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This document summarizes several drugs used to treat hypertension and tachycardia, including labetalol, esmolol, nicardipine, sodium nitroprusside, nitroglycerin, hydralazine, fenoldopam, and clevidipine. For each drug, it provides the initial dose, maximum dose, mechanism of action, site of vasodilation, onset time, duration of action, metabolism pathway, and any important notes. The drugs have different mechanisms including alpha/beta blockade, beta1 blockade, calcium channel blockade, nitric oxide effects, and D1 agonism. Nicardipine and fenoldopam are noted as preferred options in certain conditions.
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Thrombolytics and Fibrinolytics
1) The document discusses various drugs used to treat clotting disorders including anticoagulants, antiplatelets, and thrombolytics. Anticoagulants prevent clotting while antiplatelets inhibit platelet aggregation. Thrombolytics dissolve existing clots.
2) Common anticoagulants discussed are heparin, warfarin, and newer oral anticoagulants that inhibit thrombin or Factor Xa. Thrombolytics discussed include streptokinase, urokinase, anistreplase, and tissue plasminogen activators like alteplase.
3) Thrombolytics work by activating plasminogen to form plasmin,
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1. The document discusses various anticoagulants and antiplatelet drugs used in hemostasis and thrombosis including heparin, warfarin, aspirin, clopidogrel, and thrombolytics.
2. It describes the mechanisms of action, pharmacokinetics, uses, and adverse effects of these drugs.
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Drugs used in blood disorders by pharm bash
Thrombolytic drugs like streptokinase, alteplase, and urokinase are used to treat myocardial infarction by breaking up blood clots. They work by activating plasminogen into plasmin, which degrades fibrin in clots. Streptokinase is non-specific and can cause bleeding. Alteplase is fibrin-specific, reducing bleeding risk. Aminocaproic acid and tranexamic acid inhibit fibrinolysis and are used to prevent or treat bleeding from thrombolytic drugs.
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The document discusses various fibrinolytics (thrombolytics), antifibrinolytics, and antiplatelet drugs. It describes the mechanisms of fibrinolytics like streptokinase, urokinase, and recombinant tissue plasminogen activator (rt-PA) in breaking down blood clots. It also discusses antifibrinolytics like epsilon amino-caproic acid and tranexamic acid which inhibit fibrinolysis. Common antiplatelet drugs mentioned include aspirin and dipyridamole which interfere with platelet function to prevent thromboembolic disorders.
Thrombolytics notes by P. Varalakshmi
thrombolytics notes
Thrombolytic therapy is the use of drugs to break up or dissolve blood clots, which are the main cause of both heart attacks and stroke.
Antiplatelet drugs
This document summarizes different types of antiplatelet drugs. It discusses how platelet aggregation occurs through interactions between collagen, platelet receptors, and release of substances like thromboxane A2 and ADP. It then categorizes main classes of antiplatelet drugs as aspirin, dipyridamole, P2Y12 receptor blockers like clopidogrel and prasugrel, and GP IIb/IIIa receptor antagonists like abciximab, eptifibatide, and tirofiban. For each drug, it provides information on mechanism of action, pharmacokinetics, clinical uses, and side effects. The overall document provides a concise overview of the mechanisms and classes of
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Fibrinolytics such as streptokinase, urokinase, and tissue plasminogen activators activate plasminogen and break down blood clots. Antifibrinolytics like epsilon amino caproic acid and tranexamic acid compete for plasminogen binding sites to inhibit fibrinolysis. They are used to control bleeding during and after surgery or trauma. Aprotinin is a serine protease inhibitor that was previously used during cardiac surgery and liver transplantation to reduce bleeding but was withdrawn due to safety concerns like renal failure and thrombosis.
