CHEST PAIN diagnostic challenge of postoperative chest pain is distinguishing trivial disorders from myocardial ischemia and other serious problems. difficult in the postoperative period- severity of pain may correlate poorly with the seriousness of its cause.' Life-threatening disorders myocardial ischemia and infarction, arrhythmias, pulmonary edema, pneumothorax, and pulmonary embolism. Myocardial Ischemia and Infarction leading cause of death following anesthesia and surgery, (coronary artery disease) Preoperative cardiac risk factors uncompensated congestive heart failure, unstable angina, ventricular dysrhythrmas, hypertension, peripheral vascular disease, aortic stenosis, age over 70, and recent myocardial infarction. (Unstable angina, congestive heart failure, and previous myocardial infarction – highest) Risk of reinfarction - 6 to 30 % -less than three months before surgery, - 2 to 16 percent if between three and six months, and - 5 to 6 percent if longer than six months. When reinfarction occurs- mortality is approximately 50 percent. (most commonly within 24 to 72 hours after surgery (overall incidence of 0.1 to 0.7 percent in the general population.) Over 45 percent of those undergoing repair of abdominal aortic aneurysms have severe coronary artery disease Claudication may limit exercise and mask the symptoms of underlying ischemic heart disease Intraoperative factors associated with the greatest risk of perioperative cardiac morbidity are: (1) surgery involving the great vessels, thorax, or upper abdomen; (2) emergency surgery; and (3) the degree and duration of intraoperative hypotension. The postoperative period poses the greatest risk for patients with coronary artery disease changes in fluid balance, body temperature, pulmonary function, autonomic activity, and somatic stimulation create physiologic instability. Diagnosis Patients with risk factors -questioned about symptoms of ischernic heart disease before surgery. A history of angina, previous myocardial infarction, or exercise intolerance is especially important. The preoperative electrocardiogram (ECG) should be examined Medications used before surgery to treat ischemic heart disease should be reviewed. The cardiovascular effects of myocardial ischemia are predictable and progressive tachycardia, electrocardiographic ST-segment abnormalities, segmental wall-motion abnormalities, arrhythmias, hypoxemia, tachypnea, increases in pulmonary artery wedge or central venous pressures, and hypotension. Changes in blood pressure and heart rate(nonspecific) -important prognostic indices. Hypotension, a new holosystolic murmur of mitral regurgitation, an S3 gallop, and pulmonary rales suggest significant left ventricular dysfunction. Cool, pale, or cyanotic extremities suggest low diac output with peripheral vasoconstriction. The ECG remains the most important diagnostic study comparison with preoperative tracings may reveal subtle changges suggestive of myocardial ischemia. Serum levels of creatine kinase (CK) and not be useful because of the high incidence of false positive and delay in obtaining results. CK and CK-MB are related to specific procedures. Although there CK-MB activity after cystoscopy, there are marked increases in majority of patients after cholecystectomy. THERAPY Sinus tachycardia due to hypovolemia should be teated with fluids Hypertension and tachycardia from incisional pain should be treated with appropriate pain meds Hypoxemia and hypercarbia decrease myocardial oxygen delivery, increase sympathetic nervous system activity, and increase pulmonary vascular resistance. The treatment of myocardial ischemia in the postoperative patient is otherwise similar to that in nonsurgical patients except for the relative contraindications to intravenous heparin and thrombolysis administering oxygen, optimizing hematocrit with transfusions, and decreasing coronary vascular resistance while maintaining coronary perfusion pressure with pharmacologic agents. Nitroglycerin Calcium channel blockers reduce afterload. Beta-blockers decreasing contractility and heart rate. (desired negative inotropic effect of beta-blockers may precipitate congestive heart failure, especially in patients with preexisting left ventricular dysfunction.) Calcium channel blockers and nitroglycerin may cause hypotension. Nonselective beta-blockes may cause bronchospasm likely to occur 'in the 24 to 72 hours following surgery rather than during or just after the procedure. Mobilization of fluid; decreased monitoring leading to delayed intervention; and suboptimal control of incisional pain, activity, anemia, fever, and atelectasis may be contributing factors Other Common Causes of Chest Pain Preexisting esophageal disease, gastritis, or peptic ulcer disease may become symptomatic with the stress of surgery. Disease of the gallbladder and biliary system usually causes fight-upper quadrant pain but may also cause chest