This document provides an overview of the pharmacology of various cardiovascular agents, including cholinergic drugs, adrenergic drugs, catecholamines, and vasodilators. It discusses the mechanisms and therapeutic uses of specific drugs from each class, such as neostigmine, phenylephrine, dobutamine, milrinone, and levosimendan. The document also compares the effects and clinical applications of different catecholamines like norepinephrine and epinephrine.
alpha blocker, receptors, antagonist, mechanism of actionNishiThawait
Alpha blockers work by blocking alpha-adrenergic receptors in the sympathetic nervous system. They are classified as non-selective or selective alpha-1 blockers. Non-selective blockers like phenoxybenzamine irreversibly block both alpha-1 and alpha-2 receptors. Selective alpha-1 blockers like prazosin, terazosin and doxazosin are used to treat hypertension and benign prostatic hyperplasia by relaxing blood vessels and bladder neck. Tamsulosin is a selective alpha-1A blocker used for BPH. Ergot alkaloids are partial agonists and antagonists at multiple receptors and cause vasoconstriction.
The document discusses various inotropic agents used to increase the force of cardiac muscle contractions. It describes three main classes of inotropes - cardiac glycosides like digoxin, sympathomimetics like dopamine and dobutamine, and phosphodiesterase inhibitors like amrinone. For each drug, it provides details on mechanisms of action, dosages, administration, indications, contraindications, side effects and nursing considerations. The document provides an in-depth review of inotropic drugs used clinically to enhance cardiac contractility and output.
About pharmacological classification of sympathetic nervus system both sympathomimetics and sympatholytics drug and all about his pharmacokinetics and pharmacodynamics action on body
This document discusses noradrenergic transmission and classification of adrenoceptor agonists and antagonists. It describes the effects of agonists on alpha and beta receptors, including their pharmacological actions on the cardiovascular, respiratory, and other body systems. It also summarizes the clinical uses of adrenoceptor agonists and antagonists for conditions like hypertension, heart disease, glaucoma, and others. Drugs that affect neurotransmitter release and uptake like reserpine, guanethidine, and cocaine are also briefly discussed.
The document discusses various inotropic agents used to increase the force of cardiac muscle contractions including cardiac glycosides like digoxin, sympathomimetic drugs such as epinephrine, dopamine, and dobutamine, and phosphodiesterase inhibitors like amrinone. It provides details on the mechanisms of action, dosages, administration, and side effects of these different classes of inotropic drugs used to enhance cardiac contractility and output in patients with heart failure or shock.
This document discusses the physiology and pharmacology of the sympathetic nervous system and its receptors. It begins by describing epinephrine as an important regulator of heart and vascular responses to exercise and stress. It then defines sympathomimetic drugs as those that mimic epinephrine's actions. The document goes on to detail the different alpha and beta receptor subtypes, their locations, and examples of agonists and antagonists. It discusses sympathetic neurotransmission and the mechanisms of drug-induced effects. Overall, the document provides a comprehensive overview of the sympathetic nervous system and its clinical applications.
This document discusses drugs that act on the autonomic nervous system. It covers neurotransmitters in the somatic and autonomic nervous systems like acetylcholine and catecholamines. It then categorizes and describes drugs that act on the sympathetic and parasympathetic nervous systems, including sympathomimetics, sympathomolytics, parasympathomimetics, and parasympatholytics. Specific drugs are discussed in detail including their mechanisms, uses, doses, and side effects.
This document discusses various alpha and beta receptor antagonists. It provides details on their mechanisms of action, pharmacokinetics, clinical uses and side effects. Regarding alpha antagonists, it describes how they bind to alpha receptors to block catecholamine and sympathomimetic action. It also explains the differences between selective and non-selective alpha1 and alpha2 antagonists. For beta antagonists, it outlines their competitive inhibition of beta receptors and categorizes drugs as non-selective or cardioselective. The document discusses cardiovascular, respiratory, metabolic and other effects of both classes of drugs.
alpha blocker, receptors, antagonist, mechanism of actionNishiThawait
Alpha blockers work by blocking alpha-adrenergic receptors in the sympathetic nervous system. They are classified as non-selective or selective alpha-1 blockers. Non-selective blockers like phenoxybenzamine irreversibly block both alpha-1 and alpha-2 receptors. Selective alpha-1 blockers like prazosin, terazosin and doxazosin are used to treat hypertension and benign prostatic hyperplasia by relaxing blood vessels and bladder neck. Tamsulosin is a selective alpha-1A blocker used for BPH. Ergot alkaloids are partial agonists and antagonists at multiple receptors and cause vasoconstriction.
The document discusses various inotropic agents used to increase the force of cardiac muscle contractions. It describes three main classes of inotropes - cardiac glycosides like digoxin, sympathomimetics like dopamine and dobutamine, and phosphodiesterase inhibitors like amrinone. For each drug, it provides details on mechanisms of action, dosages, administration, indications, contraindications, side effects and nursing considerations. The document provides an in-depth review of inotropic drugs used clinically to enhance cardiac contractility and output.
About pharmacological classification of sympathetic nervus system both sympathomimetics and sympatholytics drug and all about his pharmacokinetics and pharmacodynamics action on body
This document discusses noradrenergic transmission and classification of adrenoceptor agonists and antagonists. It describes the effects of agonists on alpha and beta receptors, including their pharmacological actions on the cardiovascular, respiratory, and other body systems. It also summarizes the clinical uses of adrenoceptor agonists and antagonists for conditions like hypertension, heart disease, glaucoma, and others. Drugs that affect neurotransmitter release and uptake like reserpine, guanethidine, and cocaine are also briefly discussed.
The document discusses various inotropic agents used to increase the force of cardiac muscle contractions including cardiac glycosides like digoxin, sympathomimetic drugs such as epinephrine, dopamine, and dobutamine, and phosphodiesterase inhibitors like amrinone. It provides details on the mechanisms of action, dosages, administration, and side effects of these different classes of inotropic drugs used to enhance cardiac contractility and output in patients with heart failure or shock.
This document discusses the physiology and pharmacology of the sympathetic nervous system and its receptors. It begins by describing epinephrine as an important regulator of heart and vascular responses to exercise and stress. It then defines sympathomimetic drugs as those that mimic epinephrine's actions. The document goes on to detail the different alpha and beta receptor subtypes, their locations, and examples of agonists and antagonists. It discusses sympathetic neurotransmission and the mechanisms of drug-induced effects. Overall, the document provides a comprehensive overview of the sympathetic nervous system and its clinical applications.
