The document discusses various vasopressor drugs used to treat low blood pressure, including dobutamine, dopamine, epinephrine, and norepinephrine. It describes the mechanisms of action, clinical uses, dosing regimens, and adverse effects of each drug. Key points are that norepinephrine is preferred for septic shock due to fewer side effects, though clinical outcomes are similar across vasopressors. The document provides detailed information on hemodynamic effects and recommendations for use of different vasopressors in various clinical situations.
This document discusses various inotropes and vasopressors used to treat low blood pressure. It describes how vasopressors like norepinephrine work by causing vasoconstriction to raise blood pressure, while inotropes like dobutamine increase cardiac contractility. Several catecholamines are discussed in detail, including their mechanisms of action, clinical uses, dosing, and side effects. Dobutamine is an inotrope that increases heart rate and stroke volume but may increase cardiac work. Dopamine has dose-dependent effects including renal and cardiac stimulation. Epinephrine stimulates both alpha and beta receptors to increase blood pressure and heart rate. Norepinephrine is a potent vasop
Dopamine and dobutamine are endogenous catecholamines used to increase cardiac output and blood pressure. Dopamine acts through dopamine, adrenergic, and beta receptors. At low doses it increases renal blood flow but at higher doses causes vasoconstriction. Dobutamine is a synthetic catecholamine that directly stimulates beta receptors, increasing contractility and output while causing vasodilation. Both are given by continuous IV infusion and used to treat shock, heart failure, and hypotension. Side effects include arrhythmias for dopamine and hypertension for both.
Dobutamine and dopamine are commonly used inotropic agents that increase cardiac output by increasing stroke volume, though dopamine can increase afterload at higher doses. Epinephrine and norepinephrine also increase contractility through beta-1 agonism but have greater vasopressor effects. Dobutamine is preferred over dopamine when treating cardiogenic shock due to its more predictable cardiac effects. In septic shock, dobutamine with norepinephrine is recommended to increase cardiac output while maintaining blood pressure, though epinephrine is an alternative. The effects of inotropes on tissue oxygen utilization must also be considered, as agents like dopamine may impair splanchnic perfusion despite increasing cardiac output.
inotropic drugs and vassopressors drugs.pptxAhmed638947
this presentation is toalking about the Sympathomimetic drugs which are agents which in general mimic responses due to stimulation of sympathetic nerves.
These agents are able to directly activate adrenergic receptors or to indirectly activate them by increasing norepinephrine and epinephrine (mediators of the sympathoadrenal system) levels.
These drugs are used clinically to treat glaucoma, anaphylactic shock, chronic obstructive pulmonary disease, hypotension, hypertension, heart failure, nasal congestion, premature labor, attention-deficit/hyperactivity disorder, narcolepsy, and acute or chronic asthma. The α or β adrenergic antagonists block or attenuate the effect of sympathomimetics on α or β receptors. Alpha blockers are used clinically to treat hypertension and benign prostatic hyperplasia. Beta blockers are used clinically to treat ischemic heart disease, essential hypertension, cardiac arrhythmias, congestive heart failure, glaucoma, hyperthyroidism, surgical removal of pheochromocytoma, nonparkinsonian tremor, migraine headache (prophylaxis), and a wide variety of anxiety situations.
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.
Hemodynamic shock (HS) is a clinical syndrome commonly seen in hospitalized patients characterized by ineffective organ perfusion and dysfunction. The document discusses various types of shock and treatments. It describes different vasoactive drugs used to treat shock states including norepinephrine, epinephrine, dopamine, dobutamine, phenylephrine, calcium channel sensitizers, vasopressin, and phosphodiesterase inhibitors. Norepinephrine is considered the first-line vasopressor for vasodilatory shock while dobutamine is preferred for cardiogenic shock with low cardiac output.
The document summarizes key information about dopamine, including its discovery and functions as a neurotransmitter. It describes dopamine's effects at different doses when used intravenously as a drug. Low doses selectively activate dopamine receptors to increase renal and splanchnic blood flow. Intermediate doses stimulate heart rate and contractility through beta-1 receptors. High doses cause systemic and pulmonary vasoconstriction through alpha receptors. The document also discusses dopamine's clinical uses, administration, interactions, and adverse effects.
This document discusses various inotropes and vasopressors used to treat low blood pressure. It describes how vasopressors like norepinephrine work by causing vasoconstriction to raise blood pressure, while inotropes like dobutamine increase cardiac contractility. Several catecholamines are discussed in detail, including their mechanisms of action, clinical uses, dosing, and side effects. Dobutamine is an inotrope that increases heart rate and stroke volume but may increase cardiac work. Dopamine has dose-dependent effects including renal and cardiac stimulation. Epinephrine stimulates both alpha and beta receptors to increase blood pressure and heart rate. Norepinephrine is a potent vasop
Dopamine and dobutamine are endogenous catecholamines used to increase cardiac output and blood pressure. Dopamine acts through dopamine, adrenergic, and beta receptors. At low doses it increases renal blood flow but at higher doses causes vasoconstriction. Dobutamine is a synthetic catecholamine that directly stimulates beta receptors, increasing contractility and output while causing vasodilation. Both are given by continuous IV infusion and used to treat shock, heart failure, and hypotension. Side effects include arrhythmias for dopamine and hypertension for both.
