Nicotine Is Hazardous to Your Heart

that support this statement. Indeed, the average respiratory care service in an acute care setting operates 7-days-a-week, 24-h-a-day. Many hospital administrators and medical directors have opted to invest more clinical responsibilities in respiratory care services because of their service hours. This provides a greater degree of access to services without necessarily adding additional costs by hiring more staff. Other institutions have elected to invest responsibility for intubation in the RCPs and have met with success. 2 ·6 While the American Association for Respiratory Care certainly does not challenge the contention of the authors regarding the suitability of paramedics to perform this function in their institution, we do believe their success need not come at the expense of RCPs, especially in light of the fact that the two reasons given by the authors for RCPs being unsuitable for this responsibility are, to our knowledge, not supported with factual evidence. If the authors have evidence demonstrating that RCPs are not trained to perform intubation and that RCPs are unwilling to work shifts other than the standard day shift, then the American Association for Respiratory Care would like to review the data, because these claims run counter to our review of respiratory care education programs and the average staffmg patterns in respiratory care service departments in hospitals?- 11 Trudy f. Watson, RRT, 1995 President, American Association for Respiratory Care,

Dallas

R£!llrint requests: Trudy T. Watson/Sherry Milligan, AARC, 11030 Aliles Lane, Dallas, TX 15229 REFERENCES

1 National Board for Respiratory Care. Section Ill: initiate, conduct, and modifY prescribed therapeutic procedures. In: Written registry examination content outline, 1993; C.6.c.:18 2 McLaughlin AJ Jr, Scott W. Training and evaluation of respiratory therapists in emergency intubation. Respir Care 1981; 26:333-35 3 Conley JM, Smith DJ. Emergency endotracheal intubation by respiratory care personnel in a community hospital. Respir Care 1981; 26:336-38 4 Perlson R. Safe and successful delivery room intubation and resuscitation of meconium-stained newborns by respiratory therapists. Respir Care 1986; 31:689-94 5 Thalman JJ, RinaldcrGallo S, Macintyre NR. Analysis of an endotracheal intubation service provided by respiratory care practitioners. Respir Care 1993; 38:469-73 6 Zyla EL, Carlson J. Respiratory care practitioners as secondary providers of endotracheal intubation: one hospital's experience. Respir Care 1994; 39:30-3 7 Barnes TA, Durbin CG Jr. ACLS Skills for the respiratory therapist: time for a mandate. Respir Care 1992; 37:516-19 8 Kacmarek RM. The role of the respiratory therapist in emergency care. Respir Care 1992; 37:523-32 9 American Association for Respiratory Care. Clinical practice guideline: resuscitation in acute-care hospitals. Respir Care 1993; 38:1179-88 10 Buck C, Southom PA. Who should perform endotracheal intubation? A summary of issues. Respir Care 1994; 39:17-8 11 Barnes TA, Durbin CG Jr. Research on resuscitation by RCPs is long overdue. Respir Care 1994; 39:712-14

In many areas across the United States, the training curriculum for respiratory therapists (RTs) includes "hands on" endotracheal intubation training on patients. However, in Wisconsin, to the best of our knowledge, there is no teaching program for RTs that includes, as part of its regular curriculum, the above clinical "hands on" training, even though the RTs in this state are well trained and licensed in respiratory care. Despite little scientific evidence of an effect of varied training techniques on outcome of intubation by nonphysician personnel, 1•2 many believe that mannequin and textbook intubation training, in themselves, are inadequate. 3 Therefore, many hospitals have developed programs to develop and maintain RTs' skill in emergent intubation.4 At our institution, the feeling was that the relatively small number of intubations performed during in-hospital CPR alone would not enable a newly trained RT to maintain the skill needed to perform skillful intubations. This would necessitate both an intubation training and skill maintenance program for RTs at a cost that would be prohibitive when viewed in the context of accomplishing the relatively small number of intubations. Paramedics here have clinical intubation skills developed and maintained out-of-hospital; therefore, in adverse conditions not unlike in-hospital CPR only a limited testing program to ensure their intubation skill seemed to suffice. The relative availability of paramedics and RTs and their training varies significantly across the country. Furthermore, the turnover of RTs varies considerably from hospital to hospital and region to region. Endotracheal intubation on in-hospital patients is still performed by many different groups at different locations and hospitals.5 Our position is not that paramedics be selected to perform in-hospital intubations in lieu of RTs who are available and experienced in intubation and can maintain their skills at an acceptable level in an on-going fashion. Rather, we hold the position that for hospitals devoid of personnel (including RTs) with clinical experience in intubation, paramedics can safely provide an alternative and viable mechanism if they have acquired the skill as part of their previous field training and ongoing out-of-hospital clinical experience.

