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TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Carbon Monoxide (CO) is a colorless, odorless gas found in fumes produced from carbon fuels in engines, stoves, and fireplaces. CO binds to hemoglobin forming a molecule called carboxyhemoglobin (CO-Hb), which has higher affinity to O2 than hemoglobin itself which leads to symptoms of hypoxia and ischemia. Given an adequate history, clinicians can quickly initiate treatment but differentials for shortness of breath (SOB) must be sought and ruled out. Our case report will discuss the importance of CO poisoning and its involvement in thrombus formation and development of a pulmonary embolism (PE). CASE PRESENTATION: 62 year old female with history of COPD was brought to ED due to acute SOB and lethargy. Upon EMS arrival, CO level was 800. While in transport in EMS, the patient's CO-Hb level was 34 (trended to 11.4). The patient was found to have sp02 of 86% on room air (RA), and was placed on 10L nonrebreather mask. Patient was hemodynamically stable and afebrile. Labs revealed WBC 17.96, platelet 409k (clumped), troponin 0.08 ng/mL, LDH 405 units/L, and CRP 22.3 mg/L. Patient was deemed not a candidate for hyperbaric oxygen therapy. CT Head without contrast ruled out intracranial pathology and UA ruled out UTI. Chest X-ray revealed bilateral hazy opacities. CTPE revealed RUL/RML segmental and subsegmental PE as well as bilateral GGO reflecting interstitial edema in the setting of CO poisoning. Echo revealed EF of 65% with no wall motion abnormalities. COVID PCR test resulted negative making PE more likely as cause for SOB and patient was started on therapeutic Lovenox and empiric Azithromycin and Ceftriaxone. Within 24 hours, patient clinically improved and was discharged on Xarelto. DISCUSSION: PE in patients with CO poisoning should be suspected if the patient does not clinically improve with initial treatment. CO toxicity has been known to cause inflammatory and obstructive changes to arterioles and venules. Furthermore, it may induce vasospasms and increase platelet aggregation, leading to venous thrombus formation. CO poisoning may also increase oxidative stress with nitric oxide and oxygen free radicals causing further damage to endothelial lining1 and leading to further platelet dysfunction. 2 This combination of vessel wall injury and stasis in blood flow are important for development of thrombus. Treatment of given thrombus will lead to moderate resolution of symptoms. CONCLUSIONS: Treatment may be delayed in patients with coexisting PE and CO poisoning as it may be misdiagnosed. It is especially difficult to identify PE in patients with stable O2 saturation. However, the combination of endothelial damage and eventual increased platelet aggregation plays a critical role in thrombus formation in patients with CO toxicity. As a result, it is an important differential for patients with CO poisoning especially when symptoms do not respond to initial treatment. REFERENCE #1: Ruth-Sahd LA, Zulkosky K, Fetter ME. Carbon monoxide poisoning: case studies and review. Dimens Crit Care Nurs. 2011 Nov-Dec;30(6):303-14. doi: 10.1097/DCC.0b013e31822fb017. PMID: 21983502. REFERENCE #2: Ikeda H, Koga Y, Oda T, Kuwano K, Nakayama H, Ueno T, Toshima H, Michael LH, Entman ML. Free oxygen radicals contribute to platelet aggregation and cyclic flow variations in stenosed and endothelium-injured canine coronary arteries. J Am Coll Cardiol. 1994 Dec;24(7):1749-56. doi: 10.1016/0735-1097(94)90183-x. PMID: 7963124. REFERENCE #3: Sevinc A, Savli H, Atmaca H. An interesting cause of pulmonary emboli: acute carbon monoxide poisoning. Clin Appl Thromb Hemost. 2005 Jul;11(3):353-7. doi: 10.1177/107602960501100317. PMID: 16015424. DISCLOSURES: no disclosure on file for Jagadish Akella;No relevant relationships by Javed Iqbal, source=Web Response No relevant relationships by Vaishali Mehta, source=Web Response No relevant relationships by Najia Sayedy, source=Web Response

