Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/956
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Corzide (Tablet)
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DOSAGE MUST BE INDIVIDUALIZED . CORZIDE MAY BE ADMINISTERED WITHOUT REGARD TO MEALS. Bendroflumethiazide is usually given at a dose of 5 mg
daily. The usual initial dose of nadolol is 40 mg once daily whether
used alone or in combination with a diuretic. Bendroflumethiazide
in CORZIDE is 30 percent more bioavailable than that of 5 mg Naturetin
tablets. Conversion from 5 mg NATURETIN to CORZIDE represents a 30
percent increase in dose of bendroflumethiazide. The initial dose of CORZIDE (Nadolol and Bendroflumethiazide Tablets)
may therefore be the 40 mg/5 mg tablet once daily. When the antihypertensive
response is not satisfactory, the dose may be increased by administering
the 80 mg/5 mg tablet once daily. When necessary,
another antihypertensive agent may be added gradually beginning with
50 percent of the usual recommended starting dose to avoid an excessive
fall in blood pressure. Dosage Adjustment in Renal Failure���Absorbed nadolol
is excreted principally by the kidneys and, although nonrenal elimination
does occur, dosage adjustments are necessary in patients with renal
impairment. The following dose intervals are recommended:
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CORZIDE (Nadolol and Bendroflumethiazide Tablets)
for oral administration combines two antihypertensive agents: CORGARD (nadolol), a nonselective beta-adrenergic blocking agent,
and NATURETIN (bendroflumethiazide), a thiazide diuretic-antihypertensive.
Formulations: 40 mg and 80 mg nadolol per tablet combined with 5 mg
bendroflumethiazide. Inactive ingredients: cellulose, colorant (FD&C
Blue No. 2), lactose, magnesium stearate, povidone, sodium starch
glycolate, and starch.
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Nadolol Nadolol is a nonselective beta-adrenergic receptor blocking
agent. Clinical pharmacology studies have demonstrated beta-blocking
activity by showing (1) reduction in heart rate and cardiac output
at rest and on exercise, (2) reduction of systolic and diastolic blood
pressure at rest and on exercise, (3) inhibition of isoproterenol-induced
tachycardia, and (4) reduction of reflex orthostatic tachycardia. Nadolol specifically competes with beta-adrenergic receptor
agonists for available beta receptor sites; it inhibits both the betareceptors located chiefly in cardiac muscle and the betareceptors located chiefly in the bronchial and vascular musculature,
inhibiting the chronotropic, inotropic, and vasodilator responses
to beta-adrenergic stimulation proportionately. Nadolol has no intrinsic
sympathomimetic activity and, unlike some other beta-adrenergic blocking
agents, nadolol has little direct myocardial depressant activity and
does not have an anesthetic-like membrane-stabilizing action. Animal
and human studies show that nadolol slows the sinus rate and depresses
AV conduction. In dogs, only minimal amounts of nadolol were detected
in the brain relative to amounts in blood and other organs and tissues.
