American Journal of Emergency Medicine (2005) 23, 24 – 29
www.elsevier.com/locate/ajem
Inadequate hemodynamic management in patients undergoing interfacility transfer for suspected aortic dissectionB Greg Winsor RNa, Stephen H. Thomas MD, MPHa,b,*, Paul D. Biddinger MDb, Suzanne K. Wedel MDa,c a
Boston MedFlight Critical Care Transport Service, Boston, MA 02170, USA Department of Emergency Services, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA c Department of Surgery, Boston Medical Center and University School of Medicine, Boston, MA 02114, USA b
Received 20 December 2003; accepted 14 January 2004
Abstract The study goal was the analysis of effectiveness of hemodynamic management of patients undergoing interfacility transport for suspected acute aortic dissection (SAAD). Our retrospective, consecutive-case review examined 62 nonhypotensive patients transported by an air emergency medical services (EMS) service during 1998 to 2002, with referral hospital diagnosis of SAAD. Of patients with systolic blood pressure (SBP) less than 120 upon air EMS arrival, antihypertensives had been given in only 23/42 (54.8%). In 19 cases where pretransport SBP is less than 120, with no referral hospital antihypertensive therapy given, median pretransport SBP was 158 (range, 122-212). In 20/62 cases (32.3%), the air EMS agency instituted antihypertensive therapy, which was successful; of 42 cases with pretransport SBP less than 120, mean intratransport SBP decrement was 24 (95% confidence interval, 16-32). In patients undergoing transport for SAAD, pretransport hemodynamic therapy was frequently omitted and often inadequate, generating an opportunity for air EMS intervention. Education to improve SAAD care should focus upon both referral hospitals and transport services. D 2005 Elsevier Inc. All rights reserved.
1. Introduction B Parts of this project were presented at the National Association of Emergency Medical Services Physicians Annual Meeting (Panama City, Fla, 15 January 2003), and at the American College of Chest Physicians Chest 2003 Research Forum (Orlando, Fla, 25-30 October 2003). * Corresponding author. Department of Emergency Services, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Tel.: +1 617 724 4240; fax: +1 617 724 0917. E-mail address:
[email protected] (S.H. Thomas).
0735-6757/$ – see front matter D 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.ajem.2004.01.008
Aortic dissection is both common and life-threatening [1]. Authorities recommend early control of heart rate (HR) and systolic blood pressure (SBP) as soon as the diagnosis of aortic dissection is suspected to prevent propagation of the intimal flap [1-6]. In fact, elevated SBP in the setting of aortic dissection constitutes a hypertensive crisis, in which antihypertensive therapy
Inadequate hemodynamic management during interfacility transfer should be instituted immediately [1]. Because the diagnosis and treatment of suspected acute aortic dissection (SAAD) require access to advanced imaging and specialists, community hospitals may lack the resources necessary to care for SAAD patients. It is thus common for such patients to be transferred to specialty medical centers before the definitive diagnosis of aortic dissection can be made [3]. In the vast majority of circumstances, a clinical suspicion of SAAD strong enough to prompt interfacility transfer is also strong enough to warrant presumptive hemodynamic therapy. Given the serious nature of SAAD, the relative ease and safety with which referring hospitals can institute hemodynamic therapy consistent with authorities’ recommendations, and the potential for critical care transport services to institute hemodynamic therapy when referring hospital treatment is suboptimal, this study sought to address 2 questions: (1) In patients with SAAD undergoing interfacility transport, what is the frequency and effectiveness of hemodynamic therapy at the referring hospital? (2) How often, and with what effectiveness, is hemodynamic therapy instituted by interfacility critical care transport crews? Importantly, we did not set out to assess whether effective hemodynamic therapy (ie, therapy that appropriately controlled HR and SBP) was salutary in cases of aortic dissection. We believe that the extant literature support for the benefits of hemodynamic control is sufficiently strong to enable us to reasonably use as an boutcomeQ the surrogate endpoint of beffective hemodynamic control.Q In other words, this study was not designed to test whether achieving hemodynamic control was desirable; we rather took for granted the desirability of hemodynamic control in patients undergoing transport for SAAD, and designed the study to assess whether hemodynamic control was in fact being effectively provided.
