But if the blood flow is weak here, it is highly likely that it is also weak in arteries supplying the heart, raising the risk of a heart attack. In fact, some studies suggest that women with heart disease may also suffer sexual dysfunction: the clitoris, like the penis, is a vascular organ, and also relies on healthy blood flow for successful orgasms.
If you’re no longer having intercourse, you don’t need erections. Most men assume that erections are necessary for sex. No. Couples can have great sex without them. Intercourse becomes problematic for older couples. Men have erection issues and post-menopausal women develop vaginal dryness and atrophy that can make intercourse uncomfortable (or worse) even with lubricants. Many older couples jettison intercourse in favor of mutual massage, oral sex, and sex toys—and still enjoy hot sex.
In comparison, 37% of men who had received external radiotherapy as their primary therapy reported the ability to attain functional erections suitable for intercourse, along with 43% of men who had received brachytherapy as primary treatment. Pretreatment sexual health-related quality of life score, age, serum prostate-specific antigen (PSA) level, race or ethnicity, body mass index, and intended treatment details were associated with functional erections 2 years after treatment. [45]
Constriction of the trabecular smooth muscle and helicine arteries induced by sympathetic innervation makes the penis flaccid, with blood pressure in the cavernosal sinuses of the penis near venous pressure. Acetylcholine is thought to decrease sympathetic tone. This may be important in a permissive sense for adequate trabecular smooth muscle relaxation and consequent effective action of other mediators in achieving sufficient inflow of blood into the lacunar spaces. When the trabecular smooth muscle relaxes and helicine arteries dilate in response to parasympathetic stimulation and decreased sympathetic tone, increased blood flow fills the cavernous spaces, increasing the pressure within these spaces so that the penis becomes erect. As the venules are compressed against the tunica albuginea, penile pressure approaches arterial pressure, causing rigidity. Once this state is achieved, arterial inflow is reduced to a level that matches venous outflow.

Sexual functioning involves a complex interaction among biologic, sociocultural, and psychological factors, and the complexity of this interaction makes it difficult to ascertain the clinical etiology of sexual dysfunction. Before any diagnosis of sexual dysfunction is made, problems that are explained by a nonsexual mental disorder or other stressors must first be addressed. Thus, in addition to the criteria for erectile disorder, the following must be considered:
The user should stop using the vacuum pump if pain occurs... Use of a vacuum pump may bruise or rupture the blood vessels either immediately below the surface of the skin or within the deep structures of the penis or scrotum, resulting in hemorrhage and/or the formation of a hematoma. There is now sufficient information available regarding the risks, benefits, and use of vacuum pumps.

Measurement of the penile vibration perception threshold provides an inexpensive, reproducible, and painless screening test with acceptable sensitivity for detecting neuropathy. Abnormalities at the level of the sacral cord can be documented by sacral latency testing, while upper motor neuron impotence can be demonstrated with genital-cerebral evoked response testing. These latter procedures are not indicated in unselected patients with impotence.


The health care provider will ask about the firmness and duration of erections at different times (e.g., sex with partners, erections after sleep). Discussing sexual dysfunction with a health care provider is very important because many conditions causing it can be successfully treated. If a man has no diseases that cause ED and can have an erection with masturbation or early morning awakening, he likely has ED due to psychological causes.
In patients with low testosterone, testosterone treatment can improve libido and erectile dysfunction, but many men still may need additional oral medications such as sildenafil, vardenafil, or tadalafil. Some studies suggest that men with ED and low testosterone may respond better to PDE5 inhibitors when given testosterone therapy; however, this is controversial.

#4 You’re just plain turned off. It happens. Whether it’s the weight your partner has put on, the realization that you’re having period sex, or you’re just not getting what you need in the bedroom, at some point in your life, you’re going to be turned off enough to lose *or be unable to attain* your hard-on. [Read: Not attracted to your girlfriend anymore? The why and the fixes]


