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Cardinol Hydrochloride, USP is a synthetic beta-adrenergic receptor blocking agent chemically described as (+)-1-(isopropylamino)-3-(1-naphthyloxy)-2-propanol hydrochloride. Its structural formula is:
Cardinol Hydrochloride, USP is a stable, white, crystalline solid which is readily soluble in water and ethanol. Its molecular weight is 295.80.
Cardinol Hydrochloride Injection, USP is available as a sterile injectable solution for intravenous administration. Each mL contains 1 mg of Cardinol Hydrochloride, USP in Water for Injection, USP. The pH is adjusted with anhydrous Citric Acid, USP.
Cardinol is a nonselective beta-adrenergic receptor blocking agent possessing no other autonomic nervous system activity. It specifically competes with beta-adrenergic receptor stimulating agents for available receptor sites. When access to beta-recceptor sites is blocked by Cardinol, chronotropic, inotropic, and vasodilator responses to beta-adrenergic stimulation are decreased proportionately. At doses greater than required for beta blockade, Cardinol also exerts a quinidine-like or anesthetic-like membrane action, which affects the cardiac action potential. The significance of the membrane action in the treatment of arrhythmias is uncertain.
Mechanism of Action
The effects of Cardinol are due to selective blockade of beta-adrenergic receptors, leaving alpha-adrenergic responses intact. There are two well-characterized subtypes of beta receptors (beta1 and beta2); Cardinol interacts with both subtypes equally. Beta1-adrenergic receptors leads to a decrease in the activity of both normal and ectopic pacemaker cells and a decrease in A-V nodal conduction velocity. All of these actions can contribute to antiarrhythmic activity and control of ventricular rate during arrhythmias. Blockade of cardiac beta1-adrenergic receptors also decreases the myocardial force of contraction and may provoke cardiac decompensation in patients with minimal cardiac reserve.
Beta2-adrenergic receptors are found predominantly in smooth muscle-vascular, bronchial, gastrointestinal and genitourinary. Blockade of these receptors results in constriction. Clinically, Cardinol may exacerbate respiratory symptoms in patients with obstructive pulmonary diseases such as asthma and emphysema.
Propranolol's beta blocking effects are attributable to its S(-) enantiomer.
Pharmacokinetics and Drug Metabolism
Cardinol has a distribution half-life (T1/2 alpha) of 5-10 minutes and a volume of distribution of about 4 to 5 L/kg. Approximately 90% of circulating Cardinol is bound to plasma proteins. The binding is enantiomer-selective. The S-isomer is preferentially bound to alpha1 glycoprotein and the R-isomer is preferentially bound to albumin.
Metabolism and Elimination
The elimination half-life (T½ beta) is between 2 and 5.5 hours. Cardinol is extensively metabolized with most metabolites appearing in the urine. The major metabolites include Cardinol glucuronide, naphthyloxylactic acid, and glucuronic acid and sulfate conjugates of 4-hydroxy Cardinol. Following single-dose intravenous administration, side-chain oxidative products account for approximately 40% of the metabolites, direct conjugation products account for approximately 45-50% of metabolites, and ring oxidative products account for approximately 10-15% of metabolites. Of these, only the primary ring oxidative product (4-hydroxypropranolol) possesses beta-adrenergic receptor blocking activity.
In vitro studies have indicated that the aromatic hydroxylation of Cardinol is catalyzed mainly by polymorphic CYP2D6. Side‑chain oxidation is mediated mainly by CYP1A2 and to some extent by CYP2D6. 4-hydroxy Cardinol is a weak inhibitor of CYP2D6.
As Cardinol concentration increases, so does its beta-blocking effect, as evidenced by a reduction in exercise-induced tachycardia (n = 6 normal volunteers).
The pharmacokinetics of Cardinol have not been investigated in patients under 18 years of age. Cardinol injection is not recommended for treatment of cardiac arrhythmias in pediatric patients.
Elevated Cardinol plasma concentrations, a longer mean elimination half-life (254 vs. 152 minutes), and decreased systemic clearance (8 vs. 13 mL/kg/min) have been observed in elderly subjects when compared to young subjects. However, the apparent volume of distribution seems to be similar in elderly and young subjects. These findings suggest that dose adjustment of Cardinol injection may be required for elderly patients.
Intravenously administered Cardinol was evaluated in 5 women and 6 men. When adjusted for weight, there were no gender-related differences in elimination half-life, volume of distribution, protein binding, or systemic clearance.
