Appallingly little is known about the prevalence of erectile dysfunction in the United States and how this prevalence varies according to individual characteristics (age, race, ethnicity, socioeconomic status, and concomitant diseases and conditions). Data on erectile dysfunction available from the 1940's applied to the present U.S. male population produce an estimate of erectile dysfunction prevalence of 7 million.
Penile blood flow is measured using a Doppler probe and a 2.5 cm blood pressure cuff. Systolic pressures in the right and left corpora cavernosa are measured and the penile–brachial index is calculated taking a ratio of penile systolic pressure to brachial systolic pressure. These measures should be repeated before and after 3 minutes of exercising the pelvic and leg muscles. In normal men, the PBI should be 0.9 or greater. Ratios between 0.7 and 0.9 suggest vascular impotence; a ratio below 0.6 is diagnostic. Pelvic arteriography can be done if revascularization is considered.
Damage to the autonomic pathways innervating the penis may eliminate "psychogenic" erection initiated by the central nervous system. Lesions of the somatic nervous pathways may impair reflexogenic erections and may interrupt tactile sensation needed to maintain psychogenic erections. Spinal cord lesions may produce varying degrees of erectile failure depending on the location and completeness of the lesions. Not only do traumatic lesions affect erectile ability, but disorders leading to peripheral neuropathy may impair neuronal innervation of the penis or of the sensory afferents. The endocrine system itself, particularly the production of androgens, appears to play a role in regulating sexual interest, and may also play a role in erectile function.
When you become aroused, your brain sends chemical messages to the blood vessels in the penis, causing them to dilate or open, allowing blood to flow into the penis. As the pressure builds, the blood becomes trapped in the corpora cavernosa, keeping the penis erect. If blood flow to the penis is insufficient or if it fails to stay inside the penis, it can lead to erectile dysfunction.
Half of all men between the ages of 40 and 70 will experience erectile dysfunction. While the problem doesn't cause heart disease, the two often occur together – study after study has shown that men with ED are dramatically more likely to develop heart disease and have a heart attack or stroke. One German study from 2010 found men with erectile dysfunction are twice as likely to die within the next two years as those without, prompting some experts to call the phenomenon "the canary in the trousers".
Men with a rare heart condition known as long QT syndrome should not take vardenafil since this may lead to abnormal heart rhythms. The QT interval is the time it takes for the heart's muscle to recover after it has contracted. An electrocardiogram (EKG) measures the QT interval. Some people have longer than normal QT intervals, and they may develop potentially life-threatening abnormal heart rhythms, especially when given certain medications. Men with a family history of long QT syndrome should not take vardenafil, as it is possible to inherit long QT syndrome. Furthermore, vardenafil is not recommended for men who are taking medications that can affect the QT interval such as quinidine (Quinaglute, Quinidex), procainamide (Pronestyl, Procan-SR, Procanbid), amiodarone (Cordarone), and sotalol (Betapace).
Hypogonadism may be suggested by the patient's general appearance. If testosterone deficiency antedates puberty, as in Klinefelter's syndrome, eunuchoid proportions—defined as an arm span 5 cm or more in excess of height, or a sole-to-pubis length exceeding crown-to-pubis length by more than 2 cm—may be present. In postpubertal males whose testosterone levels are markedly depressed, the secondary sexual characteristics may become atrophic. Testicles less than 4 cm in length or a prostate gland that is smaller than expected may be the only clues on physical examination to a pituitary tumor with secondary hypogonadism.
Diabetes is one of the most common causes of ED. Chronically high blood sugar levels can result in nerve damage that affects your body’s ability to translate pleasurable sexual stimulation into an erection. Diabetes can also lead to issues with circulation, which reduces blood flow to the penis and makes it more difficult to keep an erection that is hard enough for intercourse.
The nerves and endothelium of sinusoids and vessels in the penis produce and release transmitters and modulators that control the contractile state of corporal smooth muscles. Although the membrane receptors play an important role, downstream signaling pathways are also important. The RhoA–Rho kinase pathway is involved in the regulation of cavernosal smooth muscle contraction. 
