WikiAnesthesia - User contributions [en]

Atropine

2024-01-05T21:31:37Z

Mccarta: Added an intro paragraph, uses, contraindications, pharmacology sections

{{Infobox drug reference
| trade_names =
| image_file =
| drug_class = Anticholinergic
| drug_class_color = anticholinergic
| uses = Treatment of bradycardia,
Antidote for acetylcholinesterase inhibitor toxicity
| contraindications = Known hypersensitivity
| routes = IV, IM, PO, oral or endotracheal inhalation, ophthalmic solution
| dosage = Treatment of bradycardia:
1 mg every 3 to 5 minutes (3mg max), repeat until obtaining desired heart rate

Treatment of acetylcholinesterase inhibitor toxicity:
2 to 3 mg every 20 to 30 min

Antisialagogue/anti-vagal:
0.5 to 1mg every 1 to 2 hours

Pediatric:
0.01 mg/kg to 0.03 mg/kg every 3 to 5 minutes. Minimum dose is 0.1 mg. Maximum dose is 0.5mg (child) or 1 mg (adolescent).
| dosage_calculation = atropine
| mechanism = Muscarinic acetylcholine antagonism
| adverse_effects =
| time_onset =
| duration =
| metabolism = Enzymatic hydrolysis in the liver
| halflife_redistribution =
| halflife_elimination =
| clearance =
| protein_binding = 14-22%
| formula = C17H23NO3
| molar_mass = 289.369 g/mol
}}

'''Atropine''' is a tertiary amine extracted from belladonna alkaloid as a racemic mixture of d and l-hyoscyamine, which vary in their potency as anticholinergic agents. It reversibly binds to peripheral muscarinic acetylcholine receptors where it acts a competitive inhibitor. Its primary uses include treatment of bradycardia or bradycardia-induced cardiac arrest, treatment of cholinergic effects of organophosphate, nerve agent, or insecticide toxicity, or in ophthalmic surgery to produce mydriasis and cycloplegia. It can also be utilized in conjunction with cholinesterase inhibitors for reversal of neuromuscular blockade in order to reduce their muscarinic effects.

==Uses==
- Treatment of bradycardia (vasovagal response, AV block, bradyarrhythmias)

- Treatment of acetylcholinesterase inhibitor toxicity (chemical nerve agents, carbamate, organophosphates)

- Perioperatively for reduction of secretions and vagal responses

- Perioperatively for prophylaxis against muscarinic effects when anticholinesterase agents (neostigmine, physostigmine, pyridostigmine) are used to reverse neuromuscular blockade

- For ophthalmic surgery, to induce mydriasis or cycloplegia

- Treatment of amblyopia

==Contraindications==

===Absolute contraindications===
- Atropine or belladonna alkaloids hypersensitivity. Note: IM/IV administration of atropine can cause flushing of face and trunk, which is not associated with a hypersensitivity response.<ref>{{Cite web|date=07/2018|title=Atropine Injection, 2mg|url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/212319s000lbl.pdf|url-status=live|access-date=01/05/2024|website=FDA Drug Safety Data}}</ref>

===Precautions===
- Coronary artery disease, acute myocardial infarct, congestive heart failure, tachycardia, or hypertension

- Chronic lung disease

- Obstructive gastrointestinal disease, including toxic megacolon, paralytic ileus, pyloric stenosis

- Obstructive urinary disease, including uropathy and prostatic hypertrophy

- Acute-angle glaucoma

- Myasthenia gravis

- Insufficient data regarding atropine use during pregnancy to determine risk of adverse developmental outcomes

==Pharmacology==

===Pharmacodynamics===

====Mechanism of action====
Atropine is a competitive inhibitor at autonomic postganglionic cholinergic receptors<ref name=":0">{{Cite web|title=Atropine|url=https://www-clinicalkey-com.laneproxy.stanford.edu/#!/topic/atropine?topic=atropine|url-status=live|access-date=1/5/2024|website=Elsevier Drug Information}}</ref>. Atropine’s activity is primarily due to the l-hyoscyamine enantiomer. Atropine binds receptors found in GI and pulmonary smooth muscle, exocrine glands, heart and eye; it does not block acetylcholine’s action at the NMJ. It does not inhibit nicotonic cholingeric receptors at typical doses. Atropine’s primary clinical effects include changes in heart rate, reduction in salivary, bronchial, and sweat gland secretions, bronchodilation, mydriasis and cycloplegia, decreased GI motility and gastric secretions, and contraction of the bladder detrusor muscle.