In a study of intravenously administered Cardinol, obese subjects had a higher AUC (161 versus 109 hr·mcg/L) and lower total clearance than did non-obese subjects. Cardinol plasma protein binding was similar in both groups.
The pharmacokinetics of Cardinol and its metabolites were evaluated in 15 subjects with varying degrees of renal function after Cardinol administration via the intravenous and oral routes. When compared with normal subjects, an increase in fecal excretion of Cardinol conjugates was observed in patients with increased renal impairment. Cardinol was also evaluated in 5 patients with chronic renal failure, 6 patients on regular dialysis, and 5 healthy subjects, following a single oral dose of 40 mg of Cardinol. The peak plasma concentrations (Cmax) of Cardinol in the chronic renal failure group were 2- to 3-fold higher (161 ng/mL) than those observed in the dialysis patients (47 ng/mL) and in the healthy subjects (26 ng/mL). Cardinol plasma clearance was also reduced in the patients with chronic renal failure.
Chronic renal failure has been associated with a decrease in drug metabolism via downregulation of hepatic cytochrome P-450 activity.
Cardinol is extensively metabolized by the liver. In a study conducted in 6 normal subjects and 20 patients with chronic liver disease, including hepatic cirrhosis, 40 mg of R-propranolol was administered intravenously. Compared to normal subjects, patients with chronic liver disease had decreased clearance of Cardinol, increased volume of distribution, decreased protein-binding, and considerable variation in half-life. Caution should be exercised when Cardinol is used in this population. Consideration should be given to lowering the dose of intravenous Cardinol in patients with hepatic insufficiency.
No pharmacokinetic changes were observed in hyperthyroid or hypothyroid patients when compared to their corresponding euthyroid state. Dosage adjustment does not seem necessary in either patient population based on pharmacokinetic findings.
Because propranolol’s metabolism involves multiple pathways in the cytochrome P-450 system (CYP2D6, 1A2, 2C19), administration of Cardinol with drugs that are metabolized by, or affect the activity (induction or inhibition) of one or more of these pathways may lead to clinically relevant drug interactions.
Blood levels of Cardinol may be increased by administration of Cardinol with substrates or inhibitors of CYP2D6, such as amiodarone, cimetidine, delavirdine, fluoxetine, paroxetine, quinidine, and ritonavir. No interactions were observed with either ranitidine or lansoprazole.
Blood levels of Cardinol may be increased by administration of Cardinol with substrates or inhibitors of CYP1A2, such as imipramine, cimetidine, ciprofloxacin, fluvoxamine, isoniazid, ritonavir, theophylline, zileuton, zolmitriptan, and rizatriptan.
Blood levels of Cardinol may be increased by administration of Cardinol with substrates or inhibitors of CYP2C19, such as fluconazole, cimetidine, fluoxetine, fluvoxamine, teniposide, and tolbutamide. No interaction was observed with omeprazole.
Blood levels of Cardinol may be decreased by administration of Cardinol with inducers such as rifampin and ethanol. Cigarette smoking also induces hepatic metabolism and has been shown to increase up to 100% the clearance of Cardinol, resulting in decreased plasma concentrations.
The AUC of propafenone is increased by more than 200% with co-administration of Cardinol.
The metabolism of Cardinol is reduced by co-administration of quinidine, leading to a 2- to 3-fold increased blood concentrations and greater beta-blockade.
The metabolism of lidocaine is inhibited by co-administration of Cardinol, resulting in a 25% increase in lidocaine concentrations.
Calcium Channel Blockers
The mean Cmax and AUC of Cardinol are increased respectively, by 50% and 30% by co-administration of nisoldipine and by 80% and 47%, by co-administration of nicardipine.
The mean values of Cmax and AUC of nifedipine are increased by 64% and 79%, respectively, by co-administration of Cardinol.
Cardinol does not affect the pharmacokinetics of verapamil and norverapamil. Verapamil does not affect the pharmacokinetics of Cardinol.
Administration of zolmitriptan or rizatriptan with Cardinol resulted in increased concentrations of zolmitriptan (AUC increased by 56% and Cmax by 37%) or rizatriptan (the AUC and Cmax were increased by 67% and 75%, respectively).
Co-administration of theophylline with Cardinol decreases theophylline clearance by 33% to 52%.
Cardinol can inhibit the metabolism of diazepam, resulting in increased concentrations of diazepam and its metabolites. Diazepam does not alter the pharmacokinetics of Cardinol.