This document discusses drugs that act on the autonomic nervous system. It covers neurotransmitters in the somatic and autonomic nervous systems like acetylcholine and catecholamines. It then categorizes and describes drugs that act on the sympathetic and parasympathetic nervous systems, including sympathomimetics, sympathomolytics, parasympathomimetics, and parasympatholytics. Specific drugs are discussed in detail including their mechanisms, uses, doses, and side effects.
This document discusses various alpha and beta receptor antagonists. It provides details on their mechanisms of action, pharmacokinetics, clinical uses and side effects. Regarding alpha antagonists, it describes how they bind to alpha receptors to block catecholamine and sympathomimetic action. It also explains the differences between selective and non-selective alpha1 and alpha2 antagonists. For beta antagonists, it outlines their competitive inhibition of beta receptors and categorizes drugs as non-selective or cardioselective. The document discusses cardiovascular, respiratory, metabolic and other effects of both classes of drugs.
The document discusses the pharmacokinetics and pharmacodynamics of intravenous anesthetic agents. It covers topics like mechanism of action, formulations, metabolism, pharmacokinetics, pharmacodynamics, doses, uses and side effects of propofol, thiopentone, ketamine, etomidate. It explains that these agents work primarily via the GABA receptor or by antagonizing NMDA receptors. Their cardiovascular, respiratory and central nervous system effects are discussed in detail.
This document discusses drugs that modulate the acetylcholinesterase enzyme. It begins by describing acetylcholine and how it is synthesized and degraded by acetylcholinesterase. It then discusses anticholinesterases, which are drugs that inhibit acetylcholinesterase, increasing acetylcholine levels. The main classes described are reversible inhibitors like carbamates and tacrine, and irreversible inhibitors like organophosphates. It provides details on the mechanisms, pharmacology, individual drug properties, uses and treatment of organophosphate poisoning with atropine and pralidoxime.
This document summarizes adrenergic agonists and antagonists. It describes the synthesis and metabolism of catecholamines like dopamine, norepinephrine, and epinephrine. It also discusses the different adrenergic receptor types (alpha and beta), their locations and functions. Various adrenergic drugs are classified and their mechanisms, effects, uses, and adverse effects outlined, including epinephrine, norepinephrine, dopamine, dobutamine, dopexamine, fenoldopam, phenylephrine, clonidine and others.
This document discusses the hormones adrenaline and noradrenaline. It describes their biosynthesis, mechanisms of action, effects on different organs, clinical uses including anaphylaxis and cardiac arrest, dosages, side effects and comparisons between the two hormones. Adrenaline acts on alpha and beta receptors and has effects like increased heart rate and bronchodilation. Noradrenaline predominantly acts on alpha receptors, causing potent vasoconstriction and increasing blood pressure without bronchodilation. Both are used to treat hypotension but noradrenaline is preferred for septic shock.
This document provides an overview of adrenergic drugs. It begins by discussing the endogenous catecholamines - norepinephrine, epinephrine, and dopamine - and their effects. It then classifies adrenergic receptors and describes the response of effector organs. The document proceeds to classify and describe the mechanisms and effects of various adrenergic drugs, including direct-acting, indirect-acting, and mixed sympathomemetics. It discusses individual drugs like epinephrine, norepinephrine, dopamine, isoproterenol, and clonidine. The document provides a detailed but technical summary of adrenergic pharmacology.
Pharmacology of the Autonomic Nervous SystemDiogo Capela
The document discusses the autonomic nervous system and pharmacology of its sympathetic and parasympathetic divisions. It describes the pre- and post-ganglionic fibers, neurotransmitters, and receptors involved. Catecholamines, adrenergic receptors, and drugs that target the sympathetic system like agonists, antagonists, and their effects are summarized. Parasympathetic muscarinic and nicotinic receptors, cholinergic drugs like direct and indirect agonists, and anticholinergic drugs are also outlined.
The document discusses the autonomic nervous system and pharmacology of drugs that act on it. It covers the cholinergic and adrenergic systems, describing receptors, endogenous neurotransmitters, and exogenous drugs that act on these systems. For the cholinergic system, it details acetylcholine, cholinoceptors, cholinomimetic and anticholinergic drugs. It provides information on mechanism of action, pharmacological effects, clinical uses and pharmacokinetics of representative drugs from each class.
This document provides an overview of the autonomic nervous system (ANS) and pharmacology of drugs that act on the cholinergic and adrenergic systems. It discusses cholinoceptors, cholinergic drugs like acetylcholine and their actions. It also covers anticholinergic drugs like atropine that act as antagonists at muscarinic receptors. Ganglionic stimulants and blockers are mentioned. Uses of cholinergic and anticholinergic drugs are summarized.
1) The document provides information on inotropes and vasopressors including their classification, sites of action, clinical effects, indications, and doses. It discusses catecholamines like adrenaline, noradrenaline, dopamine, and dobutamine. It also covers phosphodiesterase inhibitors, vasopressin, ephedrine, metaraminol, phenylephrine, methoxamine, and digoxin.
2) The document concludes with recommendations on first and second line vasopressor/inotropic agents for different clinical situations like septic shock, heart failure, cardiogenic shock, anaphylactic shock, and anesthesia-induced hypotension.
In this presentation we will discuss Parkinsonism and other movement disorders, Pathophysiology of parkinsonism and its types, drugs used in Parkinsonism and their pharmacology and briefly discuss the drugs used to treat other movement disorders like tourettes syndrome, Huntington chorea etc.
The document discusses adrenergic drugs and their mechanisms and uses. It describes how the sympathetic nervous system activates the fight or flight response through neurotransmitters like epinephrine and norepinephrine. It then covers different classes of adrenergic drugs including sympathomimetics that mimic sympathetic stimulation, vasopressors that constrict blood vessels, bronchodilators for asthma, and anorectics formerly used for weight loss. Specific drugs discussed include epinephrine, dopamine, dobutamine, ephedrine, amphetamines, and selective beta-2 agonists. A variety of conditions treated and contraindications are provided.
This document discusses vasoconstrictors which are drugs added to local anesthetics to prolong their duration and effectiveness. It classifies vasoconstrictors based on their chemical structure and mode of action. Epinephrine is described as the most commonly used vasoconstrictor due to its direct effects on alpha-1 and beta-2 receptors, which causes vasoconstriction and increased duration of anesthesia. Side effects are also discussed, noting the risks of hypertension, tachycardia and cardiac issues if overused. Maximum safe doses are provided for different local anesthetic solutions containing epinephrine or other vasoconstrictors like norepinephrine and phenylephrine.
