Sterile Dopamine Concentrate 200mg/5ml

Indications

• Cardiogenic shock
• Severe hypotension
• Reversal of hypotension from spinal or epidural anaesthesia

Dosage

Children: Neonate: Initially 3 micrograms/kg/minute (maximum dose 20 micrograms/kg/minute), adjusted according to response.

Adults: Initially 2–5 micrograms/kg/minute, titrated according to response. The maintenance dose is typically between 3-10 micrograms/kg/minute, adjusted based on individual patient response.

Mechanism of action

Dopamine acts on specific adrenergic receptors, predominantly beta1 receptors in cardiac muscle, leading to increased myocardial contractility. At low doses, it also stimulates dopaminergic receptors, resulting in vasodilation of renal and mesenteric blood vessels, which enhances renal blood flow. As doses increase, dopamine's vasopressor effects become more pronounced due to its action on alpha-adrenergic receptors, causing peripheral vasoconstriction.

Pharmacodynamics

Dopamine's pharmacodynamics are dose-dependent. At low doses (1-5 micrograms/kg/min), it primarily acts on dopaminergic receptors, promoting renal vasodilation and enhancing glomerular filtration rate. At moderate doses (5-10 micrograms/kg/min), it increases cardiac contractility without significantly affecting heart rate. At high doses (>10 micrograms/kg/min), it predominantly stimulates alpha-adrenergic receptors, leading to increased systemic vascular resistance and blood pressure.

Pharmacokinetics

Dopamine is administered intravenously and has a rapid onset of action. It is metabolized in the body by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) to inactive metabolites. Its half-life is approximately 2 minutes, necessitating continuous infusion for sustained effects. The drug is excreted primarily in the urine as metabolites.

Contra-indications

• Phaeochromocytoma
• Tachyarrhythmias
• Severe peripheral vascular disease

Adverse effects

• Angina pectoris
• Anxiety
• Arrhythmias
• Azotaemia
• Cardiac conduction disorders
• Dyspnoea
• Headache
• Hypertension
• Mydriasis
• Nausea
• Palpitations
• Piloerection
• Polyuria
• Tremor
• Vomiting

Interactions

• Sympathomimetics
• Inotropic agents
• MAO inhibitors
• Certain antidepressants

Precautions

• Use the lowest effective dose to minimize the risk of peripheral ischaemia.
• Invasive monitoring is recommended during administration in critical care settings.
• Caution in patients with pre-existing cardiovascular disease.

Pregnancy

No evidence of harm in animal studies; manufacturer advises use only if potential benefit outweighs risk.

Breast-feeding

May suppress lactation; not known to be harmful.

Storage

Store in a refrigerator (2–8°C); consult product literature for storage conditions after dilution.

Formulations

• Dopamine hydrochloride solution for infusion

Indications

• Acute heart failure
• Cardiogenic shock
• Septic shock
• Hypotension
• Renal failure (to enhance renal perfusion)

Dosage

Adults: Dopamine is typically administered as

Mechanism of action

Dopamine acts as a precursor to norepinephrine and exerts its effects through agonist action on beta-adrenoceptors, leading to positive chronotropic and inotropic effects on the heart. At low infusion rates (0.5-2 ug/kg/min), dopamine primarily stimulates dopaminergic receptors, enhancing renal and mesenteric blood flow. At higher doses (>4-6 ug/kg/min), it stimulates alpha-adrenergic receptors, causing vasoconstriction and increased afterload. The effects are mediated through increased cyclic adenosine monophosphate (cAMP) levels, enhancing calcium transport within cardiac cells.

Pharmacodynamics

Dopamine's pharmacodynamic profile includes its ability to increase heart rate and contractility via beta-1 receptor stimulation. It also improves renal perfusion at lower doses through D1 receptor activation. The physiological effects depend on the infusion rate, with lower rates promoting renal blood flow and higher rates leading to increased peripheral vascular resistance and blood pressure due to alpha-adrenergic receptor activation. The drug's action is dose-dependent, with significant implications for its clinical use in various forms of shock and heart failure.

Pharmacokinetics

Dopamine is administered intravenously and has a short half-life, typically around 2 minutes, due to rapid metabolism by monoamine oxidase and catechol-O-methyltransferase. It is distributed throughout the body, primarily affecting the central nervous system and cardiovascular system. The onset of action is immediate upon infusion, and the effects are closely tied to the infusion rate, requiring careful monitoring during administration to achieve the desired therapeutic outcomes.