Dobutamine and dopamine are commonly used inotropic agents that increase cardiac output by increasing stroke volume, though dopamine can increase afterload at higher doses. Epinephrine and norepinephrine also increase contractility through beta-1 agonism but have greater vasopressor effects. Dobutamine is preferred over dopamine when treating cardiogenic shock due to its more predictable cardiac effects. In septic shock, dobutamine with norepinephrine is recommended to increase cardiac output while maintaining blood pressure, though epinephrine is an alternative. The effects of inotropes on tissue oxygen utilization must also be considered, as agents like dopamine may impair splanchnic perfusion despite increasing cardiac output.
inotropic drugs and vassopressors drugs.pptxAhmed638947
this presentation is toalking about the Sympathomimetic drugs which are agents which in general mimic responses due to stimulation of sympathetic nerves.
These agents are able to directly activate adrenergic receptors or to indirectly activate them by increasing norepinephrine and epinephrine (mediators of the sympathoadrenal system) levels.
These drugs are used clinically to treat glaucoma, anaphylactic shock, chronic obstructive pulmonary disease, hypotension, hypertension, heart failure, nasal congestion, premature labor, attention-deficit/hyperactivity disorder, narcolepsy, and acute or chronic asthma. The α or β adrenergic antagonists block or attenuate the effect of sympathomimetics on α or β receptors. Alpha blockers are used clinically to treat hypertension and benign prostatic hyperplasia. Beta blockers are used clinically to treat ischemic heart disease, essential hypertension, cardiac arrhythmias, congestive heart failure, glaucoma, hyperthyroidism, surgical removal of pheochromocytoma, nonparkinsonian tremor, migraine headache (prophylaxis), and a wide variety of anxiety situations.
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.
Hemodynamic shock (HS) is a clinical syndrome commonly seen in hospitalized patients characterized by ineffective organ perfusion and dysfunction. The document discusses various types of shock and treatments. It describes different vasoactive drugs used to treat shock states including norepinephrine, epinephrine, dopamine, dobutamine, phenylephrine, calcium channel sensitizers, vasopressin, and phosphodiesterase inhibitors. Norepinephrine is considered the first-line vasopressor for vasodilatory shock while dobutamine is preferred for cardiogenic shock with low cardiac output.
The document summarizes key information about dopamine, including its discovery and functions as a neurotransmitter. It describes dopamine's effects at different doses when used intravenously as a drug. Low doses selectively activate dopamine receptors to increase renal and splanchnic blood flow. Intermediate doses stimulate heart rate and contractility through beta-1 receptors. High doses cause systemic and pulmonary vasoconstriction through alpha receptors. The document also discusses dopamine's clinical uses, administration, interactions, and adverse effects.
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.
Dopamine is a neurotransmitter that regulates cardiac, vascular and endocrine function. It was discovered in 1958 that dopamine acts as a neurotransmitter in addition to being a precursor for norepinephrine. Dopamine acts through D1 and D2 receptors in areas like the striatum, limbic system, thalamus and hypothalamus. At low doses, it increases blood flow and sodium excretion. At intermediate doses, it increases heart rate and contractility. At high doses, it causes vasoconstriction. Dopamine is used to treat cardiogenic and septic shock, and to prevent or reverse acute renal failure.
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 inotropes and vasopressors used to treat shock. It defines inotropes as agents that increase myocardial contractility and cardiac index, while vasopressors increase vascular tone and elevate mean arterial pressure. The main types discussed are catecholamines like dopamine, dobutamine, adrenaline and norepinephrine. Phosphodiesterase inhibitors and vasopressin are also mentioned. Clinical indications, dosages, and hemodynamic effects are provided for various drugs. The goal of treatment is to perfuse tissues and oxygenate the body through managing preload, contractility, afterload and optimizing cardiac output and systemic vascular resistance. Early recognition and treatment of shock, along with
Inotropic agents, or inotropes, are medicines that change the force of your h...jagan _jaggi
An inotrope is an agent that alters the force or energy of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction.
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.
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.
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.
A Practical Approach to Ionotropes and vasopressors Aneesh Bhandary
Vasopressors are a powerful class of drugs that induce vasoconstriction and Inotropes increase cardiac contractility. Choice of an agent should be based upon the suspected underlying etiology of shock.
This presentation deals with the practical issues and controversies surrounding the use of these agents
This document discusses various types of shock and medications used to treat shock. Shock is defined as inadequate tissue perfusion and oxygenation. Types of shock include septic, cardiogenic, hemorrhagic, and neurogenic shock. Common pressor medications discussed are dopamine, epinephrine, norepinephrine, dobutamine, and vasopressin. Each medication has different effects mediated through alpha and beta receptor stimulation, with some causing vasoconstriction and others increasing cardiac output. Norepinephrine is emerging as a preferred agent for treating septic shock.
Dopamine injection is an inotropic agent that contracts your heart muscles effectively.
This injection is one of the primary emergency drugs in emergency hospital areas to treat life-threatening medical conditions.
So, the primary use of dopamine injection is to save patient life. That’s why it is also called Life Saving Drug.
This post will describe dopamine injection uses, side effects, action, route and dose.
Dopamine belongs to a category of sympathomimetic drug or adrenergic drug. This drug contains a catechol ring, that’s why it comes in the catecholamine category.
Dopamine is a potent agonist on dopaminergic receptors (D1 and D2 receptors).
