2007 fmlg


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  • 2007 fmlg

    1. 1. ACLS PHARMACOLOGY 2007 Presented By: Enrique Escobar
    2. 2. USEFUL LINKS FOR ACLS COURSE <ul><li>http://www.skillstat.com/ECG_sim_demo.html </li></ul><ul><ul><li>ECG Simulator –Practice Recognizing Rhythms </li></ul></ul><ul><li>http://medinfo.ufl.edu/~aig/acls.shtml </li></ul><ul><ul><li>UF AIG ACLS Website- Check for Course Updates </li></ul></ul><ul><li>http://circ.ahajournals.org/content/vol112/24_suppl/ </li></ul><ul><ul><li>ACLS Guidelines 2005 – Reading over Winter Break </li></ul></ul><ul><li>Ken Grauer’s Arrhythmia Management & Cardiac Arrest Pocket Book </li></ul><ul><ul><li>Might be Offered with ACLS Course </li></ul></ul>
    3. 3. ACLS MEDICATIONS FOR SUPPORT <ul><li>Epinephrine </li></ul><ul><li>Norepinephrine </li></ul><ul><li>Isoproterenol </li></ul><ul><li>Vasopressin </li></ul><ul><li>Dopamine </li></ul><ul><li>Dobutamine </li></ul><ul><li>Milrinone </li></ul><ul><li>Nitroglycerin </li></ul><ul><li>Sodium Nitroprusside </li></ul><ul><li>Digoxin </li></ul><ul><li>Beta Blockers </li></ul><ul><li>Naloxone </li></ul><ul><li>Adenosine </li></ul><ul><li>Atropine </li></ul><ul><li>Amiodarone </li></ul><ul><li>Calcium Channel Blockers </li></ul><ul><li>Antiarrhythmics </li></ul>
    4. 5. CARDIOVASCULAR PHYSIOLOGY REVIEW <ul><li>Cardiac Output = Heart Rate x Stroke Volume </li></ul><ul><ul><li>Stroke Volume is affected by Preload, Afterload, & Contractility </li></ul></ul><ul><ul><ul><li>Preload ↑ then Stroke Volume ↑ </li></ul></ul></ul><ul><ul><ul><li>Afterload ↑ then Stroke Volume ↓ </li></ul></ul></ul><ul><ul><ul><li>Contractility ↑ then Stroke Volume ↑ </li></ul></ul></ul><ul><li>Blood Pressure = Cardiac Output x Afterload </li></ul>
    5. 6. AUTONOMIC NERVOUS SYSTEM REVIEW <ul><li>Receptors are Cholinergic if transmission across the synaptic cleft is mediated by Acetylcholine </li></ul><ul><li>Receptors are Adrenergic if transmission across the synaptic cleft is mediated by Epinephrine / Norepinephrine. </li></ul><ul><ul><li>Norepinephrine seen in postganglionic neurons of sympathetic fibers </li></ul></ul><ul><ul><li>Epinephrine seen from the Adrenal Medulla </li></ul></ul><ul><li>Parasympathetic Receptors – Nicotinic is the Pre-Ganglionic Receptor and Muscarinic is the Post Ganglionic Receptor. </li></ul><ul><ul><li>Acetylcholine binds Nicotinic and Muscarinic Receptors </li></ul></ul><ul><li>Nicotinic Receptors are the end points in somatic transmission and adrenal medulla. </li></ul>
    6. 8. ACETYLCHOLINE OVERVIEW AND EFFECTS <ul><li>Heart – Decrease in Heart Rate by Reducing the Firing Rate of the SA node and Increasing Conduction Time through the AV node. </li></ul><ul><li>Blood Vessels – Cause Mild Dilatation of Blood Vessels </li></ul>
    7. 9. CHOLINERGIC ANTAGONISTS - ATROPINE <ul><li>Atropine </li></ul><ul><ul><li>Blocks Muscarinic Receptors – Post-Ganglionic Receptors in Parasympathetic Transmission </li></ul></ul><ul><ul><li>SA Node Effects - Increase Firing Rate </li></ul></ul><ul><ul><li>AV Node Effects – Decrease Conduction Time </li></ul></ul><ul><ul><li>Overall – Increased Heart Rate, Minimal BP Effect </li></ul></ul><ul><ul><li>No Effects on Transplanted Hearts </li></ul></ul><ul><li>Indications for Atropine </li></ul><ul><ul><li>Symptomatic Bradycardia (i.e. hypotension), asystole, Pulseless Electrical Activity (PEA) if rate is slow. </li></ul></ul><ul><ul><li>Treatment of Choice for Hemodynamically Significant Bradycardia </li></ul></ul><ul><ul><li>Pacing is Preferable for Severe Bardycardia </li></ul></ul><ul><ul><li>Use of Atropine is not Benign! </li></ul></ul>Reference: Grauer Page 78
