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Tex Heart Inst J. 2007; 34(1): 41–46.
PMCID: PMC1847913

Acute Massive Pulmonary Embolism with Cardiopulmonary Resuscitation

Management and Results
Igor E. Konstantinov, MD, PhD, Pankaj Saxena, MCh, DNB, Miriam D. Koniuszko, MBBS, John Alvarez, MBBS, FRACS, and Mark A.J. Newman, MBBS, FRACS

Abstract

Patients who experience hemodynamic collapse after acute massive pulmonary embolism have a poor prognosis. Herein, we report our results with 8 patients and discuss a surgical strategy that can improve perioperative survival.

From August 1994 through May 2005, 8 consecutive patients (6 women, 2 men; age range, 27–68 yr) were urgently referred to our unit after experiencing hemodynamic collapse. All required cardiopulmonary resuscitation. Seven patients underwent pulmonary embolectomy. One patient was successfully treated with thrombolytic therapy alone under continuous monitoring by the surgical team.

There were 2 intraoperative deaths (30-day mortality rate, 28.5%). One survivor required a right ventricular assist device. Follow-up of the patients ranged from 8 months to 8 years. One patient died 8 months after the pulmonary embolectomy from long-term complications of cerebral damage that had occurred during preoperative resuscitation.

We conclude that prompt surgical management improves the early survival rates of patients who require cardiopulmonary resuscitation subsequent to massive pulmonary embolism.

Key words: Anticoagulants, cardiopulmonary bypass, cardiopulmonary resuscitation, echocardiography, transthoracic, hemodynamic processes, pulmonary artery/surgery, pulmonary embolism/complications/diagnosis/drug therapy/mortality/surgery, risk factors, thrombolytic therapy/contraindications, treatment outcome, ventricular dysfunction, right

Massive pulmonary embolism (PE) is a life-threatening condition. For clinical purposes, massive PE is defined as pulmonary embolism with either hemodynamic collapse or an occlusion of the pulmonary artery that exceeds 50% of its cross-sectional area.1–5 The overall mortality rate associated with massive PE remains at approximately 30%.6–8 If cardiopulmonary resuscitation (CPR) is required, mortality rates increase dramatically. Even in the modern era, operative deaths of patients with massive PE who require CPR may approach 75%.9 An overall mortality rate reported in the world literature is 57% for patients who require CPR, compared with 12% for those who do not.6,9–17 Herein, we present a retrospective review of the treatment and outcomes of 8 of our patients who required CPR consequent to hemodynamic collapse after massive PE.

Patients and Methods

Patients

From August 1994 through May 2005, 8 consecutive patients with suspected massive PE were referred to our cardiothoracic surgical unit after they had experienced hemodynamic collapse that required CPR. We retrospectively analyzed the patients' demographics, risk factors, methods of diagnosis, operative procedures, and postoperative morbidity and mortality rates (Table I).

Table thumbnail
TABLE I. Characteristics and Outcomes of Patients with Acute Massive Pulmonary Embolism

The average age of the patients was 45 years (range, 27–68 yr). Six patients (75%) were women. Five patients had no definitive diagnosis of massive PE before surgery, and the decision to operate on them was made on the basis of characteristic clinical scenarios. Seven of the 8 patients underwent emergency pulmonary embolectomy; one was successfully treated with thrombolytic therapy alone.

Surgical Technique

Heparin was administered to all patients during CPR upon arrival at the operating room. The heart was exposed through a median sternotomy. Mild hypothermia (32°C) was used. The ascending aorta and the right atrial appendage were cannulated for the institution of cardiopulmonary bypass (CPB). Subsequently, during total CPB, bicaval cannulation was achieved. A longitudinal incision made in the main pulmonary artery was extended into the left and right pulmonary arteries. The aorta was not cross-clamped in any patient during the procedure.

Desjardins forceps and Fogarty catheters (Edwards Lifesciences; Irvine, Calif) were used for clot removal. If the emboli extended into peripheral pulmonary arteries, a thoracoscope was also used, and CPB flow was reduced in order to better see the clots and remove them completely. The interventional radiologists placed an inferior vena caval (IVC) filter in all of the surviving patients within 24 hours of surgery.

