Airway, Breathing, Circulation
Begin Supplemental Oxygen
Give oxygen by nasal cannula or face mask, pending further evaluation.
Begin Continuous Cardiac Monitoring
Begin cardiac monitoring with pulse oximetry and treat life-threatening arrhythmias (Chapters 9 and 34).
Look for Markedly Abnormal Hemodynamics
Look for signs of shock. Altered sensorium, pale clammy skin, oliguria, and respiratory distress may result from arterial hypotension and poor peripheral perfusion.
Management of the Patient with Chest Pain and Abnormal Hemodynamics
Treatment and Disposition
Insert two large-bore (≥16-gauge) intravenous catheters. Intraosseous (IO) access is acceptable and compatible with all resuscitation infusions including thrombolytics. Obtain blood for a complete blood count (CBC), markers of cardiac injury, and basic metabolic panel (electrolytes, glucose, renal function). Begin administration of intravenous fluids based on estimate of intravascular fluid volume.
Infuse 250–500 mL of intravenous crystalloid solutions (normal saline or lactated Ringer's). Monitor the response (blood pressure, urine output, sensorium).
Central Venous Hypervolemia (with or Without Shock or Hypotension)
Pending more precise diagnosis, infuse normal saline to keep the intravenous catheter patent or place a saline lock IV.
Briefly examine the pulmonary and cardiovascular systems, and palpate the abdomen for presence of a pulsatile mass. Obtain a 12-lead electrocardiogram (ECG). Obtain arterial blood for blood gas and pH determinations. Avoid unnecessary arterial punctures if the patient is a candidate for thrombolytic therapy for acute myocardial infarction. Obtain a portable chest radiograph. Insert a urinary catheter.
Hypotension or Shock Present
Central Venous Hypovolemia
Hypovolemia is manifested by collapsed neck veins, clear lung fields on physical examination or chest X-ray, and absence of peripheral edema. Table 14–1 lists the differentiating features of the three most important conditions causing chest pain with hypotension with central venous hypovolemia.
Table 14–1. Differentiating Features of Conditions Causing Chest Pain with Hypovolemia. |Favorite Table|Download (.pdf)
Table 14–1. Differentiating Features of Conditions Causing Chest Pain with Hypovolemia.
|Myocardial infarction with vagotonia||Crushing chest pain; nausea||Bradycardia; stable hypotension||Acute infarction pattern and bradycardia||Nonspecific|
|Aortic dissection||Tearing chest pain; back pain; often history of hypertension||Tachycardia; pulse deficits; progressive hypotension||Nonspecific or may show ischemia or infarction pattern, left ventricular hypertrophy||Widened mediastinum; pleural fluid. CT scan is more sensitive than X-ray|
|Leaking upper abdominal aortic aneurysm||Chest and epigastric pain||Tachycardia; pulsatile epigastric mass||Nonspecific||CT scan or ultrasound is more sensitive than X-rays|
If the diagnosis is uncertain, treatment should be oriented primarily toward aortic dissection (Chapter 40). Type and crossmatch for 6–10 units of packed red blood cells. Expand intravascular volume with administration of intravenous crystalloid solution. Consider inserting a central venous catheter. For severe hypovolemia with shock, up to 3 L of crystalloid solution may be given rapidly (over 30–60 minutes) to restore normal hemodynamics until crossmatched blood is available. If there is no response to crystalloid solution, type-specific or universal donor blood (O negative, low antibody titer, or erythrocyte antigens) may be used pending the availability of crossmatched blood. Maintain blood pressure with continued infusion of blood and crystalloid solution. Obtain emergency vascular or thoracic surgical consultation.
Pulse deficits, an abdominal mass, or occult hematuria indicate aortic aneurysm or dissection. Obtain a portable chest X-ray and if the patient is stable consider computed tomography (CT) scan of the chest or abdomen and pelvis if indicated. Bedside ultrasound, if available, can be of great assistance in the diagnosis and management of these patients.
Management of thoracic aortic dissection consists of β-blockade (esmolol) to maintain heart rate less than 60–80 beats/min and vasodilators (nitroprusside) to maintain a systolic blood pressure less than 120 mm Hg, establishing the β-blockade first. Dissections involving the ascending aorta are managed surgically, while those not involving the ascending aorta are generally managed medically. For medical management, hospitalize the patient in an intensive care setting immediately for further evaluation and treatment.
