13 The Effects of Anesthetic Agents on Cardiac Function MICHAEL K. LOUSHIN, MD CONTENTS INTRODUCTION ANESTHESIA INDUCTION SEQUENCE INHALATIONALANESTHETICS INTRAVENOUS ANESTHETICS PHYSIOLOGIC EFFECTS OF ACUPUNCTURE ANESTHESIA AND TEMPERATURE REGULATION MYOCARDIAL PRECONDITIONING WITH INHALATIONAL AND INTRAVENOUS ANESTHETICS HEART TRANSPLANT SUMMARY COMPANION CD MATERIAL REFERENCES 1. INTRODUCTION 2. ANESTHESIA INDUCTION SEQUENCE Today, anesthesia is considered necessary for many types of A typical general anesthesia induction sequence for an adult surgeries and procedures. In general, anesthesia may provide is as follows: after establishing intravenous access and place- analgesia, amnesia, hypnosis, and muscle relaxation. The depth ment of standard American Society of Anesthesiologists (1) of administered anesthesia can vary from minimal sedation to monitors, a patient is preoxygenated with 100% oxygen. An general anesthesia (Table 1). General anesthesia typically induction dose of intravenous medications such as propofol, causes significant alterations in hemodynamics, especially dur- an opioid, and a muscle relaxant are administered (seeJPEG 1, ing induction of anesthesia. Importantly, both inhalational and on the Companion CD and description at end of chapter). After intravenous anesthetics can affect cardiovascular performance; the patient is rendered unconscious and anesthetized, direct this includes effects on cardiac output, heart rate, systemic laryngoscopy is performed, and the trachea intubated with an vascular resistance, cardiac conduction system, myocardial endotracheal tube. After confirmation of endotracheal intuba- contractility, coronary blood flow, or blood pressures. Yet, the tion, the patient is placed on an anesthesia ventilator and next choice of inhalational and intravenous anesthetics is typically ventilated with a combination of anesthetic gases, air, and associated with the patient's underlying cardiovascular status, oxygen (see JPEG 2, on the Companion CD and description at such as the presence of heart failure and hypovolemia. The end of chapter). Note, if a total intravenous anesthetic tech- primary goal of this chapter is to make commonly employed nique (such as propofol and opioid infusion) is chosen, anes- methodologies and anesthetics more familiar to the reader, with thetic gases are not administered. particular attention to the potential influences on the cardiovas- The cardiovascular depressant effects of most anesthetics cular system. typically become evident during and immediately following induction. Maintaining cardiovascular stability requires care- From: Handbook c~f Cardiac Anatomy, Physiology, and Devices Edited by: P. A. laizzo © Humana Press Inc., Totowa, NJ ful titration of medications, knowledge of clinical and basic 171 172 PART II1: PHYSIOLOGY AND ASSESSMENT/ LOUSHIN Table 1 Continuum of Depth of Sedation Definition of General Anesthesia and Levels of Sedation/Analgesia Moderate Minimal sedation sedation~analgesia Deep General (anxiolysis) ("conscious sedation") sedation~analgesia anesthesia Responsiveness Normal response to Purposeful response to Purposeful response following Unarousable even with verbal stimulation verbal or tactile stimulation repeated or painful stimulation painful stimulus Airway Unaffected No intervention required Intervention may be required Intervention often required Spontaneous ventilation Unaffected Adequate May be inadequate Frequently inadequate Cardiovascular function Unaffected Usually maintained Usually maintained May be impaired Excerpted from ASA Standards, Guidelines and Statements, 2003, of the American Society of Anesthesiologists. A copy of the full text can be obtained from ASA, 520 N. Northwest Highway, Park Ridgewood, IL 60068-2573. Table 2 F CI Minimal Alveolar Concentration (MAC) NmN I I of Inhalational Anesthetics F C -- C H MAC % Vapor pressure ] ] Agent (% of l atmosphere) (at 20°C) Nitrous Oxide I I F Br Desflurane 6.0 680 Halothane 0.75 243 Halothane Isoflurane 1.2 240 Sevoflurane 2.0 160 F H F Nitrous oxide 105 I I I Xenon 70 H C--O--C C--F I I I F CI F nitrous oxide is frequently utilized. After placement of Ameri- can Society of Anesthesiologists monitors, a high concen- Isoflurane tration of halothane or sevoflurane along with oxygen is administered via a face mask. After the patient becomes F H F unconscious, a peripheral intravenous catheter is placed, and I t I a similar adult general anesthesia and airway management H--C OmC CmF sequence follows. I Direct laryngoscopy and endotracheal intubation can often I I stimulate the upper and lower airways, which in turn may cause F F F significant changes in blood pressures and heart rate if airway Desflurane responses are not blunted. Commonly, titration of anesthetics