08644

2013

AOPXXX10.1177/1060028013508644Prom et alProm et al

Case Report

Successful Alteplase Bolus Administration for a Presumed Massive Pulmonary Embolism During Cardiopulmonary Resuscitation

Annals of Pharmacotherapy 47(12) 1730­–1735 © The Author(s) 2013 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/1060028013508644 aop.sagepub.com

Rathasen Prom, PharmD1, Ryan Dull, PharmD, BCPS2, and Bethany Delk, PharmD, BCPS, CPP1

Abstract Objective: To describe the case of a patient successfully resuscitated with bolus alteplase for a presumed massive pulmonary embolism (PE) with associated cardiac arrest. Case Summary: A 54-year-old man presented to the emergency department for evaluation of syncope following recent open reduction and internal fixation of his ankle. On arrival, his condition rapidly deteriorated and progressed to cardiopulmonary arrest. Because of noncompliance with postoperative thromboprophylaxis, there was high suspicion for PE. Following 40 minutes of advanced cardiac life support, empirical alteplase 50 mg was administered intravenously over 2 minutes with return of spontaneous circulation (ROSC) observed 6 minutes later. The diagnosis of PE using computed tomographic angiography was confirmed after fibrinolytic therapy. Although his hospital course was complicated by a gastrointestinal bleed requiring transfusion, he was discharged neurologically intact. Discussion: Clinical guidelines recommend fibrinolytic therapy for patients with PE and cardiac arrest. Data from retrospective analyses, case series, and case reports suggest that various fibrinolytic regimens may facilitate ROSC and improve neurologically intact survival without an increased risk of fatal hemorrhage. Conclusion: The choice of fibrinolytic therapy should be based on hospital availability, with prompt initiation of treatment and incorporation of an intravenous bolus. A reasonable treatment regimen is alteplase 0.6 mg/kg (maximum of 50 mg) or fixed dose of alteplase 50 mg given over 2 to 15 minutes. Resuscitation should be continued for at least 30 minutes, or until ROSC, after fibrinolytic initiation to allow time for the medication to work. Keywords fibrinolysis, thrombolysis, rtPA, alteplase, streptokinase, urokinase, tenecteplase, reteplase, pulmonary embolism, arrest, resuscitation

Introduction Pulmonary embolism (PE) represents a spectrum of clinical manifestations with varying health outcomes. Acute PE is the primary cause of mortality in patients with venous thromboembolism and is a common cause of sudden death, with nearly all cases of cardiac arrest occurring within 2 hours of symptom onset.1-3 Acute PE produces cardiac arrest in 41% of cases and is associated with a high mortality rate.3,4 The potential for sudden and fatal deterioration highlights the need for a prompt diagnosis and appropriate intervention. However, many patients with PE have no complaints or report symptoms with a broad differential such as dyspnea, chest pain, or syncope, which makes a rapid and

accurate diagnosis difficult to establish.5 Despite advances in the tools used to identify PE, the diagnosis is often not made, and it continues to pose a challenge to clinicians.6 Clinical features associated with acute PE, such as blood pressure and right ventricular (RV) function, are used to distinguish between massive and submassive subtypes.7 Submassive PE is characterized by RV dysfunction in the 1

Mission Hospitals, Asheville, NC, USA Creighton University, Omaha, NE, USA

2

Corresponding Author: Rathasen Prom, Mission Hospitals, 509 Biltmore Avenue, Asheville, NC 28806, USA. Email: [email protected]

