Starling Case Report
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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.
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COMPARISON OF DOPAMINE AND NORADRENALINE IN SHOCK TREATMENT
Dopamine and norepinephrine are both commonly used to treat shock. This randomized trial compared the effects of dopamine versus norepinephrine in 1679 patients with shock. There was no significant difference in the primary outcome of death at 28 days between the dopamine and norepinephrine groups. However, the dopamine group experienced more arrhythmic events. A subgroup analysis found that dopamine was associated with an increased rate of death in patients with cardiogenic shock specifically, but not in patients with septic or hypovolemic shock. The study concluded that while overall mortality was similar, dopamine use resulted in more adverse events than norepinephrine.
Medical procedures
Doppler ultrasound uses sound waves to measure blood flow and diagnose conditions like blood clots and heart issues. It is less invasive than tests like arteriography and venography.
The Holter monitor records heart activity through electrodes attached to the chest over hours or days to detect irregular rhythms and diagnose conditions like atrial fibrillation.
Thrombolytic drugs like t-PA and streptokinase are used to treat strokes and heart attacks by dissolving blood clots, but will not be given if the patient has recent bleeding, surgery, pregnancy or other exceptions.
Lec60[1]
1. Several substances act as vasoconstrictors or vasodilators to regulate blood flow, including norepinephrine, epinephrine, angiotensin II, vasopressin, histamine, bradykinin, ions like calcium and potassium.
2. During exercise, sympathetic nervous system discharge causes widespread vasoconstriction except in active muscles, along with increased heart rate, arterial pressure and cardiac output to elevate blood flow to muscles.
3. Coronary blood flow supplies the heart and increases during exercise to meet heightened cardiac demand, with the left coronary artery mainly supplying the left ventricle and right coronary artery mainly supplying the right ventricle.
Chf pharmacology of digitalis
Digitalis is obtained from the leaves of Digitalis purpurea. It has positive inotropic effects on the heart by enhancing myocardial activity and contractility. This increases cardiac output and shifts the stroke volume-preload curve towards normal in patients with congestive heart failure (CHF), improving cardiac function and relieving symptoms. Digitalis is used to treat CHF and cardiac arrhythmias, but it has contraindications like tachycardia, hypokalemia, and myocardial infarction.
Class drug therapy of shock
1. Shock is defined as inadequate tissue perfusion resulting in cellular dysfunction. It can occur with normal or low blood pressure and results from various causes like sepsis, hemorrhage, cardiac failure, etc.
2. Early goal-directed therapy for septic shock involves rapid fluid resuscitation, antibiotics, and vasopressors to maintain adequate perfusion. Dopamine, norepinephrine, and epinephrine are commonly used vasopressors.
3. Cardiogenic shock results from inadequate cardiac output, usually from acute myocardial infarction or myocarditis. It requires fluids, inotropes like dobutamine, and revascularization when possible.
Vasodilators
This document discusses various types of vasodilators including pulmonary, arterial, and coronary vasodilators. It describes their mechanisms of action in relaxing smooth muscle and dilating blood vessels to reduce systemic vascular resistance and blood pressure. Common vasodilators like hydralazine, ACE inhibitors, and minoxidil are used to treat conditions like hypertension, heart failure, preeclampsia, angina, and pulmonary hypertension. Side effects can include chest pain, changes in heart rate, fluid retention, headaches, and flushing.
Inotropes and vasopressors
1. This document discusses various inotropes and vasopressors used to treat shock states including dobutamine, dopamine, epinephrine, and norepinephrine.
2. It provides guidelines on administering these drugs including desired dose ranges, how to calculate infusion rates, and examples of calculating dobutamine infusion rates.
3. The document also matches different shock states, such as septic shock, cardiogenic shock, and hemorrhagic shock, with recommended first-tier and second-tier drug treatments.
Inotropes and their choice
This document discusses inotropic agents, which are drugs that affect the strength of contraction of the heart muscle. It describes positive inotropes that increase contraction and negative inotropes that decrease contraction. The choice of inotrope depends on its pharmacological effects and the specific cardiovascular condition. Positive inotropes discussed include calcium, calcium sensitizers like levosimendan, catecholamines, cardiac glycosides, and others. Negative inotropes include beta blockers, calcium channel blockers, and antiarrhythmics. The mechanisms and effects of various catecholamines like dopamine, dobutamine, epinephrine, and dopexamine are also outlined.
Recommended
COMPARISON OF DOPAMINE AND NORADRENALINE IN SHOCK TREATMENT
Dopamine and norepinephrine are both commonly used to treat shock. This randomized trial compared the effects of dopamine versus norepinephrine in 1679 patients with shock. There was no significant difference in the primary outcome of death at 28 days between the dopamine and norepinephrine groups. However, the dopamine group experienced more arrhythmic events. A subgroup analysis found that dopamine was associated with an increased rate of death in patients with cardiogenic shock specifically, but not in patients with septic or hypovolemic shock. The study concluded that while overall mortality was similar, dopamine use resulted in more adverse events than norepinephrine.
Medical procedures
Doppler ultrasound uses sound waves to measure blood flow and diagnose conditions like blood clots and heart issues. It is less invasive than tests like arteriography and venography.
The Holter monitor records heart activity through electrodes attached to the chest over hours or days to detect irregular rhythms and diagnose conditions like atrial fibrillation.
