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Stoelting's Handbook of Pharmacology and Physiology in Anesthetic Practice
Factors that Are Thought to Be Responsible for the Significantchr(10)Decrease in Lean Muscle Mass that Occurs with Aging
Table of Contents
Free Topics
10-2. Dose-Dependent Effects of Lidocaine - Table
10-4 Peak Plasma Concentrations of Local Anesthetic are Influenced by the Site of Injection for Accomplishment of Regional Anesthesia - Fig
11-3 Structure of Acetylcholinesterase - Fig
1-2 Electrolyte Compositionchr(10)of Body Fluid Compartments - Fig
1-2. Cell Membrane Composition - Table
12-1. Classification of Commonly Used and New Nondepolarizing Neuromuscular Blockers According to Duration of Action (Time to T1 = 25% of Control) after Administration of 2 × ED95a - Table
13-4. Pharmacokinetics of Antiepileptic Drugs - Table
1-4 Schematic Diagram ofchr(10)a Hypothetical Cell (Center) and its Organelles - Fig
14-10. Mean Values of Pressures Acting across Capillary Membranes - Table
14-15 Cardiac Output Can Increase Nearly Fourfold Without Greatly Increasing the Pulmonary Arterial Pressure - Fig
14-17 The Lung is Divided into Three Pulmonary Blood Flow Zones Reflecting the Impact of Alveolar Pressure (Pa), Pulmonary Artery Pressure (Ppa), and Pulmonary Venous Pressure (Ppv) on the Caliber of Pulmonary Blood Vessels - Fig
14-5 There May Be a Reversal of the Usual Relationship of Simultaneous Recordings of Radial and Aortic Blood Pressures (Prebypass) in the Early Period after Separation from Cardiopulmonary Bypass (Postbypass) - Fig
15-1. Placement of Precordial Leads - Table
15-14 Mobitz Type I (Wenckebach) - Fig
15-18 Atrial Fibrillation - Fig
15-2 Cardiac Conduction System - Fig
15-8 Cardiac Sympathetic and Parasympathetic Nerves - Fig
16-1 Schematic Depiction of a Juxtamedullary Nephron - Fig
16-5 Autoregulation - Fig
1-8 Double Helical Structurechr(10)of DNA With Adenine Bonding to Thymine (T) and Cytosine (C) tochr(10)Guanine (G) - Fig
18-6 Plasma Potassium (K+) Concentrations During the Infusion of Potassium Chloride (Kcl) Increase More in Patients Also Receiving Phenylephrine - Fig
18-8 Cardiac Glycosides - Fig
19-2 Heparin Administration - Fig
19-4. Possible Explanations for Cardioprotective Effects Produced by Perioperative ß-Adrenergic Receptor Blockade - Table
20-1. Intravenous Antihypertensive Drugs Commonly Used in the Perioperative Setting - Table
2-1. Characteristics of Nonionized and Ionized Drug Molecules - Table
2-10 Typical Time Course of Plasma Concentration Following Bolus Injection of an Intravenous Drug, With a Rapid Phase (Red), an Intermediate Phase (Blue), and a Slow Log-Linear Phase (Green) The Simulation Was Performed With the Pharmacokinetics of Fentanyl - Fig
2-16 Effect-Site Decrement Times - Fig
2-18 Dose Versus Response Relationship for Three Drugs With Potency - Fig
22-1. Diuretics and Their Sites of Action - Table
2-3. Events Responsible for Variations in Drug Responses between Individuals - Table
2-4 The Action of Agonists , Partial Agonists , Antagonists (C), and Inverse Agonists (D) Can Be Interpreted As Changing the Balance Between the Active and Inactive Forms of the Receptor In This Case, in the Absence of Agonist, the Receptor is in the Activated State 20% of the Time - Fig
24-10 The Distribution of Pulmonary Blood Flow in the Upright Position - Fig
24-12 The Heavy Line Indicated All Possible Values of Alveolar O2 (Pao2) and Co2 (Paco2) With Ventilation Perfusion (V/Q) Ratios Ranging from Zero (to the Left, Lung Base) to Infinity (to the Right, Lung Apex) for a Person Breathing Air Mixed Expired Gas is a Mixture of Ideal Alveolar Gas and Dead Space - Fig
26-3. Distinguishing Respiratory and Metabolic Acidosis versus Alkalosis - Table
27-2. Endothelial Proteins and Mediators of Hemostasis - Table
28-3. Plasma Transfusion Indications - Table