    8. 10. ALPHA ADRENORECEPTOR REVIEW <ul><li> 1 Receptors - Stimulation leads to Constriction of Vascular Smooth Muscle, primarily Skin and Splanchnic vessels. </li></ul><ul><ul><li>Increases Peripheral Vascular Resistance (PVR). </li></ul></ul><ul><li> 2 Receptors – Stimulation Inhibits NE Release </li></ul>
    9. 11. BETA ADRENORECEPTOR REVIEW <ul><li>ß1 Receptors - Stimulation Results in Increased Heart Rate, Conduction Velocity and Contractility </li></ul><ul><li>ß2 Receptors - Relaxation of Vascular Smooth Muscle, Skeletal Muscle and Bronchial Smooth Muscle. ??? Effects on PVR </li></ul><ul><li>ß3 Receptors – Not Discussed Here </li></ul>
    10. 12. EPINEPHRINE <ul><li>Stimulates  and ß Adrenergic Receptors </li></ul><ul><ul><li>Low Doses - ß Effects Predominate </li></ul></ul><ul><ul><li>High doses,  effects Predominate . </li></ul></ul><ul><li>Increases Heart Rate, Increased Contractility. </li></ul><ul><ul><li>Net Effect - Increase in Cardiac Output due to effect of ß1 Receptor </li></ul></ul><ul><li>Constricts Arterioles of Skin, Mucous Membranes, and Viscera. </li></ul><ul><ul><li>Net Effect – Increase in PVR due to effect of 1 Receptor </li></ul></ul><ul><li>If Given at “LOW” Dose, may see a Slight Drop in Diastolic Blood Pressure because of ß2 Dilatory Effects may Dominate  Receptor Effects </li></ul><ul><li>Indication – Ventricular Fibrillation, Pulseless Ventricular Tachycardia, Asystole, PEA, Severe Symptomatic Bradycardia </li></ul>Reference: Grauer Page 75
    11. 13. NOREPINEPHRINE <ul><li>Mostly See  Adrenergic Effects </li></ul><ul><li>Intensely Vasoconstricts Most Vascular Beds including Kidneys </li></ul><ul><ul><li>Net Effect - Increase in PVR via the 1 Receptor </li></ul></ul><ul><li>Can Cause a Reflex Bradycardia </li></ul><ul><ul><li>Baroreceptor Reflex in the Medulla - Increased Afferent Impulses to the Medulla resulting in Decreased Sympathetic Stimulation and Increased Parasympathetic Stimulation </li></ul></ul>
    12. 14. NOREPINEPHRINE (CONT’D) <ul><li>NE Indications </li></ul><ul><ul><li>Sepsis to improve Renal Blood Flow and Urine Output </li></ul></ul><ul><ul><li>Severe Hypotension (Systolic <70) and Low PVR who Fail to Respond to Less Potent Adrenergic Agents such as Dopamine, Phenylephrine, or Methoxamine </li></ul></ul>
    13. 16. ISOPROTERENOL <ul><li>Much Larger Preference for ß Receptors Compared with  Receptors. </li></ul><ul><ul><li>Stimulates ß1 and ß2 Equally </li></ul></ul><ul><li>Net Effect </li></ul><ul><ul><li>ß1 - Increase Heart Rate, Increase Contractility, Increase Cardiac Output, Elevates Systolic BP </li></ul></ul><ul><ul><li>ß2 – Decrease Diastolic BP, Relax Airway to Increase Flow </li></ul></ul>
    14. 17. DOPAMINE <ul><li>Binds , ß, and Dopamine Receptors. </li></ul><ul><ul><li>Effects via Adrenergic Receptors are Dose Dependent </li></ul></ul><ul><li>Low Doses (1-2 μ g/kg/min) - Activation of D1 receptors which Results in Dilation of the Renal and Mesenteric Blood Vessels </li></ul><ul><ul><li>Little Hemodynamic Effect, Urine Output is not Appreciably Increased </li></ul></ul><ul><li>Moderate Dose (2-10 μ g/kg/min) - Predominant ß1 Effect </li></ul><ul><ul><li>Increased Contractility, Some Increase in HR, Increased Cardiac Output </li></ul></ul><ul><ul><li>Modest Effect on PVR and BP </li></ul></ul><ul><li>High Dose (above 10 μ g/kg/min) - Predominant  Effect </li></ul><ul><ul><li>Increased BP </li></ul></ul>Reference: Grauer Page 77