Thrombolytics ppt
Blood clots can cause serious medical issues if they block arteries or veins. Thrombolytic drugs work by activating plasminogen into plasmin, an enzyme that breaks down fibrin in clots. The three main types of thrombolytic drugs are streptokinase, urokinase, and tissue plasminogen activators (TPA). While all three work to break down clots, TPA is more specific to clots and has fewer side effects than the other drugs. Thrombolytic drugs are used to treat conditions like heart attacks, strokes, and pulmonary embolisms but have risks of bleeding if overused or in the wrong patients.
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Thrombolytics and Fibrinolytics
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2) Common anticoagulants discussed are heparin, warfarin, and newer oral anticoagulants that inhibit thrombin or Factor Xa. Thrombolytics discussed include streptokinase, urokinase, anistreplase, and tissue plasminogen activators like alteplase.
3) Thrombolytics work by activating plasminogen to form plasmin,
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Thrombolytic drugs like streptokinase, alteplase, and urokinase are used to treat myocardial infarction by breaking up blood clots. They work by activating plasminogen into plasmin, which degrades fibrin in clots. Streptokinase is non-specific and can cause bleeding. Alteplase is fibrin-specific, reducing bleeding risk. Aminocaproic acid and tranexamic acid inhibit fibrinolysis and are used to prevent or treat bleeding from thrombolytic drugs.
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Thrombolytics notes by P. Varalakshmi
thrombolytics notes
Thrombolytic therapy is the use of drugs to break up or dissolve blood clots, which are the main cause of both heart attacks and stroke.
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Thrombolytics ppt
Blood clots can cause serious medical issues if they block arteries or veins. Thrombolytic drugs work by activating plasminogen into plasmin, an enzyme that breaks down fibrin in clots. The three main types of thrombolytic drugs are streptokinase, urokinase, and tissue plasminogen activators (TPA). While all three work to break down clots, TPA is more specific to clots and has fewer side effects than the other drugs. Thrombolytic drugs are used to treat conditions like heart attacks, strokes, and pulmonary embolisms but have risks of bleeding if overused or in the wrong patients.
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This will discuss Pharmacology of antiplatelets, thrombolytics and hemostats along with their indications and adverse effects.
Thrombolytics ppt
Thrombolytics are drugs used to lyse blood clots by activating the body's natural fibrinolytic system. The key enzyme involved is plasmin, which is generated from plasminogen by tissue plasminogen activator (t-PA) produced by endothelial cells. t-PA selectively activates fibrin-bound plasminogen within clots. Several thrombolytics are discussed, including streptokinase, urokinase, alteplase, reteplase, and tenecteplase. The document provides details on the sources, mechanisms of action, advantages and disadvantages of each thrombolytic. The main uses of thrombolytics are for acute myocardial infarction, deep vein thrombosis, pulmonary embolism
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2) Immediate reperfusion therapy with either primary percutaneous coronary intervention (PCI) or fibrinolysis is recommended for STEMI patients. The goals are to perform primary PCI within 90 minutes of first medical contact or give fibrinolysis within 30 minutes.
3) Several fibrinolytic agents are discussed including alteplase, reteplase, tenecteplase, and streptokinase. Their properties, dosages, and effectiveness are compared. Successful reperfusion is assessed by resolution of symptoms and ECG changes.
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Fibrinolytics, also known as thrombolytics, work to dissolve blood clots and are used to treat conditions like heart attacks, deep vein thrombosis, and pulmonary embolism. The main fibrinolytic agents discussed are streptokinase, tissue plasminogen activator (t-PA), and its variants reteplase and tenecteplase. These work by activating plasminogen and converting it to plasmin to break down fibrin clots. Their use comes with risks of hemorrhage, so antifibrinolytic drugs like tranexamic acid and aminocaproic acid are used to reduce bleeding when fibrinolytics are given.
