Can you take Anectine with Betaxolol?

The succinylcholine in Anectine has a major potential interaction with Allergies.

Some neuromuscular blocking agents stimulate the release of histamine, which can cause wheezing, bronchospasm, increased bronchial secretions, hypotension, tachycardia, and circulatory collapse. Hypotension may also occur due to ganglionic blockade or as a complication of positive pressure respiration. Tubocurarine appears to be the most potent inducer of histamine, followed by metocurine (no longer commercially available in the U.S.) and succinylcholine. Other agents with varying but lesser degrees of histamine-releasing properties include atracurium, mivacurium, and pancuronium (at excessive dosages). Therapy with these neuromuscular blocking agents should be administered cautiously in patients with clinically significant cardiovascular disease and/or a history of asthma or severe allergic reactions. Certain agents may prolong the QTc interval, especially during general anesthesia in pediatric patients. The initial dosage and rate of administration may need to be reduced, and hemodynamic and respiratory status carefully monitored. Neuromuscular blocking agents that appear to have little or no histamine-inducing effects include cisatracurium, doxacurium, pipecuronium, rocuronium, and vecuronium.

Betaxolol has a major potential interaction with Allergies.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) in patients with a history of allergic reactions or anaphylaxis may be associated with heightened reactivity to culprit allergens. The frequency and/or severity of attacks may be increased during beta-blocker therapy. In addition, these patients may be refractory to the usual doses of epinephrine used to treat acute hypersensitivity reactions and may require a beta-agonist such as isoproterenol.

The succinylcholine in Anectine has a major potential interaction with Asthma.

Some neuromuscular blocking agents stimulate the release of histamine, which can cause wheezing, bronchospasm, increased bronchial secretions, hypotension, tachycardia, and circulatory collapse. Hypotension may also occur due to ganglionic blockade or as a complication of positive pressure respiration. Tubocurarine appears to be the most potent inducer of histamine, followed by metocurine (no longer commercially available in the U.S.) and succinylcholine. Other agents with varying but lesser degrees of histamine-releasing properties include atracurium, mivacurium, and pancuronium (at excessive dosages). Therapy with these neuromuscular blocking agents should be administered cautiously in patients with clinically significant cardiovascular disease and/or a history of asthma or severe allergic reactions. Certain agents may prolong the QTc interval, especially during general anesthesia in pediatric patients. The initial dosage and rate of administration may need to be reduced, and hemodynamic and respiratory status carefully monitored. Neuromuscular blocking agents that appear to have little or no histamine-inducing effects include cisatracurium, doxacurium, pipecuronium, rocuronium, and vecuronium.

Betaxolol has a moderate potential interaction with Asthma.

Patients with bronchospastic disease, should, in general, not receive beta blockers, including cardioselective beta-blockers. Because of the relative beta-1 selectivity, cardioselective beta-blockers may be used in patients with bronchospastic disease who do not respond to, or cannot tolerate, other antihypertensive treatment. Because beta-1 selectivity is not absolute, the lowest possible dose of these agents should be used. Consider administering in smaller doses to avoid the higher plasma levels associated with the longer dosing intervals. If dosage must be increased, dividing the dose should be considered to achieve lower peak blood levels. It is recommended to have bronchodilators, including beta-2 agonists, readily available or administered concomitantly if necessary.

The succinylcholine in Anectine has a major potential interaction with Burns, External.

The use of succinylcholine is contraindicated in patients after the acute phase of injury following major burns. These patients are more likely to develop significant hyperkalemia which may lead to cardiac arrest. The risk of hyperkalemia typically peaks at about 7 to 10 days after injury.

Betaxolol has a major potential interaction with Cardiogenic Shock.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with hypotension or cardiogenic shock. Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to further depress cardiac output and blood pressure, which can be detrimental in these patients.

The succinylcholine in Anectine has a major potential interaction with Cardiovascular Conditions and Disorders.