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Prom et al presence of hemodynamic stability. In contrast, massive PE is defined by sustained hypotension and is associated with a high risk for mortality. The hemodynamic response to PE is dependent on thrombus size, cardiopulmonary reserve, and neurohumoral effects.8 In patients with acute PE, obstruction of blood flow causes an increase in RV afterload, leading to dilation, hypokinesis, tricuspid regurgitation, interventricular septal deviation, and ultimately ventricular failure. Septal deviation impairs left ventricular filling and end-diastolic volume, which may cause reduced cardiac output, cardiogenic shock, and cardiac arrest. The most common rhythm present on initial presentation of cardiac arrest caused by acute PE is pulseless electrical activity (PEA).3,4 Although external cardiac massage may be effective in achieving return of spontaneous circulation (ROSC) in patients with cardiac arrest and suspected or proven PE, many patients will require aggressive measures such as systemic fibrinolysis, pharmacomechanical catheter-directed therapy, or surgical pulmonary embolectomy. Among these interventions, fibrinolysis offers many useful practical features, including rapid onset of action, ease of administration, and ready availability in most hospital settings. In patients with cardiac arrest and strongly suspected or proven PE, the use of fibrinolytics during cardiopulmonary resuscitation (CPR) may improve survival.9 Clinical practice guidelines recommend fibrinolytic therapy for patients with massive PE and cardiac arrest, although few data are available to guide decisions regarding the agent, dose, rate, and frequency of administration.9,10 The purpose of this report is to describe successful bolus administration of alteplase during CPR for a presumed massive PE with associated cardiac arrest and to provide a review of the current literature.

Case Report A 54-year-old, 92-kg, white man (BMI = 25.9) presented to the emergency department (ED) for a syncopal episode, fall, and possible seizure. He had recently sustained a crush injury to his ankle necessitating open reduction and internal fixation 3 weeks prior. He was prescribed enoxaparin and warfarin for postoperative venous thromboembolism prevention, but his family reported that he had not taken a dose in weeks. He did not have other health issues and was not taking other medications. By the paramedic’s report, he was pale and diaphoretic with a systolic blood pressure of 70 mm Hg over palpation and a heart rate of 140 beats/min when the ambulance arrived at the patient’s house. Prehospital therapy was limited to intravenous normal saline. On arrival to the ED, he became unresponsive without a palpable pulse (t = 0 minutes). The cardiac monitor revealed PEA and advanced cardiac life support was initiated. The initial resuscitation included CPR, endotracheal intubation,

five 1 mg doses of epinephrine, three 1 mg doses of atropine, normal saline, and a norepinephrine infusion titrated to 20 µg/min. Within 3 minutes (t = 21 minutes) of receiving his third dose of atropine and fifth dose of epinephrine, a pulse was palpated, with a heart rate of 74 beats/min and a blood pressure of 152/125 mm Hg. This ROSC was sustained for 7 minutes, when PEA recurred (t = 28 minutes), and resuscitation was resumed. At that time, a 1 mg dose of epinephrine was administered, and the norepinephrine infusion was titrated to 30 µg/min. Five minutes later (t = 33 minutes), a transient pulse was detected with a heart rate of 113 beats/min, a blood pressure of 120/92 mm Hg, SpO2 80%, pH 6.993, pCO2 70.2, and pO2 15.6; however, hypotension and subsequent PEA recurred once again and CPR was resumed. Over the following 8 minutes, a pulse was palpated intermittently, but this was never sustained for longer than 3 minutes; CPR was ongoing, and two 1 mg doses of epinephrine were given during this time. Because of the patient’s history of recent orthopedic surgery and noncompliance with postoperative anticoagulation, there was a high clinical suspicion for a massive PE. Also, because the patient was hemodynamically unstable, he was unable to receive a confirmatory computed tomography (CT) angiogram prior to a therapeutic intervention. At t = 42 minutes into the overall resuscitation time, a single 50 mg fixed bolus of alteplase was administered intravenously via a peripheral line over 2 minutes; approximately 6 minutes later (t = 48 minutes), a sustained palpable pulse was observed. Physical exam at this time revealed a heart rate of 113 beats/min, blood pressure 55/12 mm Hg, and SpO2 97%. Then, 4 minutes later (t = 52 minutes), the patient was deemed to be more stable by the medical staff and received a chest CT angiogram, which revealed extensive bilateral PEs involving the main pulmonary arteries bilaterally, right heart strain, and bilateral infiltrates thought to represent hemorrhage, infarcts, atelectasis, and even possibly pneumonia. An echocardiogram was not performed at this time. Shortly after the CT scan (t = 59 minutes), the patient experienced another hypotensive episode with subsequent PEA necessitating a brief period of CPR. This occurred once again almost 2 hours later (t = 248 minutes), at which time CPR was performed; additionally, two 50 mEq doses of sodium bicarbonate and one 1 mg dose of epinephrine were administered, and an epinephrine infusion was started at 5 µg/min. Initial postresuscitation neurological exam revealed a Glasgow Coma Score of 4T and extensor posturing to deep painful stimulation. In addition, the patient experienced a lower gastrointestinal bleed shortly after alteplase administration, for which 2 units of packed red blood cells were given; he did not develop surgical site bleeding. A baseline hemoglobin level was not obtained, but the hemoglobin level 3 hours after alteplase administration and bleeding