It also works on adrenergic receptors (Alpha 1 and Beta 1 receptors) that mimic the effect of the sympathomimetic nervous system.
The significant therapeutic action of dopamine injection is
-Vasoconstrictor means to increase the blood flow due to stimulation of alpha 1 adrenergic receptor
-Cardiac stimulant means to increase the heart pumping due to stimulation of beta 1 adrenergic receptor
-Nephroprotective means increasing the renal blood flow due to stimulation of the D1 receptor.
Dopamine injection is always injected into a vein through an intravenous (i.v.) route of administration. This injection must be diluted in a sterile parenteral preparation such as 5% dextrose, normal saline etc.
If you receive dopamine injections, your vital organs will be closely monitored, such as your breathing, heart rate, blood pressure, blood sugar level, oxygen levels, kidney function, etc.
Dopamine injection has the potential to cause unwanted effects or side effects.
Dopamine injection is only prescribed by an expert doctor.
You may have been given dopamine injections in emergencies such as congestive heart failure, septic shock, and cardiogenic shock with oliguria.
This document summarizes various inotropic drugs used to increase cardiac contractility including cardiac glycosides like digoxin, catecholamines like dopamine and dobutamine, phosphodiesterase inhibitors like milrinone, and calcium sensitizers like levosimendan. It provides details on their mechanisms of action, pharmacokinetics, uses, dosages, and side effects. The document focuses on the inotropic and hemodynamic effects of these drugs and their roles in treating low cardiac output states and heart failure.
Pharmacology of-vasopressors-and-inotropesCorey Ahmad
The document discusses the pharmacology of vasopressors and inotropes. It describes how these drugs work via the autonomic nervous system, especially on alpha, beta, and dopamine receptors. Adrenaline is discussed as the most commonly used drug and acts on multiple receptor types. Other vasopressors mentioned include ephedrine, methoxamine, metaraminol, and phenylephrine. Inotropes given by infusion include noradrenaline, dopamine, dobutamine, dopexamine, isoprenaline, and phosphodiesterase inhibitors. A clinical case study reviews the use of ephedrine to treat hypotension during a lower segment Caesarean
This document summarizes different vasopressors and inotropes used to treat hypotension. It describes the receptor activities, physiological effects, indications, and complications of various drugs including phenylephrine, norepinephrine, epinephrine, dopamine, dobutamine, vasopressin, and phosphodiesterase inhibitors. It provides guidance on selecting agents and titrating doses based on the underlying cause of hypotension and the patient's clinical status.
The treatment for Mr. Starling's congestive heart failure condition included furosemide to reduce edema, captopril to decrease blood pressure, intravenous fluids to increase blood pressure, and dobutamine to increase contractility. While these treatments provided some improvement, his cardiac output was not improved so he was evaluated for cardiac transplantation. He ultimately received a heart transplant which involved removing his failing heart and implanting a donor heart to treat his end stage heart failure.
This document provides guidelines for the use of vasoactive medications in the treatment of sepsis and septic shock. It recommends norepinephrine as the first-choice vasopressor. It suggests adding vasopressin or epinephrine to norepinephrine to raise blood pressure targets or lower norepinephrine dosage. Dopamine should only be used in select patients due to risks of arrhythmias. Low-dose dopamine is not recommended for renal protection. Dobutamine may be used for persistent hypoperfusion despite fluids and vasopressors. The document also provides details on the use, effects, and guidelines for various vasoactive drugs to treat septic shock.
The document discusses antihypertensive agents, providing an overview and classification of types including diuretics, beta blockers, calcium channel blockers, and their mechanisms of action. It covers the indications, dosages, side effects, and toxicity management of these classes of antihypertensive drugs used to treat hypertension.
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.
The document defines important terms related to vasoactive drugs and their mechanisms of action. It discusses inotropes, vasopressors, cardiac output, stroke volume, mean arterial pressure, and circulatory shock. It also describes receptors like alpha-1, beta-1, and dopamine D1 receptors. The document provides guidelines for rational use of vasoactive drugs including starting dose, titration, monitoring, and correcting electrolyte imbalances. It also provides methods for calculating dosages of drugs like adrenaline, noradrenaline, and dopamine.
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.
Dopamine is a neurotransmitter that regulates cardiac, vascular and endocrine function. It was discovered in 1958 that dopamine acts as a neurotransmitter in addition to being a precursor for norepinephrine. Dopamine acts through D1 and D2 receptors in areas like the striatum, limbic system, thalamus and hypothalamus. At low doses, it increases blood flow and sodium excretion. At intermediate doses, it increases heart rate and contractility. At high doses, it causes vasoconstriction. Dopamine is used to treat cardiogenic and septic shock, and to prevent or reverse acute renal failure.
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 inotropes and vasopressors used to treat shock. It defines inotropes as agents that increase myocardial contractility and cardiac index, while vasopressors increase vascular tone and elevate mean arterial pressure. The main types discussed are catecholamines like dopamine, dobutamine, adrenaline and norepinephrine. Phosphodiesterase inhibitors and vasopressin are also mentioned. Clinical indications, dosages, and hemodynamic effects are provided for various drugs. The goal of treatment is to perfuse tissues and oxygenate the body through managing preload, contractility, afterload and optimizing cardiac output and systemic vascular resistance. Early recognition and treatment of shock, along with
Inotropic agents, or inotropes, are medicines that change the force of your h...jagan _jaggi
An inotrope is an agent that alters the force or energy of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction.
