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Online Letters to the Editor
It is only normal that the CVP levels of these patients would
differ related to difference in PEEP levels but their outcome
might not.
Another point that attracts our attention is the low PEEP
levels in all groups. In groups (low CVP and Pmean, either
low CVP or low Pmean), PEEP levels used are given as
5 cm H2O. In high CVP and Pmean group, PEEP levels are
given as 7.925 cm H2O. In many patients with respiratory
diseases, higher PEEP levels are needed. Were there differences in terms of Fio2 used in those three groups? Did in
any patients in any groups, reverse ratio ventilation or prone
position were used?
It is also essential at least to be informed about the types of
monitors used to screen the patients. Were all patients monitored with the same type of monitors?
Non CVP group were defined as “patients stable enough
in who it was unnecessary to insert a central venous catheter
to monitor the CVP.” A better definition is needed for “stable
enough.” Also in the result section, it is said, “respiratory and
hemodynamic parameters, as well as tissue hypoperfusion
worsened in the nonmonitored CVP group when compared
with the high CVP and high mean group (Table 3)” (1). However in Table 3 (1), no such data are given. Could it be possible
that it was forgotten?
The term “circulation protective ventilation” is not
described well. More details are needed to reproduce the
strategy in another ICU. Do the authors reject the need of
recruitment maneuvers as they state they are related with poor
Although it is said that the mean arterial pressures were
statistically significant, arterial pressures of 83.00, 82.66, and
81.00 mm Hg are not clinically different at all. Same result
can also be observed with lactate levels. Both mean arterial
pressure and lactate levels are a good sign of perfusion (3).
According the data given, perfusion was not compromised in
any of the groups. How can the authors explain these data
and reflect it on the clinic? Their comments can enlighten to
the reader.
The authors have disclosed that they do not have any potential conflicts of interest.
Guniz M. Koksal, MD, Emre Erbabacan, MD, Department
of Anesthesiology and Reanimation Istanbul University,
Cerrahpasa Medical Faculty, Istanbul, Turkey; Antonio M.
Esquinas, MD, PhD, FCCP, Intensive Care Unit, Hospital
General Universitario Morales Meseguer Murcia, Región de
Murcia, Spain
1.Long Y, Su L, Zhang Q, et al: Elevated Mean Airway Pressure and
Central Venous Pressure in the First Day of Mechanical Ventilation
Indicated Poor Outcome. Crit Care Med 2017; 45:e485–e492
2. Shojaee M, Sabzghabaei A, Alimohammadi H, et al: Effect of positive
end-expiratory pressure on central venous pressure in patients under
mechanical ventilation. Emerg (Tehran) 2017; 5:e1
3. Mikkelsen ME, Miltiades AN, Gaieski DF, et al: Serum lactate is associated with mortality in severe sepsis independent of organ failure and
shock. Crit Care Med 2009; 37:1670–1677
DOI: 10.1097/CCM.0000000000002614
The authors reply:
e thank Koksal et al (1) for their interest in our study
(2), recently published in Critical Care Medicine, of
central venous pressure (CVP) and mean airway
pressure. The data used in this study came from ICU administrative database of Peking Union Medical College Hospital. The
Department of Intensive Care Medicine is a comprehensive
30-bed ICU, equipped with same monitor. All the patients’ data,
involved internal and surgery, were applied to reflect the relationship between respiratory and circulatory, which can illustrate the
common characteristic of critically ill patients. Stable enough
patients refer to normal level of respiratory and hemodynamic
variables, as well as satisfied tissue perfusion. The patients with
stable enough status always do not need central venous catheterization to monitor CVP in ICU. Additionally, all the variables
used average within 24 hours after ICU admission, rather than
the worst value within 24 hours. Most of the shock was corrected
as soon as possible after ICU admission based on sepsis bundles
(3).Therefore, some parameters, such as mean arterial pressures,
were not have a significant difference from the figure itself. But,
the statistical and clinical significance still exists.
Lung protective ventilation modes were applied during the treatment. Recruitment maneuvers, a vital means to
maintain lung opening and get better oxygenation, was also
used in the patients with low oxygen. But, lung protective
ventilation and recruitment maneuvers do not mean always
in a higher positive end-expiratory pressure (PEEP). When
recruitment completed, it is necessary to titrate a relatively
low PEEP, rather than maintaining the open pressure of the
lungs. It is reported that acute cor pulmonale often happened during protective ventilation and caused bad prognosis in acute respiratory distress syndrome (ARDS) (4, 5).