Study objectives: The aim of the study was to measure the single-breath diffusing capacity of the lung for carbon monoxide (DLCOsb) in healthy subjects in the following two conditions originally proposed by the American Thoracic Society (ATS) guidelines: relaxation against the shutter; and full inspiration without straining. Setting: DLCOsb was measured in 76 young adults in duplicate, in the two conditions. Mouth pressure was recorded during all of the trials. Results: The mean ( SD) value of the duplicate DLCOsb measurements was higher when measured with the patient in the nonrelaxed condition than in the relaxed condition (32.65 7.65 vs 31.54 7.11 mL/min/mm Hg, respectively; p < 0.001). The mean effective alveolar volume measured during the single-breath maneuver (VAeff) was also higher in the nonrelaxed condition (VAeff: nonrelaxed condition, 5,779 1,093 mL; relaxed condition, 5,596 1,097 mL; p < 0.001), at least as a consequence of a higher inspiratory volume (Vin) in the nonrelaxed condition (nonrelaxed condition, 4,378 900 mL; relaxed condition, 4,232 902 mL; p < 0.001). Asking the subject performing a DLCOsb maneuver to relax on the shutter during apnea lowers the DLCOsb value by approximately 3.4% in comparison to full inspiration without straining, at least in part because it results in a reduced Vin. Conclusion: These data lend further support to the new European Respiratory Society/ATS Task Force recommendations (full inspiration maintained with near atmospheric intrapulmonary pressure). (CHEST 2006; 130:207–213)

Purpose Exhaled carbon monoxide and arterial blood carboxyhemoglobin concentrations increase in inflammatory pulmonary diseases. The present study was undertaken to elucidate whether arteriovenous carboxyhemoglobin (a-vHb-CO) concentration differences are also useful to define the site of inflammation, either in the lung or organs other than the lung. Materials and methods We examined concentrations of carboxyhemoglobin in both arterial and peripheral venous blood and exhaled carbon monoxide in patients with acute pulmonary inflammation including bronchial asthma (n = 18) and pneumonia (n = 33), and those in patients with extrapulmonary inflammatory diseases, including acute pyelonephritis (n = 28) and active rheumatoid arthritis (n = 16). Results The values of carboxyhemoglobin in both arterial and peripheral venous blood were significantly higher in patients with pulmonary and extrapulmonary inflammation compared with those in control subjects (n = 22). Furthermore, a-vHb-CO differences in patients with inflammatory pulmonary diseases were higher than those in patients with acute pyelonephritis and patients with rheumatoid arthritis, and than those in control subjects. The a-vHb-CO differences correlated with the WBC count of peripheral venous blood in patients with pneumonia. In patients with bronchial asthma, the a-vHb-CO differences inversely correlated with FEV 1 , although they did not correlate with WBC count of peripheral venous blood. The a-vHb-CO differences in patients with acute pyelonephritis were higher than those in patients with active rheumatoid arthritis. Conclusion The present study suggests that a-vHb-CO differences may be a useful means to define the site of inflammation, either in the lung or organs other than the lung, in patients with a fever of unknown origin. The large a-vHb-CO differences may be caused by carbon monoxide production in pulmonary inflammation.

Study objectives: To evaluate possible alterations in the diffusing capacity of the lung for carbon monoxide (DLCO) or its components, membrane diffusing capacity of the lung for carbon monoxide (DMCO) and pulmonary capillary blood volume (Vc), in habitual smokers of “crack” cocaine (with or without tobacco) and following the short-term administration of inhaled cocaine base or IV cocaine HCl. Design: Cross-sectional and longitudinal evaluation of DLCO and its components in smokers of cocaine alone, tobacco alone, and cocaine plus tobacco, and in nonsmokers and ex-smokers. Measurement of possible acute effects on DLCO and its components after experimental short-term administration of IV and smoked cocaine. Setting: University and Veterans Affairs hospital research laboratories. Participants: Convenience sample of habitual smokers of crack cocaine with or without tobacco and matched control nonsmokers and ex-smokers, and smokers of tobacco only. Measurements: DLCO ,D MCO, and Vc. Conclusions: Neither habitual cocaine smoking in cross-sectional or longitudinal analysis nor the short-term administration of inhaled alkaloidal cocaine significantly affected DLCO or its component parts. In contrast, a clear cross-sectional effect of regular tobacco smoking was demonstrated. (CHEST 2002; 122:629 – 638) Abbreviations: ANOVA analysis of variance; COHb carboxyhemoglobin; Dlco diffusing capacity of the lung for carbon monoxide; Dlco0.2 diffusing capacity of the lung for carbon monoxide at 20.9% inspired O2; Dmco membrane diffusing capacity of the lung for carbon monoxide; NHANES National Health and Nutrition Examination Survey; NIDA National Institute on Drug Abuse; Va alveolar volume; Vc pulmonary capillary blood volume