2. Methods 2.1. Design and setting We retrospectively assessed a consecutive case series of patients undergoing interfacility transport with a diagnosis of SAAD. All transports were done by Boston MedFlight (BMF) and were completed during the period of 1998 to 2002. (This period was selected as going back as far as highquality records were obtainable). During the transport period in question, BMF performed transports using 2 helicopters and 1 ground critical care vehicle. The BMF crew consists of a nurse and paramedics who provide protocol-directed care with availability of online medical control as needed. Boston MedFlight transports patients from referring hospitals throughout Massachusetts and nearby New England states to tertiary care centers in Boston.
25
2.2. Subjects During the study period, 71 patients, from 27 referring hospitals, underwent transport with a pretransport diagnosis of suspected aortic dissection. Nine of these patients were hypotensive (by a priori definition of SBP b90) before any referring hospital therapy and thus were not candidates for hemodynamic therapy. After exclusion of the 9 hypotensive patients, the final study group comprised 62 patients.
2.3. Data and analysis The study’s basic statistical methodology was a descriptive assessment of the frequency with which hemodynamic therapy was provided at the referring hospital. Standard emergency medicine [1] and cardiovascular [6] texts agree upon target ranges for SBP (100-120) and HR (60-80) during early management of aortic dissection. Thus, the current study’s design incorporated an a priori determination to define an SBP of greater than 120 and/or HR greater than 80 as the levels above which antihypertensive therapy and HR therapy were indicated. Categorical analysis was performed with Pearson’s v 2 tests. Continuous data (eg, comparison of pre- and posttransport hemodynamic values) were analyzed with parametric (t test) and nonparametric (Kruskal-Wallis test) techniques, depending on whether the particular data being assessed were distributed normally (as assessed by the ShapiroFrancia test). Data are reported as means F standard deviations, with 95% confidence intervals (CIs) for means, and also as medians with ranges and interquartile ranges (IQRs). For assessment of variables associated with the dichotomous outcome of BMF crew treatment of patients with hemodynamic therapy, we used multivariate logistic regression. Regression results are reported as odds ratios (ORs) with 95% CI for the individual variables; models were assessed with the likelihood ratio test. All statistical tests were performed with STATA version 8.0 (StataCorp, College Station, Tex). Significance was defined at the P = .05 level.
3. Results 3.1. Transport times For study patients, the time interval between request for BMF transport and arrival of the BMF crew to the patient ranged from 17 to 87 minutes (median, 31.5; IQR, 26-42). The duration of time that the transport crew spent with patients ranged from 21 to 75 minutes (median, 40; IQR, 32-50). The time interval between request for BMF transport and subsequent patient arrival at the receiving center ranged from 41 to 147 minutes (median, 72; IQR, 62-89).
26
3.2. Patient characteristics, diagnostic imaging, and receiving center diagnostic confirmation Of the 62 study patients, 37 (59.7%) were men and 25 (40.3%) were women. The median age was 71 (range, 3087; IQR, 60-78). Suspected dissections were characterized by the referral hospital as Stanford Type A in 27 patients (43.6% of 62), Type B in 10 patients (16.1%), and simply as bdissectionQ in the remaining 25 patients (40.3%). Referral hospital pretransport diagnostic imaging upon which the SAAD diagnosis was based was chest x-ray (CXR) as the sole imaging test in 8 patients (12.9% of 62), computed tomography in 47 patients (75.8%), echocardiography in 6 patients (9.7%), and cardiac catheterization in 1 patient (1.6%). There was no association between use of badvancedQ imaging (ie, beyond CXR) and likelihood of referral hospital administration of therapy for either HR (OR, 1.3; 95% CI, 0.3-6.1; P = .71) or SBP (OR, 1.5; 95% CI, 0.3-7.1; P = .70). Follow-up diagnoses obtained from the receiving centers confirmed aortic dissection (with or without associated aneurysmal dilation) in 15 patients (24.2%). There was no association between receiving hospital confirmation of aortic dissection diagnosis and referral hospital therapy for either SBP ( P = .24) or HR ( P = .75). Actually, although the results were not statistically significant, there was a tendency toward patients with ultimate diagnosis of dissection to be less likely (as compared with those in whom aortic dissection was ruled out) to receive referral hospital medication for SBP [OR and 95% CI, 0.5 (0.1-1.6)] or for HR [OR and 95% CI, 0.8 (0.3-2.7)].
3.3. Heart rate and beta-blockade therapy at referring hospitals At the time of BMF arrival at the referral hospital, patients’ HRs exceeded 80 in 26 patients (41.9% of 62). Of these 26 patients, 14 (53.9%) had received beta-blocker therapy at the referral hospital. For those 14 patients, the median HR was 88 (IQR, 83-96). In the 12 cases (46.2% of 26) where initial BMF-assessed HR exceeded 80 and no HR medication had been administered at the referral hospital, HRs ranged from 81 to 152 with median 87 (IQR, 83-97). Of the 36 cases where HR was less than 80 on BMF arrival (58.1% of 62), 13 (36.1%) had received beta-blocker medication from the referral hospital.