Nadolol has low lipophilicity as determined by octanol/water partition
coefficient, a characteristic of certain beta-blocking agents that
has been correlated with the limited extent to which these agents
cross the blood-brain barrier, their low concentration in the brain,
and low incidence of CNS-related side effects. In controlled clinical studies, nadolol at doses of 40 to 320 mg/day
has been shown to decrease both standing and supine blood pressure,
the effect persisting for approximately 24 hours after dosing. The mechanism of the antihypertensive effects of beta-adrenergic
receptor blocking agents has not been established; however, factors
that may be involved include (1) competitive antagonism of catecholamines
at peripheral (non-CNS) adrenergic neuron sites (especially cardiac)
leading to decreased cardiac output, (2) a central effect leading
to reduced tonic-sympathetic nerve outflow to the periphery, and (3)
suppression of renin secretion by blockade of the beta-adrenergic
receptors responsible for renin release from the kidneys. While cardiac output and arterial pressure are reduced
by nadolol therapy, renal hemodynamics are stable, with preservation
of renal blood flow and glomerular filtration rate. By blocking catecholamine-induced increases in heart rate, velocity
and extent of myocardial contraction, and blood pressure, nadolol
generally reduces the oxygen requirements of the heart at any given
level of effort, making it useful for many patients in the long-term
management of angina pectoris. On the other hand, nadolol can increase
oxygen requirements by increasing left ventricular fiber length and
end diastolic pressure, particularly in patients with heart failure. Although beta-adrenergic receptor blockade is useful in
treatment of angina and hypertension, there are also situations in
which sympathetic stimulation is vital. For example, in patients with
severely damaged hearts, adequate ventricular function may depend
on sympathetic drive. Beta-adrenergic blockade may worsenAV block
by preventing the necessary facilitating effects of sympathetic activity
on conduction. Beta-adrenergic blockade results in passive
bronchial constriction by interfering with endogenous adrenergic bronchodilator
activity in patients subject to bronchospasm and may also interfere
with exogenous bronchodilators in such patients. Absorption of nadolol after oral dosing is variable, averaging about
30 percent. Peak serum concentrations of nadolol usually occur in
three to four hours after oral administration and the presence of
food in the gastrointestinal tract does not affect the rate or extent
of nadolol absorption. Approximately 30 percent of the nadolol present
in serum is reversibly bound to plasma protein. Unlike many other beta-adrenergic blocking agents, nadolol is not
metabolized by the liver and is excreted unchanged, principally by
the kidneys. The half-life of therapeutic doses
of nadolol is about 20 to 24 hours, permitting once-daily dosage.
Because nadolol is excreted predominantly in the urine, its half-life
increases in renal failure . Steady state serum concentrations of nadolol are attained
in six to nine days with once-daily dosage in persons with normal
renal function. Because of variable absorption and different individual
responsiveness, the proper dosage must be determined by titration. Exacerbation of angina and, in some cases, myocardial
infarction and ventricular dysrhythmias have been reported after abrupt
discontinuation of therapy with beta-adrenergic blocking agents in
patients with coronary artery disease. Abrupt withdrawal of these
agents in patients without coronary artery disease has resulted in
transient symptoms, including tremulousness, sweating, palpitation,
headache, and malaise. Several mechanisms have been proposed to explain
these phenomena, among them increased sensitivity to catecholamines
because of increased numbers of beta receptors. Bendroflumethiazide The mechanism of action of bendroflumethiazide results
in an interference with the renal tubular mechanism of electrolyte
reabsorption. At maximal therapeutic dosage all thiazides are approximately
equal in their diuretic potency. Thiazides
increase excretion of sodium and chloride in approximately equivalent
amounts. Natriuresis causes a secondary loss of potassium and bicarbonate. The mechanism of the antihypertensive effect of thiazides
is unknown. Thiazides do not affect normal blood pressure. Onset of action of thiazides occurs in two hours and thepeak effect at about four hours. Duration of action persists for approximately
six to 12 hours. Thiazides are eliminated rapidly by the kidney.
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Nadolol Nadolol is contraindicated in bronchial asthma, sinus
bradycardia and greater than first degree conduction block, cardiogenic
shock, and overt cardiac failure . Bendroflumethiazide Bendroflumethiazide is contraindicated in anuria. It is
also contraindicated in patients who have previously demonstrated
hypersensitivity to bendroflumethiazide or other sulfonamide-derived
drugs.
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CORZIDE (Nadolol and Bendroflumethiazide Tablets) Round, biconvex tablets are white to bluish white
with dark blue specks. Each tablet has a full bisect bar. Tablet identification
numbers: 40 mg/5 mg combination embossed with KPI/283 on the scored
side and Corzide 40/5 on the other; 80 mg/5 mg combination embossed
with KPI/284 on the scored side and Corzide 80/5 on the other. Storage Keep bottle tightly closed. Store at room temperature;
avoid excessive heat. Prescribing Information
as of January 2007. Manufactured by: King Pharmaceuticals,
Inc., Bristol, TN 37620
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Exacerbation of Ischemic
Heart Disease Following Abrupt Withdrawal���Hypersensitivity
to catecholamines has been observed in patients withdrawn from beta-blocker
therapy; exacerbation of angina and, in some cases, myocardial infarction
have occurred after abrupt discontinuation
of such therapy. When discontinuing chronically administered nadolol,
particularly in patients with ischemic heart disease, the dosage should
be gradually reduced over a period of one to two weeks and the patient
should be carefully monitored. If angina markedly worsens or acute
coronary insufficiency develops, nadolol administration should be
reinstituted promptly, at least temporarily, and other measures appropriate
for the management of unstable angina should be taken. Patients should
be warned against interruption or discontinuation of therapy without
the physician's advice. Because coronary artery disease is
common and may be unrecognized, it may be prudent not to discontinue
nadolol therapy abruptly even in patients treated only for hypertension.