====Adverse effects====
- Dry mouth (xerostomia)

- Blurred vision, including photophobia and loss of visual acuity

- GI symptoms: dysphagia, constipation, nausea, vomiting

- Bradycardia (at doses of 0.4-0.6mg)

- Tachycardia (at doses of 1-2mg)

- Palpitations, arrhythmias, aystole

- Flushing

- Urinary retention

- Delirium and coma at high doses

===Pharmacokinetics===
- IV administration has a distribution half life of about 1 minute, with rapid decline in concentration within the first 8-10 minutes. <ref name=":0" />

- Crosses the blood-brain barrier and the placenta<ref name=":1">{{Cite journal|last=Ali–Melkkilä|first=T.|last2=Kanto|first2=J.|last3=Iisalo|first3=E.|date=1993-10|title=Pharmacokinetics and related pharmacodynamics of anticholinergic drugs|url=https://onlinelibrary.wiley.com/doi/10.1111/j.1399-6576.1993.tb03780.x|journal=Acta Anaesthesiologica Scandinavica|language=en|volume=37|issue=7|pages=633–642|doi=10.1111/j.1399-6576.1993.tb03780.x|issn=0001-5172}}</ref>

- Undergoes enzymatic hydrolysis in the liver into active metabolites<ref name=":1" />

- Atropine and its metabolites are primarily exreted renally, with small contributions from pulmonary and fecal routes of excretion. 13-57% of atropine is excreted unchanged in the urine.<ref name=":1" />

==Chemistry and formulation==

==History==

==References==

[[Category:Drug reference]]
[[Category:Anticholinergic]]
[[Category:Positive chronotropes]]
[[Category:Antidotes]]
<references />

Dobutamine

2024-01-08T23:22:20Z

Mccarta: Wrote general description, uses, contraindications, pharmacology, history sections

{{Infobox drug reference
| trade_names =
| drug_class = Synthetic catecholamine
| drug_class_color = cardiovascular_agonist
| uses = Low cardiac output, pharmacologic cardiac stress echocardiography
| contraindications = Corn hypersensitivity, idiopathic hypertrophic subaortic stenosis
| routes = IV
| dosage =
| dosage_calculation = dobutamine
| mechanism = beta-1 agonism (primary), beta-2 agonism and alpha-1 agonism (secondary)
| adverse_effects = Hypertension, hypotension, arrhythmia, hypokalemia, nausea, headache, chest pain
| time_onset = 1-2 minutes
| metabolism = Liver metabolism by catechol-O-methyltransferase and glucuronidation to inactive metabolites
| clearance = 90 mL/kg/min
| formula = C18H23NO3
| molar_mass = 301.38
}}

Dobutamine is a direct-acting sympathomimetic with preferential activation of beta-1 adrenergic receptors accounting for most of its ionotropic and chronotropic effects. It is also active at beta-2 and alpha-1 adrenergic receptors. Its primary indication is the treatment of low cardiac output secondary to CHF, cardiogenic shock, septic shock, or following cardiac surgery; Dobutamine is also the preferred agent for pharmacologic cardiac stress testing in patients who cannot tolerate an exercise stress test.