3.4. Systolic blood pressure and antihypertensive therapy at referring hospitals Upon BMF arrival at the referral hospital, patients’ SBPs exceeded 120 in 42 cases (67.7% of 62). Of those 42 cases, 23 (54.8%) had received antihypertensive therapy at the referral hospital. For those 23 patients, the SBP ranged from 121 to 218 (median, 158; IQR, 141-176). In the 19 cases (45.2% of 42) where initial BMF-assessed SBP exceeded
G. Winsor et al. 120 and no antihypertensive therapy had been administered at the referral hospital, SBPs ranged from 122 to 212 with median 158 (IQR, 141-180). Of the 20 cases (32.3% of 62) where SBP was less than 120 upon BMF arrival at the patient, 6 (30%) had received antihypertensive therapy from the referral hospital.
3.5. Critical care transport crew interventions for HR and SBP control The BMF crew continued HR medications, which had been started by the referral hospital in 5 patients (8.1% of 62). Continuation of antihypertensive therapy was provided in 21 (33.9% of 62) patients. In 3 patients (4.8% of 62), BMF crews continued both HR and antihypertensive therapy medications. Boston MedFlight instituted new HR therapy in 22 patients (35.5% of 62). In these 22 patients, the HR upon BMF arrival at the patient (not necessarily the HR at the time of BMF institution of HR therapy) ranged from 54 to 124 (median, 83; IQR, 71-92). For the 26 patients whose initial HR was at least 80, BMF instituted therapy for HR control in 14 cases (53.9% of 26). Boston MedFlight instituted new antihypertensive therapy in 20 (32.3% of 62) patients, including 3 patients who had already received other SBP therapy from the referral hospital. For these 20 patients, SBP on BMF arrival at the patient (not necessarily the SBP at the time of BMF institution of antihypertensive therapy) ranged from 101 to 204 (median, 158; IQR, 135-177). For the 42 patients whose initial SBP was at least 120, BMF instituted therapy for blood pressure control in 17 cases (40.5% of 42).
3.6. Effect of intratransport hemodynamic therapy The proportions of patients with HR less than 80 were similar ( P = .86) in the pre- (58.1%) and posttransport (56.5%) time frames. For the subset of patients (n = 26) whose pretransport referral hospital HRs exceeded 80, however, the posttransport HRs (median, 83; IQR, 75-93) were significantly ( P = .032) lower than pretransport HRs (median, 88; IQR, 83-96). The proportions of patients with SBP less than 120 were similar (both 32.3%, P = 1.0) in the pre- and posttransport time frames. After confirmation of normality of SBP data using the Shapiro-Francia test, t test comparison of initial vs final SBPs confirmed that the posttransport average SBP (mean, 129 F 27, 95% CI, 122-136) was significantly ( P = .0007) lower than the pretransport average SBP (mean 142 F 35.5, 95% CI, 133-151). The intratransport drop in SBP was particularly pronounced ( P b .0001) for the 42 patients whose initial SBP exceeded 120; in this group, the pretransport SBP mean was 161 F 25 (95% CI, 154-169) and the posttransport mean was 138 F 24 (95% CI, 130-145).
