Postoperative Chest Pain

Description

Postoperative chest pain can be caused/related to any part of the thorax, including the heart, lungs, esophagus, muscle, bone, and skin. Despite the possibility for innocuous causes (reflux), life-threatening causes (myocardial infarction [MI]) must be ruled out and, if identified, treated quickly.
It is a rare event that a patient complains of de novo anginal-type chest pain. Therefore, it is important to review the patient's history and assess risks to help distinguish and discern chest pain due to cardiac origin.

Epidemiology

Incidence

Postoperative MI: 0–4%, depending on coronary artery disease (CAD) risk stratification.
Those at-risk for, or have CAD: 3.9% (1) for a major perioperative cardiac event

Mortality

Patients that have an MI after noncardiac surgery have an in-hospital mortality rate of 10–15%. They also have an increased risk that persists for at least a year compared to those who did not have an MI.

Etiology/Risk Factors

Acute MI, angina: CAD, anemia secondary to surgery, hypertension (HTN), preoperative use of cocaine or other similar stimulants, recently placed coronary stents, high-risk surgery, cerebrovascular disease, use of insulin therapy for diabetes, signs of heart failure on preoperative examination, a preoperative serum creatinine >2 mg/dL, new long-standing ST-T wave changes noted intraoperatively.
Aortic dissection: s/p cardiac catheterization, aortic surgery.
Pulmonary embolism (PE): Obesity, prolonged immobility, femur fracture, pregnancy, cancer, history of prior PEs, family history of blood clots, arrhythmias, recently discontinued anticoagulation or antiplatelet medications.
Pneumothorax: Surgical injury to the chest or diaphragm, central line placement, brachial plexus block, ventilator complication.
Aspiration pneumonia: Poor motor control, extremes of age, emergency status, recent meal, morbid obesity, events during intubation or extubation, delayed gastric emptying, decreased gastric emptying, decreased lower esophageal sphincter tone.
Gastroesophageal reflux disease (GERD): History of GERD, decreased lower esophageal sphincter tone (e.g., pregnancy), certain medications (e.g., anticholinergics).
Perforated viscus: Complicated abdominal or thoracic surgery.
Costochondritis: Thoracic surgery, lateral position during surgery, repetitive minor trauma to the chest wall during surgery.

Physiology/Pathophysiology

MI: Surgery with its associated trauma, pain, hypothermia, and anemia can induce an inflammatory, hypercoagulable state that can lead to coronary plaque rupture and arterial thrombosis. ST-segment elevated MI is associated with complete thrombotic occlusion of an epicardial coronary artery. Severe imbalances in myocardial oxygen supply and demand can also result in infarction.
Angina: Chest pain results from an imbalance between myocardial oxygen supply and demand that can result from increased levels of catecholamines and cortisol. It differs from an MI in that the arteries are not completely blocked and there is little or no permanent damage to the heart; however, it could be an indicator of impending MI.
Aortic dissection: A tear in the intimal layer is followed by formation and spread of a subintimal hematoma. This produces a false lumen, which can reduce blood flow to the major arteries arising from the aorta. If the dissection involves the pericardial space, cardiac tamponade may result.
PE: Occurs when a clot breaks loose and embolizes to block pulmonary blood vessels. Deep vein thrombosis (DVTs) in the lower extremities are triggered by venostasis, hypercoagulability, and vessel wall inflammation (increased in the perioperative period). Patients who have undergone gynecologic surgery, or major trauma may have deep vein thrombosis (DVTs) that move proximally to the popliteal vessels and from there embolize to the lungs.
Pneumothorax: Occurs with the entrance of air into the pleural cavity. A tension pneumothorax (air enters, but cannot exit as a result of a "ball-valve" mechanism) results in lung collapse, respiratory compromise, and mediastinal shifting.
Perforated viscus: A hole or a tear in the wall of the gastrointestinal tract allows air to enter the abdominal cavity, which irritates the diaphragm and can cause chest pain.
Aspiration pneumonia: Occurs when material (food, foreign body) or fluid (gastric contents, blood, or saliva) enters the lungs from the pharynx into the trachea. The consequences depend on the type, amount, and pH of material aspirated. Acidic gastric contents cause alveolar–capillary breakdown, resulting in interstitial edema, intraalveolar hemorrhage, atelectasis, increased airway resistance, and commonly hypoxia.
GERD: Occurs when gastric content refluxes into the esophagus, causing symptoms with or without associated esophageal mucosal injury (i.e., esophagitis). Usually the result of lower esophageal sphincter dysfunction.
Esophageal spasm: Remains unknown; however, it is believed to relate to a loss of inhibitory innervations in the body of the esophagus (2).
Costochondritis: An inflammatory process of the costochondral or costosternal joints that causes localized pain and tenderness.

