Internal Medicine Problems as They Present to the Cardiologist

The cardiologist must be alert to both common and uncommon general internal medicine problems that present in cardiac patients, sometimes masquerading as cardiac problems. Here we discuss 6 such problems in patients who were seen by other physicians before the ultimate diagnosis was made by a consulting cardiologist.

New-Onset Hypertension in the Recovery Room

An anesthesiologist requested an emergency cardiology consultation for a middle-aged man who had been admitted postoperatively to the recovery room. The patient had new-onset hypertension after general anesthesia for foot surgery. His preoperative medical evaluation had uncovered nothing worrisome: normal blood pressure readings, no history of hypertension or heart disease, no cardiac medications, and no drug allergies. The foot surgery procedure, expected to take 1 hour, had taken 4 hours; the anesthesia record revealed normal blood pressures until the elevated pressure occurred near the end of surgery. The patient appeared to be in no distress and said that he felt “Okay.” He denied any type of pain, shortness of breath, or dizziness. His neck veins were not distended. His chest was clear. His cardiovascular examination was unremarkable except for bilateral arm blood pressures of 160/90 mmHg. There was no bradycardia.

In order to confirm his diagnosis, the cardiologist examined the abdomen. The lower abdomen was distended and exhibited bladder dullness when percussed to the umbilicus. Upon the slow removal of 1 liter of urine per catheter, the patient's blood pressure immediately returned to normal and remained so.

A distended urinary bladder can cause hypertension.^1,2 No urinary catheter had been placed because the surgery was expected to be short. The diagnostic clues were the 4-hour procedure and the rise in blood pressure near the end of surgery.

A Cardiac Patient with Acute Urinary Retention

A cardiologist was called to the emergency department to see his partner's patient. Mr. G was a banker in his 60s under treatment for stable idiopathic congestive cardiomyopathy. He'd come to the emergency department because of acute urinary retention.

The intern's impression was that Mr. G had benign prostatic hypertrophy with obstruction. He reported that he'd put in a Foley catheter and gotten out over a liter of urine, adding, “It's interesting that the catheter went in so easily.”

The cardiologist immediately asked, “Did you check the reflexes in his legs?” The reply was, “No.” On reexamining the patient, the intern and cardiologist found bilateral lower-extremity hyperreflexia and clonus, which suggested a spinal cord compression lesion and a neurogenic bladder.

An emergency neurosurgery consultation resulted in prompt drainage of an abscess in Mr. G's spinal canal. Because Mr. G's legs were weakening on the way to the operating room, any delay in surgery was reasonably certain to result in permanent paraplegia. Postoperatively, Mr. G needed 3 months of inpatient rehabilitation before he could again walk normally.

A Murmur in a Man with a Broken Arm

One evening at the Cincinnati Veterans Administration hospital, the chief medical resident asked for a cardiology consultation to evaluate a heart murmur in a newly admitted middle-aged gentleman, who wore a fresh cast on his left arm due to a recent fracture. The patient denied any history of heart disease or murmur.

On inspecting the patient's chest, the cardiologist noted a single dilated vein running vertically down the left side not far from the cardiac apex, within the 5th left intercostal space at the midclavicular line. Here, within this space, was a protuberance that felt smooth, firm, and round, but not pulsatile or tender. The resident confirmed that this was the location of the murmur in question. Auscultation over the lump revealed a localized continuous bruit characteristic of an arteriovenous fistula. Wondering whether an intercostal artery and vein had formed a fistulous connection, the cardiologist placed his index finger parasternally in the intercostal space proximal to the lump and pushed firmly while listening to the “murmur.” The continuous bruit disappeared, only to reappear when he lifted his finger. This finding was reproducible.

The cardiologist then asked the resident, “That isn't a pathologic arm fracture by any chance, is it?” The resident replied, “Yes, it is. How did you know?” They then relocated to discuss the finding. The cardiologist indicated that such an arteriovenous fistula adjacent to a bony mass suggested metastatic cancer to the chest wall, as well as to the arm. Indeed, the primary tumor turned out to be renal cell carcinoma,³ known for its angiogenesis.

Hypertensive Retinopathy in a Hypertensive Patient

A 36-year-old child psychologist with a history of stage 1 hypertension was referred for cardiac evaluation after a routine eye examination, during which he had been told that he had hypertensive retinopathy with hemorrhages and exudates. His blood pressure was (and had been) about 140/90 mmHg despite his being on an antihypertensive drug regimen; on the basis of the retinopathy, his HMO primary care physician wanted to increase his antihypertensive medication. The patient decided to get another opinion. Because this mild blood pressure elevation would not be expected to cause such retinopathy, the cardiologist took a detailed history and performed a thorough physical examination.

