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These drugs are effective in hypertension because they decrease the heart rate and cardiac output Even after continued use of -blockers, cardiac output remains lower and systemic vascular resistance higher with agents that do not have intrinsic sympathomimetic or -blocking activity The -blockers also decrease renin release and are more efficacious in populations with elevated plasma renin activity, such as younger white patients They neutralize the reflex tachycardia caused by vasodilators and are especially useful in patients with associated conditions that benefit from the cardioprotective effects of these agents These include individuals with angina pectoris, previous myocardial infarction, and stable congestive heart failure as well as those with migraine headaches and somatic manifestations of anxiety Although all -blockers appear to be similar in antihypertensive potency, controlling approximately 50% of patients, they differ in a number of pharmacologic properties (these differences are summarized in Table 11 7), including specificity to the cardiac 1-receptors (cardioselectivity) and whether they also block the 2-receptors in the bronchi and vasculature; at higher dosages, however, all agents are nonselective The -blockers also differ in their pharmacokinetics and lipid solubility which determines whether they cross the blood brain barrier and affect the incidence of central nervous system side effects and route of metabolism Labetalol and carvedilol are combined - and -blockers and, unlike most -blockers, decrease peripheral vascular resistance The side effects of all -blockers include inducing or exacerbating bronchospasm in predisposed patients (eg, those with asthma and some patients with chronic obstructive pulmonary disease [COPD]); sinus node dysfunction and atrioventricular (AV) conduction depression (resulting in bradycardia or AV block); nasal congestion; Raynaud s phenomenon; and central nervous system symptoms with nightmares, excitement, depression, and confusion Fatigue, lethargy, and impotence may occur All -blockers tend to increase plasma triglycerides The nonselective and, to a lesser extent, the cardioselective ( 1-selective) -blockers tend to depress the protective HDL fraction of plasma cholesterol As with diuretics, the changes are blunted with time and dietary changes.

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-Blockers have traditionally been considered contraindicated in patients with congestive heart failure Evolving experience suggests that they have a propitious effect on the natural history of patients with chronic stable heart failure and reduced ejection fraction (see 10) -Blockers are used cautiously in patients with type 1 diabetes, since they can mask the symptoms of hypoglycemia and prolong these episodes by inhibiting gluconeogenesis Although they may increase blood glucose levels in type 2 diabetics, the prognosis of these patients on balance is improved These drugs should also be used with caution in patients with advanced peripheral vascular disease associated with rest pain or nonhealing ulcers, but they are generally well tolerated in patients with mild claudication In treatment of pheochromocytoma, -blockers should not be administered until -blockade has been established Otherwise, blockade of vasodilatory 2-adrenergic receptors will allow unopposed vasoconstrictor -adrenergic receptor activation with worsening of hypertension For the same reason, -blockers should not be used to treat hypertension arising from cocaine use Because of the lack of efficacy in prevention of myocardial infarction and inferiority compared with other drugs in prevention of stroke and left ventricular hypertrophy, there is now increasing doubt whether -blockers should still be regarded as ideal first-line agents in the treatment of hypertension without specific compelling indications (such as active coronary artery disease) In addition to the adverse metabolic changes associated with their use, some experts have suggested that the therapeutic shortcomings of -blockers are the consequence of the particular hemodynamic profile associated with these drugs Pressure peaks in the aorta are augmented by reflection of pressure waves from the peripheral circulation These reflected waves are delayed in patients taking ACE inhibitors and thiazide diuretics, resulting in decreased systolic and pulse pressures By contrast, blockers appear to potentiate reflection of pressure waves, possibly because peripheral resistance vessels are a reflection point and peripheral resistance is not decreased by -blockers This might explain why -blockers are less effective at control of systolic and pulse pressure The ASCOT trial showed that the atenolol/bendroflumethiazide combination was inferior to the amlodipine/ perindopril combination in predominantly white patients with modestly elevated cardiovascular risk Subsequent analyses indicated that differences in blood pressure (especially the calculated central aortic systolic pressure) and HDL cholesterol contributed to the excess risk of stroke and coronary events respectively in the -blocker group Despite these concerns, the compelling indications for blockers remain, such as active coronary artery disease and impaired left ventricular function Great care should be exercised if the decision is made, in the absence of compelling indications, to remove -blockers from the treatment regimen since abrupt withdrawal can precipitate acute coronary events and severe increases in blood pressure.

The easiest screening test for hypercortisolism involves the patient obtaining a salivary cortisol at 11 pm (see below) and then dexamethasone, 1 mg orally, and collecting serum for cortisol determination at about 8 am the next morning; a cortisol level under 5 mcg/dL (< 135 nmol/L, fluorometric assay) or under 2 mcg/dL (< 54 nmol/L, high-performance liquid chromatography [HPLC] assay) excludes Cushing s syndrome with 98% certainty However, 8% of established patients with pituitary Cushing s disease have dexamethasonesuppressed cortisol levels < 2 mcg/dL Therefore, when other clinical criteria suggest hypercortisolism, further evaluation is warranted even in the face of normal dexamethasone-suppressed serum cortisol Antiseizure drugs (eg, phenytoin, phenobarbital, primidone) and rifampin accelerate the metabolism of dexamethasone, in that way causing a lack of cortisol suppression by dexamethasone Estrogens during pregnancy or as oral contraceptives or estrogen replacement therapy may also cause lack of dexamethasone suppressibility Patients with an abnormal dexamethasone suppression test require further investigation, which includes a 24-hour urine collection for free cortisol and creatinine An abnormally high 24-hour urine free cortisol (or free cortisol to creatinine ratio of > 95 mcg cortisol/g creatinine) helps confirm hypercortisolism A misleadingly high urine free cortisol excretion occurs with high fluid intake In pregnancy, urine free cortisol is increased, while 17-hydroxycorticosteroids remain normal and diurnal variability of serum cortisol is

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