Some neuromuscular blocking agents stimulate the release of histamine, which can cause wheezing, bronchospasm, increased bronchial secretions, hypotension, tachycardia, and circulatory collapse. Hypotension may also occur due to ganglionic blockade or as a complication of positive pressure respiration. Tubocurarine appears to be the most potent inducer of histamine, followed by metocurine (no longer commercially available in the U.S.) and succinylcholine. Other agents with varying but lesser degrees of histamine-releasing properties include atracurium, mivacurium, and pancuronium (at excessive dosages). Therapy with these neuromuscular blocking agents should be administered cautiously in patients with clinically significant cardiovascular disease and/or a history of asthma or severe allergic reactions. Certain agents may prolong the QTc interval, especially during general anesthesia in pediatric patients. The initial dosage and rate of administration may need to be reduced, and hemodynamic and respiratory status carefully monitored. Neuromuscular blocking agents that appear to have little or no histamine-inducing effects include cisatracurium, doxacurium, pipecuronium, rocuronium, and vecuronium.

The succinylcholine in Anectine has a major potential interaction with Cerebral Vascular Disorder.

The use of succinylcholine is contraindicated in patients with upper motor neuron injury that can be a sequelae of cerebral vasculopathy. The risk of hyperkalemia is increased in these patients.

Betaxolol has a moderate potential interaction with Cerebrovascular Insufficiency.

Beta-adrenergic blocking agents (beta-blockers), should be used with caution in patients with cerebrovascular insufficiency because of their potential effects relative to blood pressure and pulse. If signs or symptoms suggesting reduced cerebral blood flow are observed, consideration should be given to discontinuing these agents.

Betaxolol has a moderate potential interaction with COPD.

Patients with bronchospastic disease, should, in general, not receive beta blockers, including cardioselective beta-blockers. Because of the relative beta-1 selectivity, cardioselective beta-blockers may be used in patients with bronchospastic disease who do not respond to, or cannot tolerate, other antihypertensive treatment. Because beta-1 selectivity is not absolute, the lowest possible dose of these agents should be used. Consider administering in smaller doses to avoid the higher plasma levels associated with the longer dosing intervals. If dosage must be increased, dividing the dose should be considered to achieve lower peak blood levels. It is recommended to have bronchodilators, including beta-2 agonists, readily available or administered concomitantly if necessary.

Betaxolol has a major potential interaction with Diabetes Mellitus.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may mask symptoms of hypoglycemia such as tremors, tachycardia and blood pressure changes. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may inhibit catecholamine-mediated glycogenolysis, thereby potentiating insulin-induced hypoglycemia and delaying the recovery of normal blood glucose levels. Since cardioselectivity is not absolute, larger doses of beta-1 selective agents may demonstrate these effects as well. Therapy with beta-blockers should be administered cautiously in patients with diabetes or predisposed to spontaneous hypoglycemia.

The succinylcholine in Anectine has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

The use of succinylcholine has been associated with an increase in intraocular pressure. Therapy with succinylcholine should be administered cautiously in patients with narrow-angle glaucoma.

Betaxolol has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

Systemic beta-adrenergic receptor blocking agents (aka beta-blockers) may lower intraocular pressure. Therefore, patients with glaucoma or intraocular hypertension may require adjustments in their ophthalmic regimen following a dosing change or discontinuation of beta-blocker therapy.

Betaxolol has a major potential interaction with Heart Block.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to exacerbate these conditions.

The succinylcholine in Anectine has a moderate potential interaction with Heart Block.

The use of succinylcholine may exacerbate bradycardia via vagal stimulation leading to asystole, especially after a second dose. Therapy with succinylcholine should be administered cautiously in patients with bradycardia.

Betaxolol has a major potential interaction with Heart Failure.

Beta-adrenergic receptor blocking agents (aka beta-blockers) in general should not be used in patients with overt congestive heart failure (CHF). Sympathetic stimulation may be important in maintaining the hemodynamic function in these patients, thus beta-blockade can worsen the heart failure. However, therapy with beta-blockers may be beneficial and can be administered cautiously in some CHF patients provided they are well compensated and receiving digitalis, diuretics, an ACE inhibitor, and/or nitrates. Carvedilol, specifically, is indicated for use with these agents in the treatment of mild to severe heart failure of ischemic or cardiomyopathic origin. There is also increasing evidence that the addition of a beta-blocker to standard therapy can improve morbidity and mortality in patients with advanced heart failure, although it is uncertain whether effectiveness varies significantly with the different agents. Data from one meta-analysis study suggest a greater reduction of mortality risk for nonselective beta-blockers than for beta-1 selective agents.

Betaxolol has a major potential interaction with Hemodialysis.