Interactions

• antipsychotics, second generation (amisulpride, olanzapine, paliperidone, quetiapine, risperidone) + dopamine receptor agonists: Severe (decreases effects)
• benperidol + dopamine receptor agonists: Severe (decreases effects)
• droperidol + dopamine receptor agonists: Severe (decreases effects)
• flupentixol + dopamine receptor agonists: Severe (decreases effects)
• haloperidol + dopamine receptor agonists: Severe (decreases effects)
• phenothiazines + dopamine receptor agonists: Severe (decreases effects)
• pimozide + dopamine receptor agonists: Severe (decreases effects)
• sulpiride + dopamine receptor agonists: Severe (decreases effects)
• zuclopenthixol + dopamine receptor agonists: Severe (decreases effects)
• ergometrine + dopamine: Severe (increases risk of peripheral vasoconstriction)

Pregnancy

Dopamine should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Dopamine is excreted in human milk. Caution is advised when administering to nursing women.

Storage

Store in a cool, dry place away from light. Keep out of reach of children.

Indications

• Adjustment of pH in pharmaceutical formulations
• Facilitation of drug absorption
• Used in sterile preparations

Dosage

Children: Refer to specific product guidelines for dosing information, as hydrochloric acid is typically used in a controlled setting based on formulation requirements.

Adults: Refer to specific product guidelines for dosing information, as hydrochloric acid is typically used in a controlled setting based on formulation requirements.

Mechanism of action

Hydrochloric acid dissociates in aqueous solution to release hydrogen ions (H+), leading to a decrease in pH. This acidic environment promotes the activation of pepsinogen to pepsin, an enzyme essential for protein digestion. Additionally, the acidity aids in the absorption of certain minerals and drugs that require an acidic environment for optimal bioavailability.

Pharmacodynamics

The primary pharmacodynamic action of hydrochloric acid is the maintenance of gastric acidity, which is essential for normal digestive processes. The acidic environment helps in denaturing proteins, activating digestive enzymes, and providing a barrier against pathogenic microorganisms. Its effects can influence the absorption and efficacy of various medications, particularly those that are pH-dependent.

Pharmacokinetics

Hydrochloric acid does not undergo significant systemic absorption when used in its normal contexts, as it acts locally within the gastrointestinal tract. The amount of hydrochloric acid produced by the stomach varies with food intake and physiological needs. It is secreted by parietal cells in the gastric mucosa, and its secretion is regulated by neural, hormonal, and local factors. The half-life of hydrochloric acid is not applicable as it is continuously produced and neutralized within the gastrointestinal tract.

Contra-indications

• Hypersensitivity to hydrochloric acid or any of its components
• Severe renal impairment
• Active gastrointestinal bleeding

Adverse effects

• Abdominal pain
• Diarrhea
• Nausea
• Vomiting
• Esophageal irritation
• Gastric mucosal irritation
• Electrolyte imbalances

Interactions

• May interact with alkaline substances, potentially neutralizing hydrochloric acid
• Caution with antacids as they may affect the efficacy of hydrochloric acid

Precautions

• Use with caution in patients with a history of gastritis or gastric ulcers
• Monitor electrolytes in prolonged use
• Use cautiously in patients with respiratory conditions due to potential aspiration risks

Pregnancy

Hydrochloric acid is classified as a category C drug. Use during pregnancy only if clearly needed and the potential benefits justify the risks to the fetus.

Breast-feeding

There is limited data on the excretion of hydrochloric acid in human milk. Use with caution during breastfeeding.

Storage

Store in a cool, dry place away from direct sunlight and heat. Ensure the container is tightly closed.

Formulations

• Oral solutions
• Injectable forms
• Tablets

Dosage

Children: Refer to specific guidelines for pediatric dosing; consult the BNF for Children for accurate dosage information.

Adults: Refer to specific guidelines for use; dosage may vary based on the context of use.

Mechanism of action

Hydroxide ions act primarily as bases, neutralizing acids to form water and salts. They participate in various biochemical pathways, including selenium metabolism and the degradation of reactive oxygen species. Hydroxide can influence enzyme activity and stability by altering the pH of the environment, thereby affecting metabolic reactions.