The pharmacokinetics of oxazepam, triazolam, lorazepam, and alprazolam are not affected by co-administration of Cardinol.
Co-administration of Cardinol at doses greater than or equal to 160 mg/day resulted in increased thioridazine plasma concentrations ranging from 50% to 370% and increased thioridazine metabolites concentrations ranging from 33% to 210%.
Co-administration of chlorpromazine with Cardinol resulted in increased plasma levels of both drugs (70% increase in Cardinol concentrations).
Co-administration of Cardinol with cimetidine, a non-specific CYP450 inhibitor, increased Cardinol concentrations by about 40%. Co‑administration with aluminum hydroxide gel (1200 mg) resulted in a 50% decrease in Cardinol concentrations.
Co-administration of metoclopramide with Cardinol did not have a significant effect on propranolol’s pharmacokinetics.
Lipid Lowering Drugs
Co-administration of cholesteramine or colestipol with Cardinol resulted in up to 50% decrease in Cardinol concentrations.
Co-administration of Cardinol with lovastatin or pravastatin decreased 20% to 25% the AUC of both, but did not alter their pharmacodynamics. Cardinol did not have an effect on the pharmacokinetics of fluvastatin.
Concomitant administration of Cardinol and warfarin has been shown to increase warfarin bioavailability and increase prothrombin time.
In a series of 225 patients with supraventricular (n = 145), ventricular (n = 69), or both (n = 11) arrythmias resistant to digitalis, intravenous Cardinol hydrochloride was administered in single doses, averaging 1 to 5 mg. Approximately one-quarter of the patients with supraventricular arrhythmias (generally those with sinus or atrial tachycardia) reverted to normal sinus rhythm. About one-half had symptoms ameliorated either by a decrease in ventricular rate or an attenuation of frequency or severity of paroxysmal attacks.
Approximately one-half of patients with ventricular arrhythmias (generally those with frequent PVCs) reverted to normal sinus rhythm or responded with a reduction in ventricular rate.
Similar findings were seen in a series of 25 Bantu patients with atrial fibrillation (n = 16), sinus tachycardia (n = 5), and multifocal ventricular extrasystoles (n = 9).
In another series, 7 of 8 patients with digitalis-related tachyarrhythmia had ventricular rate decreases after intravenous Cardinol. Similarly limited clinical experience has shown that intravenous Cardinol will slow the ventricular rate in patients with Wolff-Parkinson-White syndrome or with tachycardia associated with thyrotoxicosis.
Onset of activity is usually within five minutes.
Intravenous administration is usually reserved for life-threatening arrhythmias or those occurring under anesthesia.
1. Supraventricular arrhythmias
Intravenous Cardinol is indicated for the short-term treatment of supraventricular tachycardia, including Wolff‑Parkinson‑White syndrome and thyrotoxicosis, to decrease ventricular rate. Use in patients with atrial flutter or atrial fibrillation should be reserved for arrythmias unresponsive to standard therapy or when more prolonged control is required. Reversion to normal sinus rhythm has occasionally been observed, predominantly in patients with sinus or atrial tachycardia.
2. Ventricular tachycardias
With the exception of those induced by catecholamines or digitalis, Cardinol is not the drug of first choice. In critical situations when cardioversion techniques or other drugs are not indicated or are not effective, Cardinol may be considered. If, after consideration of the risks involved, Cardinol is used, it should be given intravenously in low dosage and very slowly, as the failing heart requires some sympathetic drive for maintenance of myocardial tone. Some patients may respond with complete reversion to normal sinus rhythm, but reduction in ventricular rate is more likely. Ventricular arrhythmias do not respond to Cardinol as predictably as do the supraventricular arrhythmias.
Intravenous Cardinol is indicated for the treatment of persistent premature ventricular extrasystoles that impair the well‑being of the patient and do not respond to conventional measures.
3. Tachyarrhythmias of digitalis intoxication
Intravenous Cardinol is indicated to control ventricular rate in life-threatening digitalis-induced arrhythmias. Severe bradycardia may occur.
4. Resistant tachyarrhythmias due to excessive catecholamine action during anesthesia
Intravenous Cardinol is indicated to abolish tachyarrhythmias due to excessive catecholamine action during anesthesia when other measures fail. These arrhythmias may arise because of release of endogenous catecholamines or administration of catecholamines. All general inhalation anesthetics produce some degree of myocardial depression. Therefore, when Cardinol is used to treat arrhythmias during anesthesia, it should be used with extreme caution, usually with constant monitoring of the ECG and central venous pressure.
