Initial Approach

Several life-threatening conditions can cause chest pain in the critically ill, and the initial approach should focus on prompt evaluation and resuscitation of the airway, breathing, and circulation. Assess the patient’s level of consciousness, palpate the pulse, and listen to the breath sounds and heart. Obtain vital signs, including oxygen saturation by pulse oximetry, and ensure that the patient is on a cardiac monitor and has adequate intravenous (IV) access. Adhering to this algorithmic approach (Figure 27-1) in patients with chest pain will ensure that critical conditions such as hypoxemia, hypotension, tension pneumothorax, and unstable ventricular arrhythmias are quickly identified and treated. These conditions, as well as the life-threatening causes of chest pain discussed below, are covered in greater detail in other chapters in this textbook.

Figure 27-1 Approach to chest pain in the ICU. ABC, airway, breathing, circulation; CXR, chest x-ray; ECG, electrocardiogram; H + P, history and physical examination; IV, intravenous access.

History

After the initial evaluation and stabilization, obtain a more detailed history. If the patient can communicate, start with an open-ended question like “What’s going on, Mr. Jones?” Physicians typically interrupt patients within 23 seconds, but one should resist this temptation and allow the patient to describe their symptoms.¹ Physicians often neglect to ask even basic questions about the quality of chest pain in patients with aortic dissection, and this omission is associated with a delay in diagnosis.² The mnemonic OLDCAAR can help avoid this mistake (Table 27-1). Ask the bedside nurse about recent changes in the patient’s condition (e.g., changes in mental status, respiratory pattern, or recent medications). Lastly, a quick “chart dissection” should be performed, focusing on the findings noted on initial presentation, reason for ICU admission, past history, and recent progress notes.

TABLE 27-1 OLDCAAR Mnemonic for Evaluating Pain

Domain	Suggested Questions
Onset	Sudden or gradual? Maximal pain at onset?
Location	Generalized or localized? Can you point with one finger to where it hurts?
Duration	When did it start? Just now, or did the pain occur earlier, but you didn’t want to bother anyone? Is it constant or intermittent? If intermittent, is there a trigger, or is it random?
Character	Sharp? Dull? Ache? Indigestion? Pressure? Tearing? Ripping?
Associated symptoms	“Dizzy”—vertiginous or presyncopal? Diaphoresis? Palpitations? Dyspnea? Nausea or vomiting?
Alleviating/aggravating	Position? Belching? Exertion? Deep breathing? Coughing?
Radiation	To the back? Jaw? Throat? Arm? Neck? Abdomen?

Physical Examination

Inspect the chest for asymmetrical excursions, rashes, or obvious sources of pain, such as chest tubes. Palpate the chest and neck for crepitus, which can result from a pneumothorax or pneumomediastinum. Check for pulsus paradoxus and jugular venous distention. Assess for asymmetry in the carotid, femoral, or radial pulses, which can be a sign of aortic dissection. If the breath sounds are asymmetrical, hyperresonance to percussion may confirm a pneumothorax. Cardiac auscultation may reveal a friction rub from pericarditis, “crunching” sounds from mediastinal emphysema, a systolic murmur of aortic stenosis, or an aortic insufficiency murmur from a proximal aortic dissection. A focused examination also should include the abdomen to avoid missing an abdominal catastrophe masquerading as chest pain. Unfortunately, the physical examination has its limitations, and further diagnostic testing is often necessary.

Diagnostic Adjuncts

In the absence of an obvious cause of chest pain (e.g., shingles), a portable chest x-ray (CXR) and electrocardiogram (ECG) should be obtained. Serial cardiac enzymes should be strongly considered to exclude a myocardial infarction (MI). The ECG is often nonspecific but occasionally will show evidence of acute coronary syndromes (ACS), pericarditis, or pulmonary embolism (PE). The CXR is a useful screening tool for life-threatening causes of chest pain, including aortic dissection, pneumothorax, and esophageal rupture. Both the ECG and CXR should be compared with those performed prior to the onset of pain. Although the ECG or CXR may be suggestive of a diagnosis, other confirmatory studies may be necessary.

An IV contrast-enhanced computed tomography (CT) scan can help diagnose a number of causes of chest pain, including PE, aortic dissection, esophageal rupture, pneumothorax, and pneumonia. The benefits of CT scanning, however, must be weighed against the risks of transporting a critically ill patient out of the ICU and the potential for causing contrast nephropathy. Ultrasound can be rapidly performed with minimal risk to the patient and does not require transport out of the ICU. Pericarditis with associated effusion, wall motion abnormality from MI, aortic stenosis, aortic dissection, and pneumothorax are all within the diagnostic realm of ultrasound. Ultrasound has the added benefit of providing information about cardiac function.

Differential Diagnoses

Two rules to live by:

1 Do not assume the admission diagnosis is correct or all inclusive. “Premature closure,” or failing to consider alternative diagnoses after a diagnosis has been made is a common cause of medical error.³ Premature closure likely contributes to the delay in diagnosis described in hospitalized patients with aortic dissection.⁴

2 Do not be biased by the type of ICU to which the patient is admitted. Aortic dissection can present as a stroke, prompting admission to a neurologic ICU; an acute abdomen can develop in a medical ICU patient. Indeed, a review of abdominal catastrophes concluded that “delays in surgical evaluation and intervention are critical contributions to mortality rate in patients who develop acute abdominal complications in a medical ICU.”⁵

Potentially Life-Threatening Causes of Chest Pain

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.

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

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