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ED (Diagnosis (a patient's cardiac reserve should be assessed before…

- - - - It is administered before initiation of any treatment and repeated at regular intervals during treatment
- - - - erection is prolonged by a decrease in venous outflow from the corpora, which is caused by compression of subtunical venules against the tunica albuginea by the swollen corpora
      - Arterial flow into the corpora is enhanced by acetylcholine-mediated vasodilation
        
        presence of sexual stimulation to genital tissue, acetylcholine enhances the production of nitric oxide by endothelial cells and nonadrenergic–noncholinergic neurons
        
        NO conversion of cyclic guanosine triphosphate to cGMP
        
        cGMP activates a cGMP-dependent kinase, which decreases intracellular calcium concentrations in smooth muscle cells of penile arteries and cavernosal sinuses
        
        smooth muscle relaxation occurs, which enhances arterial blood flow
        
        acetylcholine or prostaglandin E enhances the activity of adenyl cyclase, which increases the conversion of cyclic adenosine triphosphate to cAMP, a potent muscle relaxant
        
        AMP decreases intracellular calcium concentrations to produce smooth muscle relaxation
    - - brain processes this information and the nervous impulse is carried down the spinal cord to peripheral cholinergic nerves that innervate the vascular supply to the corpora, resulting in an erection.
    - - Detumescence, or the progression of an erect penis to a flaccid state, results from the actions of norepinephrine, which contracts vascular smooth muscle to decrease arterial inflow to the corpora and contracts sinusoidal tissue in the corpora
- - - - pt condition
        
        Has ≥3 risk factors for cardiovascular disease
        
        complete cardiovascular workup and treadmill stress test to determine tolerance to increased myocardial energy consumption associated with increased sexual activity. Reclassify in low- or high-risk category
        
        Has mild or moderate, stable angina
        
        Had a recent myocardial infarction or stroke within the past 2-8 weeks
        
        Has moderate congestive heart failure (NYHA class III)
        
        History of stroke, transient ischemic attack, or peripheral artery disease
    - - Pt condition
        
        Has had a myocardial infarction >8 weeks ago
        
        Has mild valvular heart disease
        
        Has mild congestive heart failure (NYHA class I or II)
        
        Has well-controlled hypertension
        
        Has asymptomatic cardiovascular disease with <3 risk factors for cardiovascular disease
        
        Patient can be started on phosphodiesterase inhibitor
    - - Has unstable or refractory angina, despite treatment
      - Has uncontrolled hypertension
      - Has severe congestive heart failure (NYHA class IV)
      - Has had a recent myocardial infarction or stroke within past 2 weeks
        
        Phosphodiesterase inhibitor is contraindicated; sexual intercourse should be deferred
      - Has moderate or severe valvular heart disease
      - Has high-risk cardiac arrhythmias
      - Has obstructive hypertrophic cardiomyopathy
  - - - stimulates adenyl cyclase to increase production of cyclic adenosine monophosphate, a neurotransmitter that ultimately enhances blood flow to and blood filling of the corpora.
    - - Local adverse effects occur during the first year of therapy, including cavernosal plaques or fibrosis at the injection site (2%–12% of patients), penile pain (10%–44%), and priapism (1%–15%). Penile pain is usually mild and self-limiting, but priapism (ie, painful, drug-induced erection lasting >1 hours) necessitates immediate medical attention.