Central Venous Hypervolemia
Superficial veins (especially neck veins) are distended; pulmonary and peripheral edema may be present. See Table 14–2 for guidelines to differential diagnosis.
Table 14–2. Distinguishing Features of Conditions Causing Chest Pain, Hypotension, or Shock in Association with Distended Neck Veins. |Favorite Table|Download (.pdf)
Table 14–2. Distinguishing Features of Conditions Causing Chest Pain, Hypotension, or Shock in Association with Distended Neck Veins.
|Diagnosis||Helpful Distinguishing Features|
|Tension pneumothorax||Hyperresonant hemithorax with decreased breath sounds; chest X-rays diagnostic, trachea deviates away from affected side|
|Cardiac tamponade||Faint heart sounds; ECG with diffuse low voltage or electrical alternans. Pulmonary edema rare. Echocardiography diagnostic|
|Cardiogenic shock (arrhythmogenic)||ECG or cardiac monitor shows severe bradycardia or tachycardia (ventricular rate <50 beats/min, usually <40 beats/min, usually >180 beats/min). Signs of myocardial ischemia may also be present|
|Cardiogenic shock (myocardial)||Pulmonary edema almost always present. ECG almost always shows pattern diagnostic of infarction|
|Pulmonary embolism (massive)||Physical examination, ECG, and chest X-ray show signs of right heart strain. Chest X-ray may show infiltrates, effusion, or truncation of pulmonary vasculature. Confirm diagnosis by ventilation–perfusion scanning, spiral CT scan of chest or pulmonary arteriography|
(See Chapter 24) Consider tension pneumothorax immediately because this condition may be quickly and reliably differentiated from the others and is easy to treat. Look for marked respiratory distress, tracheal deviation away from the affected side, and a hyperresonant hemithorax with markedly decreased or absent breath sounds on the affected side. Chest X-ray confirms the diagnosis, but treatment should not be delayed to obtain a chest X-ray. Treatment consists of the insertion of a thoracostomy tube if one is readily available (Chapter 7). Otherwise, a 14-gauge needle inserted in the second intercostal space at the midclavicular line or in the fourth intercostal space at the anterior axillary line relieves tension in the chest until a thoracostomy tube can be inserted. Hospitalize the patient for further care.
(See Chapter 24) Cardiac tamponade should also be diagnosed early because treatment is reasonably effective but differs markedly from that for cardiogenic shock, heart failure, or pulmonary embolism. Look for hypotension, jugular venous distension, and muffled heart sounds (Beck triad). Electrocardiographic manifestations may include low voltage on all leads, electrical alternans, or diffuse ST-segment elevation typical of pericarditis. A narrow pulse pressure and pulsus paradoxus may also be present. Pulmonary edema is rare. Because acute tamponade does not cause cardiomegaly, chest X-ray is not helpful. Definitive diagnosis by noninvasive methods is best done by bedside emergency ultrasound or formal echocardiography. Attempt volume expansion with intravenous administration of 500–1000 mL of crystalloid solution over 20–30 minutes if the diagnosis is confirmed (this therapy is disastrous for cardiogenic shock). If the initial trial succeeds in elevating the blood pressure, volume expansion may be repeated once in a patient whose systolic blood pressure subsequently drops to less than 90 mm Hg.
Obtain emergency cardiothoracic consultation for therapeutic pericardiocentesis, which should be performed in the operating room or under echocardiographic or fluoroscopic guidance. If rapid, progressive hypotension develops and the patient fails to respond to volume expansion perform immediate pericardiocentesis (under ultrasound guidance if available) (Chapter 6). Hospitalize the patient at once in an intensive care unit.
Cardiogenic Shock (Arrhythmogenic)
See Chapter 35 for further details on the diagnosis and treatment of cardiac arrhythmias.
