Dyspnea in a man with a history of hypertension and emphysema
An elderly patient was reluctant to undergo further testing. Luckily, clinicians convinced him otherwise.
Mr. T, 86 years old, has an extensive medical history. When he arrived complaining of a number of symptoms (primarily shortness of breath), we were unable to come up with an immediate diagnosis.
Five days before visiting the clinic, Mr. T experienced sudden onset of dyspnea while sitting at home. He measured his pulse at 100 beats per minute. After driving himself to the clinic, the patient still felt short of breath but no worse than at onset. The dyspnea, described as mild in severity, was not made worse by exertion or position. Mr. T reported no cough, hemoptysis, or wheeze. There was also no chest pain, palpitations, orthopnea, or paroxysmal nocturnal dyspnea. He experienced no fever, chills, diaphoresis, dizziness, blurred vision, or nausea.
The patient’s medical history revealed mild emphysema and hypertension but no coronary artery disease or MI. The history was remarkable for renal cell cancer leading to left nephrectomy (but no active malignancy) and thyroid nodule with hypothyroidism. (Mr. T had been placed on thyroid supplementation four months earlier.) He also had a known arteriovenous malformation of the cecum. There had been no recent travel or periods of immobility. He quit smoking 20 years ago. Psychiatric history was significant for mild anxiety.
Mr. T was a thin elderly man in no acute distress. His respiratory rate was measured at 16 breaths per minute in the office. BP was 124/68 mm Hg while sitting and pulse was 96 beats per minute and regular. A head, eyes, ears, nose, and throat exam was benign. His voice was notably hoarse, but this was not a new clinical finding. No palpable thyromegaly, nodules, jugular venous distension, or carotid bruits were detected.
Auscultation of the patient’s lungs revealed mildly diminished breath sounds bilaterally, but there were no rales, rhonchi, or wheeze. Heart auscultation revealed borderline tachycardia but no murmur or ventricular filling gallop. Atrial gallop was not present, and his second heart sound was not accentuated. The lower extremities were nontender, nonedematous, and nonerythematous. Peripheral pulses were 1+.
ECG revealed regular rhythm with ventricular rate of 90 beats per minute. However, P waves were inverted in the inferior, septal, and lateral leads (a new finding in comparison with a previous reading). Mr. T’s ECG also showed a newly short P-R interval (Figure 1). There were no ST- or T-wave changes. Chest x-ray found emphysematous changes but no infiltrate or consolidation. No pleural effusion was present.
Laboratory studies were ordered. Chemistries, including magnesium and phosphorus, were within normal range. Mr. T had a blood urea nitrogen of 25.9 mg/dL and a creatinine of 1.5 mg/dL. Thyroid-stimulating hormone and throxine were back to normal from labs drawn four months ago.
At this point, our working differential diagnosis was varied (Table 1). The list included chronic obstructive pulmonary disease exacerbation or atrial infarct (with the subsequent tachycardia making our elderly patient feel ill at ease).
A D-dimer determination revealed mild elevation at 0.62 ng/mL (upper range of normal, 0.40). Mr. T underwent a ventilation-perfusion (VQ) lung scan, which was chosen over spiral CT in light of an iodine allergy. The patient was not feeling ill at the time and did not want to undergo the scan until the next day. After a review of risks, he agreed to the VQ scan that day. The results pointed to a high probability for PE.
The patient was admitted and started on IV heparin and warfarin (Coumadin) 5 mg daily. He was later discharged on warfarin alone and was seen regularly in our Coumadin clinic to monitor his prothrombin time. After a month on anticoagulant therapy, he was clinically and symptomatically improved.
Because many symptoms for PE are common among patients without such a diagnosis, the need for additional testing is heightened. Dyspnea and tachypnea are found in 73% and 70% of PE presentations, respectively. Additional symptoms, in decreasing order of prevalence, are pleuritic chest pain, cough, and hemoptysis. Other signs are rales, tachycardia, atrial gallop, accentuated second heart sound, and circulatory collapse. The modified Wells criteria assist in clinical assessment for PE (Table 2). Since Mr. T’s score was zero, his probability was low or considered unlikely, despite the common symptom of dyspnea.
The next step in a low-likelihood PE patient is quantitative D-dimer testing. D-dimer has an excellent negative predictability (levels are normal in only 25% of patients without PE). Of those without PE, D-dimer can be elevated with malignancy and recent surgery as well as in hospitalized patients. Furthermore, there is an indirect relationship between specificity and increasing age.