The Heart in Oxygen Debt

CHEST

editorials VOLUME 108 I NUMBER 4 I OCTOBER, 1995

"Steering Clear" of Automobile Accidents in Patients With Sleep Disorders ktomobile accidents are the third leading cause of death in the United States. Although the exact numbers will never b e known, sleepiness has been implicated as a causative or contributing factor in many of these cases. Patients with sleep disorders such as narcolepsy and obstructive sleep apnea have an increased number of automobile accidents likely due to poor vigilance and excessive s le epiness associated with these disorders. In a r ecent issue of CHEST, Findley and colleagues 1 demonstrated that a test of vigilance, "Steer Clear," may assist in identifYing patients with sleep apnea or narcolepsy who are at risk for having automobile accidents. This study is unique in that other tests of sleepiness or vigilance have never been directly compared to the number of automobile accidents in a controlled fashion. The study shows that patients who did poorly on "Steer Clear" had a higher number of automobile accidents compared to two control groups. In the sleep apnea group, severity of disease as assessed by oxygen saturation indices and apnea-hypopnea indices (AHI) also correlated with poor performance on "Steer Clear." These findings are important for all physicians who diagnose and treat patients with sleep disorders. We, as physicians, have an obligation to society to keep patients who are a t high risk for automobile accidents off the road. The medico-legal implications are enormous. A r ecent statement by the American Thoracic Society2 regarding driving risk in sleep apnea patients advocates "educating and warning [high-risk] individuals on driving risks associated with sleepiness." However, to date, we have no objective guidelines to determine which patients are at risk. Tests of sleepiness such as the multiple s le ep latency test (MSLT) and maintenance of wakefulness test ( MWT) are time-consuming, expensive, and have poor correlation with automobile accident risk. Numerous studies have also shown that severity of disease as measured b y objective parameters such as MSLT, AHI, saturation indices, or arousal indices are not good predictors of vigilance or sleepiness in individual patients.3.4 The development of devices such as "Steer Clear"

is the first step towards resolution of this dilemma. The advantage of "Steer Clear" is that it is relatively easy to use, inexpensive, and would be available to any physician with a computer to repetitively assess patients following treatment initiation. Ideally, patients who score over a certain percentage would be advised not to drive, and if they continued to do so, they would be eligible to have their license suspended if necessary. Retesting after treatment would provide an objective means to assess the patient's readiness to go back on the road. Nancy A Gallop, MD, FCCP Charleston, South Carolina Deput)' Editor, CHEST; Assistant Professor, Medical University of South Carolina. R EFERENCES

1 Findley LJ, Unverzagt M, Guchu R, e t al. Vigilance and automobile accidents in patients with sleep apnea or n arcolepsy. Chest 1995; 108:619-24 2 Aldrich M. Automobile accidents in patients with sleep disorders. Sleep 1989; 12(6)487-94 3 Findley L, Unverzagt M, Suratt P . Automobile accidents involving patients with obstructive sleep apnea. Am R ev Respir Dis 1988; 138:337-40 4 American Thoracic Society. Sleep apnea, sleepiness, and driving risk. Am J Respir Crit Care Med 1994; 150:1463-73

The Heart in Oxygen Debt

unassisted ascent of Mount Everest is Thea te"natural" stament to the fact that the human heart is an

obligate aerobe that appears to be resistant to hypoxemia. In this issue of CHEST, Cargill, Kiely, and Lipworth (see page 899) study noninvasive measures of left ventricular systolic performance in eight healthy male volunteers subjected to brief episodes of hypoxemia. "Myocardial contractility" is difficult to study by noninvasive techniques as all measurements are load dependent in the in situ heart. Nevertheless, Doppler estimates of myocardial performance and cardiac output appear to be reproducible measures given certain limitations. This study is of interest on two levels. Myocardial performance during ischemia is dependent partly on oxygen delivery as well as metabolites and tissue turgor. In patients with coronary artery disease, left ventricular (LV) systolic performance appears to be variCHEST I 108 I 4 I OCTOBER, 1995