Thrombolytic drugs like t-PA and streptokinase are used to treat strokes and heart attacks by dissolving blood clots, but will not be given if the patient has recent bleeding, surgery, pregnancy or other exceptions.
Lec60[1]
1. Several substances act as vasoconstrictors or vasodilators to regulate blood flow, including norepinephrine, epinephrine, angiotensin II, vasopressin, histamine, bradykinin, ions like calcium and potassium.
2. During exercise, sympathetic nervous system discharge causes widespread vasoconstriction except in active muscles, along with increased heart rate, arterial pressure and cardiac output to elevate blood flow to muscles.
3. Coronary blood flow supplies the heart and increases during exercise to meet heightened cardiac demand, with the left coronary artery mainly supplying the left ventricle and right coronary artery mainly supplying the right ventricle.
Chf pharmacology of digitalis
Digitalis is obtained from the leaves of Digitalis purpurea. It has positive inotropic effects on the heart by enhancing myocardial activity and contractility. This increases cardiac output and shifts the stroke volume-preload curve towards normal in patients with congestive heart failure (CHF), improving cardiac function and relieving symptoms. Digitalis is used to treat CHF and cardiac arrhythmias, but it has contraindications like tachycardia, hypokalemia, and myocardial infarction.
Class drug therapy of shock
1. Shock is defined as inadequate tissue perfusion resulting in cellular dysfunction. It can occur with normal or low blood pressure and results from various causes like sepsis, hemorrhage, cardiac failure, etc.
2. Early goal-directed therapy for septic shock involves rapid fluid resuscitation, antibiotics, and vasopressors to maintain adequate perfusion. Dopamine, norepinephrine, and epinephrine are commonly used vasopressors.
3. Cardiogenic shock results from inadequate cardiac output, usually from acute myocardial infarction or myocarditis. It requires fluids, inotropes like dobutamine, and revascularization when possible.
Vasodilators
This document discusses various types of vasodilators including pulmonary, arterial, and coronary vasodilators. It describes their mechanisms of action in relaxing smooth muscle and dilating blood vessels to reduce systemic vascular resistance and blood pressure. Common vasodilators like hydralazine, ACE inhibitors, and minoxidil are used to treat conditions like hypertension, heart failure, preeclampsia, angina, and pulmonary hypertension. Side effects can include chest pain, changes in heart rate, fluid retention, headaches, and flushing.
Inotropes and vasopressors
1. This document discusses various inotropes and vasopressors used to treat shock states including dobutamine, dopamine, epinephrine, and norepinephrine.
2. It provides guidelines on administering these drugs including desired dose ranges, how to calculate infusion rates, and examples of calculating dobutamine infusion rates.
3. The document also matches different shock states, such as septic shock, cardiogenic shock, and hemorrhagic shock, with recommended first-tier and second-tier drug treatments.
Inotropes and their choice
This document discusses inotropic agents, which are drugs that affect the strength of contraction of the heart muscle. It describes positive inotropes that increase contraction and negative inotropes that decrease contraction. The choice of inotrope depends on its pharmacological effects and the specific cardiovascular condition. Positive inotropes discussed include calcium, calcium sensitizers like levosimendan, catecholamines, cardiac glycosides, and others. Negative inotropes include beta blockers, calcium channel blockers, and antiarrhythmics. The mechanisms and effects of various catecholamines like dopamine, dobutamine, epinephrine, and dopexamine are also outlined.
Ionotropes and vasopressor use in the ED
This document discusses the use of inotropes and vasopressors in the emergency department for management of shock. It provides an overview of different drug classes including their mechanisms of action, dosages, and side effects. Case studies are presented to demonstrate how these drugs may be used in scenarios involving hypotension, shock, and heart block. Key drugs discussed include norepinephrine, dopamine, adrenaline, metaraminol, and isoprenaline. The document emphasizes the importance of determining the type of shock and selecting an appropriate drug to increase cardiac output, systemic vascular resistance, or both depending on the clinical situation.
Inotropes and vasopressors in cardiogenic shock
Cardiogenic shock is defined as hypotension and hypoperfusion due to left ventricular dysfunction. Inotropes and vasopressors may be used to increase cardiac output and blood pressure to improve organ perfusion. Dobutamine is an inotrope that also causes vasodilation. Norepinephrine is a potent vasopressor with weak inotropic effects. Levosimendan is a calcium sensitizer that increases contractility while also causing vasodilation. Guidelines recommend considering short-term inotropes for hypotension and hypoperfusion, and norepinephrine if additional vasopressor support is needed. Close monitoring is important due to risks of arrhythmias and ischemia.
Vasodilators and vasoconstrictors
Vasoactive drugs act on vascular smooth muscle to cause vasoconstriction or vasodilation. Vasoconstrictors such as endothelin, angiotensin II, and ADH cause contraction through increasing calcium levels or sensitivity. Vasodilators such as calcium channel blockers, ACE inhibitors, and nitrates cause relaxation through decreasing calcium, increasing cGMP/cAMP, or inhibiting phosphodiesterases. The vascular endothelium releases various mediators like prostanoids, nitric oxide, and C-type natriuretic peptide that regulate vascular tone. RAAS activation leads to vasoconstriction and sodium retention through angiotensin II, while drugs blocking RAAS cause indirect vasodilation.
