Potential Treatments

A complete discussion of the treatment options available is beyond the scope of this chapter; however, some basic principals are briefly outlined (75). One of the physician's most important tasks is to identify whether hypotensive syncope is primary or secondary in nature, and to determine if there are any potentially reversible causes (such as drugs, anemia, or volume depletion) (see Table 6).

It is equally important to educate the patient and their family about the nature of the problem. Teaching the patient to avoid aggravating factors (such as extreme heat, dehydration, and alcohol consumption), as well as recognizing any prodromal symptoms and assuming a recumbent position at their onset, are extremely helpful measures.

Nonpharmacologic therapies that are useful include sleeping with the head of the bed upright (approx 6-12 inches), and elastic support hose (at least 30-40 mm/Hg ankle counter-pressure). Biofeedback has also proven useful in selected patients.

Pharmacotherapy should be used cautiously, and should be tailored to fit the needs of the patient based on the type of autonomic disorder being treated, as well as coexisting symptoms and conditions. It should also be remembered that virtually any drug used in treatment can occasionally worsen symptoms (a "prosyncopal" effect).

In neurocardiogenic syncope, a number of reports have found that beta-blocker

Neurocardiogenic

— Blood Pressure Heart Rate

Dysautonomy Response

Blood Pressure Heart Rate

Postural Orthostatic Tachycardia

— Blood Pressure Heart Rate

Fig. 3. Response Patterns During Tilt-Table Testing.

Blood Pressure Heart Rate therapy is effective, presumably because its negative inotropic effects lessen the degree of cardiac mechanoreceptor activation associated with abrupt falls in venous return

(92). The increase in peripheral vascular resistance that accompanies unopposed beta blockade may also contribute to its therapeutic effects. We have not found beta blockade as useful in other forms of reflex syncope, and it may be detrimental in the dysautonomic syndromes. A useful agent in patients with dysautonomic syncope (and in younger patients with neurocardiogenic syncope) is the mineral corticoid agent fludrocortisone

(93). It results in fluid and sodium retention, and also appears to raise pressure via an

Table 6

Pharmacologic Agents That May Cause or Worsen Orthostatic Intolerance

Angiotensin-converting enzyme inhibitors

Alpha-receptor blockers

Calcium-channel blockers

Beta-blockers

Phenothiazines

Tricyclic antidepressants

Bromocriptine

Ethanol

Opiates

Diuretics

Hydralazine

Ganglionic blocking agents indirect vasoconstrictive effect resulting from sensitization of peripheral alpha receptors. Since the drug may cause hypokalemia and hypomagnesemia, serum potassium and magnesium levels must be periodically monitored.

Since failure to properly vasoconstrict the peripheral vessels is common to all of these disorders, vasoconstrictive substances can be employed. Initially, we employed the amphetamine-like agent, methylphenidate, with excellent results (94). However, the fact that it is a controlled substance with potent CNS-stimulating activity tended to limit our use of the drug. An excellent alternative is the new peripherally acting alpha agonist, midodrine. It has virtually no CNS effects or cardiac stimulation, and provides identical degrees of peripheral alpha-receptor stimulation. Several studies have demonstrated the efficacy of midodrine in both neurocardiogenic and dysautonomic disorders (95-97).

It has been found that the alpha-2-receptor blocking agent, clonidine, can actually elevate blood pressure in dysautonomic patients for whom hypotension is secondary to a severe post-ganglionic sympathetic lesion (98). In patients with severe autonomic failure, the post-junctional vascular alpha-2 receptors that are plentiful in the venous system are actually hypersensitive. Although, in normal individuals, clonidine acts on the CNS to lessen sympathetic output and blood pressure, in autonomic failure, some patients exhibit little or no sympathetic output, thus permitting its peripheral actions to become manifest.

Interestingly, a number of patients with autonomic failure will be anemic. A brilliant study by Hoeldtke and Streeten demonstrated that subcutaneous injections of erythropoi-etin while raising blood count will also produce dramatic increases in blood pressure (99). This pressure effect seems to occur independent of the red cell effect (100).

A series of both animal and human studies have demonstrated that the neurotransmitter serotonin (5-hydroxytryptamine) plays an essential role in the central regulation of blood pressure and heart rate. It has been postulated that some patients with autonomic disorders may have disturbances in central serotonin production or regulation (101). The observation that serotonin reuptake inhibitors can be effective in both the treatment of neurocardiogenic syncope and orthostatic hypotension supports this concept (102,103).

The exact role of pacemaker therapy in the treatment of these disorders remains controversial, and is beyond the scope of this discussion. However, a number of investigators have found that in selected patients pacemaker therapy can be effective in reducing symptoms and may sometimes eliminate syncope altogether (104). The recent North American Vasovagal Pacemaker Study demonstrated that pacing using a rate-drop hysteresis algorithm was effective in preventing syncope (105). More recently, the VASIS trial, using DDI pacing with simple rate hysteresis, yielded similar results (106).

It should be considered that in dysautonomic disorders (as opposed to the reflex syncopes), hypotensive syncope is only one aspect of a broader constellation of symptoms relating to autonomic failure. The physician should therefore not give the patient unrealistic expectations as to what symptoms can and cannot be eliminated. Both physician and patient should remain aware that these disorders can be progressive in nature, and that therapies may need to be altered over time.

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