Antidepressants hypertension with

A cerebral hemorrhage is the result of rupture of a sclerosed or otherwise diseased blood vessel in the brain. The brain cells in the vicinity of the burst vessel are deprived of blood and therefore nutrients. They will mostly die within several minutes. The symptoms may be mild to severe, including loss of speech and memory, as well as an inability to walk. It is believed that atherosclerosis, combined with hypertension, predisposes a person to such a CVA. Intracranial bleeding can also result from a head injury or from the interaction of certain antidepressant drugs with other drugs or even particular foods. 

The amphetamines and the anorexiants should not be given during or within 14 days after administration of monoamine oxidase inhibitors (see Chap. 31) because the patient may experience hypertensive crisis and intracranial hemorrhage. When guanethidine is administered with the amphetamines or the anorexiants, the antihypertensive effect of guanethidine may decrease. Coadministration of the amphetamines or the anorexiants with the tricyclic antidepressants may decrease the effects of the amphetamines or the anorexiants. 

The antidiarrheal drugs cause an additive CNS depression when administered with alcohol, antihistamines, narcotics, and sedatives or hypnotics. There are additive cholinergic effects when administered with other drugp having anticholinergic activity, such as antidepressants or antihistamines. Concurrent use of the antidiarrheals witii a monoamine oxidase inhibitor increases the risk of a hypertensive crisis. 

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

Tricyclic antidepressants are cardiotoxic, inducing tachycardias and an increased tendency for ventricular arrhythmias with high doses. This dose dependent cardiotoxicity gives these agents a low therapeutic index. Overdoses are characterized by cardiac conduction disturbances, hyperpyrexia, hypertension, confusion, hallucinations, seizures and coma and there is a high mortality rate in suicide attempts. Depressed patients should therefore not be given more than one week supply of these drugs. 

Tricyclic antidepressants are notorious for their risk to be involved in drug-drug interactions. Additive anticholinergic effects can be expected in combination with antihistamines, antipsychotics and anticholinergic-type anti-Parkinson agents. Hepatic enzyme-inducing agents increase their hepatic metabolism while enzyme inhibitors may potentiate the effects of tricyclics. Concomitant use with monoamine oxidase inhibitors will produce hypertension, hyperpyrexia and convulsions. 

The MAOIs are as effective as the heterocyclic antidepressants and the newer agents, such as the SSRIs. However, at least two forms of life-threatening toxicity (hepatotoxicity and dietary tyramine-induced hypertensive crisis ) have been associated with their chronic use. For this reason, the MAOIs are not considered first-line agents in the treatment of depression. They are generally reserved for treatment of depressions that resist therapeutic trials of the newer, safer antidepressants. However, a new transdermal formulation of selegiline undergoing clinical trials demonstrates antidepressant efficacy without concerns of liver toxicity or dietary tyramine-induced hypertension. 

Can antidepressants such as tricyclics or buproprion augment the effect of stimulants on nondepressed children with ADHD Randomized controlled trials have yet to address this question. Nonetheless, such combinations are common in clinical practice. One case report showed leukopenia in a child treated with a combination of MPH and tricyclics for 4 months, although the doses were not specified (Burke et ah, 1995). Another case report indicated that obsessive-compulsive symptoms developed secondary to the combination of MPH and tricyclics (Pataki et ah, 1993). On a cautionary note, MPH has been found to interact with guanethidine to produce paradoxical hypotension. Patients on monoamine oxidose (MAO) inhibitors are likely to develop hypertensive crises if given a stimulant. 

Coadministration of beta-blockers can potentiate rebound hypertension upon discontinuation of medications, and it is therefore recommended that the beta-blocker be withdrawn before the tt2 agonist (Physicians Desk Reference, 2001). Tricyclic antidepressants may also produce changes in sinus node and AV conduction, and it is recommended that they be used cautiously in combination with tt2 agonists (Physicians Desk Reference, 2001). However, in child psychiatric practice, there has been debate about whether there are adverse interactions related to concomitant use of tricyclics and tt2 agonists. Finally, the tt2 agonists may potentiate the effects of CNS depressants (e.g., barbiturates) or other medications that produce sedation, so lower doses of each may be warranted. 