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.
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.
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.
A Practical Approach to Ionotropes and vasopressors Aneesh Bhandary
Vasopressors are a powerful class of drugs that induce vasoconstriction and Inotropes increase cardiac contractility. Choice of an agent should be based upon the suspected underlying etiology of shock.
This presentation deals with the practical issues and controversies surrounding the use of these agents
This document discusses various types of shock and medications used to treat shock. Shock is defined as inadequate tissue perfusion and oxygenation. Types of shock include septic, cardiogenic, hemorrhagic, and neurogenic shock. Common pressor medications discussed are dopamine, epinephrine, norepinephrine, dobutamine, and vasopressin. Each medication has different effects mediated through alpha and beta receptor stimulation, with some causing vasoconstriction and others increasing cardiac output. Norepinephrine is emerging as a preferred agent for treating septic shock.
Dopamine injection is an inotropic agent that contracts your heart muscles effectively.
This injection is one of the primary emergency drugs in emergency hospital areas to treat life-threatening medical conditions.
So, the primary use of dopamine injection is to save patient life. That’s why it is also called Life Saving Drug.
This post will describe dopamine injection uses, side effects, action, route and dose.
Dopamine belongs to a category of sympathomimetic drug or adrenergic drug. This drug contains a catechol ring, that’s why it comes in the catecholamine category.
Dopamine is a potent agonist on dopaminergic receptors (D1 and D2 receptors).
It also works on adrenergic receptors (Alpha 1 and Beta 1 receptors) that mimic the effect of the sympathomimetic nervous system.
The significant therapeutic action of dopamine injection is
-Vasoconstrictor means to increase the blood flow due to stimulation of alpha 1 adrenergic receptor
-Cardiac stimulant means to increase the heart pumping due to stimulation of beta 1 adrenergic receptor
-Nephroprotective means increasing the renal blood flow due to stimulation of the D1 receptor.
Dopamine injection is always injected into a vein through an intravenous (i.v.) route of administration. This injection must be diluted in a sterile parenteral preparation such as 5% dextrose, normal saline etc.
If you receive dopamine injections, your vital organs will be closely monitored, such as your breathing, heart rate, blood pressure, blood sugar level, oxygen levels, kidney function, etc.
Dopamine injection has the potential to cause unwanted effects or side effects.
Dopamine injection is only prescribed by an expert doctor.
You may have been given dopamine injections in emergencies such as congestive heart failure, septic shock, and cardiogenic shock with oliguria.
This document summarizes various inotropic drugs used to increase cardiac contractility including cardiac glycosides like digoxin, catecholamines like dopamine and dobutamine, phosphodiesterase inhibitors like milrinone, and calcium sensitizers like levosimendan. It provides details on their mechanisms of action, pharmacokinetics, uses, dosages, and side effects. The document focuses on the inotropic and hemodynamic effects of these drugs and their roles in treating low cardiac output states and heart failure.
Pharmacology of-vasopressors-and-inotropesCorey Ahmad
The document discusses the pharmacology of vasopressors and inotropes. It describes how these drugs work via the autonomic nervous system, especially on alpha, beta, and dopamine receptors. Adrenaline is discussed as the most commonly used drug and acts on multiple receptor types. Other vasopressors mentioned include ephedrine, methoxamine, metaraminol, and phenylephrine. Inotropes given by infusion include noradrenaline, dopamine, dobutamine, dopexamine, isoprenaline, and phosphodiesterase inhibitors. A clinical case study reviews the use of ephedrine to treat hypotension during a lower segment Caesarean
This document summarizes different vasopressors and inotropes used to treat hypotension. It describes the receptor activities, physiological effects, indications, and complications of various drugs including phenylephrine, norepinephrine, epinephrine, dopamine, dobutamine, vasopressin, and phosphodiesterase inhibitors. It provides guidance on selecting agents and titrating doses based on the underlying cause of hypotension and the patient's clinical status.
The treatment for Mr. Starling's congestive heart failure condition included furosemide to reduce edema, captopril to decrease blood pressure, intravenous fluids to increase blood pressure, and dobutamine to increase contractility. While these treatments provided some improvement, his cardiac output was not improved so he was evaluated for cardiac transplantation. He ultimately received a heart transplant which involved removing his failing heart and implanting a donor heart to treat his end stage heart failure.
This document provides guidelines for the use of vasoactive medications in the treatment of sepsis and septic shock. It recommends norepinephrine as the first-choice vasopressor. It suggests adding vasopressin or epinephrine to norepinephrine to raise blood pressure targets or lower norepinephrine dosage. Dopamine should only be used in select patients due to risks of arrhythmias. Low-dose dopamine is not recommended for renal protection. Dobutamine may be used for persistent hypoperfusion despite fluids and vasopressors. The document also provides details on the use, effects, and guidelines for various vasoactive drugs to treat septic shock.
The document discusses antihypertensive agents, providing an overview and classification of types including diuretics, beta blockers, calcium channel blockers, and their mechanisms of action. It covers the indications, dosages, side effects, and toxicity management of these classes of antihypertensive drugs used to treat hypertension.
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.