Severe Bradydysrhythmia (Heart Rate Usually <40 Beats/Min)
Give atropine, 0.5 mg intravenously; if necessary, repeat every 5–10 minutes up to a total dose of 0.04 mg/kg. An external transcutaneous pacemaker (Chapter 7) may be applied to increase the heart rate until a percutaneous transvenous pacemaker can be inserted, if indicated. Epinephrine infusion can be used for patients that do not respond to atropine. Begin an infusion at 2–10 μg/min and titrate to patient response. Assess intravascular volume and support as needed. Dopamine can be used to support blood pressure and increase myocardial contractility. Infuse at a rate of 10–20 μg/kg/min by continuous intravenous infusion. It may be administered with epinephrine or administered alone. Titrate the dose to patient response. Consider IV glucagon, 3 mg initially, followed by infusion at 3 mg/hour for patients with hypotension and bradycardia from either B-blocker or calcium channel blocker overdose.
Severe Tachydysrhythmia (Heart Rate Usually >150 Beats/Min)
Immediate cardioversion is the treatment of choice for tachydysrhythmia-induced shock. Deliver 50–100 J of synchronized direct current counter shock initially, and increase the shock by 50–100 J increments if there is no response. (If the patient is STABLE ie, no alteration in mental status, no chest pain, no shock or hypotension see Chapter 34).
Cardiogenic Shock (Myocardial Infarction)
(See also Chapter 34) In patients with no evidence of pulmonary edema, ensure adequate intravascular volume; give intravenous crystalloid solution, 250–500 mL over 30 minutes. If blood pressure improves, maintain the infusion at a rate of 100–200 mL/h. Avoid unnecessary arterial punctures in patients who may be candidates for thrombolytic therapy.
Give dobutamine 5–20 mcg/kg/min IV continuous infusion, dopamine 5–20 mcg/kg/min IV continuous infusion; increase by 1–4 mcg/kg/min q10–q30 minutes to optimal response, or a combination of both if no change in blood pressure occurs or if severe shock or pulmonary edema is present initially. Dobutamine is the drug of choice for treatment of cardiogenic shock due to pump failure. Caution: Observe for signs of dysrhythmia.
Give morphine, 2–4 mg intravenously every 5–20 minutes, until pain and dyspnea are controlled. If hypotension is a concern, then fentanyl may be used for pain. Carefully monitor the patient's respiratory status.
Nitroglycerin should generally be avoided in patients in cardiogenic shock or blood pressure less than 90 mm Hg systolic.
Consider aspirin 325 mg orally if aortic dissection is unlikely. In patients with aspirin allergy or expected deferred catheterization clopidogrel may be used.
Obtain cardiology consultation immediately if an acute infarction pattern is evident on the 12-lead ECG. Emergency reperfusion therapy with thrombolytic agents or percutaneous coronary intervention has been shown to be of benefit in decreasing the mortality rate and the size of the infarct. If thrombolytic therapy is to be used (Chapter 35), it should be initiated in the emergency department by the emergency physician, avoiding the delay necessitated by obtaining cardiologic consultation or transporting the patient to the coronary care unit. Hospitalize the patient immediately in a coronary care or intensive care unit.
Massive Pulmonary Embolism
(See Chapter 33) Because massive pulmonary embolism is a difficult diagnosis to confirm rapidly, every attempt should be made to exclude other causes of chest pain with shock. Consider an emergency echocardiogram if available. Findings consistent with massive pulmonary embolism include right ventricular hypokinesis and dilation. Right ventricular dysfunction from pulmonary embolism predicts increased mortality and the need for thrombolytic therapy.
Administer 250–500 mL of normal saline over 20–30 minutes in an effort to elevate systolic blood pressure. The dose may be repeated if the trial is successful and if heart failure does not develop. In the rare patient with hypotension without central venous hypervolemia, a fluid challenge should also be given, but a larger dose (500–1000 mL of normal saline instead of 300–500 mL) may be administered.
Give dopamine (see above). If clinical signs strongly suggest pulmonary embolism and thoracic dissection has been ruled out (computerized tomography may be useful in definitively establishing either of these diagnoses), begin heparin (unfractionated or a low-molecular-weight heparin) (see Pulmonary Embolism, below, and Chapters 33 and 34). Obtain pulmonary consultation, and consider thrombolytic therapy.
Hypotension or Shock Not Present
Central Venous Hypervolemia
Superficial veins (especially neck veins) are distended. Pulmonary and peripheral edema is common. Blood pressure is normal or (more commonly) elevated.
