- Email: [email protected]
Monitored arterial and end-tidal carbon dioxide during in-flight mechanical ventilation
ORIGINAL RESEARCH
Monitored Arterial and End-tidal Carbon Dioxide During In-flight Mechanical Ventilation Cheryl J. Erler, RN, MS,’ William F. Rutherford, Stahl, RN, BS*
1. Associate Professor, West Lafayette, Ind. 2. Life Line Methodist Ind.
Purdue
Hospital,
3. Health Services Research, pital, Indianapolis, Ind.
University,
Abstract
Introduction
Indianapolis,
Introduction: Mechanical ventilation with monitored arterial carbon dioxide tension is necessary for optimum pulmonary support and hemodynamic stability. Ongoing monitor-
The most common method of ventilation in the prehospital setting is intubation and manual ventilation with a bag valve device. Although it is a lie-saving technique, previous studies have established that manual ventilation frequently results in low tidal volumes (vt), loss of minute ventilation, acidosis, and a.lkalosis.l-3Low tidal volumes are reportedly advantageous with certain pulmonary diseases; however, the low volumes are associated with permissive hypercapnia and have not been studied in multisystem trauma patients because of the physiologic effects of acidosis.4.5 Both acidosis and alkaIosis prompt a plethora of consequences. Acidosis results in decreased systemic vascular re sistance, decreased cardiac contractility, increased cerebral blood flow, and a shift in the oxyhemoglobin curve to the right.4,6 Myocardial consequences of alkalosis include decreased cardiac output, coronary artery vasospasmand ischemia, and various cardii arrhythmias.sJ In addition, alkalosis also decreases cerebral blood flow and may result in localized cerebral edema, rebound increased intracranial pressure, and &ii the oxyhemoglobin curve to the left.810 Although hyperreaction with resulting respiratory alkalosis has been common practice in early treatment of trauma patients with
Methodist
Hos-
Key Words: capnography, arterial blood gases, tidal volume, ventilation, air transport Address for correspondence and reprints: Cheryl J. Erler, RN, MS, Associate Professor, Purdue University, JNSN 1337, West Lafayette, IN 47907. Submitted: January 30, 1996 Revised: July 27, 1996 Accepted: August 281996 Presented at the Air Medical Transport Conference in Long Beach, California, October 16, 1995. Copyright Associates.
0 1996
1067-991
X/96/$5.00
Reprint
MD,* Angela Fiege, RN, BS,* David R. Nelson, MS,3 Ann
by the Air Medical
Journal
ing is necessary to ensure adequate ventilation parameters. The prospective study purpose was to (1) compare mechanical ventilation to historic manual ventilation, (2) evaluate the effectiveness of institutional tidal volume parameters, (3) determine the effect of institutional tidal volume manipulation on end-tidal carbon dioxide tension, and (4) explore the relationship between in-flight end-tidal carbon dioxide tension and arterial carbon dioxide tension. Methods: Randomized groups were mechanically ventilated (tidal volume = 12 cc/kg, rate = 14/min) with a target arterial carbon dioxide tension between 30 and 35 ton. Group I was monitored with in-line end-tidal carbon dioxide tension, and group II was monitored with arterial carbon dioxide tension by means of inflight arterial blood gas. Results: Arterial carbon dioxide tension varied less with monitored mechanical than with manual ventilation @ = 0.001). The gradient between arterial and end-tidal carbon dioxide tension was 5.3 * 4.4 (mean + standard deviation [SD]). End-tidal and arterial carbon dioxide tension positively correlated (r = 0.76, p = 0.001) yet end-tidal carbon dioxide tension accounted for only 58% variation of arterial carbon dioxide tension (r’ = 0.58). Conclusion: Mechanical ventilation is more precise but inconsistent in achieving a target arterial carbon dioxide tension with current
+ 0
No. 74lIl77907
ventilation parameters. End-tidal carbon dioxide tension is a reasonable estimate of, but cannot exclusively replace, arterial carbon dioxide tension in critically ill patients.
Air Medical Journal
154
October-December
1996
171
neurologic insult, there is controversy about the range of arterial carbon dioxide tension (PaCOd values that provide therapeutic benefit and whether any pos sible benefits are worth the associated risks.11 Although mechanical ventilation is undeniably more predictable in ensuring ventilation parameters than manual ventilation, punctilious surveillance is necessary to evaluate its ongoing pulmonary and hemodynamic effects. Blind or unwary ventilation exposes patients to unnecessary risks and complications. Traditionally, arterial blood gas (ABG) analysis has been used to ascertain a PaCOzvalue and determine the effective ness of ventilation maneuvers. However, ABG analysis is invasive and intermittent, and typically there is a time delay between sampling and accessibility of re sults. Most recently, capnography, a noninvasive technique for end-tidal carbon dioxide (ETCOd measurement, has become widely accepted in various settings as a method to monitor ventilation. Capnography has been shown to be effective in early detection of potentially disastrous events such as hypoventilation, esophageal intubation, and ventilator disconnection.12 ETC02, defined as the maximal CO2 concentration detected at the end of the expiratory cycle,is expressedas a percentage (ETCO2, or in millimeters of mercury or torr (PetCO2).13ETC02 represents the general effects of three body functions: metabolism, circulation, and ventilation. When CO2 production and CO2 transport remain constant, changes in EICOs repro sent a variation in ventilation.ls This real time measurement permits the earliest detection of alveolar ventilation and may allow substitution for the traditional and more cumbersome ABG measurement used to detect PaC02 values.14 ‘Ihe accuracy and reliability of the re lationship between ETC02 and PaC02, referred to as P(a-ET)COs gradient, varies in different populations and clinical settings. Most reported studies have explored the P(a-BT)COs in healthy subjects and mechanically ventilated patients 172
ABG Values Historic controls (n PH PaC02 Pa02 Values
q
Group Vent+ETCO+ 7)
7.3 f 0.22 40.3 f 18.6 233.2 + 164.6
are expressed
as mean
(n
q
I I-STAT
p
15)
7.4 f 0.10 32.7 i 6.4 355.9 * 97.8
Value
Vent, c 7.4 30.2 501.8
0.01 0.001 0.10
= + + +
Group II i-STAT x 2 7) 0.25 2.3 123.1
p
Value 0.74 0.001 0.60
f SD.