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event was 11.0; a heparin drip was not started for this reason. He was subsequently transferred to the intensive care unit. On hospital day 2, a lower-extremity ultrasound revealed a small deep-vein thrombosis in a gastrocnemius vein, and an inferior vena cava filter was placed the following day. An echocardiogram performed on day 3 demonstrated a left ventricular ejection fraction of 45% to 50% with severely reduced RV function. He was extubated on day 3, and vasopressors were weaned off by day 4. The patient was hospitalized for 14 days, after which he was transferred to an inpatient rehabilitation center without any neurological sequelae. He was not discharged on anticoagulant therapy because of the lower gastrointestinal bleed.

Discussion The management approach to patients who present with acute PE is tailored according to the PE subtype (low-risk, submassive, and massive) based on risk for adverse shortterm outcomes, clinical characteristics, bleeding risk, and presence of contraindications.7 Whereas those with low-risk PE can be adequately treated with therapeutic anticoagulation alone and certain individuals with submassive PE may benefit from adjunctive fibrinolytics, patients with massive PE should be considered for aggressive therapy to reduce the risk of short-term mortality.10-12 This is especially true in the setting of acute PE complicated by cardiac arrest, a finding associated with up to a 95% mortality rate.3 Of the available treatment options, which include fibrinolysis, pharmacomechanical catheter-directed therapy, or surgical pulmonary embolectomy, fibrinolysis is often the most practical choice. It displays a rapid onset of action, can be administered easily and during CPR, is available in most hospital settings, and has reported efficacy in PE-associated cardiac arrests.3,4,13-38 Fibrinolytic therapy, however, is still not widely used for PE-associated cardiac arrests; it has classically been contraindicated because of a concern for life-threatening bleeding and lack of quality evidence demonstrating efficacy.39 Additionally, when it is considered, it is often as a last resort.23 An English language literature search was performed with MEDLINE/PubMed from January 1986 to September 2013 using the search terms fibrinolysis, thrombolysis, rtPA, alteplase, streptokinase, urokinase, tenecteplase, reteplase, pulmonary embolism, arrest, and resuscitation to identify relevant articles. References of the retrieved articles were also assessed to identify other important articles. The American Heart Association advanced cardiac life support guidelines recommend against the routine administration of fibrinolytics in undifferentiated cardiac arrests, given the lack of efficacy and higher risk of bleeding in such situations.9 However, when an acute PE is