pain. Acute pancreatitis can simulate myocardial infarction clinically and produce ECG abnormalities suggesting subendocardial ischemia. Chest-wall trauma due to preoperative injury or surgical intervention can cause severe chest pain. Anterior chest-wall trauma may cause contusion of the right ventricle or biventricular injury and myocardial rupture if severe. Right ventricular contusion can lead to ischemic ECG changes, heart block, and dysrhythmias as well as right-heart failure. Echocardiogram can be helpful in showing a dilated hypokinetic right ventricle, tricuspid regurgitation, and sometimes hemopericardium. Diaphragmatic irritation is common during abdominal surgery and can cause upper-abdominal discomfort or chest pain radiating to the shoulders. Pleurodesis - creates a sterile pleuritis and can be painful enough to require general anesthesia. Costochondritis or Teitze's syndrome, caused by inflammation of the cartilaginous joints between the ribs and the sternum, is characterized by local tenderness and chest discomfort aggravated by respiration. Treatment includes nonsteroidal anti-inflammatory drugs, narcotics, and infiltration with local anesthestics. Chest pain due to pulmonary embolism is variable and may be absent, making diagnosis difficult. The symptoms of pericardial inflammation are difficult to distinguish from those of pulmonary embolism, pleuritis, and myocardial infarction, and may include chest pain, malaise, and dyspnea. Fever, rales, pericardial rubs, or effusions may be present. Characteristic ECG changes include transient global STsegment elevations followed by T wave inversion. The etiologies of pericarditis include trauma, tumor, infection, drug and myocardial infarction. Pericarditis occurring of an acute myocardial infarction is caused by an immune response to myocardial injury. However, when it develops several weeks months after the infarction, it is termed Dressler's syndrome. DYSPNEA as an "abnormally fortable. awareness of breathing The dyspneic patient is usually agitated and exhibits rapid breathing. Tachypnea, abnormal auscultatory findings, sternal tractions, and the use of accessory muscles may be presentor cyanosis may also be evident, and hypertension and tachacardia are common. Hypoxemia is common after general anesthesia because respiratory response to hypoxia is markedly depressed by residual thetics. In this setting, hypoxia can occur without dyspnea patients may experience dangerously low arterial oxygen without an increase in minute ventilation. Supplemental oxygen should therefore be administered to all patients after general thesia. Cardiac Dysfunction Dyspnea due to heart failure is caused by a decrease compliance from increased lung water, hypoxemia from intrapulmonary pulmonary shunting, and an increase in physiologic deadspace Decreased compliance increases the work of breathing. metabolic acidosis may further stimulatecenter to increase minute ventilation. Respiratory distress due to hypervolemia often develops 24 to 48 hours after surgery when interstitial fluid is being returned the vascular space. Diuresis is first-line treatment in severe volume overload and pulmonary edema may mechanical ventilation, positive end-expiratory pressure, or therapy. Antiarrhythmics or electrical cardioversion patients with new atrial fibrillation on examination and an enlarged cardiac may be helpful echocardiogram is the fluid. Airway Obstruction common sites of postoperative airway obstruction are the pharynx. Risk factors include obesity, a large tongue, the airway, a history of sleep apnea, abnormal airway and residual sedation. Surgical complications that may -airway obstruction include excessive bleeding, softng after pharyngeal or cervical surgery, and failure to I packs after airway or dental surgery. Patients with obstruction exhibit snoring, use of respiratory accessory muscles, work of breathing. Despite an increase in respiratory end tidal volume and minute ventilation result in hypoventilation Progressive hypercarbia and hypoxemia lead to obrespiratory failure, and cardiac arrest if untreated. oxygen should always be administered while efforts to identify and relieve the obstruction. examination should include inspection for tracheal deviation or swelling. The posterior oropharynx should be cleared of secretions, and other foreign matter, and a stable airway established. Alert and responsive patients can assist in obstruction by changing position, expectorating any foreign matter from the airway, and cooperating with placement of an nasopharyngeal airwav. Sedated patients have a higher risk pharyngeal tongue against the posterior pharyngeal wall, therapeutic subluxation of the jaw and placement of airway Lower Airway: Larynx, Trachea, and Bronchi The most common site of obstruction in the larynx is at the level of the vocal cords. In parathyroid and thyroid surgery, transient or permanent injury to