3-17 Cross-Section of the Spinal Cord, Showing the Dorsal (Posterior) and Ventral (Anterior) Roots - Fig
3-2. Chemicals that Act at Synapses as Neurotransmitters - Table
3-21 Neurotransmitters of the Autonomic Nervous System - Fig
3-23 The Effects of Different Warming Techniques on Mean Body Temperature Plotted According to the Elapsed Hours of Treatment (Top) and Changes in Mean Body Temperature According to the Volume of Fluid Administered (Bottom) - Fig
3-3 Athe Elements of the Action - Fig
3-8. Events that Contribute to Decreases in Body Temperature During Surgery - Table
3-9 The Pyramidal Tracts are Major Pathways for Transmission of Motor Signals from the Cerebral Cortex to the Spinal Cord - Fig
4-10 Cerebral Blood Flow Measured in the Presence of Normocapnia and in the Absence of Surgical Stimulation - Fig
4-14 The Effects of Increasing Concentrations (MAC) of Halothane, Isoflurane, Desflurane, and Sevoflurane on Cardiac Index (L/Min) When Administered to Healthy Volunteers - Fig
4-20 Responses to Submucosally Injected Epinephrine in Patients Receiving Sevoflurane (SEVO) or Isoflurane (ISO) Anesthesia - Fig
4-22 Impact of Surgical Stimulation on the Resting Paco2 (Mm Hg) During Administration of Isoflurane or Halothane - Fig
4-3. Comparative Solubilities of Inhaled Anesthetics - Table
5-4. Circulatory Effects of Ketamine - Table
5-5 The Principal Metabolite of Midazolam is 1-Hydroxymidazolam - Fig
6-1. Components of Pain - Table
6-5 The Synaptic Mechanism Underlying Peripheral, Nociceptive, Stimuli-Induced, and Persistent Heterosynaptic Potentiation of Dorsal Horn Neurons Transmitters and Mediators Released from Primary Afferents and Surrounding Microglial Cells, Including Substance P, Neurotrophins, and Cytokines May Act at a Distance on Dorsal Horn Neurons to Produce Long-Lasting Heterosynaptic Potentiation of Glutamatergic Transmission - Fig
6-7 Visceral Innervation - Fig
7-3. Time Course of Opioid Withdrawal - Table
7-5. Clinical Uses of Fentanyl - Table
9-1. Characteristics of Commonly Prescribed Nonsteroidal Antiinflammatorychr(10)Drugs - Table
9-3. Comparative Pharmacology of Endogenous and Synthetic Corticosteroids - Table
Acknowledgment
Alkalinization of Local Anesthetic Solutions Shortens the Onset of Neural Blockade
Antiarrhythmic Drug Pharmacology
Barbiturates
Benzodiazepines
Blood Volume
Calcium channel blockers
Cardiac Glycosides
Cardiac Physiology
Cell Structure and Function
Chronic Respiratory Disease is Divided into Obstructive and Restrictive
Clinical Uses
Comparative Pharmacology of Gaseous Anesthetic Drugs
Components of the Systemic Circulation
Distribution
Distribution of Ventilation
Functional Anatomy
Graft Versus Host Disease (GVHD) is a Potentially Fatal Complication that Occurs More Commonly after a Bone Marrow or Stem Cell Transplant
Hemostasis and History
How Nerves Work
Intracellular pH Regulation
Introduction
Ketamine
Limitations of Acetylcholinesterase Inhibitors
Lipid Disorders
Mechanism of Action
Mechanism of Drug Action
Metabolism Converts Pharmacologically Active, Lipid-Soluble Drugs into Water-Soluble and Usually Inactive Metabolites; Exceptions are Metabolism to Active Compounds As for Diazepam and Opioids (Morphine-6-Glucuronide is More Potent Than Morphine; Codeine is a Prodrug Metabolized to Morphine)
Metabolism of Amide Local Anesthetics
Molecular Structure
Muscle Types
Neostigmine Acts by Inhibiting Acetylcholinesterase and Preventing the Breakdown of Acetylcholine
Opioid Allergy
Osmosis
Osmotic diuretics
Patient-Controlled Analgesia
Peripheral Nerve Physiology of Pain
Pharmacokinetic Models
Pharmacokinetics of inhaled anesthetics
Platelet Glycoprotein Iib/Iiia Antagonists
Potency of Nondepolarizing Neuromuscular Blockers
Preface
Proarrhythmic Effects Describe Bradyarrhythmias or Tachyarrhythmias that Represent New Cardiac Arrhythmias Associated With Antiarrhythmic Drug Treatment
