15 mg, 30 mg, and 60 mg.
D1 and D2 receptors.
Hepatic metabolism; metabolites are excreted in urine and feces.
85%.
By binding to specific sites on muscle cells as an agonist at the oxytocin receptor.
1–20 μg/kg/min.
Tachycardia, chest pain, dizziness, metallic taste, nausea and vomiting, abdominal pain.
Hemabate.
0.05–0.2 μg/kg/min.
Caution in those with uterine conditions.
0.5–40 μg/kg/min, titrated to effect.
Acts within 2–3 minutes.
It is a potent bronchodilator.
Syntocinon.
0.01–0.1 μg/kg/min.
Increases heart rate, contractility, and cardiac output.
Through enzymatic degradation; minimally renally excreted (0.7%).
0.001–0.002 u/min, do not exceed 5 u per day.
Increased cardiac output, coronary artery vasodilation, and decreased diastolic blood pressure.
Associated rise in mortality.
85%.
3-methoxy-4-hydroymandelic acid (VMA) and metadrenaline.
0.1–1 mg/mL.
0.5–6 μg/kg/min, titrated to effect.
Approximately 1 hour.
By direct stimulation of β receptors.
20 minutes.
α and β adrenoreceptors.
To cause sustained uterine contraction following caesarean section.
Hepatic metabolism by catechol-O-methyltransferase.
A naturally occurring catecholamine and neurotransmitter.
12.5/50 mg/mL.
50 μg/kg over 10 minutes.
To cause uterine contraction and stop post-partum hemorrhage in patients unresponsive to oxytocin and ergometrine.
1 hour.
Mainly α effects.
Stimulates uterine contraction; mechanism not elucidated.
Decreased renal vessel resistance and increased renal blood flow.
Increased cardiac output and inhibition of Na+/K+ ATPase.
It is a clear colorless solution at a concentration of 2 mg/mL for dilution.
A long-acting synthetic analogue of oxytocin.
30 mg t.d.s.
Induction of labour, following caesarean section, and following abortion.
Holding measure in complete heart block while awaiting pacing.
Bronchodilation due to β2 receptor stimulation.
Hyperstimulation, nausea, vomiting, rash, anaphylaxis, and amniotic fluid embolism following overdose.
30 mg t.d.s.
Following caesarean section, second line treatment of uterine atony after oxytocin/carbetocin, and following abortion.
It is a direct and indirect α1 agonist with some small action at β receptors.
Increased heart rate, contractility, and cardiac output.
By mitochondrial monoamine oxidase (MAO) in the liver, brain, and kidney, and by cytoplasmic catechol-O-methyltransferase (COMT).
Synthetic β1 and β2 agonist.
Hepatic metabolism.
A synthetic β agonist, primarily β1 > β2.
Increases heart rate, contractility, and cardiac output while decreasing afterload.
It is inactivated.
It binds to troponin C, stabilizing troponin C and actin-myosin cross-bridges, increasing contractility and vasodilatation without increasing Ca2+ concentration.
Increased systemic vascular resistance and potent bronchodilation.
Blood glucose and free fatty acids increase.
By inhibiting PDE III, which increases intracellular cAMP and Ca2+ release.
Headache.
0.09–0.4 L/kg.
Hypertension, bradycardia, headache, and peripheral ischemia.
85 to 100 minutes.
By mitochondrial monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT).
200/800 mg in 5 mL.
α and β agonist.
Agonist at G protein-coupled oxytocin receptor, stimulating uterine contraction.
Cardiac arrest.
To cause uterine contraction and reduce bleeding.
65%.
Urine output may increase with increased cardiac output.
Acts within 1 minute.
A synthetic β2, D1, and D2 agonist.
As an inotrope and diuretic.
Selective phosphodiesterase III inhibitor.
Increased systemic vascular resistance (SVR) and blood pressure, with potential severe hypertension in patients with cardiac disease.
70%.
250 μg/mL.
Increases heart rate, contractility, and cardiac output; may increase myocardial O2 demand.
Nausea and vomiting.
It slightly increases AV nodal conduction; consider co-administration of digoxin if necessary.
Headache, dizziness, tinnitus, and reported cerebrovascular accidents (CVA).
It is contraindicated in patients on monoamine oxidase inhibitors (MAOIs).
To cause uterine contraction.
100 μg IV over 1 minute, given immediately following parturition; can only give 1 dose.
6–12 μg/kg over 10 minutes.
It increases renal blood flow, causing diuresis.
0.375–0.75 μg/kg/min.
30 mg/mL.
Increases stroke volume, contractility, and cardiac index; no increase in cardiac oxygen consumption; decreases SVR, PVR, and PCWP.
To maintain blood pressure (BP) and systemic vascular resistance (SVR), especially in sepsis.
Increased heart rate, cardiac output, blood pressure, and coronary artery blood flow.
Bronchospasm – relatively contraindicated in asthmatics.
Vanillylmandelic acid (VMA).
Hepatic metabolism via COMT.
Hepatic and renal metabolism.
Severe hepatic/renal failure, ventricular outflow obstruction, severe hypotension/tachycardia, history of torsades de pointes.
May precipitate arrhythmias.
Stimulates uterine and vascular smooth muscle contraction by binding to 5HT receptors and stimulates D2 receptors at the chemoreceptor trigger zone (CTZ) causing emesis.
0.01 μg/kg/min, titrated to effect.
Hyperglycemia, hypokalemia, nausea, and vomiting.
2.5 hours.
Via COMT in the liver, kidney, and plasma.
Can cause hypotension.
Increases BP and SVR, may decrease cardiac output, causes peripheral vasoconstriction, and increases myocardial oxygen consumption.
Sweating and flushing.
Mainly β effects.
As an inotrope in low cardiac output states and for cardiac stress testing.
Caution with MAOIs as it can precipitate hypertensive crisis.
Increases systemic vascular resistance (SVR) and blood pressure, can cause severe hypertension, bradycardia, and arrhythmias.
Effective within 1–2 minutes.
250 μg IM or directly into uterine muscle, repeat every 15 min as necessary, with a max dose of 2 g.
0.5 mg/mL.
Inotrope for low cardiac output states, especially following cardiac surgery.
Headache and dizziness.
Severe nausea and vomiting.
In fixed cardiac output states or pheochromocytoma.
It causes the release of noradrenaline from nerve terminals.
75%.
Cardiovascular collapse and pulmonary edema (rare).
Hypotension, nasal decongestant, and nocturnal enuresis.
Increases basal metabolic rate, glycogenolysis, and plasma glucose.
Increases stroke volume, contractility, and cardiac index; decreases systemic vascular resistance (SVR).
0.5 mg IM or 0.125 mg by slow IV injection.
4 hours.