889

able depending on the type of ischemic insult. The greatest fall in LV systolic performance appears to be . the result of both hypoxemia and the build-up of metabolites as shown by occluding an artery with a percutaneous transluminal coronary angioplasty balloon. LV performance was less affected by pacing induced ischemia compared with ischemia created by a perfusion balloon (ischemia with washout of metabolites). 1 Myocardial performance is difficult to isolate as both systole and diastole must be taken into account. The in vivo assessment of myocardial performance is load dependent and thus direct myocardial contractility cannot be measured accurately with noninvasive techniques. Systolic ejection time intervals and aortic peak and mean acceleration times are also load dependent and variable, and it may not always closely correspond to left ventricular performance. 2·3 For example, a person with a dilated cardiomyopathy and impaired left ventricular function could have normal aortic peak acceleration time intervals. The use of continuous wave Doppler to assess stroke volume is becoming more widely accepted as a valid technique. 4 Two-dimensional echocardiography (2DECO) is more reliable to look at aortic cross-sectional diameter than M-mode echocardiography, and visualized optimal continuous wave Doppler interrogation of aortic flow is equivalent to invasive measures of cardiac output. 5 These Doppler techniques may be difficult to perform in a patient with high respiratory rates and with endomorphic physiognomy. In the present study, M-mode measurements were obtained with good reproducibility. The increasing use of Doppler echocardiography to assess hemodynamic data is laudable and easily applicable to the critical care units. The current study is important as various studies have examined the effect of hypoxemia on cardiac output with mixed results. In a well-controlled study using Doppler echocardiography, Phillips et al 6 have measured stroke volume using cross-sectional area and aortic-flow velocity integral at controlled levels of isocapnic hypoxemia, and noted that cardiac output does increase slightly in normal persons mostly as a result of heart rate. This physiologic response to hypoxemia makes adaptive sense. To compensate for falling tissue oxygen delivery by decreased Sa0 2, increased oxygen delivery could compensate. In the setting of ARDS and sepsis when patients are often subjected to hypoxemia, direct hypoxemia probably does not lead to myocardial depression but could contribute to the increased cardiac output and peripheral vasodilatation. Because the 1ight and left ventricles are interdependent, the performance of the left ventricle during hypoxemia is particularly interesting as it related to acute hypoxic pulmonary vasoconstriction. The study of anoxia on pulmonary pressures in man was of particular interest during; wartime. An invasive study was 890

reported by Motley et al 7 who subjected five men to 10% Oz/N 2 mixture while collecting pressure measurements within the pulmonary artery and right ventricle. Sa02 was decreased from 94 to 74% as compared with the severe hypoxemia group in the current study. Hypoxemia did cause acute hypoxic pressure response that doubled the mean residual volume pressures (7.9 to 14 mm Hg), and PA pressures with inc;eases in both rulmonary vas~ular resistance ~ 120 to 25o dynes·s·cm - ) and systemic vascular resistance (1,216 to 1,407 dynes·s·cm- 5 ). Heart rate and respiration rate increased with increases in minute ventilation from 7.2 to 11 Umin. Cardiac output, measured by Fick, was not significantly altered (5.7 to 5.2 Umin) and heart rate increased from 67 to 80 beats/min. Hypoxemia usually causes hyperventilation and pulmonary hypertension with compensatory rise in right heart pressures. We know now that hypoxic pulmonary vasoconstriction is a unique feature that distinguishes the pulmonary from systemic circulation. Acute hypoxic pulmona1y vasoconstriction is an adaptive mechanism that diverts blood from hypoxic alveoli and reduces intrapulmonary shunting. The response occurs within seconds of hypoxemia and can be prolonged for hours. It is a physiologically significant as shown by paradoxical nitroglycerin induced hypoxemia when normal pulmonary vasoconstlictor response is blunted and ventilation perfusion mismatch occurs. 8 The degree of acute pulmonary vasoconstriction is greatest in normal persons compared with patients with COPD and bronchitis. 9 It would be of interest to study the performance of residual volume during hypoxemia by similar methods using 2D-ECO or transesophageal Doppler echocardiography of the pulmonmy artery velocity integral. In the hypoxemic patient, many metabolic and hemodynamic variables contribute to myocardial performance. Seen globally, both right and left ventricular ionotropic and lusitropic effects need to be accounted. For now, it is encouraging to hear that the heart is an obligate aerobe that can go into oxygen debt without much usury to LV systolic performance. Jiho Han, MD Kenneth A Ellenbogen, MD Richrrwnd, Virginia Division of Cardiology, Medical College of Virginia, and Cardiac Physiology, McGuire- VA Hospital, Ricbmond. REFERENCES

l Bmyne B, Bronzwaer JGF, Heyndrickx GR, et aL Comparative

effects of ischemia and hypoxemia on left ventricular systolic and diastolic function in humans. Circulation 1993; 88:461-71 2 Noble MI, Trenchard D, Guz A. Left ventricular ejection in conscious dogs-measurement and significance of the maximum acceleration of blood from the left ventricle. Circ Res 1966; Editorials