with pulmonary or cardiac disease. To date there is a paucity of clinical studies regarding capnography and mechanical ventilation during in-flight transport of critically ill patients. The purpose of this prospective study was to (1) compare mechanical ventilation by means of either monitored ETCOz or PaC02 to historic controls (manual ventilation with in-flight ABGs), (2) evaluate the effectiveness of institutional Vt parameters in achieving a target PaC02 range, (3) evaluate the effect of Vt manipulation on ETC02 and PaCO,, and (4) explore the relationship between in-flight ETC02 and PaCO2. Methods This study is the third part of an ongoing investigation designed to determine the efficacy of ventilation strategies used during the prehospital transport of critically ill patients. The first part of the study, conducted from 1990 to 1991, involved a retrospective review of 187 patients manually ventilated during transport. Study findings were congruent with the literature and reflected inconsistent and extreme values of PaC02.1s In 1992, a prospective study (part II) was designed to explore the effect of unmonitored manual ventilation on in-flight ABG values. Early analysis in part II showed blatant PaC02 abnormalities after 15 minutes of in-flight manual ventilation.16 Because of the abnormalities with unmonitored manual ventilation, part II was suspended and part III of the study was postponed until mechanical ventilation, capnography, and portable ABG analysis capability were in place.
The study (part III) was conducted at a level I trauma center from December 1994 to April 1995. The data were collected in two Eurocopter BK-117 helicopters by a flight team that included either a nurse and paramedic or a nurse and emergency medicine resident. All crew members were skilled in use of mechanical ventilation, capnography, and in-flight ABG techniques. The study was approved by the institutional review board at Methodist Hospital and the committee on human subjectsreview at Purdue University. Study subjects included critically ill patients over 15 years of age who required intubation and mechanical ventilation during air transport. Subjects with obvious chest injury and those receiving resuscitative drugs such as sodium bicarbonate and alpha-adrenergic agents were excluded from the study. In addition, sub jects known to have preexisting chronic pulmonary disease were eliminated from the study population because of disease influence on the P(a-ET)C02 gradient and dependability of capnography. All subjects were ventilated with an IMPACT Univent model 750 volume-cycled transport ventilator (IMPACT Instrumentation, Inc., West Caldwell, NJ.) according to the hospital’s institutional guidelines that include Vt = 12 cc/kg of ideal body weight, ventilation rate = 14, and percentage of inspired oxygen = 100%.Before liftoff to the receiving haspital, subjects were randomized into group I or II by selection of a sealed envelope containing one of two study proto ~01s. The target PaC02 range for the study was 30 to 35 torr.
October-December
1996
15:4
Air Medical
Journal
Blood Gases (p Historic controls (n PaCO2 <30 30-35 135
range
q
Group
I + ETCOI
(I?=
15)
ventilation 7)
18-71.4 torr n=3 n=O n=4
20.8-40.3 n=lO n=3 n=2
Comparison Group ETCOs+
Vent,
Values
are expressed
Group Ventilation
II + PaCOs
(n = 7) torr
18.9-46 n=4 n=2 n=l
torr
of Final PaCO,
I I-STAT
Vent
Group II + I-STAT
(n=15) PaCO2
0.001)
q
p
x 2
Value
(n = 7)
32.7
zt 6.4
as mean
f SD.
30.2
ETCO, vs PaCO,
* 2.3
0.07
Relationship
minutes of ventilation, a second i-STAT determination was made. Respiratory acidosis and alkalosis were treated by manipulation of the Vt. For both groups I and II, Vt was increased to 15 cc/kg for ETCO;! and PaCOz values >35 torr. Vt was decreased to 10 cc/kg for ETC02 and PaC02 ~30 torr. The dependent variables were ETCO;! and PaC02, and the independent variable was Vt. Demographic variables included age, weight, gender, and mechanism of injury. Instrumentation to measure PaC02 by means of in-flight ABG analysis was the i-STAT system. Estimates of reliability reported for the i-STAT are 0.9785 to 0.9946. In-line El’C02 was measured with monitored capnography using a ProPaq PAOlOGEL (Protocol System, Inc., Beaverton, Ore.). Internal product validation test results for the ProPaq COz report accuracy within 10%. Results
50 45 $
10
15
20
25
30
35
40
45
50
ETCO, (torr) r=O.76,p=0.001
In group I, ETCOz values were noted by means of in-line capnography after 10 minutes of mechanical ventilation, and Vt changes were made for ETCOa values outside the target range. Ten minutes after changes in ventilation were initiated, both ETCO, measured by means of capnography and ABG analysis with the i-STAT system values (i-STAT CorporaAir Medical Journal
15:4
October-December
tion, Princeton, N.J.) were simultaneously determined and recorded. After 10 minutes of mechanical ventilation in group II, PaCOzvalues were determined by ABG analysis by means of i-STAT and Vt adjustments were made on the basis of the PaC02 level. As in group I, ventilation changes were made for PaC02 values outside the target range. After 10
1996
The sample comprised 22 subjects ranging from ages 16 to 90, with a mean age of 48 years. The 15 males and seven fe males required mechanical ventilation for a variety of reasons including motor vehicle accidents, gunshot wounds, falls, bums, and neurologic insults of medical origin. All subjects in both groups I and II were compared with historic controls from part II of the study. Historic controls (tl = 7) included patients with inflight ABG analysis after 15 minutes of unmonitored manual ventilation. F-tests were used to compare variance of pH, PaC02, and PaOz between the historic controls and the two treatment groups. Group I subjects, those with mechanical ventilation and in-line ETCOz, showed less variation in pH, less variation in PaC02, and no diierence in PaOz compared with historic controls. Group II subjects varied significantly less in PaCOz than historic controls; however, no difference in variation was detected for pH and Pa02 (Table 1). There were more subjects in the target PaC02 range in both groups I and II than historic control subjects with un-