Pharmacodynamics

Hydroxide ions can impact biological processes by changing the local pH, which influences enzyme activity, ion transport, and the solubility of other compounds. Their ability to neutralize acids can help regulate physiological pH, contributing to homeostasis in living organisms.

Pharmacokinetics

As an inorganic ion, hydroxide does not undergo traditional pharmacokinetic processes like absorption, distribution, metabolism, or excretion. Instead, it is rapidly equilibrated in biological fluids and participates in acid-base reactions, having immediate effects on the local environment.

Pregnancy

There is limited information regarding the use of hydroxide during pregnancy. Consult a healthcare professional for advice.

Breast-feeding

Limited data is available on the excretion of hydroxide in breast milk. Consult a healthcare professional before use.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Pain management
• Vaccination
• Antibiotic therapy
• Hormonal therapies
• Anesthesia
• Nutritional support
• Chemotherapy

Dosage

Children: Refer to specific drug guidelines for paediatric dosing, as it requires careful consideration of weight and age.

Adults: Refer to specific drug guidelines for adult dosing, as it varies widely depending on the medication and clinical condition.

Mechanism of action

The mechanism of action of injected drugs varies widely based on the specific medication being administered. Generally, injected drugs enter the bloodstream directly, allowing them to circulate rapidly throughout the body. For instance, antibiotics may work by inhibiting bacterial cell wall synthesis, while analgesics may modulate pain pathways in the central nervous system. Each drug has unique pathways through which it achieves its therapeutic effects.

Pharmacodynamics

Pharmacodynamics refers to the effects of drugs on the body and their mechanisms of action. For injectable medications, effects can be immediate or delayed, depending on the drug's formulation and route of administration. Factors influencing pharmacodynamics include receptor affinity, drug concentration, and the presence of other substances that may enhance or inhibit the drug's effects. For example, some injectable drugs may require specific receptors to exert their effects, while others may have a broader range of action.

Pharmacokinetics

Pharmacokinetics involves the absorption, distribution, metabolism, and excretion (ADME) of injected drugs. After administration, drugs are rapidly absorbed into the bloodstream, leading to quick therapeutic effects. The distribution depends on factors such as blood flow, tissue permeability, and protein binding. Drugs are metabolized primarily in the liver and excreted through the kidneys or bile. The pharmacokinetic profile can vary widely based on the drug's chemical nature, dosage, and individual patient factors.

Pregnancy

Safety during pregnancy depends on the specific injection and its active ingredients. It is essential to consult a healthcare professional for guidance.

Breast-feeding

The safety of injections during breastfeeding varies by the specific medication. It is recommended to seek advice from a healthcare provider.

Storage

Store injections as per manufacturer's guidelines, usually in a cool, dry place away from direct sunlight. Some may require refrigeration.

Indications

• Food preservation
• Antioxidant in pharmaceutical formulations
• Reducing agent in chemical processes
• Component in certain injectable medications

Dosage

Children: Refer to the specific product information or clinical guidelines for dosing recommendations, as dosages can vary based on formulation and intended use.

Adults: Refer to the specific product information or clinical guidelines for dosing recommendations, as dosages can vary based on formulation and intended use.

Mechanism of action

Metabisulphite acts as a reducing agent through its ability to donate electrons, leading to the reduction of other compounds. It reacts with free radicals and other reactive species, thus preventing oxidative damage to cells and tissues. The sulfite ion can also interact with thiol groups in proteins, altering their structure and function, which can have both beneficial and adverse effects depending on the context.

Pharmacodynamics

The pharmacodynamics of metabisulphite involve its antioxidant properties, which help protect cells from oxidative stress. By scavenging free radicals, it contributes to the stabilization of various compounds, prolonging their efficacy. However, its potential to induce oxidative stress and trigger allergic reactions in susceptible individuals is also recognized, necessitating caution in its use.

Pharmacokinetics

Metabisulphite is rapidly absorbed when administered, and its pharmacokinetic profile is influenced by the route of administration. It is metabolized to sulfite and further to sulfate in the liver. The elimination half-life is relatively short, with renal excretion being the primary route of elimination. Individuals with compromised renal function may have altered clearance rates, requiring careful monitoring.