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General: Nadolol Nadolol should be used with caution in patients with impaired
renal function . Bendroflumethiazide Periodic determination of serum
electrolytes to detect possible electrolyte imbalance should be performed
at appropriate intervals. All patients receiving
thiazide therapy should be observed for clinical signs of fluid or
electrolyte imbalance, namely: hyponatremia, hypochloremic alkalosis,
and hypokalemia. Serum and urine electrolyte determinations are particularly
important when the patient is vomiting excessively or receiving parenteral
fluids. Warning signs or symptoms of fluid and electrolyte imbalance
may include: dryness of the mouth, thirst, weakness, lethargy, drowsiness,
restlessness, muscle pains or cramps, muscular fatigue, hypotension,
oliguria, tachycardia, and gastrointestinal disturbances, such as
nausea and vomiting. Hypokalemia may develop,
especially with brisk diuresis or when severe cirrhosis is present. Interference with adequate oral electrolyte intake will
also contribute to hypokalemia. Hypokalemia can sensitize or exaggerate
the response of the heart to the toxic effects of digitalis (e.g.,
increased ventricular irritability). Concurrent administration of
a potassium-sparing diuretic or potassium supplements may be indicated
in these patients. Any chloride deficit is
generally mild and usually does not require specific treatment except
under extraordinary circumstances (as in liver disease or renal disease).
Dilutional hyponatremia may occur in edematous patients in hot weather;
appropriate therapy is water restriction, rather than administration
of salt, except in rare instances when the hyponatremia is life-threatening.
In actual salt depletion, appropriate replacement is the therapy of
choice. Hyperuricemia may occur or frank gout
may be precipitated in certain patients receiving thiazide therapy. Latent diabetes mellitus may become manifest during thiazide
administration. The antihypertensive effect
of thiazide diuretics may be enhanced in the postsympathectomy patient. If progressive renal impairment becomes evident, as indicated
by a rising nonprotein nitrogen or blood urea nitrogen (BUN), a careful
reappraisal of therapy is necessary with consideration given to withholding
or discontinuing diuretic therapy. Thiazides
may decrease serum PBI levels without signs of thyroid disturbance. Calcium excretion is decreased by thiazides. Pathological
changes in the parathyroid gland with hypercalcemia and hypophosphatemia
have been observed in a few patients on prolonged thiazide therapy.
The common complications of hyperparathyroidism such as renal lithiasis,
bone resorption, and peptic ulceration have not been seen. Thiazides
should be discontinued before carrying out tests for parathyroid function. Thiazides have been shown to increase the urinary excretion
of magnesium; this may result in hypomagnesemia.<br/>Information for Patients: Patients, especially those with evidence of coronary
artery insufficiency, should be warned against interruption or discontinuation
of therapy without the physician's advice. Although cardiac
failure rarely occurs in properly selected patients, patients being
treated with beta-adrenergic blocking agents should be advised to
consult the physician at the first sign or symptom of impending failure. The patient should also be advised of a proper course
in the event of an inadvertently missed dose. The patient should be informed of symptoms that would suggest potential
adverse effects and told to report them promptly.<br/>Laboratory Tests: Serum electrolyte levels should be regularly monitored
(see WARNINGS, Bendroflumethiazide , also PRECAUTIONS , General , Bendroflumethiazide ).<br/>Drug Interactions: Nadolol When administered concurrently the following drugs may
interact with beta-adrenergic receptor blocking agents: Anesthetics, general���exaggeration of the hypotension induced by general anesthetics
(see WARNINGS , Nadolol , Major Surgery). Antidiabetic drugs (oral agents and
insulin)���hypoglycemia or hyperglycemia; adjust dosage
of antidiabetic drug accordingly (see WARNINGS, Nadolol, Diabetes and Hypoglycemia). Catecholamine-depleting drugs
(e.g., reserpine)���additive effect; monitor closely
for evidence of hypotension and/or excessive bradycardia (e.g., vertigo,
syncope, postural hypotension). Response to Treatment for Anaphylactic Reaction���While taking beta-blockers, patients with a history of severe
anaphylactic reaction to a variety of allergens may be more reactive
to repeated challenge, either accidental, diagnostic, or therapeutic.