The document defines important terms related to vasoactive drugs and their mechanisms of action. It discusses inotropes, vasopressors, cardiac output, stroke volume, mean arterial pressure, and circulatory shock. It also describes receptors like alpha-1, beta-1, and dopamine D1 receptors. The document provides guidelines for rational use of vasoactive drugs including starting dose, titration, monitoring, and correcting electrolyte imbalances. It also provides methods for calculating dosages of drugs like adrenaline, noradrenaline, and dopamine.
One health condition that is becoming more common day by day is diabetes.
According to research conducted by the National Family Health Survey of India, diabetic cases show a projection which might increase to 10.4% by 2030.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
2. Vasopressors are a powerful class of drugs that induce
vasoconstriction and thereby elevate mean arterial
pressure (MAP).
Vasopressors differ from inotropes, which increase
cardiac contractility; however, many drugs have both
vasopressor and inotropic effects.
Although many vasopressors have been used since the
1940s, few controlled clinical trials have directly
compared these agents or documented improved
outcomes due to their use .
Thus, the manner in which these agents are commonly
used largely reflects expert opinion, animal data, and
the use of surrogate end points such as tissue
oxygenation as a proxy for decreased morbidity and
mortality.
3. Catecholamines are drugs that promote blood
flow and blood pressure by stimulating
adrenergic receptors
4. Despite differences in adrenergic receptor
activation and physiological responses, no
catecholamine drug has proven superior to the
others for improving clinical outcomes.
5.
6. Dobutamine is primarily a β1-receptor agonist,
but also has weak β2- receptor agonist activity.
The β1-receptor stimulation produces an
increase in heart rate and stroke volume, while
the β2-receptor stimulation produces
peripheral vasodilatation.
Because the increase in stroke volume is
accompanied by a decrease in systemic
vascular resistance, the blood pressure is
usually unchanged or slightly increased .
The response to dobutamine, however, can
vary widely in critically ill patients.
7. The cardiac stimulation produced by
dobutamine is often accompanied by an
increase in cardiac work and myocardial O2
consumption .
These effects can be deleterious in heart failure
because cardiac work and myocardial energy
needs are already heightened in the failing
myocardium.
8. Dobutamine has been used to augment cardiac
output in patients with decompensated heart
failure due to systolic dysfunction.
However, the unfavorable effects of
dobutamine on myocardial energetics has
created a preference for other inodilators in
decompensated heart failure.
Dobutamine remains the preferred inotropic
agent for the treatment of myocardial
depression associated with septic shock but it
usually must be combined with a
vasoconstrictor agent (e.g., norepinephrine) to
raise the blood pressure.
9. Dosing Regimen
Dobutamine is started at an infusion rate of 3–5
μg/kg/min (without a loading dose), and this
can be increased in increments of 3–5
μg/kg/min, if necessary, to achieve the desired
effect.
The usual dose range is 5–20 μg/kg/min.
Therapy should be driven by hemodynamic
end-points, and not by pre-selected dose rates.
10. Adverse Effects
Dobutamine produces only mild increases in
heart rate (5-15 beats/min) in most patients,
but it occasionally causes significant
tachycardia (rate increases > 30 beats/min) ,
which can be deleterious in patients with
coronary artery disease.
Like all positive inotropic agents, dobutamine
is contraindicated in patients with
hypertrophic cardiomyopathy.
11. Dopamine is an endogenous catecholamine
that serves as a precursor for norepinephrine.
When given as an exogenous drug, dopamine
produces a variety of dose-dependent effects,
as described next.
12. Actions
At low infusion rates (≤ 3 μg/kg/min),
dopamine selectively activates dopamine-
specific receptors in the renal and splanchnic
circulations, which increases blood flow in
these regions .
Low-dose dopamine also directly affects renal
tubular epithelial cells, causing an increase in
both urinary sodium excretion (natriuresis) and
urine output that are independent of the
changes in renal blood flow .
The renal effects of low-dose dopamine are minimal
or absent in patients with acute renal failure .
13. At moderate infusion rates (3 – 10 μg/kg/min),
dopamine stimulates β- receptors in the heart
and peripheral circulation, producing an
increase in myocardial contractility and heart
rate, along with peripheral vasodilatation.
The increase in stroke volume produced by
dopamine is greater than dobutamine at
equivalent infusion rates.
14. At high infusion rates (> 10 μg/kg/min),
dopamine produces a dose dependent
activation of α-receptors in the systemic and
pulmonary circulations, resulting in
progressive pulmonary and systemic
vasoconstriction.
This vasopressor effect increases ventricular
afterload, and can reduce the stroke volume
augmentation produced by lower doses of
dopamine.
15. Clinical Uses
Dopamine can be used to manage patients with
cardiogenic shock and septic shock, although
other measures are favored in these conditions
(i.e., mechanical assist devices are preferred for
cardiogenic shock, and norepinephrine is
preferred for septic shock).
Low-dose dopamine is NOT recommended as
a therapy for acute renal failure.
16. Dosing Regimen
Dopamine is usually started at a rate of 3 – 5
μg/kg/min (without a loading dose), and the infusion
rate is increased in increments of 3 – 5 μg/kg/min to
achieve the desired effect.
The usual dose range is 3 – 10 μg/kg/min for
increasing cardiac output, and 10 – 20 μg/kg/min for
increasing blood pressure.
Dopamine infusions should be delivered into large,
central veins, because extravasation of the drug
through peripheral veins can produce extensive tissue
necrosis.