Cardinol is contraindicated in 1) cardiogenic shock; 2) sinus bradycardia and greater than first-degree block; 3) bronchial asthma; and 4) in patients with known hypersensitivity to Cardinol hydrochloride.
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, some have been shown to be highly beneficial when used with close follow-up in patients with a history of failure who are well compensazted and are receiving additional therapies, including diiuretics as needed. Beta-adrenergic blocking agents do not abolish the inotropic action of digitalis on heart muscle.
Nonallergic Bronchospasm (e.g., Chronic Bronchitis, Emphysema)
In general, patients with bronchospastic lung disease should not receive beta blockers. Cardinol should be administered with caution in this setting since it may block bronchodilation produced by endogenous and exogenous catecholamine stimulation of beta-receptors.
The necessity or desirability of withdrawal of beta-blocking therapy prior to major surgery is controversial. It should be noted, however, that the impaired ability of the heart to respond to reflex adrenergic stimuli in propranolol-treated patients might augment the risks of general anesthesia and surgical procedures.
Cardinol is a competitive inhibitor of beta-receptor agonists, and its effects can be reversed by administration of such agents, e.g., dobutamine or isoproterenol. However, such patients may be subject to protracted severe hypotension.
Diabetes and Hypoglycemia
Beta-adrenergic blockade may prevent the appearance of certain premonitory signs and symptoms (pulse rate and pressure changes) of acute hypoglycemia, especially in labile insulin-dependent diabetics. In these patients, it may be more difficult to adjust the dosage of insulin.
Cardinol therapy, particularly in infants and children, diabetic or not, has been associated with hypoglycemia especially during fasting, as in preparation for surgery. Hypoglycemia has been reported after prolonged physical exertion and in patients with renal insufficiency.
Beta-adrenergic blockade may mask certain clinical signs of hyperthyroidism. Therefore, abrupt withdrawal of Cardinol may be followed by an exacerbation of symptoms of hyperthyroidism, including thyroid storm. Cardinol may change thyroid-function tests, increasing T4 and reverse T3, and decreasing T3.
Cardinol should be used with caution in patients with impaired hepatic or renal function.
Cardinol is not indicated for the treatment of hypertensive emergencies.
Beta-adrenergic receptor blockade can cause reduction of intraocular pressure. Patients should be told that Cardinol might interfere with the glaucoma screening test. Withdrawal may lead to a return of elevated intraocular pressure.
Risk of 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.
There have been reports of exacerbation of angina and, in some cases, myocardial infarction, following abrupt discontinuance of Cardinol therapy. Therefore, when discontinuance of Cardinol is planned, the dosage should be gradually reduced over at least a few weeks, and the patient should be cautioned against interruption or cessation of therapy without a physician’s advice. If Cardinol therapy is interrupted and exacerbation of angina occurs, it is usually advisable to reinstitute Cardinol therapy and take other measures appropriate for the management of angina pectoris. Since coronary artery disease may be unrecognized, it may be prudent to follow the above advice in patients considered at risk of having occult atherosclerotic heart disease who are given Cardinol for other indications.
Clinical Laboratory Tests
In patients with hypertension, use of Cardinol has been associated with elevated levels of serum potassium, serum transaminases and alkaline phosphatase. In severe heart failure, the use of Cardinol has been associated with increases in Blood Urea Nitrogen.
Caution should be exercised when Cardinol is administered with drugs that have an effect on CYP2D6, 1A2, or 2C19 metabolic pathways. Co-administration of such drugs with Cardinol may lead to clinically relevant drug interactions and changes in its efficacy and/or toxicity (see CLINICAL PHARMACOLOGY, DRUG INTERACTIONS.
Propafenone has negative inotropic and beta-blocking properties that can be additive to those of Cardinol.
Quinidine increases the concentration of Cardinol and produces a greater degree of clinical beta-blockade and may cause postural hypotension.
Disopyramide is a Type I antiarrhythmic drug with potent negative inotropic and chronotropic effects and has been associated with severe bradycardia, asystole and heart failure when administered with Cardinol.
Amiodarone is an antiarrhythmic agent with negative chronotropic properties that may be additive to those seen with Cardinol.
The clearance of lidocaine is reduced when administered with Cardinol. Lidocaine toxicity has been reported following co-administration with Cardinol.
Caution should be exercised when administering Cardinol with drugs that slow A-V nodal conduction, e.g., digitalis, lidocaine and calcium channel blockers.