Indoor group water-pipe tobacco smoking, commonly referred to as water-pipe smoking (WPS), especially in coffee shops, has gained worldwide popularity. We performed a comprehensive laboratory and clinical evaluation of the acute effects of active and passive indoor group WPS.This comparative study evaluated pre- and post-30-min active and passive indoor group WPS. The outcome parameters were carboxyhemoglobin (COHb), nicotine, and cotinine levels; CBC count; and cardiorespiratory parameters. Exhaled breath condensate (EBC) cytokines and endothelial function (using the EndoPat device [Itamar Medical Ltd]) were measured only in active smokers. Statistical methods used were Student t test, Wilcoxon signed rank test, Fisher exact test, analysis of variance, and Newman-Keuls post hoc test where relevant.Sixty-two volunteers aged 24.9±6.2 years were included; 47 were active smokers, and 15 were passive smokers. COHb level increased postactive WPS (active smokers, 2.0%±2.9% vs 17.6%±8.8%; P.00001); six subjects (12.7%) had a25% increase, and two subjects (4.2%) had a40% increase. Plasma nicotine level increased postactive WPS (active smokers, 1.2±4.3 ng/mL vs 18.8±13.9 ng/mL; P.0001); plasma cotinine and urinary nicotine and cotinine levels also increased significantly. EBC IL-4, IL-5, IL-10, IL-17, and γ-interferon decreased significantly with postactive smoking; endothelial function did not change. WPS was associated with adverse cardiorespiratory changes. In passive smokers, COHb level increased (0.8%±0.25% vs 1.2%±0.8%, respectively, P=.003) as did respiratory rate.One session of active indoor group WPS resulted in significant increases in COHb and serum nicotine levels (eightfold and 18-fold, respectively) and was associated with adverse cardiorespiratory health effects. The minor effects found in passive smokers suggest that they too may be affected adversely by exposure to WPS. The results call for action to limit the continuing global spread of WPS in coffee shops.ClinicalTrials.gov; No.: NCT1237548; URL: www.clinicaltrials.gov.

Introduction Measurement of oxygen saturation by pulse oximetry (SpO 2 ) is frequently performed during exercise testing of patients with COPD to monitor for hypoxemia. The purpose of this study was to assess the accuracy and precision of pulse oximetry during exercise. We hypothesized that the SpO 2 would more closely reflect oxygen saturation as measured by co-oximetry (SaO 2 ) when it was corrected for carboxyhemoglobin (COHb). We also hypothesized that SpO 2 would more closely reflect SaO 2 when the pulse rate by oximeter was equivalent to the heart rate by ECG. Finally, we hypothesized that SpO 2 would be a better measure of SaO 2 at maximal workloads than at rest or submaximal workloads. Methods Eight white men with severe COPD (mean ± SD FEV 1 , 0.91±0.37) underwent progressive, symptom-limited exercise testing by cycle ergometry. SaO 2 was measured from arterial blood at each workload using a co-oximeter. SpO 2 and pulse rate were obtained by a pulse oximeter (Ohmeda 3700). Heart rate was continuously monitored by ECG. Results Reliable oximetric values as determined by a dicrotic notch in each waveform and adequate signal intensity were obtained in all eight patients. SpO 2 was a moderately accurate measure of SaO 2 (bias, 1.7%; precision, 2.9). The bias actually increased (4.1%) when SpO 2 was corrected for COHb. Accuracy of SpO 2 was not improved when pulse rate by oximetry and heart rate by ECG were equivalent, nor was the accuracy improved at maximal workloads relative to submaximal workloads during the exercise test. Conclusion Oxygen saturation as measured by pulse oximetry (SpO 2 ) in patients with COPD undergoing exercise testing is not sufficiently accurate to replace SaO 2 as the gold standard for oxygen saturation. ( CHEST 1996; 109:1151–55 )

We have shown that in patients with COPD, myocardial efficiency during exercise is enhanced following acute elevations of plasma phosphate (Pi). A decrease in Hb-O2 affinity (increase in P50) was not responsible for the improvement. We postulated that the physiologic benefit was due to the acute reversal of a subclinical myocardial Pi depletion. To further test this hypothesis in a chronic state, we studied nine stable hypoxemic (PaO2 = 64 +/- 2 mm Hg [+/- SEM]) patients with COPD over five weeks: two weeks at normal plasma Pi; and three weeks at elevated plasma Pi, induced by etidronate disodium (Didronel; 750 mg orally daily). Administration of etidronate disodium increased (p less than 0.05) plasma level of Pi (4.4 +/- 0.2 to 5.8 +/- 0.1 mg/dl), RBC level of Pi (3.1 +/- 0.2 to 4.1 +/- 0.2 mg/dl), RBC level of 2,3-DPG (16.2 +/- 1.1 to 21.3 g+/- 1.3 mumol/g of Hb) and P50 (23.7 +/- 0.5 to 26.0 +/- 0.8 mm Hg). At the end of the treatment, the widening of the C(a-v)O2 with exercise (7.1 +/- 0.8 to 8.9 +/- 0.6 ml/dl) was less pronounced than under control conditions (6.9 +/- 0.4 to 10.1 +/- 0.6 ml/dl; p less than 0.02); concomitantly, the crossover point (COP; the PaO2 below which a rightward-shifted Hb-O2 curve causes the C(a-v)O2 to become narrower rather than wider) increased (37 +/- 2 to 49 +/- 1 mm Hg). Indicators of myocardial work efficiency were not affected by etidronate disodium at rest or during exercise. We postulate that during exercise the potential beneficial effect of the rightward shift of the Hb-O2 curve upon cardiac function was negated by the fall of PaO2 to or below the COP level, a situation which would limit increases in tissue O2 extraction.