Inadequate hemodynamic management during interfacility transfer
4. Discussion The estimated incidence of aortic dissection is between 5 and 30 cases per million persons per year [4], although the increased likelihood of disease in older patients means that this potentially lethal diagnosis is often considered, and not infrequently diagnosed, in the acute care setting [1]. Untreated, mortality can be as high as 1% per hour and can reach more than 21% to 25% in 24 hours [5,6]. Unfortunately, failure to recognize and treat acute dissection in a timely and effective manner is a major contributor to mortality [7]. Once the diagnosis of aortic dissection is suspected, survival is improved with control of blood pressure and HR either as definitive therapy or as a bridge to surgical repair [8]. Aggressive medical management is recommended in cases of aortic dissection to attain the therapeutic goals of SBP between 100 and 120, mean arterial pressure between 60 and 75 mm Hg, and HR between 60 and 80 beats per minute [1,5,6,9]. In the absence of contraindications, all patients suspected of having aortic dissection should receive immediate intravenous treatment utilizing beta-blocking agents (eg, esmolol, metoprolol, or a mixed alpha- and beta-blocking agent such as labetalol) to control HR and contractility, in combination with vasodilators (usually sodium nitroprusside) administered to achieve blood pressure control [1,6,10-14]. Although therapies are continually evolving, with new approaches such as endovascular stenting, emergent surgical intervention is typically indicated in Stanford type A (ie, ascending) dissections, whereas Stanford type B (ie, descending-only) dissections tend to be medically managed [1,6,15]. Importantly, in either case, the early benefits of hemodynamic therapy are clear. In fact, the benefits of early provision of critical hemodynamic therapy are sufficiently established that this study used the provision of such therapy as a surrogate endpoint for assessing quality of care. Thus, this study was not designed, powered, or focused on determining whether provision of effective hemodynamic therapy had salutary effects on patient outcome; we believe this question has already been sufficiently answered in previous literature. Although much has been published regarding establishing the diagnosis of aortic dissection (eg, optimal imaging techniques), the issue of adequacy of medical management of SAAD patients has received less attention. Because SAAD represents an urgent diagnosis with potential for increasing mortality rate with the passage of hours, early and aggressive provision of hemodynamic therapy is particularly important. The delays entailed in interfacility transport are not trivial: the current study found a time interval of 72 minutes between initial referral hospital request for BMF transport and ultimate patient arrival at the receiving center. Of course, this retrospective study could not assess the time lapse between referral hospital suspicion of aortic dissection and request for BMF transport. Regardless, it is clear that the typical transport involves
27
time delays that can place the patient at potentially grave risk if hemodynamic therapy is not properly instituted before patient arrival at the receiving hospital. With the ever-increasing regionalization of critical care and associated transport services, the issue of pretertiary care center hemodynamic therapy of patients with SAAD is likely to arise even more frequently in the near future. The current study identified potentially serious lapses in referral hospital hemodynamic care for patients with SAAD. The suboptimal SAAD therapy at referral hospitals translated into an opportunity for vital medical intervention by the study critical care service; such intervention was often provided, but like the referral hospital care, BMF provision of hemodynamic therapy was characterized by room for improvement. The HR data are subject to difficulties in retrospective assessment, because HR therapy in SAAD is aimed both at treating the HR and preventing reflex tachycardia associated with vasodilator therapy. Even considering this limitation, it is difficult to conceive of an acceptable explanation for the fact that the initial BMF-recorded HR at referral hospitals exceeded the study’s liberal cutoff (of 80) in 42% of cases. None of the patients who did not receive beta-blockade had contraindications (eg, congestive heart failure or heart block). In fact, of the patients whose initial BMF-recorded pretransport HR was less than the cutoff of 80, in nearly two thirds of cases, the HR was within the acceptable range without benefit of any beta-blocker therapy at the referral hospital. Although the fact that the HR went untreated in most patients has important implications for therapeutic dP/ dt considerations (minimization of rate of change in pressure), the HR data in this study were perhaps most important as a corollary finding to infrequent referral hospital provision of SBP therapy. As was the case with HR therapy results, referral hospital SBP treatment data revealed that appropriate medication was provided in a surprisingly low proportion of patients. This was especially noteworthy considering the generous cutoff (120) used to define the SBP treatment threshold. Even if the technical capabilities of referral hospitals did not allow for nitroprusside infusion (eg, inability to place indwelling arterial lines), the assessment for referral hospital SBP treatment included therapy with any agent (other than analgesics) that could lower SBP. Thus, the finding that SBP exceeded the treatment threshold in more than two thirds of cases—not to mention the fact that SBPs ranged as high as 212 in untreated patients—represents an area of potentially substantial improvement in care. Even when patients were treated with antihypertensive therapy at the referral hospital, the SBP remained above the treatment threshold in more than half of the cases. As with the findings for the HR, even when the initial BMF arrival SBP was below the treatment threshold, this had usually occurred (in 70% of cases) without the benefit of antihypertensive therapy administered at the referral hospital.