Calcium Channel Blockers
Caution should be exercised when patients receiving a beta-blocker are administered a calcium-channel-blocking drug with negative inotropic and/or chronotropic effects. Both agents may depress myocardial contractility or atrioventricular conduction.
There have been reports of significant bradycardia, heart failure, and cardiovascular collapse with concurrent use of verapamil and beta‑blockers.
Co-administration of Cardinol and diltiazem in patients with cardiac disease has been associated with bradycardia, hypotension, high degree heart block, and heart failure.
When combined with beta-blockers, ACE inhibitors can cause hypotension, particularly in the setting of acute myocardial infarction.
ACE inhibitors have been reported to increase bronchial hyperreactivity when administered with Cardinol.
The antihypertensive effects of clonidine may be antagonized by beta-blockers. Cardinol should be administered cautiously to patients withdrawing from clonidine.
Prazosin has been associated with prolongation of first dose hypotension in the presence of beta-blockers.
Postural hypotension has been reported in patients taking both beta-blockers and terazosin or doxazosin.
Patients receiving catecholamine-depleting drugs, such as reserpine, with Cardinol should be closely observed for excess reduction of resting sympathetic nervous activity, which may result in hypotension, marked bradycardia, vertigo, syncopal attacks, or orthostatic hypotension. Administration of reserpine with Cardinol may also potentiate depression.
Patients on long-term therapy with Cardinol may experience uncontrolled hypertension if administered epinephrine as a consequence of unopposed alpha-receptor stimulation. Epinephrine is therefore not indicated in the treatment of Cardinol overdose.
Isoproterenol and Dobutamine
Propranolol is a competitive inhibitor of beta-receptor agonists, and its effects can be reversed by administration of such agents, e.g., dobutamine or isoproterenol. Also, Cardinol may reduce sensitivity to dobutamine stress echocardiography in patients undergoing evaluation for myocardial ischemia.
Non-Steroidal Anti-Inflammatory Drugs
Non-steroidal anti-inflammatory drugs (NSAIDs) have been reported to blunt the antihypertensive effect of beta-adrenoreceptor blocking agents.
Administration of indomethacin with Cardinol may reduce the efficacy of Cardinol in reducing blood pressure and heart rate.
The hypotensive effects of MAO inhibitors or tricyclic antidepressants may be exacerbated when administered with beta-blockers by interfering with the beta blocking activity of Cardinol.
Methoxyflurane and trichloroethylene may depress myocardial contractility when administered with Cardinol.
Administration of Cardinol with warfarin increases the concentration of warfarin. Therefore, the prothrombin time should be monitored.
Hypotension and cardiac arrest have been reported with the concomitant use of Cardinol and haloperidol.
Thyroxine may result in a lower than expected T3 concentration when used concomitantly with Cardinol.
In dietary administration studies in which mice and rats were treated with Cardinol hydrochloride for up to 18 months at doses of up to 150 mg/kg/day, there was no evidence of drug-related tumorigenesis. On a body surface area basis, this dose in the mouse and rat is, respectively, about equal to and about twice the maximum recommended human oral daily dose (MRHD) of 640 mg Cardinol hydrochloride. In a study in which both male and female rats were exposed to Cardinol hydrochloride in their diets at concentrations of up to 0.05% (about 50 mg/kg body weight and less than the MRHD), from 60 days prior to mating and throughout pregnancy and lactation for two generations, there were no effects on fertility. Based on differing results from Ames Tests performed by different laboratories, there is equivocal evidence for a genotoxic effect of Cardinol hydrochloride in bacteria (S. typhimurium strain TA 1538).
In a series of reproductive and developmental toxicology studies, Cardinol hydrochloride was given to rats by gavage or in the diet throughout pregnancy and lactation. At doses of 150 mg/kg/day, but not at doses of 80 mg/kg/day (equivalent to the MRHD on a body surface area basis), treatment was associated with embryotoxicity (reduced litter size and increased resorption rates) as well as neonatal toxicity (deaths). Cardinol hydrochloride also was administered (in the feed) to rabbits (throughout pregnancy and lactation) at doses as high as 150 mg/kg/day (about 5 times the maximum recommended human oral daily dose). No evidence of embryo or neonatal toxicity was noted.
