Does significant arterial hypoxemia alter vital signs?

ELSEVIER

Does Significant Arterial Hypoxemia Alter Vital Signs? David N. Thrush, Michael Hodges,f Department Tampa,

of Anesthesiology,

MD,* John B. Downs, MD,? Robert A. Smith, MS, RRT§ University

of South

Florida

College

of Medicine,

FL.

Objective: To determine the cardiovascular and respiratory effects of arterial hypoxemia in adult volunteers. Design: Prospective, subject-controlled. Setting: University-affiliated hospital. Subjects: 16 awake, unsedated, unanesthetized adult volunteers. Interventions: Inspired oxygen concentration (FrO,) was decreased in decrements to reduce pulse oximetm values to a range of 95 % to 90 %, 89 % to 85 %, 84 % to 80 %, and 79% to 70%. Measurements and Main Results: Heart rate (HR), blood pressure (BP), respirator? rate (RR), artm’al blood PH, gas tensions, and oxyhemoglobin saturation were determined during normoxia and each level of oxyhemoglobin desaturation. FIO, was reduced from 21% to 10%. Arterial blood oxyhemoglobin saturation and oxygen tension ranged from 100% to 71% and 103 to 35 mmHg, respectively. There were no significant changes in RR, BP, or HR dumng the study. Conclusions: HR, BP, and RR are not reliable indicators of arterial hypoxemia in awake volunteers. If this finding is also true for sedated or anesthetized patients, then continuous monitoring with pulse oximetry should be used whenever patients are at risk for arterial hypoxemia. Stable HR, BP, and RR may not eliminate the possibility of significant arterial hypoxemia and impending catastrophic events. 0 1997 by Elsevier Science Inc.

Study

Keywords: Blood pressure, heart rate, hypoxemia, rate, vital signs.

+Professor and Chairman Research Support

SRegistered Respiratory

respiratory

Introduction

*Associate Professor

IDirector,

monitoring,

Therapist

Address reprint requests to Editorial Office, Department of Anesthesiology, University of South Florida College of Medicine, MDC 59, 12901 Bruce B. Downs Boulevard, Tampa, FL 33612-4799, USA. Presented in part at the Annual Meeting of the American Society of Anesthesiologists, New Orleans, October 19-23, 1996. Received for publication December 12, 1996; revised manuscript accepted for publication February 26, 1997.

Arterial hypoxemia secondary to sedation and/or analgesia must be rapidly recognized and corrected to avoid brain damage, cardiac arrest, and death. Pulse oximetry is used widely for this purpose during administration of anesthesia, but it is less commonly employed in areas other than operating rooms (OR) by non-anesthesiologists. In these situations, reliance on physical signs such as skin color, heart rate (HR), blood pressure (BP), and respiratory rate (RR) may be the only means of detecting arterial hypoxemia. It has been demonstrated that skin color does not correlate with the degree of hypoxemia. Although previous studies have demonstrated circulatory and respiratory changes that were attributed to arterial hypoxemia, these responses were variable and may have been complicated by factors other than hypoxemia.‘-’ If physical signs are unreliable, arterial hypoxemia may go undetected until significant physiologic impairment has occurred. Therefore, we wished to determine the effects of progressive arterial hypoxemia on vital signs of awake, unsedated, unanesthetized adult volunteers.

Journal of Clinical Anesthesia 9:35.5-357, 1997 0 1997 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010

0952.8180/97/$17.00 PII S0952-8180(97)00061-5

Table 1.

Variables

Reflecting

Cardiopulmonary

Function

in 16 Adult Volunteers Arterial

lOO-96%

FIO, (%) PaO, (mmHg)

21 96 + 73 t 124 + 77 2 94 k 14? 7.42 -c 39 +

HR @pm) SBP (mmHg) DBP (mmHg) MAP (mm@4 RR (breaths/min) Pa PaCO, (mmHg) Note: Data are represented *p < 0.05 compared

8 9 11 9

blood

89435%

+ 1* + + + +

13 * 1*

9* 12 13 6

10

94 ? 9

2 0.03 5

15 t 3 7.43 t 0.02 37 k 4

Normoxia

oxyhemoglobin

95-90% 15 71 74 120 78

During

52 77 128 76 96 16 7.44 39

+ f + + + ? 2 2

4* 10 13 6 7 5 0.02 3

and Progressive

Arterial

Hypoxemia

saturation 84-80%

79-70%

12 +- 1”

11 * 1*

46 ? 3” 76 2 9

41 2 3* 71 t 6

127 t 17 74 2 94t 15 ? 7.45 ? 36 5

7 10 4 0.03 4

117 +- 7 74 90 16 7.44 37

? k ? + +

5 4 3 0.02 3

as means 2 SD.

to variables obtained while volunteers

breathed room air.