173
monitored manual ventilation (Table 2). PaC02 variation was greater for subjects monitored with PaCOz as compared with subjects monitored with ETCOz. However, there was a greater percentage of subjects within the target range with monitored PaCOz.No statistically signitlcant differences were found between the PaC02 (p = 0.07) for group I and the second PaC02 for group II. No statistical difference was found in the post-ventilation change in PaCOz between group I subjects whose ventilation adjustments were based on ETC08 and group II subjects whose ventilation adjustments were based on preliminary i-STAT ABGs (Table 3). Estimated weights were used to determine the Vt based on cubic centimeters per kilogram. Ten subjects had actual recorded weights. The Pearson product correlation between estimated weight and ETCOBwas Y = 4.84, which was statistically significant @ = 0.002) when the weight was inaccurately underestimated or overestimated by 20 kg. With the use of the sign test, no statistical diierence was found (p = 0.50) be tween the number of subjects in group I with PaC02 values withii 30 to 35 torr in the second ETC02 after Vt manipulation compared with the first ElC02. No difference was found in mean scores with the use of a t-test (p = 0.76) or by SD with the use of the F-test (p = 0.38) between the first ETC02 and second ETC02 (p = 0.76) reading obtained after Vt manipulation. Mean values for first ETC02 recordings were (26.5 f 8.1 tot-r) compared with the second ETCO;! (32.7 f 6.4 torr) recordings. The P(a-ET)CO, gradient was 5.3 f 4.4 torr, ranging from a minimum of -1 and a maximum of 17.7 torr. The Pearson product moment correlation between ETCO, and PaCOswas r = 0.76, which was signiticant (p = 0.001). With the use of 72analysis, ETC02 accounted for 58% (r” = 0.58) of the variation of PaCO, (Fii 1). Discussion
Study findings reflect less extreme PaCOs values with mechanical ventila-
174
tion and monitored ETCOz and PaC02 compared with previous study PaCO, values reported with manual ventilation. There are more patients within the target PaC02 range with mechanical ventilation; however, a number of subjects continue to be outside the study range. Me chanical ventilation is more precise but still inconsistent in achieving target PaC02 with the use of the current ventilation parameters. Estimated weights as a basis for Vt determination resulted in less target variation in PaC02 values when weight was erroneously estimated by 20 kg. As weight was overestimated, ETCO, values were higher; conversely, when weight was overestimated, ETCOz values were less. In general, a Vt of 12 cc/kg was typ ically too high to achieve a target PaCOs during the study time allotted. This finding is consistent with studies that report higher PaCO, values with lower Vt.4*5 A change in Vt of 2 cc/kg did not effect the PaCOzsignificantly. The average flight and total transport time was 30 minutes. A longer time interval between Vt changes and ETC02 or PaC02 determinations may be needed to more adequately reflect significant PaC02. Also, larger changes in Vt may be required to generate the desired PaCOzchanges. In this study of patients who were me chanically ventilated during air transport, there is an overall positive correlation be tween ETC02 and PaC02 (r = 0.76) (Figure 1). The study correlation coefficient is similar to that found by Hoffman et al.17 who reported a correlation coefficient of r = 0.78 in critically ill patients undergoing changes in mechanical ventilation. A similar correlation is reported by Thrush and Mentisis who determined that ETCO, was a good indicator of PaC02 (r = 0.76) and may be used to safely and effectively wean patients from mechanical ventilation after coronary artery bypass surgery. A positive but less significant correlation (r = 0.61) was reported for extubated postoperative patients and trauma patients with chest injuries who were being observed for possible mechanical ventilation sup-
port-19A higher correlation coefficient (r = 0.87, p < 0.01) was reported in extubated postoperative surgical patients who had no influencing systemic diseases.14 Morris and KinkadeZc reported a similar correlation coefficient (r = 0.84) for a pop ulation of patients both intubated and nonintubated during air transport. The r statistic when squared can be directly interpreted as the portion of the variability in the dependent variable that is explained or accounted for by the inde pendent variable.21The value 1 - 12rep resents the portion of the variable of ETC02 that cannot be explained by the variable PaC02. In this study 12 = 0.58. This means that 42%of the variability of ETCO2 is not dependent on the variability of the PaC02. This substantiates that individual PaC02 and ETC02 values often vary independently of each other. There was a greater disparity between ETCO, and PaC02 at higher PaC02 levels (Figure 1). This finding is consistent with other studies that reflect a tendency for ETCO, to underestimate the PaC02 at higher levels.14,z-24 The results support other studies that report overall statistically signilicant correlation but recognize significant clinical changes in ETCO, that fail to correlate with PaC02.22-24Christensen et al.24 reported ElCO2 values showed a moderately acceptable correlation with PaC02 measurements in head injury and neurosurgical patients who were hyperventilated; however, changes in ETCO, and PaC02 failed to correlate simultaneously.24 Graybeal and Russell23 report ETC02 does not provide a reliable continuous monitor of PaC02 that is capable of pre dieting changes in magnitude and direction in a study of multisystem trauma patients. Laze11 and Burrows25 report unreliability in children with cyanotic congenital heart disease, and other studies have cited inconsistencies in ETC02 prediction of PaC02 during cardiopulmonary resuscitation.13~26 The gradient between ETC02 and PaC02, the P(a-ET)CO,, is considered a reflection of alveolar dead space with a small component of the gradient depen-
