CHEST PAIN diagnostic challenge of postoperative chest pain is

Document Sample
CHEST PAIN diagnostic challenge of postoperative chest pain is Powered By Docstoc
diagnostic challenge of postoperative chest pain is distinguishing trivial disorders from myocardial ischemia and other serious
difficult in the postoperative period- severity of pain may correlate poorly with the seriousness of its cause.' Life-threatening disorders
           myocardial ischemia and infarction,
           pulmonary edema,
           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,
         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.

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
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.

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.

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
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.

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

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
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

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

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
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

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.

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.

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.
Foger ED, Davis KB, Carpenter JA et at: Risk of noncardiac opera,um in patients with defined coronary disease: The coronary artery
sorgery study (CASS) registry experience. Ann Thorac Surg 41:4250- 1986.
Hertzer NR, Beven EG, Young JR et at: Coronary artery disease in peripheral vascular patients. A classification of 1000 coronary
angio grams and results of surgical management. Ann Surg 199:223-233 1984.
Goldman L: Cardiac risks and complications of noncardiac surgery. Un Intern Med 98:504-513, 1983.
Rao TLK, Jacobs KH, EI-Etr AA: Reinfarction following anesthesia m patients with myocardial infarctions. Anesthesiology
Dershwitz M, Sherman EP: Acute myocardial infarction symptoms masked by epidural morphine? J Clin Anesth 3:146-148, 1991.
Mangano DT, Browner WS, Hollenberg M et at: Association of peri
,perative myocardial ischemia with cardiac morbidity and mortality in
men undergoing noncardiac surgery. N Engl J Med 323:1781-1-1990.
15. Marriott HKL: Myocardial infarction, in Practical Echocardiograph 7th ed. Baltimore, Williams & Wilkins, 1983, pp 373-401.
Weinfurt PT: Electrocardiographic monitoring: An overview. J Chn Monit 6:132-138, 1990.
17. Kotter G, Konly K, Kalbfleisch I et at: Myocardial ischemia during cardiovascular surgery as detected by an ST-segment trend
monitoring system. J Cardiothorac Anesth 1:190-199, 1987.
18. Roger MC, Abildskov JA, Preston JB: Neurogenic ECG changes in critically ill patients: An experimental model. Crit Care Med
1:192, 1973.
Presswitz W, Neumier D: Creatine-kinase and CK-MB isoenzyme activity in serum of patients after surgical operations, polytrauma
and other damage to skeletal muscle. Clin Biochem 12:225, 1979.
20. Buja LM, Parkey RW, Dees JH et at: Morphologic correlates of 99-technetium stannous pyrophosphate imaging of acute
myocardial infarcts in dogs. Circulation 52:596-607, 1975.
21. Holman BL, Wynne J: Infarct avid (hot-spot) myocardial scintigraphy. Radiol Clin N Am 18:487-499, 1980.
22. Pflugfelder PW, Wisenberg G, Prato FS et at: Early detection of canine myocardial infarction by magnetic resonance imaging in
vivo. Circulation 71:587-594, 1985.
23 McNamara MT, Higgins CB, Schectmarm N et at: Detection and characterization of acute myocardial infarction in man with use of
gated magnetic resonance. Circulation 71:717-724, 1985.
Lieberman RW, Orkin FK, Jobes DR et at: Hemodynamic predictors of myocardial ischemia during halothane anesthesia for coronary
artery revascularization. Anesthesiology 59:36-41, 1983.
Prys-Roberts C, Meloche R, Foex P: Studies of anaesthesia in relation to hypertension: 1. Cardiovascular responses to treated and
untreated patients. Br J Anaesth 43:122-137, 1971.
Steen PA, Tinker JH, Tarban S: Myocardial reinfarction after anesthesia and surgery. JAMA 239:2566-2570, 1978.
London MJ, Hollenberg M, Wong WG et at: Intraoperative myocardial ischemia: Localization by continuous 12-lead
electrocardiography. Anesthesiology 69:232-241, 1988.
van Daele ME, Sutherland GR, Mitchell MM et at: Do changes in pulmonary capillary wedge pressure adequately reflect myocardial
ischemia during anesthesia: A correlative preoperative hemodynamic, electrocardiographic, and transesophageal echocardiographic
study Circulation 81:865-871, 1990.
Smith IS, Cahalan MK, Benefiel DJ et at: Intraoperative detection of myocardial ischemia in high-risk patients: Electrocardiography
versus two-dimensional transesophageal echocardiography. Circulation 72: 1015-1021, 1985.
30. Buffington CW, Coyle RJ: Altered load dependence of postischernic myocardium. Anesthesiology 75:464-474, 1991.
MacIntyre PE, Pavlin EG, Dwersteg JF: Effect of meperidine on oxygen consumption, carbon dioxide production, and respiratory gas
exchange in postanesthesia shivering. Anesth AnaIg 66:751-755, 1987.
32 Gibbs CP, Schwartz DJ, Wynne JW et at: Antacid pulmonary aspira tion in the dog. Anesthesiology 51:380-385, 1979.
33. Radnay PA, Duncalf D, Novakoric M et at: Common bile duct presure changes after fentanyl, morphine, meperidine, butorphanol
and naloxone. Anesth Analg 63:441-444, 1984.
34. Engle MA, Gay WA Jr, Kaminsky ME et at: The postpericardiotom% syndrome then and now. Curr Prob Cardiol 312:1-40, 1978.
35. Kassanoff AH, Martirossian MG: Postpericardiotomy and postmyocardial infarction syndrome presenting as noncardiac pulmonar~
edema. Chest 99(6):1410-1414, 1991.
36 Walton K, Holt PJ: Rheumatic symptoms after cardiac surgery: A prospective study. Br Med J 197(6640):21-24, 1988.
37. Miller RH, Horneffer PJ, Gardner TJ et at: The epidemiology of the postpericardiotomy syndrome: A common complication of
cardiac surgery. Am Heart J 116(5):1323-1329, 1988.