Internal Medicine Case Studies

A 78-year-old man with a past history remarkable only for gout is seen because of the acute onset of chest pain. He describes a 4-day prodrome of rhinorrhea, nonproductive cough, myalgias, and anorexia. Approximately 8 hours before he is seen in the emergency room (ER), he began to notice the gradual onset of sharp substernal chest pain, worse with inspiration, relieved by sitting up, and associated with diaphoresis.

The pain is slightly worse with exertion but is not relieved by sublingual nitroglycerin (NTG) administered in the ER, although morphine sulfate and oxygen do seem to alleviate his discomfort. His temperature is 101◦F (38.5◦C), his heart rate is 105 beats per minute and regular, his respiratory rate is 17 per minute, and his blood pressure is 105/65 mmHg. The remainder of the physical examination is normal. The electrocardiogram (ECG) is interpreted by the ER staff to show “sinus tachycardia with ST-segment elevations inferiorly and nonspecific ST- and T-wave changes elsewhere.” An arterial blood gas determination performed on room air shows normal arterial oxygenation. The chest radiographic study is normal.

The ER staff starts an IV heparin drip and a platelet glycoprotein IIb-IIIa inhibitor infusion for the treatment of a presumed acute coronary syndrome (ACS) An IV NTG infusion and oxygen therapy are instituted but, despite these measures, the pain continues. The cardiac catheterization team is called to consider coronary angiography. Antacid therapy does not relieve the pain and only morphine sulfate seems to offer relief. Blood tests reveal a normal troponin, normal electrolytes, normal D-dimer, and normal renal function. The hemoglobin is normal but the white blood cell count is mildly elevated.

The patient is taken to the catheterization laboratory and his coronary angiogram reveals diffuse, mild, nonobstructive coronary artery disease (CAD). The IIb-IIIa inhibitor AQ3 is discontinued. When the patient is transferred to the coronary care unit, the ECG shows continued “evolution” with ST-segment elevations of less than 2 mm in leads I, II, III, aVL, aVF, and V2 to V6 that do not respond to IV NTG. The patient’s chest pain persists.

Further increments of NTG are given in an IV infusion and the patient’s blood pressure begins to decrease. After 2 hours, the patient continues to writhe in pain, complains of feeling dizzy and having a severe headache, and vomits after the fifth dose of IV morphine sulfate. You are asked to see the patient and your examination reveals sinus tachycardia, a blood pressure of 82/50 mmHg (no pulsus paradoxus), a respiratory rate of 16 per minute, a temperature of 101◦F (38.5◦C), clear lung fields, and no elevation in the jugular venous pressure, but a three-component pericardial friction rub is heard over the precordium. The hemoglobin level is stable.

1. What is the most likely clinical diagnosis of this patient’s chest pain?
2. On the basis of your clinical impression of this patient’s presentation, what features would be expected on the ECG?
3. Is a normal troponin helpful in acute MI?
4. What is the most effective treatment for acute pericarditis?
5. What is the most likely cause of the hypotension in this patient?

1. What is the most likely clinical diagnosis of this patient’s chest pain?

The most likely clinical diagnosis of this patient’s chest pain is acute idiopathic or viral pericarditis. Relatively common causes of acute chest pain that must be considered are MI or ACS, pericarditis, aortic dissection, pneumonia, pulmonary embolus, costochondritis, and pneumothorax. The pertinent features of the history and physical examination that lead to this diagnosis are that the pain was preceded by a viral prodrome and was very clearly positional and exacerbated by inspiration, which strongly suggests pericardial pain. Pericardial pain does not improve with NTG, but the lack of response to NTG does not exclude an acute MI. The patient’s vital signs were stable except for a slight fever and tachycardia that are also very frequent in either acute pericarditis or MI. The absence of tachypnea, together with the normal examination findings and normal D-dimer, make acute pulmonary embolization unlikely. Acute costochondritis is often positional but associated with exquisite pain on palpation of the involved costochondral junction, and is not associated with ECG changes. If the examination and chest radiographic findings are normal and there is no past history of smoking, forceful coughing, or trauma, the likelihood of acute pneumothorax is low.

The remaining two diagnoses, acute pericarditis versus MI, can often be differentiated on the basis of the history and physical examination findings, the ECG, and troponin. The sharp quality of the substernal chest pain, which is associated more with the recumbent position, deep breathing, and coughing, and which is improved by sitting up, is atypical for MI but a classic symptom of pericarditis. The ECG was initially more consistent with pericarditis but an acute MI could not be excluded. The absence of significant coronary obstruction strongly argued against an acute MI, a finding confirmed by the normal troponin.

2. On the basis of your clinical impression of this patient’s presentation, what features would be expected on the ECG?

Sinus tachycardia and ST-segment elevation are often the earliest ECG findings, although the absence of ECG changes does not exclude the diagnosis of pericarditis. The typical changes of acute pericarditis often evolve over hours or days and are thought to be caused by a myocardial current of injury due to inflammation. The ECG in acute pericarditis evolves usually through four stages over several days. There is early diffuse ST-segment elevation in stage 1. This differs from the ST-segment elevation of acute MI, which is usually localized (anterior, inferior, or lateral), with the ST segments convex upward. In pericarditis, the ST-segment elevation is concave upward and usually involves all the leads except aVR and V1. Stage 2 is defined by normalization of the ST segments and stage 3 is characterized by the development of diffuse T-wave inversions. In stage 4, the T waves return to their normal configuration. PR segment depression is also common in the early phases of acute pericarditis even in the absence of ST-segment elevation and is strongly suggestive of acute pericarditis. An important exception is in pericarditis following an acute MI, in which typical ECG changes of pericarditis may not be present or may be atypical.

3. Is a normal troponin helpful in excluding an acute MI?

A normal troponin 8 or more hours after the onset of chest pain generally excludes acute MI but does not exclude ACS. However, a mildly elevated troponin may be present with acute myopericarditis. Myocarditis is an inflammatory disease of the cardiac muscle, which can be caused by a variety of different illnesses, many of which are infectious. Typically, myocarditis is associated with cardiac enzyme elevation that reflects myocardial necrosis. When chest pain occurs in the setting of myocarditis it may be associated with concomitant pericarditis and is called myopericarditis.

4. What is the most effective treatment for acute pericarditis?

In the treatment of idiopathic or viral pericarditis, the goals of therapy are relief of pain and resolution of inflammation. First-choice therapy is the administration of nonsteroidal antiinflammatory drugs (NSAIDs) or aspirin. The administration of AQ4 colchicine alone or in combination with NSAIDs might be another therapeutic alternative. The use of corticosteroids is usually reserved for patients with pericarditis secondary to autoimmune disease.

5. What is the most likely cause of the hypotension in this patient?

The hypotension in this patient is most likely due to the cumulative effects of the medications he has been given (morphine and NTG). The accumulation and potentiation of medications, especially in the elderly, is a common clinical problem in the acute care setting. The combination of morphine and NTG in this patient may have induced sufficient vasodilation to cause hypotension.

Bleeding is also a possible cause of the hypotension. The administration of IV heparin, aspirin, and platelet glycoprotein IIb-IIIa inhibitor agents may result in gastrointestinal bleeding and melanotic stools. The absence of jugular venous distention and a paradoxical pulse argues against tamponade, but these findings may be absent with vasodilation or volume depletion. A more worrisome possibility is hemorrhagic pericarditis, especially because a new friction rub is heard. If the hypotension does not resolve quickly with discontinuation of NTG and morphine, an echocardiogram is indicated to exclude cardiac tamponade.