October-December
1996 154
Air Medical Journal
dent on venous admixture.z2 The most correlation of ETC02 and PaC02. Under normal circumstances, ETCO, reportsignificant influences that disturb corre lation estimates are alterations in ventila- edly offers good clinical resemblance to PaCO,. Correlation tends to be higher in tion/perfusion (VA/Q) relationships, namely increased dead space ventila- mechanically ventilated patients without tion.‘* In this study P(a-ET)CO, was 5.3 pulmonary disease and lower in multisysf 4.4 (mean +_SD). In the absence of lung tern trauma patients or patients with exdisease or ventilation perfusion mis- isting lung disease. Clinical problems match, P(a-ET)C02 reportedly ranges that could increase dead space and influfrom 3 to 4.8 torrz2; in awake healthy vol- ence ETCO, and PaC02 correlation inunteers, -0.9 + -1.8 torrrs; in postopera- clude pulmonary contusion and pneutive cardiac surgery patients, 5.4 f 5.2 mothorax. Trauma patients rarely sustain torr27; in a group of extubated postopera- an isolated injury, and, more often, multitive patients, 2.8 + 5.2 torrr4; and in me- ple systems are usually involved. Limitations of the study include a chanically ventilated patients in a neuro surgical intensive care unit, 6.9 f 4.4 small sample size and limited control for torr.28 The study P(a-ET)CO, was higher influencing variables such as possible chest injury. Pneumothorax is the secthan the gradient reported for healthy subjects but similar to that reported for ond most common chest injury and may other neurologically compromised and be unrecognized in the initial patient asmechanically ventilated patients. Russell sessment. In addition, the study did not examine the possible effect of extreme and GraybeaW report a much higher temperatures on capnography or the gradient, P(a-EI’)CO, of -14 f -11, and conclude that trends in P(a-ET)C02 are physiologic effect of age or altitude on Vt and the P(a-ET)C02. not reliable and concordant direction ABGs are mainly dependent on Vt changes in ETCOz and PaCO, are not and ventilation frequency. Other study ensured. There is a widely reported range for limitations include lack of control for the
effect of airway pressure, alveolar dead space, or ventilation/perfusion (V/Q) mismatch. Although studies have shown a positive correlation between the physic logic dead space to Vt ratio, study changes in Vt may coincide with poor correlation between ETCOa and PaCOZ. The study did not retrospectively identify subjects with a positive correlation between ETCO2 and PaC02 or those subjects without significant correlation. Capnometry represents a reasonable estimate of PaC02 in some clinical populations. However, ETC02 cannot be used exclusively to replace PaC02 in critically ill patients. Future studies need to explore the influence of pathologic conditions present and pharmacologic modalities used in the pre-hospital setting that influence the P(a-ET)COs and dependability of capnography. In addition, future studies need to be directed toward continued efforts to identify ventilation parameters that provide pulmonary support and optimize tissue oxygenation and he modynamic stability.
References 1.
Gervais HW, Eberle B, Konietzke D, Hermes HJ, Dick W. Comparison of blood gases of ventilated patients during transport. Crit Care Med 1987;15:76@3. 2. Braman SS, Dunn SM. Amico CA, Milman RP. Complications of intrahospital transport of critically ill patients. Ann Intern Med 1987;4:46973. 3. Hurst JM, Davis L, Branson RD, et al. Comparison of blood gases during transport using two methods of ventilatory support. J Trauma 1989;29%3740. 4. McIntyre RC, Haenel JB, Moore FA, Read RR, Burch JM, Moore EE. Cardiopulmonary effects of permissive hypercapnia in the management of adult respiratory distress syndrome. J Trauma 1994;37:433-8. 5. Lee PC, Helsmoortel CM, Cohn SM, Fink MP. Are low tidal volumes safe? Chest 1990,97:4364. 6. Feihl F, Pert-et C. Permissive hypercapnia: How permissive should we be? Am J Respir Crit Care Med 1994;150:172237. 7. Kerr, ME, Brucia J. Hyperventilation in the head-injured patient: An effective treatment modality? Heart Lung 1993;22:51&22. 8. Moore, C, Flood C. Hyperventilation in head injury: Does it do more harm than good? Axone
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9.
10.
11.
12.
13.
14.
15.
16.
1993;15:3@3. Duffy RD, Becker DP. State of the art manage ment of severe closed-head injury. J Intens Care Med 1988;3:291302. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg 1991;75:731-9. EliasJones AC, Punt JA, Tumbull AE, Jaspan T. Management and outcome of severe head injury in the Trent region 198590. Arch Dis Child 1992;67:14305. Wren KR. Ventilation monitoring during monitored anesthesia care: a review. J Am Assoc Nurs Anestb 1994;62:5216. Trill0 G, van-Planta M, Kette F. ETCOZ monitoring during low flow states: clinical aims and limits. Resusitation 1994;1:1-8. Bondgard F, Wu Y, Lee TS, Klein S. Capnographic monitoring of extubated postoperative patients. J Invest Surg 1994;7:25964. Erler CJ, Rutherford WF, Rodman G, Mounts J, Schutz D, Eccles B. Inadequate respiratory sup port in head injury patients. Air Med J 1993;12:223-6. Rutherford WF, Erler CJ, Mounts J. In-flight
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17.
18.
19.
20.
21.
22.
23.
