Letters to the Editor

Letters to the Editor

The Revised Uniform Anatomical Gift Act (2006) and constitutional civil rights in the United States To the Editor: We agree with Iltis et al (1) that the enactment of the 2006 Revised Uniform Anatomical Gift Act and its subsequent 2007 amendment represents a serious transgression on civil liberties in the United States. If organs are removed from donors without fulfilling the legal definition of death (2), then enforcement of the Revised Uniform Anatomical Gift Act can also be a direct violation of the Fourteenth Amendment of the United States Constitution (1868): “No State shall make or enforce any law which shall abridge the privileges or immunities of citizens of the United States; nor shall any State deprive any person of life, liberty, or property, without due process of law; nor deny to any person within its jurisdiction the equal protection of the laws.” The revisions to the federal policies and state legislations were made on the recommendations of several concurring reports from governmental committees, health regulatory agencies, and prestigious private professional organizations (3). These entities represented a select group of shareholders (e.g., transplant professionals and advocates) but were also without a proportionate representation of the principal stakeholder (i.e., the general public) (4). The disproportionate representation served the objective of maximizing opportunities for procuring human organs for transplantation. Although organ transplantation can save human lives, organ procurement and transplantation activities take place within financially prosperous, domestic, and globally competitive markets (5). We had previously outlined at least two steps to resolve the societal challenges created by the Revised Uniform Anatomical Gift Act (6). First, doctors and hospitals must fulfill their legal obligations to patients or surrogate decision makers by disclosing organ donation legislations particularly the sections 14 (c) and 21 (b). They must also disclose that patients have the right to document preferences about the use of life support systems for preserving organs at the end of life. Second, a broad-based societal discussion must be initiated to 1830

resolve the infringement of the Revised Uniform Anatomical Gift Act on an individual’s autonomy. We think that the US Congress is the proper authority to initiate such a discussion and to ensure the respect of diverse personal values, cultures, and religious practices in a pluralistic society. The authors have not disclosed any potential conflicts of interest. Joseph L. Verheijde, PhD, MBA, PT, Department of Biomedical Ethics, Department of Physical Medicine and Rehabilitation, Mayo Clinic Hospital, Phoenix, AZ, Bioethics, Policy, and Law Program, Arizona State University, Tempe, AZ; Mohamed Y. Rady, MD, PhD, FCCM, Department of Critical Care Medicine, Mayo Clinic Hospital, Phoenix, AZ, Bioethics, Policy, and Law Program, Arizona State University, Tempe, AZ; Joan L. McGregor, PhD, Department of Philosophy, Arizona State University, Tempe, AZ

REFERENCES 1. Iltis A, Rie M, Wall A: Organ donation, patients’ rights, and medical responsibilities at the end of life. Crit Care Med 2009; 37:1– 6 2. Miller FG, Truog RD: Rethinking the ethics of vital organ donations. Hastings Cent Rep 2008; 38:38 – 46 3. DuBois JM, DeVita M: Donation after cardiac death in the United States: How to move forward. Crit Care Med 2006; 34:3045–3047 4. Mongoven AM: Duties to stakeholders amidst pressures from shareholders: Lessons from an advisory panel on transplant policy. Bioethics 2003; 17:319 –340 5. Hauboldt RH, Hanson SG, Bernstein GR: 2008 U.S. organ and tissue transplant cost estimates and discussion. Available at: http:// www.milliman.com/expertise/healthcare/ publications/rr/. Accessed December 10, 2008 6. Verheijde JL, Rady MY, McGregor JL: The United States Revised Uniform Anatomical Gift Act (2006): New challenges to balancing patient rights and physician responsibilities. Philos Ethics Humanit Med 2007; 2:19. Available at: http://www.peh-med.com/content/2/1/19

ysis focused on the rule of law as it exists today regarding premortem interventions on potential donors and end-of-life decision making, including the legal and ethical standards to which critical care professionals and healthcare institutions are held, rather than on the current debate about the definition of death and the dead donor rule. We conclude (as did Dr. Greer in his accompanying editorial [1]) that better public education at the time of joining a donor registry or signing a donor card would be necessary to further advance meaningful informed consent for the vast majority of the American people who favor transplantation as a publicly desirable medical therapy while protecting those citizens not wanting aggressive life and organ preservation techniques before they die. As Uniform Anatomical Gift Act is a nongovernmental model statute without the force of law, it will need to be amended in those states that enacted the earlier versions and changed in those states that have not yet revised the existent statute to preserve the authority of patients and their surrogates and the integrity of medical professionals. Such revisions are likely to be necessary for continued federal funding of organ donation activities by United Netword for Organ Sharing and local organ procurement organizations. The authors have not disclosed any potential conflicts of interest.