==Uses==

*Low cardiac output secondary to congestive heart failure, cardiogenic shock, septic shock, or following cardiac surgery<ref name=":0">{{Citation|title=Dobutamine in Dextrose Injection|url=http://dx.doi.org/10.31003/uspnf_m27790_06_01|publisher=U.S. Pharmacopeial Convention|access-date=2024-01-08}}</ref>

*Stress echocardiography, preferred alternative test for evaluation of myocardial ischemia if the patient is unable to exercise, though this use is off-label<ref>{{Cite journal|last=Pellikka|first=Patricia A.|last2=Arruda-Olson|first2=Adelaide|last3=Chaudhry|first3=Farooq A.|last4=Chen|first4=Ming Hui|last5=Marshall|first5=Jane E.|last6=Porter|first6=Thomas R.|last7=Sawada|first7=Stephen G.|date=2020-01|title=Guidelines for Performance, Interpretation, and Application of Stress Echocardiography in Ischemic Heart Disease: From the American Society of Echocardiography|url=http://dx.doi.org/10.1016/j.echo.2019.07.001|journal=Journal of the American Society of Echocardiography|volume=33|issue=1|pages=1–41.e8|doi=10.1016/j.echo.2019.07.001|issn=0894-7317}}</ref>

==Contraindications==

===Absolute contraindications===

*Corn hypersensitivity, as premixed bags contain dextrose

*Idiopathic hypertrophic subaortic stenosis

===Precautions===

*Acute myocardial infarction and coronary artery disease, as dobutamine may worsen myocardial ischemia
*Atrial fibrillation, ventricular arrhythmias, as dobutamine increases AV conduction and can precipitate or worsen ectopic activity<ref>{{Cite journal|last=David|first=Shukri|last2=Zaks|first2=Jeffrey M.|date=1986-02|title=Arrhythmias Associated with Intermittent Outpatient Dobutamine Infusion|url=http://dx.doi.org/10.1177/000331978603700203|journal=Angiology|volume=37|issue=2|pages=86–91|doi=10.1177/000331978603700203|issn=0003-3197}}</ref>
*Hypertension
*Hypotension and hypovolemia
*Renal failure, as continuous infusions may result in myoclonia<ref>{{Cite journal|last=Wierre|first=L.|last2=Decaudin|first2=B.|last3=Barsumau|first3=J.|last4=Vairon|first4=M. X.|last5=Horrent|first5=S.|last6=Odou|first6=P.|last7=Azar|first7=R.|date=2004-04-21|title=Dobutamine-induced myoclonia in severe renal failure|url=http://dx.doi.org/10.1093/ndt/gfh132|journal=Nephrology Dialysis Transplantation|volume=19|issue=5|pages=1336–1337|doi=10.1093/ndt/gfh132|issn=0931-0509}}</ref>
*Premature neonates, as dobutamine has been shown to be less effective than dopamine in this population<ref name=":0" />
*Geriatric patients
*Pregnancy and breast feeding<ref name=":0" />
*Sulfite hypersensitivity, as some preparations include sulfites<ref name=":0" />

==Pharmacology==

===Pharmacodynamics===

====Mechanism of action====
Dobutamine is a direct-acting synthetic catecholamine. It is formulated as a racemic mixture of 2 enantiomers, the positive enantiomer is predominantly a beta-agonist (beta-1 greater than beta-2), while the negative enantiomer has partial alpha-1 agonist effects. Dobutamine binding to beta-1 adrenergic receptors enhances voltage-gated calcium channel expression on cardiac myocytes and increases myocardial contractility, leading to larger stroke volumes and increased cardiac output. This increased cardiac output activates baroreceptors, which decrease systemic vascular resistance, resulting in minimal change to arterial blood pressure. Dobutatmine also has minor beta-2 and alpha-1 adrenergic stimulatory effects. <ref>{{Cite journal|last=Ruffolo|first=Robert R.|date=1987-10|title=Review: The Pharmacology of Dobutamine|url=http://dx.doi.org/10.1097/00000441-198710000-00005|journal=The American Journal of the Medical Sciences|volume=294|issue=4|pages=244–248|doi=10.1097/00000441-198710000-00005|issn=0002-9629}}</ref>

