Acute Coronary Syndromes

ACS include unstable angina and ST-segment and non–ST-segment elevation MI. The “classic” symptoms of ACS include chest pressure radiating to the left arm, nausea, and diaphoresis, but the history has several limitations with regard to the diagnosis of ACS. Although certain features (pain radiating down the right arm or both arms) are associated with a higher likelihood of ACS, and other characteristics (pleuritic, positional, or sharp pain) with a lesser likelihood, none of these can reliably confirm or exclude the diagnosis.^6,7 Further complicating matters, diabetes, smoking, dyslipidemia, hypertension, and a family history predict the development of heart disease over years in asymptomatic patients but may be less useful in predicting ACS in patients with acute chest pain.⁸ Reduction in pain after the administration of nitroglycerin is also not a reliable indicator of cardiac chest pain.⁹ Thus, ACS should almost never be excluded as a cause of chest pain based on the history alone.

Physical examination findings in patients with ACS include signs of left ventricular dysfunction, such as hypotension, jugular venous distention (JVD), and an S₃ heart sound. The ECG should be examined for ST-segment elevation or depression, Q waves, and T wave inversions. The ECG has a low sensitivity for diagnosing MI, but yield increases with serial ECGs. Given the limitations of the ECG and history and examination findings, cardiac enzymes should be measured in most ICU patients with chest pain.

All patients suspected of having ACS should be placed on oxygen and, if not contraindicated, treated with aspirin (or clopidogrel in the setting of aspirin allergy). Sublingual nitroglycerin and IV morphine should be used to relieve pain if the systolic pressure is above 90 mm Hg. Further treatment of ACS is primarily dictated by ECG findings and may include emergency percutaneous intervention or fibrinolysis in the setting of ST-segment elevation.

Pulmonary Embolism

Approximately 1% to 2% of ICU patients develop deep vein thrombosis (DVT) or PE, but the true incidence is probably higher.¹⁰ Unrecognized PE carries a high mortality, but survival improves dramatically with prompt diagnosis and treatment. Chest pain due to PE is usually pleuritic and often associated with dyspnea, hemoptysis, cough, or syncope.¹¹ ICU patients usually have risk factors for PE including immobility, advanced age, recent surgery or trauma, malignancy, and central venous catheterization. Do not be deterred from working up PE in patients receiving subcutaneous heparin, as two-thirds of those with DVT and PE are receiving prophylaxis at the time of diagnosis.¹⁰

Physical examination findings are generally nonspecific in PE. Unexplained tachypnea or tachycardia may be the only diagnostic clues. Hypoxia is often present but is not a universal finding, and its absence cannot exclude PE. A large PE may present as hypotension or cardiovascular collapse. Signs of pulmonary hypertension and right heart failure, such as a loud second heart sound (P₂), JVD, or an S₄ heart sound may be present. Lung examination may reveal crackles, decreased breath sounds, wheezing, rhonchi, or a pleural friction rub.

An elevated arterial-alveolar gradient may be noted on blood gas analysis, but this is a nonspecific finding in the critically ill. The ECG is often normal, but it may show sinus tachycardia, nonspecific ST-segment and T-wave changes, or a right bundle branch block.¹² The CXR can be normal but more commonly reveals nonspecific findings such as pleural effusion, infiltrates, or atelectasis.¹³ Although D-dimer testing has been used to rule out venothromboembolic disease in outpatients with a low likelihood of this diagnosis, the D-dimer assay does not appear to be a particularly useful diagnostic tool in the ICU setting.¹⁴ The sensitivity of transthoracic echocardiography (TTE) for PE varies considerably, but the test can be useful in patients who have larger clots that are of hemodynamic significance.¹⁵ In such cases, TTE can be performed rapidly at the bedside when patients are unsafe for transport out of the ICU. TTE has the added benefit of assessing the response to thrombolytics by evaluating right heart function and changes in pulmonary artery pressure.¹⁵ A ventilation/perfusion scan can be time consuming and difficult to perform in mechanically ventilated patients; its interpretation may be obscured by other lung pathology.¹⁶ An IV contrast-enhanced CT of the chest can be performed rapidly, and newer scanners have high sensitivity and specificity, making this the diagnostic study of choice in most ICU patients.

