Pulmonary

Hemorrhage

During Cardiac Surgery

David N. Thrush, MD, and Diane Jeffries, MD

P

ULMONARY HEMORRHAGE rarely occurs in cardiac surgical patients, but it may be a life-threatening event when it does occur. The most frequent cause of intraoperative hemoptysis is catheter-induced perforation of the pulmonary artery (PA). Less frequently, pulmonary hemorrhage occurs in patients with chronic pulmonary hypertension, mitral valve disease, and in children with congenital anomalies. A hemorrhagic lung syndrome with bleeding from the pulmonary parenchyma has also been reported to occur during pulmonary embolectomy. Rarely is intraoperative hemorrhage severe and uncontrollable. Therefore, a patient is presented who had massive and uncontrollable hemorrhagic pulmonary edema immediately after discontinuation of cardiopulmonary bypass (CPB). CASE REPORT

An &year-old woman (weight 55 kg, height 155 cm) required coronary artery revascularization as a result of progressive chest pain and dyspnea on exertion over a period of more than 3 months. Although no previous myocardial infarction was documented, she had an episode of pulmonary edema 2 months earlier following a hysterectomy. Subsequently, cardiac catheterization showed severe atherosclerotic coronary artery disease with total occlusion of the left anterior descending coronary artery, subtotal occlusion of a large ramus vessel, and total occlusion of a large dominant right coronary artery. Mild mitral regurgitation, secondary to an ischemic papillary muscle, also was noted. PA pressure (PAP) was 35/13 mm Hg with a pulmonary capillary wedge pressure (PCWP) of 12 mm Hg. Although a V wave initially was not appreciated, after injection of contrast material, the PCWP increased to 30 mm Hg, and a 52 mm Hg V wave was observed. Thermodilution cardiac index (CI) was 2.8 Wminlm’ with an ejection fraction of 73%. The patient’s past medical history showed a recent episode of upper gastrointestinal bleeding, which required a 2-U blood transfusion prior to cardiac operation. However, no diagnostic procedures were performed to elucidate the etiology of the bleeding. At the time of operation, the patient’s medications included nitroglycerin paste, isosorbide dinitrate, and nifedipine. Physical examination showed a blood pressure of 120/54 mm Hg, a regular pulse rate of 84 beats/min, and a normal respiratory rate and pattern. Pulmonary auscultation showed minimal bibasilar rales. No murmur, S, gallop, or peripheral edema was noted. The remainder of the physical examination was unremarkable. Routine laboratory reports showed a hemoglobin of 10.3 g/dL and a hematocrit of 31%. Electrocardiographic interpretation noted a sinus rhythm with T wave inversion in leads III and AVF. A chest radiograph demonstrated a small right pleural effusion. Preanesthetic medication consisted of 3 mg of morphine sulfate and 0.3 mg of scopolamine, intramuscularly, 30 minutes prior to induction of anesthesia. A left radial arterial catheter, 16-gauge intravenous (IV), and a right internal jugular Oximetric PA catheter were inserted without difficulty. Initial PAP was 42/21 mm Hg with a PCWP of 18 mm Hg. An infusion of nitroglycerin (NTG) was begun to improve the patient’s hemodynamic profile. After she was transported from the preinduction area to the operating room, her PAP increased to 72/36 mm Hg with a PCWP of 32 mm Hg, without apparent cause. Increasing the NTG infusion and applying 100% 0, facilitated return of PAP to baseline levels. Preinduction CI was 2.5 L/min/m2. IV induction of general anesthesia was accomplished smoothly with 250 ug of sufentanil and 10 mg of vecuronium, titrated slowly over 10 minutes. Postinduction CI was Journalof Cardiothoracic and VascularAnesthesia,

2.4 L/mitt/m2 and SvO, was 89%. CPB was initiated without complications. Three aortocoronary artery bypass grafts were constructed with saphenous veins, total aortic cross-clamp time was 43 minutes, and initial CPB time was 70 minutes. During weaning from CPB bright red, frothy blood filled the endotracheal tube and breathing circuit. The pulmonary edema was so perfuse that it was impossible to ventilate the patient, and CPB was reinstituted. Rigid bronchoscopy was unsuccessful in determining the origin of the bleeding, which appeared to come from both right and left mainstem bronchi. Therefore, a left-sided double-lumen endotracheal tube was inserted. On multiple occasions, lOO-mL aliquots of blood were suctioned from both the left and right lungs. Eventually, the total amount of blood expelled from the lungs was approximately 2 L. Fiberoptic examination down both sides of the double-lumen tube showed diffuse bleeding from both bronchi. Hemoglobin concentration of the pulmonary edema fluid was 4.8 g/dL, with a corresponding systemic hemoglobin concentration of 7.8 g/dL. An intraoperative chest radiograph showed the PA catheter positioned in the main PA. Increments of 10, 20, and 30 cm H,O of positive end-expiratory pressure (PEEP) were added to the controlled ventilation pattern in an attempt to control the pulmonary hemorrhage. Bleeding subsided only when 30 cm II,0 of PEEP was applied. Rather suddenly at this point, a decrease in myocardial contractility and large amounts of air were noted in the saphenous vein grafts. Despite repeated evacuation of air from the vein grafts, air continued to accumulate. After meticulous inspection, no visible source of air entry into the heart was found. Weaning from CPB was unsuccessful, and the patient died. Gross examination of the lungs showed diffuse bilateral hemorrhage. Each lung was approximately three times heavier than normal. Even with thorough and extensive investigation, a PA rupture was not noted on autopsy. Microscopic examination demonstrated diffusely blood-filled alveoli with multiple areas of alveolar capillary disruption. DISCUSSION