====Adverse effects====

*Hypertension
*Hypotension due to decreased systemic vascular resistance
*Tachycardia
*Rapid ventricular response or premature ventricular contractions
*Hypokalemia
*Nausea
*Headaches
*Chest pain
*Palpitations
*Shortness of breath

===Pharmacokinetics===

*Onset of action: 1-2 minutes, though peak effect can take up to 10 minutes
*Plasma half-life: 2 minutes
*Metabolized in the liver catechol-O-methyltransferase and by glucuronidation to inactive metabolites, excretion of metabolites via the kidneys

==Chemistry and formulation==

==History==
Dobutamine was developed by Drs. Tuttle and Mills in 1975, after they modified the structure of isoproterenol. <ref>{{Cite journal|last=Tuttle|first=R R|last2=Mills|first2=J|date=1975-01|title=Dobutamine: development of a new catecholamine to selectively increase cardiac contractility.|url=http://dx.doi.org/10.1161/01.res.36.1.185|journal=Circulation Research|volume=36|issue=1|pages=185–196|doi=10.1161/01.res.36.1.185|issn=0009-7330}}</ref>

==References==

[[Category:Drug reference]]
<references />

Isoprenaline

2024-01-09T20:06:39Z

Mccarta: Wrote general information, uses, contraindications, pharmacodynamics sections

{{Infobox drug reference
| trade_names = Isuprel
| drug_class = Synthetic catecholamine
| drug_class_color =
| uses =
| contraindications = Tachyarrhythmia, tachycardia
| routes = IV, IM, subcutaneous, inhalation
| dosage = Treatment of AV block or cardiac arrest:
IV - 0.02-0.06 mg, then 0.01-0.2 mg depending on ventricular rate
IM - 0.2 mg, then 0.02-1 mg depending on ventricular rate
Subcutaneous - 0.2 mg, then 0.15-0.2 mg depending on ventricular rate
Treatment of hypovolemic and septic shock, low cardiac output, CHF:
IV - 0.5-5 mcg/min continuous infusion, titrate to goal HR, CVP, SBP, or urine output
Treatment of cardiogenic shock:
IV - 0.5-20 mcg/min continuous infusion
Treatment of bronchospasm:
IV - 0.01-0.02 mg PRN
Treatment of symptomatic bradycardia:
IV - 20-60 mcg initial bolus, then 10-20 mcg as needed until goal HR and rhythm response met
Treatment of ventricular tachyarrhythmia in patients with short QT or Brugada syndrome:
IV - 2-10 mcg/min continuous infusion
| dosage_calculation = isoprenaline
| mechanism = Beta agonism
| adverse_effects = Tachycardia, hypertension, hypotension, ventricular arrhythmia, Adam-stokes syndrome, angina, skin necrosis
| time_onset = Immediate
| duration = 10-15 minutes
| metabolism = Liver metabolism by COMT
| formula = C11H17NO3
| molar_mass = 211.258 g/mol
}}

Isoprenaline (also known as isopreterenol) is a direct-acting synthetic catecholamine. It has agonist activity at both beta-1 and beta-2 adrenergic receptors. Its approved uses are in the treatment of AV block and cardiac arrest secondary to heart block, when pacemaker therapy is not available or ineffective. However, it is also used clinically in the treatment of symptomatic bradycardia, bronchospasm, shock, arrhythmia secondary to conduction abnormalities, and intraprocedurally to induce arrhythmia or syncope.

==Uses==

*AV block not requiring pacing
*Cardiac arrest from heart block when pacemaker therapy is unavailable
*Bradycardia, especially in cardiac transplant patients
*Acute bronchospasm
*Cardiogenic shock
*Hypovolemic and septic shock, congestive heart failure
*For electrophysiological procedures: to provoke ventricular arrhythmias
*For tilt table testing: to provoke syncope
*Treatment of beta-blocker overdose
*Short QT syndrome
*Torsades de pointes
*Electrical storm in patients with Brugada syndrome