Such patients may be unresponsive to the usual doses of epinephrine
used to treat allergic reaction. Bendroflumethiazide When administered concurrently the following drugs may interact with
thiazide diuretics: Alcohol, barbiturates, or narcotics���potentiation
of orthostatic hypotension may occur. Amphotericin B, corticosteroids, or corticotropin
(ACTH)���may intensify electrolyte imbalance, particularly
hypokalemia. Monitor potassium levels; use potassium replacements
if necessary. Anticoagulants (oral)���dosage adjustments of anticoagulant
medication may be necessary since bendroflumethiazide may decrease
their effects. Antigout medications���dosage adjustments of antigout
medication may be necessary since bendroflumethiazide may raise the
level of blood uric acid. Other antihypertensive medications (e.g., ganglionic
or peripheral adrenergic blocking agents)���dosage
adjustments may be necessary since bendroflumethiazide may potentiate
their effects. Antidiabetic drugs (oral agents and insulin)���since
thiazides may elevate blood glucose levels, dosage adjustments of
antidiabetic agents may be necessary. Calcium salts���increased serum
calcium levels due to decreased excretion may occur. If calcium must
be prescribed monitor serum calcium levels and adjust calcium dosage
accordingly. Cardiac
glycosides���enhanced possibility of digitalis toxicity
associated with hypokalemia. Monitor potassium levels; use potassium
replacement if necessary. Cholestyramine resin and colestipol HCl���may delay or decrease absorption of bendroflumethiazide.
Sulfonamide diuretics should be taken at least one hour before or
four to six hours after these medications. Diazoxide���enhanced
hyperglycemic, hyperuricemic, and antihypertensive effects. Be cognizant
of possible interaction; monitor blood glucose and serum uric acid
levels. Lithium
salts���may enhance lithium toxicity due to reduced
renal clearance. Avoid concurrent use; if lithium must be prescribed
monitor serum lithium levels and adjust lithium dosage accordingly. MAO inhibitors���dosage adjustments of one or both
agents may be necessary since hypotensive effects are enhanced. Nondepolarizing muscle relaxants,
preanesthetics and anesthetics used in surgery (e.g., tubocurarine
chloride and gallamine triethiodide)���effects of these
agents may be potentiated; dosage adjustments may be required. Monitor
and correct any fluid and electrolyte imbalances prior to surgery
if feasible. Nonsteroidal
anti-inflammatory agents���in some patients, the administration
of a nonsteroidal anti-inflammatory agent can reduce the diuretic,
natriuretic, and antihypertensive effect of loop, potassium-sparing
or thiazide diuretics. Therefore, when bendroflumethiazide and nonsteroidal
anti-inflammatory agents are used concomitantly, the patient should
be observed closely to determine if the desired effect of the diuretic
is obtained. Methenamine���possible decreased effectiveness due to alkalinization of
the urine. Pressor
amines (e.g., norepinephrine)���decreased arterial
responsiveness, but not sufficient to preclude effectiveness of the
pressor agent for therapeutic use. Use caution in patients taking
both medications who undergo surgery. Administer preanesthetic and
anesthetic agents in reduced dosage, and if possible, discontinue
bendroflumethiazide one week prior to surgery. Probenecid or sulfinpyrazone���increased dosage of these agents may be necessary since bendroflumethiazide
may have hyperuricemic effects.<br/>Drug and Laboratory Test Interactions: Bendroflumethiazide may produce false-negative results
with the phentolamine and tyramine tests; may interfere with the phenolsulfonphthalein
test due to decreased excretion; and it may cause diagnostic interference
of serum electrolyte levels, blood and urine glucose levels, and a
decrease in serum PBI levels without signs of thyroid disturbance.<br/>Carcinogenesis, Mutagenesis, Impairment of Fertility: Nadolol In chronic oral toxicologic studies (one to two years)