Drugs used in the treatment of angina pectoris
Drugs are used to treat angina pectoris by two main strategies - reducing oxygen demand on the heart and increasing oxygen delivery. Nitrates are commonly used to treat angina by both strategies. They reduce preload and afterload, thereby reducing oxygen demand, and can also increase delivery by reducing coronary vasospasm. Calcium channel blockers and beta blockers also reduce oxygen demand. Myocardial revascularization can increase delivery by improving blood flow through coronary bypass grafting or angioplasty.
Renin angiotensin system
This document discusses drugs that inhibit the renin-angiotensin system for treating hypertension and other conditions. It describes how ACE inhibitors work by inhibiting the angiotensin converting enzyme and decreasing angiotensin II formation, while also increasing bradykinin levels. Angiotensin receptor blockers competitively block the angiotensin II receptor. Both classes lower blood pressure by vasodilation and reduced sodium retention. They are used to treat hypertension, heart failure, diabetic nephropathy, and myocardial infarction. Adverse effects include hypotension, hyperkalemia, and cough with ACE inhibitors.
Anti-Anginal drugs
This document discusses various drugs used to treat angina pectoris, which is chest pain due to myocardial ischemia. It describes several classes of antianginal drugs that work by either increasing oxygen supply to the heart or decreasing oxygen demand. These include organic nitrates like glyceryl trinitrate, beta-blockers, calcium channel blockers, and ACE inhibitors. The document provides details on the mechanisms and sites of action of these drug classes as well as their adverse effects. Alternative treatment methods for ischemic heart disease like rotational atherectomy are also mentioned.
Congestive Heart Failure and Drugs used in CCF by Dr. Pawan
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs or receive blood returning to the heart. It is classified as left or right, chronic or acute, and low or high output failure. Common causes include hypertension, heart attacks, congenital heart disease, and cardiomyopathy. Treatment involves reducing the workload on the heart through medications like diuretics, ACE inhibitors, beta-blockers, and vasodilators to decrease preload and afterload and manage fluid retention and edema. The goal is to improve symptoms and prolong life for patients with congestive heart failure.
Vasopressors in Sepsis
This document summarizes recommendations for vasopressor therapy in sepsis and septic shock. It discusses the pathophysiology of sepsis and progression to septic shock. Early sepsis is characterized by hypovolemia, lactic acidosis, and increased oxygen extraction. Late-stage septic shock involves vasoplegia, reduced stroke volume, microcirculatory failure, and mitochondrial dysfunction leading to multi-organ failure. The document recommends norepinephrine as the initial vasopressor and considers epinephrine, vasopressin, and dobutamine as adjunctive therapies. It cautions against the use of dopamine and phenylephrine based on their adverse effects.
Vasopressors Presentation_final
This document discusses types of shock, goals of therapy for different shock states, and vasopressor pharmacology. It defines hypovolemic, cardiogenic, septic, neurogenic, and combined shocks. The goals for hypovolemic shock are to increase preload with fluids, while cardiogenic shock aims to increase cardiac output with drugs like dopamine or dobutamine. Septic and neurogenic shock goals are to first increase preload then increase afterload with vasopressors like norepinephrine, phenylephrine, and vasopressin. Norepinephrine is usually the initial vasopressor, while other drugs like dopamine, epinephrine, vasopressin may be used as adjunct
Vasodilators and antihypertensive agents-Dr.Jibachha Sah,M.V.Sc,Lecturer
Dr. Jibachha Sah,M.V.Sc( Veterinary pharmacology, TU,Nepal),posted lecturer notes on AUTONOMIC AND SYSTEMIC PHARMACOLOGY for B.V.Sc & A.H. 6 th semester veterinary students of College of veterinary science,Nepal Polytechnique Institute, Bharatpur, Bhojard, Chitwan, Nepal.I hope this lecture notes may be beneficial for other Nepalese veterinary students. Please send your comment and suggestion .Email:jibachhashah@gmail.com,moble,00977-9845024121
Vasoactive drugs
This document discusses vasoactive drugs, which affect vasomotor tone by causing vasoconstriction or vasodilation. It describes several classes of vasoactive drugs including vasodilators like hydralazine and nitroglycerin that work by different mechanisms in the arteries and veins. Vasoconstrictors like phenylephrine and vasopressin are also discussed. Many vasoactive drugs have direct effects on the heart by acting on receptors in the cardiovascular system. Inodilators like milrinone cause both vasodilation and increased cardiac contractility. Specific drugs such as dopamine, norepinephrine, and epinephrine are explained in terms of their vascular and cardiac effects.
Vasodilator Lecture
This document discusses various drug treatments for congestive heart failure. It describes how beta blockers, ACE inhibitors, angiotensin II inhibitors, vasodilators like nitrates, and other drugs work to impact factors like preload, contractility, cardiac output, and afterload. It outlines the mechanisms of action, hemodynamic effects, advantages, and potential undesirable side effects of different classes of heart failure drugs.