Purified Protein Concentrates
Recombinant Coagulation Products are Used to Manage Bleeding in Hemophilia
Regulation of Systemic Blood Pressure
Renal Blood Flow
Synthetic Noncatecholamines
Systemic Circulation Supplies Blood to All the Tissues of the Body Except the Lungs
Thermoregulation
Total Body Fluid Composition
Part I: Basic Principles of Physiology and Pharmacology
1. Basic Principles of Physiology
1-1 Body Fluid Compartmentschr(10)and the Percentage of Body Weight Represented by Each Compartmentchr(10)The Location Relative to the Capillary Membrane Divides Extracellularchr(10)Fluid into Plasma or Interstitial Fluid - Fig
1-1. Total Body Water by Age and Gender - Table
1-2 Electrolyte Compositionchr(10)of Body Fluid Compartments - Fig
1-2. Cell Membrane Composition - Table
1-3 Diagrammatic Representation of Osmosis Depicting Water Molecules (Open Circles) and Solute Molecules (Solid Circles) Separated by a Semipermeable Membrane Water Molecules Move Across the Semipermeable Membrane to the Area of Higher Concentration of Solute Molecules - Fig
1-3. Predicted Relationship between Diffusion Distance and Time - Table
1-4 Schematic Diagram ofchr(10)a Hypothetical Cell (Center) and its Organelles - Fig
1-4. Diameters of Ions, Molecules, and Channels - Table
1-5 Schematic Depictionchr(10)of Phagocytosis (Ingestion of Solid Particles) and Pinocytosis (Ingestionchr(10)of Dissolved Particles) - Fig
1-6 Sodium-Potassium Adenosine Triphosphatase is an Enzymechr(10)Present in All Cells that Catalyzes the Conversion of Adenosine Triphosphatechr(10)(ATP) to Adenosine Diphosphate (ADP) - Fig
1-7 The Five Major Typeschr(10)of Protein Ion Channels are Calcium, Sodium, Nonselective, Chloride,chr(10)and Potassium Flow of Ions through These Channels (Calcium and Sodiumchr(10)into Cells and Potassium Outward) Determines the Transmembrane Potentialchr(10)of Cells - Fig
1-8 Double Helical Structurechr(10)of DNA With Adenine Bonding to Thymine (T) and Cytosine (C) tochr(10)Guanine (G) - Fig
Blood Volume
Body Composition
Cell Structure and Function
Constituents of Body Fluid Compartments
Dehydration
Fluid Management
Introduction
Osmosis
Tonicity of Fluids
2. Basic Principles of Pharmacology
2-1 The Interaction of a Receptor With an Agonist May Be Portrayed As a Binary Bound Versus Unbound Receptor The Unbound Receptor is Portrayed As Inactive - Fig
2-1. Characteristics of Nonionized and Ionized Drug Molecules - Table
2-10 Typical Time Course of Plasma Concentration Following Bolus Injection of an Intravenous Drug, With a Rapid Phase (Red), an Intermediate Phase (Blue), and a Slow Log-Linear Phase (Green) The Simulation Was Performed With the Pharmacokinetics of Fentanyl - Fig
2-11 Fentanyl and Alfentanil Arterial Concentrations (Circles) and Electroencephalographic (EEG) Response (Irregular Line) to an Intravenous Infusion Alfentanil Shows a Less Time Lag Between the Rise and Fall of Arterial Concentration and the Rise and Fall of EEG Response Than Fentanyl Because It Equilibrates With the Brain More Quickly - Fig
2-12 The Three Compartment Model from an Added Effect Site to Account for the Equilibration Delay Between the Plasma Concentration and the Observed Drug Effect The Effect Site Has a Negligible Volume - Fig
2-13 Plasma (Black Line) and Effect-Site (Red Line) Concentrations Following a Bolus Dose of Fentanyl or Alfentanil - Fig
2-14 Fentanyl Infusion Rate to Maintain a Plasma Concentration of 1 chr(956)G/Hr The Rate Starts Off Quite High Because Fentanyl is Avidly Taken Up by Body Fat - Fig
2-15 Context-Sensitive Half-Times As a Function of the Duration of Intravenous Drug Infusion for Each Fentanyl, Alfentanil, Sufentanil, Propofol, Midazolam, and Thiopental - Fig
2-16 Effect-Site Decrement Times - Fig
2-17 Drug Exposure (Dose, Concentration, Etc) Versus Drug Effect Relationship - Fig
2-18 Dose Versus Response Relationship for Three Drugs With Potency - Fig