Tadalafil should not be used with alpha-blockers (except Flomax), medicines used to treat high blood pressure, and benign prostate hypertrophy (BPH) because the combination of tadalafil and an alpha-blocker may lower the blood pressure greatly and lead to dizziness and fainting. Examples of alpha-blockers include tamsulosin (Flomax), terazosin (Hytrin), doxazosin (Cardura), alfuzosin (Uroxatral), and prazosin (Minipress). Tamsulosin (Flomax) is the only alpha-blocker that patients can use safely with tadalafil. When tadalafil (20 mg) was given to healthy men taking 0.4 mg of Flomax daily, there was no significant decrease in blood pressure and so patients on this dose of tamsulosin (Flomax) can be prescribed tadalafil. The only alpha-blocker not tested with tadalafil is alfuzosin (Uroxatral), and no recommendations can be made regarding the interaction between the two.
However, a review of a United Kingdom medical record database found no evidence that the use of 5-alpha reductase inhibitors independently increase the risk for ED. In 71,849 men with benign prostatic hyperplasia (BPH), the risk of ED was not increased with the use of finasteride or dutasteride only (odds ratio [OR] 0.94), or a 5-alpha reductase inhibitor plus an alpha blocker (OR 0.92) compared with an alpha blocker only. In addition, the risk of ED was not increase in 12 346 men prescribed finasteride 1 mg for alopecia, compared with unexposed men with alopecia (OR 0.95). The risk of ED did increase with longer duration of BPH, regardless of drug exposure. 
Endocrine evaluation consisting of a morning serum testosterone is generally indicated. Measurement of serum prolactin may be indicated. A low testosterone level merits repeat measurement together with assessment of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin levels. Other tests may be helpful in excluding unrecognized systemic disease and include a complete blood count, urinalysis, creatinine, lipid profile, fasting blood sugar, and thyroid function studies.
Acetylcholine released by the parasympathetic nerves is thought to act primarily on endothelial cells to release a second nonadrenergic-noncholinergic carrier of the signal that relaxes the trabecular smooth muscle. Nitric oxide released by the endothelial cells, and possibly also of neural origin, is currently thought to be the leading of several candidates as this nonadrenergic-noncholinergic transmitter; but this has not yet been conclusively demonstrated to the exclusion of other potentially important substances (e.g., vasoactive intestinal polypeptide). The relaxing effect of nitric oxide on the trabecular smooth muscle may be mediated through its stimulation of guanylate cyclase and the production of cyclic guanosine monophosphate (cGMP), which would then function as a second messenger in this system.
The vacuum device creates a vacuum to pull blood into the penis. Unlike a normal erection, the inflow of blood does not continue once the individual removes the vacuum device. The rubber band placed at the base of the penis constricts the penis to prevent the blood from leaving the penis. As there is no inflow or outflow of blood when the rubber band is in place, it is uncommon for the tip of the penis (the glans) to appear a little blue and the penis to be cooler. Once intercourse is completed, the individual removes the rubber band and the blood drains out of the penis.
I'm a college guy who has only had sex a handful of times, and I've noticed a bit of a reccurring issue. During any foreplay and all that good stuff, I have a nice big erection, but as soon as I'm about to stick it in, the erection disappears like a frightened turtle. Then once the 30 seconds of embarrassing made-up explanations concludes, the erection is back.
Estimates of the prevalence of impotence depend on the definition employed for this condition. For the purposes of this consensus development conference statement, impotence is defined as male erectile dysfunction, that is, the inability to achieve or maintain an erection sufficient for satisfactory sexual performance. Erectile performance has been characterized by the degree of dysfunction, and estimates of prevalence (the number of men with the condition) vary depending on the definition of erectile dysfunction used.
The motivation and expectations of the patient and his partner and education of both are critical in determining which therapy is chosen and in optimizing its outcome. If single therapy is ineffective, combining two or more forms of therapy may be useful. Penile prostheses should be placed only after patients have been carefully screened and informed. Vascular surgery should be undertaken only in the setting of clinical investigation and extensive clinical experience. With any form of therapy for erectile dysfunction, long-term followup by health professionals is required to assist the patient and his partner with adjustment to the therapeutic intervention. This is particularly true for intracavernosal injection and vacuum constriction therapies. Followup should include continued patient education and support in therapy, careful determination of reasons for cessation of therapy if this occurs, and provision of other options if earlier therapies are unsuccessful.