the recurrent laryngeal nerve can cause unilateral vocal cord paralysis. Recurrent laryngeal nerve injury may necessitate postoperative tracheal intubation. Obstruction of the trachea or bronchi can be extrinsic or intrinsic. Reactive Airway Disease characterized by tachypnea, expiratory wheezing that may progress to loss of breath sounds, use of accessory muscles, intercostal retractions, nasal flaring, and increased sympathetic nervous system activity. Chest x-rays demonstrate hyperinflation with air-trapping. Arterial blood gas measurements and serum theophylline levels should be performed as indicated. Hypoxemia and hypocarbia are early findings; hypercarbia and respiratory acidosis supervene as the patient fatigues or bronchospasm worsens. Pulmonary Edema Pulmonary edema is an increase in lung water resulting in decreased lung compliance, increased work of breathing, and intrapulmonary shunting. Clinical manifestations include dyspnea, tachypnea, agitation, coughing, rales, wheezing, jugular venous distentions if associated with heart failure, cyanosis, and pink frothy sputum. Postoperative pulmonary edema can be cardiac or noncardiac in origin. Cardiac pulmonary edema due to hypervolemia or ischemic, hypertensive, or valvular heart disease. Treatment is dictated by the underlying disease. Noncardiac pulmonary edema can occur after reexpansion of a collapsed lung. Noncardiac edema can also be the result of inspiratory efforts made against an obstructed airway, adult respiratory distress syndrome, sepsis, and hypervolemia. Intravenous administration of naloxone can rarely provoke pulmonary edema Therapy includes oxygen administration, proper positioning, diuresis, fluid restriction, vasodilator therapy, and assisted or controlled ventilation with positive end-expiratory pressure. Retained Secretions Retained secretions are common after surgery and can cause ventilatory compromise. Factors predisposing patients to accumulate and retain secretions include preexisting inflammatory disease in the airways, as in pneumonia, bronchitis, and asthma; unopposed parasympathetic tone produced by acetylcholinesterase inhibitors used to reverse muscle relaxants; impaired mucociliary function in smokers and after inhalation anesthesia; and inability to generate an effective cough due to muscle weakness, sedation, or splinting. Such patients may exhibit dyspneap agitation, hypercarbia, and hypoxia. Restricted Lung Mechanics The causes of restricted lung mechanics vary but share similar pathophysiology. Lung expansion is impeded by compression due to pleural effusion, hemothorax, and pleural tumors; limited diaphragmatic excursion seen with bowel distention, obesity, ascites, and suboptimal positioning; and restricted chest-wall mobility due to surgical dressings, term pregnancy, chest restraints, positioning, and obesity. Muscle Weakness tive dyspnea may be caused by muscle weakness. effects of muscle relaxants are potentiated by a variety of including antibiotics such as aminoglycosides, polymyxins, lincomycins; residual inhalational anesthetics, magnesium; anesthetics; calcium channel blockers; and quinidine. delayed recovery and prolonged paralysis may occur with hypokalemia hypermagnesemia, hypocalcemia, respiratory acidosis, metabolic alkalosis, and hypothermia. Patients with myasthenia gravis, Eaton-Lambert syndromes and myotonia are more sensitive to muscle relaxants and can experience postoperative weakness even if such agents are not administered during surgery. All patients with neuromuscular disorders should be monitored for weakness in the postoperative period, and provisions should be immediately available if assisted ventilation is required. An uncommon cause of ventilatory failure is paralysis of the diaphragm caused by surgical trauma to the phrenic nerve in head and neck surgery, cardiac surgery, regional nerve block or certain positions. However, unilateral phrenic nerve dysfunction rarely causes significant respiratory compromise in patients with otherwise normal lung functional Trauma Direct trauma to the chest can cause rib fractures, pneumothorax, and pulmonary contusion. Dyspnea is common and may be associated with hypoxemia, airway obstruction, splinting, chest-wall tenderness, flail chest, and multiple organ system injury. Cardiac contusion, aortic dissection, and tracheal or bronchial lacerations should also be considered. Lung contusions usually produce local hemorrhage and pulmonary thrombosis. The severity of hypoxemia produced by pulmonary contusion parallels the extent of parenchymal involvement and airway compromise. Most contusions improve rapidly if the airways are clear of blood. Central venous access was placed in the subclavian or internal jugular veins. Treatment consists of ventilatory support until pulmonary function is self-supporting. A pneumothorax of more than 20% or associated with respiratory distress requires placement of a chest tube Blunt injury to the phrenic nerve frequently causes transient dysfunction and does not compromise pulmonary function unless there is bilateral involvement, other pulmonary injury, or preexisting lung disease. Pain Pain is a potent respiratory stimulant that increases respiratory rate and minute ventilation and decreases tidal volumes. The breathing pattern changes to minimize pain, frequently resulting in abnormal ventilatory mechanics that increase the work of breathing and total body oxygen consumption. . Adverse Drug Reactions Adverse drug reactions have been classified as predictable and unpredictable. 