    15. 18. DOPAMINE (CONT’D) <ul><li>Indications </li></ul><ul><ul><li>Symptomatic Bradycardia (i.e.hypotension) not responding to Atropine (pacing unavailable) </li></ul></ul><ul><ul><li>Cardiogenic Shock </li></ul></ul><ul><ul><li>If you have Severe Bradycardia (ie slow ventricular escape with a barely palpable pulse) – physicians favor Epinephrine Infusion </li></ul></ul>
    16. 19. ADRENERGIC ANTAGONISTS <ul><li> Blockers – Not Part of ACLS Protocol </li></ul><ul><li>ß Blockers – Can Block ß1 and/or ß2. Can be Combined with  Blockers. </li></ul><ul><ul><li>Metoprolol, Atenolol, and Esmolol are ß1 Selective </li></ul></ul><ul><ul><li>Propanolol is ß1 and ß2 Selective </li></ul></ul><ul><ul><li>Esmolol, Metoprolol, and Propanolol are IV Agents </li></ul></ul><ul><ul><li>Propanolol, Atenolol, and Metoprolol are Oral Agents </li></ul></ul><ul><li>Indications for ß Blockers </li></ul><ul><ul><li>Acute Myocardial Infarction (MI) – Mortality Reduced because of lower risk of Ventricular Fibrillation </li></ul></ul><ul><ul><li>Drug Choice for Benign Premature Ventricular Contractions (PVCs), Selected Cases of Refractory Ventricular Tachycardia(VT) and Ventricular Fibrillation (V Fib) (Due to Excess Sympathetic Tone) </li></ul></ul><ul><ul><li>Supraventricular Tachycardias (SVTs) </li></ul></ul>Reference: Grauer Page 89
    17. 20. BETA BLOCKERS <ul><li>What Effects will They Have? </li></ul><ul><ul><li>SA Node Effects - Decreased Firing Rate </li></ul></ul><ul><ul><li>AV Node Effects – Increased Conduction Time </li></ul></ul><ul><ul><li>Overall – Decreased Heart Rate, Decreased Contractility, Decreased BP </li></ul></ul>
    18. 21. NITRATES <ul><li>Nitrates are used for their ability to relax vascular smooth muscle. Nitroglycerin is the initial treatment of choice for suspected ischemic-type pain or discomfort. </li></ul><ul><li>Action of Nitroglycerin is Mediated through Local Endothelial Production of Nitric Oxide, particularly in the Venous Capacitance System. </li></ul><ul><li>Sub Lingual, Oral, Topical and IV. </li></ul><ul><li>Can Drop the BP so Check BP Before Administration </li></ul><ul><li>Can Produce Tachycardia, Paradoxical Bradycardia, Hypoxemia caused by Increased Pulmonary V entilation-Perfusion Mismatch, and Headache. </li></ul><ul><li>Avoid if Patient has used Viagra or Levitra within Past 24 Hours </li></ul>
    19. 22. NITRATES
    20. 23. NARCAN (NALOXONE) <ul><li>Competitive Opioid Receptor Antagonist. </li></ul><ul><li>Reverses Effects of Opioids. </li></ul><ul><li>ACLS – Used Primarily for Respiratory Distress/Arrest Due to Opioid Overdose. </li></ul><ul><li>Duration of Action is TWO HOURS. It may Run Out Before the Opioid is Out of The System </li></ul>
    21. 24. CALCIUM CHANNEL BLOCKERS <ul><li>Two Main Categories: Dihydropyridine (Amlodipine) and Non-Dihydropyridine (Verapamil, Diltiazem) </li></ul><ul><li>Non-Dihydropiridines are used in ACLS. By Blocking Certain Calcium Channels they: </li></ul><ul><ul><li>Decrease the Force of Cardiac Contraction </li></ul></ul><ul><ul><li>Decrease the Rate of SA Node Firing </li></ul></ul><ul><ul><li>Increase Conduction Time Through the AV Node </li></ul></ul><ul><ul><li>Relax Vascular Smooth Muscle. </li></ul></ul><ul><li>Can be Used to Treat HTN, Coronary Spasms, SVTs (A Fib, A Flutter, PSVT, and MAT) </li></ul><ul><li>DO NOT GIVE an IV ß Blocker with IV Verapamil/Diltiazem (Excessive Bradycardia or Asystole) </li></ul>