Study objectives There are large reported differences for the carboxyhemoglobin (COHb) half-life (COHb t 1/2 ) in humans breathing 100% atmospheric O 2 following CO inhalation in tightly controlled experiments compared to the COHb t 1/2 observed in clinical CO poisoning (range, 36 to 131 min, respectively). Other reports have suggested that the COHb t 1/2 may be affected by gender differences, age, and lung function. We wished to test the hypothesis that the COHb t 1/2 might also be influenced by CO poisoning vs experimental CO exposure, by a history of loss of consciousness (LOC), concurrent tobacco smoking, and by Pa o 2 . The purpose of the present study was to measure the COHb t 1/2 in a cohort of CO-poisoned patients and to determine if those listed factors influenced the COHb t 1/2 . Design Retrospective chart review from 1985 to 1995. We calculated the COHb t 1/2 of CO-poisoned patients who were treated with high-flow supplemental atmospheric pressure O 2 delivered by nonrebreather face mask or endotracheal tube. Setting Hyperbaric medicine department of a tertiary-care teaching hospital. Patients Of 240 CO-poisoned patients, 93 had at least two COHb measurements > 2% (upper limit of normal) with recorded times of the measurements, permitting calculation of the COHb t 1/2 . Results The COHb t 1/2 was 74 ± 25 min (mean ± 1 SD) with a range from 26 to 148 min. By stepwise multiple linear regression analysis, the Pa o 2 influenced the COHb t 1/2 ( R 2 = 0.19; p 1/2 was not influenced by gender, age, smoke inhalation, history of LOC, concurrent tobacco smoking, degree of initial metabolic acidosis (base excess), or initial COHb level. Conclusions The COHb t 1/2 of 93 CO-poisoned patients treated with 100% O 2 at atmospheric pressure was 74 ± 25 min, considerably shorter than the COHb t 1/2 reported in prior clinical reports (approximately 130 ± 130 min) and was influenced only by the patient's Pa o 2 .

To assess whether the breath carbon monoxide (CO) concentration can be used to determine a patient's smoking habits in a respiratory outpatient clinic.To provide a normal range for smokers and nonsmokers, 41 outpatients and 24 healthy subjects were questioned on their smoking habits and asked to provide two breaths into a CO monitor (EC50 Smokerlyser; Bedfont Instruments; Kent, UK). In a subsequent single-blind study, 51 different outpatients were not told of the purpose of the study and were assessed by extensive questionnaire, spirometry, and Smokerlyser estimation.The Chest Clinic and Pulmonary Medicine Department at the Northern General Hospital, Sheffield, UK.Phase 1 involved 41 outpatients attending the Chest Clinic and 24 nonoutpatient colleagues. In phase 2, an additional 51 different outpatients were studied.The mean (SD) breath CO levels were 17.4 (11.6) parts per million (ppm) for smokers and 1.8 (1.3) ppm for nonsmokers (p0.001). A level of 6 ppm was taken as the cutoff, as this gave a selectivity of 96% and a sensitivity of 94% for outpatients. Of the 51 study patients, 5 admitted to smoking in the administered questionnaire. Eight denied smoking but had a mean breath CO6 ppm (7.5 to 42 ppm). Of these, three admitted to smoking after being explained the implication of the reading.Breath CO concentration provides an easy, noninvasive, and immediate way of assessing a patient's smoking status. A reading6 ppm strongly suggests that an outpatient is a smoker.

Study objectives To evaluate the accuracy and quantitate the error of pulse oximetry measurements of arterial oxygenation in patients with severe carbon monoxide (CO) poisoning. Design Retrospective review of patient clinical records. Setting Regional referral center for hyperbaric oxygen therapy. Patients Thirty patients referred for treatment of acute severe CO poisoning who demonstrated carboxyhemoglobin (COHb) levels >25%, with simultaneous determinations of arterial hemoglobin oxygen saturation by pulse oximetry (SpO2) and arterial blood gas (ABG) techniques. Measurements and results COHb levels and measurements of arterial oxygenation from pulse oximetry, ABG analysis, and laboratory CO oximetry were compared. SpO2 did not correlate with COHb levels. SpO2 consistently overestimated the fractional arterial oxygen saturation. The difference between arterial hemoglobin oxygen saturation (SaO2) calculated from ABG analysis and SpO2 increased with increasing COHb level. Conclusions Presently available pulse oximeters overestimate arterial oxygenation in patients with severe CO poisoning. An elevated COHb level falsely elevates the SaO2 measurements from pulse oximetry, usually by an amount less than the COHb level, confirming a prior observation in an animal model. Accurate assessment of arterial oxygen content in patients with CO poisoning can currently be performed only by analysis of arterial blood with a laboratory CO-oximetry.