Sympathomimetic drugs mimic the actions of norepinephrine and epinephrine. They can act directly on alpha and beta adrenoceptors or indirectly by releasing norepinephrine from neurons. These drugs have many therapeutic uses including treating hypotension, cardiogenic shock, congestive heart failure, bronchial asthma, glaucoma, and more. The most important classes are epinephrine, norepinephrine, dopamine, dobutamine, and selective beta-2 agonists. They work by various mechanisms like increasing cardiac output, relaxing bronchioles, and constricting blood vessels.
Dr. Viraj Shinde's document provides an overview of sympathommimetic drugs. It defines them as drugs that mimic the actions of norepinephrine or epinephrine. It discusses the sympathetic and parasympathetic nervous systems, classification of sympathommimetic drugs, examples like epinephrine, mechanisms of action, therapeutic uses, and adverse effects. Receptor types, locations, agonists, and antagonists are outlined. The document also covers neurotransmitters, their criteria and the neurotransmission process. Specific drugs discussed include dopamine, isoproterenol, dobutamine, fenoldopam, phenylephrine, clonidine, and beta-2 selective agents.
Dr. Viraj Ashok Shinde's document discusses sympathommimetic drugs. It defines them as drugs that partially or completely mimic the actions of norepinephrine or epinephrine. It describes the sympathetic and parasympathetic nervous systems, classifications of sympathommimetic drugs, examples like epinephrine, mechanisms of action, therapeutic uses, and side effects. The summary provides an overview of the key topics covered in the document.
The term inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle (myocardial contractility). However, it can also refer to pathological conditions. For example, enlarged heart muscle (ventricular hypertrophy) can increase inotropic state, whereas dead heart muscle (myocardial infarction) can decrease it.
This document provides information on antihypertensive drugs. It defines hypertension as elevated blood pressure and discusses its classification. The mechanisms involved in hypertension development include increased heart rate, stroke volume, cardiac output, peripheral vascular resistance, and vasoconstriction. Antihypertensive drug classes include those that inhibit the renin-angiotensin-aldosterone system, sympathetic nervous system, calcium channels, and drugs that cause vasodilation or diuresis. Specific drug mechanisms and examples from each class are described along with their advantages and adverse effects in summarizing the pharmacology of antihypertensive treatment options.
This document discusses the adrenergic system including adrenoceptor physiology, adrenergic agonists and antagonists. It describes the different types of adrenoceptors (alpha and beta), their locations and responses. It then discusses various adrenergic agonists like epinephrine, norepinephrine, phenylephrine, clonidine and dexmedetomidine and provides their mechanisms of action and dosages. Finally it covers various adrenergic antagonists like phentolamine, labetalol, esmolol, metoprolol and propranolol, describing their receptor selectivities, durations of action and dosages.
Adrenaline and noradrenaline are catecholamines that act as hormones and neurotransmitters. They are synthesized from tyrosine and phenylalanine through a series of enzymatic reactions. Adrenaline acts on alpha-1, alpha-2, and beta receptors and causes effects like increased heart rate, vasoconstriction, bronchodilation and glycogenolysis. Noradrenaline predominantly acts on alpha-1 and beta-1 receptors, causing potent vasoconstriction with little bronchodilation. Both are used to treat hypotension, cardiac arrest and anaphylaxis. Their administration must be closely monitored due to risks of hypertension, arrhythmias and tissue necrosis from vasoconstrict
The document discusses the pharmacokinetics and pharmacodynamics of intravenous anesthetic agents. It covers topics like mechanism of action, formulations, metabolism, pharmacokinetics, pharmacodynamics, doses, uses and side effects of propofol, thiopentone, ketamine, etomidate. It explains that these agents work primarily via the GABA receptor or by antagonizing NMDA receptors. Their cardiovascular, respiratory and central nervous system effects are discussed in detail.
This document discusses drugs that modulate the acetylcholinesterase enzyme. It begins by describing acetylcholine and how it is synthesized and degraded by acetylcholinesterase. It then discusses anticholinesterases, which are drugs that inhibit acetylcholinesterase, increasing acetylcholine levels. The main classes described are reversible inhibitors like carbamates and tacrine, and irreversible inhibitors like organophosphates. It provides details on the mechanisms, pharmacology, individual drug properties, uses and treatment of organophosphate poisoning with atropine and pralidoxime.
This document summarizes adrenergic agonists and antagonists. It describes the synthesis and metabolism of catecholamines like dopamine, norepinephrine, and epinephrine. It also discusses the different adrenergic receptor types (alpha and beta), their locations and functions. Various adrenergic drugs are classified and their mechanisms, effects, uses, and adverse effects outlined, including epinephrine, norepinephrine, dopamine, dobutamine, dopexamine, fenoldopam, phenylephrine, clonidine and others.
This document discusses the hormones adrenaline and noradrenaline. It describes their biosynthesis, mechanisms of action, effects on different organs, clinical uses including anaphylaxis and cardiac arrest, dosages, side effects and comparisons between the two hormones. Adrenaline acts on alpha and beta receptors and has effects like increased heart rate and bronchodilation. Noradrenaline predominantly acts on alpha receptors, causing potent vasoconstriction and increasing blood pressure without bronchodilation. Both are used to treat hypotension but noradrenaline is preferred for septic shock.
This document provides an overview of adrenergic drugs. It begins by discussing the endogenous catecholamines - norepinephrine, epinephrine, and dopamine - and their effects. It then classifies adrenergic receptors and describes the response of effector organs. The document proceeds to classify and describe the mechanisms and effects of various adrenergic drugs, including direct-acting, indirect-acting, and mixed sympathomemetics. It discusses individual drugs like epinephrine, norepinephrine, dopamine, isoproterenol, and clonidine. The document provides a detailed but technical summary of adrenergic pharmacology.
Pharmacology of the Autonomic Nervous SystemDiogo Capela
The document discusses the autonomic nervous system and pharmacology of its sympathetic and parasympathetic divisions. It describes the pre- and post-ganglionic fibers, neurotransmitters, and receptors involved. Catecholamines, adrenergic receptors, and drugs that target the sympathetic system like agonists, antagonists, and their effects are summarized. Parasympathetic muscarinic and nicotinic receptors, cholinergic drugs like direct and indirect agonists, and anticholinergic drugs are also outlined.