highly suspected or proven, the guidelines state that it is reasonable to administer fibrinolytics.9 No randomized trial has evaluated the efficacy and safety of fibrinolysis in PE-associated cardiac arrest, and cardiac arrest patients have been excluded from randomized studies of fibrinolysis in acute PE. The guidelines’ recommendations are based on evidence from retrospective analyses, case series, and case reports, where fibrinolysis appeared to increase chances of ROSC and improve survival in PE-associated cardiac arrest.3,4,13-38 In two retrospective analyses that included both a fibrinolysis and control group, ROSC was more frequently achieved in those who received fibrinolytics (range = 67%-81%) compared with those who did not receive such therapy (43%).4,30 Although the use of fibrinolytics also yielded a nonsignificantly lower mortality rate (81% vs 93%; P = .15) in one of those studies (n = 66), the mortality rate was similar between those who received and those who did not receive fibrinolysis (90% vs 95%; P > .99) in the other analysis (n = 42).4,30 A thorough review of retrospective analyses and case series involving PE-associated cardiac arrest patients revealed varying mortality rates ranging from 22% to 90% with the use of fibrinolytics.4,20,23,30,36 Fibrinolysis may be effective even in cases of prolonged CPR and delayed administration (15 to 60 minutes from the start of CPR).14,16,19,20,33,37 A retrospective analysis by Er et al, however, showed that PE-associated cardiac arrest patients who achieved ROSC and survived to hospital discharge received fibrinolytics significantly sooner than those who did not have ROSC (13.6 minutes vs 24.6 minutes; P < .001) and those who did not survive to hospital discharge (11 minutes vs 22.5 minutes; P < .001), respectively.23 One reason that has been cited for not administering fibrinolytics for PE-associated cardiac arrest is expected neurological damage following prolonged CPR.4 Use of fibrinolytics during CPR, however, may help preserve neurological function in PE-associated cardiac arrest survivors.3 Published cases revealed good or intact neurological status for the majority of survivors, even in cases of prolonged CPR up to 90 minutes and delayed fibrinolytic administration up to 60 minutes.4,14,15,18-21,23-25,27-29,33,35,37 These findings are consistent with experimental studies that showed that fibrinolytics may reduce the cerebral no-reflow phenomenon and improve microcirculatory reperfusion.40,41 The occurrence of major bleeding complications (total, intracranial, and fatal) is a serious concern of fibrinolysis during CPR. Because performing external cardiac massage may cause injuries to the abdominal and thoracic cavities, use of fibrinolysis had previously been contraindicated during previous, ongoing, or prolonged (>10 minutes) CPR for fear that such treatment may exacerbate or produce life-threatening hemorrhage in those areas.14,19,20,23,30 Retrospective analyses of patients with PE- or myocardial infarction– associated cardiac arrests have related fibrinolysis with a nonsignificant 2.5-fold increased risk of total major

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Prom et al bleeding, with no association between the duration of CPR (10 minutes) and bleeding.30,42 In prospective studies of undifferentiated cardiac arrest patients receiving CPR, fibrinolysis was not associated with an excess risk of nonintracranial major bleeding; intracranial bleeding, however, was more frequent in patients who received fibrinolysis compared with placebo.43-45 There does not appear to be a heightened risk of fatal bleeding when fibrinolysis is used during CPR.3 The risk of bleeding may be increased in patients receiving an oral or injectable anticoagulant (besides intravenous unfractionated heparin) prior to cardiac arrest and fibrinolytic administration. There is currently no published experience with the new targetspecific oral anticoagulants and vitamin K antagonists, whereas limited data exist with prophylactic and therapeutic doses of low-molecular-weight heparin.18,19,21,22,32,46 Alteplase is the only FDA-approved tissue plasminogen activator for PE and is the most commonly used and investigated agent.10 The FDA-approved regimen is an infusion of 100 mg over 2 hours. In the setting of cardiac arrest, however, the ability to administer alteplase as a bolus is attractive, given that CPR will likely not be continued for the duration of the 2 hour alteplase infusion in cases where ROSC has not been obtained. One alteplase dose that has been evaluated and compared with the FDA-approved 100 mg over 2 hours regimen is 0.6 mg/kg (maximum 50 mg) bolus dose given over 2 to 15 minutes.47-49 In a randomized, double-blind, double-dummy trial in hemodynamically stable PE patients, the incidence of death or recurrent PE and death was similar between patients assigned to a 0.6 mg/kg bolus dose and to 100 mg over 2 hours.48 Follow-up assessments of RV function (3 hours; 20-28 hours), lung perfusion scan scores (20-28 hours), and qualitative and quantitative angiographic exams were also comparable between the 2 groups.48 In another randomized, multicenter, double-blind trial in angiographically documented acute massive PE patients, decreases in total pulmonary resistance (30 minutes; 1 hour; 12 hours) and mean pulmonary artery pressure (1 hour; 12 hours), increases in cardiac index (1 hour; 12 hours), and improvements in lung perfusion defect were also similar between patients who received 0.6 mg/kg (maximum 50 mg) bolus and 100 mg over 2 hours.49 Rates of major and other important bleeding were comparable between patients in each treatment group.48,49 The most recent American College of Chest Physician guidelines state that bolus administration is indicated in PE-associated cardiac arrest.10 Various alteplase dosing schemes have been used successfully in the literature in PE-associated cardiac arrest while receiving CPR. Many cases used some form of bolus dosing, including giving a single bolus of 50 mg, 100 mg, or 0.6 to 1 mg/kg (maximum dose of 100 mg) or a double bolus of 50 mg (total 100 mg) separated by15 to 30 minutes.4,18-21,30 Alternatively, regimens that involved administering a 10 mg to 25 mg initial bolus followed by a 1 to