ABG abnormalities with manual hyperventilation. Air Med J 1993;12:352. Hoffman RA, Kreiger BP, Kramer MR. Endtidal carbon dioxide in critically ill patients during changes in mechanical ventilation. Am Rev Respir Dis 1989;140:1265. Thrush DN, Mentis SW. Weaning with endtidal CO2 and pulse oximetry. J Clin Anesth 1991;3:45&60. Liu SY, Lee TS, Bondgard F. Accuracy of capnography in nonintubated surgical patients. Chest 1992;102:1512-5. Morris M, Kinkade S. The effect of capnometry on manual ventilation technique. Air Med J 1995;14:7982. Polit DF, Hungler BP. Essentials of nursing re search. 3rd ed. Philadelphia: Lippincott, 1993:304. Russell GB, Graybeal JM. Reliability of the arte rial to end-tidal carbon dioxide gradient in mechanically ventilated patients with multisystem trauma. J Trauma 1994;36:317-22. Graybeal JM, Russell GB. Capnometry in the surgical ICU: an analysis of the arterial-to-end tidal carbon dioxide difference. Respir Care 1993;38:923-8. 175
24. Christensen hU, Bloom J, Sutton RR Comparing arterial and end-tidal carbon dioxide values in hyperventilated surgical patients. Am J Crlt Care 1995;4:11621. 25. Lazzell VA, Burrows FA. Stability of the intraop erative arterial to end-tidal carbon dioxide partial pressure difference in children with congen-
176
ital heart disease. Can J Anaesth 1991;38:859-65. 26. Cantineau JP, Merckx P, Lambert Y, Sorldne M, Bertrand C, Duvaldestin P. Effect of epinephrine on end-tidal carbon dioxide pressure during prehospital cardiopulmonary resuscitation. fun J Emerg Med 1994;12:267-70. 27. Bermudez J, Ikhtiger M. Increases in arterial
to end-tidal COz tension differences after cardiopuhnonary bypass. Anesth Analg 1987;66:699. 28. Russell GB, Graybeal JM. End-tidal carbon dioxide in nemointensive care patients. J Neurow-g Anaesth 1992;4:245.
October-December
1996
15:4
Air Medical
Journal
Monitored Arterial and End-tidal Carbon Dioxide During In-flight Mechanical Ventilation Cheryl J. Erler, RN, MS,’ William F. Rutherford, Stahl, RN, BS*
1. Associate Professor, West Lafayette, Ind. 2. Life Line Methodist Ind.
Purdue
Hospital,
3. Health Services Research, pital, Indianapolis, Ind.
University,
Abstract
Introduction
Indianapolis,
Introduction: Mechanical ventilation with monitored arterial carbon dioxide tension is necessary for optimum pulmonary support and hemodynamic stability. Ongoing monitor-
The most common method of ventilation in the prehospital setting is intubation and manual ventilation with a bag valve device. Although it is a lie-saving technique, previous studies have established that manual ventilation frequently results in low tidal volumes (vt), loss of minute ventilation, acidosis, and a.lkalosis.l-3Low tidal volumes are reportedly advantageous with certain pulmonary diseases; however, the low volumes are associated with permissive hypercapnia and have not been studied in multisystem trauma patients because of the physiologic effects of acidosis.4.5 Both acidosis and alkaIosis prompt a plethora of consequences. Acidosis results in decreased systemic vascular re sistance, decreased cardiac contractility, increased cerebral blood flow, and a shift in the oxyhemoglobin curve to the right.4,6 Myocardial consequences of alkalosis include decreased cardiac output, coronary artery vasospasmand ischemia, and various cardii arrhythmias.sJ In addition, alkalosis also decreases cerebral blood flow and may result in localized cerebral edema, rebound increased intracranial pressure, and &ii the oxyhemoglobin curve to the left.810 Although hyperreaction with resulting respiratory alkalosis has been common practice in early treatment of trauma patients with
Methodist
Hos-
Key Words: capnography, arterial blood gases, tidal volume, ventilation, air transport Address for correspondence and reprints: Cheryl J. Erler, RN, MS, Associate Professor, Purdue University, JNSN 1337, West Lafayette, IN 47907. Submitted: January 30, 1996 Revised: July 27, 1996 Accepted: August 281996 Presented at the Air Medical Transport Conference in Long Beach, California, October 16, 1995. Copyright Associates.
0 1996
1067-991
X/96/$5.00
Reprint
MD,* Angela Fiege, RN, BS,* David R. Nelson, MS,3 Ann
by the Air Medical
Journal
ing is necessary to ensure adequate ventilation parameters. The prospective study purpose was to (1) compare mechanical ventilation to historic manual ventilation, (2) evaluate the effectiveness of institutional tidal volume parameters, (3) determine the effect of institutional tidal volume manipulation on end-tidal carbon dioxide tension, and (4) explore the relationship between in-flight end-tidal carbon dioxide tension and arterial carbon dioxide tension. Methods: Randomized groups were mechanically ventilated (tidal volume = 12 cc/kg, rate = 14/min) with a target arterial carbon dioxide tension between 30 and 35 ton. Group I was monitored with in-line end-tidal carbon dioxide tension, and group II was monitored with arterial carbon dioxide tension by means of inflight arterial blood gas. Results: Arterial carbon dioxide tension varied less with monitored mechanical than with manual ventilation @ = 0.001). The gradient between arterial and end-tidal carbon dioxide tension was 5.3 * 4.4 (mean + standard deviation [SD]). End-tidal and arterial carbon dioxide tension positively correlated (r = 0.76, p = 0.001) yet end-tidal carbon dioxide tension accounted for only 58% variation of arterial carbon dioxide tension (r’ = 0.58). Conclusion: Mechanical ventilation is more precise but inconsistent in achieving a target arterial carbon dioxide tension with current
+ 0
No. 74lIl77907
ventilation parameters. End-tidal carbon dioxide tension is a reasonable estimate of, but cannot exclusively replace, arterial carbon dioxide tension in critically ill patients.