There are no adequate and well-controlled studies in pregnant women. Intrauterine growth retardation has been reported for neonates whose mothers received Cardinol hydrochloride during pregnancy. Neonates whose mothers received Cardinol hydrochloride at parturition have exhibited bradycardia, hypoglycemia, and respiratory depression. Adequate facilities for monitoring such infants at birth should be available. Cardinol should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Cardinol is excreted in human milk. Caution should be exercised when Cardinol is administered to a nursing woman.
Safety and effectiveness of Cardinol in pediatric patients have not been established.
Clinical studies of intravenous Cardinol did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Elderly subjects have decreased clearance and a longer mean elimination half‑life. These findings suggest that dose adjustment of Cardinol injection may be required for elderly 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 the decreased hepatic, renal or cardiac function, and of concomitant disease or other drug therapy.
In a series of 225 patients, there were 6 deaths. Cardiovascular events (hypotension, congestive heart failure, bradycardia, and heart block) were the most common. The only other event reported by more than one patient was nausea.
Other adverse events for intravenous Cardinol, reported during post-marketing surveillance include cardiac arrest, dyspnea, and cutaneous ulcers.
The following adverse events have been reported with use of formulations of sustained- or immediate-release oral Cardinol and may be expected with intravenous Cardinol.
Nausea, vomiting, epigastric distress, abdominal cramping, diarrhea, constipation, mesenteric arterial thrombosis, ischemic colitis.
Cardinol is not significantly dialyzable. In the event of overdose or exaggerated response, the following measures should be employed:
Hypotension and bradycardia have been reported following Cardinol overdose and should be treated appropriately. Glucagon can exert potent inotropic and chronotropic effects and may be particularly useful for the treatment of hypotension or depressed myocardial function after a Cardinol overdose. Glucagon should be administered as 50-150 mcg/kg intravenously followed by continuous drip of 1-5 mg/hour for positive chronotropic effect. Isoproterenol, dopamine, or phosphodiesterase inhibitors may also be useful. Epinephrine, however, may provoke uncontrolled hypertension. Bradycardia can be treated with atropine or isoproterenol. Serious bradycardia may require temporary cardiac pacing.
The electrocardiogram, pulse, blood pressure, neurobehavioral status and intake and output balance must be monitored. Isoproterenol and aminophylline may be useful for bronchospasm.
Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.
The usual dose is 1 to 3 mg administered under careful monitoring, such as electrocardiography and central venous pressure. The rate of administration should not exceed 1 mg (1 mL) per minute to diminish the possibility of lowering blood pressure and causing cardiac standstill. Sufficient time should be allowed for the drug to reach the site of action even when a slow circulation is present. If necessary, a second dose may be given after two minutes. Thereafter, additional drug should not be given in less than four hours. Additional Cardinol hydrochloride should not be given when the desired alteration in rate or rhythm is achieved.
Transfer to oral therapy as soon as possible.
Each mL contains 1 mg of Cardinol Hydrochloride, USP in Water for Injection, USP. The pH is adjusted with anhydrous Citric Acid, USP. Supplied as: 1 mL vials in boxes of 10 (NDC 0143-9872-10).
Store at 20° to 25°C (68° to 77°F). Protect from freezing or excessive heat.
Manufactured by: HIKMA FARMACÊUTICA (PORTUGAL), S.A.
Estrada do Rio da Mó, 8, 8A e 8B – Fervença – 2705-906 Terrugem SNT, PORTUGAL
Distributed by: WEST-WARD PHARMACEUTICAL CORP.
Eatontown, NJ 07724 USA
Depending on the reaction of the Cardinol after taken, if you are feeling dizziness, drowsiness or any weakness as a reaction on your body, Then consider Cardinol not safe to drive or operate heavy machine after consumption. Meaning that, do not drive or operate heavy duty machines after taking the capsule if the capsule has a strange reaction on your body like dizziness, drowsiness. As prescribed by a pharmacist, it is dangerous to take alcohol while taking medicines as it exposed patients to drowsiness and health risk. Please take note of such effect most especially when taking Primosa capsule. It's advisable to consult your doctor on time for a proper recommendation and medical consultations.Is Cardinol addictive or habit forming?
Medicines are not designed with the mind of creating an addiction or abuse on the health of the users. Addictive Medicine is categorically called Controlled substances by the government. For instance, Schedule H or X in India and schedule II-V in the US are controlled substances.
Please consult the medicine instruction manual on how to use and ensure it is not a controlled substance.In conclusion, self medication is a killer to your health. Consult your doctor for a proper prescription, recommendation, and guidiance.
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The information was verified by Dr. Rachana Salvi, MD Pharmacology