The document discusses the autonomic nervous system and pharmacology of drugs that act on it. It covers the cholinergic and adrenergic systems, describing receptors, endogenous neurotransmitters, and exogenous drugs that act on these systems. For the cholinergic system, it details acetylcholine, cholinoceptors, cholinomimetic and anticholinergic drugs. It provides information on mechanism of action, pharmacological effects, clinical uses and pharmacokinetics of representative drugs from each class.
This document provides an overview of the autonomic nervous system (ANS) and pharmacology of drugs that act on the cholinergic and adrenergic systems. It discusses cholinoceptors, cholinergic drugs like acetylcholine and their actions. It also covers anticholinergic drugs like atropine that act as antagonists at muscarinic receptors. Ganglionic stimulants and blockers are mentioned. Uses of cholinergic and anticholinergic drugs are summarized.
1) The document provides information on inotropes and vasopressors including their classification, sites of action, clinical effects, indications, and doses. It discusses catecholamines like adrenaline, noradrenaline, dopamine, and dobutamine. It also covers phosphodiesterase inhibitors, vasopressin, ephedrine, metaraminol, phenylephrine, methoxamine, and digoxin.
2) The document concludes with recommendations on first and second line vasopressor/inotropic agents for different clinical situations like septic shock, heart failure, cardiogenic shock, anaphylactic shock, and anesthesia-induced hypotension.
In this presentation we will discuss Parkinsonism and other movement disorders, Pathophysiology of parkinsonism and its types, drugs used in Parkinsonism and their pharmacology and briefly discuss the drugs used to treat other movement disorders like tourettes syndrome, Huntington chorea etc.
The document discusses adrenergic drugs and their mechanisms and uses. It describes how the sympathetic nervous system activates the fight or flight response through neurotransmitters like epinephrine and norepinephrine. It then covers different classes of adrenergic drugs including sympathomimetics that mimic sympathetic stimulation, vasopressors that constrict blood vessels, bronchodilators for asthma, and anorectics formerly used for weight loss. Specific drugs discussed include epinephrine, dopamine, dobutamine, ephedrine, amphetamines, and selective beta-2 agonists. A variety of conditions treated and contraindications are provided.
This document discusses vasoconstrictors which are drugs added to local anesthetics to prolong their duration and effectiveness. It classifies vasoconstrictors based on their chemical structure and mode of action. Epinephrine is described as the most commonly used vasoconstrictor due to its direct effects on alpha-1 and beta-2 receptors, which causes vasoconstriction and increased duration of anesthesia. Side effects are also discussed, noting the risks of hypertension, tachycardia and cardiac issues if overused. Maximum safe doses are provided for different local anesthetic solutions containing epinephrine or other vasoconstrictors like norepinephrine and phenylephrine.
Sympathomimetic drugs mimic the actions of norepinephrine and epinephrine. They can act directly on alpha and beta adrenoceptors or indirectly by releasing norepinephrine from neurons. These drugs have many therapeutic uses including treating hypotension, cardiogenic shock, congestive heart failure, bronchial asthma, glaucoma, and more. The most important classes are epinephrine, norepinephrine, dopamine, dobutamine, and selective beta-2 agonists. They work by various mechanisms like increasing cardiac output, relaxing bronchioles, and constricting blood vessels.
Dr. Viraj Shinde's document provides an overview of sympathommimetic drugs. It defines them as drugs that mimic the actions of norepinephrine or epinephrine. It discusses the sympathetic and parasympathetic nervous systems, classification of sympathommimetic drugs, examples like epinephrine, mechanisms of action, therapeutic uses, and adverse effects. Receptor types, locations, agonists, and antagonists are outlined. The document also covers neurotransmitters, their criteria and the neurotransmission process. Specific drugs discussed include dopamine, isoproterenol, dobutamine, fenoldopam, phenylephrine, clonidine, and beta-2 selective agents.
Dr. Viraj Ashok Shinde's document discusses sympathommimetic drugs. It defines them as drugs that partially or completely mimic the actions of norepinephrine or epinephrine. It describes the sympathetic and parasympathetic nervous systems, classifications of sympathommimetic drugs, examples like epinephrine, mechanisms of action, therapeutic uses, and side effects. The summary provides an overview of the key topics covered in the document.
The term inotropic state is most commonly used in reference to various drugs that affect the strength of contraction of heart muscle (myocardial contractility). However, it can also refer to pathological conditions. For example, enlarged heart muscle (ventricular hypertrophy) can increase inotropic state, whereas dead heart muscle (myocardial infarction) can decrease it.
This document provides information on antihypertensive drugs. It defines hypertension as elevated blood pressure and discusses its classification. The mechanisms involved in hypertension development include increased heart rate, stroke volume, cardiac output, peripheral vascular resistance, and vasoconstriction. Antihypertensive drug classes include those that inhibit the renin-angiotensin-aldosterone system, sympathetic nervous system, calcium channels, and drugs that cause vasodilation or diuresis. Specific drug mechanisms and examples from each class are described along with their advantages and adverse effects in summarizing the pharmacology of antihypertensive treatment options.
This document discusses the adrenergic system including adrenoceptor physiology, adrenergic agonists and antagonists. It describes the different types of adrenoceptors (alpha and beta), their locations and responses. It then discusses various adrenergic agonists like epinephrine, norepinephrine, phenylephrine, clonidine and dexmedetomidine and provides their mechanisms of action and dosages. Finally it covers various adrenergic antagonists like phentolamine, labetalol, esmolol, metoprolol and propranolol, describing their receptor selectivities, durations of action and dosages.
Adrenaline and noradrenaline are catecholamines that act as hormones and neurotransmitters. They are synthesized from tyrosine and phenylalanine through a series of enzymatic reactions. Adrenaline acts on alpha-1, alpha-2, and beta receptors and causes effects like increased heart rate, vasoconstriction, bronchodilation and glycogenolysis. Noradrenaline predominantly acts on alpha-1 and beta-1 receptors, causing potent vasoconstriction with little bronchodilation. Both are used to treat hypotension, cardiac arrest and anaphylaxis. Their administration must be closely monitored due to risks of hypertension, arrhythmias and tissue necrosis from vasoconstrict
How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
A workshop hosted by the South African Journal of Science aimed at postgraduate students and early career researchers with little or no experience in writing and publishing journal articles.
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
7. BETHANECHOL
Not hydrolyzed by acetylcholinesterase but hydrolyzed by other
esterases.
No nicotinic actions.
Has longer duration of action than acetylcholine.
Therapeutic uses: post operative non-obstructive urinary retention &
post-operative ileus.
8. PILOCARPIN
E
- A natural alkaloid, not hydrolyzed by
acetylcholinesterase.