    23. 26. DIGOXIN <ul><li>Half-Life is 36 Hours in Young Adult, 5 Days in Old Adult with Renal Failure </li></ul><ul><li>Inhibits the Na/K pump. This Leads to an Increase in Intracellular Na, thereby Driving the Na/Ca Exchanger, Resulting in Increased Intracellular Ca. </li></ul><ul><ul><li>Increases contractility, decreases the speed of conduction and firing of SA node </li></ul></ul><ul><li>Increases Vagal (Parasympathetic) Tone </li></ul><ul><li>With toxicity, can see Atrial Tachycardia with 2:1 or 3:1 block. Can also see Ventricular arrhythmias. </li></ul><ul><li>Indications – Limited </li></ul><ul><ul><li>Rapid A Fib / A Flutter – Slows the Ventricular Response </li></ul></ul><ul><ul><li>Does not convert A Fib any better than Placebo (50% Spontaneous Conversion within 24 Hours) </li></ul></ul><ul><ul><li>Less Likely to Work if Sympathetic Tone is Increased </li></ul></ul>Reference: Grauer Page 88
    24. 27. ADENOSINE <ul><li>Half life of 10 Seconds. </li></ul><ul><li>Activates the Inward Rectifier K Current and Inhibits the Ca Current, Resulting in Hyperpolarization of the Cell and Suppression of Action Potentials. </li></ul><ul><li>When Bolused, Directly Inhibits the AV Node, Usually Halting Conduction. </li></ul><ul><li>Warn Patients that They will Feel Flushed, Chest Pressure, and Shortness of Breath for a Few Seconds. </li></ul><ul><li>Indications </li></ul><ul><ul><li>Tachyarrhythmias with Reentry Mechanism (Especially involving AV Node) </li></ul></ul><ul><ul><li>Drug of Choice for Paroxysmal SVT </li></ul></ul><ul><ul><li>May be Used Diagnostically in SVTs of Unknown Etiology </li></ul></ul>Reference: Grauer Page 85
    25. 28. VASOPRESSIN <ul><li>In Vivo – Released from Posterior Pituitary in Response to Increased Plasma Osmotic Pressure or Decreased ECF Volume </li></ul><ul><li>Very Powerful Vasoconstrictor </li></ul><ul><li>Indications </li></ul><ul><ul><li>V Fib, Pulseless V Tachycardia, Asystole, PEA (Pulseless Cardiac Arrest) </li></ul></ul>
    26. 29. ANTIARRHYTHMICS <ul><li>There are Many Antiarrhythmics and the Different Mechanisms of Action are Way Beyond the Scope of This Class </li></ul><ul><li>All Interact with Electrolyte Channels in Atrial Muscle and/or Ventricular Muscle and/or SA Node and/or AV Node and/or Purkinjie Fibers </li></ul><ul><li>Brief Strong Points </li></ul><ul><ul><li>Magnesium – Treatment of Choice for Torsades de Pointes </li></ul></ul><ul><ul><li>Amiodarone – Cardiac Arrest for Refractory V Fib and Sustained V Tachycardia – Antiarrhythmic of 1 st Choice </li></ul></ul><ul><ul><ul><li>Also SVTs (Atrial Tachycardias, Wolf Parkinson White (WPW) Rhythms, A Fib/ A Flutter </li></ul></ul></ul>
    27. 30. ANTIARRHYTHMICS <ul><li>Class I – Sodium Channel Blockers: Procainamide, Lidocaine, Flecainide, Propafenone </li></ul><ul><li>Class II – ß Blockers </li></ul><ul><li>Class III – K Channel Blockers: Amiodarone, Sotalol, Ibutilide. </li></ul><ul><li>Class IV – Calcium Channel Blockers: Non Dihydropyridines. </li></ul><ul><li>Other – Adenosine, Digoxin, Magnesium Sulfate </li></ul>