2-19 Concentration Versus Response Curves for Drugs With Differing Efficacies - Fig
2-2 The Simple View of Receptor Activation Also Explains the Action of Antagonist In This Case, the Antagonist (Red) Binds to the Receptor, but the Binding Does Not Cause Activation - Fig
2-2. The Time to Peak Effect and t chr(189) ke0 following a Bolus Dose - Table
2-20 Analysis to Determine the Ld50, the Ld99, and the Therapeutic Index of a Drug - Fig
2-21 Interaction Between Fentanyl and Isoflurane or Desflurane on the Minimum Alveolar Concentration Required to Suppress Movement to Noxious Stimulation - Fig
2-22 Interaction of Propofol With Alfentanil on the Concentration Required to Suppress Response to Intubation, Maintain Nonresponsiveness During Surgery, and Then Awaken from Anesthesia - Fig
2-3 Receptors Have Multiple States, and They Switch Spontaneously Between Them In This Case, the Receptor Has Just Two States - Fig
2-3. Events Responsible for Variations in Drug Responses between Individuals - Table
2-4 The Action of Agonists , Partial Agonists , Antagonists (C), and Inverse Agonists (D) Can Be Interpreted As Changing the Balance Between the Active and Inactive Forms of the Receptor In This Case, in the Absence of Agonist, the Receptor is in the Activated State 20% of the Time - Fig
2-5 The Central Volume is the Volume that Intravenously Injected Drug Initially Mixes into - Fig
2-6 The Relationship Between Drug Rate of Metabolism Can Be Computed As the Rate of Liver Blood Flow Times the Difference Between the Inflowing and Outflowing Drug Concentrations This is a Common Approach to Analyzing Metabolism or Tissue Uptake Across an Organ in Mass-Balance Pharmacokinetic Studies - Fig
2-7 The Relationship Between Liver Blood Flow (Q), Clearance, and Extraction Ratio For Drugs With a High Extraction Ratio, Clearance is Nearly Identical to Liver Blood Flow - Fig
2-8 Standard One- , Two- , and Three-Compartment (C) Mammillary Pharmacokinetic Models I Represents Any Input into the System (Bolus or Infusion) - Fig
2-9 The Relationship Between Volume and Clearance and Half-Life Can Be Envisioned by Considering Two Settings: a Big Volume and a Small Clearance and a Small Volume With a Big Clearance Drug Will Be Eliminated Faster in the Latter Case - Fig
Absorption is Not Particularly Relevant for Most Anesthetic Drugs
Distribution
Drug Interactions
Hepatic Clearance
Introduction
Ionization
Metabolism Converts Pharmacologically Active, Lipid-Soluble Drugs into Water-Soluble and Usually Inactive Metabolites; Exceptions are Metabolism to Active Compounds As for Diazepam and Opioids (Morphine-6-Glucuronide is More Potent Than Morphine; Codeine is a Prodrug Metabolized to Morphine)
Pharmacodynamics
Pharmacokinetic Models
Pharmacokinetics is the Quantitative Study of the Absorption, Distribution, Metabolism, and Excretion of Injected and Inhaled Drugs and Their Metabolites (What the Body Does to a Drug)
Protein Binding
Receptor Action
Receptor Theory
Receptor Types
Renal Clearance
Route of Administration and Systemic Absorption of Drugs
Stereochemistry
Part II: Neurologic System
10. Local Anesthetics
10-1 Local Anesthetics Consist of a Lipophilic and Hydrophilic Portion Separated by a Connecting Hydrocarbon Chain - Fig
10-1. Comparative Pharmacology of Local Anesthetics - Table
10-2 Ester and Amide Local Anesthetics - Fig
10-2. Dose-Dependent Effects of Lidocaine - Table
10-3 Local Anesthetics Slow the Rate of Depolarization of the Nerve Action Potential Such that the Threshold Potential is Not Reached As a Result, an Action Potential Cannot Be Propagated in the Presence of Local Anesthetic and Conduction Blockade Results - Fig
10-3. Clinical Uses of Local Anesthetics - Table
10-4 Peak Plasma Concentrations of Local Anesthetic are Influenced by the Site of Injection for Accomplishment of Regional Anesthesia - Fig