Acute exacerbation of congestive heart failure is the most common cause. It occasionally results from acute myocardial infarction (acute cardiogenic pulmonary edema), and less commonly from acute myocarditis or pericardial effusion.
Nitroglycerin may be quickly administered either sublingually (0.4 mg) or transdermally (nitroglycerin ointment 1.25–2.5 cm) (½–1 inch). An intravenous nitroglycerin infusion may be started in the emergency department. Monitor the blood pressure closely, and if hypotension develops, place the patient in the Trendelenburg position and decrease the infusion rate. Avoid nitrates in patients taking any selective phosphodiesterase 5 inhibitor (sildenafil [Viagra], tadalafil [Cialis], or vardenafil [Levitra]).
Give furosemide, 0.5–1.0 mg/kg, by bolus intravenous injection. The initial effect of rapid preload reduction is of immediate benefit; diuresis occurs later.
Give morphine, 2–4 mg intravenous, and repeat every 5–10 minutes until pain and dyspnea are relieved.
Give aspirin, 160–325 mg chewed, if not contraindicated. If the patient has an allergy to aspirin, use clopidogrel, 75 mg orally.
Angiotensin-Converting Enzyme (ACE) Inhibitors
Captopril and enalapril are associated with reduced admission rates to the intensive care unit and decreased endotracheal intubation rates. Acutely, reduction in preload and afterload has been reported. For oral or sublingual captopril, a one-time dose of 12.5 or 25 mg is given; enalapril is given as a 1.25 mg intravenous infusion over 5 minutes. Avoid using ACE inhibitors in patients who are hypotensive, pregnant, hyperkalemic, or have renal insuffiency.
Positive Pressure Ventilation
If the patient continues to deteriorate, consider early noninvasive positive pressure ventilation (BiPAP or CPAP); this approach may even prevent the need for endotracheal intubation.
Short-term inotropic therapy can improve hemodynamic parameters. These agents may be beneficial for patients who are unable to receive conventional therapy. Milrinone or dobutamine are reasonable choices.
Has been shown by meta-analysis to actually increase mortality but can be considered in patients who cannot tolerate nitroglyerin. It is costly and has no additive benefit to nitroglycerin.
Hospitalize the patient immediately in an intensive care setting.
Management of the Patient with Severe Chest Pain and Normal Hemodynamics
The patient is in acute distress because of chest pain but is neither hypotensive nor in shock.
Differential Diagnosis by Location and Quality of Pain
Evaluation of patients who complain of chest pain but are not in severe distress should proceed in a systematic fashion. The single most useful means of evaluation is the carefully elicited history supplemented by examination of the heart, lungs, abdomen, and peripheral vessels in conjunction with electrocardiography and chest X-ray. Consider most of the diagnostic possibilities at least briefly in every patient who presents with chest pain (Table 14–3).
Table 14–3. Diagnostic Clues to Cause of Chest Pain.a |Favorite Table|Download (.pdf)
Table 14–3. Diagnostic Clues to Cause of Chest Pain.a
|Cause||Previous Attacks of Similar Pain||Location||Character||Onset||Duration||Common Associated Findings||Signs||Other Abnormalities||Other Comments|
|Angina||Usually||Restrosternal, radiating to arms, neck, back, or epigastrium||Squeezing, dull ache||Often with stress or exercise||2–10 min up to 20–30 min||Occasionally dyspnea; dizziness and syncope rare||Often none. S4, occasionally||ECG often normal between attacks||Relieved by nitroglycerin|
|Acute myocardial Infarction||In some cases||Restrosternal, radiating to arms, neck, back, or epigastrium||Squeezing, dull ache, increase with time||No precipitating factor necessary||>30 min||Nausea and vomiting, diaphoresis, dyspnea||Heart failure, restlessness, shock; cardiac examination often normal||ECG may be diagnostic or normal||Elevated CK, CK-MB isoenzymes and Troponin I or T. Normal isoenzymes levels on one determination do not exclude diagnosis|
|Mitral valve prolapse||Usually||Variable||Variable||Variable||Variable; usually hours||Dyspnea, dizziness common; syncope in some||Midsystolic click or murmur in most cases||ECG may shown inverted T waves on leads II, III, and aVF. Echocardiogram is diagnostic||Arrhythmia or sudden death may occur. Usually seen in young women, high-arched palate or chest or spine deformities may be present|