28 Thus, the patterns for referral hospital treatment of HR and SBP were similar. Abnormalities in the hemodynamic parameters were present at an alarming rate upon BMF arrival at the referral hospital; even when patients had been treated, titration to commonly accepted hemodynamic endpoints had frequently been insufficient. Furthermore, when patients’ hemodynamic parameters were within the target ranges, this tended to have occurred in the absence of therapy, rather than as a result of referral hospital pharmacological intervention. Interestingly, hemodynamic therapy by the referring hospitals tended to produce median HR and SBP (upon BMF arrival at referring hospitals) that were essentially the same as those in untreated patients. Whether this represents inadequate therapy, resistance to therapy (eg, from anxiety-mediated tachycardia refractory to beta-blockade) or some other shortcoming will have to be addressed in a prospective analysis that can control for more factors than those accounted for in our study. After the referral hospital phase of hemodynamic therapy, the study focused upon the interventions provided by the critical care transport service providing interfacility transport. Even when hemodynamic therapy had been started at the referral hospital, the critical care transport crews needed to be familiar with principles for titration of such therapy: in nearly half of the transports, BMF crews titrated HR, antihypertensive therapy, or both therapies. In addition, the crews instituted beta-blocker therapy for HR in over a third of patients transported, and antihypertensive therapy was begun in a similar proportion of transports. The effectiveness of HR therapy as titrated, and as instituted by BMF, was reflected partially by the intratransport drop in HR, and perhaps more importantly, by the fact that the intratransport improvement in SBP control was not associated with reflex tachycardia. The critical care transport service’s main effect on hemodynamics was the reduction of SBP, in both the overall patient population, and most importantly, in the subgroup in whom the initial BMF SBP exceeded the treatment threshold value of 120. Considering the mean transport time of about 30 minutes, the average intratransport SBP drop of 23 represented appropriately aggressive therapy. However, room for improvement in intratransport SBP management was indicated by the findings that the posttransport average SBP remained higher than the target range, and that two thirds of patients still had SBP over the target range at the end of transport. Interpretation of the study’s results is subject to limitations of the design. Most importantly, a retrospective study such as this one is inherently left with questions that cannot be answered. Although we relied upon data that were entered prospectively, in the manner dictated by BMF patient care protocols, the retrospective nature of the study meant that we were not able to assess why hemodynamic treatment was not instituted. We were also not able to track the hemodynamic data occurring at the referral hospital,
G. Winsor et al. other than the SBP and HR noted upon arrival of BMF at the referral institution. Furthermore, we were unable to assess the impact of nonhemodynamic medications, specifically analgesics, which would have been administered at the referring hospital and which could have clearly had salutary effects on both SBP and HR. In a retrospective study such as this, we were not able to assess the timing, dosage, or results of analgesics that were administered before BMF arrival at the referring hospitals. One potential explanation for referral hospital nonprovision of hemodynamic treatment is that patients were not thought to have sufficiently high chance of having the diagnosis of aortic dissection to warrant therapy. There are a number of reasons this argument is not likely to be true. First, patients in whom there was referral hospital advanced imaging—and associated diagnostic certainty—were no more likely to receive hemodynamic therapy than those in whom the pretransport diagnosis of SAAD was assigned based only on CXR. Second, patients in whom hemodynamic therapy was provided usually did not meet the target ranges for HR and SBP. Finally, it is reasonable to expect that hemodynamic therapy should be provided to any patient warranting resource-intensive interfacility transport for (expensive) SAAD workup at a tertiary care center. When considered with the finding that nontreated patients lacked contraindications to hemodynamic intervention, we conclude that the suboptimal SAAD therapy was not because of lack of indication, or presence of contraindication, to medical treatment. An additional limitation to the study is that we did not correlate hemodynamic intervention with outcome. Given the widespread acceptance of the principles of hemodynamic intervention, the multitude of factors (not easily tracked in a retrospective study) potentially affecting outcome, and the fact that aortic dissection was actually only present in a fourth of our study population, it was felt that the study endpoints of SBP and HR were of sufficient clinical import to serve as valuable outcome measures. Despite the limitations as noted above, the study’s results make a strong case for inadequacy of referral hospital intervention to manage SBP and HR in patients with SAAD. Limitations in meeting hemodynamic treatment objectives could be related to referral hospital staff education, time, and/or other resources required to initiate therapy before transport. In addition, although the study transport service often instituted or titrated therapy, and the results were generally positive with respect to BMF intervention, the results clearly left room for improvement. Limitations to achieving appropriate hemodynamic control in the transport environment could be related to the provider education or the time and resources (eg, arterial catheters) required to initiate and manage therapy, but as was the case with suboptimal referral hospital hemodynamic therapy, the frequency with which hemodynamic goals went unmet almost certainly indicates there is room for better patient care.