Ana S. Iltis, PhD, Center for Health Care Ethics, St. Louis University, St Louis, MO; Michael A. Rie, MD, Anesthesiology Critical Care Service, Department of Anesthesiology, University of Kentucky College of Medicine, Lexington, KY; Anji Wall, BBE, Center for Health Care Ethics, St. Louis University, St Louis, MO

DOI: 10.1097/CCM.0b013e3181a09595

REFERENCE The authors reply: We thank Verheijde and colleagues for their concerns about potential organ donor civil liberties and discussion of how Uniform Anatomical Gift Act 2006 and 2007 were created. The force of our anal-

1. Greer DM: Respecting patients’ rights at the end of life: Problems with the 2006 Uniform Anatomical Gift Act. Crit Care Med 2009; 37:372–373 DOI: 10.1097/CCM.0b013e3181a1ab8a

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Free radicals mediate postshock contractile impairment in cardiomyocytes—Translating experimental studies into clinical practice To the Editor: The study by Tsai et al (1) demonstrated that electrical shock generates free radicals inside the cardiomyocyte, and causes contractile impairment and associated decrease of Ca21 transient. They also concluded that ascorbic acid decreases damage to the cardiomyocyte after electrical shock by eliminating free radicals. Transient ST segment changes in the electrocardiogram are common after direct current shock and have been reported in 39% of successful defibrillation attempts (2). Only about 2.5% had a pulse after defibrillation attempts in postshock and in 10% of the patients who had a subsequent return of spontaneous circulation after the defibrillation attempt, which was due to myocardial stunning (3). On the basis of this evidence, the current European Resuscitation Council guidelines recommend restarting cardiopulmonary resuscitation immediately after defibrillation, without doing a pulse check. Myocardial stunning should not be regarded as a single entity because this has been observed in a wide variety of experimental settings (4): a. stunning after a single, completely reversible episode of regional ischemia in vivo; b. stunning after multiple, completely reversible episodes of regional ischemia in vivo; c. stunning after a partly reversible episode of regional ischemia in vivo (subendocardial infarction); d. stunning after global ischemia in vitro; e. stunning after global ischemia in vivo; and f. stunning after exercise-induced ischemia (high-flow ischemia). Pathogenesis of myocardial stunning has not yet been fully established. There are two hypotheses in the development of stunning, namely, generation of oxygenderived free radicals and by a transient calcium overload. Myocardial stunning is a type of myocardial reperfusion injury. Multiple attempts to individually target known mediators of myocardial stunning in patients using antioxidant therapy, calcium-channel blockers, sodium– hydrogen exchange inhibitors, and anti-inflammaCrit Care Med 2009 Vol. 37, No. 5

tory drugs have been largely disappointing, which lead to rethinking for a reevaluation of the current procedure for translating experimental interventions into clinical therapy like the one by Tsai et al. Radhakrishnan Ramaraj, MD, Department of Internal Medicine, University of Arizona Medical Centre, Tucson, AZ

REFERENCES 1. Tsai MS, Sun S, Tang W, et al: Free radicals mediate postshock contractile impairment in cardiomyocytes. Crit Care Med 2008; 36: 3213–3219 2. Reddy RK, Gleva MJ, Gliner BE, et al: Biphasic transthoracic defibrillation causes fewer ECG ST-segment changes after shock. Ann Emerg Med 1997; 30:127–134 3. Rea TD, Shah S, Kudenchuk PJ, et al: Automated external defibrillators: To what extent does the algorithm delay CPR? Ann Emerg Med 2005; 46:132–141 4. Bolli R, Marban E: Molecular and cellular mechanisms of myocardial stunning. Physiol Rev 1999; 79:609 – 634 DOI: 10.1097/CCM.0b013e3181a0965d

The authors reply: Myocardial stunning after electrical shock is associated with high fatality rate in the early hours after successful resuscitation. Many studies concentrate on investigating the underlying mechanism and potential resolutions, including waveform design of defibrillator and various pharmaceutical interventions. Although the mechanism of electrical shock–induced myocardial injury has not yet been fully explored, free radicals generated after electrical shock are documented to be involved in the pathogenesis of postshock myocardial dysfunction. In addition to the beneficial effect of antioxidants on the postshock contractile function of cardiomyocte in our study, there are plenty of published articles demonstrating improved myocardial function in different experimental models receiving antioxidant therapy (1–3). In patients with STelevation myocardial infarct, antioxidant treatment can reduce the incidence of reperfusion arrhythmia (4). Dr. Ramaraj raises an important point about translating experimental studies into clinical practice, which is a general but crucial concern among laboratory experiments. On the basis of our findings on cardiomyocyte, experiments that evaluate the cardioprotective effect of antioxidants on rats with ventricular fibrillation-induced cardiac arrest are ongoing. From experi-