Antianginal drugs
This document discusses different types of drugs used to treat angina pectoris. It describes 5 main classes of antianginal drugs: 1) Nitrates like glyceryl trinitrate that work by releasing nitric oxide to cause vasodilation. 2) Beta blockers like propranolol that reduce cardiac workload and oxygen demand. 3) Calcium channel blockers like verapamil and nifedipine that relax arteries by decreasing intracellular calcium. 4) Potassium channel openers like nicorandil that activate potassium channels to cause vasodilation. 5) Other drugs like trimetazidine that reduce angina frequency through non-hemodynamic mechanisms. The document provides details on the mechanisms and uses
9 cardiac glycosides
This document discusses treatments for congestive heart failure (CHF), focusing on digitalis glycosides and other positive inotropic agents. It provides details on:
- The mechanisms of action and molecular effects of digitalis glycosides, which increase cardiac contractility and output, lowering venous pressure and edema.
- Other positive inotropic drugs used in acute CHF like dobutamine and phosphodiesterase inhibitors.
- Drugs that reduce cardiac preload and edema like diuretics and angiotensin converting enzyme inhibitors, which lower blood pressure and sympathetic tone.
The document explains the benefits, side effects and clinical uses of various CHF drugs in detail through multiple sections and diagrams.
Vasopressors and inotropes
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.
Ionotrops 3
This document discusses ionotropes, which are drugs that increase the force of contraction of the myocardial muscle. Positive ionotropes stimulate smooth muscle contraction in capillaries and arteries, causing vasoconstriction and increased blood pressure, improving tissue perfusion and oxygenation. The document categorizes ionotropes based on their effects on contractility, heart rate, systemic vascular resistance, mean arterial pressure and other factors. It also discusses how different ionotropes work through receptors and second messengers like cAMP to increase contractility. The combinations of various ionotropes with different receptor specificities and hemodynamic effects are described.
Vasodilators
This document discusses various vasodilators used to treat conditions like hypertension, heart failure, and peripheral vascular disease. It describes different classes of vasodilators including direct-acting vasodilators like calcium channel blockers and drugs that increase cyclic nucleotides, and indirect vasodilators that interfere with the sympathetic nervous system or renin-angiotensin system. Specific vasodilators discussed in detail include nitroglycerin, hydralazine, minoxidil, diazoxide, nitric oxide, and natriuretic peptides. Their mechanisms of action, pharmacological effects, uses, and adverse effect profiles are summarized.
Types of Angina,Nitrates and Nitrites
Angina is chest pain due to reduced blood flow to the heart muscle. There are three main types: atherosclerotic angina caused by plaque buildup, vasospastic angina occurring at rest from artery spasm, and unstable angina with increased attacks. Nitrates like nitroglycerin are used to treat angina by dilating blood vessels and reducing oxygen demand on the heart. They work by increasing nitric oxide which causes smooth muscle relaxation. While effective for angina relief, nitrates can cause side effects like headaches and low blood pressure, and tolerance can develop with regular use.
Class cardiotonic
The document discusses various drugs that can increase the force of myocardial contraction, known as positive inotropic drugs, including cardiac glycosides like digoxin, beta-adrenergic agonists, and phosphodiesterase inhibitors. It provides details on the mechanisms of action and effects of these drugs, such as how cardiac glycosides inhibit the sodium-potassium ATPase pump to increase intracellular calcium levels. A variety of conditions are also listed where these positive inotropic drugs may be used, including congestive heart failure, shock, and cardiac emergencies.
Emergency drugs
This document summarizes several emergency drugs including their trade names, chemical classes, functional classes, and mechanisms of action. Epinephrine increases heart rate and blood pressure through effects on the sympathetic nervous system. Furosemide is a loop diuretic that inhibits sodium reabsorption in the kidneys, decreasing blood pressure and edema. Sodium bicarbonate breaks down into ions that increase bicarbonate levels and neutralize gastric acid. Dopamine and dobutamine are catecholamines that increase cardiac output and blood pressure through effects on adrenergic receptors. Atropine blocks muscarinic receptors to reduce muscarinic effects. Hydrocortisone suppresses inflammation. Morphine depresses pain
Inotropes and Vasopressors.pptx
This document provides an overview of inotropes and vasopressors. It discusses how inotropes such as dobutamine work to increase cardiac contractility as positive inotropes, while drugs like calcium channel blockers act as negative inotropes. Vasopressors like norepinephrine work mainly through alpha receptors to increase blood pressure. The document reviews the mechanisms and indications for various inotropes and vasopressors. It also discusses factors like preload, afterload and contractility that influence cardiac output, and how drugs can be used to optimize these factors in conditions like cardiogenic shock. Monitoring of parameters like blood pressure, cardiac output and central venous pressure is important when using these
Inotropesfs
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.
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Ionotropes and vasopressor use in the ED
This document discusses the use of inotropes and vasopressors in the emergency department for management of shock. It provides an overview of different drug classes including their mechanisms of action, dosages, and side effects. Case studies are presented to demonstrate how these drugs may be used in scenarios involving hypotension, shock, and heart block. Key drugs discussed include norepinephrine, dopamine, adrenaline, metaraminol, and isoprenaline. The document emphasizes the importance of determining the type of shock and selecting an appropriate drug to increase cardiac output, systemic vascular resistance, or both depending on the clinical situation.
