| Abstract|| |
A 57-year-old man presented with chest pain and shortness of breath 1 month after left ventricular aneurysmectomy and ventricular septal defect closure for post-infarct left ventricular aneurysm and ventricular septal defect. Echocardiography revealed a large recurrent ruptured inferior left ventricular aneurysm with high-velocity flow into a 5 cm posterolateral pericardial effusion. Thirty minutes earlier, the patient had eaten a full meal. Rapid sequence induction was performed with midazolam, ketamine, and succinylcholine. Moderate hypotension was treated effectively and the patient tolerated controlled transition to cardiopulmonary bypass. The ventricular defect was oversewn and reinforced with bovine pericardium. The patient had a difficult but ultimately successful recovery. Options for anesthetic management in the setting of tamponade and a full stomach are discussed, with a brief review of the evidence relating to this clinical problem.
Keywords: Full stomach, Pericardial tamponade, Rapid sequence induction, Ruptured ventricular aneurysm, Ventricular rupture
|How to cite this article:|
Maxwell BG, Harrington KB, Kelly NE. Anesthetic management for reentry sternotomy in a patient with a full stomach and pericardial tamponade from left ventricular rupture. Ann Card Anaesth 2013;16:51-3
|How to cite this URL:|
Maxwell BG, Harrington KB, Kelly NE. Anesthetic management for reentry sternotomy in a patient with a full stomach and pericardial tamponade from left ventricular rupture. Ann Card Anaesth [serial online] 2013 [cited 2021 Jan 21];16:51-3. Available from: https://www.annals.in/text.asp?2013/16/1/51/105371
| Introduction|| |
Pericardial tamponade, ventricular rupture, and aspiration risk, each present management challenges to the anesthesiologist that, when combined, constitute a demanding scenario. We describe anesthetic management for left ventricular rupture repair in a patient who presented with full stomach, and pericardial tamponade.
| Case Report|| |
A 57-year-old man with a history of hypertension and cocaine use presented to a referring hospital with chest pain and shortness of breath. He provided a written, informed consent for the publication of this case description. One month earlier, the patient had presented with similar symptoms in the setting of cocaine use and had been diagnosed with a post-infarct ventricular septal defect (VSD) and inferior wall left ventricle (LV) aneurysm. He underwent LV aneurysmectomy with primary multi-layer ventricular closure as well as VSD closure with a bovine pericardial patch. His postoperative recovery was delayed due to a slow wean of intra-aortic balloon pump and inotropic support, but was eventually discharged home 2 weeks prior to his re-presentation with chest pain.
After initial optimization, he was transferred back to our institution. A transthoracic echocardiogram (TTE) performed on arrival revealed preserved LV function, no residual VSD, and a large recurrent inferior LV aneurysm with a pericardial effusion measuring approximately 5 cm in diameter in the posterolateral dimension. There was a high-velocity bidirectional jet visualized on color Doppler between the lateral wall of the LV and the pericardial space. The appearance of the atria and vena cava were consistent with elevated filling pressures. The patient was scheduled for emergency redo sternotomy and probable redo LV aneurysmectomy. Approximately 30 min prior to TTE examination, the patient had consumed a full meal including steak, mashed potatoes, and green peas. Urine toxicology was negative for stimulant use. He was also noted to have very poor dentition and multiple loose front teeth. The patient was brought to the operating room, where peripheral intravenous access options were determined to be inadequate (no successful venous access larger than a 22-gauge catheter). Arterial access was obtained in the right radial artery with a 20-gauge catheter. Central venous access was obtained in the right internal jugular vein using a 9-French, 10 cm introducer sheath (Arrow PSI CDC-09903-1A, Arrow International, Reading, Pennsylvania, USA) and 7-French, 16 cm, triple-lumen catheter (Arrow AGB CDC-42703-XP1A, Arrow International, Reading, Pennsylvania, USA). All lines were placed under local anesthesia without sedation. The patient remained calm and cooperative. Given the recent VSD patch closure, a pulmonary artery catheter was not placed. Pre-induction vital signs without vasopressor support were a heart rate of 95 beats per minute, arterial blood pressure 90/72 mmHg, and central venous pressure of 23 mmHg. Transcutaneous defibrillation pads were applied, and autologous cross-matched units of packed red blood cells were in the room prior to induction. Both groins were prepped in anticipation of femoral venous and arterial cannulation immediately after induction for institution of cardiopulmonary bypass prior to redo sternotomy. After adequate pre-oxygenation, rapid sequence induction was performed with intravenous midazolam (2 mg), ketamine (120 mg), succinylcholine (100 mg), and epinephrine (5 mcg) with concomitant volume administration (250 ml of 5% albumin). Cricoid pressure was maintained from loss of eyelash reflex to endotracheal tube cuff inflation. The patient did experience moderate hypotension on induction with narrowing of the pulse pressure (nadir arterial blood pressure 69/61 mmHg) but did not require significant resuscitation maneuvers after induction.