mental study to clinical practice, we still have a long way to go. The authors have not disclosed any potential conflicts of interest. This study was supported, in part, by a Grant-in-Aid from the American Heart Association, Dallas, TX (to WT). Min-Shan Tsai, MD, The Weil Institute of Critical Care Medicine, Rancho Mirage, CA, Department of Emergency Medicine, National Taiwan University Hospital, Taipei, Taiwan; Wanchun Tang, MD, FCCM, The Weil Institute of Critical Care Medicine, Rancho Mirage, CA, The Keck School of Medicine of the University of Southern California, Los Angeles, CA

REFERENCES 1. Kapla´n P, Matejovicova´ M, Herijgers P, et al: Lack of the effect of superoxide dismutase and catalase on Na 1 , K 1 -ATPase activity in stunned rabbit hearts. Physiol Res 2008; 57: S61–S66 2. Kals J, Starkopf J, Zilmer M, et al: Antioxidant UPF1 attenuates myocardial stunning in isolated rat hearts. Int J Cardiol 2008; 125: 133–135 3. Kaplan P, Matejovicova M, Herijgers P, et al: Effect of free radical scavengers on myocardial function and Na1, K1-ATPase activity in stunned rabbit myocardium. Scand Cardiovasc J 2005; 39:213–219 4. Hicks JJ, Montes-Cortes DH, CruzDominguez MP, et al: Antioxidants decrease reperfusion induced arrhythmias in myocardial infarction with ST-elevation. Front Biosci 2007; 12:2029 –2037 DOI: 10.1097/CCM.0b013e3181a1aa07

Posttraumatic stress disorder–related symptoms after critical care: The role of sedation and family To the Editor: We read with great interest the article by Granja et al (1). We want to compliment the authors for evaluating several aspects of posttraumatic stress disorder (PTSD) in post–intensive care unit (ICU) patients. This problem is not often addressed but, nonetheless, has significant implications for the recovery phase of critically ill patients after discharge from the ICU and hospital. We like to comment on the authors’ conclusions and add some observations from our post-ICU outpatient clinic. The authors state that an association may exist between amnesia in the early 1831

phase of critical illness and PTSD-related symptoms. They hypothesize that the “early amnesia” may be due to brain dysfunction occurring at peak illness severity. We question this theory for several reasons. First, the observation that early amnesia is related to PTSD could be explained by differences in severity of illness but also by concomitant use of sedative medications. Patients with a higher Simplified Acute Physiology II Score are likely to have received more analgosedative medications and mechanical ventilation and probably had more profound neurologic disturbances before admission. Furthermore, approximately one fourth of these patients underwent surgery and will have received general anesthesia and postoperative analgesia. In addition, the occurrence of delirium during ICU stay may have been of influence. Specific data concerning these aspects are not reported, and we would like to ask the authors to provide additional information. The role of the family in the process of recollection and interpretation of memories of the ICU stay was not mentioned by the authors. From our experience with the follow-up of ICU patients at the postICU outpatient clinic, we feel that the influence of the relatives, especially the spouse, in the post-ICU period is significant. We frequently observe discrepancies in reported feelings or physical complaints between the patient and the spouse. Patients seem less concerned about the physical and mental consequences they may experience often due to the lack of recollection, whereas the spouses experience an intense period of anxiety and fear. The emotions of the spouse may also be reflected in the questionnaires and may overestimate the true PTSD symptoms of the patient. To evaluate this phenomenon, separate questionnaires for patients and spouses could be used. In addition, family members may also be of help when patients have PTSDrelated symptoms. It has been shown that lack of social support is one of the major risk factors for development of PTSD (2). Finally, the 23% observed incidence of PTSD-related symptoms at 6 months could underestimate the incidence 1–3 months after hospital discharge. Posttraumatic stress reactions are known to resolve spontaneously in the first months after the event (3). In our group of ICU patients with sepsis and multiple organ dysfunction syndrome, we have noted 1832