Inotropes and vasopressors in cardiogenic shock
Cardiogenic shock is defined as hypotension and hypoperfusion due to left ventricular dysfunction. Inotropes and vasopressors may be used to increase cardiac output and blood pressure to improve organ perfusion. Dobutamine is an inotrope that also causes vasodilation. Norepinephrine is a potent vasopressor with weak inotropic effects. Levosimendan is a calcium sensitizer that increases contractility while also causing vasodilation. Guidelines recommend considering short-term inotropes for hypotension and hypoperfusion, and norepinephrine if additional vasopressor support is needed. Close monitoring is important due to risks of arrhythmias and ischemia.
Vasodilators and vasoconstrictors
Vasoactive drugs act on vascular smooth muscle to cause vasoconstriction or vasodilation. Vasoconstrictors such as endothelin, angiotensin II, and ADH cause contraction through increasing calcium levels or sensitivity. Vasodilators such as calcium channel blockers, ACE inhibitors, and nitrates cause relaxation through decreasing calcium, increasing cGMP/cAMP, or inhibiting phosphodiesterases. The vascular endothelium releases various mediators like prostanoids, nitric oxide, and C-type natriuretic peptide that regulate vascular tone. RAAS activation leads to vasoconstriction and sodium retention through angiotensin II, while drugs blocking RAAS cause indirect vasodilation.
Drugs used in the treatment of angina pectoris
Drugs are used to treat angina pectoris by two main strategies - reducing oxygen demand on the heart and increasing oxygen delivery. Nitrates are commonly used to treat angina by both strategies. They reduce preload and afterload, thereby reducing oxygen demand, and can also increase delivery by reducing coronary vasospasm. Calcium channel blockers and beta blockers also reduce oxygen demand. Myocardial revascularization can increase delivery by improving blood flow through coronary bypass grafting or angioplasty.
Renin angiotensin system
This document discusses drugs that inhibit the renin-angiotensin system for treating hypertension and other conditions. It describes how ACE inhibitors work by inhibiting the angiotensin converting enzyme and decreasing angiotensin II formation, while also increasing bradykinin levels. Angiotensin receptor blockers competitively block the angiotensin II receptor. Both classes lower blood pressure by vasodilation and reduced sodium retention. They are used to treat hypertension, heart failure, diabetic nephropathy, and myocardial infarction. Adverse effects include hypotension, hyperkalemia, and cough with ACE inhibitors.
Anti-Anginal drugs
This document discusses various drugs used to treat angina pectoris, which is chest pain due to myocardial ischemia. It describes several classes of antianginal drugs that work by either increasing oxygen supply to the heart or decreasing oxygen demand. These include organic nitrates like glyceryl trinitrate, beta-blockers, calcium channel blockers, and ACE inhibitors. The document provides details on the mechanisms and sites of action of these drug classes as well as their adverse effects. Alternative treatment methods for ischemic heart disease like rotational atherectomy are also mentioned.
Congestive Heart Failure and Drugs used in CCF by Dr. Pawan
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs or receive blood returning to the heart. It is classified as left or right, chronic or acute, and low or high output failure. Common causes include hypertension, heart attacks, congenital heart disease, and cardiomyopathy. Treatment involves reducing the workload on the heart through medications like diuretics, ACE inhibitors, beta-blockers, and vasodilators to decrease preload and afterload and manage fluid retention and edema. The goal is to improve symptoms and prolong life for patients with congestive heart failure.
Vasopressors in Sepsis
This document summarizes recommendations for vasopressor therapy in sepsis and septic shock. It discusses the pathophysiology of sepsis and progression to septic shock. Early sepsis is characterized by hypovolemia, lactic acidosis, and increased oxygen extraction. Late-stage septic shock involves vasoplegia, reduced stroke volume, microcirculatory failure, and mitochondrial dysfunction leading to multi-organ failure. The document recommends norepinephrine as the initial vasopressor and considers epinephrine, vasopressin, and dobutamine as adjunctive therapies. It cautions against the use of dopamine and phenylephrine based on their adverse effects.
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This document discusses types of shock, goals of therapy for different shock states, and vasopressor pharmacology. It defines hypovolemic, cardiogenic, septic, neurogenic, and combined shocks. The goals for hypovolemic shock are to increase preload with fluids, while cardiogenic shock aims to increase cardiac output with drugs like dopamine or dobutamine. Septic and neurogenic shock goals are to first increase preload then increase afterload with vasopressors like norepinephrine, phenylephrine, and vasopressin. Norepinephrine is usually the initial vasopressor, while other drugs like dopamine, epinephrine, vasopressin may be used as adjunct
Vasodilators and antihypertensive agents-Dr.Jibachha Sah,M.V.Sc,Lecturer
Dr. Jibachha Sah,M.V.Sc( Veterinary pharmacology, TU,Nepal),posted lecturer notes on AUTONOMIC AND SYSTEMIC PHARMACOLOGY for B.V.Sc & A.H. 6 th semester veterinary students of College of veterinary science,Nepal Polytechnique Institute, Bharatpur, Bhojard, Chitwan, Nepal.I hope this lecture notes may be beneficial for other Nepalese veterinary students. Please send your comment and suggestion .Email:jibachhashah@gmail.com,moble,00977-9845024121
Vasoactive drugs
This document discusses vasoactive drugs, which affect vasomotor tone by causing vasoconstriction or vasodilation. It describes several classes of vasoactive drugs including vasodilators like hydralazine and nitroglycerin that work by different mechanisms in the arteries and veins. Vasoconstrictors like phenylephrine and vasopressin are also discussed. Many vasoactive drugs have direct effects on the heart by acting on receptors in the cardiovascular system. Inodilators like milrinone cause both vasodilation and increased cardiac contractility. Specific drugs such as dopamine, norepinephrine, and epinephrine are explained in terms of their vascular and cardiac effects.