Air Medical Journal
154
October-December
1996
171
neurologic insult, there is controversy about the range of arterial carbon dioxide tension (PaCOd values that provide therapeutic benefit and whether any pos sible benefits are worth the associated risks.11 Although mechanical ventilation is undeniably more predictable in ensuring ventilation parameters than manual ventilation, punctilious surveillance is necessary to evaluate its ongoing pulmonary and hemodynamic effects. Blind or unwary ventilation exposes patients to unnecessary risks and complications. Traditionally, arterial blood gas (ABG) analysis has been used to ascertain a PaCOzvalue and determine the effective ness of ventilation maneuvers. However, ABG analysis is invasive and intermittent, and typically there is a time delay between sampling and accessibility of re sults. Most recently, capnography, a noninvasive technique for end-tidal carbon dioxide (ETCOd measurement, has become widely accepted in various settings as a method to monitor ventilation. Capnography has been shown to be effective in early detection of potentially disastrous events such as hypoventilation, esophageal intubation, and ventilator disconnection.12 ETC02, defined as the maximal CO2 concentration detected at the end of the expiratory cycle,is expressedas a percentage (ETCO2, or in millimeters of mercury or torr (PetCO2).13ETC02 represents the general effects of three body functions: metabolism, circulation, and ventilation. When CO2 production and CO2 transport remain constant, changes in EICOs repro sent a variation in ventilation.ls This real time measurement permits the earliest detection of alveolar ventilation and may allow substitution for the traditional and more cumbersome ABG measurement used to detect PaC02 values.14 ‘Ihe accuracy and reliability of the re lationship between ETC02 and PaC02, referred to as P(a-ET)COs gradient, varies in different populations and clinical settings. Most reported studies have explored the P(a-BT)COs in healthy subjects and mechanically ventilated patients 172
ABG Values Historic controls (n PH PaC02 Pa02 Values
q
Group Vent+ETCO+ 7)
7.3 f 0.22 40.3 f 18.6 233.2 + 164.6
are expressed
as mean
(n
q
I I-STAT
p
15)
7.4 f 0.10 32.7 i 6.4 355.9 * 97.8
Value
Vent, c 7.4 30.2 501.8
0.01 0.001 0.10
= + + +
Group II i-STAT x 2 7) 0.25 2.3 123.1
p
Value 0.74 0.001 0.60
f SD.
with pulmonary or cardiac disease. To date there is a paucity of clinical studies regarding capnography and mechanical ventilation during in-flight transport of critically ill patients. The purpose of this prospective study was to (1) compare mechanical ventilation by means of either monitored ETCOz or PaC02 to historic controls (manual ventilation with in-flight ABGs), (2) evaluate the effectiveness of institutional Vt parameters in achieving a target PaC02 range, (3) evaluate the effect of Vt manipulation on ETC02 and PaCO,, and (4) explore the relationship between in-flight ETC02 and PaCO2. Methods This study is the third part of an ongoing investigation designed to determine the efficacy of ventilation strategies used during the prehospital transport of critically ill patients. The first part of the study, conducted from 1990 to 1991, involved a retrospective review of 187 patients manually ventilated during transport. Study findings were congruent with the literature and reflected inconsistent and extreme values of PaC02.1s In 1992, a prospective study (part II) was designed to explore the effect of unmonitored manual ventilation on in-flight ABG values. Early analysis in part II showed blatant PaC02 abnormalities after 15 minutes of in-flight manual ventilation.16 Because of the abnormalities with unmonitored manual ventilation, part II was suspended and part III of the study was postponed until mechanical ventilation, capnography, and portable ABG analysis capability were in place.
The study (part III) was conducted at a level I trauma center from December 1994 to April 1995. The data were collected in two Eurocopter BK-117 helicopters by a flight team that included either a nurse and paramedic or a nurse and emergency medicine resident. All crew members were skilled in use of mechanical ventilation, capnography, and in-flight ABG techniques. The study was approved by the institutional review board at Methodist Hospital and the committee on human subjectsreview at Purdue University. Study subjects included critically ill patients over 15 years of age who required intubation and mechanical ventilation during air transport. Subjects with obvious chest injury and those receiving resuscitative drugs such as sodium bicarbonate and alpha-adrenergic agents were excluded from the study. In addition, sub jects known to have preexisting chronic pulmonary disease were eliminated from the study population because of disease influence on the P(a-ET)C02 gradient and dependability of capnography. All subjects were ventilated with an IMPACT Univent model 750 volume-cycled transport ventilator (IMPACT Instrumentation, Inc., West Caldwell, NJ.) according to the hospital’s institutional guidelines that include Vt = 12 cc/kg of ideal body weight, ventilation rate = 14, and percentage of inspired oxygen = 100%.Before liftoff to the receiving haspital, subjects were randomized into group I or II by selection of a sealed envelope containing one of two study proto ~01s. The target PaC02 range for the study was 30 to 35 torr.
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Blood Gases (p Historic controls (n PaCO2 <30 30-35 135
range
q
Group
I + ETCOI
(I?=
15)
ventilation 7)
18-71.4 torr n=3 n=O n=4
20.8-40.3 n=lO n=3 n=2
Comparison Group ETCOs+
Vent,
Values
are expressed
Group Ventilation
II + PaCOs
(n = 7) torr
18.9-46 n=4 n=2 n=l
torr
of Final PaCO,
I I-STAT
Vent
Group II + I-STAT
(n=15) PaCO2
0.001)
q
p
x 2
Value
(n = 7)
32.7
zt 6.4
as mean
f SD.