|Aortic stenosis||May have occurred||Like angina||Like angina||Like angina||Like angina||Syncope, dyspnea||Systolic ejection murmur transmitted to carotid arteries; delayed carotid pulse||ECG usually shows left ventricular hypertrophy. Echocardiography and angiocardiography are diagnostic||More common in older men|
|Aortic regurgitation||May have occurred||Like angina||Like angina||Like angina||May be prolonged||Dyspnea||Diastolic murmur transmited to carotid arteries. Water-hammer and Quincke's pulse. Wide arterial pulse pressure||ECG may be normal or may show left ventricular hypertrophy. Echocardiographyand angiocardiography are diagnostic||History of rheumatic heart disease, connective tissue disease, or syphilis|
|Pericarditis||May have occurred||Retrosternal||Variable; often pleuritic and relieved by sitting||Variable||Hours to days||Variable||Pericardial friction rub in many||ECG may be diagnostic, nonspecific, or normal. Echocardiography often shows fluid||Recent history of upper respiratory Infection|
|Aortic dissection||No||Retrosternal and back||Tearing, maximal at onset||Sudden||Variable||Myocardial infarction, stroke, limb ischemia, syncope||Stroke, absent pulses, hematuria, shock||Chest X-ray may show widened mediastinum or be normal. ECG may show acute myocardial infarction. Pulsatile abdominal mass||Angiography or CT scan is definitive. Hypertension or connective tissue disease may be present|
|Pleurisy||In some cases||Variable; usually lateral thorax||Pleuritic||Usually sudden||Variable||Subjective dyspnea||Often none. Occasionally friction rub, low-grade fever||Occasionally pleural effusion||Negative lung scan, spiral chest CT scan, or pulmonary angiogram|
|Pneumothorax||May have occurred||Variable||Variable often pleuritic||Usually sudden||Variable||Dyspnea and cough; shock if tension pneumothorax is present||Tachycardia, lung collapse with or without mediastinal shift||Chest X-ray is diagnostic but needs careful examination|
|Pneumomediastinum||No||Retrosternal||Variable; often pleuritic||Usually sudden||Variable||Dyspnea||Mediastinal crunch||Chest X-ray is diagnostic. Pneumothorax common||Consider esophageal perforation as cause|
|Pulmonary hypertension||Usually||Retrosternal||Like angina||Like angina||Variable||Dyspnea, fatigue, exercise syncope||Loud P2, right ventricular lift||ECG show right heart strain. Chest X-rays shows signs of pulmonary hypertension|
|Pulmonary embolism||May have occurred||Variable; usually lateral thorax||Usually strong pleuritic component||Usually sudden||Minutes to hours||Dyspnea, cough, and tachypnea; hemoptysis sometimes||Friction rub or splinting in some||Hypoxemia and hypocapnia. Chest X-ray usually abnormal, but findings are not specific||Abnormal ventilation–perfusion radionucleotide lung scan, spiral CT chest, or pulmonary angiogram|
|Pneumonia||Rare||Over affected lobe||Pleuritic||Variable||Variable||Fever and chills, cough, dyspnea, sputum production||Fever, rales with or without consolidation, friction rub||Infiltrates on chest X-ray; purulent sputum|
|Esophagitis Esophageal spasm Hiatal hernia||Usually||Retrosternal or epigastrium||Changes with eating||Usually gradual||Variable||Gastrointestinal symptoms||None||Positive barium swallow or endoscopy||Relieved by antacids, H2 blockers, or proton pump inhibitors|
|Perforated esophagus||No||Retrosternal||Severe||Usually sudden||Variable||Variable||Subcutaneous emphysema, mediastinal crunch||Chest X-ray usually shows pneumomediastinum, pneumothorax, or pleural effusion. Esophagogram or esophagoscopy is diagnostic||History of severe retching or vomiting or esophageal trauma or instrumentation.|
|Perforated duodenal ulcer||No, or milder pain of ulcer||Retrosternal to epigastrium||Severe||Variable||Variable||Variable||Epigastric pain. May have prominent findings of peritoneal irritation||Free air in peritoneum; elevated amylase||Rare as cause of chest pain|
|Pancreatitis||May have occurred||Retrosternal to epigastrium||Variable||Variable||Hours to days||Vomiting, anorexia||Epigastric or upper quadrant tenderness||Markedly elevated serum lipase or amylase||Rare as cause of chest pain|