Carboxyhemoglobin (COHb) levels were measured in patients who came to an emergency department complaining of acute chest pain. For subjects not receiving prior oxygen therapy, those with cocaine-related chest pain (n = 10) had a higher mean COHb level than a comparison group (n = 28) with nonischemic chest pain (4.50 +/- 2.40 vs 2.73 +/- 0.66; p0.05). Four of the seven (57 percent) who smoked crack had COHb levels greater than 4.5 percent, while only one of six (17 percent) smokers of only tobacco had such a level. These findings suggest an additional mechanism, the formation of COHb, which could aggravate cocaine-induced cardiotoxicity.

Inhaling motor vehicle exhaust fumes is a common method used by people attempting to commit suicide; however, the decreased carbon monoxide concentrations found in the exhaust of late-model automobiles equipped with catalytic converters are changing the clinical presentation of exhaust inhalation.

Thirty-one critically ill patients with acute respiratory failure and circulatory shock were divided into three groups. Group 1 included 11 patients with an inserted mixed venous saturation (SvO2) catheter using three-reference wavelengths and characterized by one transmitting and one detecting fiberoptic filament (Oximetrix opticath catheter); group 2 included eight patients with an inserted SvO2 catheter using two-reference wavelengths and characterized by one transmitting and one detecting fiberoptic filament; (Edwards sat-one catheter); group 3 included 12 patients with an inserted SvO2 catheter using two-reference wavelengths and characterized by one transmitting and two detecting fiberoptic filaments. Once calibration procedures were performed, SvO2 measured by the catheter and by an hemoximeter OSM 3 (reference value) were compared following each therapeutic intervention. Over a period of 1.5 to 6 hours during which the hematocrit value remained unchanged, 119 measurements were obtained in group 1, 91 in group 2 and 181 in group 3. The dispersion of SvO2 values was much more pronounced with the two-reference wavelength systems using either one or two detecting fiber optic filaments, and the correlation coefficient was significantly higher with the three-reference wavelength system (r = 0.970 for the Oximetrix catheter vs r = 0.855 for the Edwards catheter and r = 0.826 for the Spectramed catheter, p less than 0.001). After 24 hours, the spontaneous drifts in the two-reference wavelength systems, using either one or two detecting fiber optic filaments (expressed as the SvO2 value measured by the catheter minus the reference SvO2 value) were significantly higher than the spontaneous drift in the three-reference wavelength system (9.3 +/- 7 percent for the Edwards catheter and +/- 6 +/- 4.1 percent for the Spectramed catheter vs 3.3 +/- 3.1 percent for the Oximetrix catheter, p less than 0.05). This study shows that a three-wavelength system is more accurate than a two-wavelength system for measuring acute changes in SvO2. The addition of a second detecting fiber optic filament does not seem to improve the accuracy of the system when SvO2 changes occur in conditions of stable hematocrit.

Carboxyhemoglobin level (%COHB) obtained during pulmonary function testing was used as a measure of recent tobacco smoking among persons claiming to be nonsmokers and ex-smokers. Asbestos disability applicants and reference routine clinical patients had similar mean %COHB (2.09 ± 1.34 and 1.99 ± 0.88, respectively) and proportions with abnormally elevated %COHB (35 and 46 percent, respectively, had %COHB >2 percent). However, comparisons of persons claiming to be ex-smokers and nonsmokers showed that the ex-smokers had higher mean %COHB (p

A radioaerosol procedure using 99m Tc-DTPA (diethylene triamine penta acetate) was used to evaluate the permeability of the pulmonary epithelium in smokers and nonsmokers. The average clearance of this indicator from the lungs of smokers without significant airway obstruction exceeded that found in normal subjects by an average factor of more than five. This abnormality was observed throughout all lung regions. 99m Tc-DTPA clearance decreased rapidly during the week after smoking was discontinued. It is concluded that smoking results in a rapidly reversible increase in pulmonary epithelial permeability.