Hemoptysis is a rare complication of CPB, and pulmonary hemorrhage occurs even more rarely. Bleeding from the lungs can occur following PA rupture, pulmonary embolus, amniotic fluid embolus, pulmonary hypertension, and as a consequence of severe congestive heart failure. The present patient had several risk factors that increased the likelihood of PA catheter-induced rupture, such as advanced age, pulmonary hypertension, and a possibility of PA catheter migration during CPB.L.2However, clinical and pathological evidence suggested that the diffuse bilateral bleeding was a fulminant hemorrhagic pulmonary edema, secondary to diffuse disruption of the alveoli-capillary membrane. Hormonal or vasoactive substances released during CPB could have caused such a phenomenon.

From the Department ofAnesthesiology,

University of South Florida

of Surgeq The Tampa General Hospital, Tampa, FL Address reprint requests to David N. Thrash, MD, Department of Anesthesiology, The Tampa General Hospital, PO Box 1289, Tampa, FL 33601. Copyright 0 1991 by W B. Saunders Company 1053-0770/9110504-0014$03.00/0 College of Medicine,

Vol5, No 4 (August), 1991: pp 377-378

and the Department

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THRUSH AND JEFFRIES

Once the presumptive diagnosis of hemorrhagic pulmonary edema was made, PEEP was instituted to control formation and/or egress of the edema. Although the hemorrhage was reduced significantly, air was soon noted in the coronary arteries and vein grafts and continued to appear in spite of repeated venting with a 25gauge needle. Cardiac function visibly deteriorated, and severe ST segment elevation was noted. Termination of CPB was not possible without extreme hypotension and a decrease in the SVO?. Systemic arterial air embolism has been associated with penetrating chest trauma, transthoracic needle lung biopsy, transbronchial lung biopsy, driving accidents, and cesarean section. Mechanical ventilation with PEEP rarely has been implicated as an etiologic factor.‘-’ Air can enter the venous circulation whenever the operative field is elevated above the heart and an open vessel exists. Large amounts of entrained air can cause a physical impediment to pulmonary outflow, car pulmonale, and cardiovascular collapse. When such an eventuality is expected, monitoring with a precordial Doppler, capnograph, and aspiration of central venous air may provide diagnostic evidence. Treatment includes head-down and left lateral decubitus positioning, aspiration of venous air, and vasoactive support. In the absence of a patent foramen ovale, systemic air embolization usually does not occur. In this case, all suture lines were secure, no holes were found in the heart or great vessels, and vascular pressures precluded atmospheric air entrainment. Air can enter the systemic arterial circulation by traversing the pulmonary capillary bed or by entering through a pulmonary arteriovenous shunt. The amount of air aspirated from the saphenous vein grafts was so large that it could not have traversed a normal pulmonary capillary

network, and a pulmonary arteriovenous shunt would have caused preoperative arterial hypoxemia, which was not noted. Finally, autopsy findings precluded a patent foramen ovale or another intracardiac right-to-left shunt as the source of air. Mechanical ventilation with PEEP rarely has been implicated as a cause of air embolism. Massive air embolization during positive-pressure ventilation is most often reported to occur in premature infants. However, the same phenomenon was reported in a 95year-old woman who developed massive air embolism as a result of positive-pressure ventilation during resuscitation for a spontaneous pneumothorax. Chest radiograph during the event demonstrated large amounts of air filling the right and left ventricles and great vesseis. Cardiac arrest was attributed to acute car pulmonale and/or air in the PA.’ Extremely high pulmonary venous pressures probably secondary to the ischemic mitral regurgitation and/or a distended left ventricle during CPB provided the need for the high airway pressure. It is believed that the high airway pressure required to maintain ventilation and inhibit egress of the massive pulmonary hemorrhage ultimately caused air to enter the pulmonary capillaries and veins. Air subsequently migrated through the heart and into the coronary arteries, causing left ventricular dysfunction and the inability to wean the patient from CPB. High ainvay pressures may cause pulmonary capillary air entrainment, especially if the alveolar capillary membrane is disrupted. Therefore, PEEP, which may be required to accomplish acceptable ventilation and oxygenation, should be limited to a level necessary to inhibit the pulmonary edema from tilling the airways.

REFERENCES

1. Carlson TA, Goldenberg IF, Murray PD, et al: Catheterinduced delayed recurrent pulmonary artery hemorrhage: Intervention with therapeutic embolism of the pulmonary artery. JAMA 261:1943-1945,1989 2. Spodick DH: Analysis of flow-directed pulmonary artery catheterization. JAMA 261:1946-1947,1989 3. Baker BK, Awwad EE: Computed tomography of fatal

cerebral air embolism following percutaneous aspiration biopsy of the lung. J Comput Assist Tomogr 12:1082-1083, 1988 4. Marini JJ, Culver BH: Systemic gas embolism complicating mechanical ventilation in the adult respiratory distress syndrome. Ann Intern Med 110:699-703,1989 5. Godwin JE, Heffner JE: Combating cardiopulmonary collapse from venous air emboli. J Crit Ill 4:17-24, 1989

Pulmonary hemorrhage during cardiac surgery.

Pulmonary Hemorrhage During Cardiac Surgery David N. Thrush, MD, and Diane Jeffries, MD P ULMONARY HEMORRHAGE rarely occurs in cardiac surgical p...
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