==Contraindications==

===Absolute contraindications===

*Tachyarrhythmias, including atrial fibrillation, atrial flutter, ventricular fibrillation
*Digitalis toxicity-induced AV block
*Tachycardia
*Pheochromocytoma

===Precautions===

*Diabetes mellitus, as it induces glycogenolysis and insulin resistance
*Hyperthyroidism, as it can induce thyroid storm<ref>{{Citation|last=Cannon|first=Ayana|title=Isoproterenol (Isuprel, Medihaler-ISO)|date=2011|url=http://dx.doi.org/10.1016/b978-1-4377-1720-4.00535-5|work=Essence of Anesthesia Practice|pages=613|publisher=Elsevier|access-date=2024-01-09|last2=Bernstein|first2=Wendy K.}}</ref>
*Children with refractory asthma, as its use in this population can result in clinical deterioration, myocardial necrosis, congestive heart failure, and death<ref>{{Cite journal|last=Boniol|first=Scott|last2=Slatkin|first2=Neal E.|last3=Stambler|first3=Nancy|last4=Israel|first4=Robert J.|date=2021-05-20|title=Rescue-free laxation response with methylnaltrexone treatment in cancer patients with opioid-induced constipation: The impact of baseline ECOG status.|url=http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e24083|journal=Journal of Clinical Oncology|volume=39|issue=15_suppl|pages=e24083–e24083|doi=10.1200/jco.2021.39.15_suppl.e24083|issn=0732-183X}}</ref>
*Recent myocardial infarction, ischemic heart disease
*Hypovolemia causing hypotension
*Hypertension
*Sulfite hypersensitivity

==Pharmacology==

===Pharmacodynamics===

====Mechanism of action====
Isoprenaline is a potent nonselective beta agonist. Upon binding beta-1 adrenergic receptors, it increases intracellular calcium in cardiac myocytes, with positive ionoptropic, lusitropic, chronotropic, and dromotropic effects. Beta-1 activation also activates the RAAS system in the kidney.<ref>{{Cite journal|last=Biazi|first=Giuliana R.|last2=Frasson|first2=Isabele G.|last3=Miksza|first3=Daniele R.|last4=de Morais|first4=Hely|last5=de Fatima Silva|first5=Flaviane|last6=Bertolini|first6=Gisele L.|last7=de Souza|first7=Helenir M.|date=2018-05-15|title=Decreased hepatic response to glucagon, adrenergic agonists, and cAMP in glycogenolysis, gluconeogenesis, and glycolysis in tumor‐bearing rats|url=http://dx.doi.org/10.1002/jcb.27027|journal=Journal of Cellular Biochemistry|volume=119|issue=9|pages=7300–7309|doi=10.1002/jcb.27027|issn=0730-2312}}</ref> Upon binding beta-2 adrenergic receptors, it increases intracellular cAMP and PKA, inactivating myosin light chain kinase. Thus, agonism of these beta-2 receptors results in the relaxation of smooth muscle, peripheral vasodilation, bronchial dilation, and uterine smooth muscle relaxation. Isoprenaline also induces hepatic glycogenolysis and release of glucagon from the pancreas via beta-2 adrenergic activity.<ref>{{Cite journal|last=Matera|first=Maria Gabriella|last2=Page|first2=Clive|last3=Rinaldi|first3=Barbara|date=2018-06|title=β2-Adrenoceptor signalling bias in asthma and COPD and the potential impact on the comorbidities associated with these diseases|url=http://dx.doi.org/10.1016/j.coph.2018.04.012|journal=Current Opinion in Pharmacology|volume=40|pages=142–146|doi=10.1016/j.coph.2018.04.012|issn=1471-4892}}</ref>

====Adverse effects====

*Headache
*Dizziness
*Nausea
*Flushing
*Fatigue
*Diaphoresis
*Mild tremor
*Weakness
*Blurred Vision
*Tachycardia
*Hypertension
*Hypotension
*Ventricular arrhythmia or PVCs
*Adams-Stokes syndrome
*Dyspnea
*Hypokalemia
*Hyperglycemia
*Angina
*Skin necrosis