The right ventricular systolic function is sensitive to PEEP
in ARDS patients undergoing mechanical ventilation (6).
Lower PEEP decreased the right ventricular pressure load.
Therefore, the higher PEEP used to open the lungs and lower
PEEP to maintain the recruitment status. In the article, “
Circulatory Protective Ventilation” was put forwarded and
suggested from four aspects, such as volume protection,
heart function protection, vascular tone protection organ,
and tissue perfusion protection. How to achieve these four
aspects? The following targets may give the clinicians easier
to operate in the daily work: (7, 2) 1) plateau pressure less
than 27 cm H2O, 2) driving pressure less than 18 cm H2O,
3) Paco2 less than 48 mm Hg, 4) CVP as lower as possible.
By the way, the respiratory, hemodynamic variable, and tissue perfusion had worsened in the high CVP and high Pmean
group compared with the nonmonitored CVP group, which
was shown in Tables 1 and 3.
The authors have disclosed that they do not have any potential conflicts of interest.
Yun Long, MD, Longxiang Su, MD, Dawei Liu, MD,
Department of Critical Care Medicine, Peking Union Medical
College Hospital, Peking Union Medical College & Chinese
Academy of Medical Sciences, Beijing, China
November 2017 • Volume 45 • Number 11
Copyright © 2017 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
Online Letters to the Editor
1. M Koksal G, Erbabacan E, Esquinas A: When, Who, and How is Elevated
Mean Airway Pressure and Central Venous Pressure in the First Day of
Mechanical Ventilation a Sign? Crit Care Med 2017; 45:e1203–e1204
2. Long Y, Su L, Zhang Q, et al: Elevated mean airway pressure and central venous pressure in the first day of mechanical ventilation indicated
poor outcome. Crit Care Med 2017; 45:e485–e492
3.Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis Campaign
Guidelines Committee including the Pediatric Subgroup: Surviving
sepsis campaign: International guidelines for management of severe
sepsis and septic shock: 2012. Crit Care Med 2013; 41:580–637
4.Boissier F, Katsahian S, Razazi K, et al: Prevalence and prognosis of
cor pulmonale during protective ventilation for acute respiratory distress syndrome. Intensive Care Med 2013; 39:1725–1733
5.Bouferrache K, Vieillard-Baron A: Acute respiratory distress syndrome, mechanical ventilation, and right ventricular function. Curr
Opin Crit Care 2011; 17:30–35
6.Schmitt JM, Vieillard-Baron A, Augarde R, et al: Positive end-expiratory pressure titration in acute respiratory distress syndrome patients:
Impact on right ventricular outflow impedance evaluated by pulmonary artery Doppler flow velocity measurements. Crit Care Med 2001;
7.Paternot A, Repessé X, Vieillard-Baron A: rationale and description
of right ventricle-protective ventilation in ARDS. Respir Care 2016;
DOI: 10.1097/CCM.0000000000002661
The Use of Tidal Volume Challenge Test in
Critically Ill Patients: Caution Needed
To the Editor:
e read with interest the article by Myatra et al (1) in
a recent article in Critical Care Medicine, where the
authors reported that in 20 patients with acute circulatory, two of whom had acute respiratory distress syndrome
(ARDS), the absolute change (ΔPPV6–8) in pulse pressure variation (PPV) after increasing tidal volume (Vt) from 6 to 8 ml/lkg
predicted body weight (PBW) (tidal volume challenge) reliably predicts fluid responsiveness (sensitivity 94% and specificity 100%) during low Vt (6 ml/lkg) ventilation. However, we
are not convinced by their conclusion that this “tidal volume
challenge test” may reliably identify the true fluid responders
during low Vt. Will this approach work in patients with ARDS
ventilated with a low Vt?