Contra-indications

• Hypersensitivity to metabisulfite or any other sulfite compounds
• Asthma or a history of sulfite sensitivity

Adverse effects

• Allergic reactions, including anaphylaxis
• Respiratory distress in sensitive individuals
• Skin reactions such as rashes or urticaria

Interactions

• May interact with certain medications that can cause allergic reactions
• Possible enhancement of the effects of other sulfite-containing medications

Precautions

• Use with caution in patients with asthma or sulfite sensitivity
• Monitor for respiratory reactions in susceptible individuals

Pregnancy

Safety during pregnancy has not been established; use only if clearly needed.

Breast-feeding

Safety during breastfeeding is not well established; use with caution.

Storage

Store in a cool, dry place, away from light and moisture.

Formulations

• Powder for solution
• Tablet form
• Inhalation solution

Indications

• Cryotherapy for the destruction of abnormal tissue
• Treatment of warts, moles, and other skin lesions
• Nitrogen narcosis in diving

Dosage

Children: Refer to the BNF for Children for appropriate dosing recommendations in paediatric patients.

Adults: For cryotherapy, the dosage and duration depend on the specific condition being treated and should be determined by the healthcare provider. Refer to specific guidelines for each condition.

Mechanism of action

In cryotherapy, the mechanism of action involves three stages: heat transfer, cell injury, and inflammation. The boiling point of liquid nitrogen is -196°C, which initiates heat transfer, leading to cell injury during the thawing process. The inflammation stage follows, characterized by edema and erythema, resulting from cellular death and contributing to local cell destruction. Additionally, nitrogen can cause direct toxic effects on brain functions, leading to nitrogen narcosis, which impairs cognitive abilities and motor functions due to its impact on nerve conduction.

Pharmacodynamics

Nitrogen's pharmacodynamics relate to its behavior in cryotherapy and asphyxiation. In cryotherapy, it induces tissue destruction through rapid cooling, leading to apoptosis of abnormal cells. In high-pressure environments, nitrogen narcosis affects the central nervous system, producing symptoms similar to alcohol intoxication, ultimately decreasing reasoning, decision-making abilities, and manual dexterity.

Pharmacokinetics

Nitrogen does not undergo metabolism in the traditional sense, as it is an inert gas at physiological conditions. Its pharmacokinetics involve physical principles of gas exchange and partial pressures. In the case of nitrogen narcosis, the effects are influenced by the partial pressure of nitrogen in the bloodstream, which increases with depth during diving. Nitrogen is primarily eliminated from the body through respiration.

Adverse effects

• Narcotic effect at high pressures
• Stupor or euphoria
• Decreased motor function and manual dexterity
• Asphyxiation due to oxygen displacement

Precautions

• Careful monitoring in environments with high nitrogen pressures
• Avoidance of rapid ascents in diving to prevent nitrogen narcosis
• Use in controlled settings to prevent asphyxiation risks

Pregnancy

Nitrogen is generally considered safe in terms of direct effects during pregnancy; however, the safety of exposure in high-pressure environments should be assessed.

Breast-feeding

Nitrogen is not known to affect breastfeeding; however, caution is recommended in environments where nitrogen levels may displace oxygen.

Storage

Store in a cool, dry place away from heat sources; liquid nitrogen should be handled with care due to extreme cold.

Formulations

• Liquid nitrogen
• Nitrogen gas (compressed)