2 hour infusion to provide a total dose of about 90 to 110 mg have also been implemented.4,13-16,24 Even though most regimens included a bolus, an infusion of 100 mg over 2 to 3 hours has also been used successfully.22,36 Despite the apparent differences in these dosing strategies, times to ROSC were similar among the groups and ranged from 3 minutes to 35 minutes but sometimes took as long as 90 minutes.4,13-16,18-22,24,30,36 Because of a lack of head-tohead comparisons, it is not known which regimen has the most favorable efficacy-to-safety profile. Prompt initiation of therapeutic anticoagulation is recommended in patients who present with acute PE in the absence of cardiac arrest.7 In situations where fibrinolytic therapy is considered, an intravenous unfractionated heparin infusion is the preferred anticoagulant because it may be easily reversed in the event of major bleeding.50 The heparin infusion may either be temporarily suspended or continued during fibrinolytic administration; the efficacy and safety of either strategy as compared with the other is unknown, however, and the FDA recommends withholding heparin administration during the FDA-approved 2 hour alteplase infusion.10,50 There is currently no consensus or recommendation regarding the anticoagulation approach in PE-associated cardiac arrest where fibrinolysis is used. Many strategies have been used in case reports, case series, and retrospective analyses, including initiating heparin with or without a bolus around the time of fibrinolytic commencement or starting the heparin infusion toward or at the end of the fibrinolytic administration.4,14,15,18,21,24,27,30 A reasonable approach could be to start or resume heparin without a bolus at the end of the fibrinolytic infusion and after the activated partial thromboplastin time is less than 80 seconds, regardless of whether a heparin bolus was given prior to fibrinolytic administration.49 In the event of major bleeding, the heparin infusion should be discontinued; additionally, protamine may be considered to reverse the effects of heparin.50 There is also evidence supporting the use of other fibrinolytics in PE-associated cardiac arrests. Streptokinase, urokinase, tenecteplase, and reteplase have successfully resuscitated patients in such situations.25-29,33,36 Streptokinase and urokinase, like alteplase, are both FDA approved for treating acute PE and are typically infused over 12 to 24 hours; however, bolus administration was used in the PE-associated cardiac arrest cases.7,38 Tenecteplase and reteplase, in contrast, do not carry an FDA-indication for but have been investigated in acute PE.51,52 Tenecteplase 0.5 mg/kg bolus injection has led to improvements in RV function in hemodynamically stable PE patients, whereas reteplase has shown efficacy and safety comparable to that of alteplase 100 mg over 2 hours in acute massive PE when administered as two boluses of 10 units (total 20 units) given 30 minutes apart.51,52 Both tenecteplase and reteplase may be administered quickly, with adminis­ tration times being over 5 seconds and 2 minutes, respectively.53,54

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The overall evidence suggests that fibrinolysis may be beneficial in achieving ROSC, reducing mortality, and preserving neurological function in PE-associated cardiac arrest patients, even in cases of prolonged CPR and delayed fibrinolytic administration. This efficacy does not appear to be counterbalanced by an excess risk of fatal bleeding. The quality of the current literature, however, precludes any firm conclusions from being made. Because the majority of publications comprise case series and case reports (including our reported case), selective reporting of positive cases may exist, and the true amount of times when fibrinolysis was utilized unsuccessfully would be unknown. Despite limitations of current evidence, fibrinolytics should be strongly considered in patients who present with cardiac arrest and a confirmed or high suspicion for acute PE because of the high mortality risk. In the absence of such suspicion, fibrinolysis should not be routinely administered, given its lack of efficacy and higher bleeding risk in undifferentiated cardiac arrests. The fibrinolytic choice should be based on hospital availability, some type of bolus should be incorporated, and the treatment should be initiated as soon as possible to improve efficacy. A reasonable treatment regimen is a weight-based bolus dose of alteplase of 0.6 mg/kg (maximum of 50 mg) or fixed dose of alteplase 50 mg given over 2 to 15 minutes because of efficacy and safety comparable to that of the FDA-approved regimen of alteplase 100 mg over 2 hours in patients with acute hemodynamically stable or angiographically massive PE. Resuscitation should be continued for at least 30 minutes, or until ROSC, after fibrinolytic initiation to allow adequate time for the medication to work. In patients who achieve ROSC without the use of a fibrinolytic and diagnostic testing confirms an acute PE, we favor using the FDA-approved regimen of alteplase 100 mg over 2 hours. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.