Indeed the main explanation for the poor predictive performance of PPV during a low Vt is that respiratory changes
in pleural pressure (ΔPpl) are too low, such that PPV is low
even in responders (false negatives) (2). More recently, Lansdorp et al (3) recruited 20 ventilated patients following coronary artery bypass grafting surgery, clearly showing that Vt is
a relevant determinant of ΔPpl: the higher the Vt, the higher
the ΔPpl. Hence, we agree with the authors that, in non-ARDS
patients, raising the Vt (from 6 to 8 ml/kg PBW) increases
the magnitude of ΔPpl (and then of PPV in responders),
avoiding some of the false negatives observed during low Vt.
Unfortunately, this is not necessarily the case in patients with
ARDS, in whom the magnitude of ΔPpl (2) was mostly determined by chest wall elastance (Ecw) (R2 = 0.84) or the ratio
Critical Care Medicine
of Ecw to respiratory system elastance (Ers, R2 = 0.69), but to
a lesser extent by Vt (R2 = 0.12). Given that ΔPpl = Vt × ERS ×
(Ecw/ERS) (2), the inadequacy of Vt as a determinant of ΔPpl
(2, 4) (and of PPV (2)) can be accounted for by the great
variability of Ecw/ERS (range, 0.08–0.80) (2, 5) reported for
ICU populations with ARDS and renders tidal volume challenge test questionable at best in such a population. In short,
the clinician should be cautioned against using the tidal volume challenge test to identify responders masked by low Vt
in patients with ARDS, in particular when the Ecw or Ecw/
ERS is “too low” such that increases in Vt (i.e., 6–8 ml/Kg) will
fail to produce sufficient increases in ΔPpl (2) to induce significant changes in PPV values (ΔPPV6–8) in responders. The
question of how low is “too low” remains unsettled, however.
Future studies are required to determine a cutoff value for
Ecw or Ecw/ERS, below which the use of this test should be
In addition, we disagree with the authors’ interpretation (1)
that the low ability of PPV to predict fluid responsiveness in
ARDS patients was related to low respiratory system compliance (CRS, reciprocal of ERS). As well demonstrated in our study
(2), a low Ecw/ERS, rather than a low CRS (or high ERS), induces
reduced pleural pressure swings (ΔPpl) and therefore low ΔPP
values in responders. The highly variable relation between
ERS and ΔPpl is mainly due to great variations in Ecw (2, 4)
(ΔPpl = ΔPaw × Ecw/ERS, where ΔPaw is the airway driving pressure) and explains why a low CRS is not a key factor
accounting for the decreased magnitude of ΔPpl and the consequent low ΔPP values in responders.
The authors have disclosed that they do not have any potential conflicts of interest.
Yang Liu, MD, Medical Intensive Care Unit, Pingjin Hospital,
Logistics College of the Chinese People’s Armed Police
Forces, Tianjin, China; Yu-ming Li, MD, PhD, Tianjin Key
Laboratory of Cardiovascular Remodeling and Target Organ
Injury, Institute of Cardiovascular Disease and Heart Center,
Pingjin Hospital, Logistics College of the Chinese People’s
Armed Police Forces, Tianjin, China
1.Myatra SN, Prabu NR, Divatia JV, et al: The Changes in Pulse
Pressure Variation or Stroke Volume Variation After a “Tidal Volume
Challenge” Reliably Predict Fluid Responsiveness During Low Tidal
Volume Ventilation. Crit Care Med 2017; 45:415–421
2. Liu Y, Wei LQ, Li GQ, et al: Pulse pressure variation adjusted by respiratory changes in pleural pressure, rather than by tidal volume, reliably
predicts fluid responsiveness in patients with acute respiratory distress syndrome. Crit Care Med 2016; 44:342–351
3.Lansdorp B, Hofhuizen C, van Lavieren M, et al: Mechanical ventilation-induced intrathoracic pressure distribution and heart-lung interactions. Crit Care Med 2014; 42:1983–1990
4.Loring SH, O’Donnell CR, Behazin N, et al: Esophageal pressures
in acute lung injury: Do they represent artifact or useful information about transpulmonary pressure, chest wall mechanics, and lung
stress? J Appl Physiol (1985) 2010; 108:515–522
5.Gattinoni L, Pelosi P, Suter PM, et al: Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different
syndromes? Am J Respir Crit Care Med 1998; 158:3–11
DOI: 10.1097/CCM.0000000000002645
Copyright © 2017 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.
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