Ten patients with bronchial asthma and ten control subjects were exposed to sidestream cigarette smoke (passive smoking) for one hour in an environmental chamber. All subjects showed the same increase in carboxyhemoglobin as a result of the exposure: 0.40 percent. The asthmatic group demonstrated a significant linear decrease in pulmonary function during this exposure. After one hour of smoke, FEV1 decreased 21.4 percent, FEF25-75% decreased 19.2 percent, and FVC decreased 20.0 percent in the asthmatic patients. These alterations were readily reversible in all subjects when given inhalations of metaproterenol following the exposure. The control subjects showed no change in pulmonary function when exposed to identical conditions. These data show that nonsmokers with bronchial asthma are at risk when exposed to sidestream cigarette smoke in an environmental chamber.

In order to investigate the mechanism of polycythemia in chronic obstructive pulmonary disease (COPD), serum and urinary levels of erythropoietin and medullary erythroid progenitors were studied in 21 patients; nine were nonpolycythemic (hematocrit, 39 ± 4 percent; red blood cell [RBC] mass, 28 ± 5 ml/kg; forced expiratory volume in one second [FEV 1 ], 0.6 ± 0.1 L), and 12 patients were polycythemic (hematocrit, 52 ± 7 percent; RBC mass, 46 ± 7 ml/kg; FEV 1 , 0.9 ± 0.3 L). Hypoxia was severe in both groups, with mean arterial oxygen pressure of 47 mm Hg. The following parameters of tissue oxygenation were not significantly different between the two groups: arterial and mixed-venous oxygen saturations; cardiac output; oxygen utilization coefficient; 2, 3-diphosphoglycerate, and carboxyhemoglobin level. The level of erythropoietin was measured by bioassay in vitro. The level was increased in the serum of 85 percent (18) and in the urine of 38 percent (8) of the patients. There was no significant difference between the nonpolycythemic and polycythemic groups. Without exogenous erythropoietin, none of the subjects showed spontaneous colonies of erythroid progenitors. The addition of one unit of erythropoietin induced a similar normal proliferation of erythroid progenitors in both groups. The absence of adaptative polycythemia in the nonpolycythemic group with severe hypoxia was seemingly related neither to a quantitative deficit of erythropoietin nor to a lack of sensitivity of erythroid progenitors to its action.

This study of 130 subjects was performed to obtain more data about the smoking habits and levels of carboxyhemoglobin in various types of pipe and cigar smokers. These smokers may be divided by history into primary or secondary smokers and also into current inhalers and noninhalers. Prior studies of carboxyhemoglobin levels have yielded conflicting results, presumably due to differences in current habits of inhalation, which were often not taken into account. Cigarette, primary pipe, and secondary pipe inhalers had similar carboxyhemoglobin levels that were significantly higher than nonsmokers (5.6, 5.0, 5.4, and 1.0 percent, respectively). Cigar inhalers had markedly elevated concentrations of carboxyhemoglobin (13.8 and 11.8 percent in primary and secondary inhalers, respectively). Most secondary cigar and pipe smokers inhaled, whereas most primary smokers did not. Intentional inhalation, rather than past smoking history, is the most important factor in determining the carboxyhemoglobin level for each type of smoke.

Hyperlipemia in an acyanotic patient with diabetic ketoacidosis, alcoholism, and pancreatitis produced a falsely elevated concentration of methemoglobin (19 percent) and a lower-than-expected oxygen saturation measured with an automated spectrophotometer (IL-282 CO-Oximeter). In addition, there was a "normal" hemoglobin level despite a low hematocrit reading. In vitro studies showed that hyperlipemia corresponding to triglyceride levels of 500 mg/100 ml and greater produced erroneously high values for methemoglobin and total hemoglobin and "negative" values for carboxyhemoglobin. These abnormalities disappeared when the excessive lipids were removed by washing the erythrocytes in physiologic saline solution.

In two seriously ill patients, cyanosis developed shortly after a topical anesthetic spray (Cetacaine) was used. In both cases the presence of methemoglobinemia was suggested by a discrepancy between the arterial oxygen tension and the oxygen saturation of hemoglobin, as measured spectrophotometrically. The characteristic responses of the spectrophotometric oximeter to blood containing different concentrations of methemoglobin are described. Physicians administering this topical anesthetic spray (Cetacaine) should be aware of the possible development of methemoglobinemia.

Ten patients with bronchial asthma and ten control subjects were exposed to sidestream cigarette smoke (passive smoking) for one hour in an environmental chamber. All subjects showed the same increase in carboxyhemoglobin as a result of the exposure: 0.40 percent. The asthmatic group demonstrated a significant linear decrease in pulmonary function during this exposure. After one hour of smoke, FEV1 decreased 21.4 percent, FEF25-75% decreased 19.2 percent, and FVC decreased 20.0 percent in the asthmatic patients. These alterations were readily reversible in all subjects when given inhalations of metaproterenol following the exposure. The control subjects showed no change in pulmonary function when exposed to identical conditions. These data show that nonsmokers with bronchial asthma are at risk when exposed to sidestream cigarette smoke in an environmental chamber.