|Cholecystitis||Usually||Right upper quadrant; occasionally epigastrium or retrosternal||Variable||Usually sudden||Hours to days||Vomiting, anorexia, fever||Epigastric or right upper quadrant tenderness||Abnormal liver function tests. Sonography usually diagnostic||Rare as cause of chest pain|
|Musculoskeletal disorder (eg, Tietze's syndrome, stitch), rib fracture||Variable||Costochondral junction; retrosternal and lateral||Pleuritic ache, “sticking” sensation||Gradual to sudden||Variable; fleeting for stitch||Splinting||Tender (or, rarely, swollen), costosternal junction, especially first and second ribs. Point tenderness over affected ribs||None.||Relieved by lidocaine-corticosteriod injection.|
Retrosternal discomfort, especially if it is a tightness, pressure, or “squeezing” pain, should suggest serious underlying disease, for example, myocardial infarction, unstable angina due to atherosclerosis or valvular heart disease, pericarditis, dissection of the aorta, or pulmonary embolism. When the abovementioned diagnoses are excluded, esophageal disease (eg, spasm, esophagitis) is the most common cause of retrosternal distress (see below). Because esophageal disease is relatively benign and rarely requires hospitalization, the more serious causes of retrosternal discomfort must be excluded with a high degree of certainty before concluding that the pain is of esophageal origin.
Pain that is markedly worse on inspiration should suggest pleurisy associated with pneumonia, pulmonary embolism, or isolated pleuritis. The pain of pneumothorax, pneumomediastinum, ruptured esophagus, and pericarditis frequently has a pleuritic component. The fleeting pain of a “stitch in the side” is often pleuritic in nature as well. Chest pain due to myocardial infarction may have a pleuritic component.
One of the most serious causes of pleuritic chest pain, pulmonary embolism, is also one of the most difficult to diagnose given the widely varied presentations of the disease with nonspecific history and physical examination findings. Because of the increased mortality associated with misdiagnosis, consider pulmonary embolism in all patients presenting with pleuritic chest pain (Chapters 33 and 35).
Back or Abdominal Pain with Chest Pain
Abdominal pain that is inferior to the xiphoid process and associated with chest pain should suggest intra-abdominal disease, dissecting aortic aneurysm, or possibly myocardial ischemia. In stable patients, CT scan of the chest and abdomen with intravenous contrast can reliably exclude the diagnosis of dissecting or ruptured aortic aneurysm. Even after aortic catastrophes are excluded, patients with chest pain often require hospitalization or admission to an observation unit to rule out myocardial ischemia.
Musculoskeletal disease with chest pain (Tietze's syndrome, rib fracture) is usually associated with marked tenderness localized over the affected site. Patients with chest pain referred from intrathoracic structures may also have some associated tenderness of superficial structures. Most patients with chest pain from musculoskeletal disorders can receive treatment in the emergency department and be discharged for outpatient follow-up care.
An emerging method of evaluation of chest pain in the Emergency Department is the Chest Pain Unit. Various structures can be utilized, but most are protocol-driven observation units intending to screen low risk patients for cardiac origin of chest pain. Often located in the ED proper, the Chest Pain Unit is a virtual observation unit holding patients in preparation for some form of noninvasive stress testing.
The protocols usually include serial electrocardiograms, serial markers of cardiac injury, telemetry, and risk stratification. Certain exclusion criteria typically apply: existing coronary artery disease, diabetes mellitus, stimulant induced chest pain, and sometimes female patients. These populations are thought to have higher likelihood of silent ischemia, reduced exercise tolerance, or increased risk of adverse events when undergoing stress testing.
The Chest Pain Unit will likely grow in sophistication and see more widespread use in the future of emergency medicine. In centers with large indigent populations who may have difficulty obtaining outpatient follow up, emergency physicians will increasingly incorporate this observational method. As an alternative to hospital admission, this diagnostic modality offers a cost-effective means of observing and testing low-risk patients.