in mice, rats, and dogs, nadolol did not produce any significant toxic
effects. In two-year oral carcinogenicity studies in rats and mice,
nadolol did not produce any neoplastic, preneoplastic, or nonneoplastic
pathologic lesions. In fertility and general reproductiveperformance
studies in rats, nadolol caused no adverse effect. Bendroflumethiazide Studies have not been performed to evaluate carcinogenic
potential, mutagenesis, or whether this drug adversely affects fertility
in males or females.<br/>Pregnancy:<br/>Teratogenic Effects: Nadolol Category C. In animal reproduction studies with nadolol,
evidence of embryo- and fetotoxicity was found in rabbits, but not
in rats or hamsters, at doses 5 to 10 times greater (on a mg/kg basis)
than the maximum indicated human dose. No teratogenic potential was
observed in any of these species. There are
no adequate and well-controlled studies in pregnant women. Nadolol
should be used during pregnancy only if the potential benefit justifies
the potential risk to the fetus. Neonates whose mothers are receiving
nadolol at parturition have exhibited bradycardia, hypoglycemia, and
associated symptoms. Bendroflumethiazide Category C.
Animal reproduction studies have not been conducted with bendroflumethiazide.
It is also not known whether this drug can cause fetal harm when administered
to a pregnant woman or can affect reproduction capacity. Bendroflumethiazide
should be given to a pregnant woman only if clearly needed.<br/>Nonteratogenic Effects: Thiazides cross the placental barrier and appear
in cord blood. The use of thiazides in pregnant women requires that
the anticipated benefit be weighed against possible hazards to the
fetus. These hazards include fetal or neonatal jaundice, thrombocytopenia,
and possibly other adverse reactions which have occurred in the adult.<br/>Nursing Mothers: Both nadolol and bendroflumethiazide are excreted
in human milk. Because of the potential for serious adverse reactions
in nursing infants from both drugs, a decision should be made whether
to discontinue nursing or to discontinue therapy taking into account
the importance of CORZIDE (Nadolol and Bendroflumethiazide Tablets)
to the mother.<br/>Pediatric Use: Safety and effectiveness in pediatric patients have
not been established.<br/>Geriatric Use: Clinical studies of Corzide did not include sufficient
numbers of subjects aged 65 and over to determine whether they respond
differently from younger subjects. Other reported clinical experience
has not identified differences in responses between the elderly and
younger patients. In general, dose selection for an elderly patient
should be cautious, usually starting at the low end of the dosing
range, reflecting the greater frequency of decreased hepatic, renal,
or cardiac function, and of concomitant disease or other drug therapy.
This drug is known to be substantially excreted by the kidney, and
the risk of toxic reaction to this drug may be greater in patients
with impaired function. Because elderly patients are more likely to
have decreased renal function, care should be taken in dose selection,
and it may be useful to monitor renal function.
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In the event of overdosage, nadolol may cause excessive
bradycardia, cardiac failure, hypotension, or bronchospasm. In addition to the expected diuresis, overdosage of bendroflumethiazide
may produce varying degrees of lethargy which may progress to coma
with minimal depression of respiration and cardiovascular function
and without significant serum electrolyte changes or dehydration.
The mechanism of thiazide-induced CNS depression is unknown. Gastrointestinal
irritation may occur. Transitory increase in BUN has been reported,
and serum electrolyte changes may occur, especially in patients with
impaired renal function.