To determine the prevalence of carboxyhemoglobin levels in banked blood exceeding Air Quality Standards (level of carboxyhemoglobin greater than 1.5 percent), we analyzed banked blood for the level of carboxyhemoglobin from 101 randomly selected samples. Of 101 units of banked blood, 49 (49 percent) had carboxyhemoglobin levels greater than 1.5 percent, and 36 (36 percent) had levels of 2.0 percent or more. We suggest that it may be undesirable to use blood with increased carboxyhemoglobin content when multiple transfusions are necessary, particularly in patients with cardiac or pulmonary disease. Labeling banked blood for carboxyhemoglobin content would be useful in order to help avoid multiple or consecutive transfusions of blood with high levels of carboxyhemoglobin.

Eleven hypoxic (arterial oxygen pressure [PaO2] less than or equal to 61 mm Hg), polycythemic (hematocrit reading greater than or equal to 54 percent) patients were studied to determine the effect of the carboxyhemoglobin level on their response to therapy with supplemental oxygen. Five nonsmokers with a mean carboxyhemoglobin level of 2.8 percent showed an excellent response to therapy with supplemental oxygen, with a decrease in hematocrit reading from 57 percent to 48 percent (P less than 0.0025) as the PaO2 increased from 53 mm Hg to 69 mm Hg (P less than 0.01) and the arterial oxygen saturation (SaO2) increased from 86 percent to 94 percent (P less than 0.0025). Six smokers with a mean carboxyhemoglobin level of 13 percent showed an incomplete response to therapy with supplemental oxygen, with a decrease in hematocrit reading from 62 percent to 57 percent (P less than 0.0025) as the PaO2 increased from 53 mm Hg to 69 mm Hg (P less than 0.0025) and the SaO2 increased from 82 percent to 88 percent (P less than 0.001). In spite of similar values for the PaO2, the smokers had higher hematocrit readings before and during therapy with oxygen (P less than 0.01), presumably due to superimposed desaturation by carboxyhemoglobin. We concluded that polycythemia in hypoxic smokers is due to additive effects of hypoxia and a high carboxyhemoglobin level. The former is responsive to therapy with oxygen, while the latter is not. To achieve a "complete" response to therapy with supplemental oxygen, hypoxic polycythemic smokers should quit smoking.

A reservoir nasal cannula which stores oxygen during exhalation and delivers it as a bolus during inhalation has been reported to conserve oxygen delivery in patients with chronic obstructive pulmonary disease (COPD) at rest. We compared the effects upon arterial oxygen saturation (SaO2) of the reservoir cannula and a standard nasal cannula in hypoxemic obstructed and restricted patients at rest and during exercise. The SaO2 was monitored by ear oximeter. While at rest, 13 obstructed and four restricted patients breathed oxygen from the reservoir cannula at 0.5, 1.0, 1.5, and 2.0 L/min and from a standard cannula at 0.5, 1.0, 2.0, 3.0, and 4.0 L/min. Mean SaO2 was significantly higher with the reservoir cannula compared to the standard cannula at 1.0 and 2.0 L/min (p less than 0.0006) and tended to be higher at 0.5 L/min (p less than 0.1). Seven obstructed patients walked on a level treadmill at 0.75 mph while breathing oxygen at 0.5 and 1.5 L/min from the reservoir cannula and at 1.0 and 3.0 L/min from the standard cannula. The SaO2 during exercise with the reservoir cannula was comparable to that with the standard cannula at approximately half of the oxygen flow rate. The ratio of the oxygen flow rate of the standard to the reservoir cannula to produce 90 percent saturation was estimated and found to be 2.5 +/- 0.8 (mean +/- SD) for patients at rest and 2.9 +/- 1.8 during exercise. We conclude that in hypoxemic patients at rest and during exercise, the reservoir cannula uses less than half the oxygen of a standard cannula to produce similar improvement in SaO2 and thus has advantages of a reduced cost of ambulatory therapy with low-flow oxygen and a longer time permitted away from a stationary source of oxygen.