Therapy with beta-adrenergic receptor blocking agents (aka beta-blockers) should be administered cautiously in patients requiring hemodialysis. When given after dialysis, hemodynamic stability should be established prior to drug administration to avoid marked falls in blood pressure. The hemodynamic status should be closely monitored before and after the dose.

The succinylcholine in Anectine has a major potential interaction with Hemorrhagic Stroke.

The use of succinylcholine is contraindicated in patients after the acute phase of injury following major burns, multiple trauma, extensive denervation of skeletal muscle, or upper motor neuron injury. has been associated with an elevation in potassium levels due to rapid release of potassium from intracellular sites. Therapy with succinylcholine should be administered cautiously in patients with hyperkalemic states such as extensive soft-tissue trauma, burns, chronic abdominal infections, and subarachnoid hemorrhage.

Betaxolol has a moderate potential interaction with High Cholesterol.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may alter serum lipid profiles. Increases in serum VLDL and LDL cholesterol and triglycerides, as well as decreases in HDL cholesterol, have been reported with some beta-blockers. Patients with preexisting hyperlipidemia may require closer monitoring during beta-blocker therapy, and adjustments made accordingly in their lipid-lowering regimen.

The succinylcholine in Anectine has a major potential interaction with History (Familial) - Musculoskeletal Disorder.

The use of succinylcholine is contraindicated in patients with a personal or family history of skeletal muscle myopathies. Acute rhabdomyolysis with hyperkalemia followed by ventricular arrhythmias, cardiac arrest, and death have been reported following the administration of succinylcholine in apparently healthy children who were later found to have undiagnosed skeletal muscle myopathy, most frequently Duchenne muscular dystrophy. Immediate treatment of hyperkalemia should be instituted whenever a healthy appearing infant or child develops cardiac arrest with no obvious cause soon after administration of succinylcholine.

The succinylcholine in Anectine has a major potential interaction with History - Musculoskeletal Disorder.

The use of succinylcholine is contraindicated in patients with a personal or family history of skeletal muscle myopathies. Acute rhabdomyolysis with hyperkalemia followed by ventricular arrhythmias, cardiac arrest, and death have been reported following the administration of succinylcholine in apparently healthy children who were later found to have undiagnosed skeletal muscle myopathy, most frequently Duchenne muscular dystrophy. Immediate treatment of hyperkalemia should be instituted whenever a healthy appearing infant or child develops cardiac arrest with no obvious cause soon after administration of succinylcholine.

The succinylcholine in Anectine has a major potential interaction with Hyperkalemia.

The use of succinylcholine is contraindicated in patients after the acute phase of injury following major burns, multiple trauma, extensive denervation of skeletal muscle, or upper motor neuron injury. has been associated with an elevation in potassium levels due to rapid release of potassium from intracellular sites. Therapy with succinylcholine should be administered cautiously in patients with hyperkalemic states such as extensive soft-tissue trauma, burns, chronic abdominal infections, and subarachnoid hemorrhage.

Betaxolol has a moderate potential interaction with Hyperthyroidism.

When beta-adrenergic receptor blocking agents (aka beta-blockers) are used to alleviate symptoms of hyperthyroidism such as tachycardia, anxiety, tremor and heat intolerance, abrupt withdrawal can exacerbate thyrotoxicosis or precipitate a thyroid storm. To minimize this risk, cessation of beta-blocker therapy, when necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks. Patients should be advised not to discontinue treatment without first consulting with the physician. Close monitoring is recommended during and after therapy withdrawal.

Betaxolol has a major potential interaction with Hypotension.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with hypotension or cardiogenic shock. Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to further depress cardiac output and blood pressure, which can be detrimental in these patients.

Betaxolol has a major potential interaction with Ischemic Heart Disease.

Heightened sensitivity to catecholamines may occur after prolonged use of beta-adrenergic receptor blocking agents (aka beta-blockers). Exacerbation of angina, myocardial infarction and ventricular arrhythmias have been reported in patients with coronary artery disease following abrupt withdrawal of therapy. Cessation of beta-blocker therapy, whenever necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks in patients with coronary insufficiency. Patients should be advised not to discontinue treatment without first consulting with the physician. In patients who experience an exacerbation of angina following discontinuation of beta-blocker therapy, the medication should generally be reinstituted, at least temporarily, along with other clinically appropriate measures.