Jeffery S171Llle, MD, and Kesavan Kutty, MD, FCCP, St. Joseph's Hospital, Milwaukee REFERENCES

1 Stratton SJ, Kane G, Gunter CS, et al. Prospective study of manikin-only versus manikin and human subject endotracheal intubation training of paramedics. Ann Emerg Med 1991; 20:1314-18 2 Stewart RD, Paris PM, Pelton GH, et al. Effect of varied training techniques on field endotracheal intubation success rates. Ann Emerg Med 1984; 13:1032-36 3 Hauswald M, Tuohy GF, Philip von der Heydt. Adequate training for endotracheal intubation [letter]. Ann Emerg Med 1992; 21:1168-69 4 Boudin KM. Strategies for maintaining ACLS skills in hospitals. Respir Care 1995; 40:550-66 5 Buck C, Southom PA. Who should perform endotracheal intubation? A summary of issues. Respir Care 1994; 39:17-8

To the Editor:

We appreciate the thoughtful comments and interest of Ms. Watson in our article entitled, "Endotracheal Intubation by Paramedics During In-Hospital CPR" (CHEST 1995; 107:1655-61); we agree that the availability of qualified individuals to perform intubation during in-hospital cardiopulmonary resuscitation (CPR) is difficult in many areas. We would like to respond to her comments and areas of concern. 584

Nicotine Is Hazardous to Your Heart To the Editor:

We read with interest the case report by Ottervanger et a1 (CHEST 1995; 107:1765-6) entitled "Acute Myocardial Infarction Communications to the Ed~or

While Using the Nicotine Patch." In the Discussion, they speculate the causal relation between nicotine patch and acute myocardial infarction and cite many articles with respect to adverse effects of nicotine on the cardiovascular system. Our viewpoint is that even if it is just coincidental, it is important to warn those who use the nicotine patch, physicians and patients alike, about this veryserious adverse cardiovascular effect of nicotine through this case report. In fact, nicotine has been reported 1-3 in many studies to cause many cardiovascular problems such as myocardial infarction, arrhythmia, and aortic aneurysm, particularly when combined with a high level of cholesterol and hypertension. Unfortunately, this information has been generally overwhelmed by the more obvious pulmonary complications due to smoking. In our laboratory, we have performed studies of nicotine on isolated rabbit heart, aorta, and pulmonary artery with perfusion and tissue bath techniques, respectively 4 The preliminary findings have shown that nicotine behaves like low dose epinephrine. It causes significant dose-related myocardial contraction and endotheliumindependent vasoconstriction (Tables 1 and 2). Apparently, if these results can be extrapolated to a clinical condition, increased myocardial oxygen consumption secondary to increased contractility and heart rate, and decrease of coronary blood flow due to vasoconstriction will cause imbalance between oxygen demand and supply of the heart and lead to arrhythmia, and myocardial ischemia or infarction or both. Other than mediated by catecholamines, nicotine may have direct positive inotropic and vasoconstrictive effect through adrenergic receptors. In our laboratory, these increased inotropic and vasoconstrictive effects can be antagonized by 13- and a-adrenergic blocking agents, respectively. Quillen et al3 show that cigarette smoking C'Onstricts coronary arteries and myocardial resistance vessels. Although nicotine absorption via transdermal patch is slower and lesser than cigarette smoking, the net serum concentration of nicotine will make a difference. Based on dose-related response in our studies, we believe that with or without concurrent smoking, it is the total dose of nicotine that is responsible for myocardial complications as in the case report (CHEST 1995; 107:1765-66). Most people, including patients and the media, are very familiar with the serious pulmonary consequences of tobacco smoking such as lung cancer and COPD. As a matter of fact, from a medical point of view, the adverse effects of nicotine on the cardiovascular system is as bad as on the pulmonary, or even worse.2 Unfortunately, it has been understated and the public is not well informed. It is advisable for the US Food and Drug Administration to consider including boxed warning labels on nicotine patches relating to cardiovas-

