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2007 fmlg Presentation Transcript

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