Vasodilator Lecture
This document discusses various drug treatments for congestive heart failure. It describes how beta blockers, ACE inhibitors, angiotensin II inhibitors, vasodilators like nitrates, and other drugs work to impact factors like preload, contractility, cardiac output, and afterload. It outlines the mechanisms of action, hemodynamic effects, advantages, and potential undesirable side effects of different classes of heart failure drugs.
Antianginal drugs
This document discusses different types of drugs used to treat angina pectoris. It describes 5 main classes of antianginal drugs: 1) Nitrates like glyceryl trinitrate that work by releasing nitric oxide to cause vasodilation. 2) Beta blockers like propranolol that reduce cardiac workload and oxygen demand. 3) Calcium channel blockers like verapamil and nifedipine that relax arteries by decreasing intracellular calcium. 4) Potassium channel openers like nicorandil that activate potassium channels to cause vasodilation. 5) Other drugs like trimetazidine that reduce angina frequency through non-hemodynamic mechanisms. The document provides details on the mechanisms and uses
9 cardiac glycosides
This document discusses treatments for congestive heart failure (CHF), focusing on digitalis glycosides and other positive inotropic agents. It provides details on:
- The mechanisms of action and molecular effects of digitalis glycosides, which increase cardiac contractility and output, lowering venous pressure and edema.
- Other positive inotropic drugs used in acute CHF like dobutamine and phosphodiesterase inhibitors.
- Drugs that reduce cardiac preload and edema like diuretics and angiotensin converting enzyme inhibitors, which lower blood pressure and sympathetic tone.
The document explains the benefits, side effects and clinical uses of various CHF drugs in detail through multiple sections and diagrams.
Vasopressors and inotropes
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.
Ionotrops 3
This document discusses ionotropes, which are drugs that increase the force of contraction of the myocardial muscle. Positive ionotropes stimulate smooth muscle contraction in capillaries and arteries, causing vasoconstriction and increased blood pressure, improving tissue perfusion and oxygenation. The document categorizes ionotropes based on their effects on contractility, heart rate, systemic vascular resistance, mean arterial pressure and other factors. It also discusses how different ionotropes work through receptors and second messengers like cAMP to increase contractility. The combinations of various ionotropes with different receptor specificities and hemodynamic effects are described.
Vasodilators
This document discusses various vasodilators used to treat conditions like hypertension, heart failure, and peripheral vascular disease. It describes different classes of vasodilators including direct-acting vasodilators like calcium channel blockers and drugs that increase cyclic nucleotides, and indirect vasodilators that interfere with the sympathetic nervous system or renin-angiotensin system. Specific vasodilators discussed in detail include nitroglycerin, hydralazine, minoxidil, diazoxide, nitric oxide, and natriuretic peptides. Their mechanisms of action, pharmacological effects, uses, and adverse effect profiles are summarized.
Types of Angina,Nitrates and Nitrites
Angina is chest pain due to reduced blood flow to the heart muscle. There are three main types: atherosclerotic angina caused by plaque buildup, vasospastic angina occurring at rest from artery spasm, and unstable angina with increased attacks. Nitrates like nitroglycerin are used to treat angina by dilating blood vessels and reducing oxygen demand on the heart. They work by increasing nitric oxide which causes smooth muscle relaxation. While effective for angina relief, nitrates can cause side effects like headaches and low blood pressure, and tolerance can develop with regular use.
Class cardiotonic
The document discusses various drugs that can increase the force of myocardial contraction, known as positive inotropic drugs, including cardiac glycosides like digoxin, beta-adrenergic agonists, and phosphodiesterase inhibitors. It provides details on the mechanisms of action and effects of these drugs, such as how cardiac glycosides inhibit the sodium-potassium ATPase pump to increase intracellular calcium levels. A variety of conditions are also listed where these positive inotropic drugs may be used, including congestive heart failure, shock, and cardiac emergencies.
Emergency drugs
This document summarizes several emergency drugs including their trade names, chemical classes, functional classes, and mechanisms of action. Epinephrine increases heart rate and blood pressure through effects on the sympathetic nervous system. Furosemide is a loop diuretic that inhibits sodium reabsorption in the kidneys, decreasing blood pressure and edema. Sodium bicarbonate breaks down into ions that increase bicarbonate levels and neutralize gastric acid. Dopamine and dobutamine are catecholamines that increase cardiac output and blood pressure through effects on adrenergic receptors. Atropine blocks muscarinic receptors to reduce muscarinic effects. Hydrocortisone suppresses inflammation. Morphine depresses pain
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This document provides an overview of inotropes and vasopressors. It discusses how inotropes such as dobutamine work to increase cardiac contractility as positive inotropes, while drugs like calcium channel blockers act as negative inotropes. Vasopressors like norepinephrine work mainly through alpha receptors to increase blood pressure. The document reviews the mechanisms and indications for various inotropes and vasopressors. It also discusses factors like preload, afterload and contractility that influence cardiac output, and how drugs can be used to optimize these factors in conditions like cardiogenic shock. Monitoring of parameters like blood pressure, cardiac output and central venous pressure is important when using these
Inotropesfs
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.