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nadolol and bendroflumethizaide
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Corzide (Tablet)
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Nadolol Most adverse effects have been mild and transient and
have rarely required withdrawal of therapy. Cardiovascular���Bradycardia
with heart rates of less than 60 beats per minute occurs commonly,
and heart rates below 40 beats per minute and/or symptomatic bradycardia
were seen in about 2 of 100 patients. Symptoms of peripheral vascular
insufficiency, usually of the Raynaud type, have occurred in approximately
2 of 100 patients. Cardiac failure, hypotension, and rhythm/conduction
disturbances have each occurred in about 1 of 100 patients. Single
instances of first degree and third degree heart block have been reported;
intensification of AV block is a known effect of beta-blockers (see
also CONTRAINDICATIONS , WARNINGS, and PRECAUTIONS ). Central Nervous System���Dizziness
or fatigue has been reported in approximately 2 of 100 patients; paresthesias,
sedation, and change in behavior have each been reported in approximately
6 of 1000 patients. Respiratory���Bronchospasm has been reported in approximately
1 of 1000 patients . Gastrointestinal���Nausea, diarrhea, abdominal discomfort, constipation, vomiting,
indigestion, anorexia, bloating, and flatulence have been reported
in 1 to 5 of 1000 patients. Miscellaneous���Each of the following
has been reported in 1 to 5 of 1000 patients: rash; pruritus; headache;
dry mouth, eyes, or skin; impotence or decreased libido; facial swelling;
weight gain; slurred speech; cough; nasal stuffiness; sweating; tinnitus;
blurred vision. Reversible alopecia has been reported infrequently. The following adverse reactions have been reported in
patients taking nadolol and/or other beta-adrenergic blocking agents,
but no causal relationship to nadolol has been established. Central Nervous System���Reversible mental depression progressing to catatonia; visual
disturbances; hallucinations; an acute reversible syndrome characterized
by disorientation for time and place, short-term memory loss, emotional
lability with slightly clouded sensorium, and decreased performance
on neuropsychometrics. Gastrointestinal���Mesenteric arterial
thrombosis; ischemic colitis; elevated liver enzymes. Hematologic���Agranulocytosis;
thrombocytopenic or nonthrombocytopenic purpura. Allergic���Fever combined
with aching and sore throat; laryngospasm; respiratory distress. Miscellaneous���Pemphigoid
rash; hypertensive reaction in patients with pheochromocytoma; sleep
disturbances; Peyronie's disease. The
oculomucocutaneous syndrome associated with the beta-blocker practolol
has not been reported with nadolol. Bendroflumethiazide Gastrointestinal���Nausea,
vomiting, cramping and anorexia are not uncommon; diarrhea, constipation,
gastric irritation, abdominal bloating, jaundice (intrahepatic cholestatic
jaundice), hepatitis, and sialadenitis occasionally occur; and pancreatitis
has been reported. Central Nervous System���Dizziness, vertigo, paresthesia,
headache, and xanthopsia occasionally occur. Hematologic���Leukopenia,
agranulocytosis, thrombocytopenia, hemolytic anemia, and aplastic
anemia have been reported. Dermatologic-Hypersensitivity���Purpura,
exfoliative dermatitis, pruritus, ecchymosis, urticaria, necrotizing
angiitis (vasculitis, cutaneous vasculitis), respiratory distress
including pneumonitis, fever, and anaphylactic reactions occasionally
occur; photosensitivity and rash have been reported. Cardiovascular���Orthostatic
hypotension may occur and may be potentiated by coadministration with
certain other drugs (e.g., alcohol, barbiturates, narcotics, other
antihypertensive medications, etc.; see PRECAUTIONS, Drug Interactions). Other���Muscle spasm, weakness, or restlessness is not uncommon;
hyperglycemia, glycosuria, metabolic acidosis in diabetic patients,
hyperuricemia, allergic glomerulonephritis, and transient blurred
vision occasionally occur. Whenever adverse
reactions are moderate or severe, thiazide dosage should be reduced
or therapy withdrawn.