17. Adverse Effects
Sinus tachycardia and atrial fibrillation are
reported in 25% of patients receiving dopamine
infusions .
Other adverse effects of dopamine include
increased intraocular pressure , splanchnic
hypoperfusion, and delayed gastric emptying,
which could predispose to aspiration
pneumonia.
18. EXTRAVASATION OF VASOPRESSORS:
The risk of tissue necrosis from extravasation of
dopamine is a concern with all vasopressor
(vasoconstrictor)drug infusions, and eliminating
this risk is the reason that large, central veins are
recommended for all vasopressor drug infusions.
If dopamine or any other vasopressor drug escapes
from a peripheral vein into the surrounding
tissues, the tendency for ischemic tissue necrosis
can be reduced by injecting phentolamine (an α-
receptor antagonist) into the involved area.
The recommended injectate is a solution
containing 5 – 10 mg phentolamine in 15 mL of
isotonic saline.
19. Epinephrine is an endogenous catecholamine
that is released by the adrenal medulla in
response to physiological stress.
It is the most potent natural β-agonist.
20. Actions
Epinephrine stimulates both α-adrenergic and β-
adrenergic receptors (β1 and β2 subtypes), and
produces dose-dependent increases in heart rate,
stroke volume, and blood pressure.
Epinephrine is a more potent β1- receptor agonist than
dopamine, and produces a greater increase in stroke
volume and heart rate than comparable doses of
dopamine.
The α-receptor stimulation produces a nonuniform
peripheral vasoconstriction, with the most prominent
effects in the subcutaneous, renal, and splanchnic
circulations.
Epinephrine also has several metabolic effects,
including lipolysis, increased glycolysis, and increased
lactate production (from β-receptor activation), and
hyperglycemia from α-receptor-mediated inhibition of
insulin secretion.
21. Clinical Uses
Epinephrine plays an important role in the
resuscitation of cardiac arrest and it is the drug of
choice for hemodynamic support in anaphylactic
shock.
Epinephrine is also used for hemodynamic
support in the early postoperative period
following cardiopulmonary bypass surgery.
Although epinephrine is as effective as other
catecholamines in septic shock concerns about side
effects have limited its popularity in septic shock.
22. Dosing Regimen
The dosing regimens for epinephrine in cardiac
arrest is 1 mg IV every 3–5 minutes.
Vasopressor effect can increase coronary
perfusion pressure, but cardiac stimulation is
counter productive.
Dosing for anaphylactic shock is:
23.
24. Epinephrine infusions are not preceded by a
loading dose.
The initial infusion rate is usually 1 – 2 μg/min
(or 0.02 μg/kg/min), and the rate is then
increased in increments of 1 – 2 μg/min to
achieve the desired effect .
The usual dose range for augmenting cardiac
output or correcting hypotension is 5 – 15
μg/min.
25. Adverse Effects
Epinephrine creates a greater risk of unwanted
cardiac stimulation (which can be deleterious in
patients with coronary artery disease) than the
other catecholamine drugs .
Other adverse effects include hyperglycemia,
increased metabolic rate, and splanchnic
hypoperfusion (which can damage the mucosal
barrier in the bowel).
Epinephrine infusions are accompanied by an
increase in serum lactate levels but this is not an
adverse effect because it reflects an increased rate
of glycolysis (not tissue hypoxia), and the lactate
can be used as an
alternative fuel source.
26. Norepinephrine is an endogenous
catecholamine that normally functions as an
excitatory neurotransmitter.
When used as an exogenous drug,
norepinephrine functions as a vasopressor
27. Actions
The principal action of norepinephrine is α-receptor-
mediated peripheral vasoconstriction.
However, the adrenergic response to norepinephrine is
altered in patients with septic shock .
For example, norepinephrine infusions are usually
accompanied by a decrease in renal blood flow but in
patients with septic shock, renal blood flow is
increased by norepinephrine infusions .
Similar alterations may also occur with splanchnic
blood flow (i.e., normally reduced, but not in septic
shock)
Norepinephrine is also a weak β1-receptor agonist, but
the effects of norepinephrine on stroke volume and
heart rate can be comparable to dopamine (a more
potent β1-receptor agonist) in patients with septic
Shock.
28. Clinical Uses
Norepinephrine is the preferred catecholamine for
circulatory support in patients with septic shock.
This preference is not based on improved outcomes,
because the mortality rate in septic shock is the same
regardless of the catecholamine used for circulatory
support.
Instead, norepinephrine is favored in septic shock
because it has fewer adverse effects
than dopamine or epinephrine .
29. Dosing Regimen
Norepinephrine infusions are usually started at a
rate of 8 – 10 μg/min, and the dose rate is then
titrated upward or downward to maintain a mean
blood pressure of at least 65 mm Hg.
The effective dose rate in septic shock varies
widely in individual patients, but is usually below
40 μg/min.
Hypotension that is refractory to norepinephrine
usually prompts the addition of dopamine or
vasopressin, but there is no evidence that this
practice improves outcomes
30. Adverse Effects
Adverse effects of norepinephrine include local
tissue necrosis from drug extravasation, and
intense systemic vasoconstriction with organ
dysfunction when high dose rates are required.
However, whenever high doses of a
vasoconstrictor drug are required to correct
hypotension, it is difficult to distinguish
between adverse drug effects and adverse
effects of the circulatory shock.
31. Phenylephrine is a potent vasoconstrictor that has very
few applications in the ICU.