30.2
ETCO, vs PaCO,
* 2.3
0.07
Relationship
minutes of ventilation, a second i-STAT determination was made. Respiratory acidosis and alkalosis were treated by manipulation of the Vt. For both groups I and II, Vt was increased to 15 cc/kg for ETCO;! and PaCOz values >35 torr. Vt was decreased to 10 cc/kg for ETC02 and PaC02 ~30 torr. The dependent variables were ETCO;! and PaC02, and the independent variable was Vt. Demographic variables included age, weight, gender, and mechanism of injury. Instrumentation to measure PaC02 by means of in-flight ABG analysis was the i-STAT system. Estimates of reliability reported for the i-STAT are 0.9785 to 0.9946. In-line El’C02 was measured with monitored capnography using a ProPaq PAOlOGEL (Protocol System, Inc., Beaverton, Ore.). Internal product validation test results for the ProPaq COz report accuracy within 10%. Results
50 45 $
10
15
20
25
30
35
40
45
50
ETCO, (torr) r=O.76,p=0.001
In group I, ETCOz values were noted by means of in-line capnography after 10 minutes of mechanical ventilation, and Vt changes were made for ETCOa values outside the target range. Ten minutes after changes in ventilation were initiated, both ETCO, measured by means of capnography and ABG analysis with the i-STAT system values (i-STAT CorporaAir Medical Journal
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tion, Princeton, N.J.) were simultaneously determined and recorded. After 10 minutes of mechanical ventilation in group II, PaCOzvalues were determined by ABG analysis by means of i-STAT and Vt adjustments were made on the basis of the PaC02 level. As in group I, ventilation changes were made for PaC02 values outside the target range. After 10
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The sample comprised 22 subjects ranging from ages 16 to 90, with a mean age of 48 years. The 15 males and seven fe males required mechanical ventilation for a variety of reasons including motor vehicle accidents, gunshot wounds, falls, bums, and neurologic insults of medical origin. All subjects in both groups I and II were compared with historic controls from part II of the study. Historic controls (tl = 7) included patients with inflight ABG analysis after 15 minutes of unmonitored manual ventilation. F-tests were used to compare variance of pH, PaC02, and PaOz between the historic controls and the two treatment groups. Group I subjects, those with mechanical ventilation and in-line ETCOz, showed less variation in pH, less variation in PaC02, and no diierence in PaOz compared with historic controls. Group II subjects varied significantly less in PaCOz than historic controls; however, no difference in variation was detected for pH and Pa02 (Table 1). There were more subjects in the target PaC02 range in both groups I and II than historic control subjects with un-
173
monitored manual ventilation (Table 2). PaC02 variation was greater for subjects monitored with PaCOz as compared with subjects monitored with ETCOz. However, there was a greater percentage of subjects within the target range with monitored PaCOz.No statistically signitlcant differences were found between the PaC02 (p = 0.07) for group I and the second PaC02 for group II. No statistical difference was found in the post-ventilation change in PaCOz between group I subjects whose ventilation adjustments were based on ETC08 and group II subjects whose ventilation adjustments were based on preliminary i-STAT ABGs (Table 3). Estimated weights were used to determine the Vt based on cubic centimeters per kilogram. Ten subjects had actual recorded weights. The Pearson product correlation between estimated weight and ETCOBwas Y = 4.84, which was statistically significant @ = 0.002) when the weight was inaccurately underestimated or overestimated by 20 kg. With the use of the sign test, no statistical diierence was found (p = 0.50) be tween the number of subjects in group I with PaC02 values withii 30 to 35 torr in the second ETC02 after Vt manipulation compared with the first ElC02. No difference was found in mean scores with the use of a t-test (p = 0.76) or by SD with the use of the F-test (p = 0.38) between the first ETC02 and second ETC02 (p = 0.76) reading obtained after Vt manipulation. Mean values for first ETC02 recordings were (26.5 f 8.1 tot-r) compared with the second ETCO;! (32.7 f 6.4 torr) recordings. The P(a-ET)CO, gradient was 5.3 f 4.4 torr, ranging from a minimum of -1 and a maximum of 17.7 torr. The Pearson product moment correlation between ETCO, and PaCOswas r = 0.76, which was signiticant (p = 0.001). With the use of 72analysis, ETC02 accounted for 58% (r” = 0.58) of the variation of PaCO, (Fii 1). Discussion
Study findings reflect less extreme PaCOs values with mechanical ventila-
174
tion and monitored ETCOz and PaC02 compared with previous study PaCO, values reported with manual ventilation. There are more patients within the target PaC02 range with mechanical ventilation; however, a number of subjects continue to be outside the study range. Me chanical ventilation is more precise but still inconsistent in achieving target PaC02 with the use of the current ventilation parameters. Estimated weights as a basis for Vt determination resulted in less target variation in PaC02 values when weight was erroneously estimated by 20 kg. As weight was overestimated, ETCO, values were higher; conversely, when weight was overestimated, ETCOz values were less. In general, a Vt of 12 cc/kg was typ ically too high to achieve a target PaCOs during the study time allotted. This finding is consistent with studies that report higher PaCO, values with lower Vt.4*5 A change in Vt of 2 cc/kg did not effect the PaCOzsignificantly. The average flight and total transport time was 30 minutes. A longer time interval between Vt changes and ETC02 or PaC02 determinations may be needed to more adequately reflect significant PaC02. Also, larger changes in Vt may be required to generate the desired PaCOzchanges. In this study of patients who were me chanically ventilated during air transport, there is an overall positive correlation be tween ETC02 and PaC02 (r = 0.76) (Figure 1). The study correlation coefficient is similar to that found by Hoffman et al.17 who reported a correlation coefficient of r = 0.78 in critically ill patients undergoing changes in mechanical ventilation. A similar correlation is reported by Thrush and Mentisis who determined that ETCO, was a good indicator of PaC02 (r = 0.76) and may be used to safely and effectively wean patients from mechanical ventilation after coronary artery bypass surgery. A positive but less significant correlation (r = 0.61) was reported for extubated postoperative patients and trauma patients with chest injuries who were being observed for possible mechanical ventilation sup-
