Product Name
Chemical Name
Ritodrine HCl
Therapeutic Category
Miscellaneous drugs
Pharmacologic Category
Uterine Relaxant - Beta-2 Adrenergic Agonist
Pharmaceutical Form
Ritodrine HCl 10mg
uncomplicated premature labour
Adult: Start oral therapy 30-60 mins before termination of IV infusion at 10 mg every 2 hr for 24 hr. Subsequently, 10-20 mg every 4-6 hr according to patient's response. Max oral dose 120 mg daily.
uncomplicated premature labour
Adult: Given as IV infusion, initially 0.05 mg/min. Increase by 0.05 mg/min every 10 min until patient responds. Usual rate: 0.15-0.35 mg/min. As IM inj: 10 mg every 3-8 hr. Maintain for 12-48 hr after the contractions have stopped.
Ritodrine is used to stop premature labor.
Adverse Reactions
Tachycardia, palpitation, headache, nervousness, anxiety, nausea, vomiting.
Potentially Fatal: Rarely, anaphylaxis, arrhythmia, pulmonary oedema, hypokalaemia.
Antepartum haemorrhage, eclampsia and severe preeclampsia, intrauterine foetal death, cardiac disease. Threatened miscarriage, placenta praevia and cord compression.
Warnings / Precautions Drug
CV risk factors, concurrent steroids, hyperthyroidism, myocardial insufficiency, arrhythmias, hypertension, DM, bronchial asthma treated with beta-agonists, lactation. Monitor plasma glucose and potassium. Monitor maternal pulse throughout infusion; adjust rate to avoid maternal heart beat exceeding 140 beats/min. Monitor patient's hydration status to reduce risk of pulmonary oedema. Discontinue treatment if there are signs of pulmonary oedema.
May enhance neuromuscular blockade produced by pancuronium and vecuronium.
Potentially Fatal: Potassium-depleting drugs may increase risk of hypokalaemia.
 Either animal-reproduction studies have not demonstrated a foetal risk but there are no controlled studies in pregnant women or animal-reproduction studies have shown an adverse effect (other than a decrease in fertility) that was not confirmed in controlled studies in women in the 1st trimester (and there is no evidence of a risk in later trimesters).
Mechanism of Action
A selective β2-adrenoceptor agonist with its main action on the uterus, causing relaxation. It reduces the intensity and frequency of contractions. Heart rate is also increased while diastolic pressure is reduced. May cause bronchial relaxation but this is not clinically significant in its usage.
Pharmacodynamics / Kinetics
Absorption: Rapid absorption from the GI tract (oral). Bioavailability: about 30% of an oral dose.
Distribution: Crosses the placenta.
Metabolism: Hepatic: By conjugation with glucuronic acid or sulfate.
Excretion: 70-90% of a dose is excreted in the urine within 10-12 hr.