19:139-147 3 Berk MR, Evans J, Knapp C, et al. Influence of alterations in loading produced by lower body negative pressure on aortic blood flow acceleration. JAm Coli Cardiol1990; 15:1069-74 4 Bouchard A, Blumlein S, Schiller, e t al. Measurement of left ventJicular stroke volume using continuous wave Doppler echocardiography of the ascending aorta and M-mode echocardiography of the aortic valve. J Am Coli Cardiol 1987; 9:75-83 5 Gorcsan J, Snow FR, Paulsen W, etal. Noninvasive estimation of left atrial pressure in patients with congestive heart failure and mitral regurgitation by Doppler echocardiography. Am Heart J 1991; 121:858-63 6 Phillips BA, McConnell JW, Smith MD, eta!. The effects of hypoxe mia on cardiac output: a dose-response curve. Chest 1988; 93:471-75 7 Motley HL, Coumand A, Werko L, e t al. The influence of short periods of induced acute anoxia upon pulmonmy artery pressures in man. Am J Physiol 1947; 150:315-20 8 Weygandt GR, Kopman EA, Ludbrook PA. Mechanism of nitroglycerin-induced hypoxemia. Cathet Cardiovasc Diagn 1980; 6:387-95 9 Weitzenblum E, Schrijen F , Mohan-KumarT, eta!. Variability of the pulmonary vascular response to acute hypoxia in chronic bronchitis. Chest 1988; 94:772-78

Justifying the Use of Blood Cultures When Diagnosing Community-Acquired Pneumonia chalasani and colleagues (see page 932) have reported on their study of the use of blood cultures in community-acquired pneumonia (CAP). In their retrospective study, the authors find that relatively few patients with CAP have positive blood cultures, almost all positive isolates are Streptococcus pneum.oniae and rarely do positive cultures lead to alterations in antibiotic therapy. The authors recommend prospective studies to see if blood cultures really are useful in an age when the cost of medical procedures must be justified. The authors have excluded from the study the subgroups of patients most likely to have bacteremic pneumonia-those with AIDS, myeloma, sickle cell anemia, and hematologic malignancy. They recognize that the use of blood cultures in these high-risk groups is without question. The present study comes a year after the American Thoracic Society published their consensus statement on Guidelines for the Initial Management of Adults with Community-Acquired Pneumonia. 1 In the statement, a panel rejects the use of sputum Gram's stain or "use of clinical syndromes to predict microbial etiology." Empirical antibiotic therapy is recommended in all patients with CAP. It is beyond the scope of this editorial to review the complex and conflicting literature on the value of clinical and microbiologic data in the specific diagno-

sis of CAP. It is fair to say that most infectious disease physicians believe that their training and skills are useful in determining causes of infection. The use of history-taking, physical examination, and review of Gram's stain, or other appropriate examinations of body fluids is an infectious disease tradition that grew out of Oslerian bedside teaching and was enhanced by clinical-microbiologic correlates exhaustively elucidated by Maxwell Finland and others. The major textbooks of medicine and infectious disease still recommend unequivocally the use of blood cultures, sputum Gram's stain, and clinical evaluation in an attempt to determine the specific cause of CAP.2-4 Will prospective studies really show that such an approach is just one more example of cost ineffectiveness-academic teachings unsupported by outcome data? Certainly, depending on hospital setting, there will be patients with CAP who will have positive blood cultures for less common organisms. Chalasani found one patient with bacteremic Escherichia coli pneumonia. Other series have found Gram-negative rods to cause between .5.9%5 and 20%6 of CAP. Bacteremic Gram-negative pneumonia is well described both as a community-acquired and nosocomial infection. 7 Bacteremic community-acquired E coli may occur in association with urinary tract infection.8 Bacteremic Klebsiella pneum.oniae pneumonia has been described in the alcoholic. Acinetobacter pneumonias have occurred as a bacteremic community-acquired infection.9 Chalasani et al found three patients with pneumonia caused by Hemophilus influenzae. This organism has also been implicated frequently in lifethreatening community-acquired pneumonia and occurs most commonly in patients with COPD and those on steroids.10.1 1 About 20 to 50% of strains are 13-lactamase producing and might require modification of an empirical antibiotic regimen. Chalasani et al found one patient with bacteremic 13-hemolytic streptococcal pneumonia. 13-Hemolytic streptococci (both Group A and B) do cause bacteremic pneumonia, which often requires specific, high-dose penicillin therapy.12 All infectious disease specialists will have their anecdotes of unusual pathogens causing bacteremic CAP, for example Bacillus, Pasteurella, and Francisella species. In many cases, a blood culture may have saved the day. Additionally, most admit, that a few patients who may have appeared to have CAP initially were diagnosed later by blood and other appropriate cultures as having endocarditis or urosepsis. Whatever prospective studies may show about the use of blood cultures, sputum Gram's stain, or clinical syndromes, we cannot afford to rely on empirical therapy for bacterial pneumonia. The cephalosporinerythromycin approach is doomed to failure. Simple guidelines will not work for a disease that is now more complicated than ever-a disease in which more CHEST 1108 I 4 I OCTOBER, 1995

891