Cardiac Arrest during anesthesia induction in a patient with LV aneurysm

Introduction

Out of all mechanical complications of acute myocardial infarction (MI), rupture of the free wall of the LV is catastrophic. The precise incidence of aneurysm and pseudo aneurysm of heart is unknown. LV pseudo aneurysm is formed if cardiac rupture is contained by pericardium, organizing thrombus, and hematoma. This condition calls for an urgent surgical repair.¹ Hemodynamic stability and proper monitoring are very important in these patients during induction of anesthesia. Hypertension can lead to rupture, and cardiac tamponade and hypotension to LV pump failure or reduce coronary perfusion and cardiovascular collapse.

Case Report

A 58 years old male with a history of hypertension and diabetes presented with retrosternal chest pain with breathlessness, and was admitted in a local hospital where he was diagnosed as infero-lateral wall myocardial infarction. He was managed conservatively with antiplatelets, statin and Beta-blockers and was planned for coronary angiography (CAG). On the day of CAG, he developed suddenly hypotension and shock, 2 D (dimention) – Echo showed pericardial collection of fluid with presence of a clot over right ventricular surface with a postero-lateral aneurysm suggestive of a sealed cardiac rupture. After 7 days he came to our institute for further management. 

All blood investigations such as complete blood count, renal and liver function tests, coagulation profiles, and electrolytes were within normal limits. Chest X-ray showed enlarged cardiac shadow. ECG showed anterolateral infarction, left ventricular hypertrophy and left anterior fascicular block.  2D-Echo showed Left Ventricular Ejection Fraction (LVEF) -20-25%; severe Left Ventricular Systolic Dysfunction (LVSD), Grade I Left Ventricular Diastolic Dysfunction (LVDD), inferoposterior LV free wall rupture with defect measuring 4.5 cm- resulting in pseudo aneurysm of 5x9 cm and minimal pericardial effusion. Surgery was planned for aneurysm repair (Direct Closure) and CAG on the table.

Pre-op patient was on Tab.Ecosprin 75mg OD, Tab. Ivabrad 5mg OD , Tab. Angispan TR 2.5 mg OD, Tab. Dytor 5 mg BD, Tab. Aldactone 25 mg BD (withhold Tab. Ivabrad 5 mg & Tab. Angispan TR 2.5 mg if Systolic Blood Pressure (SBP<100 mm of Hg).

On arrival in OT after CAG (right femoral artery sheath in situ) which had revealed Single Vessel Coronary Artery Disease (SVCAD) 100% occlusion in mid-segment of Left Circumflex artery, Baseline Arterial Blood Pressure (ABP) – 130/80 mm Hg, Heart Rate – 70/min, Oxygen Saturation (SpO2) -98% on room air. Intra-op Monitoring: ECG, ABP, Pulmonary Artery Pressure (PAP), SpO2, End Tidal Carbon Dioxide (RTCO2) and Cerebral oximetry was carried out.

Patient was induced with Inj.Midazolam (0.05mg/ kg), Inj. Buprenorphine 2mcg/kg, Inj.Etomidate (0.3mg/kg) Inj.Vecuronium (0.1mg/kg) and Sevoflurane through mask. It was unanticipated difficult intubation. During attempt SBP went up to 190 mm Hg. Nitroglycerine (NTG) infusion was (25mg/250ml) started before next attempt.

Soon, ABP fell down to 64/32 mm Hg. NTG was stopped, Domamine (200mg/50ml) and Noradrenaline (2mg/50ml) infusions were started at 20ml/hr but the patient was not responding, and soon arrested, Cardio-Pulmonary Rescuscitation (CPR) was started. 100% O2 through mask was given. Inj. Adrenaline 1 mg bolus was given. Patient was intubated with bougie on 3rd attempt. Patient developed ventricular fibrillation, Direct Current (DC) Shock with 200J was given twice. CPR was continued, Noradrenaline and dopamine infusions were further increased, and adrenaline boluses were given intermittently. With CPR, Mean BP was maintained around 50 mm Hg. Sodabicarb 100 ml and Inj. calcium gluconate 1 gm were given.

Meanwhile chest was opened with continuous CPR, Rhythm came back. Simultaneously Left femoral artery was cannulated by the surgeons. Patient was taken on cardiopulmonary bypass (CPB). On opening pericardium, there was no hemopericardium but size of pseudo aneurysm was enlarged.