Inotropes and vasopressors
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.
Cardiac medications
This document provides an overview of various cardiac medications, including their classifications, mechanisms of action, indications for use, dosages, and potential adverse effects. It discusses drugs that work on the cardiovascular system like beta blockers, calcium channel blockers, ACE inhibitors, diuretics, inotropes, antiarrhythmics, and anticoagulants. The document also provides a case study example and discusses preparation for cardiac catheterization.
CARDIOVASCULAR PHARMACOLOGY.ppt
1. The document discusses cardiovascular pharmacology, focusing on drugs used to treat hypertension and heart failure.
2. Several classes of antihypertensive drugs are described, including diuretics, beta-blockers, ACE inhibitors, calcium channel blockers, and vasodilators.
3. Drugs used to treat heart failure that are mentioned include diuretics, ACE inhibitors, beta-blockers, and vasodilators.
Vasopressors
Vasopressors used in operative room, ICU, and critical care set up. there dose, side effect and interaction.
Inotropes
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.
Inotropes
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.
Congestive heart failure
Congestive heart failure (CHF) is a condition where the heart cannot pump enough blood to meet the body's needs. It can be caused by systolic or diastolic dysfunction. Common symptoms include fatigue, weight gain, cough, and shortness of breath. Treatment includes drugs that increase cardiac contractility, reduce fluid retention, block the renin-angiotensin system, dilate blood vessels, and reduce heart rate. New drugs like ivabradine and sacubitril/valsartan may also help lower hospitalization rates.
recent trends in heart failure.pptx
The document summarizes recent trends in the management of heart failure. It discusses the epidemiology and classification of heart failure. The mainstay of treatment involves neurohumoral modulation using ACE inhibitors, ARBs, beta-blockers, and MRAs. Other management principles include preload and afterload reduction, increasing contractility cautiously, and reducing heart rate. Newer drugs like sacubitril/valsartan, dapagliflozin, and vericiguat are improving outcomes, while others like omecamtiv mecarbil and istaroxime are under investigation.
THE USE OF INOTROPIC DRUGS IN CARDIAC SURGERY
This document provides information on various inotropic drugs used in cardiac surgery, including their indications, mechanisms of action, dosages, and side effects. It discusses sympathomimetic drugs like dopamine, dobutamine, and adrenaline that have positive inotropic effects by stimulating cardiac contraction directly. It also mentions the negative inotrope propranolol and vasopressors like adrenaline and noradrenaline. The aim of using inotropes in cardiac surgery is to optimize cardiac output while using the minimum effective dose to achieve desired outcomes and allow weaning off the drugs.
inotropic drugs and vassopressors drugs.pptx
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.
Hypensive urgency and emergency
This document discusses hypertensive urgency and emergency. Hypertensive urgency is severely elevated blood pressure without target organ damage, with symptoms like headache and dizziness. Treatment involves slowly lowering blood pressure over hours to days. Hypertensive emergency is elevated blood pressure that results in organ damage to the brain, heart, or kidneys, requiring immediate treatment to lower blood pressure within minutes to hours to prevent further damage. Specific treatments depend on the affected organ and may include drugs like labetalol, nicardipine, and sodium nitroprusside. The main difference between urgency and emergency is that emergency involves organ damage while urgency does not.
Critical Medications
This document provides summaries of common emergency medications used to treat critical patients. It lists indications, dosages, and considerations for oxygen, epinephrine, atropine, adenosine, amiodarone, dopamine, lidocaine, diltiazem, procainamide, nitroglycerine, magnesium sulfate, and calcium chloride. The document aims to describe the actions and importance of these frequently prescribed critical medications.
inotropes
Dopamine is a chemical precursor of norepinephrine that stimulates alpha, beta, and dopaminergic receptors. At low doses, it causes vasodilation and increased renal blood flow. At intermediate doses, it increases heart rate and cardiac output. At high doses, it increases blood pressure through alpha receptor stimulation. Dobutamine is a synthetic catecholamine that stimulates beta1 and beta2 receptors, causing increased contractility and cardiac output without affecting renal blood flow. Nitroglycerin dilates coronary arteries to improve blood flow and reduces preload, helping to lower blood pressure and myocardial oxygen demand in conditions like hypertension and heart failure.
Inotropes especially noradrenaline PACU.pptx
This document provides information on various inotropic agents including catecholamines like epinephrine, norepinephrine, and dopamine. It discusses their physiology, mechanisms of action, indications, and dosing. Non-catecholamine inotropes described include phosphodiesterase inhibitors, levosimendan, omecamtiv mecarbil, and vasopressin. The document explains how each agent affects cardiac contractility, vascular tone, and blood pressure through different adrenergic receptor pathways and non-receptor mediated mechanisms. Clinical applications include treating shock, heart failure, and hypotension during anesthesia.
Haemodynamic drug infusions
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.