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37. Landy C, Plancade D, Gagnon N, et al. Complication of intraosseous administration of systemic fibrinolysis for a massive pulmonary embolism with cardiac arrest. Resuscitation. 2012;83:e149-e150. 38. Zhu T, Pan K, Shu Q. Successful resuscitation with thrombolysis of a presumed fulminant pulmonary embolism during cardiac arrest. Am J Emerg Med. 2013;31:453 e1-e3. 39. Spohr F, Bottiger BW. Safety of thrombolysis during cardiopulmonary resuscitation. Drug Saf. 2003;26:367-379. 40. Fischer M, Bottiger BW, Popov-Cenic S, et al. Thrombolysis using plasminogen activator and heparin reduces cerebral noreflow after resuscitation from cardiac arrest: an experimental study in the cat. Intensive Care Med. 1996;22:1214-1223. 41. Bottiger BW, Martin E. Thrombolytic therapy during cardiopulmonary resuscitation and the role of coagulation activation after cardiac arrest. Curr Opin Crit Care. 2001;7:176-183. 42. Kurkciyan I, Meron G, Sterz F, et al. Major bleeding complications after cardiopulmonary resuscitation: impact of thrombolytic treatment. J Intern Med. 2003;253:128-135. 43. Bottiger BW, Bode C, Kern S, et al. Efficacy and safety of thrombolytic therapy after initially unsuccessful cardiopulmonary resuscitation: a prospective clinical trial. Lancet. 2001;357:1583-1585. 44. Abu-Laban RB, Christenson JM, Innes GD, et al. Tissue plasminogen activator in cardiac arrest with pulseless electrical activity. N Engl J Med. 2002;346:1522-1528. 45. Bottiger BW, Arntz HR, Chamberlain DA, et al. Thrombolysis during resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 2008;359:2651-2662. 46. Hannig KE, Husted SE, Grove EL. Cardiac arrest caused by multiple recurrent pulmonary embolism. Case Rep Med. 2011;2011:425090. 47. Levine M, Hirsh J, Weitz J, et al. A randomized trial of a single bolus dosage regimen of recombinant tissue plasminogen activator in patients with acute pulmonary embolism. Chest. 1990;98:1473-1479. 48. Goldhaber SZ, Agnelli G, Levine MN. Reduced dose bolus alteplase vs conventional alteplase infusion for pulmonary embolism thrombolysis: an international multicenter randomized trial. The Bolus Alteplase Pulmonary Embolism Group. Chest. 1994;106:718-724. 49. Sors H, Pacouret G, Azarian R, et al. Hemodynamic effects of bolus vs 2-h infusion of alteplase in acute massive pulmonary embolism: a randomized controlled multicenter trial. Chest. 1994;106:712-717. 50. Piazza G, Goldhaber SZ. Fibrinolysis for acute pulmonary embolism. Vasc Med. 2010;15:419-428. 51. Becattini C, Agnelli G, Salvi A, et al. Bolus tenecteplase for right ventricle dysfunction in hemodynamically stable patients with pulmonary embolism. Thromb Res. 2010;125: e82-e86. 52. Tebbe U, Graf A, Kamke W, et al. Hemodynamic effects of double bolus reteplase versus alteplase infusion in massive pulmonary embolism. Am Heart J. 1999;138:39-44. 53. TNKase (tenecteplase) [product information]. San Francisco, CA: Genentech, Inc; 2011. 54. Retavase (reteplase) [product information]. Bedminster, NJ: EKR Therapeutics, Inc; 2009.

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Successful alteplase bolus administration for a presumed massive pulmonary embolism during cardiopulmonary resuscitation.

To describe the case of a patient successfully resuscitated with bolus alteplase for a presumed massive pulmonary embolism (PE) with associated cardia...
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