There have been some studies to suggest that a placebo effect that improves ED may work for some men. One study found that men taking an oral placebo pill showed as much improvement in ED symptoms as men who took actual medication to improve ED. Conversely, men who were given therapeutic suggestions to improve ED did not see signs of symptom improvement.
One study examined the role of testosterone supplementation in hypogonadal men with ED. These men were considered nonresponders to sildenafil, and their erections were monitored by assessing nocturnal penile tumescence (NPT). After these men were given testosterone transdermally for 6 months, the number of NPTs increased, as did the maximum rigidity with sildenafil.  This study suggests that a certain level of testosterone may be necessary for PDE5 inhibitors to function properly.
Vardenafil and tadalafil belong to the same group of chemical compounds as sildenafil, namely phos-phodiesterase type 5 (PDE-5) inhibitors. Some men cannot benefit from sildenafil or the two newer PDE-5 inhibitors because they have low levels of nitric oxide. British investigators reported in late 2002 that three different types of compounds are being studied as possible medications for men with low levels of nitric oxide. They are Rho-kinase inhibitors, soluble guanylate cyclase activators, and nitric oxide-releasing PDE-5 inhibitors.
Look, ED can have many causes. Most of the time, it’s physiological. But there are also lots of psychological reasons why someone may experience ED. Treating ED isn’t all about medication. Dealing with some of these psychological issues can help you battle ED, too. I’m talking about depression, anxiety, loss of desire, sense of inadequacy, guilt, fatigue, anger, relationship dysfunction. Working through these types of psychological challenges can help you achieve the happy, healthy manhood you deserve.
Among their findings, the panel concluded that (1) the term "erectile dysfunction" should replace the term "impotence"; (2) the likelihood of erectile dysfunction increases with age but is not an inevitable consequence of aging; (3) embarrassment of patients and reluctance of both patients and health care providers to discuss sexual matters candidly contribute to underdiagnosis of erectile dysfunction; (4) many cases of erectile dysfunction can be successfully managed with appropriately selected therapy; (5) the diagnosis and treatment of erectile dysfunction must be specific and responsive to the individual patient's needs and that compliance as well as the desires and expectations of both the patient and partner are important considerations in selecting appropriate therapy; (6) education of health care providers and the public on aspects of human sexuality, sexual dysfunction, and the availability of successful treatments is essential; and (7) erectile dysfunction is an important public health problem deserving of increased support for basic science investigation and applied research.
For the past few months I’ve been dating a lovely man but our relationship is at risk because he can’t get it up. He says he fancies me and always seems turned on. Sometimes he gets hard - but when we try for sex he loses his erection. On the few occasions he has got hard, he doesn’t orgasm. I’ve always been a very sexual person and would like a lot of sex. We’re hardly having any. I find it difficult to orgasm even if he tries other things because I keep thinking. Why can’t he have proper sex with me?
To reach the largest audience, communications strategies should include informative and accurate newspaper and magazine articles, radio and television programs, as well as special educational programs in senior centers. Resources for accurate information regarding diagnosis and treatment options also should include doctors' offices, unions, fraternal and service groups, voluntary health organizations, State and local health departments, and appropriate advocacy groups. Additionally, since sex education courses in schools uniformly address erectile function, the concept of erectile dysfunction can easily be communicated in these forums as well.
The circulatory system plays a central role in obtaining and sustaining erections. Augmentation of blood flow to the corporal bodies depends on the intravascular pressure in the penile artery. Vascular lesions—typically atherosclerotic, but occasionally fibrotic—and systemic hypotension will limit flow to the corpora. In certain patients, blood flow at rest may be sufficient to obtain an erection but not sufficient to maintain it during intercourse, when the pelvic musculature places greater demands on a compromised blood supply.
While pills for ED are convenient, some men sustain stronger erections by injecting medication directly into the penis. Drugs approved for this purpose work by widening the blood vessels, causing the penis to become engorged with blood. Another option is inserting a medicated pellet into the urethra. The pellet can trigger an erection within 10 minutes.