Persistent Bleeding After Cardiopulmonary Bypass
• Reversing heparin effects: Protamine should be used to return ACT to baseline (usually 1 mg per 100 U of heparin is needed with additional doses of 25–50 mg if inadequate). Administering protamine too rapidly may result in severe hypotension or pulmonary hypertension.
• Persistent bleeding after bypass: Often occurs after prolonged durations of bypass (>2 hr) and usually is caused by inadequate surgical control of bleeding sites, incomplete reversal of heparin, thrombocytopenia, platelet dysfunction, hypothermia-induced coagulation defects, undiagnosed preoperative hemostatic defects, newly acquired factor deficiency, or hypofibrinogenemia. Platelet, fresh-frozen plasma, or cryoprecipitate transfusion should be considered. Accelerated fibrinolysis confirmed by elevated fibrin degradation products (>-32 mg/mL) or evidence of clot lysis should be treated with ε-aminocaproic acid or tranexamic acid.
• Antifibrinolytic therapy: Should be considered for patients who are undergoing a repeat operation; who refuse blood products, such as Jehovah’s Witnesses; who are at high risk for postoperative bleeding because of recent administration of glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, or tirofiban); who have preexisting coagulopathy; and who are undergoing long and complicated procedures involving the heart or aorta.
• Chest tube drainage: In the first 2 hours after surgery of more than 250 to 300 mL/hr (10 mL/kg/hr)—in the absence of a hemostatic defect—is excessive and may require surgical reexploration. Intrathoracic bleeding at a site not adequately drained may cause cardiac tamponade, requiring immediate reopening of the chest, and is associated with severe hypotension on anesthetic induction.
Anesthetic Management of Carotid Surgery
• Indications for carotid endarterectomy (CEA): CEA is recommended for transient ischemic attacks associated with ipsilateral severe carotid stenosis (>70% occlusion), severe ipsilateral stenosis in a patient with minor (incomplete) stroke, and 30% to 70% occlusion in a patient with ipsilateral symptoms (usually an ulcerated plaque). For asymptomatic lesions with greater than 60% stenosis, stenting is generally recommended.
• Anesthetic management: Maintain adequate perfusion to the brain and heart. Neurologic deficits should be defined, and other disease states should be optimized. Most patients are elderly, have hypertension, have generalized arteriosclerosis, and often have diabetes. Intraoperatively, avoid tachycardia and wide swings in arterial pressure. Regional anesthesia with superficial cervical plexus blocks allow the patient to be awake and neurologically examined during surgery. Propofol or etomidate can be used for induction of GA as they reduce CMRO2 more than CBF. Isoflurane appears to provide the greatest protection against cerebral ischemia. Keep MAP at or slightly above preoperative levels. Intraoperative hypertension is common and should be treated with a vasodilator like nitroglycerin, nicardipine, or nitroprusside; phenylephrine is used for hypotension. Bradycardia or complete heart block can be caused by manipulation of the carotid baroreceptor and is treated with atropine. Maintain normocapnia.
• Neurologic monitoring: EEG and SSEP monitoring may be used.
• Complications The perioperative mortality rate is 1% to 4% and is primarily attributable to cardiac complications. The perioperative morbidity rate is 4% to 10% and is principally neurologic. Wound hematoma can compromise the airway. Damage to the recurrent laryngeal nerve can cause hoarseness, and damage to the hypoglossal nerve can cause ipsilateral deviation of the tongue. Denervation of the ipsilateral carotid baroreceptor can cause postoperative hypertension, and denervation of the carotid body can blunt the ventilatory response to hypoxemia.
Cardiac Tamponade
• Causes: Cardiac tamponade exists when increased pericardial pressure impairs diastolic filling of the heart and can be caused by pericardial effusions from viral, bacterial, or fungal infections; malignancies; bleeding after cardiac surgery; trauma; uremia; myocardial infarction (MI); aortic dissection; hypersensitivity or autoimmune disorders; drugs; or myxedema.
• Signs and symptoms: Decreased cardiac output (CO) from a reduced stroke volume (SV) with increase in central venous pressure (CVP). Equalization of diastolic pressure occurs in all chambers of the heart. Increase in sympathetics causes increased heart rate and contractility to help maintain CO. Acute cardiac tamponade usually presents as sudden hypotension, tachycardia, and tachypnea. Physical examination may show jugular venous distention, narrowed arterial pulse pressure, muffled heart sounds, friction rub, or pulsus paradoxus. ECG may show decreased voltage in all leads and nonspecific ST- and T-wave abnormalities. Electrical alternans may be seen with a large pericardial effusion.
• Anesthetic considerations: Symptomatic cardiac tamponade requires evacuation either by pericardiocentesis or surgically (usually for postoperative cardiac tamponade or for large recurrent pericardial effusions). Pericardiocentesis may be done with local anesthetic and small doses of ketamine (10 mg IV boluses) if supplemental analgesia is needed. Induction can precipitate severe hypotension and cardiac arrest. Have an epinephrine infusion immediately available. Pericardiocentesis before induction may improve CO and allow safe induction and intubation. Large-bore IV access is mandatory because the patients require large fluid boluses to supplement CO. Avoid cardiac depression, vasodilation, slowing of the heart, high airway pressures, and deep anesthesia.
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