Except for the hypertensive retinopathy, the patient's history was quite ordinary. He was married, had 3 children under the age of 6, and had never felt better in his entire life. His examination was also unremarkable, except for his blood pressure of 140/90 mmHg in both arms and a definitely enlarged spleen with a nontender, rounded edge, 2 fingerbreadths below the left costal margin. A complete blood count revealed a white blood cell count (WBC) of 100,000/mm³ with promyelocytes and metamyelocytes. A subsequent Philadelphia chromosome test was positive.

On the next day, a hematologist did a bone marrow biopsy and prescribed imatinib immediately to treat chronic myelogenous leukemia (CML). In the 8 years since, the patient has had no hematologic or cytogenetic evidence of CML. On hearing about the WBC, the patient's ophthalmologist agreed that the retinopathy was consistent with the hyperviscosity syndrome and should resolve once the WBC returned to normal. When this resolution indeed occurred, it was strong presumptive evidence in favor of a cause-and-effect relationship.

Hyperviscosity syndrome due to an increased number of white cells is a rare complication of both CML⁴ and chronic lymphocytic leukemia.⁵

Acute Myocardial Infarction and Ventricular Tachycardia

A cardiologist received a “casual” admission in 1974. The patient was a 50-year-old janitor with severe chest pain who had arrived at the emergency department by ambulance. His electrocardiogram (ECG) revealed an acute inferior myocardial infarction and multiple short runs of monomorphic ventricular tachycardia (VT). When neither lidocaine nor intravenous procainamide suppressed the arrhythmia, quinidine and β-blockers were tried. The short runs of asymptomatic VT continued. The patient had no other complications of his acute myocardial infarction. Because the patient appeared anxious and had a slight tremor, the cardiologist recommended thyroid function tests, but these were not done.

After 9 days of monitoring in the coronary care unit, the patient was transferred to the regular floor, where a T₄ of 19 μg/dL confirmed thyrotoxicosis. This was thought to be related to the ventricular arrhythmia, because thyrotoxicosis can increase the heart's sensitivity to catecholamines. Three days later, the patient's temperature spiked to 102 °F. On the assumption that an infection was present, the on-call resident ordered a complete blood count and cultures of the urine, blood, sputum, and throat. After suggesting that the resident also consider life-threatening thyroid storm,⁶ the cardiologist recommended urgent consultation with an endocrinologist regarding emergency therapy.⁷ The endocrinologist agreed with the diagnosis of thyroid storm. After appropriate thyroid treatment, the fever and ventricular arrhythmia disappeared.

Thyroid storm or thyroid crisis, although rare, is an exacerbation of hyperthyroidism that can be life-threatening. It can cause heart failure and arrhythmias and can be precipitated by acute illness manifested by fever and other symptoms. The precipitating event here was probably the patient's acute myocardial infarction.

Ventricular Tachycardia without Acute Myocardial Infarction

In 1982, a Chicago cardiologist spoke at a suburban community hospital on the subject of sudden cardiac death. Afterward, a general internist asked if he'd be willing to see a dying patient in the coronary care unit. The internist explained that this 65-year-old woman had passed out with a cardiac arrest at home. She had been resuscitated by her son and then by paramedics. At the hospital, no evidence of acute myocardial infarction could be found, but she had been shocked for sustained VT 35 times over the previous 3 days. Her doctors had tried all the usual antiarrhythmic drugs without success.

The patient was comatose, intubated, and being fed through a nasogastric tube. Her standard laboratory studies showed normal electrolyte levels and euthyroidism. The ECG revealed recurrent torsades de pointes VT. Because she had not had a test of her serum magnesium level and one could not be obtained promptly at that hospital, she was transferred safely by ambulance to a tertiary-care facility.

The magnesium level was 0.04 mg/dL (normal range, 1.8–3 mg/dL). The torsades resolved with the intravenous administration of magnesium sulfate 3 g per day, although it took 3 days for the patient's serum magnesium level to increase to the normal range. Subsequent cardiac catheterization revealed an old total occlusion of the left anterior descending coronary artery, with akinesia of the anterior wall of the left ventricle. The remaining coronary arteries had no obstructive atherosclerotic disease. During an electrophysiologic study, no VT could be induced once the magnesium level was normal. The cause of the hypomagnesemia was never discovered. She was discharged from the hospital, alert and doing well on magnesium supplement tablets. Over many subsequent years, she never had documented VT or another episode of syncope.

Conclusion

The clinical cardiologist must not ignore his or her roots in internal medicine. In each of these 6 cases, other physicians were taking care of the patient, but it was the cardiologist who diagnosed the general medical disorders that were critical. Patients would not ordinarily seek the care of a clinical cardiologist for urinary retention, a neurogenic bladder, renal cell carcinoma, CML, thyroid storm, or hypomagnesemia unrelated to diuretic therapy.