PTSD-like symptoms up to 20% at 1–3 months, which usually resolved after 6 months (,5%). Therefore, the results of Granja et al may not apply to earlier phases after hospital discharge. In conclusion, we feel that there are important limitations to the early illness amnesia hypothesis. We, therefore, fully agree with the authors that more detailed research is warranted to support this hypothesis. The authors have not disclosed any potential conflicts of interest. Maartje C. van Rijk, MD, PhD, Bastiaan H. J. Wittekamp, MD, David H. T. Tjan, MD, Arthur R. H. van Zanten, MD, PhD, Department of Intensive Care, Gelderse Vallei Hospital, Ede, The Netherlands

REFERENCES 1. Granja C, Gomes E, Amaro A, et al: Understanding posttraumatic stress disorder-related symptoms after critical care: The early illness amnesia hypothesis. Crit Care Med 2008; 36: 2801–2809 2. Brewin CR, Andrews B, Valentine JD: Metaanalysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. J Consult Clin Psychol 2000; 68:748 –766 3. Marshall RD, Spitzer R, Liebowitz MR: Review and critique of the new DSM-IV diagnosis of acute stress disorder. Am J Psychiatry 1999; 156:1677–1685 DOI: 10.1097/CCM.0b013e3181a096e8

The authors reply: We thank van Rijk et al for their letter as it provides an excellent opportunity to have an additional discussion of our results. We must stress although that most of the potential limitations to our study that are mentioned in their letter (e.g., the lack of information regarding previous psychiatric or neurologic disorders or sedation strategies before intensive care unit [ICU] admission) have already been acknowledged in our original paper (see Limitations section). Nevertheless, in contrast with the opinion of van Rijk et al, we do not believe that critically ill patients with a higher Simplified Acute Physiology II Score receive more analgosedative medications and mechanical ventilation before ICU admission. Furthermore, some studies (Weinert and Sprenkle [1]) failed to find an association between sedative exposure and ability to recall and, even if there is one, it is more likely to affect the memories for future, rather than for retrospective, events. Therefore, the argument that the “early

amnesia” found in our study may be due to drugs taken before ICU admission does not seem to be a stronger alternative explanation to our hypothesis. On the other hand, critically ill patients with a higher Simplified Acute Physiology II Score are indeed more likely to present profound neurologic disturbances. We believe that it is reasonable to assume that these disturbances are explained by acute brain dysfunction, which is highly prevalent (up to 80% [1–3]) among critically ill patients. Regarding the possible bias introduced by the family in the recollection of patient’s memories, this bias should equally affect the memories of events occurring both before and during ICU stay and, therefore, it is not likely to affect our main conclusions. Finally, according to the experience of van Rijk et al, prevalence rates of posttraumatic stress disorder–related symptoms at 6 months after ICU discharge may underestimate those at an earlier period, which would just strengthen the importance of our findings. Nevertheless, it should be noticed that other authors have reported that the prevalence of a formal posttraumatic stress disorder diagnosis may be similar at 2 and 6 months (1). In conclusion, we must wait for new evidence to emerge, to clarify the validity of our hypothesis and elucidate the true factors affecting the development of posttraumatic stress disorder in patients needing intensive care. Cristina Granja, MD, PhD, Augusta Amaro, MD; Emergency and Intensive Care Medicine Department, Hospital Pedro Hispano, Matosinhos, Portugal; Ernestina Gomes, MD, Antonio Carneiro MD, Intensive Care Unit, Hospital Santo Antonio, Porto, Portugal; Orquídea Ribeiro, BSc, Altamiro CostaPereira, MD, PhD, Biostatistics and Medical Informatics Department, Faculty of Medicine of Porto, Portugal; Christina Jones, BSc, MPhil, PhD, PG Dip Psych, Whiston Hospital, Intensive Care Research Group, Liverpool, UK

REFERENCES 1. Weinert CR, Sprenkle M: Post-ICU consequences of patient wakefulness and sedative exposure during mechanical ventilation. Intensive Care Med 2008; 34:82–90 2. Ely EW, Margolin R, Francis J, et al: Evalua-

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tion of delirium in critically ill patients: Validation of the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). Crit Care Med 2001; 29:1370 –1379 3. Ebersoldt M, Sharshar T, Annane D: Sepsisassociated delirium. Intensive Care Med 2007; 33:941–950 DOI: 10.1097/CCM.0b013e3181a1abf3