===Pharmacokinetics===

*Poor substrate for MAO, not taken up by neurons to the same extent as epinephrine and norepinephine. This, duration of action of isoprenaline is longer than epinephrine.
*Instead, it is metabolized in the liver and other tissues by catechol-O-methyltransferase (COMT) to the 3-O-methyl isoproterenol metabolite, which is subsequently conjugated with sulfate
*Excretion occurs via the urine
*Onset of action: immediate
*Duration of action 10-15 minutes
*Plasma half-life: 2.5-5 minutes

==Chemistry and formulation==
Isoprenaline hydrochloride (also called isoproterenol hydrochloride) is 3,4-Dihydroxy-alpha- (isopropylamino) methyl benzyl alcohol hydrochloride, a synthetic sympathomimetic amine that is structurally related to epinephrine but acts almost exclusively on beta adrenergic receptors.

==History==

==References==

[[Category:Drug reference]]
<references />

Milrinone

2024-01-09T21:41:46Z

Mccarta: Wrote general, indications, contraindications, pharmacology sections.

{{Infobox drug reference
| trade_names =
| drug_class = Positive inotrope
| drug_class_color = cardiovascular_agonist
| uses =
| contraindications = Milrinone hypersensitivity
| routes = Intravenous
| dosage =
| dosage_calculation = milrinone
| mechanism = Phosphodiesterase inhibitor
| adverse_effects = Hypotension, arrhythmia, headache, syncope, bronchospasm
| time_onset = 2-10 minutes
| duration = variable, 1.5-5 hours
| metabolism = Liver glucuronidation
| halflife_elimination = 2.4 hours (heart failure patients)
| clearance = 0.14 L/kg/hr (heart failure patients)
| protein_binding = 70%
| volume_distribution = 0.45 L/kg
| formula = C12H9N3O
| molar_mass = 211.22 g/mol
}}

Milrinone is a phosphodiesterase III inhibitor, which increases cardiac contractility and induces both peripheral and pulmonary vasodilation. Its primary indication is for short-term treatment of acute decompensated heart failure with reduced ejection fraction. Milrinone is more likely to cause hypotension and less likely to cause arrhythmias when compared to other inotropes, such as dobutamine and dopamine.<ref>{{Cite journal|last=Jentzer|first=Jacob C.|last2=Coons|first2=James C.|last3=Link|first3=Christopher B.|last4=Schmidhofer|first4=Mark|date=2014-11-28|title=Pharmacotherapy Update on the Use of Vasopressors and Inotropes in the Intensive Care Unit|url=http://dx.doi.org/10.1177/1074248414559838|journal=Journal of Cardiovascular Pharmacology and Therapeutics|volume=20|issue=3|pages=249–260|doi=10.1177/1074248414559838|issn=1074-2484}}</ref>

== Uses ==

* Short-term treatment of acute decompensated heart failure with reduced ejection fraction<ref name=":0">{{Cite book|title=Milrinone injection package insert|publisher=Baxter Healthcare Corporation|year=2018|location=Deerfield, IL}}</ref>
* Treat of cerebral vasospasm after aneurysmal subarachnoid hemorrhage<ref>{{Cite journal|last=Fraticelli|first=Amanda Tarabini|last2=Cholley|first2=Bernard P.|last3=Losser|first3=Marie-Reine|last4=Saint Maurice|first4=Jean-Pierre|last5=Payen|first5=Didier|date=2008-03|title=Milrinone for the Treatment of Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage|url=http://dx.doi.org/10.1161/strokeaha.107.492447|journal=Stroke|volume=39|issue=3|pages=893–898|doi=10.1161/strokeaha.107.492447|issn=0039-2499}}</ref>
* Treatment of persistent pulmonary hypertension of the newborn in patients with poor response to nitric oxide

== Contraindications ==

=== Absolute contraindications ===

* Milrinone hypersensitivity
* Corn hypersensitivity, as some formulations contain dextrose<ref name=":0" />