FIO, = inspired oxygen concentration; PaO, = arterial oxygen tension; HR = heart rate; SBP = systolic blood pressure; DBP = diastolic blood pressure; MAP = mean arterial pressure; RR = respiratory rate; pHa = arterial blood pH; PaCO, = arterial carbon dioxide tension.

Materials

and Methods

Participants signed an informed consent approved by the Institutional Review Board of the University of South Florida College of Medicine. Chest leads (Model 78354A, Hewlett-Packard, Waltham, MA) were placed appropriately on seated participants to monitor their electrocardiogram (EGG) and HR. After infiltration with local anesthetic, a 20-gauge catheter was inserted percutaneously into a radial artery and maintained patent with heparinized saline. Sampled arterial blood was assayed for arterial blood pH (pHa) , PaO,, and PaCO, using standard electrodes (Model 1306, Instrumentation Laboratories, Lexington, MA), and oxyhemoglobin saturation (SaO,) with a co-oximeter (Model 482, Instrumentation Laboratories, Lexington, MA). A pneumatic cuff was positioned appropriately around the uncatheterized arm and connected to a monitor for automated determination of systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial blood pressure (MAP) (Dinamapm Plus Model 8700, Critikon, Tampa, FL). A fingertip probe was attached to a pulse oximeter (Oxyshuttle, Critikon, Tampa, FL) for monitoring arterial oxygen saturation (SpO,) Inspired oxygen concentration (FIO,) was monitored with a calibrated oxygen analyzer, incorporating a galvanic fuel cell (Ohmeda 5100, Boulder, CO). Awake, unsedated, unanesthetized subjects breathed air through a mouthpiece (16 mL dead space) attached to a nonrebreathing circuit, and their nostrils were closed with a nose clip. Inspired oxygen concentration (FIO,) was decreased in decrements by blending nitrogen with air flowing into the breathing circuit to reduce SpO, to the following levels: 95% to 90%, 89% to 85%, 84% to SO%, and 79% to 70%. When SpO, was stable for 60 seconds, data were collected. Respiratory rate was determined visually by an investigator. After each period of oxygen desaturation, volunteers breathed room air for 10 minutes. Respiratory and hemodynamic variables observed at each level of desaturation as determined by the co-oximeter were summarized as means -C SD and compared to 356

J. Clin. Anesth., vol. 9, August 1997

control values (room air) with an analysis of variance repeated measures and Dunnett’s test (p 5 0.05).

for

Results Titrating the FIO, to a given SpO, required eight to ten minutes of breathing hypoxic gas mixtures. During that period, SpO, varied above and below the target SpO, range despite minimal or no changes in the inspired hypoxic gas mixture. When SpO, stabilized (t2%), data were collected and stratified according to the following levels of arterial blood oxyhemoglobin saturation: 100% to 96%, 95% to 90%, 89% to 85%, 84% to SO%, and 79% to 70% for analysis. Arterial oxyhemoglobin saturation and PaO, ranged from 98% to 71% and 103 to 35 mmHg, respectively, as FIO, varied from 21% to 10% in 16 adult participants. However, there were no significant differences in HR, BP, RR, pHa, or PaCO, (Table I).

Discussion Decreasing FIO, to 10% produced significant arterial hypoxemia, but it was not associated with any discernible hemodynamic or respiratory response. These findings are in contrast to previous studies that have concluded that hypoxemia increases HR, BP, and minute ventilation. The degree of hypoxemia necessary to produce a response, the type of response observed, either circulatory or respiratory, and the amount of rebreathing has varied in prior studies.re4 As a consequence, it is difficult to discern which level of hypoxemia will stimulate a response and which stimulus, or combination of stimuli, are responsible. For example, Dripps and Comroe reported a significant change in HR and minute ventilation when healthy volunteers breathed progressively lower concentrations of oxygen.’ Heart rate increased when FIO, was reduced from 21% to 18%, with progressive increases as FIO, was reduced further. The most dramatic increase in HR, 21 2 10 beats/minute, was observed with 10% inspired oxygen.

Vital signs during hypoxmia: Thrush et al.