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Please find the power point on Pharmacology of Anticoagulants, antiplatelets . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Thrombolysis In Acute MI Current Status Kiernan Med Clin N Am 2007 91 617 637
This document summarizes the current status of thrombolysis in acute myocardial infarction. It discusses the historical use of fibrinolytic agents like streptokinase and tissue plasminogen activator. It also reviews large randomized controlled trials from the 1980s that demonstrated a reduction in mortality with thrombolytic therapy compared to placebo when administered within 12 hours of symptom onset. Specifically, the GISSI-1 trial showed an 18% relative reduction in mortality, and the ISIS-2 trial showed reductions of 23% with aspirin alone and 42% with aspirin and streptokinase. The greatest benefit is seen when thrombolysis is administered very early, within the first 2-3 hours of symptoms.
ppt Presentation of thrombolytics drugs by Dr xrshad Danish
Thrombosis is the formation of a blood clot within a blood vessel. A thrombus can form in any vessel when blood flow is slowed. Thrombolytics are drugs used to dissolve blood clots and reopen vessels. Examples include streptokinase, urokinase, and tissue plasminogen activators like alteplase, reteplase, and tenecteplase. These drugs work by activating plasmin which degrades the clot. Their use requires weighing the risks of bleeding against the benefits of clot lysis. Aminocaproic acid and tranexamic acid can inhibit fibrinolysis and are used to prevent or treat bleeding risks from thrombolytics.
Anticoagulantpresentation sp10-95slides2
This document summarizes drugs used to treat blood dysfunctions related to thrombosis, bleeding, and anemia. It describes the formation of blood clots and the drugs used to regulate clotting, focusing on platelet activation and aggregation inhibitors like aspirin, clopidogrel, abciximab, eptifibatide, and tirofiban. It also discusses the coagulation cascade and anticoagulants like heparin and warfarin that inhibit coagulation factors to prevent unwanted clotting.
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This ppt is important for UG MBBS, PG Pharmacology and any other healthcare person interested in Antiplatelet drugs.
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This document summarizes fibrinolytics and antiplatelet drugs. It discusses the fibrinolytic system and lists fibrinolytics such as streptokinase, urokinase, alteplase, and newer recombinant tissue plasminogen activators. It also discusses their uses for conditions like myocardial infarction and mechanisms of action. The document then discusses antiplatelet drugs, focusing on mechanisms of platelet aggregation and inhibition. It lists classes of antiplatelet drugs like aspirin, dipyridamole, clopidogrel, and abciximab and their uses, mechanisms, and side effects. Finally, it lists common uses of antiplatelet drugs for conditions like coronary artery disease and angioplasty.
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Fibrinolytics such as streptokinase, urokinase, alteplase, reteplase, and tenecteplase activate the natural fibrinolytic system and lyse thrombi to recanalize occluded blood vessels. They are used to treat myocardial infarction, deep vein thrombosis, pulmonary embolism, and peripheral arterial occlusion. Antifibrinolytics like epsilon amino-caproic acid and tranexamic acid inhibit plasminogen activation and clot dissolution to prevent or control bleeding caused by fibrinolytics or surgical procedures. The timing of fibrinolytic administration is critical for heart attack treatment, with better outcomes seen within 1-3 hours of symptom onset.
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Fibrinolytics and antifibrinolytics
Fibrinolytics such as streptokinase, urokinase, and alteplase work by activating the natural fibrinolytic system to lyse thrombi and recanalize occluded blood vessels. They activate plasminogen to plasm in order to dissolve blood clots through the process of fibrinolysis. Streptokinase is the least expensive but also the least specific and can cause allergic reactions. Urokinase is non-antigenic and adverse effects are rare. Alteplase is fibrin-specific, rapid-acting, and has a lower risk of bleeding but is more expensive. Fibrinolytics are used to treat conditions like myocardial infarction, deep vein thrombosis, and pulmonary
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Magnesium plays an important physiological role as an intracellular and extracellular cation. It is involved in many metabolic processes and acts as a physiological antagonist to calcium. Hypomagnesemia can occur due to inadequate intake, excess renal losses, or redistribution. It can manifest as cardiovascular, neuromuscular, or psychiatric symptoms. Magnesium sulfate is used to treat and prevent eclampsia and preeclampsia by reducing cerebral vasospasm. It is also used for cardiovascular indications such as arrhythmias. Magnesium can impact anesthesia by potentiating neuromuscular blockade and decreasing acetylcholine release.