The MAO-B inhibitor, l-deprenyl, has been approved by the FDA for use in Parkinson s disease. At the lower dose range, it does not interact with tyramine. As mentioned earlier, there is preliminary evidence of antidepressant efficacy for a transdermal delivery system for selegiline. This formulation does not interact with tyramine to produce a hypertensive crisis (181). 

This antidepressant can interact with other drugs via its two mechanisms of action serotonin and NE uptake inhibition. The former action means that the same pharmacodynamic interactions will occur with venlafaxine as with SSRIs, including the serotonin syndrome. At higher doses, venlafaxine is also prone to the same pharmacodynamic interactions as NSRIs such as secondary amine TCAs like desipramine and with newer NSRIs such reboxetine. Thus, the combination of high-dose venlafaxine plus an MAOl could produce a hypertensive crisis as well as the serotonin syndrome. 

MAOIs have the most serious pharmacodynamic interactions of any antidepressant class. As discussed earlier, they can cause a hypertensive crisis and the serotonin syndrome. They potentiate the hypertensive effects of most sympathomimetic amines, as well as tyramine, which is the reason for the avoidance of over-the-counter preparations containing such agents, in addition to the tyramine-free diet ( 508, 509). The serotonin syndrome occurs most often when MAOIs are used in combination with SSRIs and venlafaxine but it can also occur when MAOIs are used with tryptophan, 5-hydroxytryptophan, and some narcotic analgesics. In addition, MAOIs can also significantly potentiate the sedative and respiratory depressant effects of narcotic analgesics. 

The adverse effects of TCAs are also similar to those reported in adults (see Chapter 7). The secondary amine TCAs (e.g., desipramine, nortriptyline) are generally as well tolerated as newer antidepressants. Increased blood pressure may be more likely to occur in children than in adults but hypertension per se is rare ( 135). The most common cardiovascular effect is mild tachycardia. Despite their generally favorable adverse effect profile, secondary amine TCAs can cause serious toxicity in children and adolescents just as in adults when a taken in an overdose or when a high TCA plasma level occurs as a result of slow metabolism ( 136). For that reason, most clinicians reserve TCAs for the child or adolescent who has at least a moderate depressive disorder unresponsive to a trial of one or more newer antidepressants. In such instances, TDM should be done at least once to ensure plasma concentrations greater than 450 ng/mL do not develop ( 137). Such levels are associated with an increased risk of the following ... 

Five cases (ages 36, 48, 48 and 60 and one unknown three males and two females) reported intermittent ineffectiveness with sertraline, including complaints of does not seem to be working, anxiety attack, or worsening depression. In four cases, symptoms occurred after sertraline was added to the continuing St. John s wort therapy. In contrast to reports with other antidepressants, these cases did not report hypertension or possible serotonin syndrome. It is uncertain if the occasional events were possibly associated with the patients unstable psychiatric status following sertraline therapy, or due to potential sertraline-related adverse events. 

Serotonin syndrome SSRIs, second generation antidepressants, MAOIs, linezolid, tramadol, meperidine, fentanyl, ondansetron, sumatriptan, MDMA, LSD, St. John s wort, ginseng Hypertension, hyperreflexia, tremor, clonus, hyperthermia, hyperactive bowel sounds, diarrhea, mydriasis, agitation, coma onset within hours Sedation (benzodiazepines), paralysis, intubation and ventilation consider 5-HT2 block with cyproheptadine or chlorpromazine... 

Monoamine oxidase inhibitors (eg, tranylcypromine, phenelzine) are older antidepressants that are occasionally used for resistant depression. They can cause severe hypertensive reactions when interacting foods or drugs are taken (see Chapters 9 and 30), and they can interact with the selective serotonin reuptake inhibitors (SSRIs). 

One old-fashioned augmentation strategy that has fallen out of favor in recent years is to combine with great caution a TCA and an MAO inhibitor (the cautious combo in Fig. 7—30). Given its potential dangers (e.g., sudden hypertensive episodes, orthostatic hypotension, drug and dietary interactions, obesity), as well as the wide variety of other antidepressant combinations available today, this combination is rarely necessary or justified. 

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