Mechanism of action

Dopamine is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system. Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings. In the brain, dopamine acts as an agonist to the five dopamine receptor subtypes (D1, D2, D3, D4, D5). Dopamine acts on cardiac beta-1-adrenergic receptors and has dosage-dependent effects on peripheral receptors. Dopamine receptors are activated at a low infusion rate (0.5-2 ug/kg/min). At a rate > 4-6 ug/kg/min, peripheral alpha-adrenergic receptors are activated, and vasoconstriction and increased afterload may occur. The effects that dopamine produces in the body are directly related to its actions on alpha, beta, and dopaminergic receptor sites. When these receptors are stimulated cyclic adenosine monophosphate levels increase, increasing calcium transport into the cell. The amount of dopamine determines which receptors are predominantly stimulated. At infusion rates more than 5 to 10 ug/kg/minute, alpha-receptor stimulation predominates, resulting in peripheral vasoconstriction, with a rise in blood pressure. At infusion rates greater than 20 ug/kg/minute, the vasoconstrictive effect can be greater than the beta1 effect. The cardiovascular effects of dopamine are mediated by several distinct types of receptors that vary in their affinity for dopamine. At low concentrations, the primary interaction of dopamine is with vascular D1 receptors, especially in the renal, mesenteric, and coronary beds. By activating adenylyl cyclase and raising intracellular concentrations of cyclic AMP, D1 receptor stimulation leads to vasodilation. Infusion of low doses of dopamine causes an increase in glomerular filtration rate, renal blood flow, and Na+ excretion. Activation of D1 receptors on renal tubular cells decreases sodium transport by cAMP-dependent and cAMP-independent mechanisms. Increasing cAMP production in the proximal tubular cells and the medullary part of the thick ascending limb of the loop of Henle inhibits the Na+-H+ exchanger and the Na+,K+-ATPase pump. The renal tubular actions of dopamine that cause natriuresis may be augmented by the increase in renal blood flow and the small increase in the glomerular filtration rate that follow its administration. The resulting increase in hydrostatic pressure in the peritubular capillaries and reduction in oncotic pressure may contribute to diminished reabsorption of sodium by the proximal tubular cells. At somewhat higher concentrations, dopamine exerts a positive inotropic effect on the myocardium, acting on beta1 adrenergic receptors. Dopamine also causes the release of norepinephrine from nerve terminals, which contributes to its effects on the heart. Tachycardia is less prominent during infusion of dopamine than of isoproterenol. Dopamine usually increases systolic blood pressure and pulse pressure and either has no effect on diastolic blood pressure or increases it slightly. Total peripheral resistance usually is unchanged when low or intermediate doses of dopamine are given, probably because of the ability of dopamine to reduce regional arterial resistance in some vascular beds, such as mesenteric and renal, while causing only minor increases in others. At high concentrations, dopamine activates vascular alpha1 receptors, leading to more general vasoconstriction. For more Mechanism of Action (Complete) data for DOPAMINE (9 total), please visit the HSDB record page.

Pharmacodynamics

Dopamine is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). It is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system, especially in the nigrostriatal tract, and in a few peripheral sympathetic nerves. Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings.

Mechanism of action

In cryotherapy, mechanism of action could be classified into three stages: 1. heat transfer, 2. cell injury and 3. inflammation. Boiling point of liquid nitrogen is -196°C, which is the responsible for creating the initial stage which is heat transfer. The second stage is cell injury which is induced during thawing conditions of the cells. The last step in the cryotherapy is the inflammation stage which is characterized by edema and erythema. Inflammation occurs as a result of cellular death and it helps in local cell destruction. ... Nitrogen also has a direct toxic action of its own, affecting brain functions and inducing a stupor or euphoria. Nitrogen narcosis ("rapture of the deep" or "the martini effect") results from a direct toxic effect of high nitrogen pressure on nerve conduction and produces effects similar to alcohol intoxication. Complex reasoning, decision-making ability, motor function, and manual dexerity decrease. Individuals vary in this response widely, but it typically can be noticed among divers at depths exceeding 100 ft (30 m). For example, certain individuals experience no effect at depths of < or = 130 ft, whereas others feel some effect at around 80 ft. Nonetheless, the narcotic effect increases with increasing depth so that each additional 50 ft incrementally produces the effect of "another martini". A simple asphyxiant, nitrogen's main toxicty arises from its ability to displace O2 and generate an atmosphere that does not support the chemical reactions needed for maintenance of life. The displacement of O2 can be complete or incomplete, leading to varying degrees of hypoxia. Nitrogen is an inert substance and does not exert a direct toxicological effect. Nitrogen acts by the physiological effect of simple asphyxia on the target species within a Controlled Atmosphere Treatment (CAT) bubble. The biocide action of nitrogen is due to its displacement of oxygen from an atmospheric oxygen level of 20.8% to levels < 0.2% v/v in the CAT bubble. The level of oxygen is the critical factor. Victims exposed to atmospheres deficient in oxygen, i.e. < 19%, will begin to display signs and symptoms of oxygen-deficient exposure of air due to an increase in nitrogen.