Magnesium and anaesthesia
This document discusses magnesium and its role in anaesthesia. It begins by describing magnesium's physiological functions, distribution in the body, and homeostasis. It then covers the pharmacology of magnesium sulfate, causes and manifestations of hypo- and hypermagnesemia, and treatment of magnesium deficiencies and toxicities. The document also discusses the use of magnesium sulfate for preeclampsia/eclampsia prevention and treatment, as well as its applications in cardiovascular anesthesia and management of other conditions like asthma and tetanus.
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Thrombolytics are drugs used to lyse blood clots by activating the body's natural fibrinolytic system. The key enzyme involved is plasmin, which is generated from plasminogen by tissue plasminogen activator (t-PA) produced by endothelial cells. t-PA selectively activates fibrin-bound plasminogen within clots. Several thrombolytics are discussed, including streptokinase, urokinase, alteplase, reteplase, and tenecteplase. The document provides details on the sources, mechanisms of action, advantages and disadvantages of each thrombolytic. The main uses of thrombolytics are for acute myocardial infarction, deep vein thrombosis, pulmonary embolism
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3) Several fibrinolytic agents are discussed including alteplase, reteplase, tenecteplase, and streptokinase. Their properties, dosages, and effectiveness are compared. Successful reperfusion is assessed by resolution of symptoms and ECG changes.
Fibrinolytic agents
Fibrinolytics, also known as thrombolytics, work to dissolve blood clots and are used to treat conditions like heart attacks, deep vein thrombosis, and pulmonary embolism. The main fibrinolytic agents discussed are streptokinase, tissue plasminogen activator (t-PA), and its variants reteplase and tenecteplase. These work by activating plasminogen and converting it to plasmin to break down fibrin clots. Their use comes with risks of hemorrhage, so antifibrinolytic drugs like tranexamic acid and aminocaproic acid are used to reduce bleeding when fibrinolytics are given.
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Antiplatelets and fibrinolytics are used to treat thrombosis. Aspirin is the main antiplatelet drug and works by inhibiting platelet aggregation. Other antiplatelets include clopidogrel, dipyridamole, and GPIIb/IIIa inhibitors. Fibrinolytics such as streptokinase, alteplase, and tenecteplase dissolve blood clots by activating the body's fibrinolytic system. Antiplatelets are used to prevent arterial thrombosis and reduce risks of heart attack and stroke. Fibrinolytics are primarily used for heart attacks to restore blood flow in acute myocardial infarction. Both antiplatelets and fibrinolytics have benefits but also risks like bleeding that require consideration
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Alteplase is a thrombolytic agent produced through recombinant DNA technology. It is used to treat heart attacks, pulmonary embolisms, and strokes by breaking up blood clots through the conversion of plasminogen to plasmin. The drug has a short half-life of 4-8 minutes and is administered via intravenous infusion over hours. Side effects include bleeding and hemorrhaging while drug interactions can increase the risk of bleeding when combined with other anticoagulants. Patients are counseled about monitoring for signs of bleeding after treatment.
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Please find the power point on Pharmacology of Anticoagulants, antiplatelets . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
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This document summarizes the current status of thrombolysis in acute myocardial infarction. It discusses the historical use of fibrinolytic agents like streptokinase and tissue plasminogen activator. It also reviews large randomized controlled trials from the 1980s that demonstrated a reduction in mortality with thrombolytic therapy compared to placebo when administered within 12 hours of symptom onset. Specifically, the GISSI-1 trial showed an 18% relative reduction in mortality, and the ISIS-2 trial showed reductions of 23% with aspirin alone and 42% with aspirin and streptokinase. The greatest benefit is seen when thrombolysis is administered very early, within the first 2-3 hours of symptoms.