89 Predictable reactions account for about 80 percent of such drug responses and are dose-dependent, due to direct drug toxicity, or related to a predictable secondary effect such as druginduced histamine release. Unpredictable reactions are associated with unexpected immunologic responses due to anaphylactic (antibody-mediated) or anaphylactoid mechanisms. Aspiration Residual sedation, nausea, obesity, gastric distention, pregnancy, recent food ingestion, cholinergic agents, or bowel irritation may lead to passive regurgitation or vomiting in the postoperative period. Precautions should be taken to minimize the risk of aspiration and the extent of pulmonary injury should it occur. Prophylactic therapy is aimed at decreasing gastric volume, increasing gastric pH, and identifying those patients who require airway precautions Nonparticulate antacids like sodium citrate can be used to increase gastric pH. Gastric volume can be reduced by evacuating the ach with a nasogastric tube, increasing gastric emptying with clopramide, and decreasing acid secretion with H2 blockers. Patients in whom nausea is expected should be extubated only when they are awake and capable of protecting their airways. The clinical manifestations of aspiration depend on the position and quantity of the aspirate and underlying pulmonary tion. Chunks of food can obstruct large atelectasis, ventilation-perfusion mismatch acidic aspirate with pH under 2.5 inhibits ciliary causes a severe chemical pneumonitis. Dyspnea and respiratory distress begin abruptly The mouth and oropharynx should be suctioned immediately the head down to minimize further aspiration. Oxygen therapy crucial to treat the increased intrapulmonary shunting and hy Intubation is indicated if respiratory failure becomes im Steroids are not recommended, and prophylactic antibiotics controversial. SUMMARY 1. The differential diagnosis of postoperative chest pain is extensive and requires meticulous review or the sumptoms, medical history, physical exmamination, current medications, laboratory data and intraoperative anesthetic and surgical management. 2. Myocardial ischemia must be differentiated from causes of chest pain, including preexisting esophageal diseasse, gastritis, or peptic ulcer; gallbladder and biliary system disease; pancreatitis; pulmonary embolism; pericarditis, including postpericardiotomy syndrome; pneumottiorax; cliest wall trauma; diaphragm irritation resulting from abdominal surgery; and costochondritis 3. Preoperative cardiac risk gestive heart failure, unstable angina, ventricular dysrhythia hypertension, peripheral vascular disease, aortic stenosis, age 70, and a history of a previous myocardial infarction. Intraoperative risk factors include surgery involving the great vessels, or upper abdomen, emergency surgery, and the degree and duration of intraoperative hypotension. 4. The postoperative period poses the greatest risk for with underlying coronary artery disease undergoing no surgery. Postoperative myocardial ischemia occurs in more than 40 percent of high-risk patients and carries a threefold increase is risk of an adverse cardiac event. Most ischemic events within 24 to 72 hours after surgery. 5. The presentation of postoperative myocardial infarction can be atypical, and electrocardiographic and serum enzyme abnormal r ities can be nonspecific and misleading. Continuous intraoperative and postoperative monitoring is recommended in high-rise mi The treatment of postoperative myocardial ischemia is the same in other patients except for the relative contraindications and thrombolytic therapy. 6. Postperative dyspnea include pneumo dial tamponade, upper- and lowerway disease, noncardiac pulmonary tricted lung mechanics, preexisting dysfunction, muscle weakness, trauma, pain, adverse reactions and aspiration. Careful analysis of the history, and laboratory data establish the individual natient Other causes of posto pleural effusion, pericar obstruction, reactive air retained secretions, restricted I%mmlee JE, Boettner RB: Myocardial infarction during and following anesthesia and operation. South Med J 65:886-889, 1972. Gc4dman L, Caldera DL, Nussbaum SR et at: Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 297: ~S45-850, 1977. 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