- Marked muscarinic actions:
◦ Eye: loss of accommodation, miosis and lowering the
intraocular pressure (IOP).
◦ Secretary glands: stimulates sweating, salivation and
lacrimation.
-Therapeutic uses:
◦ Glucoma.
◦ Reverse cycloplagic and mydriatic effect of atropine.
-Side effects: CNS disturbance -----> crosses the BBB,
sweating and salivation.
10. NEOSTIGMIN
E
o Synthetic anticholinergic.
o poorly absorbed.
o Polar compound ----> doesn’t cross BBB/CNS.
o Therapeutic uses:
◦ Antidote for tubocurarine poisoning.
◦ Myasthenia gravis.
◦ In the OT for reversal of NMJ blockers.
11. PHYSOSTIGMI
NE
o An alkaloid.
o Well absorbed and penetrate the BBB.
o Therapeutic uses:
◦ Glaucoma.
◦ Atropine poisoning.
◦ Alzheimer s disease.
o Side effects:
◦ CNS: convulsions.
◦ Heart: bradycardia.
◦ Paralysis of skeletal muscles (when overdosed).
12. Edrophonium
The actions of edrophonium are similar to those of neostigmine.
More rapidly absorbed and has a short duration of action.
Used in the diagnosis of myasthenia gravis.
Intravenous injection of edrophonium leads to rapid increase in muscle strength.
Caution: care must be taken, because excess drug may provoke a cholinergic crisis.
Atropine is the antidote.
13. - TACRINE, -
DONEPEZIL,
-
RIVASTIGMI
NE -
GALANTAMI
NE
Patients with Alzheimer's disease have a deficiency
of cholinergic neurons in the CNS ----> development of
anticholinesterases as possible remedies for the loss
of cognitive function
Tacrine
◦ The first to become available.
◦ Replaced by other agents because of hepatotoxicity.
15. ECHOTHIOPHATE
Organophosphate covalently binds via its phosphate group to the serine-oh group
at the active site of acetylcholinesterase.
permanently inactivated
Restoration of acetylcholinesterase activity requires the synthesis of new enzyme
molecules.
The loss of an alkyl group = aging--> impossible for chemical reactivators, such as
pralidoxime, to break the bond between the remaining drug and the enzyme.
17. Major effects
of agonist
binding at
adrenergic
receptors
Alpha-1 receptor:
◦ Smooth muscle contraction, mydriasis
◦ Gq coupled-receptors
Alpha-2 receptor:
◦ Mixed smooth muscle effects
◦ Gi coupled-receptors
Beta-1 receptor:
◦ Gs coupled-receptors
◦ Increased cardiac chronotropic and inotropic effects
Beta-2 receptor: Gs coupled & Gi + Bronchodilation
Beta-3 receptor: Gs coupled & Gi + Increased lipolysis
18. Contraindications
Alpha-1 receptor agonists are relatively contraindicated:
hypertension, bradycardia, prostatic hyperplasia
Alpha-2 receptor agonists cautious with hypotension.
Geriatric patients may be at increased risk of falls due to
the sedating and hypotensive effects.
Beta-1 receptor agonists : arrhythmias.
Beta-2 receptor agonists : hypokalemia.
Norepinephrine :. When dosing halothane or
cyclopropane, there is an increased risk of dangerous
arrhythmias.
Epinephrine :angle-closure glaucoma
20. PHENYLEPHRINE
Direct-acting sympathomimetic amine
Related to epinephrine and ephedrine
Short onset of action (1 to 3 minutes)
Short duration of action (5 to 20 minutes)
Phenylephrine dosing can be via weight-based or non-
weight based infusion with typical dose ranges of 0.1 to 1.5
mcg/kg per minute.
21. ALPHA-2
RECEPTOR
AGONISTS
Methyldopa: hypertension & gestational hypertension.
Clonidine: hypertension & attention deficit hyperactivity
disorder (ADHD).
◦ Non- FDA approved indications : sleep disorders, post-
traumatic stress disorder (PTSD), anxiety, restless leg
syndrome, hot flashes associated with menopause
Dexmedetomidine: sedation in the intensive care unit , no
respiratory depression
22. Dexmedetomidine
Binding to the presynaptic alpha-2 adrenoceptors
Inhibits the release of norepinephrine ---> terminate the
propagation of pain signals.
Activation of the postsynaptic alpha-2 adrenoceptors ---
> sympathetic activity decreases blood pressure and heart
rate.
Volume of distribution : 118 L
◦ Protein binding :94%
◦ Metabolism: Hepatic
◦ Route of elimination: The majority of metabolites are excreted
in the urine
Load: 1 mcg/kg IV over 10 minutes
◦ Maintenance 0.6 mcg/kg/hr IV titrate to effect (usually 0.2-1
mcg/kg/hr)
24. BETA-1
RECEPTOR
AGONISTS
Dobutamine:
Beta-1 adrenergic receptors, with negligible effects on beta-2 or
alpha receptors.
no release of endogenous norepinephrine, as does dopamine.
Cardiac Decompensation
◦ 0.5-1 mcg/kg/min IV continuous infusion initially, then 2-20
mcg/kg/min; not to exceed 40 mcg/kg/min
Absorption: Onset: 1-10 min
Duration: 10 min
Time to peak effect: ~15 min
Distribution : Vd: 0.2 L/kg
Metabolism in tissues and liver by catechol-O-methyl transferase
Excretion: Urine
32. Epinephrine
Lower doses the beta-agonist effects may predominate;
Ongoing up-titration ---> increasing alpha-agonist effects
as well.
Clinical uses
(1) bradycardia and bradycardic shock (given inotropic effects).
(2) septic shock
(3) Low doses (below 5-10 mcg/kg/min)--> the predominant
effect inotrope, low-output cardiogenic shock.
- Compared to dobutamine/milrinone, low-dose epinephrine has a
touch of alpha-activity ----> prevent hypotension.
4) first-line agent for anaphylaxis.
33. Midodrine
Oral alpha-1 agonist = pure vasopressor.
Accelerated weaning from vasopressors
◦ According to some experts, may be useful to facilitate
discontinuation of low dose IV vasopressors; prospective data are
limited.
◦ Re-evaluate therapy regularly, at each transition of care.
◦ Dose : starting dose is 10 mg PO q8hr. Dose range is 5-40 mg q8hr
Liver Cirrhosis
In diuretic resistant patients
Hypotensive patients.
Hepatorenal syndrome (type 1)
Alternative to terlipressin
Cleared by the kidney ----> caution in renal impairment.