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Thrombosis is the formation of a blood clot within a blood vessel. A thrombus can form in any vessel when blood flow is slowed. Thrombolytics are drugs used to dissolve blood clots and reopen vessels. Examples include streptokinase, urokinase, and tissue plasminogen activators like alteplase, reteplase, and tenecteplase. These drugs work by activating plasmin which degrades the clot. Their use requires weighing the risks of bleeding against the benefits of clot lysis. Aminocaproic acid and tranexamic acid can inhibit fibrinolysis and are used to prevent or treat bleeding risks from thrombolytics.
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Antiplatelet Drugs
This ppt is important for UG MBBS, PG Pharmacology and any other healthcare person interested in Antiplatelet drugs.
PHARMACOLOGY - Fibrinolytic Drugs
Streptokinase and tissue plasminogen activator (t-PA) are fibrinolytic drugs that activate plasminogen to induce fibrinolysis. Streptokinase forms a complex with plasminogen to activate it, while t-PA activates plasminogen bound to fibrin hundreds of times more than free plasminogen. The major toxicity of these drugs is hemorrhage from lysis of physiological thrombi and a systemic lytic state. Contraindications include recent surgery, bleeding disorders, and hypertension. Aminocaproic acid inhibits fibrinolysis by competing for lysine binding sites on plasminogen and plasmin.
Fibrinolytics & antiplatelets
This document summarizes fibrinolytics and antiplatelet drugs. It describes the fibrinolytic system and how fibrinolytics like streptokinase, urokinase, alteplase work to activate plasminogen and lyse clots. Newer fibrinolytics like reteplase and tenecteplase are discussed. Antiplatelet drugs discussed include aspirin, dipyridamole, clopidogrel, abciximab and how they inhibit platelet aggregation by blocking TXA2 synthesis, increasing cAMP, or blocking ADP/GP-IIb-IIIa receptors. Their uses for coronary artery disease and procedures are highlighted.
Fibrinolytic and antiplatelet drugs
This document summarizes fibrinolytics and antiplatelet drugs. It discusses the fibrinolytic system and lists fibrinolytics such as streptokinase, urokinase, alteplase, and newer recombinant tissue plasminogen activators. It also discusses their uses for conditions like myocardial infarction and mechanisms of action. The document then discusses antiplatelet drugs, focusing on mechanisms of platelet aggregation and inhibition. It lists classes of antiplatelet drugs like aspirin, dipyridamole, clopidogrel, and abciximab and their uses, mechanisms, and side effects. Finally, it lists common uses of antiplatelet drugs for conditions like coronary artery disease and angioplasty.
Fibrinolytics & antifibrinolytics
Fibrinolytics such as streptokinase, urokinase, alteplase, reteplase, and tenecteplase activate the natural fibrinolytic system and lyse thrombi to recanalize occluded blood vessels. They are used to treat myocardial infarction, deep vein thrombosis, pulmonary embolism, and peripheral arterial occlusion. Antifibrinolytics like epsilon amino-caproic acid and tranexamic acid inhibit plasminogen activation and clot dissolution to prevent or control bleeding caused by fibrinolytics or surgical procedures. The timing of fibrinolytic administration is critical for heart attack treatment, with better outcomes seen within 1-3 hours of symptom onset.
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The document discusses anticoagulants and their use in preventing blood clots. It describes tests like PT, INR, and PTT that are used to monitor anticoagulant therapy and provides normal ranges. PT measures clotting factors while INR standardizes PT results between labs. PTT evaluates heparin therapy and clotting factors. Warfarin users should have an INR of 2.0-3.0 for basic needs or 2.5-3.5 if at high risk of clots.