Stress echo.pptx
Stress echocardiography uses ultrasound imaging during physical or pharmacological stress to detect abnormalities in heart wall motion that indicate reduced blood flow to the heart muscle. It can be used to diagnose coronary artery disease, assess heart valve function, and determine heart muscle viability. The document describes different stress techniques, pharmacological agents, protocols, safety, and interpretation of stress echocardiography. Dobutamine stress echocardiography is useful for detecting ischemia and assessing viability while vasodilator stress is better for perfusion imaging. Low dose dobutamine can identify hibernating myocardium through improvement or a biphasic response in segmental wall motion.
seminar on Management of shock
Management of shock involves positioning, airway support, vascular access, fluid resuscitation, monitoring, and medication therapy. The type of shock determines specific treatment, which may include fluid boluses, vasoactive drugs, and treating the underlying cause. Septic shock, the most common distributive shock, results from infection and involves a complex inflammatory response. Treatment focuses on antibiotics, fluids, and vasopressors like dopamine or norepinephrine to support blood pressure. The goal is to identify and treat shock early before organ dysfunction occurs.
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Starling Case Report
- 1. THE CASE OF MR. STARLING The treatment for Mr. Starling’s CHF condition Presented by: Ingvild Kummen Yoav Litani Daniela Levy Khitam Hajuj
- 2. TREATMENT METHODS USED: Furosemide (diuretic, to treat edema and decrease preload) Captopril (ACE inhibitor, to decrease preload) Intravenous fluids (to increase blood pressure) Dobutamine (to increase contractility) Cardiac transplantation
- 3. FUROSEMIDE Diuretic Venodilator Mechanism: Inhibits loop of Henle and proximal and distal convoluted tubule sodium and chloride resorption. furosemide itself stimulates the release of renin, thereby increasing levels of angiotensin 2 3 4 5 as well as of prostaglandins from the kidney. The effects on these two vasoactive hormonal systems have been associated with arterial vasoconstriction and venous vasodilation observed after systemic administration of the drug.
- 4. CAPTOPRIL ACE inhibitor Mechanism: Inhibits the Angiotensin Converting Enzyme that is found in the lung thus inhibits the conversion of Angiotensin I to Angiotensin II. Angiotensin II has many mechanism to increase blood pressure. By blocking the conversion to Angiotenstin II, Captopril decreases the blood pressure.
- 5. RENIN ANGIOTENSIN SYSTEM
- 6. EFFECTS ON MR. STARLING’S VALUES Blood pressure decreases from 102/85 to 80/60 mmHg In addition Mr. Starling reports that is feeling is somewhat improved:“though I don’t feel great, I feel so much better that I now realize how sick I was.” * the administered drugs did not solve the problem since the cardiac output was not improved
- 7. INTRAVENOUS FLUIDS Normal intravenous transfusion is giving a liquid substance directly into the patient's vein. In this case a "Normal Saline" solution was given. The normal saline is a solution of sodium chloride at 0.9% concentration which is isotonic. It was given in order to elevate the decreased blood pressure. The intravenous route is the fastest way to deliver fluids and medications throughout the body.
- 8. DOBUTAMINE Positive ionotropic agent Mechanism: Stimulates β¹ receptors of the sympathetic nervous system. By increasing the contractility, Dobutamine increases the cardiac output while decreases the end systolic volume. Dobutamine is used for congestive heart failure, but it is not useful in case of cardiac ischemia because it increases the oxygen demand of the myocardium. Dobutamine decreases systemic vascular resistance while increasing
- 9. DOBUTAMINE Dobutamine Dopamine Dobutamine has many similarities with Dopamine. Dobutamine has the extra ring section which means it is too bulky to activate dopamine receptors and cause norepinephrine release i.e. it is a selective beta-1 receptor agonist.
- 10. EFFECTS ON MR. STARLING’S VALUES The right atrial pressure decreases from 12 to 20 mmHg The decrease in right atrial pressure reflects the fact that more blood is ejected from the heart with each beat as a result of increased contractility and increased stroke volume. The cardiac output increases from 2,2 to 4,2 L/min The cardiac index increases from 1,2 (cardiogenic shock) to 2,4 L/min/m² The heart rate decreases from 120 to 100 beats pr minute (indirect effect) The brachial artery pressure goes from 100/90 to 120/70 mmHg The Systemic vascular resistance decreases from 2600 to 1400 dyn*sec/cm5
- 11. EFFECTS ON MR. STARLING’S VALUES
- 12. CARDIAC TRANSPLANT Heart transplantations are administered to patients with end stage heart failure. As Mr. sterling still suffered from reoccurring sessions of pulmonary edema and hypotenstion despite the previous heart treatment, he became a suitable candidate for a heart transplantation. The most common procedure is to take a working heart from a recently deceased organ donor (allograft) and implant it into the patient. The patient's own heart may either be removed (orthotopic procedure) or, less commonly, left in to support the donor heart (heterotopic procedure). The patient is also given immunosuppressant medication so that their immune system will not reject the new heart.
- 13. CARDIAC TRANSPLANT The procedure begins with the surgeons performing a median sternotomy to expose the mediastinum. The pericardium is opened, the great vessels are dissected and the patient is attached to cardiopulmonary bypass. The failing heart is removed by transecting the great vessels and a portion of the left atrium. The pulmonary veins are not transected; rather a circular portion of the left atrium containing the pulmonary veins is left in place. The donor heart is trimmed to fit onto the patients remaining left atrium and the great vessels are sutured in place. The new heart is restarted, the patient is weaned from cardiopulmonary bypass and the chest cavity is closed.