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Nadolol Cardiac Failure���Sympathetic stimulation
may be a vital component supporting circulatory function in patients
with congestive heart failure, and its inhibition by beta-blockade
may precipitate more severe failure. Although beta-blockers should
be avoided in overt congestive heart failure, if necessary, they can
be used with caution in patients with a history of failure who are
well compensated, usually with digitalis and diuretics. Beta-adrenergic
blocking agents do not abolish the inotropic action of digitalis on
heart muscle. IN PATIENTS WITHOUT A HISTORY
OF HEART FAILURE, continued use of beta-blockers can, in some cases,
lead to cardiac failure. Therefore, at the first sign or symptom of
heart failure, the patient should be digitalized and/or treated with
diuretics, and the response observed closely, or nadolol should be
discontinued (gradually, if possible). Exacerbation of Ischemic
Heart Disease Following Abrupt Withdrawal���Hypersensitivity
to catecholamines has been observed in patients withdrawn from beta-blocker
therapy; exacerbation of angina and, in some cases, myocardial infarction
have occurred after abrupt discontinuation
of such therapy. When discontinuing chronically administered nadolol,
particularly in patients with ischemic heart disease, the dosage should
be gradually reduced over a period of one to two weeks and the patient
should be carefully monitored. If angina markedly worsens or acute
coronary insufficiency develops, nadolol administration should be
reinstituted promptly, at least temporarily, and other measures appropriate
for the management of unstable angina should be taken. Patients should
be warned against interruption or discontinuation of therapy without
the physician's advice. Because coronary artery disease is
common and may be unrecognized, it may be prudent not to discontinue
nadolol therapy abruptly even in patients treated only for hypertension. Nonallergic Bronchospasm
(e.g., chronic bronchitis, emphysema)���PATIENTS WITH
BRONCHOSPASTIC DISEASES SHOULD IN GENERAL NOT RECEIVE BETA-BLOCKERS.
Nadolol should be administered with caution since it may block bronchodilation
produced by endogenous or exogenous catecholamine stimulation of betareceptors. Major Surgery���Because beta-blockade impairs the ability of the
heart to respond to reflex stimuli and may increase the risks of general
anesthesia and surgical procedures, resulting in protracted hypotension
or low cardiac output, it has generally been suggested that such therapy
should be withdrawn several days prior to surgery. Recognition of
the increased sensitivity to catecholamines of patients recently withdrawn
from beta-blocker therapy, however, has made this recommendation controversial.
If possible, beta-blockers should be withdrawn well before surgery
takes place. In the event of emergency surgery, the anesthesiologist
should be informed that the patient is on beta-blocker therapy. The
effects of nadolol can be reversed by administration of beta-receptor
agonists such as isoproterenol, dopamine, dobutamine, or levarterenol.
Difficulty in restarting and maintaining the heart beat has also been
reported with beta-adrenergic receptor blocking agents. Diabetes and Hypoglycemia���Beta-adrenergic blockade may prevent the appearance of premonitory
signs and symptoms (e.g., tachycardia and blood pressure changes)
of acute hypoglycemia. This is especially important with labile diabetics.
Beta-blockade also reduces the release of insulin in response to hyperglycemia;
therefore, it may be necessary to adjust the dose of antidiabetic
drugs. Thyrotoxicosis���Beta-adrenergic blockade may mask certain clinical signs
(e.g., tachycardia) of hyperthyroidism. Patients suspected of developing
thyrotoxicosis should be managed carefully to avoid abrupt withdrawal
of beta-adrenergic blockade which might precipitate a thyroid storm. Bendroflumethiazide Thiazides should be used with caution in
severe renal disease. In patients with renal disease, thiazides may
precipitate azotemia. Cumulative effects of the drug may develop in
patients with impaired renal function. Thiazides
should be used with caution in patients with impaired hepatic function
or progressive liver disease, since minor alterations of fluid and
electrolyte balance may precipitate hepatic coma. Sensitivity reactions may occur in patients with or without a history
of allergy or bronchial asthma. The possibility
of exacerbation or activation of systemic lupus erythematosus has
been reported. Lithium generally should not
be given with diuretics; diuretic agents reduce the renal clearance
of lithium and add a high risk of lithium toxicity. Refer to the package
insert for lithium preparations before use of such concomitant therapy.
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Corzide
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