and opioids administration is used to blunt these airway and F I associated sympathetic responses. F FmC--F 3. INHALATIONAL ANESTHETICS I I Commonly used inhalational anesthetics include nitrous 0 C H H--C oxide, isoflurane, desflurane, halothane, and sevoflurane I I (Fig. 1). Each of these inhalational anesthetics has a specific H F C--F minimum alveolar concentration (MAC) at which general I anesthesia is considered induced (Table 2). MAC is defined as Sevofiurane F the minimum alveolar concentration of an inhaled anesthetic required to prevent movement in 50% of patients in response Fig. 1. Chemical structure of commonly administered inhalational to a surgical incision. It is important to note that infants have anesthetics. a higher MAC than adults, and pregnant women and elderly patients have lower MAC requirements. MAC is additive, that is, the 0.5 MAC of nitrous oxide and science in physiology and pharmacology, and diligent monitor- the 0.5 MAC of isoflurane result in 1 MAC total anesthesia. ing of vital signs (JPEG 3). More specifically, the brain anesthetic partial pressure is Typically, induction of general anesthesia in children by dependent on factors such as inspired (F~) and alveolar (FA) placement of an intravenous catheter for preinduction may be concentration of anesthetic gas. The brain (F~) concentration traumatic to the child or difficult because of noncooperation. of anesthetic is dependent on FA and F~: Instead, initial mask induction with halothane, sevoflurane, or Fl <"-" FA ~ FB CHAPTER 13 / ANESTHESIAAND CARDIOVASCULAREFFECTS 173 Table 3 Cardiovascular Effects of Inhalational Anesthetics Heart Blood Systemic Cardiac Sensitize Coronary rate pressure vascular resistance output to epinephrine dilation Desflurane + - - - 0/- 0/+ + Halothane 0 - - 0/- - +++ + Isoflurane + ..... 0/+ ++ Sevoflurane 0 - - - 0/- 0/+ 0 Nitrous oxide + 0 0 0 0 0 0, no change; +, increased; ++, more increased; +++, most increased; -, decreased; --~ more decreased; ---, most decreased. Anesthetic uptake is determined by its blood solubility, car- Volatile anesthetics may also cause specific cardiac dys- diac output, and the difference between alveolar and venous rhythmias. Specifically, volatile anesthetics have been reported partial pressure (2). The greater the uptake of anesthetic gas, the both to slow the rate of sinoatrial node discharge and to increase slower is the rate of induction. Inhalational anesthetics with ventricular and His bundle conduction times (11), which may lower blood:gas solubility (i.e., desflurane and sevoflurane) increase the development of nodal rhythms. Further, volatile will cause faster induction and emergence from general anes- anesthetics may increase ventricular automaticity by altering thesia. potassium and calcium ion channels (11). It has been reported that halothane increases the incidence of 3.1. Blood Pressure ventricular dysrhythmias, especially when coadministered with and Systemic Vascular Resistance epinephrine; in contrast, the coadministration of epinephrine All volatile anesthetics (e.g., isoflurane, desflurane, sevo- with isoflurane, desflurane, or sevoflurane has minimal effects flurane, and halothane) cause dose-dependent effects on car- on increasing the incidence of ventricular dysrhythmias (12- diovascular function. For example, these agents cause a dose- 14). Furthermore, halothane may blunt the reflex increases in dependent decrease in mean arterial blood pressure (3-6). The heart rates that typically accompany decreases in blood pres- relative decrease in mean arterial blood pressure is considered sure; it may also slow conduction from the sinoatrial node, to be caused by decreases in systemic vascular resistance, resulting in junctional ventricular rhythms. myocardial contractility, sympathetic output, or a combination Sevoflurane and desflurane are also known to blunt sympa- of these. In particular, isoflurane, desflurane, and sevoflurane thetic baroreflex sensitivity partially. Importantly, isoflurane cause greater decreases in systemic vascular resistance com- is well known to cause significant decreases in systemic vas- pared to halothane (Table 3). Further, increasing doses of hal- cular resistances and thus in blood pressure. Yet, the baro- othane result in small changes in system vascular resistance (7), receptor response remains partially intact, and cardiac output and decreases in mean arterial pressure. Yet, halothane admin- is maintained relatively stable with isoflurane via associated istration is associated with decreases in cardiac output. increases in heart rate. In general, volatile anesthetics decrease systemic vascular resistance by causing peripheral vasodilation, thus increasing 3.3. Coronary Blood Flow blood flow to cutaneous and skeletal