Care Society Acute Hypercapnic Respiratory Failure Guideline Development Group, On behalf of the British Thoracic Society Standards of Care Committee. BTS/ICS guideline for the ventilatory management of acute hypercapnic respiratory failure in adults. Thorax 2016;71 Suppl 2:ii1-35. [PubMed] [Free full text]
  34. Brochard L, Martin GS, Blanch L, Pelosi P, Belda FJ, Jubran A, et al. Clinical review: Respiratory monitoring in the ICU - a consensus of 16. Crit Care 2012;16:219. [Free full text]
  35. Sanz F, Dean N, Dickerson J, Jones B, Knox D, Fernández-Fabrellas E, et al. Accuracy of PaO2 /FiO2 calculated from SpO2 for severity assessment in ED patients with pneumonia. Respirology 2015;20:813-8. [PubMed]
  36. Pisani L, Roozeman JP, Simonis FD, Giangregorio A, van der Hoeven SM, Schouten LR, et al. Risk stratification using SpO2/FiO2 and PEEP at initial ARDS diagnosis and after 24 h in patients with moderate or severe ARDS. Ann Intensive Care 2017;7:108. [Free full text]
  37. Brown SM, Duggal A, Hou PC, Tidswell M, Khan A, Exline M, et al; National Institutes of Health (NIH)/National Heart, Lung, and Blood Institute (NHLBI) Prevention and Early Treatment of Acute Lung Injury (PETAL) Network. Nonlinear Imputation of PaO2/FIO2 From SpO2/FIO2 Among Mechanically Ventilated Patients in the ICU: A Prospective, Observational Study. Crit Care Med 2017;45:1317-24. [PubMed] [Free full text]
  38. Tusman G, Bohm SH, Suarez-Sipmann F. Advanced Uses of Pulse Oximetry for Monitoring Mechanically Ventilated Patients. Anesth Analg 2017;124:62-71. [PubMed]
  39. Janssens J, Borel J, Pépin J, on behalf of the SomnoNIV Group. Nocturnal monitoring of home non-invasive ventilation: the contribution of simple tools such as pulse oximetry, capnography, built-in ventilator software and autonomic markers of sleep fragmentation. Thorax 2011;66:438-45 [PubMed] [Free full text]
  40. McSwain SD, Hamel DS, Smith PB, Gentile MA, Srinivasan S, Meliones JN, Cheifetz IM: End-tidal and arterial carbon dioxide measurements correlate across all levels ofphysiologic dead space. Respir Care 2010;55:288-93. [PubMed] [Free full text]
  41. Kerslake I, Kelly F. Uses of capnography in the critical care unit. BJA Educ 2017;5: 178–83.
  42. Kim S-M, Park KS, Nam H, et al. Capnography for Assessing Nocturnal Hypoventilation and Predicting Compliance with Subsequent Noninvasive Ventilation in Patients with ALS. Morty R, ed. PLoS ONE. 2011;6(3):e17893. [PubMed] [Free full text]
  43. Piquilloud L, Thevoz D, Jolliet P, Revelly J-P. End-tidal carbon dioxide monitoring using a naso-buccal sensor is not appropriate to monitor capnia during non-invasive ventilation. Ann Intensive Care 2015;5:2. [Free full text]
  44. Aarrestad S, Tollefsen E, Kleiven AL, Qvarfort M, Janssens JP, Skjønsberg OH. Validity of transcutaneous PCO2 in monitoring chronic hypoventilation treated with non-invasive ventilation. Respir Med 2016;112:112-8. [PubMed] [Free full text]
  45. Clouser R, Stevens P, Hamlin M, Allen GB. Minimization of Arterial Blood Gas Sampling in Mechanically Ventilated Patients Via Continuous SpO2 and End Tidal CO2 Monitoring. A Choosing Wisely Project. Am J Respir Crit,Care Med 2018;197:A6827.
  46. Sood P, Paul G, Puri S. Interpretation of arterial blood gas. Indian J Crit Care Med 2010;14:57-64. [PubMed] [Free full text]
  47. Köhnlein T,Windisch W, Köhler D, Drabik A, Geiseler J,Hartl S, et al. Non-invasive positive pressure ventilation for the treatment of severe stable chronic obstructive pulmonary disease: a prospective, multicentre, randomised, controlled clinical trial. Lancet Respir Med 2014;2:698–705. [PubMed]
  48. Budweiser S, Jörres RA, Riedl T, Heinemann F, Hitzl AP, WindischW, et al. Predictors of survival in COPD patients with chronic hypercapnic respiratory failure receiving noninvasive home ventilation. Chest 2007;131:1650–8. [PubMed]
  49. Roberts CM, Brown JL, Reinhardt AK, Kaul S, Scales K, Mikelsons C, et al. Non-invasive ventilation in chronic obstructive pulmonary disease: management of acute type 2 respiratory failure. Clin Med (Lond) 2008;8:517-21. [PubMed] [Free full text]
  50. Lim BL, Kelly AM. A meta-analysis on the utility of peripheral venous blood gas analyses in exacerbations of chronic obstructive pulmonary disease in the emergency department. Eur J Emerg Med 2010;17:246-8. [PubMed]
  51. Byrne AL, Bennett M, Chatterji R, Symons R, Pace NL, Thomas PS. Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta-analysis. Respirology 2014;19:168-175. [PubMed] [Free full text]
  52. Carron M, Freo U, BaHammam AS, Dellweg D, Guarracino F, Cosentini R, et al. Complications of non-invasive ventilation techniques: a comprehensive qualitative review of randomized trials. Br J Anaesth 2013;110:896 – 914. [PubMed] [Free full text]
  53. Pasquina P, Adler D, Farr P, Bourqui P, Bridevaux PO, Janssens JP. What does built-in software of home ventilators tell us? An observational study of 150 patients on home ventilation. Respiration 2012;83:293–9. [PubMed] [Free full text]
  54. Funcke S, Sander M, Goepfert MS, Groesdonk H, Heringlake M, Hirsch J, et al. The ICU-CardioMan Investigators. Practice of hemodynamic monitoring and management in German, Austrian, and Swiss intensive care units: the multicenter cross-sectional ICU-CardioMan Study. Ann Intensive Care 2016;6:49. [Free full text]
  55. Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C, et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med 2014;40:1795–1815. [PubMed] [Free full text]
  56. Cheifetz IM, Myers TR. Respiratory therapies in the critical care setting. Should every mechanically ventilated patient be monitored with capnography from intubation to extubation? Respir Care 2007;52:423-38;discussion 438-42. [PubMed] [Free full text]
  57. Eddleston J, Goldhill D, Morris J; Council of the Intensive Care Society. Levels of critical Care in adult patients. Intensive Care Society Standards. London: Intensive Care Society; 2009.pp 1-12. [cited 2018 June 3]. Available from: https://www.ics.ac.uk/AsiCommon/Controls/BSA/Downloader.aspx?iDocumentStorageKey=74ca75c6-67c4-4400-96a2-4e7e14b8d9a3&iFileTypeCode=PDF&iFileName=Levels%20of%20Critical%20Care%20for%20Adult%20Patients