Timing of Resuscitation

Five patients presented at our emergency department with ongoing CPR having been administered en route by paramedics; the other 3 patients experienced in-hospital cardiac arrest.

Patient 4 (Table I) was admitted with acute shortness of breath and palpitations. After ventilation–perfusion (V/Q) scanning, he was given heparin for anticoagulation. However, on the next day, he began to bleed from the upper gastrointestinal tract, so the heparin was discontinued. On the following day, he developed severe hypoxia that led to cardiac arrest; he was resuscitated and was referred for cardiothoracic surgery. He was urgently brought to the operating room with ongoing CPR. During surgery, multiple bilateral clots were found in his peripheral pulmonary arteries. The patient could not be weaned from CPB, and he died.

Patient 5 was transferred to our hospital with suspected pulmonary embolism. A V/Q scan showed a marked reduction of perfusion to the middle and lower lobes of the right lung, and to the lingula and lower lobe of the left lung. An IVC filter was placed. Heparin and warfarin were administered. Despite these measures, the patient's hypoxia worsened on day 4 of her hospital stay. A 2nd V/Q scan showed persistence of the previously noted defects and their extension into both upper lobes. The patient was taken to surgery and developed cardiac arrest on the operating table, requiring CPR. We removed the clots from her right pulmonary artery and left lobar branches, and she recovered.

A hepatic hydatid cyst was ruptured during its removal from Patient 7. This resulted in a complicated postoperative course with prolonged immobilization. On postoperative day 8, she developed severe hypoxia and hemodynamic collapse that required CPR. After endotracheal intubation and resuscitation, transthoracic echocardiography (TTE) showed severe right ventricular (RV) dilatation, and the patient underwent emergency thromboembolectomy. She survived.

Morbidity and Death

Patients 4 and 6 had no clots in their main, left, or right pulmonary arteries, but they had multiple clots in their peripheral arteries. Both patients died in the operating room of persistent hypoxia and severe RV failure upon discontinuation of CPB. Therefore, the operative death rate was 28.6% (2/7).

Patient 1 was discharged from the hospital. Unfortunately, she had severe hypoxic cerebral damage, and she died 8 months later.

Patient 2, who had a large thrombus in his main pulmonary artery (Fig. 1), developed severe RV failure. He required postoperative RV support with a Bio-Medicus® pump (Medtronic, Inc.; Minneapolis, Minn) and delayed sternal closure. On postoperative day 2, he was weaned from the pump and his chest was closed.

figure 10FF1
Fig. 1 Patient 2. A thrombus in the shape of the inferior vena caval bifurcation was retrieved from the pulmonary artery.

The overall postoperative hospital stay ranged from 8 to 77 days (mean, 24 days; median, 11 days).

Follow-Up

The follow-up periods of the 6 survivors ranged from 8 months to 8 years (mean, 50 mo), with 1 death (patient 1) at 8 months. All 6 patients were prescribed warfarin as an anticoagulant postoperatively for 6 months, and an IVC filter was placed in all. As of January 2007, all 5 surviving patients remained asymptomatic and were doing well.

Discussion

Three of our patients had severe RV dysfunction during the attempt to wean them from CPB support. In 1 patient, a very large thrombus (Fig. 1) was removed from the central pulmonary arteries. Despite severe RV dysfunction, his oxygenation improved considerably. Therefore, we believed that most of the obstruction was removed and that the RV failure was reversible. This patient was successfully supported with a RV assist device. In contrast, 2 other patients had no thrombi in their central pulmonary arteries, but they had multiple thrombi in the peripheral arteries, rendering complete surgical thrombectomy impossible. Furthermore, persistent severe hypoxia after weaning from CPB made successful recovery unlikely for these patients even if RV assist devices had been used. Both patients died in the operating room. Our operative mortality rate of 28.6% compares favorably with the previously reported mortality rates of patients with massive PE who required preoperative CPR.9 Very prompt transfer to the operating room and institution of CPB may explain our comparatively good results.