Caution: reflex bradycardia
34. inodilators (milrinone,
dobutamine)
◦ Dobutamine stimulates mostly beta-receptors, with very little
stimulation of alpha-receptors.
◦ Milrinone inhibits intracellular adenylyl cyclase, thereby
increasing intracellular cyclic AMP levels.
Physiologic effect :
◦ Primary effect is positive inotropy, with positive
chronotropy as well
◦ Secondary effect is peripheral vasodilation.
◦ Cardiac output is increased due to both inotropic effect
and vasodilation.
◦ Effect on blood pressure is variable
Clinical use
(1) low-output cardiogenic shock = risk of exacerbating
hypotension.
(2) septic shock with inadequate cardiac output (as an add-on
agent)
35. vasopressin
Stimulates V1 and V2 receptors, causing vasoconstriction
and renal water retention.
Physiologic effects:
◦ Increases systemic vascular resistance (SVR).
◦ Cause venoconstriction, which may increase preload.
◦ Dominant effect on cardiac output is often to cause a reduction (but this
may depend on the heart's ability to tolerate increased afterload
Clinical use:
• Vasodilatory shock (particularly sepsis). low doses (0-0.06
U/min), either as primary or secondary agent.
• Front-line agent for hepatorenal syndrome (HRS) in countries
lacking terlipressin (such as the United States).
• Central diabetes insipidus (only very low doses are needed, e.g.
0.01 units/minute or less).
• Variceal gastrointestinal hemorrhage (theoretically an attractive
agent, but pragmatically it's impossible to titrate adequately).
The main difference between adrenergic and cholinergic is that adrenergic involves the use of neurotransmitter adrenaline and noradrenalin whereas cholinergic involves the use of neurotransmitter Acetylcholine.
Another key difference is that adrenergic receptors are present in sympathetic nervous system while cholinergic receptors are present in parasympathetic nervous system.
Adrenergic receptor binding induces improved activity of the heart and overall body performance while cholinergic receptor binding is responsible for down regulating this effect.
Adrenergic receptors are of two types i.e. alpha and beta receptors while the two types of cholinergic receptors are nicotinic and muscarinic receptor.
Adrenergic receptor works by G-protein coupling while Cholinergic are intropic-ligand gated and metabotropic receptors.
Cholinergic agonists are of two types:
Direct-acting cholinergic agonists: directly bind to cholinergic receptors.
Indirect-acting cholinergic agonists: increase the availability of acetylcholine at the cholinergic receptors... Anticholinesterases are the agents which inhibit ChE, protect Ach from hydrolysis- produce cholinergic effects and potentiates Ach. Reversible: Carbamates: Physostigmine, Neostigmine, Pyridostigmine, Edrophonium, Rivastigmine, Donepeizil, Galantamine Acridine: Tacrine
mimic the actions of acetylcholine. Acetylcholine is one of the most common neurotransmitters in our body, and it has actions in both the central and peripheral nervous systems.
The peripheral nervous system consists of the autonomic nervous system (which regulates involuntary processes including digestion and breathing) and the somatic nervous system, which transmits signals from the central nervous system and external stimuli to skeletal muscle and also mediates hearing, sight, and touch. The autonomic nervous system can be further broken down into the sympathetic and parasympathetic nervous systems. The parasympathetic nervous system regulates various organ and gland functions at rest, including digestion, defecation, lacrimation, salivation, and urination, and primarily uses acetylcholine as its main neurotransmitter.
adverse effects include blurred vision, cramps and diarrhea, low blood pressure and decreased heart rate, nausea and vomiting, salivation and sweating, shortness of breath, and increased urinary frequency
Cholinergic Agonists
18. Direct-Acting Cholinergic Agonists • Cholinergic agonists (parasympathomimetics) mimic the effects of acetylcholine by binding directly to cholinoceptors. • These agents may be broadly classified into two groups: 1. choline esters, which include acetylcholine synthetic esters of choline, such as carbachol and bethanechol. 2. Naturally occurring alkaloids, such as pilocarpine constitue the second group.
19. • All of the direct-acting cholinergic drugs have longer durations of action than acetylcholine. • Some of the more therapeutically useful drugs pilocarpine and bethanechol preferentially bind to muscarinic receptors and are sometimes referred to as muscarinic agents. • As a group, the direct-acting agonists show little specificity in their actions, which limits their clinical usefulness.
20. A. Acetylcholine: is a quaternary ammonium compound that cannot penetrate membranes. it is therapeutically of no importance because of its multiplicity of actions and its rapid inactivation by the cholinesterases. • Acetylcholine has both muscarinic and nicotinic activity. Its actions include
21. 1. Decrease in heart rate and cardiac output: The actions of acetylcholine on the heart mimic the effects of vagal stimulation. For example, acetylcholine, if injected intravenously, produces a brief decrease in cardiac rate (negative chronotropy) and stroke volume as a result of a reduction in the rate of firing at the sinoatrial (SA) node. * normal vagal activity regulates the heart by the release of acetylcholine at the SA node
22. 2. Decrease in blood pressure: Injection of acetylcholine causes vasodilation and lowering of blood pressure by an indirect mechanism of action. Acetylcholine activates M3 receptors found on endothelial cells lining the smooth muscles of blood vessels This results in the production of nitric oxide from arginine Nitric oxide then diffuses to vascular smooth muscle cells to stimulate protein kinase G production, leading to hyperpolarization and smooth muscle relaxation
23. • Other actions: A. In the gastrointestinal tract, acetylcholine increases salivary secretion and stimulates intestinal secretions and motility. Bronchiolar secretions are also enhanced. In the genitourinary tract, the tone of the detrusor urinae muscle is increased, causing expulsion of urine. • B. In the eye, acetylcholine is involved in stimulating ciliary muscle contraction for near vision and in the constriction of the pupillae sphincter muscle, causing miosis (marked constriction of the pupil). Acetylcholine (1% solution) is instilled into the anterior chamber of the eye to produce miosis during ophthalmic surgery.
24. B. Bethanechol: is structurally related to acetylcholine, in which the acetate is replaced by carbamate and the choline is methylated. • It is not hydrolyzed by acetylcholinesterase (due to the addition of carbonic acid), although it is inactivated through hydrolysis by other esterases. • It lacks nicotinic actions (due to the addition of the methyl group) but does have strong muscarinic activity. • Its major actions are on the smooth musculature of the bladder and gastrointestinal tract. It has a duration of action of about 1 hour.
