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Cardiac Surgery, Immediate Postoperative Management

Basics

Description

Cardiac surgery presents unique challenges due to cardiopulmonary bypass (CPB), surgical trauma, anesthesia, and pre-existing cardiac comorbidities. Prompt recognition and treatment are essential to minimizing early postoperative morbidity and mortality.

Pathophysiology

Pathophysiologic effects of CPB:

  • Fluid and electrolyte disturbances: Increased fluid and rapid shifts increase exchangeable sodium, decrease exchangeable potassium, deplete phosphate, and cause hyperglycemia.
  • Inflammatory response: Precipitated by blood contact with bypass equipment, operative trauma, and anesthesia. Inflammation results in platelet-endothelial cell interaction, coronary vasospasm, capillary leak, and the "post-pump syndrome" characterized by fever, leukocytosis, coagulopathy, hypoxemia, pulmonary capillary leak, renal dysfunction, and cognitive dysfunction.
  • Transient depression of ventricular function: Secondary to ischemia and reperfusion-induced free radicals. LV function is generally, worst 4-5 hr post-CPB, significantly recovered by 8-10 hr, and fully recovered by 24-48 hr. Off-pump surgery is associated with less dysfunction.
  • Hypothermia: Predisposes to dysrhythmias, increases systemic vascular resistance (SVR), impairs coagulation, and causes shivering, which increases O2 consumption and CO2 production.
  • NOTE: SVR drops during re-warming, requiring volume/vasopressor support.
  • Respiratory insufficiency: Results from V/Q mismatch (atelectasis), decreased respiratory drive (anesthetics), and mechanical effects of sternotomy. Resultant hypercarbia precipitates/exacerbates catecholamine surge.
  • Bleeding: Results from residual heparin effects, incomplete surgical hemostasis, HTN, hypothermia, platelet dysfunction, thrombocytopenia (hemodilution), and clotting factor depletion (consumption or hemodilution), HTN

Treatment

Medication

  • Reinstitute medications for comorbid diseases
  • Anticoagulation for valves, atrial fibrillation/flutter, and other conditions and in patients with high thromboembolic risk
  • Aspirin, lipid-lowering agents for CABG patients (clopidogrel commonly used as well)
  • Endocarditis prophylaxis; mechanical valves
  • β-Blockers for atrial fibrillation prophylaxis; amiodarone in high-risk patients.
  • Diltiazem (1 mo) to prevent spasm if radial artery graft used
  • Vasoactive medications for hypotension: Dobutamine and dopamine when low-output Norepinephrine 1st-line in vasodilatory states
  • IV fluids for volume support
  • Short-acting IV antihypertensives: Nitroprusside for rapid onset/offset Esmolol when β-blocker indicated
  • Diuretics transiently, if volume overloaded
  • DVT prophylaxis
  • Insulin infusion if hyperglycemic
  • Opiates, acetaminophen for pain control