Five patients survived surgery. Unfortunately, one sustained hypoxic brain injury—despite witnessed cardiac arrest and in-hospital CPR—possibly from preoperative resuscitation that was inadequate because of complete pulmonary artery obstruction. Cardiac arrest occurred while the patient was recovering from a cesarean section in an obstetrics unit. Although this patient was transferred to a rehabilitation ward after discharge from the hospital, she never recovered normal neurocognitive function, and she died of pneumonia 8 months later.

Finally, 1 patient (Patient 8) was managed conservatively. She had experienced hemodynamic collapse at home while recuperating from orthopedic surgery, and she underwent CPR initially performed by a family member and then by paramedics en route to the hospital. She had recovered completely by the time she arrived at the hospital. A computed tomographic scan showed a large thrombus in the left pulmonary artery (Fig. 2A). We suspect that this thrombus was dislodged from the main pulmonary artery into the left pulmonary artery during CPR. This occurrence enabled unobstructed blood flow into the right lung, with consequent restoration of normal oxygen saturation and normal hemodynamics. The patient was admitted to the cardiothoracic surgical ward and was given reteplase. Two days later, a computed tomographic scan confirmed complete lysis of the thrombus (Fig. 2B). An IVC filter was placed, and the patient received warfarin as an anticoagulant.

figure 10FF2
Fig. 2 Patient 8. Computed tomographic scans of the chest show a massive pulmonary embolus A) before thrombolysis and B) after the resolution of the thrombus.

Pulmonary embolism is an important cause of morbidity and death worldwide.18–20 Furthermore, the risk of death is dramatically higher in those patients who require CPR because of massive PE. Cardiac arrest increases mortality rates after massive PE by 3 to 7 times.21 This trend is well documented in the surgical literature.9,22 For instance, in a 2005 report of 11 patients who underwent pulmonary embolectomy for acute massive PE, the mortality rate in those who received preoperative CPR was 75% (3 of 4 patients). In contrast, all of the patients who did not require preoperative CPR survived the operation. Imaging was performed on all patients before surgery.9

Similarly, Leacche and colleagues22 reported an overall operative mortality rate of only 6% in their series of 47 patients with massive PE. However, in 6 (11%) of their patients who required CPR before surgery, operative death was substantially higher. Two of the 6 patients (33%) died during surgery.

About two thirds of patients with fatal PE develop cardiac arrest within 1 to 2 hours after the clinical presentation.1,23 Therefore, rapid attendance by cardiothoracic surgeons appears to be crucial to successful outcomes. In our study, the definitive diagnosis of PE was not established in 5 of the 8 patients (62.5%) (patients 1, 2, 3, 6, and 7).

It should be emphasized that massive PE is a clinical diagnosis. A combination of jugular venous distention, low oxygen saturation, recent surgery with a period of immobilization, and clear bilateral lung sounds with no pneumothoraces makes massive PE the most likely differential diagnosis. If a patient's condition permits, we perform further evaluation; however, hemodynamic collapse with ongoing CPR makes further imaging impractical or impossible. Therefore, a high index of suspicion combined with rapid deterioration necessitates emergency surgery.

Three of our 5 patients had undergone recent surgery with a period of immobilization, and TTE performed on 2 of these 3 showed severe RV dilatation with ventricular septal deviation, an underfilled left ventricle, and no pericardial effusion. The 2 other patients were being treated for deep venous thrombosis; one of them (Patient 2) also had testicular cancer and a large IVC thrombus diagnosed by ultrasonography. Although transesophageal echocardiography (TEE) can be very helpful as a diagnostic tool in stable patients, none of our patients was sufficiently stable immediately after CPR for placement of a TEE probe. Sudden deterioration followed by cardiac arrest strongly suggested massive PE. In each of these cases, the decision to operate was made very early during the event, which we believe partially explains the better outcomes in our patients. It is known that attempts to stabilize a critically ill patient who has massive PE are often frustrating, and the patient's condition deteriorates during this time. Prompt surgical intervention with CPB can be life-saving.