CPB time: 2 hours 20 minutes. Aortic cross-clamp time: 40 minutes. Intra-Aortic Balloon Pump (IABP) was inserted while coming off CPB. Intra – op patient was transfused 5 Whole Blood, 6 Packed Cells, 2 Single Donor Platelets and 8 Fresh Frozen Plasma units.  Patient was shifted to ICU with Inj. Dopamine (200mg/50ml) @ 5 ml/hr, Inj. Noradrenaline (2mg/50ml) @ 5 ml/hr & Inj. Adrenaline (1mg/50ml) @ 5ml/hr.

Course in the ICU – On day 1, he had little gastrointestinal bleed for which bowel wash was given and antacid was started. He was conscious, oriented, following verbal commands. There was no neurological deficit. He was extubated uneventfully after 24 hours. He had retained secretions for which mini-tracheostomy was done under aseptic precautions. Tapering of Inotropes was done with stable hemodynamics; all invasive lines were removed and patient was mobilized in next 7 days. On 7thday, he complained of mild pain and swelling of left lower limbs.  Venous Doppler of left Lower Limb revealed Deep Vein Thrombosis(DVT). Anticoagulant was continued. 2D Echo was done to see Pulmonary Artery Pressure (PAP), which was normal. DVT stockings were used. Rest of the course was uneventful. Minitracheostomy was removed on 10th post –op day. The patient was shifted from intensive care unit to the ward on 11th post op day and was discharged from the hospital on 17^th post op day.

Post-op Echo showed LVEF – 25 %, moderate LVSD, GR I LVDD, Trivial to mild localized pericardial effusion-lateral to LV 6 mm;

Discussion

Left ventricular pseudo aneurysm is a type of rare, lethal condition developing from rupture of the ventricular free wall, but enclosed by the adherent pericardium or scar tissue.² The incidence of LV pseudo aneurysm was 0.23%, as reported by Csapo et al.³ Though mortality rates in patients who underwent surgery was approximately 23%, but untreated pseudo aneurysms had an approximately 30% to 45% risk of rupture, so surgical resection is considered the most appropriate way of management of LV pseudo aneurysm.

Though non-specific, LV pseudo aneurysm usually presents with symptoms such as congestive heart failure and chest discomfort (chest pain or dyspnea), syncope or cough.² Because of nonspecific symptoms, diagnosis of LV pseudo aneurysm is always made tardily, and may even be reported 4 months after infarction.⁴

Frances et al after reviewing the data from 290 patients hasreported that the most common etiology of LV pseudo aneurysm is myocardial infarction followed by cardiac surgery.⁵ If the etiology is myocardial infarction these patients usually present with LV pseudo aneurysm within 2 months of the event.⁶ The risk factors for the LV pseudo aneurysms are old age, female sex, hypertension and inferior and lateral wall involvement in the myocardial infarction. The common location for LV pseudo aneurysm is postero-inferior followed by postero-lateral and anterior wall, in contrast to a true LV aneurysm which is more commonly located in the anterior and apical walls.⁵

Once the diagnosis is confirmed, urgent surgical intervention is necessary in acute LV pseudo aneurysm as the risk of rupture outweighs the risk of surgery.⁷ However, Small retrospective studies have shown that patients with incidental finding of chronic small LV pseudo aneurysm less than 3 cm in size and patients with increased surgical risk can be managed conservatively.

In our case, initially we thought patient collapsed because of rupture of pseudo aneurysm and cardiac tamponade due to a rise in ABP following failed first intubation attempt. But on opening pericardium we found though pseudo aneurysm had enlarged in size, there was no hemopericardium or cardiac tamponade. Cardiovascular collapse was due to hypotension and not hypertension.

Induction of anesthesia should be accomplished with minimal or no compromise in cardiac function. Cardiac depressant drugs such as thiopental should be avoided. Even inhalational agents also should be used cautiously. Histamine releasing neuro-muscular blocking agents also should be avoided.⁸

In our case, while trying to avoid hypertension and possible rupture of pseudo aneurysm we started NTG infusion (25mg/250ml) in small doses. Even with transient NTG, preload had been reduced and hypotension occurred reducing forward flow from LV to the aorta and distension of the LV cavity. It facilitated flow of more blood from LV cavity to low resistance pseudo aneurysm. However, due to adherent pericardium (7days) it did n’t rupture. Hypotension led to reduction in coronary perfusion and LV pump failure. As heart was already bad (2D echo) the patient arrested. Pre-op insertion of Intra-Aortic Balloon Pump (IABP) might have helped in improving left ventricular function and after load reduction.

Conclusion

Both hypertension and hypotension are dangerous in a patient with pseudo aneurysm during induction of anesthesia. There are more reports about rupture of pseudo aneurysm and cardiac tamponade as a cause of collapse in these patients. The present case has shown that hypotension is equally or even more dangerous in these patients

especially after several days history of MI and low EF.