Prevantative Measures

Cardiac events: Patients on beta-blockers or statins prior to surgery should receive their dose in the perioperative period. Patients with recently placed bare metal stents should wait at least 6 weeks and those with drug-eluting stents should wait at least 1 year before discontinuing dual platelet therapy to decrease the risk of acute stent thrombosis. Treat postoperative anemia, hypothermia, hypotension or HTN, and pain aggressively to decrease myocardial oxygen demand/supply mismatch.
PE: Early ambulation, mechanical and/or pharmacologic thromboprophylaxis have been demonstrated to be effective.
GERD: Administer acid reflux medication in the perioperative period.

MI or angina: Variable and can include tachycardia or bradycardia, hypotension or HTN, tachypnea, diaphoresis, and a fourth heart sound. Sign of CHF include S3 heart sound (gallop), pulmonary rales, lower extremity edema, and elevated jugular venous pressure. EKG changes: ST-segment elevation (2 mm in leads V1, V2 or V3 and 1 mm in the other leads) or depression (1 mm) in at least 2 contiguous leads, or symmetric inversion of T waves (1 mm) in at least 2 contiguous leads (3). New Q waves in two neighboring leads may be seen.
Aortic dissection: Hypertension (secondary to release of catecholamines), hypotension (excessive vagal tone), cardiac tamponade, hypovolemia, syncope, altered mental status. Dyspnea may be caused by CHF or tracheal/bronchial compression. Dysphagia form esophageal compression. A new diastolic murmur and a decrease in oxygen saturation may occur. A CT scan of the aortic vessels should be considered.
PE: Unilateral leg swelling from DVT, hypoxemia (<95%), and pulse >94 bpm. Massive PE causes hypotension due to acute cor pulmonale. Wheezing may be present. EKG changes: Prominent S wave in lead I; Q wave and inverted T wave in lead III pattern due to right ventricular strain. May also see peaked P waves in lead II, new right bundle branch block, right axis deviation, or new onset atrial fibrillation. Decreased oxygen saturation. D-dimer is a unique degradation product produced by plasmin-mediated proteolysis of cross-linked fibrin; levels are increased in PEs (nonspecific). A high resolution CT angiograph is a sensitive diagnostic tool; if it is not available, then a V/Q scan should be performed (less sensitive and specific). A duplex ultrasound of a DVT can also aid with diagnosis.
Pneumothorax: Decreased or absent breath sounds on the affected side with dyspnea, decreased pulse oximetry. When large, hypotension can result.
Aspiration pneumonia: Tachypnea, tachycardia; decreased breath sounds, rales, dullness to percussion over the area of consolidation; and hypoxemia. Chest radiograph is usually normal initially; a CT scan of the chest may yield results more quickly.
Perforated viscus: Rebound abdominal tenderness and fever. Hypotension secondary to significant blood loss or septic shock. An abdominal radiograph would show free air.
Costochondritis: Pain on palpation of the affected costochondral joints.
ECGs: Can be uninterpretable if the patient has known bundle branch block, chronic ST-segment changes, or is pacer dependant.
Blood troponin level: To identify infarction; a typical rise and gradual fall is a sign of cardiac ischemia or PE.
Transthoracic or esophageal echocardiogram (TTE or TEE): New wall motion abnormalities on echocardiography are likely due to MI. New right ventricular dysfunction may also suggest PE.
Radionuclide scan: New fixed cardiac defects on radionuclide scan is likely due to myocardial infarct.
Chest x-ray: Can rule out pneumothorax, check for enlarged mediastinum (aortic dissection), or infiltrate formation (aspiration pneumonia). for PE, the film may initially be normal; occasionally there may be dilation of the pulmonary vessels proximal to an embolism along with collapse of distal vessels. After 24–72 hours, the loss of pulmonary surfactant can cause atelectasis and pulmonary infiltrates which may appear like pneumonia. Aspiration pneumonia typically has a delayed presentation on radiography.
Arterial blood gas: Hypoxia and possible respiratory acidosis in pneumonia, pneumothorax, and PE.
White blood cell count (WBC): Increased with bacterial infections associated with aspiration pneumonia, as well as PE, and perforated viscus (if associated with sepsis). However, it can also be elevated after trauma and major operations.
Barium swallow: If a trial of proton pump inhibitors does not work and chest pain of an esophageal origin is still suspected, then a barium swallow can be done to rule out diffuse esophageal spasm or to detect hiatal hernias (associated with GERD).
Esophagogastroduodenoscopy (EGD): Can be done to rule out esophagitis and peptic ulcer disease. Esophageal manometry can be used to further detect diffuse esophageal spasm, and monitor the lower esophageal sphincter (which can help detect GERD).