10-4. Dosage Chart for Common Continuous Nerve Blocks - Table
10-5 Fetal-Maternal Arterial (Fa/Ma) Lidocaine Ratios are Greater During Acidemia Compared With a Normal pH - Fig
10-6 Addition of Epinephrine to the Solution Containing Lidocaine or Prilocaine Decreases Systemic Absorption of the Local Anesthetic by About One-Third - Fig
10-7 American Society of Regional Anesthesia and Pain Medicine Recommendations for Managing Last Cv, Cardiovascular - Fig
10-8 Therapeutic and Diagnostic Recommendations in Cocaine-Associated Chest Pain - Fig
Adverse Effects of Local Anesthetics
Alkalinization of Local Anesthetic Solutions Shortens the Onset of Neural Blockade
Cocaine Toxicity
Introduction
Liposomal Local Anesthetics
Mechanism of Action
Metabolism of Amide Local Anesthetics
Metabolism of Ester Local Anesthetics
Methemoglobinemia
Molecular Structure
Neural tissue toxicity
Pharmacokinetics
Racemic Mixtures or Pure Isomers
Structure-Activity Relationships
Treatment of Last
Tumescent Liposuction
Use of Vasoconstrictors
Uses of Local Anesthetics
11. Neuromuscular Physiology
11-1 Schematic Depiction of Skeletal Muscle Innervation - Fig
11-2 The Synaptic Vesicle Exocytosis-Endocytosis Cycle - Fig
11-3 Structure of Acetylcholinesterase - Fig
11-4 Subunit Composition of the Nicotinic Acetylcholine Receptor (Nachr) in the Endplate Surface of Adult Mammalian Muscle - Fig
Introduction
Motor Units
Muscle Types
Neuromuscular Transmission and Excitation-Contraction Coupling
The neuromuscular junction
12. Neuromuscular Blocking Drugs and Reversal Agents
12-1 Acceleromyographic Recording During the Course of Neuromuscular Blockade Induced by a Nondepolarizing Agent - Fig
12-1. Classification of Commonly Used and New Nondepolarizing Neuromuscular Blockers According to Duration of Action (Time to T1 = 25% of Control) after Administration of 2 Ã ED95a - Table
12-2 Mechanomyographic Recording During Recovery from 10 mg/Kg Succinylcholine - Fig
12-2. Dose-Response Relationships and Pharmacodynamic Parameters for Nondepolarizing Neuromuscular Blocking Drugs in Human Subjectsa - Table
12-3 Structural Relationship of Succinylcholine, a Depolarizing Neuromuscular Blocking Agent, to Acetylcholine - Fig
12-3. Pharmacokinetic Parameters for Neuromuscular Blocking Drugs - Table
12-4 Chemical Structures of the Steroidal Neuromuscular Blockers Pancuronium, Vecuronium, and Rocuronium - Fig
12-5 Gamma-Cyclodextrin (A) and Sugammadex (Modified gamma-Cyclodextrin) (B) - Fig
Adverse Effects of Neuromuscular Blockers
Characteristics of Nondepolarizing and Depolarizing Neuromuscular Block
Drugs for Reversal of Neuromuscular Blockade
Introduction
Limitations of Acetylcholinesterase Inhibitors
Monitoring of neuromuscular function
Pharmacology of Nondepolarizing Neuromuscular Blockers
Pharmacology of Succinylcholine
Potency of Nondepolarizing Neuromuscular Blockers
Principles of Action of Neuromuscular Blockers at the Neuromuscular Junction
Structure of Neuromuscular Blocking Drugs
Sugammadex: A Novel Selective Relaxant-Binding Agent
13. Antiepileptic and Other Neurologically Active Drugs
13-1. Classification of Epileptic Seizures - Table
13-2. Antiepileptic Drugs Used to Treat Epilepsy - Table
13-3. Side Effects of Antiepileptic Drugs - Table
13-4. Pharmacokinetics of Antiepileptic Drugs - Table
13-5. Side Effects of Phenytoin - Table
13-6. Side Effects of Levodopa - Table
13-7. Clinical Uses of Doxapram - Table
Anticholinergic drugs
Antiepileptic Drugs
Antipsychotic drugs
Benzodiazepines Display Anxiolytic
Central Nervous System Stimulants
Centrally Acting Muscle Relaxants
Drugs Used for Treatment of ParkinsonâS Disease
Major Antiepileptic Drugs
Mechanism of Drug Action
Mechanism of Seizure Activity
Peripheral Decarboxylase Inhibitors
Pyridoxine
Status epilepticus
3. Neurophysiology
3-1 Anatomy of a Neuron - Fig
3-1. Classification of Peripheral Nerve Fibers - Table