port-19A higher correlation coefficient (r = 0.87, p < 0.01) was reported in extubated postoperative surgical patients who had no influencing systemic diseases.14 Morris and KinkadeZc reported a similar correlation coefficient (r = 0.84) for a pop ulation of patients both intubated and nonintubated during air transport. The r statistic when squared can be directly interpreted as the portion of the variability in the dependent variable that is explained or accounted for by the inde pendent variable.21The value 1 - 12rep resents the portion of the variable of ETC02 that cannot be explained by the variable PaC02. In this study 12 = 0.58. This means that 42%of the variability of ETCO2 is not dependent on the variability of the PaC02. This substantiates that individual PaC02 and ETC02 values often vary independently of each other. There was a greater disparity between ETCO, and PaC02 at higher PaC02 levels (Figure 1). This finding is consistent with other studies that reflect a tendency for ETCO, to underestimate the PaC02 at higher levels.14,z-24 The results support other studies that report overall statistically signilicant correlation but recognize significant clinical changes in ETCO, that fail to correlate with PaC02.22-24Christensen et al.24 reported ElCO2 values showed a moderately acceptable correlation with PaC02 measurements in head injury and neurosurgical patients who were hyperventilated; however, changes in ETCO, and PaC02 failed to correlate simultaneously.24 Graybeal and Russell23 report ETC02 does not provide a reliable continuous monitor of PaC02 that is capable of pre dieting changes in magnitude and direction in a study of multisystem trauma patients. Laze11 and Burrows25 report unreliability in children with cyanotic congenital heart disease, and other studies have cited inconsistencies in ETC02 prediction of PaC02 during cardiopulmonary resuscitation.13~26 The gradient between ETC02 and PaC02, the P(a-ET)CO,, is considered a reflection of alveolar dead space with a small component of the gradient depen-
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Air Medical Journal
dent on venous admixture.z2 The most correlation of ETC02 and PaC02. Under normal circumstances, ETCO, reportsignificant influences that disturb corre lation estimates are alterations in ventila- edly offers good clinical resemblance to PaCO,. Correlation tends to be higher in tion/perfusion (VA/Q) relationships, namely increased dead space ventila- mechanically ventilated patients without tion.‘* In this study P(a-ET)CO, was 5.3 pulmonary disease and lower in multisysf 4.4 (mean +_SD). In the absence of lung tern trauma patients or patients with exdisease or ventilation perfusion mis- isting lung disease. Clinical problems match, P(a-ET)C02 reportedly ranges that could increase dead space and influfrom 3 to 4.8 torrz2; in awake healthy vol- ence ETCO, and PaC02 correlation inunteers, -0.9 + -1.8 torrrs; in postopera- clude pulmonary contusion and pneutive cardiac surgery patients, 5.4 f 5.2 mothorax. Trauma patients rarely sustain torr27; in a group of extubated postopera- an isolated injury, and, more often, multitive patients, 2.8 + 5.2 torrr4; and in me- ple systems are usually involved. Limitations of the study include a chanically ventilated patients in a neuro surgical intensive care unit, 6.9 f 4.4 small sample size and limited control for torr.28 The study P(a-ET)CO, was higher influencing variables such as possible chest injury. Pneumothorax is the secthan the gradient reported for healthy subjects but similar to that reported for ond most common chest injury and may other neurologically compromised and be unrecognized in the initial patient asmechanically ventilated patients. Russell sessment. In addition, the study did not examine the possible effect of extreme and GraybeaW report a much higher temperatures on capnography or the gradient, P(a-EI’)CO, of -14 f -11, and conclude that trends in P(a-ET)C02 are physiologic effect of age or altitude on Vt and the P(a-ET)C02. not reliable and concordant direction ABGs are mainly dependent on Vt changes in ETCOz and PaCO, are not and ventilation frequency. Other study ensured. There is a widely reported range for limitations include lack of control for the
effect of airway pressure, alveolar dead space, or ventilation/perfusion (V/Q) mismatch. Although studies have shown a positive correlation between the physic logic dead space to Vt ratio, study changes in Vt may coincide with poor correlation between ETCOa and PaCOZ. The study did not retrospectively identify subjects with a positive correlation between ETCO2 and PaC02 or those subjects without significant correlation. Capnometry represents a reasonable estimate of PaC02 in some clinical populations. However, ETC02 cannot be used exclusively to replace PaC02 in critically ill patients. Future studies need to explore the influence of pathologic conditions present and pharmacologic modalities used in the pre-hospital setting that influence the P(a-ET)COs and dependability of capnography. In addition, future studies need to be directed toward continued efforts to identify ventilation parameters that provide pulmonary support and optimize tissue oxygenation and he modynamic stability.
References 1.
Gervais HW, Eberle B, Konietzke D, Hermes HJ, Dick W. Comparison of blood gases of ventilated patients during transport. Crit Care Med 1987;15:76@3. 2. Braman SS, Dunn SM. Amico CA, Milman RP. Complications of intrahospital transport of critically ill patients. Ann Intern Med 1987;4:46973. 3. Hurst JM, Davis L, Branson RD, et al. Comparison of blood gases during transport using two methods of ventilatory support. J Trauma 1989;29%3740. 4. McIntyre RC, Haenel JB, Moore FA, Read RR, Burch JM, Moore EE. Cardiopulmonary effects of permissive hypercapnia in the management of adult respiratory distress syndrome. J Trauma 1994;37:433-8. 5. Lee PC, Helsmoortel CM, Cohn SM, Fink MP. Are low tidal volumes safe? Chest 1990,97:4364. 6. Feihl F, Pert-et C. Permissive hypercapnia: How permissive should we be? Am J Respir Crit Care Med 1994;150:172237. 7. Kerr, ME, Brucia J. Hyperventilation in the head-injured patient: An effective treatment modality? Heart Lung 1993;22:51&22. 8. Moore, C, Flood C. Hyperventilation in head injury: Does it do more harm than good? Axone
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to end-tidal COz tension differences after cardiopuhnonary bypass. Anesth Analg 1987;66:699. 28. Russell GB, Graybeal JM. End-tidal carbon dioxide in nemointensive care patients. J Neurow-g Anaesth 1992;4:245.
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