Initial treatment of patients with confirmed PE involves anticoagulation with subcutaneous low-molecular-weight heparin or IV unfractionated heparin. Patients with hemodynamic instability due to PE may require thrombolysis or surgical embolectomy.¹⁷

Thoracic Aortic Dissection

Aortic dissection results from a tear in the aortic intima, allowing blood to dissect between the intima and adventitia. The Stanford system classifies dissections as type A (involving the ascending aorta) or type B (not involving the ascending aorta). Risk factors include hypertension, advanced age, atherosclerosis, cocaine use, intraaortic catheterization, Ehlers-Danlos syndrome, Turner syndrome, and giant cell arteritis.¹⁸ Patients younger than 40 years are more likely to have Marfan syndrome, bicuspid aortic valve, prior aortic surgery, or aortic aneurysm.¹⁹ The mortality rate is as high as 1% to 2% per hour from symptom onset, and the history remains critical to early diagnosis.¹⁹ Clinicians correctly suspect aortic dissection in more than 90% of cases when questions about quality, radiation, and intensity of the pain are asked. If one or more of these questions is omitted, the correct diagnosis is missed in over half of cases.² Many patients complain of sudden onset of chest pain that radiates to the back or abdomen. Contrary to popular belief, patients more commonly describe their pain as sharp, rather than “tearing.”¹⁹ Dissection can extend into any of the major aortic branches, causing a multitude of clinical presentations owing to ischemia of the brain, heart, kidney, spinal cord, or gut.

Certain physical examination findings should raise the suspicion of aortic dissection. About one third of patients have pulse deficits in the carotid, radial, or femoral arteries, and some have focal neurologic deficits related to cerebral or spinal cord ischemia.¹⁸ Hypotension often occurs with type A dissection, whereas hypertension is more commonly seen in type B dissection.²⁰ A significant difference in systolic blood pressure (>20 mm Hg) between the upper extremities may be seen with dissection, but this is not a pathognomonic finding. A diastolic murmur of aortic insufficiency can result from retrograde dissection into the aortic valve.

The ECG may be normal or show nonspecific ST-segment or T-wave changes or left ventricular hypertrophy (LVH) from hypertension. Rarely, the ECG reveals evidence of an MI from dissection into a coronary artery. Over 90% of patients will have some abnormality on CXR, such as widening of the mediastinum, an abnormal aortic contour, pleural effusion, or displacement of intimal aortic calcification from the outer border of the aortic knob.²¹ Therefore, it behooves the clinician to scour the CXR for these findings when considering aortic dissection as a cause of chest pain. The diagnosis can be confirmed with CT, magnetic resonance imaging (MRI), or transesophageal echocardiography, all of which have high sensitivity and specificity. The choice of diagnostic study will depend on physician preference and the risks involved. Initial management should focus on blood pressure control, usually with beta-blockers and a potent vasodilator such as nitroprusside.²⁰

Pneumothorax

Pneumothorax is caused by air entry from the alveolar space or the atmosphere into the potential space between the parietal and visceral pleura. Pneumothorax in the ICU is often iatrogenic and results from mechanical ventilation (particularly with acute respiratory distress syndrome), attempts at central venous catheterization, thoracentesis, tracheostomy, or bronchoscopy.²² Virtually any lung pathology can contribute to a pneumothorax, but a ruptured bleb from chronic obstructive pulmonary disease is the most common culprit. Patients with pneumothorax typically complain of sudden onset of ipsilateral pleuritic chest pain with associated dyspnea.

Chest examination may reveal palpable crepitus, decreased breath sounds, decreased chest wall excursion, or hyperresonance to percussion on the affected side. Vital signs may be significant for tachycardia, hypoxia, or tachypnea. Patients with a tension pneumothorax classically have tracheal deviation, JVD, and hypotension. Patients on mechanical ventilation can have increased peak inspiratory airway pressures. The signs of pneumothorax are nonspecific, and any significant deterioration in a patient on a ventilator should prompt a diagnostic evaluation for pneumothorax.