Actions
Phenylephrine in a pure α-receptor agonist that
produces widespread vasoconstriction.
The consequences of this vasoconstriction can include
bradycardia, a decrease in cardiac stroke output
(usually in patients with cardiac dysfunction), and
hypoperfusion of the kidneys and bowel
32. Clinical Uses
The principal use of phenylephrine is for the
reversal of severe hypotension produced by spinal
anesthesia.
However, pure α-receptor agonists are not
universally favored in this situation because they
can aggravate the decrease in cardiac stroke output
that occurs in spinal shock .
Phenylephrine is not recommended for
hemodynamic support in septic shock, although a
clinical study comparing phenylephrine and
norepinephrine for the early management of septic
shock showed no differences in hemodynamic
effects or clinical outcomes with the use of either
drug.
33. Dosing Regimen
Phenylephrine can be given as intermittent IV
doses. The initial IV dose is 0.2 mg, which can
be repeated in increments of 0.1 mg to a
maximum dose of 0.5 mg .
Adverse Effects
The principal adverse effects of phenylephrine
are bradycardia, low car-diac output, and renal
hypoperfusion.
These effects are magnified in hypovolemic
patients.
34. The following drugs can be added to vasopressor
therapy with catecholamines in selected situations.
Vasopressin
Antidiuretic hormone (ADH) is an osmoregulatory
hormone that is also called vasopressin because it
produces vasoconstriction.
35. Actions
The vasoconstrictor effects of vasopressin are
mediated by specialized vasopressin (V1) receptors
located on vascular smooth muscle.
Vasoconstriction is most prominent in skin,
skeletal muscle, and splanchnic circulations .
Exogenous vasopressin does not increase blood
pressure in healthy volunteers, but it can produce
significant increases in blood pressure in patients
with hypotension caused by peripheral
vasodilatation.
This type of hypotension occurs in septic shock,
anaphylactic shock, autonomic insufficiency, and
the hypotension associated with spinal and general
anesthesia.
36. Other actions of vasopressin include enhanced water
reabsorption in the distal renal tubules (mediated by
V2 receptors), and stimulation of ACTH release by the
anterior pituitary gland (mediated by V3 receptors).
These actions are clinically silent when vasopressin is
administered in the recommended doses.
37. Clinical Uses
Vasopressin can be used in the following clinical
situations.
In the resuscitation of cardiac arrest, vasopressin can
be given as a single IV dose (40 units) to replace the
first or second dose of epinephrine.
In cases of septic shock that are resistant, or refractory,
to hemodynamic support with norepinephrine or
dopamine, a vasopressin infusion can be used to raise
the blood pressure and reduce the catecholamine
requirement (catecholamine sparing effect) .
Unfortunately, there is no survival benefit associated
with the this practice .
In cases of hemorrhage from esophageal or gastric
varices, vasopressin infusions can be used to promote
splanchnic vasoconstriction and reduce the rate of
bleeding.
38. Dosing Regimen
The plasma half-life of exogenous vasopressin
is 5 – 20 min , so vasopressin must be given by
continuous infusion to produce prolonged
effects.
In septic shock, the recommended infusion rate
is 0.01 – 0.04 units/min, and a rate of 0.03
units/min is most popular.
39. Adverse Effects
Adverse effects are uncommon with infusion
rates < 0.04 units/hr .
At higher infusion rates, unwanted effects can
include consequences of excessive
vasoconstriction (e.g., impaired renal and
hepatic function), along with excessive water
retention and hyponatremia.
40. Terlipressin
Terlipressin is a vasopressin analogue that has two
advantages over vasopressin.
First, it is a selective V1 receptor agonist, and does not
produce the
side effects associated with stimulation of the other
vasopressin receptors.
Secondly, terlipressin has a much longer duration of
action than vasopressin, and a single IV dose of 1 – 2
mg can raise the blood pressure for 5 hours .
41. The long duration of action allows terlipressin
to be given by intermittent IV dosing.
Terlipressin is a potent splanchnic
vasoconstrictor, and may prove valuable in the
management of variceal bleeding.
However, there is an increased risk of
splanchnic ischemia with terlipressin, and
ischemic effects cannot be reversed for 5 hours
after the drug is administered.
Like vasopressin, there is no survival
advantage associated with the addition of
terlipressin in patients with septic shock
42. Despite adequate volume replacement, if the patient is
hypotensive and perfusion of vital organs is jeopardized,
vasoactive agents may be administered to improve cardiac output
and blood pressure.
It is useful to understand the receptors through which adrenergic
agents exert their effect.
• Three broad groups of agents may be identified:
1. Predominant b -agonists (dobutamine, dopexamine, isoprenaline)
2. Predominant a -agonists (phenylephrine)
3. Those with mixed b - and a -effects (adrenaline and noradrenaline).
43. In general, when the heart is failing, and the peripheral
vascular resistance is normal, an agent with predominant
inotropic effect (especially a b -1 selective agent) would be a
good choice.
If there is vasodilatation, a vasoconstrictor with
predominant a -agonist activity is appropriate.
Familiarize with doses and effects of commonly used
inotropes and vasopressors.
Consider practical aspects of vasopressor infusion:
– Infuse through large veins preferably central veins.
– Use multi-lumen catheters and use dedicated lumen for
vasopressor infusion.
– No other drug bolus or infusion should be given through the
same lumen.