Fibrinolytics and antifibrinolytics
Fibrinolytics such as streptokinase, urokinase, and alteplase work by activating the natural fibrinolytic system to lyse thrombi and recanalize occluded blood vessels. They activate plasminogen to plasm in order to dissolve blood clots through the process of fibrinolysis. Streptokinase is the least expensive but also the least specific and can cause allergic reactions. Urokinase is non-antigenic and adverse effects are rare. Alteplase is fibrin-specific, rapid-acting, and has a lower risk of bleeding but is more expensive. Fibrinolytics are used to treat conditions like myocardial infarction, deep vein thrombosis, and pulmonary
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Thrombolysis In Acute MI Current Status Kiernan Med Clin N Am 2007 91 617 637
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ppt Presentation of thrombolytics drugs by Dr xrshad Danish
ppt Presentation of thrombolytics drugs by Dr xrshad Danish
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Magnesium plays an important physiological role as an intracellular and extracellular cation. It is involved in many metabolic processes and acts as a physiological antagonist to calcium. Hypomagnesemia can occur due to inadequate intake, excess renal losses, or redistribution. It can manifest as cardiovascular, neuromuscular, or psychiatric symptoms. Magnesium sulfate is used to treat and prevent eclampsia and preeclampsia by reducing cerebral vasospasm. It is also used for cardiovascular indications such as arrhythmias. Magnesium can impact anesthesia by potentiating neuromuscular blockade and decreasing acetylcholine release.
Magnesium and anaesthesia
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Emergency medications drugs
This document provides guidelines for critical care medication administration at Lucile Packard Children's Hospital. It lists various drugs used in continuous infusions or bolus administrations, including usual dosing, administration details, dose ranges, mechanisms of action, and important nursing considerations for each drug. The guidelines cover a range of drug classes and indications, such as analgesics, sedatives, paralytics, pressors, inotropes, antiarrhythmics and more.
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.
A new perspective on hyperkalemia
This document discusses hyperkalemia and its management. It defines hyperkalemia as a potassium level greater than 5.5 meq/L. It describes the symptoms and signs of hyperkalemia including cardiac arrhythmias and EKG abnormalities. It discusses various treatments for acute hyperkalemia including calcium gluconate, sodium bicarbonate, insulin with glucose, beta-2 agonists, dialysis, and potassium-binding resins. It also addresses approaches to evaluating the underlying cause of hyperkalemia such as assessing renal potassium handling and aldosterone function.
A New Perspective on Hyperkalemia
This document discusses hyperkalemia and its management. It begins with definitions of potassium levels and types of hyperkalemia. Mechanisms of hyperkalemia include extracellular shifts, reduced renal excretion, and decreased gastrointestinal secretion. Clinical signs include cardiac and neuromuscular symptoms. Management focuses on stabilizing the myocardium, shifting potassium into cells, and promoting excretion. Strategies include calcium gluconate, sodium bicarbonate, insulin with glucose, beta-agonists, dialysis, and cation exchange resins. Addison's disease and progesterone are also discussed in relation to potassium handling.
Electrolyte imbalance
This document discusses electrolyte imbalances and provides information on the composition and regulation of sodium, potassium, calcium, magnesium, and other electrolytes in the body. It details the causes, signs and symptoms, and treatment approaches for various electrolyte abnormalities including hyperkalemia, hypokalemia, hyponatremia, hypernatremia, hypocalcemia, hypercalcemia, hypomagnesemia, and hypermagnesemia. Treatment involves correcting underlying causes, restoring electrolyte levels at appropriate rates, and addressing any associated fluid volume abnormalities.
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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.
supraventricular tachyarrythmias on the go .pptx
This document discusses the classification, mechanism of action, dosing, and side effects of various drugs used to treat supraventricular tachyarrhythmias. It covers class I-IV antiarrhythmic drugs based on the Vaughan Williams classification system. Specific drugs discussed include amiodarone, adenosine, propafenone, vernakalant, flecainide, ibutilide, and others. Treatment approaches for atrial fibrillation, including rate and rhythm control, are reviewed. The document also covers topics like torsades de pointes, vagal maneuvers, bleeding risk assessment, and AF screening in the general population.
supraventricular tachyarrythmias on the go .pptx
This document discusses the classification, mechanism of action, dosing, and side effects of various drugs used to treat supraventricular tachyarrhythmias. It covers class I-IV antiarrhythmic drugs based on the Vaughan Williams classification system. Specific drugs discussed include amiodarone, adenosine, propafenone, vernakalant, flecainide, ibutilide, and others. Treatment approaches for atrial fibrillation, including rate and rhythm control, are reviewed. The document also covers topics like torsades de pointes, vagal maneuvers, bleeding risk assessment, and AF screening in the general population.