=== Precautions ===

* Idiopathic hypertrophic subaortic stenosis
* Acute myocardial infarction
* Atrial fibrillation or flutter
* Renal impairment or failure
* Hypovolemia
* Hypokalemia
* Pregnancy or breast-feeding

== Pharmacology ==

=== Pharmacodynamics ===

==== Mechanism of action ====
Milrinone is an inotrope and vasodilator without significant chronotropic activity. Milrinone selectively inhibits phosphodiesterase III, preventing the breakdown of cAMP in cardiac myocytes and smooth muscle cells. This preserved cAMP increases protein kinase A activity, leading to phosphorylation of calcium ion channels in the sarcoplasmic reticulum and increasing calcium availability in myocyte sarcomere. The aforementioned increased calcium availability results in enhanced cardiac inotropy and chronotropy. In vascular smooth muscle cells, phosphodiesterase III inhibition promotes vasodilation and reduces systemic vascular resistance. Similarly, it decreases pulmonary vascular resistance. <ref>{{Cite journal|last=Dobashi|first=Shintaro|last2=Watanabe|first2=Ippei|last3=Nakanishi|first3=Rine|last4=Hisatake|first4=Shinji|last5=Kiuchi|first5=Shunsuke|last6=Kabuki|first6=Takayuki|last7=Oka|first7=Takashi|last8=Fujii|first8=Takahiro|last9=Ikeda|first9=Takanori|date=2019-12-21|title=Comparing the effects of milrinone and olprinone in patients with congestive heart failure|url=http://dx.doi.org/10.1007/s00380-019-01543-6|journal=Heart and Vessels|volume=35|issue=6|pages=776–785|doi=10.1007/s00380-019-01543-6|issn=0910-8327}}</ref>

==== Adverse effects ====

* Ventricular or Atrial arrhythmia<ref>{{Cite journal|last=Chong|first=Luke Yong Zheng|last2=Satya|first2=Kumar|last3=Kim|first3=Bernard|last4=Berkowitz|first4=Robert|date=2018-01|title=Milrinone Dosing and a Culture of Caution in Clinical Practice|url=http://dx.doi.org/10.1097/crd.0000000000000165|journal=Cardiology in Review|volume=26|issue=1|pages=35–42|doi=10.1097/crd.0000000000000165|issn=1061-5377}}</ref>
* Sudden cardiac death
* Headache
* Syncope
* Hypotension
* Injection site reaction
* Tremor
* Bronchospasm and anaphylactic shock

=== Pharmacokinetics ===

* Onset of action typically within 2 minutes, though peak effect is closer to 10 minutes in patients with heart failure<ref name=":0" />
* Duration of action: highly variable, but generally 1.5-5 hours
* Metabolized in the liver via glucuronidation to an O-glucuride metabolite
* Milrinone and metabolite are cleared in the urine
* Elimination half-life: 2.4 hours

== Chemistry and formulation ==
Milrinone is a bipyridine.

== History ==

== References ==

[[Category:Drug reference]]

Dopamine

2024-01-09T22:29:24Z

Mccarta: Wrote general, uses, contraindications, pharmacology sections

{{Infobox drug reference
| trade_names =
| drug_class = Endogenous catecholamine
| drug_class_color = cardiovascular_agonist
| uses = Treatment of hypotension and bradycardia
| contraindications = pheochromocytoma, ventricular tachycardia, ventricular fibrillation, corn or sulfite hypersensitivities
| routes = Intravenous
| dosage =
| dosage_calculation = dopamine
| mechanism = Dopaminergic and adrenergic agonism
| adverse_effects = Arrhythmia and ectopy, tachycardia, hypotension, hypertension, headahce, vomiting, dyspnea, peripheral vasoconstriction and tissue necrosis
| time_onset = 5 minutes
| duration = 10 minutes
| metabolism = MAO and COMT activity in liver, kidneys, plasma
| formula = C8H11NO2
| molar_mass = 153.18 g/mol
}}

Dopamine is a catecholamine with dopaminergic and adrenergic activity. Its primary indication is for the treatment of hypotension and bradycardia in the setting of shock and cardiac arrest. It is also used in the treatment of symptomatic bradycardia that is not responsive to atropine or pacing. It may be used as a palliative infusion for patients with chronic heart failure.