44. Use infusion or syringe pumps or other infusion
controllers.
Invasive arterial pressure should be measured.
Dobutamine and other inodilators may be given
through peripheral line.
Volume defi cit should always be corrected as much as
possible before resorting to vasopressors which would
lead to a false sense of security by increasing blood
pressure while underlying hypovolemia and resultant
low perfusion will lead to subsequent organ
dysfunction.
45. All inotropes and vasopressors should be titrated so
that tissue perfusion is restored with the lowest dose of
drug and to the desired end points with minimal or no
side effects:
– Titrate to clinical improvements in heart rate (HR)
and mean arterial pressure (MAP).
– Titrate inotropes to desired cardiac output.
46. Do not aim for supranormal cardiac output:
– Titrate vasopressors to MAP of 65–70 mmHg.
– In patients with long-standing hypertension, renal
failure, recent cerebral infarct, and increased intra-
abdominal pressure, a higher MAP may be desirable.
– In trauma with active bleeding, a lower MAP till bleeding
source is controlled is advisable.
– Aiming for higher MAP than desired may result in
unnecessary vasoconstriction.
– Titrate to achieve adequacy of organ perfusion
• Urine output more than 0.5 mL/Kg/h
• ScvO 2 more than 70%
• Reduction in lactate levels over time (e.g., 20% over 2 h)
• Watch for side effects: tachycardia, arrhythmias, cardiac
ischemia
47.
48.
49.
50. – It is a myo fi lament calcium sensitizer. It increases
myocardial contractility without increasing myocardial
ATP consumption, thereby improving contraction at low
energy cost.
– It causes normal or improved diastolic relaxation and
vasodilatation.
– It has been studied in acute decompensated heart failure,
during and after cardiac surgery, and postmyocardial
infarction.
51. MILRINONE: Milrinone is a phosphodiesterase
inhibitor that enhances myocardial contractility and
relaxation via the same mechanism as dobutamine (i.e.,
cyclic AMP-mediated calcium influx into cardiac
myocytes).
Milrinone has similar effects on cardiac performance as
dobutamine, but
is more likely to produce hypotension .
52. Digitalis glycosides
– The digitalis glycosides have long been used as
inotropic agents.
– However, today their role in the treatment of acute
heart failure or cardiogenic shock is limited to control
of the ventricular rate response in fast atrial fi
brillation.
– The onset of action of effects of digoxin takes 90 min
after an intravenous loading dose, and peak effect
occurs at 2–6 h.
– The effects of digoxin are modest and unpredictable,
and it has a narrow therapeutic index
53. • Agents used in septic shock
The Surviving Sepsis Campaign makes the following
evidence-based recommendations in patients with sepsis:
– Vasopressors
• Recommend to maintain MAP ³ 65 mmHg.
• Recommend noradrenaline centrally administered as the
initial vasopressors of choice.
• Suggest that dopamine, adrenaline, phenylephrine, or
vasopressin should not be administered as the initial
vasopressor in septic shock.
• Vasopressin at dose of 0.03 unit/min may be
subsequently added to noradrenaline with anticipation of
an effect equivalent to noradrenaline alone
54. Use adrenaline as the fi rst alternative agent in septic
shock when blood pressure is poorly responsive to
noradrenaline
Recommend not to use low-dose dopamine for renal
protection.
Recommend to insert an arterial catheter in patients
requiring vaso pressors, as soon as practical.
– Inotropic therapy
• Recommend the use of dobutamine in patients with
myocardial dysfunction as supported by elevated cardiac fi
lling pressures and low cardiac output.
• Do not increase cardiac index to predetermined
supranormal levels.
55. • All inotropic and vasopressor drugs may increase myocardial oxygen
demand.
• Increasing blood pressure by use of vasopressors does not lead to
increased perfusion all the time; in certain circumstances like
hypovolemia, it might lead to decreased fl ow to end organs.
• Tachycardia may occur, especially in volume-depleted patients.
• Arrhythmias.
• Catecholamines also have signi fi cant neurohumoral and metabolic
effects, which might be deleterious, for example, hyperglycemia and
hyperlactatemia induced by adrenaline and suppression of prolactin by
dopamine.
56. All attempts should be made to treat underlying cause
of low perfusion state whenever feasible and
vasopressors should be weaned off at the earliest.
• If necessary, additional fl uid challenges may be used
judiciously in order to wean off vasopressors
57. The following broad recommendations can be
made:
Smaller combined doses of inotropes and vasopressors may
be advantageous over a single agent used at higher doses to
avoid dose-related adverse effects.
The use of vasopressin at low to moderate doses may allow
catecholamine sparing, and it may be particularly useful in
settings of catecholamine hyposensitivity and after
prolonged critical illness.
In cardiogenic shock complicating AMI, current guidelines
based on expert opinion recommend dopamine or
dobutamine as first-line agents with moderate hypotension
(systolic blood pressure 70 to 100 mm Hg) and
norepinephrine as the preferred therapy for severe
hypotension (systolic blood pressure 70 mm Hg).
58. Routine inotropic use is not recommended for end-
stage HF. When such use is essential, every effort
should be made to either reinstitute stable oral
therapy as quickly as possible or use destination
therapy such as cardiac transplantation or LV
assist device support.
Large randomized trials focusing on clinical
outcomes are needed to better assess the clinical
efficacy of these agents