Cardiac Medications
This document provides an overview of various cardiovascular medications, including their uses, dosages, and key effects. It discusses medications that alter hemodynamics such as heart rate, preload, afterload, and contractility. Specific drugs covered include antiarrhythmics like amiodarone and diltiazem, preload enhancers and reducers, vasopressors like dopamine and epinephrine, afterload reducers like nitroprusside, inotropes like dobutamine, and anticoagulants like heparin. Important considerations for each drug class and specific medications are outlined, such as dosing protocols, hemodynamic impacts, and monitoring parameters.
Pharmacology of Antidysrhythmic and Vasoactive Medications
Atropine is indicated for symptomatic sinus bradycardia. Nitroglycerin should not be given topically with cardioversion or concurrently with Viagra due to risk of excessive hypotension. The appropriate dose of vasopressin for pulseless VT/VF is 40 units IV push.
Drugs And The Kidney
The document discusses drugs and their effects on the kidney. It covers normal kidney function, estimation of renal function, loop and thiazide diuretics, nephrotoxic drugs such as NSAIDs and aminoglycosides, and prescribing considerations in kidney disease. The ALLHAT trial found thiazide-type diuretics were superior to other antihypertensives in preventing cardiovascular disease due to their lower cost and greater efficacy.
ACE Inhibitors
1. ACE inhibitors work by inhibiting the angiotensin converting enzyme and reducing angiotensin II levels, leading to vasodilation and sodium excretion.
2. Common ACE inhibitors include lisinopril, enalapril, ramipril, and benazepril. They are used to treat hypertension, heart failure, myocardial infarction, and diabetic nephropathy.
3. Potential side effects include dry cough, hypotension, hyperkalemia, angioedema, and renal dysfunction. ACE inhibitors can also cause fetal harm during pregnancy.
Antianginal Drugs
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload on the heart. Calcium channel blockers and beta blockers are also outlined as treatments that decrease oxygen demand. Combination therapies are noted to provide additive effects in managing angina.
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Pharmacology of Antidysrhythmic and Vasoactive Medications
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Antihypertensive
- 1. NeurologyResidents.Net Ahmed Koriesh, MD Drips for Hypertension/Tachycardia Drug Initial Dose Max Dose MOA Dilator Onset (min) Duration Metabolism Notes Labetalol 10mg q10min then 1-2mg/min 8mg/min α and β blocker Arterial 2 2-4 hours Hepatic Avoid in bradycardia & decompensated HF Esmolol 500mcg/kg load 25-50mcg/kg/min 300mcg/kg/min β1 blocker ↓COP 1 15 min RBC esterase Avoid in bradycardia & decompensated HF Nicardipine 5mg/hr 15mg/hr CCB Arterial 10 4-6 hours Hepatic DOC in ischemic stroke and HTN encephalopathy Sodium Nitroprusside 0.5mcg/kg/min 5mcg/kg/min Nitrate Arterial/ Venous 1 1 min Kidney Causes coronary steal, tolerance, cyanide toxicity Nitroglycerine 5mcg/min 400mcg/min Nitrate Venous 3 15 min Hepatic Tolerance in 24h Hydralazine 10-20mg boluses Arterial 10 3 hours Hepatic Variable effect – avoid in acute conditions Fenoldopam 0.1mcg/kg/min 1.6mcg/kg/min D1 agonist Arterial 5 1 hour Hepatic Sulfa allaergy Clevidipine 1mg/hr 16mg/hr CCB Arterial 1 10 min RBC esterase Lipid emulsion Can’t use > 96h MOA: mechanism of action – DOC: drug of choice