== Uses ==

* Hemodynamic support or treatment of hypotension from shock (septic, cardiogenic, anaphylactic, or neurogenic), open-heart surgery, or renal failure
* Treatment of symptomatic bradycardia unresponsive to atropine and/or external pacing
* Treatment of chronic heart failure

== Contraindications ==

=== Absolute contraindications ===

* Pheochromocytoma
* Ventricular tachycardia
* Ventricular fibrillation
* Corn or sulfite hypersensitivities

=== Precautions ===

* Asthma
* Hypovolemia
* Occlusive vascular disease
* Raynaud’s phenomenon
* Thromboangiitis obliterans
* Geriatric patients
* Pregnancy or breast-feeding

== Pharmacology ==

=== Pharmacodynamics ===

==== Mechanism of action ====
Dopamine is an endogenous catecholamine, the metabolic precursor to norepinephrine in the catecholamine synthetic pathway. Dopamine’s affinity for its receptors is dose-dependent. Low infusion rates (0.5 to 2 micrograms/kg per minute) act on dopaminergic D1 and D2 receptors in the visceral vasculature to produce vasodilation and increased blood flow to the kidneys, intestines, heart, and brain. Intermediate infusion rates (from 2 to 10 micrograms/kg/min) continue to stimulate dopaminergic receptors, but also activates beta-1 receptors, increasing myocardial contractility and electrical conductivity in the heart leading to increased cardiac output. Higher doses cause potent vasoconstriction and increased blood pressure via the adrenergic receptors alpha-1, beta-1, and beta-2.<ref name=":0">{{Citation|title=Dopamine Hydrochloride and Dextrose Injection|url=http://dx.doi.org/10.31003/uspnf_m28028_05_01|publisher=U.S. Pharmacopeial Convention|access-date=2024-01-09}}</ref> <ref>{{Cite journal|last=Overgaard|first=Christopher B.|last2=Džavík|first2=Vladimír|date=2008-09-02|title=Inotropes and Vasopressors|url=http://dx.doi.org/10.1161/circulationaha.107.728840|journal=Circulation|volume=118|issue=10|pages=1047–1056|doi=10.1161/circulationaha.107.728840|issn=0009-7322}}</ref><ref>{{Cite journal|last=Stratton|first=Leeanne|last2=Berlin|first2=David A.|last3=Arbo|first3=John E.|date=2017-02|title=Vasopressors and Inotropes in Sepsis|url=http://dx.doi.org/10.1016/j.emc.2016.09.005|journal=Emergency Medicine Clinics of North America|volume=35|issue=1|pages=75–91|doi=10.1016/j.emc.2016.09.005|issn=0733-8627}}</ref>

==== Adverse effects ====

* Ventricular arrhythmias
* Atrial fibrillation
* PVCs and PACs
* Sinus tachycardia
* Hypotension
* Hypertension
* Headache
* Vomiting
* Dyspnea
* Anxiety
* Piloerection
* Azotemia
* Peripheral vasoconstriction and tissue necrosis

=== Pharmacokinetics ===

* Widely distributed throughout the body, but does not cross the blood-brain barrier
* Metabolized in the liver, kidneys, and plasma by monoamine oxidase and catechol-O-methyltransferase<ref name=":0" />
* 25% is taken up into adrenergic nerve terminals, where it is hydroxylated to form norepinephrine<ref name=":0" />
* Excretion of metabolites and conjugates in the urine
* Onset of action: 5 minutes
* Duration of action: 10 minutes

== Chemistry and formulation ==
Dopamine is the prototypical endogenous catecholamine.

== History ==

== References ==

[[Category:Drug reference]]