"Data shows the longer you ride, the higher your chance of developing ED in terms of distance per week," Gittens says. If you cycle for exercise or socialization, you don't have to necessarily give it up, just make some modifications. Gittens suggests riding for shorter distances, giving yourself a rest every once in a while, finding a comfortable seat, and getting a bike that’s sized appropriately.
Although erectile dysfunction increases progressively with age, it is not an inevitable consequence of aging. Knowledge of the risk factors can guide prevention strategies. Specific antihypertensive, antidepressant, and antipsychotic drugs can be chosen to lessen the risk of erectile failure. Published lists of prescription drugs that may impair erectile functioning often are based on reports implicating a drug without systematic study. Such studies are needed to confirm the validity of these suggested associations. In the individual patient, the physician can modify the regimen in an effort to resolve the erectile problem.
Inside the cell, NOS catalyzes the oxidation of L-arginine to NO and L-citrulline. Endogenous blockers of this pathway have been identified. The gaseous NO that is produced acts as a neurotransmitter or paracrine messenger. Its biologic half-life is only 5 seconds. NO may act within the cell or diffuse and interact with nearby target cells. In the corpora cavernosa, NO activates guanylate cyclase, which in turn increases cyclic guanosine monophosphate (cGMP). Relaxation of vascular smooth muscles by cGMP leads to vasodilation and increased blood flow.
For the patient whose history suggests organic impotence, further history, physical and laboratory data will help identify the cause. The classification listed in Table 187.2 is based on the pathophysiologic scheme presented above, and includes mechanical problems that can interfere with erection. Vascular disease is the most common cause of impotence. In advanced cases, Lehriche's syndrome of aortoiliac occlusion will be suggested by bilateral thigh or calf claudication, loss of muscle mass in the buttocks and legs, and impotence. However, the majority of patients with vascular impotence have less severe vascular disease and many will have occlusive disease of the hypogastric-cavernous bed only. Even among patients without claudication, vascular disease is still a likely cause of impotence, especially if risk factors for atherosclerosis are present. Nonatherosclerotic disease is a consideration in the patient with a history of trauma or radiation to the pelvis, both of which cause fibrosis of vessels.

Besides treating the underlying causes such as potassium deficiency or arsenic contamination of drinking water, the first line treatment of erectile dysfunction consists of a trial of PDE5 inhibitor (such as sildenafil). In some cases, treatment can involve prostaglandin tablets in the urethra, injections into the penis, a penile prosthesis, a penis pump or vascular reconstructive surgery.[1]
On the horizon is gene therapy that would deliver genes that produce products or proteins that may not be functioning properly in the penile tissue of men with ED. Replacement of these proteins may result in improvement in erectile function. Experimental animal models have demonstrated improvement in erectile function with gene therapy. Human studies may also demonstrate success with this therapy. Gene therapy may take a long time for regulatory approval and public acceptance.

The drugs are worth trying, but don’t expect miracles. Everyone has heard of Viagra, but Cialis is actually more popular because it’s effective longer—24 to 36 hours instead of three to five. Erection drugs improve erections in around two-thirds of men. They don’t work for about one-third. When they work, they do not produce porn-star erections. Over time, many men need larger doses. But as dosage increases, side effects become more likely, notably, headache and nasal congestion. Finally, the drugs have no effect on arousal, so men may raise erections but don't feel particularly interested in sex. Many men feel disappointed with the drugs. Fewer than half refill their prescriptions.
Ultrasound with Doppler imaging (ultrasound plus evaluation of blood flow in the arteries and veins) can provide additional information about blood flow of the penis and may help in the evaluation of patients prior to surgical intervention. This study is typically performed after the injection of a chemical that causes the arteries to open up, a vasodilator (prostaglandin E1), into the corpora cavernosa in order to cause dilation of blood vessels and promote blood flow into the penis. The rate of blood flow into the penis can be measured along with an evaluation of problems with compression of the veins.
The cost to you for ED drug therapy varies considerably, depending on the pharmacy price, prescription co-pays, and your level of health plan coverage. Nationally, the out-of-pocket cost per pill ranges from approximately $15 to $20. Even if private insurance covers it, you may be limited to four doses per month. Here are a few things you can do to contain costs:
The association between low testosterone and ED is not entirely clear. Although these 2 processes certainly overlap in some instances, they are distinct entities. Some 2-21% of men have both hypogonadism and ED; however, it is unclear to what degree treating the former will improve erectile function. [17] About 35-40% of men with low testosterone see an improvement in their erections with testosterone replacement; however, almost 65% of these men see no improvement. [15]
The symptoms of erectile dysfunction include difficulty achieving an erection, trouble maintaining an erection, and a reduced interest in sex. Because male sexual arousal is a fairly complex process, it can sometimes be difficult to identify a specific cause. Arousal starts in the brain but it also involves the nerves, muscles, and blood vessels and can be impacted by hormones and emotions. If a problem develops with any of these things, erectile dysfunction could be the consequence.
The severity of ED has been correlated with the extent of CVD. Banks et al reported that the risk of future CV events increased progressively according to ED severity.28 This was shown in both men with and without known CVD at baseline and after controlling for confounders. Solomon and colleagues found an inverse correlation between international index of erectile function (IIEF) scores and plaque burden seen on coronary angiography.29 In addition, Yaman et al demonstrated a significant correlation between ED severity on IIEF questionnaires and coronary artery calcification.30
The various PDE5 inhibitors for the treatment of ED share several common side effects, including headache, flushing, nasal congestion, nausea, dyspepsia (stomach discomfort), and diarrhea. Differences exist in side effects of the different PDE5 inhibitors, and thus it is important to be familiar with the prescribing information of the PDE5 inhibitor you are prescribed.
Since endothelial dysfunction, CVD and ED are closely associated in epidemiological studies, the question for clinicians is whether to recommend the man presenting with ED undergo a cardiovascular (CV) evaluation. Clearly, based on numerous studies, ED can be considered at least a ‘marker’ for possible further vascular disease or CVD.15 In their report, Vlachopoulos and coworkers make the point that the man presenting with ED, the clinician, is offered an opportunity to attempt to improve the health of the man by addressing lifestyle modification, and consider further vascular evaluation owing to the clear relationship between endothelial dysfunction, ED and CVD.19
Factors that mediate contraction in the penis include noradrenaline, endothelin-1, neuropeptide Y, prostanoids, angiotensin II, and others not yet identified. Factors that mediate relaxation include acetylcholine, nitric oxide (NO), vasoactive intestinal polypeptide, pituitary adenylyl cyclase–activating peptide, calcitonin gene–related peptide, adrenomedullin, adenosine triphosphate, and adenosine prostanoids.