Differential Diagnosis

Cardiac: Acute MI, angina, aortic dissection
Pulmonary: Embolism, pneumothorax, aspiration pneumonia
Gastrointestinal: Acid reflux, esophagitis, esophageal spasm, perforated viscus
Musculocutaneous: Costochondritis

MI and hemodynamically stable: Consult a cardiologist and possibly an intensivist. Medical management includes supplemental oxygen, morphine to adequately treat the patient's pain (decreases sympathetic stimulation and has preload-reducing properties), nitroglycerin (decreases cardiac preload and causes coronary vasodilation), IV beta-blockers (decreases myocardial O₂ consumption; may not be appropriate in patients with decompensated CHF, severe COPD, severe hypotension from shock), and aspirin 325 mg (decreases platelet aggregation). IV unfractionated heparin may be given (to decrease thrombin formation) if suspicion of plaque rupture is high and the bleeding risks are acceptable. The cardiologist may also recommend starting an ACE inhibitor and a statin.
MI and hemodynamically unstable: Consult a cardiologist; cardiac catheterization with percutaneous coronary intervention may be necessary. Patients that have recently discontinued antithrombotic medications for cardiac stent placement should be catheterized immediately to rule out acute stent thrombosis.
Aortic dissection: Consult a thoracic surgeon, keep the heart rate between 60 and 80 bpm (beta-blockers), and systolic BP between 100 and 120. Treat pain adequately to maintain pulse and BP within a target range. Urgent surgical intervention may be necessary depending on the location and type of dissection.
PE: Supplemental oxygen promotes pulmonary vascular dilation; vasoconstrictive agents and IV fluids should be given to treat hypotension. Anticoagulation with heparin, either unfractionated or low molecular weight, may be given to prevent clot progression; thrombolytic therapy may be considered. Consultation with the surgeon and an intensivist should be done prior to heparin and thrombolytic therapy since there is a great risk of major bleeding in postoperative patients.
Small pneumothorax: Typically resolves on its own without intervention. If large, a chest tube should be placed to decompress the air around the lung and allow for re-expansion.
Perforated viscus: Requires surgical intervention.
Aspiration pneumonia: Suction upper airway for any gastric content, provide supplemental oxygen, and consider intubation if signs of respiratory failure or poor oxygenation are present. Consider a pulmonary/critical care consult on the basis of severity.
GERD or esophagitis: Antacids, H₂ blockers, or proton pump inhibitors.
Costochondritis: Patient reassurance and adequate pain control.

Devereaux PJ , Goldman DJ , et al. Perioperative cardiac events in patients undergoing noncardiac surgery: A review of the magnitude of the problem, the pathophysiology of the events and methods to estimate and communicate risk. CMAJ. 2005;173(6):627–634.
Krieger-Grubel C , Hiscock R , Nandurkar S , et al. Physiology of diffuse esophageal spasm (DES)-when normal swallows are not normal. Neurogastroenterol Motil. 2010;22:1056–e279.
Devereaux PJ , Goldman L , Yusuf S , et al. Surveillance and prevention of major perioperative ischemic cardiac events in patients undergoing noncardiac surgery: A review. CMAJ. 2005;173(7):779–788.
Priebe HJ. Myocardial infarction-aetiology and prevention. Br J Anaesth. 2005;95(1):3–19.

Adesanya AO , de Lemos JA , Grilich NB. Management of perioperative myocardial infarction in noncardiac surgical patients. Chest. 2006;130:584–596.

See Also (Topic, Algorithm, Electronic Media Element)

Myocardial Infarction
Pneumothorax
Aortic Dissection
Aspiration Pneumonia
Gastroesophageal Reflux Disease
Anemia

ICD9

338.18 Other acute postoperative pain
786.50 Chest pain, unspecified

ICD10

G89.18 Other acute postprocedural pain
R07.9 Chest pain, unspecified

Postoperative chest pain can be caused by many different etiologies. It is critical to immediately rule out and treat the life-threatening causes.
Review the patient's medical history and intraoperative record for clues on the cause of postoperative chest pain. for example, does the patient have known CAD or GERD?
Perform a physical examination and order diagnostic testing as indicated
Implement treatment quickly and consult specialists as appropriate.

Philip Levin , MD

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Basics ⬇

Incidence

Mortality

Diagnosis ⬆ ⬇

Treatment ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