Transesophageal echocardiography confirmed the large pericardial fluid collection with bidirectional flow into a portion of the pericardial space from a 2.6 cm defect at the posterior-lateral wall of the LV [Figure 1]. Extensive loculations and organized thrombus were visualized within the pericardial space, which correlated to absent flow in approximately two-thirds of the area of the fluid collection [Figure 2]. There was no flow appreciated across the prior VSD.
|Figure 1: Left-rotated mid-esophageal four-chamber view demonstrating a ventricular defect (D) in the posterior-lateral wall and a large, complex pericardial fluid collection (P). LA = Left atrium; LV = Left ventricle; RV = Right ventricle|
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|Figure 2: Left-rotated trans-gastric short-axis view of the left ventricle (LV) demonstrating the aneurysm defect (D) with high velocity flow in systole into the pericardial space (P). L = Liver|
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Cardiopulmonary bypass (CPB) was instituted through bifemoral cannulation within 15 min of induction and repeat sternotomy was performed. After extensive dissection of dense adhesions was carried out and the heart arrested, approximately 500 ml of blood, thrombus, and fibrotic tissue was evacuated from the posterior-lateral pericardial space. The LV defect was confirmed by gross inspection (approximately 3 × 3 cm), oversewn, and reinforced with a bovine pericardial patch. The prior VSD patch was confirmed to be intact. An intra-aortic balloon pump (IABP) was placed empirically and the patient was weaned from CPB. His postoperative course was complicated by coagulopathy, multiple transfusions, and a slow wean of the IABP (postoperative day 4) and inotropes (postoperative day 6). He eventually made a full recovery and was discharged home on postoperative day 17.
| Discussion|| |
Pericardial tamponade (manifested in this case by a pericardial effusion, elevated central venous pressures, narrowed pulse pressure, and echocardiographic evidence of restricted filling) is a surgical emergency with a high risk of decompensation on induction of general anesthesia. Traditional induction strategies carry the potential disadvantages of reducing preload, contractility, and systemic vascular resistance (SVR), which are poorly tolerated in presence of tamponade. Inhalation induction with maintenance of spontaneous ventilation has been recommended.  If intravenous induction with paralysis is used, a gradual induction strategy with agents that preserve hemodynamics is preferred.
When tamponade occurs in a patient with a full stomach, no ideal induction strategy exists. One must minimize aspiration risk and the adverse hemodynamic consequences of a rapid sequence induction strategy. Awake subxiphoid pericardiocentesis under local anesthesia prior to induction may help provide a margin of safety, but this was not an option in our patient because of prior pericardial dissection, adhesions, and the possibility of worsened bleeding and exsanguination with decompression of the tamponade. The need for re-entry sternotomy in this patient further complicated the clinical challenges. Because rapid chest entry is not possible in a patient like ours with prior sternotomy, rapid initiation of CPB is not a viable backup plan, should hemodynamic compromise occur on induction. The most conservative option for preventing death upon induction is to place CPB cannulas in the femoral vessels under local anesthesia for transition to bypass prior to or coincident with induction. This strategy is utilized by some even when the possibility of acute tamponade exists, for example, in laser lead removal.  An intermediate strategy would include placing wires in the femoral vessels if adequate local anesthesia for cannula placement could not be provided or the patient is less cooperative.
Induction with ketamine as the primary anesthetic agent may have offered important advantages in this situation in preserving myocardial contractility, SVR (and therefore maintaining coronary perfusion pressure), and venous return. ,, Compared to propofol, etomidate is less likely to decrease SVR, but often still decreases venous return significantly. , Empiric administration of low-dose epinephrine supported the patient during the transition to an anesthetized state, we believe it may be preferable to the post-hoc treatment of hypotension. No clear evidence favors colloid over crystalloid, but empiric volume administration at the time of anesthetic induction was used in the belief that it may help counter any decrements in venous return. In our patient, adequate local anesthesia and reassurance were crucial in allowing awake central venous access. In a less cooperative patient, awake femoral venous cannulation may be a less stimulating site for obtaining access for possible rapid volume administration if large-bore peripheral venous access cannot be obtained.
In addition, this case illustrates the importance of communication and coordinating management strategies between the perfusionist, surgical, and anesthesia teams.
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Bryan G Maxwell
Department of Anesthesiology, Stanford University Medical Center, 300 Pasteur Drive, H3586 MC 5640, Stanford, CA 94305-5640
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2]