Chest Pain

Published on 22/03/2015 by admin

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Last modified 22/03/2015

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27 Chest Pain

Chest pain in the intensive care unit (ICU) is a somewhat different entity from chest pain seen in the office, inpatient ward, or emergency department. The keys to management of chest pain in the ICU are rapid assessment and treatment of immediately life-threatening conditions, careful consideration of the differential diagnosis, a logical evaluation plan, and empirical treatment while pursuing a definitive diagnosis.

image 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?

image Differential Diagnoses

Two rules to live by:

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.

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

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