Carboxyhemoglobin level (%COHB) obtained during pulmonary function testing was used as a measure of recent tobacco smoking among persons claiming to be nonsmokers and ex-smokers. Asbestos disability applicants and reference routine clinical patients had similar mean %COHB (2.09 +/- 1.34 and 1.99 +/- 0.88, respectively) and proportions with abnormally elevated %COHB (35 and 46 percent, respectively, had %COHB greater than 2 percent). However, comparisons of persons claiming to be ex-smokers and nonsmokers showed that the ex-smokers had higher mean %COHB (p less than 0.001 by analysis of variance) and proportions with elevated %COHB. This study suggests that disability applicants and routine clinical patients do not differ in veracity of self-stated smoking information, but many persons claiming to be ex-smokers are actually not.

The rate of clearance from the lung of the hydrophilic tracer molecule 99mTc DTPA was used to investigate the short-term effects on lung epithelial function when smokers switched to cigarettes with lower yields of tobacco smoke constituents. Two separate studies were performed. In the first study, subjects smoked conventional mid- and low-tar cigarettes. The second study used two specially manufactured cigarettes with similar tar and nicotine yields, but differing carbon monoxide yields. Neither study demonstrated any significant improvement in 99mTc DTPA clearance. The yields of carbon monoxide determined under standard machine smoking conditions implied that there would be a 44 percent reduction in exposure to carbon monoxide when subjects switched from smoking conventional mid-tar to low-tar cigarettes. However, measurements of carboxyhemoglobin showed that the smokers compensated for the lower yields and their exposure was reduced by only 11 percent. Similarly, in the second study, the subjects reduced their exposure by 7 percent instead of the expected 44 percent. Urine nicotine/cotinine excretion measurements in this study indicated that there was no complimentary increase in nicotine absorption suggesting the possibility that subjects may be able to regulate their intake of individual components of the cigarette smoke. Thus, the unexpected result from this study was the finding that cigarette smokers could, in some way, regulate their intake of smoke from cigarettes of different composition so as to maintain a constant exposure of smoke constituents.

The effects of smoking and inhalation of carbon monoxide on the systolic time intervals and blood pressure were examined in ten healthy smokers with a mean age of 24.3 years. Each subject smoked a low-nicotine cigarette with a ventilated filter (0.1 mg nicotine, 1.1 vol percent CO), and a high-nicotine plain cigarette (2.6 mg nicotine, 4.5 vol percent CO), as well as a cigar in random sequence and in a standardized way. Cigar smoke was not inhaled. The product heart rate x blood pressure was increased and the left ventricular ejection time index (LVETc) prolonged following smoking the high-nicotine cigarette, whereas changes after smoking the low-nicotine cigarette and the cigar were not as pronounced. These changes are presumably caused by nicotine-induced catecholamine release. Inhalation of CO did not affect cardiac performance acutely as shown by unchanged systolic time intervals. When a high-nicotine cigarette was smoked after the subject received a beta blocker, a significant prolongation of the pre-ejection period index (PEPc) occurred as a result of the increased afterload. Thus, the effects of catecholamines on parameters of myocardial contractility (PEPc, PEP/LVET) were presumably offset by the increased afterload. We conclude that the acute hemodynamic changes of smoking in healthy subjects depend upon the amount of nicotine absorbed.

Mild to moderately severe hypoxemia was documented in 19 of 21 mostly asymptomatic firemen who were exposed to dense smoke containing polyvinylchloride and other pulmonary irritants. The hypoxemia was transient, with nearly complete reversibility within 24 hours. Subsequent tests for pulmonary function one month later demonstrated that this transient hypoxemia was not related to previous underlying pulmonary disease. The potential for serious complications of inhalation of smoke, particularly smoke from burning plastics, is heightened by the frequent lack of symptoms associated with this type of exposure, despite the development of moderately severe hypoxemia in addition to carboxyhemoglobinemia. Precautionary measures should include uninterrupted use of an effective breathing apparatus by firemen exposed to smoke and to noxious fumes and temporary oxygen supplementation, even in asymptomatic firemen, following exposure to dense smoke.

Although marijuana is now consumed extensively, little is known of its biologic effects on the lung. To study this problem, the intrapulmonary inactivation of an aerosolized challenge of Staphylococcus aureus was quantified in rats exposed to graded amounts of fresh marijuana smoke. Controls inactivated 85.1 percent ± 0.3 percent of the bacteria six hours after inoculation. Following an in vivo accumulative exposure to smoke from progressively increasing numbers of marijuana cigarettes for periods of ten minutes each hour for five consecutive hours, intrapulmonary bacterial inactivation was impaired in a dose-dependent manner. Evaluation of the effects of parenterally administered delta-9-tetrahydrocannabinol (THC) or of exposure to fresh smoke from THC-extracted marijuana placebo cigarettes indicated that the cytotoxin in marijuana was not related to the primary psychomimetic component. Thus, marijuana smoke is toxic to the lung and impairs the pulmonary antibacterial defense system in a dose-dependent manner.