In the same study, the respiratory response to hypoxemia was characterized by “extreme individual variability”; and when Dripps and Comroe combined their data with two other similar studies,“” the increase in minute ventilation was negligible until the FIO, was reduced to 10%. The authors of this study concluded that the circulatory response was more sensitive than the respiratory response to hypoxemia, and that both were more pronounced at very low FIO,.’ The three methods used by Dripps and Comroe’ to deliver the hypoxic gas mixtures may explain why our results are different and may illustrate how other stimuli contributed to previous observations. In the first group of patients, a nonrebreathing system fitted to a small rubber mask, which just covered the nose and mouth, was used for delivering 21%, 187 O, and 16% oxygen. In the second group of patients, an army gas mask or an aviation-type half mask were used when lower concentrations were delivered (14.5%, 12%, lo%, and 8%). In the first group, the amount of dead space and rebreathing was minimal. In the latter group, the two masks had a dead space of 400-500 mL and 200 mL, respectively; and at end inspiration, the atmosphere within the mask contained 0.5% to 2.0% CO,. Consequently, when FIO, levels below 16% were delivered, subjects rebreathed up to 2.0% (or 14 mmHg) CO,. The most dramatic response occurred at these lower FIO, levels, when significant rebreathing occurred; and it may have been partially or solely responsible for the dramatic changes in ventilation and circulation. In contrast, we used a nose clip applied to the subject’s nares while he or she breathed through a mouthpiece attached to a nonrebreathing system with minimal dead space. Since rebreathing was minimized, the respiratory and circulatory responses, which were previously observed by Dripps and Comroe, did not occur. When FIO, was reduced in the study by Dripps and Comroe,’ the increase in minute ventilation was secondary to an increase in tidal volume (Vr), with no change in RR. Similarly, RR did not change in the current study, and although Vr and minute ventilation were not measured, stable PaCO, values throughout the present study period indicate that hyperventilation secondary to an increase in Vr and minute ventilation did not occur. Our results are also dissimilar to those of Shock and Soley.* They reported that minute ventilation in healthy college students increased 5% and 30% when FIO, levels were reduced to 17% and 12%, respectively. When 2% CO, was mixed with 21%, 17%, and 12% oxygen, minute ventilation increased 27%, 37%, and 97%, respectively. They reported that the increase in minute ventilation due to both gases could be estimated by adding the average effect of the two gases administered separately. Despite these findings, they concluded that marked individual differences made predictions of the respiratory response of an individual subject “impossible”. The apparatus and method of administering the hypoxic gas mixtures is not mentioned in the report; therefore, it is not possible to determine if rebreathing occurred. It is noteworthy that in subjects breathing 2% CO,, the increase in minute ventilation was more pronounced as the FIO, level was lowered.

Caplan et al.” studied adverse anesthetic outcomes based on information contained in the closed-claim files of insurance companies, and they reported that hemodynamic changes caused by esophageal intubation and hypoxemia probably occurred after some degree of irreversible damage to vital organs had been done. They concluded that indirect tests of ventilation, such as HR and BP, may delay diagnosis of arterial hypoxemia. Our results support this conclusion. Our study has limitations that may impact direct clinical application. Subjects were awake, unsedated, unanesthetized healthy volunteers without any significant cardiovascular and respiratory disease. Less healthy or sedated, anesthetized patients might respond differently to arterial hypoxemia. The lowest FIO, level delivered during the study was 10%. Further decreases in the FIO, might have resulted in a more significant response. Inspired oxygen concentration was decreased for several minutes prior to and during data collection. Although unlikely, it is possible that prolonging this period might result in hemodynamic or respiratory changes. With the advent of pulse oximetry, reliance on physical signs as indicators of arterial hypoxemia is not necessary. The American Society of Anesthesiologists (ASA) has specific guidelines for monitoring oxygenation and ventilation during anesthesia. These guidelines include oximetry and capnography. Similar guidelines are being developed for non-anesthesiologists, who may administer sedatives, analgesics, and muscle relaxants in non-OR locations, such as the Gastrointestinal Lab, Emergency Room, and Radiology Department. Rapid detection of respiratory and cardiovascular depression secondary to anesthetic drugs must be recognized and treated rapidly to prevent hypoxic brain injury, cardiac arrest, and death. Our study demonstrates that HR, BP, and RR are not reliable indicators of arterial hypoxemia in awake volunteers. If this finding is also true for sedated or anesthetized patients, then continuous monitoring with pulse oximetry should be used whenever patients are at risk for arterial hypoxemia in or out of the OR. Lack of change in HR, BP, and RR may not be used as evidence of normoxia in the time frame preceding cardiovascular collapse.

References 1. Dripps RD, Comroe JH: The effect of inhalation of high and low oxygen concentrations on respiration, pulse rate, ballistocardiogram and arterial oxygen saturation (oximeter) of normal individuals. Am JPhysioZ 1947;149:277-91. 2. Shock NW, Soley MH: Effect of lowered oxygen tension of inspired air on the respiratory response of normal subjects to carbon dioxide. Am JPhysiol 1942;137:256-8. 3. Horvath SM, Dill DB, Corwin W: Effects on man of severe oxygen lack. Am J Physiol 1943;138:659-68. 4. Ellis MM: Respiratory volumes of men during short exposures to constant low oxygen tensions attained by rebreathing. Am JPhysiol 1919;50:267-79. 5. Caplan RA, Posner KL, Ward RJ, Cheney Fw: Adverse respiratory evene in anesthesia: a closed claims analysis. Anesthmiology 1990; 72828-33. J. Clin. Anesth., vol. 9, August 1997

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