Additional Treatment

General Measures

  • Postoperative Complications
  • HTN: Present in most patients without LV dysfunction. PVR increased due to catecholamine surge/RAS activation from CPB and hypothermia. Resolution of capillary leak expands intravascular volume. Treatment minimizes graft/anastomosis damage, pulmonary edema, and bleeding Treatment goal: G 10% above upper limit of normal MAP. Nitroprusside and esmolol commonly used
  • Hypotension: Potential etiologies: Vasodilation from rewarming; inflammatory reaction to CPB; diastolic dysfunction; low-output syndrome Treatment is volume expansion and vasoactive drugs.
  • Low-output syndrome: Most common among patients with preoperative LV dysfunction, long CPB run, perioperative MI. Clinical features include: Cold extremities, systolic BP (SBP) <90 mm Hg, but may be >100 if SVR elevated Urine output <30 mL/h Cardiac index <2.0 L/min/m2 Low early postoperative cardiac index associated with increased mortality Mixed venous O2 <50% (except in sepsis) Acidosis generally present Define etiology; use Swan-Ganz catheter, echo to identify decreased preload, LV contractility, or RV function, tamponade, sepsis, or arrhythmia: Nonuniform compression from clot can complicate distinction between tamponade and LV dysfunction. Echo is essential. Vasoactive medications: Dopamine and dobutamine 1st choices for low output; norepinephrine if low SVR. If severe/persistent, intraaortic balloon counterpulsation, ECMO, other devices
  • RV failure: Can precipitate LV failure Fluid administration to ensure preload Minimize airway pressures Pulmonary vasodilators may be useful
  • Perioperative MI: Symptoms unreliable Risk factors: Age, long CPB run, elevated LVEDP, left main disease. Diagnose by ECG, cardiac biomarkers; echo may be confirmatory. No routine postoperative biomarkers unless intraoperative hemodynamic instability or new ECG changes.
  • Arrhythmias: Supraventricular: Atrial tachyarrhythmias particularly common in valvular procedures Sinus tachycardia: Can be normal response to catecholamines, but evaluate for other precipitants (hypovolemia, infection, low-output syndrome). Atrial fibrillation (AF): 10-30% occurrence postoperatively Risk factors: Advanced age, history of AF, DM, and long CPB/cross-clamp time Commonly occurs around post-op day 2. Prophylactic β-blocker, amiodarone if high-risk 80% return to sinus rhythm within 1-3 days following digoxin or β-blocker. IV diltiazem, esmolol for rate control; cardioversion for hemodynamic compromise (required in about 10%) Atrial flutter may convert to sinus rhythm using atrial epicardial pacing. Burst pace 15-30 sec @ 300-600 bpm Ibutilide most effective at converting new atrial flutter (but can cause torsade de pointes); cardiovert if unstable. Ventricular: Frequent ectopy (>6 bpm) in 1st 12 hr postop suggests ischemia. Ectopy common postoperative days 3-5. Variable use of pharmacotherapy (procainamide, lidocaine) to suppress. Ventricular tachycardia: Re-entrant circuits often from revascularizing nonviable myocardium; sustained VT usually requires amiodarone. Cardiovert if unstable. Note: Wide complex tachycardia with rates 250-300 bpm suggests accessory pathway. Procainamide is drug of choice, but cardioversion more widely used. Avoid lidocaine and verapamil. Bradyarrhythmias/conduction defects: Conduction defects in up to 45% of patients Prevalent in aortic valve replacement (AVR) Majority transient, particularly hemiblocks; some related to incomplete washout of cardioplegia or operative trauma AV nodal transection during AVR a well-known cause of permanent AV block Right bundle branch block the most common conduction defect; AF with slow ventricular response, sinus bradycardia, and junctional rhythm are less common Bradycardia: Temporary atrial pacing Dyssynchrony: AV sequential pacing High-grade block: Epicardial pacing Interrogate/reactivate ICDs and pacemakers
  • Pulmonary: Pulmonary complications the most significant cause of morbidity and major cause of mortality after CPB. Atelectasis (70% of patients): Primarily left lower lobe (intraoperative compression). Altered mechanics contribute to atelectasis and result in V/Q mismatch and hypoxemia: Decreased chest wall movement due to incisional pain or decreased compliance post-sternotomy Phrenic nerve damage may require up to 6 wk for recovery; may be permanent. Decreased respiratory drive (medications) Exacerbation of obstructive lung disease: CPB can induce bronchospasm. Pleural effusions: Often resolve spontaneously or with diuresis Repeat thoracentesis if large or persistent Adult respiratory distress syndrome (ARDS) (<2% occurrence; 80% mortality): Early clues: Decreased pulmonary compliance (high airway pressures) and difficulty maintaining oxygenation Management: Low tidal volume ventilation (permissive hypercapnia), and euvolemia. Mortality: Primarily multisystem organ failure Pneumonia: Increased risk with prolonged intubation. Peak incidence ~4 days after surgery. Diagnosis and appropriate antibiotics critical. Ventilator management: Tidal volumes (Vt) 8-10 mL/kg typically used to prevent atelectasis; low Vt in ARDS. Goal PaO2> 65; wean FiO2 aggressively Early (fast-track) extubation often possible, particularly for off-pump cases.
  • Infection: Noninfectious postop fever common (atelectasis, phlebitis, pleuropericarditis, post-pump syndrome); suspect infection if temperature >38.5 C. Incisional: Leg: Occurs in 1% of patients; common in obese women, thigh incisions Sternal/mediastinitis: Occurs in 0.4-5% of patients; diabetics with bilateral IMA grafts at greatest risk. Infective endocarditis: Perioperative antibiotic prophylaxis in appropriate patients. CABG: No increased risk for native valves Prosthetic valve: Rare, but serious disease.
  • Neurologic: Cerebral injury: Likely microembolic (air, thrombus, atheromatous debris) Delirium/encephalopathy: Up to 2/3 of patients; generally resolves. Some have mild long-term cognitive disorder Major cerebrovascular accident incidence ~2% (3% have minor/transient deficits) Peripheral nerve injury: Brachial plexus, ulnar and median nerves; usually temporary, may require up to 6 mo for recovery. Phrenic and recurrent laryngeal nerve injury; can cause respiratory failure from diaphragmatic/vocal cord palsy Visual symptoms common: Floaters, decreased acuity, spots, and stripes Incisional pain: Thoracotomy generally more than sternotomy; secondary to muscle incision. Persistent pain: Evaluate for fracture, subluxation, infection Leg incisions often require pain control
  • Hematologic: Blood loss and hemodilution: Transfuse as needed; target HCT often >30, but sparse evidence for this goal. Aminocaproic acid, aprotinin, DDAVP, platelets, fresh-frozen plasma, and cryoprecipitate all can be helpful. Recombinant factor VIIa for severe refractory bleeding Monitor for heparin-induced thrombocytopenia Anticoagulation (AC): Warfarin indications: High risk for thromboembolism; presence of atrial fibrillation; presence of intracardial thrombi Valve replacement: Risk with mechanical valve > bioprosthetic valve; mitral > aortic; duration of AC for bioprosthetic valves by patient risk factors At least 3 mo if no contraindication INR target/longer duration based on valve position/risk factors; lifelong AC with mechanical valves Increased INR (2.5-3.5) in 1st 3 mo, in MVR, and high-risk patients; adjunctive aspirin therapy based on valve site and patient risk factors
  • Endocrine/Metabolic: Electrolyte disturbances: Hyperkalemia, hypomagnesemia, hypophosphatemia essential to correct. Hypocalcemia rarely requires correction unless hypotensive Hyperglycemia: Surgical trauma and CPB induce catecholamine and cortisol: Tight control (typically with insulin infusion) improves mortality, wound healing Insulin requirements may be significant in immediate postoperative period
  • Renal: Incidence of postop renal dysfunction up to 30%, but rarely requires dialysis. Etiology: CPB (loss of pulsatile perfusion), hypotension, vasoconstriction Greatest incidence (and morbidity/mortality) in older patients, long CPB runs and cross-clamp times, preoperative renal dysfunction Mannitol, furosemide, and dopamine may reduce ischemic insults intraoperatively.
  • Gastrointestinal: Serious complications rare, often ischemic