Inadequate hemodynamic management during interfacility transfer In fact, our transport service, in recognizing the scope of the problem and in considering the scope of the solution, has determined that BMF itself may be an important part of improving the care given patients with SAAD. For example, the transport program’s educational newsletter, which goes to all referral hospitals in our area, contains a detailed account of our study’s results and emphasizes the importance of improving SAAD at both the referral hospital and the transport phases. In addition, it is being stressed to the transport crew that the necessity for speed in preparing patients for transport does not obviate the importance for focusing on important details of hemodynamic care for SAAD patients. For some issues, such as stressing the need for arterial catheterization in patients likely to require nitroprusside, referring hospital interventions can occur whereas the transport vehicle is still en route to the patient and thus no time is lost. This and other issues relevant to proper pretransport SAAD care, as well as the ready availability of physician medical consultation from the transport service and/or receiving hospital personnel, is being added to the materials discussed at our program’s regular bpublic relationsQ visits to hospitals in our service area. Finally, BMF will work with receiving hospital physicians to disseminate our findings and educate them on the importance of explicitly discussing hemodynamic management with referring hospital physicians. To bclose the loop,Q we plan to repeat our study after these plans are implemented to see if our systemwide interventions have resulted in improvement in our region’s care for patients with SAAD. The bpostinterventionQ study will assess the endpoints of this study and will also incorporate the ability to prospectively assess parameters (eg, timing and results of analgesia provision), which were not easily measured in the current article.
5. Conclusion Appropriate pretransport SBP and HR control was infrequently achieved in patients with suspected aortic dissection undergoing interfacility transfer; this represents an area of potentially useful community hospital education. The inadequacy of referring institution hemodynamic therapy of SAAD creates an important opportunity for critical care transport service intervention in a time-critical
29
illness; our transport service frequently instituted such potentially lifesaving care, but just as was the case with referral hospital care, there was room for improvement in BMF care of these patients. Further study in our area will include reassessment of hemodynamic care for SAAD after appropriate educational efforts are undertaken. Other referring and receiving hospitals and critical care transport services may be well served to focus attention on the basic, yet crucial, patient intervention of hemodynamic therapy in the setting of possible aortic dissection.
References [1] Ankel F. Aortic dissection. In: Marx J, et al, editors. Rosen’s emergency medicine. 5th ed. St. Louis (Mo)7 Mosby; 2003. p. 1171 - 6. [2] Perez L, Wise L. A standardized treatment protocol for blood pressure management in transport patients with a reported diagnosis of acute aortic dissection or symptomatic aortic aneurysm. Air Med J 1999; 18:111 - 3. [3] Mitchell A, Tallon J. Air medical transport of suspected aortic emergencies. Air Med J 2002;21:34 - 7. [4] Mehta R, O’Gara P, Bossone E, et al. Acute type A aortic dissection in the elderly: clinical characteristics, management, and outcomes in the current era. J Am Coll Cardiol 2002;40:685 - 92. [5] Khan I, Nair C. Clinical, diagnostic and management perspectives of aortic dissection. Chest 2002;122:311 - 28. [6] Isselbacher E. Diseases of the aorta. In: Braunwald E, editor. Heart disease: a textbook of cardiovascular medicine. 6th ed. Philadelphia (Pa)7 WB Saunders; 2001. p. 1422 - 56. [7] Dmowski A, Carey M. Aortic dissection. Am J Emerg Med 1999;17: 372 - 5. [8] Rosman H, Patel S, Borzak S, et al. Quality of history taking in patients with aortic dissection. Chest 1998;114:793 - 5. [9] Frakes M. Esmolol: a unique drug with ED applications. J Emerg Nurs 2001;27:47 - 51. [10] Sullivan P, Wolfson A, Leckey R, et al. Diagnosis of acute thoracic aortic dissection in the emergency department. Am J Emerg Med 2000;18:46 - 50. [11] Finkelmeier B, Marolda D. Aortic dissection. J Cardiovasc Nurs 2001; 15:15 - 24. [12] Umana J, Lai D, Mitchell R, et al. Is medical therapy still the optimal treatment strategy for patients with acute type B aortic dissections? J Thorac Cardiovasc Surg 2002;124:896 - 910. [13] Varon J, Marik P. The diagnosis and management of hypertensive crisis. Chest 2000;118:214 - 27. [14] Karmy-Jones R, Aldea G, Boyle E. The continuing evolution in the management of thoracic aortic dissection. Chest 2000;117:1221 - 3. [15] Januzzi J, Sabatine M, Choi J, et al. Refractory systemic hypertension following type B aortic dissection. Am J Cardiol 2001;88:686 - 8.