Management of Erectile Dysfunction
By age 70, more than two-thirds of men have some erectile dysfunction, yet most of these men are still desirous of participating in intercourse. A goal-directed approach suggests that clinicians identify etiologies for which they can implement specific cure (e.g., testosterone deficit, medication-induced erectile dysfunction), and offer functional restoration of sexual function generically to all others, by tools such as external vacuum devices, intraurethral and injectable prostaglandins, and oral agents. Primary care clinicians are encouraged to include sexual history as part of their initial patient evaluation, do a focussed physical examination (seeking signs of androgen deficit, thyroid dysfunction, prolactin excess, or physical genital abnormality such as Peyronie's disease), and consider laboratory tests pertinent only to those diagnoses for which there is a specific treatment.
After exclusion of specifically correctable disorders, clinicians may offer vacuum devices, intracavernosal injections (e.g., Caverject, Edex), transure-thral delivery systems (MUSE), and oral agents (Viagra) to patients and their partners as initial therapy. Since some couples will opt for surgical implantation of prostheses, this method should also be explained. Of course, psychogenic impotence may benefit from counseling. Although vascular and neurologic etiologies are common in erectile dysfunction, tools for correction of these maladies are either unavailable or in the category of "investigational;" hence, available tools for rapid restoration of sexual function take priority.
Stern MG, et al. J Clin Outcomes Management 1998;5:36-56.
Clinical Scenario: The ECG in the figure was obtained from an 80-year-old woman who presented with "fatigue." What valvular lesion should be carefully listened for in view of the findings seen in this tracing?
Interpretation: The rhythm is irregularly irregular, and atrial activity is absent. This defines the rhythm as atrial fibrillation-in this case with a controlled ventricular response. The QRS and QT intervals are normal. The mean QRS axis is +80°. There is no evidence of left ventricular hypertrophy (LVH). There are minimal, nonspecific ST-T wave abnormalities present that do not appear to be acute.
Other than the rhythm, the most remarkable finding on this tracing is the presence of a tall (and clearly predominant) R wave in lead V1. This abnormal finding that should always suggest consideration of five possible diagnoses:
1. Right bundle branch block (RBBB)
2. Wolff-Parkinson-White (WPW) syndrome
3. Posterior infarction
4. Right ventricular hypertrophy (RVH)
5. Normal variant
In this particular case, the first two entities in the above differential list can be excluded because the QRS complex is narrow. This ECG is clearly not a normal variant. Posterior infarction almost always occurs in association with evidence of inferior infarction (since the right coronary artery most often provides the blood supply to both of these areas of the heart). There is no indication of inferior infarction in this tracing. Therefore, by the process of elimination, a diagnosis of RVH should be strongly suspected as the cause for the tall R wave in lead V1 of this ECG. The finding of a nearly vertical QRS axis and persistent S waves in lateral precordial leads is consistent with this diagnosis.
The valvular lesion that should be suspected with the ECG finding of atrial fibrillation and RVH is mitral stenosis.