On rare occasions, massive PE may be misdiagnosed despite a very typical clinical presentation. For instance, we recently encountered a patient with a very typical clinical picture of massive PE 2 weeks postpartum. Ongoing CPR and persistently low oxygen saturation despite massive inotropic support made further evaluation impossible. Her hemodynamic instability was life-threatening; therefore, she was taken to the operating room as a last resort, with a presumed diagnosis of massive PE. No embolism was found, and the patient died. The autopsy showed no cause of death. It is possible that she had acute viral myocarditis superimposed on postpartum heart failure with sudden and dramatic hemodynamic collapse.

Acute dilatation of the RV with accompanying ischemia leads to RV dysfunction. Right ventricular dilatation and hypokinesia are associated with higher death rates and an increased risk of recurrent PE.24 Prompt institution of CPB is crucial—it provides immediate circulatory support and enables surgeons to use the best method for removing mechanical obstructions from the pulmonary arteries. We prefer sternotomy with aortic and right atrial cannulation for the following reasons. Foremost, patients with massive PE may have residual IVC, iliac, or femoral venous clots, which make femoral venous cannulation difficult and venous return through a small cannula ineffective. Second, midline sternotomy provides very fast access, which speeds the establishment of CPB. We believe that this approach is faster than cannulation of the femoral vessels in obese patients. Five of our patients were obese. Femoral cannulation in those patients would have necessitated placement of a small femoral venous cannula that inevitably would have impeded venous return. Third, we learned from treating the very 1st patient in our series that standard closed-chest CPR can be ineffective in a patient with massive PE, despite cardiac arrest witnessed in the hospital and immediate, uninterrupted CPR delivered by a qualified team. A very large embolus completely occluded this patient's pulmonary artery, making closed-chest CPR ineffective. In addition, we believe that avoiding global myocardial ischemia and maintaining good myocardial perfusion throughout the procedure is important for a successful outcome.

Conclusion

Massive pulmonary embolism is a difficult clinical entity to treat, because even standard CPR is highly unlikely to be successful in the case of mechanical obstruction to blood flow with severe hypoxia. Prompt surgical management can save some of the patients who require CPR after massive PE and associated hemodynamic collapse.

The absence of thromboemboli within the main pulmonary artery in combination with the presence of multiple peripheral thrombi is a bad prognostic sign. On rare occasions, a selected patient with this condition can be treated conservatively with thrombolytic therapy. We highly recommend, however, that the thrombolysis be given in the cardiothoracic surgical unit under the continuous monitoring of a qualified team, in case the need for emergency surgery arises.

Editorial Commentary

This report of 6 successful results of pulmonary embolectomy reveals the evolving aggressive surgical treatment of a highly fatal vascular complication and disease. Emergency treatment using cardiopulmonary bypass has replaced the early techniques suggested by Trendelenburg a century ago. Few patients survived those heroic efforts.

In 1961, we reported the 1st use of cardiopulmonary bypass for acute massive pulmonary embolism.1 Since then, surgical treatment of this disease has improved greatly. Often, the emboli have migrated out of the main pulmonary artery and have lodged peripherally. Opening both pleural spaces permits manual compression of both lungs to dislodge the emboli. The authors used a thoracoscope to ensure the completeness of the removal.

Thrombolytic agents are currently used in less desperate situations, but treatment should be monitored constantly and abandoned if circulatory collapse threatens. Diagnosis of pulmonary embolism is enhanced by noninvasive ultrasonography and other techniques, but awareness of physical findings is still essential.

Denton A. Cooley, MD, President
Texas Heart Institute at St. Luke's Episcopal Hospital, Houston

Reference

1. Cooley DA, Beall AC Jr, Alexander JK. Acute massive pulmonary embolism. Successful surgical treatment using temporary cardiopulmonary bypass. JAMA 1961;177:283–6. [PubMed]

Footnotes

Address for reprints: Igor E. Konstantinov, MD, Department of Cardiothoracic Surgery, Sir Charles Gairdner Hospital, Hospital Avenue, Nedlands, Perth, WA 6009, Australia. E-mail: igorkonst/at/hotmail.com

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