Surgery

Reexploration for persistent, uncontrolled bleeding or if tamponade suspected secondary to thrombus. Reexploration can, in some cases, be done in ICU.

In-Patient Considerations

Discharge Criteria

Hemodynamic stability, normal sinus rhythm or rate-controlled atrial fibrillation, ability to ambulate and eat, and presence of adequate family support to provide basic needs for convalescence.

Ongoing Care

Follow-Up Recommendations

Patient Monitoring

In the 1st weeks to months after discharge, patients should be seen by cardiac surgeon, cardiologist, and primary care provider. Patients monitored for:

  • Emotional/mental well-being, attitude
  • Healing at sternal, extremity wound sites
  • Activity level/reconditioning/return to work
  • Return of CBC indices to baseline
  • Proper medication regimen
  • Risk factor control

Patient Education

  • Modification of cardiac risk factors
  • Proper diet, activity, and coping with stress
  • Education regarding AC, other medications

Prognosis

6 wk to several months generally to regain or improve exercise tolerance if postoperative course uncomplicated. Patients should not drive or lift >20 lbs for 4-6 wk after sternotomy.

Additional Reading

1

Eagle KA. ACC/AHA 2004 guideline update for coronary artery bypass graft surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999 Guidelines for Coronary Artery Bypass Graft Surgery). Circulation. 2004;110(14):e340-437. [View Abstract] 2

Gray RJ, Sethna DH.

Medical management of the patient undergoing cardiac surgery. In: Libby PBraunwald's Heart disease: A Textbook of Cardiovascular Medicine, 8th ed.Philadelphia: WB Saunders, 2008;1993-2009. 3

Morris DC, Clements SD, Pepper J.

Management of the patient after cardiac surgery. In: Fuster V et al., Hurst's the Heart, 12th ed.New York: McGraw-Hill, 2008;1519-1528. 4

Morris DC, St.

Claire D Jr. Management of patients after cardiac surgery. Curr Probl Cardiol. 1999;24:161-228. [View Abstract] 5

Weissman C.

Pulmonary complications after cardiac surgery. Semin Cardiothorac Vasc Anesth 2004;8:185-211. [View Abstract]

Clinical Pearls

  • Preoperative status the most important predictor of postop morbidity and mortality.
  • Ascertaining etiology of postop hypotension can be difficult given many potential causes, but is essential to proper management.
  • Pulmonary complications represent the major cause of postop morbidity and a major source of mortality in cardiac surgery patients.