CXRs are often performed in the semiupright or supine position in the ICU, and the classic finding of a visceral pleural line is often seen only on upright CXR. In supine patients, a deep sulcus sign may be seen where the costophrenic angle extends more inferiorly than normal as air collects in this space. Alternatively, a sharp delineation of the cardiac silhouette from the lucency of an anteromedial pneumothorax may be seen. In an experienced operator’s hands, ultrasound can effectively rule out a pneumothorax in seconds.²³

Because of a high rate of conversion to tension pneumothorax in patients on mechanical ventilation, prompt diagnosis and treatment are critical. Treatment involves evacuation of air from the pleural space, usually through tube thoracostomy. In patients with hemodynamic compromise from a suspected tension pneumothorax, treatment with immediate needle thoracostomy, followed by tube thoracostomy, should not be delayed while waiting for a CXR.

Esophageal Rupture

A full-thickness tear of the esophagus carries high mortality, owing to the intense inflammatory response to gastric contents in the mediastinum, secondary bacterial infection, and subsequent sepsis and multisystem organ failure. Most cases of esophageal perforation are caused by upper gastrointestinal tract endoscopy.²⁴ The risk of esophageal injury from a diagnostic endoscopy is low but increases dramatically when interventions such as dilation or stent placement are performed. Esophageal rupture may be caused by other procedures commonly performed in the ICU, including nasogastric or tracheal intubation. Spontaneous rupture of the esophagus (Boerhaave syndrome) occurs from a sudden increase in intraluminal pressure, usually from vomiting or retching. Patients with esophageal disease such as cancer, Barrett’s esophagus, strictures, prior radiation, and varices are particularly vulnerable to rupture. With thoracic perforations, the pain localizes to the substernal or epigastric area, but it may occur in the neck with cervical perforations. Other associated symptoms include dysphagia, odynophagia, and dyspnea.

The patient is often febrile. Crepitus can be felt in the neck with perforation of the cervical esophagus. Mediastinal emphysema can sometimes be detected by a crunching sound on cardiac auscultation, termed Hamman’s sign. A CXR often reveals subcutaneous emphysema, pneumomediastinum, pneumothorax, or pleural effusion. The CXR is abnormal in almost 90% of cases but may be normal early after the perforation occurs.²⁴ A water-soluble contrast study of the esophagus or a CT scan of the chest can be performed in cases where there is a high clinical suspicion and the CXR is nondiagnostic.

Treatment may involve operative repair, endoscopic therapies, or conservative management with broad-spectrum antibiotics and close observation.

Aortic Stenosis

Aortic stenosis causes left ventricular outflow obstruction, which leads to left ventricular hypertrophy. Aortic stenosis may result from a congenitally abnormal (bicuspid) valve or rheumatic heart disease in young adults or from valvular calcification in the elderly. Clinical manifestations of aortic stenosis, including angina, congestive heart failure, and syncope, occur when the hypertrophied left ventricle can no longer overcome the valvular stenosis, or when the hypertrophy itself causes diastolic dysfunction or excessive myocardial oxygen demand.

Physical examination features of aortic stenosis include narrow pulse pressure, slow rise of the carotid pulse, a systolic murmur at the right second intercostal space, and an S₄ heart sound. CXR and ECG may show signs left ventricular hypertrophy, but the diagnostic study of choice is a Doppler echocardiogram.

Definitive therapy involves valve replacement. Temporizing management focuses on cautiously decreasing afterload with vasodilators. Angina and congestive heart failure are treated with oxygen and the careful administration of nitrates, morphine, and diuretics. Close hemodynamic monitoring is essential with vasodilators because of the risk of hypotension.

Miscellaneous

Other causes of potentially life-threatening chest pain in the ICU include pneumonia and acute abdominal processes. Pneumonia is often accompanied by pleuritic chest pain or shoulder pain referred from diaphragmatic irritation. A perforated ulcer can sometimes present as a chest pain, and the diagnosis is often made when free air is incidentally discovered under the diaphragm on an upright CXR.

Esophageal Disorders

In patients with noncardiac chest pain, gastroesophageal reflux disorder and esophageal motility disorders (e.g., esophageal spasm) are common. Esophageal disease is associated with pain precipitated by lying flat, postprandial pain, heartburn, or dysphagia. Owing to the shared innervation of the heart and esophagus, visceral pain originating from these two organs can be similar in character. Relief of symptoms after a “GI cocktail” cannot be relied upon to identify chest pain as noncardiac in origin.²⁵ Confirmatory tests including esophageal manometry and esophageal pH monitoring can be performed, but a trial of a proton pump inhibitor may be a more practical diagnostic approach.²⁶ Lastly, a nasogastric tube with the distal tip in the esophagus can produce chest pain; this is easily remedied by advancing the tube distally into the stomach.