25. • Actions: Bethanechol directly stimulates muscarinic receptors, causing increased intestinal motility and tone. It also stimulates the detrusor muscles of the bladder whereas the trigone and sphincter are relaxed, causing expulsion of urine. • Therapeutic applications: In urologic treatment, bethanechol is used to stimulate the atonic bladder, particularly in postpartum or postoperative, nonobstructive urinary retention. Bethanechol may also be used to treat neurogenic atony ( poor muscular condition ). as well as megacolon (Hypertrophy and dilation of the colon associated with prolonged constipation). • Adverse effects: Bethanechol causes the effects of generalized cholinergic stimulation. These include sweating, salivation, flushing, decreased blood pressure, nausea, abdominal pain, diarrhea, and bronchospasm.
26. C. Carbachol (carbamylcholine): has both muscarinic as well as nicotinic actions (lacks a methyl group present in bethanechol. • Like bethanechol, carbachol is an ester of carbamic acid and a poor substrate for acetylcholinesterase. • It is biotransformed by other esterases, but at a much slower rate.
27. • Actions: Carbachol has profound effects on both the cardiovascular system and the gastrointestinal system because of its ganglion-stimulating activity, and it may first stimulate and then depress these systems. It can cause release of epinephrine from the adrenal medulla by its nicotinic action. Locally instilled into the eye, it mimics the effects of acetylcholine, causing miosis and a spasm of accommodation in which the ciliary muscle of the eye remains in a constant state of contraction.
28. • Therapeutic uses: Because of its high potency, receptor nonselectivity, and relatively long duration of action, carbachol is rarely used therapeutically except in the eye as a miotic agent to treat glaucoma by causing pupillary contraction and a decrease in intraocular pressure. • Adverse effects: At doses used ophthalmologically, little or no side effects occur due to lack of systemic penetration (quaternary amine).
29. D. Pilocarpine: is alkaloid with a tertiary amine and is stable to hydrolysis by acetylcholinesterase. • Compared with acetylcholine and its derivatives, it is far less potent, but it is uncharged and penetrate the CNS at therapeutic doses. • Pilocarpine exhibits muscarinic activity and is used primarily in ophthalmology. Actions of pilocarpine and atropine on the iris and ciliary muscle of the eye
34. Pilocarpine -Origin of the Drug -South American Shrub - Pilocarpus jaborandi -Isolated in 1875 -Chemical Structure + - Cholinergic Parasympathomimetic agent
35. Reaction Mechanism - Pilocarpine binds to muscarinic receptor - Activates receptor binds G-protein - Removal of GDP and addition of GTP to G-protein - Dissociation of G-protein from muscarinic receptor - Separation of G-protein into alpha and beta-gamma subunits - Alpha subunit interacts with and activates Phospholipase C - Phosphatidyl inositol biphosphate (PIP) complex - Phospholipase breaks down PIP into inositol 1,4,5-triphosphate (IP3)and diacylglycerol (both 2o) - IP3 interacts with ER membrane which releases Ca2+
36. Muscle Action - Ca2+ binds to calmodulin forming a complex - This complex binds to caldesmon - When caldesmon is bound by Ca2+/calmodulin complex this allows myosin-actin interactions to occur -The muscle (pupil)contracts Marieb Fig 16-7
37. GTP GDP Muscarinic Receptor G- Protein subunits , , Phospholipase C Phosphatidyl inositol biphosphate (PIP) complex Inositol 1,4,5 - triphosphate (IP3) + diacylglycerol Endoplasmic Reticulum Ca2+ Calmodulin/ Ca2 Reaction Sequence caldesmon Myosin-actin interactio (Muscle Contraction)
38. • Actions: Applied topically to the cornea, pilocarpine produces a rapid miosis and contraction of the ciliary muscle. Pilocarpine is one of the most potent stimulators of secretions (secretagogue) such as sweat, tears, and saliva, but its use for producing these effects has been limited due to its lack of selectivity. The drug is beneficial in promoting salivation in patients with xerostomia resulting from irradiation of the head and neck. Sjgoren's syndrome: which is characterized by dry mouth and lack of tears, is treated with oral pilocarpime tablets and cevimeline, a cholinergic drug that also has the drawback of being nonspecific. The opposing effects of atropine, a muscarinic blocker, on the eye.
39. • Therapeutic use in glaucoma: Pilocarpine is the drug of choice in the emergency lowering of intraocular pressure of both narrow-angle (also called closed-angle) and wide-angle (also called open-angle) glaucoma. Pilocarpine is extremely effective in opening the trabecular meshwork around Schlemm's canal, causing an immediate drop in intraocular pressure as a result of the increased drainage of aqueous humor. • Adverse effects: Pilocarpine can enter the brain and cause CNS disturbances. It stimulates profuse sweating and salivation.
Three areas on the
acetylcholinesterase molecule are capable of binding inhibitory ligands: two
are located in the active center of the enzyme (the acyl pocket and a choline
subsite, referred to collectively as the “esteratic” site), whereas the third is a
peripheral “anionic” site.
Reactivation of acetylcholinesterase • Pralidoxime can reactivate inhibited acetylcholinesterase. However, it is unable to penetrate into the CNS. • The presence of a charged group allows it to approach an anionic site on the enzyme, where it essentially displaces the phosphate group of the organophosphate and regenerates the enzyme. • If given before aging of the alkylated enzyme occurs, it can reverse the effects of echothiophate, except for those in the CNS.
Pralidoxime is a weak acetylcholinesterase inhibitor and, at higher doses, may cause side effects similar to other acetylcholinsterase inhibitors
PYRIDOSTIGMINE AND AMBENOMIUM: ARE OTHER CHOLINESTERASE INHIBITORS THAT ARE USED IN THE CHRONIC MANAGEMENT OF MYASTHENIA GRAVIS. ADVERSE EFFECTS OF THESE AGENTS ARE SIMILAR TO THOSE OF NEOSTIGMINE. D. DEMECARIUM: IS ANOTHER CHOLINESTERASE INHIBITOR USED TO TREAT CHRONIC OPEN-ANGLE GLAUCOMA (PRIMARILY IN PATIENTS REFRACTORY TO OTHER AGENTS) CLOSED-ANGLE GLAUCOMA AFTER IRREDECTOMY. IT IS ALSO USED FOR THE DIAGNOSIS AND TREATMENT OF ACCOMMODATIVE ESOTROPIA. MECHANISMS OF ACTIONS AND SIDE EFFECTS ARE SIMILAR TO THOSE OF NEOSTIGMINE.
Alpha-1 Receptor
Phospholipase C is activated, which leads to the formation of inositol triphosphate (IP3) and diacylglycerol (DAG). As a result, intracellular calcium rises.