The succinylcholine in Anectine has a major potential interaction with Malignant Hyperthermia.

The use of succinylcholine is contraindicated in patients with a personal or family history of malignant hyperthermia. Succinylcholine administration has been associated with acute onset of malignant hyperthermia, especially during the concomitant use of volatile anesthetics. If malignant hyperthermia occurs, anesthesia should be discontinued and supportive measures rendered promptly, including rapid cooling, inhalation of 100% oxygen, control of acidosis, support of circulation, and assurance of adequate urinary output. In addition, intravenous dantrolene sodium is recommended.

The succinylcholine in Anectine has a moderate potential interaction with Myasthenia Gravis.

Depolarizing agents, including succinylcholine, should be used with caution in patients with known neuromuscular junction disease. The succinylcholine-induced neuromuscular blockade may be prolonged in patients with myasthenia gravis (MG). Care should be exercised when using this agent in patients with existing, previously diagnosed MG.

Betaxolol has a moderate potential interaction with Myasthenia Gravis.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may potentiate muscle weakness consistent with certain myasthenic symptoms such as diplopia, ptosis, and generalized weakness. Several beta-blockers have been associated rarely with aggravation of muscle weakness in patients with preexisting myasthenia gravis or myasthenic symptoms. Use cautiously in patients with myasthenia gravis.

The succinylcholine in Anectine has a major potential interaction with Myopathy.

The use of succinylcholine is contraindicated in patients with a personal or family history of skeletal muscle myopathies. Acute rhabdomyolysis with hyperkalemia followed by ventricular arrhythmias, cardiac arrest, and death have been reported following the administration of succinylcholine in apparently healthy children who were later found to have undiagnosed skeletal muscle myopathy, most frequently Duchenne muscular dystrophy. Immediate treatment of hyperkalemia should be instituted whenever a healthy appearing infant or child develops cardiac arrest with no obvious cause soon after administration of succinylcholine.

Betaxolol has a major potential interaction with Peripheral Arterial Disease.

Due to their negative inotropic and chronotropic effects on the heart, beta-adrenergic receptor blocking agents (aka beta-blockers) reduce cardiac output and may precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may attenuate catecholamine-mediated vasodilation during exercise by blocking beta-2 receptors in peripheral vessels. Therapy with beta-blockers should be administered cautiously in patients with peripheral vascular disease. Close monitoring for progression of arterial obstruction is advised.

Betaxolol has a moderate potential interaction with Pheochromocytoma.

Administration of beta-blockers alone in the setting of pheochromocytoma has been associated with a paradoxical increase in blood pressure due to the attenuation of beta receptor-mediated vasodilatation in skeletal muscle. In patients with pheochromocytoma, an alpha-blocking agent should be initiated prior to the use of any beta-blocking agent. Caution should be taken in the administration of these agents to patients suspected of having pheochromocytoma.

Betaxolol has a moderate potential interaction with Psoriasis.

The use of beta-blockers in psoriatic patients should be carefully weighed since the use of these agents may cause an aggravation in psoriasis.

The succinylcholine in Anectine has a major potential interaction with Pulmonary Impairment.

Neuromuscular blocking agents can cause respiratory depression and paralysis. Therapy with neuromuscular blocking agents should be administered cautiously in patients with pulmonary impairment. Treatment of respiratory paralysis consists of positive-pressure artificial respiration with oxygen and maintenance of a patent airway until the recovery of normal respiration is assured.

Betaxolol has a major potential interaction with Renal Dysfunction.

Betaxolol and its metabolites are eliminated by the kidney. Patients with renal impairment may be at greater risk for adverse effects from betaxolol due to decreased drug clearance. Therapy with betaxolol should be administered cautiously in patients with renal impairment. Dosage adjustments are recommended for patients with severe renal dysfunction (CrCl < 10 mL/min) or undergoing dialysis.

Betaxolol has a major potential interaction with Sinus Node Dysfunction.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to exacerbate these conditions.

Betaxolol has a moderate potential interaction with Tachyarrhythmia.

Beta-adrenergic blockade in patients with Wolff-Parkinson-White syndrome and tachycardia has been associated with severe bradycardia requiring treatment with a pacemaker. In one case, this result was reported after an initial dose of 5 mg propranolol. The use of beta-adrenergic receptor blocking agents (aka beta-blockers) should be administered cautiously in these patients.