Rebound hypertension

For treatment of hypertensive rebound after withdrawal of clonidine, 0.2 mg is given initially, followed by 0.2 mg hourly until the DBP falls below 110 mm Hg or a total of 0.7 mg has been administered a single dose may be sufficient. 

Geriatric Considerations - Summary The alphaj-adrenergic agonist effect of tizani-dine lowers blood pressure in a manner similar to clonidine but is less potent. Older adults are at risk of hypotension and when discontinued, this drug should be tapered to avoid hypertensive rebound. 

A number of other reports describe similar cases of hypertensive rebound (a sudden and serious rise in blood pressure) within 24 to 72 hours of stopping the elonidine, apparently worsened by the presenee of propranolol. The symptoms resemble those of phaeochromoeytoma, and inelude tremor, apprehension, flushing, nausea, vomiting, severe head-aehe, and a serious rise in blood pressure. One patient died from a eerebel-lar haemorrhage. ... 

The normal additive hypotensive effects of these drugs result from the two acting in concert at different but complementary sites in the cardiovascular system. Just why antagonism sometimes occurs is unexplained. The hypertensive rebound following elonidine withdrawal is thought to be due to an increase in the levels of circulating catecholamines. With the beta (vasodilator) effects blocked by a beta blocker, the alpha (vasoconstrictor) effects of the catecholamines are unopposed and the hypertension is further exaggerated. 

When clonidine is withdrawn abmpdy, patients may experience a rebound hypertensive phenomenon, whereia blood pressure rises rapidly to a level higher than the predmg level. These patients may experience symptoms of headache, tachycardia, agitation, and nervousness. If rebound hypertension occurs, resumption of clonidine therapy or adrninistration of phentolamine reduces the blood pressure. For clonidine withdrawal, the dose should be reduced gradually over a two-week period. The principal side effects are sedation, dry mouth, drowsiaess, di22iQess, and fatigue. 

Centrally acting a2-Receptor agonists Sedation, dry mouth, rebound hypertension... 

Should it be necessary to discontinue antihypertensve therapy, the nurse should never discontinue use of the drug abruptly. The dosage is gradually reduced over 2 to 4 days to avoid rebound hypertension (a rapid rise in blood pressure). 

Never discontinue use of this drug except on the advice of the primary care provider. These drug control but do not cure hypertension. Skipping doses of the drug or voluntarily discontinuing the drug may cause severe, rebound hypertension. 

Clonidine Rebound hypertension on acute drug cessation... 

Abrupt cessation may lead to rebound hypertension, which is thought to result from a compensatory increase in norepinephrine release that follows discontinuation of presynaptic a-receptor stimulation. 

Side effects. Lassitude, dry mouth rebound hypertension after abrupt cessation of clonidine therapy. 

Abrupt termination of continuous treatment can be followed by rebound hypertension (particularly with short ti/2 p-blockers). 

Rebound hypertension also has occurred following discontinuation of the transdermal patch. 

Adverse reactions may include Stevens-Johnson syndrome pericardial effusion T-wave changes rebound hypertension (following gradual withdrawal in children) decreased initial hematocrit, hemoglobin and erythrocyte counts nausea vomiting temporary edema alkaline phosphatase/serum creatinine/BUN increase, hypertrichosis. 

Discontinuing therapy If therapy needs to be discontinued, especially in patients who have been receiving high doses for long periods, the dose should be decreased slowly to minimize the risk of withdrawal and rebound hypertension, tachycardia, and hypertonia. 

NaHCOs and CaCOs can neutralize HCl rapidly, depending on particle size and crystal structure, and effectively. NaHCOs acts rapidly but absorption of unneutralized NaHCOs produces risks for alkalosis and sodium retention which may lead to edema, hypertension or heart failure. Also neutralized antacids may cause alkalosis by permitting the absorption of endogenous NaHCOs. Ca + may stimulate the secretion of gastrin and HCl and calcium-containing antacids have been associated with rebound acid hypersecretion. 

Patients with malignant-accelerated hypertension can usually be managed by oral therapy. Patients who are seen in a nursing home or clinic, whose BP is found to be above some arbitrary danger level like a BP of 180/120 should not automatically be given nifedipine sublingually. Indiscriminate use of nifedipine sublingually could lead to a major catastrophe like myocardial infarction or cerebrovascular episodes. Nifedipine activates sympathetic response and leads to precipitous drops of blood pressure followed by rebound hypertension. 

Do not discontinue abruptly may require taper rapid withdrawal may produce rebound hypertension or angina... 

Abrupt withdrawal may result in rebound hypertension associated with nervousness, agitation, anxiety, insomnia, hand tingling, tremor, flushing, and diaphoresis. 

Abrupt withdrawal, including a large reduction in dosage or interruption in drug delivery, may produce rebound pulmonary hypertension as evidenced by dyspnea, dizziness, and asthenia. 

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