When sexually stimulated there is a release of a chemical, nitric oxide (NO) in the blood vessels of the corpus cavernosum. The NO stimulates the production of a compound called cGMP, which causes relaxation of the smooth muscle in the blood vessels supplying the corpus cavernosum. PDE 5 is an enzyme that breaks down cGMP. By inhibiting the breakdown of cGMP by PDE5, these medications allow cGMP to build up in the penis. cGMP causes muscles in the corpora cavernosa of the penis to relax. When the muscle is relaxed, more blood can flow into the penis and fill the spaces in the penis. As the penis fills with blood, the veins in the penis are compressed, and this results a hard erection. When the effect on PDE5 decreases, the cGMP levels go down and the muscle in the penis contracts, causing less blood to flow into the penis and allowing the veins to open up and drain blood out of the penis.
It doesn't really matter what they are — sexual turnoffs vary wildly from person to person. But if the person you're getting it on with is doing stuff that's taking you out of the mood — even if it's stuff you feel like you're supposed to enjoy — it's time to swallow your pride and say something. Keeping it a secret might be saving you an awkward conversation in the short term, but in the long term, it could be seriously undermining your sex life. 
Another approach is vacuum therapy. The man inserts his penis into a clear plastic cylinder and uses a pump to force air out of the cylinder. This forms a partial vacuum around the penis, which helps to draw blood into the corpora cavernosa. The man then places a special ring over the base of the penis to trap the blood inside it. The only side effect with this type of treatment is occasional bruising if the vacuum is left on too long.
Erections occur in response to tactile, olfactory, and visual stimuli. The ability to achieve and maintain a full erection depends not only on the penile portion of the process but also on the status of the peripheral nerves, the integrity of the vascular supply, and biochemical events within the corpora. The autonomic nervous system is involved in erection, orgasm, and tumescence. The parasympathetic nervous system is primarily involved in sustaining and maintaining an erection, which is derived from S2-S4 nerve roots.
There have been rare reports of priapism (prolonged and painful erections lasting more than six hours) with the use of PDE5 inhibitors such as sildenafil, vardenafil, and tadalafil. Patients with blood cell diseases such as sickle cell anemia, leukemia, and multiple myeloma have higher than normal risks of developing priapism. Untreated priapism can cause injury to the penis and lead to permanent impotence. Therefore, if your erection lasts four hours, you should seek emergency medical care.
In some cases, ED can be a warning sign of more serious disease. One study suggests ED is a strong predictor of heart attack, stroke, and death from cardiovascular disease. The researchers say all men diagnosed with ED should be evaluated for cardiovascular disease. This does not mean every man with ED will develop heart disease, or that every man with heart disease has ED, but patients should be aware of the link.
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