Alpha-2 Receptor
Adenylate cyclase is inactivated, which leads to a decrease in intracellular cyclic adenosine monophosphate (cAMP).
Beta-1 Receptor
Adenylate cyclase is activated, and intracellular cAMP increases.
Beta-2 Receptor
The adenylate cycle becomes activated through the Gs-protein-coupled receptors, and there is an increase in intracellular cAMP. Gi protein-coupled receptors are also activated, and this will decrease intracellular cAMP
Beta-adrenoceptors normally bind to norepinephrine released by sympathetic adrenergic nerves, and to circulating epinephrine. Therefore, β-agonists mimic the actions of sympathetic adrenergic stimulation acting through β-adrenoceptors
They are a class of drugs that act on the beta-2 adrenergic receptors. This causes the smooth muscles of the airways to relax, which is why they are effective in treating conditions that cause acute bronchospasm.
Norepinephrine is safe for short periods of time through a large peripheral vein. Ongoing peripheral infusion also appears safe, but this should ideally be done within the context of a well-designed protocol involving frequent monitoring of the extremity and preparation for management of extravasation reaction. Ongoing infusion should be avoided in deep ultrasound-guided peripheral IVs, where it may be impossible to monitor the tissue surrounding the end of the IV cannula.
Phenylephrine and epinephrine have not been reported to cause tissue necrosis. Peripheral infusion of these agents appears to be generally safe, although this should still ideally be done via a well-functioning cannula proximal to the wrist.
Vasopressin should arguably be avoided for peripheral administration, because if it extravasates there is no vasodilatory agent which can counteract its action.
(shown in the cat trial to be an adequate alternative to norepinephrine). It seems to work especially well in patients with inappropriately low heart rate and/or low cardiac output, who likely have a poor sympathetic response to sepsis.
Causes chronotropy and inotropy, thereby increasing the cardiac output.
Increases systemic vascular resistance and also causes venoconstriction (increasing preload).
Stabilizes mast cells, blocking the pathophysiology of anaphylaxis.
Beta-2 agonist stimulation causes bronchodilation, decreases potassium levels, and stimulates the generation of aerobic lactate production by the liver. This is often feared, but lactate may be used as a metabolic fuel by the heart, so this mechanism of action is probably beneficial (in the absence of profound pre-existing metabolic acidosis).
The main concern is that at high doses for long periods of time, it may promote a stress cardiomyopathy.
It causes lactate production which isn't dangerous (may be physiologically beneficial). However, practitioners must be aware of this issue; otherwise they may senselessly chase lactate values.
Epinephrine causes a small decrease in potassium, which is generally not a problem. Effects on potassium may be useful in patients with hyperkalemia and bradycardia (e.g., BRASH syndrome
, depending on how responsive the heart is to inotropy. If the heart responds strongly (with increased stroke volume and heart rate), it is possible for these drugs to increase blood pressure. However, if the heart is already working as hard as it can, then the vasodilator effect may be dominant, causing a drop in blood pressure. Overall, the effect on blood pressure is unpredictable.
Milrinone causes a bit more vasodilation, so it might be better for cardiogenic shock. However, milrinone is renally eliminated, which can make it difficult to titrate in patients with renal failure.
Dobutamine is easier to titrate due to its short half-life, so it is often a preferred agent if the patient's response to inotropy isn't entirely predictable.
Prolonged infusion of dobutamine may cause desensitization of beta-receptors and reduced efficacy. This may be a problem, but it can also help wean the patient off dobutamine once the infusion has been running for a long time (it may be easier to wean off than would be expected).
Pro/Con
Vasopressin may preferentially cause vasoconstriction of post-glomerular arterioles in the kidney, causing improvement in renal function.
It may cause some pulmonary vasodilation, which can be helpful in the context of pulmonary hypertension.
Vasopressin shouldn't generally be given peripherally (if it extravasates, there is no antidote).
Vasopressin can cause digital ischemia, especially when combined with norepinephrine
Mechanism/physiology
Dopamine hits a variety of receptors at different dose ranges (“dirty” drug).
It's often difficult to figure out what it is doing to your patient. For example, low-dose dopamine can actually cause hypotension (due to a predominant effect of vasodilation), which can make it difficult to wean off the dopamine.
Reasons dopamine should be abandoned:
Dopamine increases mortality in RCTs: Dopamine increased mortality compared to norepinephrine in the subgroup of patients with cardiogenic shock.(20200382) It also increased mortality compared to epinephrine among septic children.(26323041)
It's often impossible to figure out what dopamine is doing (given the variety of different effects at different doses in different patients). This makes it impossible to titrate in any rational fashion (up-titration may cause dopamine to function via a different mechanism entirely).
Dopamine has unique adverse endocrine effects.
Dopamine may directly stimulate diuresis via action on dopamine-receptors, thereby falsely suggesting that renal perfusion is adequate.
There is a relatively high risk of tissue necrosis if it extravasates.
Better agents exist: there is nothing dopamine does that can't be achieved with the use of norepinephrine and/or epinephrine.
Dopamine may cause greater malperfusion of the gut compared to norepinephrine
PYRIDAZINONE-DINITRILE DERIVATIVE
INCREASES CALCIUM SENSITIVITY TO MYOCYTES BY BINDING TO TROPONIN C IN A CALCIUM DEPENDENT MANNER. THIS INCREASES CONTRACTILITY WITHOUT RAISING CALCIUM LEVELS. IT ALSO RELAXES VASCULAR SMOOTH MUSCLE BY OPENING ADENOSINE TRIPHOSPHATE SENSITIVE POTASSIUM CHANNELS.
LEVOSIMENDAN IS USED TO MANAGE ACUTELY DECOMPENSATED CONGESTIVE HEART FAILURE.
HALF-LIFE :ELIMININATION HALF-LIFE IS APPROXIMATELY 1 HOUR.
All the vasodilators that are useful in hypertension relax smooth muscle of arterioles, thereby decreasing systemic vascular resis-tance. Sodium nitroprusside and the nitrates also relax veins. Decreased arterial resistance and decreased mean arterial blood pressure elicit compensatory responses, mediated by baroreceptors and the sympathetic nervous system (Figure 11–4), as well as renin, angiotensin, and aldosterone. Because sympathetic reflexes are intact, vasodilator therapy does not cause orthostatic hypoten-sion or sexual dysfunction.
Vasodilators work best in combination with other antihyper-tensive drugs that oppose the compensatory cardiovascular responses.