Tahle 1-The Effects of Nicotine on Myocardial Contractility* Nicotine, pm 1 10 30 100 1,000 PDT,% 100.5±2.1 105.0±2.0 136.7±5.3 163.2±10.7 202.7± 23.6 dT/dt,% 99.8±2.2 117.3±6.9 183.0±7.5 253.7±23.0 289.8±27.9 *Data represent Mean±SE, n=6; PDT=peak developed tension; dT/dt=delta tension/delta time.

Table 2-The Vasoactive Effects of Nicotine on Pulmonary Artery and Aorta* Nicotine, pM PA(E+) PA (E-) AO(E+) AO(E-)

3 18.8±5.7 4.2±2.1 9.7:'::3.1 3.3±2.2

10 113.3:'::21.9 ll5.7±4l.7 67.8±5.2 101.8:'::30.3

30 291.3:'::46.2 289.8±62.8 270.0±30.4 262.5±47.3

100 375.3:'::42.7 340.7:'::56.3 379.2:'::25.7 378.8:'::63.2

*Data represent Mean:'::SE as force (g)/wet tissue (g); n=6; PA= pulmonary artery; AO=aorta; E=endothelium.

cular complications, particularly for patients with coronary disease. 5 It is about time, we believe, to face and emphasize these serious cardiovascular problems associated with nicotine and to educate as well as warn the public of this issue.

Tai-Shion Lee, MD, FCCP, and Xiuhua Hou, MD; Department of Anesthesiology, Harbor-UCLA Medical Center, Torrance, California REFERENCES 1 Benowitz NL. Smoking-induced coronary vasoconstriction: implications for therapeutic use of nicotine. JAm Coil Cardiol1993; 22:648-49 2 Report of the Surgeon General. The health consequences of smoking: cardiovascular disease. Washington, DC: US Dept of Health and Human Services; 1983, Publication CDC 3 Quillen JE, Rossen JD, Oskarsson HJ, eta!. Acute effect of cigarette smoking on the coronary circulation: constriction of epicardial and resistance vessels. J Am Coil Cardiol 1993; 22:642-47 4 Lee TS, Hou X. Direct vasoactive effects of nicotine on isolated aorta and pulmonary artery [slide presentation]. Presented at the 61st Annual International Scientific Assembly of the American College of Chest Physicians, November 1, 1995, New York City. Chest 1995; 108(suppl 3):120S 5 Fiore MC, Jorenby DE, Baker TB, et a!. Tobacco dependence and the nicotine patch. JAMA 1992; 268:2687-94

Nutritional State and Exercise Tolerance in Patients With COPD To the Editor: Falange and colleagues (CHEST 1995; 107:1206-12) recently claimed that malnutrition impairs maximal exercise performance in patients with COPD. We think that this conclusion cannot be supported because the FEV1 of the malnourished patients was 25% predicted vs 40% predicted in the normal weight and overweight groups. We hope that Palange et a! will reanalyze their data using appropriate statistical techniques to determine whether nutritional status had a significant effeet on exercise performance of their patients, independent of FEV1. Nutritional status does affect exercise performance to some extent in COPD. Gray-Donald et al1 showed that maximal exercise capacity was reduced in underweight COPD patients. In their patients, the range of FEV1 among the three weight groups was only 31 to 36% predicted, 1 so the effects of nutritional status were more readily apparent. There was no relation between body weight and walk distance, 1•2 although Schols et al 2 found that the 6-min walk distance correlated with the serum albumin and the creatinineheight index. Palange et a! raise an interesting therapeutic point. They speculate that patients with COPD might benefit from oxygen administration during exercise, even if they are not hypoxemic. Two reports show 25 to 40% improvement in exercise distance or duration at submaximal exercise; 3•4 this is mediated at least in part by reductions in breathlessness. In assessing the effects of malnutrition or other interventions on exercise performance, it is important to note whether the effect is apparent in maximal or submaximal exercise.

Jing Win Liu, MD, FCCP, Pulrrwnary Division, Department of Medicine, CHEST I 109 I 2 I FEBRUARY, 1996

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