Obtaining pulmonary artery catheter data is too labor intense to be reliable To the Editor: I am writing with reference to the Special Article: Point of View, entitled, “The Pulmonary Artery Catheter: In Medio Virtus” by Jean-Louis Vincent et al (1). Although I fully appreciate and agree with the viewpoints stated by the esteemed physicians contributing to this article, I cannot resist sharing a nursing perspective. I am a clinical nurse specialist and responsible for teaching hemodynamic monitoring to our new nursing staff. I am also involved in pulmonary artery catheter (PAC) monitoring skills competency for our seasoned staff. Unlike SvO2 and cardiac output readings, pressure monitoring with the PAC requires tedious attention to detail. Besides zeroing and calibrating, the most simplistic aspects of insuring system accuracy, a square wave test must be completed to assess dynamic response. If the test is unsatisfactory (not uncommon), then measures are required to improve it including removing air bubbles, clots, and kinks or perhaps applying a dampening device. To obtain accurate pressures, readings must be taken manually at end expiration, a point that varies considerably between spontaneous breathing and mechanical ventilation. For the central venous pressure and pulmonary artery occlusion pressure measures, the “a” wave has to be identified and defined. All of these highly technical skills are mind boggling to new orientees and far too time consuming for busy intensive care unit nurses. In addition, with reduced use of the PAC, it becomes even more difficult for nurses to recall all the inexorable

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details for getting the data right. I have far more fear about the potential harm that can come from applying erroneous PAC information to a patient’s care than harm from having no PAC information at all. The author has not disclosed any potential conflicts of interest. Deborah Tuggle, RN, MN, CCNS, Jewish Hospital, Louisville, KY

REFERENCE 1. Vincent J-L, Pinsky MR, Sprung CL, et al: The pulmonary artery catheter: In medio virtus. Crit Care Med 2008; 36:3093–3096 DOI: 10.1097/CCM.0b013e3181a097ba

The authors reply: We thank Ms. Tuggle for her comments on our recent publication, The Pulmonary Artery Catheter: In Medio Virtus (1). She brings up one of the more important technical limitations to our ability to adequately interpret pulmonary artery catheter data, namely the proper identification of intrapulmonary vascular pressures at the passive end of expiration. We have emphasized this point before (2). This fundamental limitation is the reason for the development of Web-based pulmonary artery catheter vascular pressure measure training applications (e.g., http://www.thoracic.org/sections/clinicalinformation/critical-care/hemodynamicmonitoring/pulmonary-artery-catheterprimary/index.html). Importantly, the bedside caregiver needs to record a vascular pressure profile during breathing either to a strip chart or monitor screen freeze frame and measure the pressure directly, rather than use an electronic monitor readout of the estimated pressure value. One measures intrapulmonary vascular pressures (e.g., central venous, pulmonary artery, and pulmonary artery occlusion pressures) at passive end expiration to minimize the influence of intrathoracic pressure, not to abolish it. Referencing pulmonary artery catheter pressures to airway pressure often improves the accuracy in identifying end

expiration (3). The primary reasons for measuring pulmonary artery catheter pressures are to assess right ventricular afterload, pulmonary vascular resistance, and the hydrostatic determinants of pulmonary edema, rather than to determine ventricular filling pressures and predict volume responsiveness (4). Furthermore, measures of SvO2 and cardiac output reflect the primary targets of resuscitation, based on a number of positive clinical trials (5). Thus, these very real technical limitations in the estimation of intrapulmonary vascular pressures should have less of an impact on its utility if treatment algorithms focus more on optimizing oxygen delivery to the tissues and guiding therapy based on this priority (2). Michael R. Pinsky, MD, Dr hc, Department of Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA; John J. Marini, MD, Department of Pulmonary and Critical Care Medicine, Regions Hospital, St Paul, MN; Didier Payen, MD, Department of Anesthesiology and Intensive Care, Centre Hospitalier Universitaire Lariboisiere, Paris, France; Jean-Louis Vincent, MD, PhD, FCCP, Department of Intensive Care Medicine, Erasme Hospital, Universite´ Libre de Bruxelles, Belgium

REFERENCES 1. Vincent JL, Pinsky MR, Sprung CL, et al: The pulmonary artery catheter: In medio virtus. Crit Care Med 2008; 36:3093–3096 2. Pinsky MR, Vincent JL: Let us use the PAC correctly and only when we need it. Crit Care Med 2005; 33:1119 –1122 3. Rizvi K, deBoisblanc BP, Truwit JD, et al: Effect of airway pressure display on interobserver agreement in the assessment of vascular pressures in patients with acute lung injury and acute respiratory distress syndrome. Crit Care Med 2005; 33:98 –103 4. Michard F, Teboul JL: Predicting fluid responsiveness in ICU patients: A critical analysis of the evidence. Chest 2002; 121:2000 –2008 5. Pinsky MR: Hemodynamic evaluation and monitoring in the ICU. Chest 2007; 132:2020 –2029 DOI: 10.1097/CCM.0b013e3181a1aa7f

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