Musculoskeletal Disorders

The chest wall is a common source of pain in patients without a cardiorespiratory etiology of their symptoms. Pain from costochondritis is often reproduced with palpation or with arm movement. Up to 15% of patients with MI also have chest wall tenderness, so this finding does not exclude ACS.²⁷ Most cases of costochondritis are self-limiting and treated with nonsteroidal antiinflammatory drugs (NSAIDs). ICU patients may have other causes of chest wall pain, including rib fractures, chest tubes, postoperative pain after cardiothoracic surgery, or an intercostal muscle strain from coughing.

Pericarditis

Pericarditis is a relatively rare cause of chest pain in the inpatient setting.²⁸ The condition most commonly results from viral or idiopathic causes, but other etiologies include bacterial infections, malignancy, tuberculosis, uremia, autoimmune diseases, transmural MI, and cardiac surgery. Chest pain from pericarditis is typically pleuritic, sharp, retrosternal, and radiates to the back, neck, or arms. The pain is often relieved by sitting forward and exacerbated by lying flat. Although uncomplicated pericarditis is not generally life threatening, pericardial inflammation can lead to pericardial effusion and cardiac tamponade if the effusion is large or acute.

A pericardial friction rub is highly specific for pericarditis and is present in the majority of cases. A pericardial rub sounds similar to hair being rubbed together and is best heard with the diaphragm of the stethoscope over the left sternal border, with the patient sitting forward. Beck’s triad (JVD, hypotension, muffled heart tones) is the classic description of pericardial tamponade, but unexplained tachycardia and tachypnea may be early signs. Pulsus paradoxus, or a fall in systolic blood pressure by more than 10 mm Hg with inspiration, is often seen in tamponade but is nonspecific.

ECG findings can clinch the diagnosis of pericarditis. Both MI and pericarditis may result in ST-segment elevation, but with pericarditis, ST-segment depression is typically absent in the reciprocal leads. Absence of Q waves, concave ST-segment elevation, and PR depression strongly favor pericarditis.²⁸ Careful ECG review, auscultation, and history are key to distinguishing ACS from pericarditis and avoiding the potentially fatal complication of administering thrombolytics to a patient with pericarditis and precipitating hemotamponade. Electrical alternans and low voltage on the ECG, coupled with cardiomegaly on CXR, strongly favor pericardial effusion. Although the ECG and CXR findings of pericardial effusion can be useful, echocardiography should be performed to confirm the diagnosis.

Treatment is aimed at the underlying etiology. NSAIDs relieve pain and inflammation in cases of viral or idiopathic pericarditis. Pericardiocentesis is performed for therapeutic purposes in the case of tamponade and for diagnostic purposes if tuberculosis, bacterial infection, or malignancy is suspected. An IV fluid challenge may be a helpful temporizing measure in hypovolemic patients with tamponade.

Psychiatric Disorders

A significant number of patients with noncardiac chest pain suffer from panic disorder.²⁹ In addition to chest pain, panic attacks can cause other symptoms that mimic MI, including diaphoresis, dyspnea, palpitations, and a sense of impending doom. A self-report of anxiety helps clue into the diagnosis of underlying panic disorder. Severe illness and its treatment with invasive procedures in the ICU can provoke profound psychological distress. The development of posttraumatic stress disorder is well described in ICU survivors, particularly in patients who experience episodes of extreme fear.³⁰ Thus, the diagnosis of chest pain due to panic attack may not be acutely life threatening, but this condition should not be considered benign and must be treated. Benzodiazepines are helpful in this regard. Psychiatric patients with cardiac or pulmonary disease can be especially challenging to diagnose, and a thorough, empathetic history is essential.

Herpes Zoster

Reactivation of the varicella-zoster virus from thoracic sensory ganglia causes a painful, dermatomal rash across the chest. The pain of shingles may precede the rash by several days, which can delay the diagnosis. The rash is characterized by vesicles that crust over after approximately one week. Oral acyclovir reduces the duration of herpetic neuralgia. Immunocompromised hosts are at high risk of complications from zoster infections and often require more aggressive treatment with IV acyclovir.