3-10 Dermatome Map that May Be Used to Evaluate the Level of Sensory Anesthesia Produced by Regional Anesthesia - Fig
3-11 Cerebral Blood Flow is Influenced by Pao2, Paco2, and Mean Arterial Pressure (MAP) - Fig
3-12 The Electroencephalogram Consists of Alpha, Beta, Theta, and Delta Waves - Fig
3-13 Cerebral Spinal Fluid Fluxes in and Out of the Ventricles With the Cardiac Cycle - Fig
3-14 Schematic Diagram of the Eye - Fig
3-15 The Chemoreceptor Trigger Zone and Emetic Center Respond to a Variety of Stimuli Resulting in Nausea and Vomiting 5-Ht3, 5-Hydroxytryptamine; Gi, Gastrointestinal - Fig
3-16 The Peripheral Nervous System Connects the Body Tissues to the Spinal Cord and Central Nervous System - Fig
3-17 Cross-Section of the Spinal Cord, Showing the Dorsal (Posterior) and Ventral (Anterior) Roots - Fig
3-18 Anatomy of the Sympathetic Nervous System - Fig
3-19 Anatomy of a Sympathetic Nervous System Nerve - Fig
3-2 Basic Structure of the Synapse - Fig
3-2. Chemicals that Act at Synapses as Neurotransmitters - Table
3-20 Anatomy of the Parasympathetic Nervous System - Fig
3-21 Neurotransmitters of the Autonomic Nervous System - Fig
3-22 Graphic Representation of the Typical Triphasic Core Temperature Pattern that Occurs after Induction of Anesthesia Note that the Phase 3 Plateau May Not Occur, Particularly During Regional Anesthesia or During Combined Regional and General Anesthesia - Fig
3-23 The Effects of Different Warming Techniques on Mean Body Temperature Plotted According to the Elapsed Hours of Treatment (Top) and Changes in Mean Body Temperature According to the Volume of Fluid Administered (Bottom) - Fig
3-3 Athe Elements of the Action - Fig
3-3. Responses Evoked by Autonomic Nervous System Stimulation - Table
3-4 Schematic Diagram Showing G Protein-Coupled Receptors, the Ã2-Adrenergic Receptor, Which Upregulates Adenylyl Cyclase, and the M2 Muscarinic Receptor, Which Downregulates Adenylyl Cyclase (AC) The Effects of These G Protein-Coupled Receptors are Then Mediated through the Intercellular Concentration of Cyclic Amp - Fig
3-4. Classification and Characterization of Adrenergic and Cholinergic Receptors - Table
3-5 Structure of the Synapse - Fig
3-5. Mechanism of Action of Drugs that Act on the Autonomic Nervous System - Table
3-6 Brain Anatomy - Fig
3-6. Clinical Assessment of Autonomic Nervous System Function - Table
3-7 The Sensorimotor Cortex Consists of the Motor Cortex, Pyramidal (Betz) Cells, and Somatic Sensory Cortex - Fig
3-7. Causes of Hyperthermia - Table
3-8 Schematic Diagram of a Cross-Section of the Spinal Cord Depicting Anatomic Laminae I to IX of the Spinal Cord Gray Matter and the Ascending Dorsal, Lateral, and Ventral Sensory Columns of the Spinal Cord White Matter - Fig
3-8. Events that Contribute to Decreases in Body Temperature During Surgery - Table
3-9 The Pyramidal Tracts are Major Pathways for Transmission of Motor Signals from the Cerebral Cortex to the Spinal Cord - Fig
3-9. Immediate Adverse Consequences of Perioperative Hypothermia - Table
Autonomic Nervous System Controls Visceral Functions of the Body
Central Nervous System
How Nerves Work
Introduction
Peripheral nervous system
Thermoregulation
4. Inhaled Anesthetics
4-1 Inhaled Anesthetics Introduced into Clinical Practice Beginning With the Successful Use of Nitrous Oxide in 1844 for Dental Anesthesia Followed by Recognition of the Anesthetic Properties of Ether in 1846 and of Chloroform in 1847 Modern Anesthetics, Beginning With Halothane, Differ from Prior Anesthetics in Being Fluorinated and Nonflammable - Fig
4-1. Physical and Chemical Properties of Inhaled Anesthetics - Table
4-10 Cerebral Blood Flow Measured in the Presence of Normocapnia and in the Absence of Surgical Stimulation - Fig
4-11 The Effects of Increasing Concentrations (MAC) of Halothane, Isoflurane, Desflurane, and Sevoflurane on Mean Arterial Pressure (Mm Hg) When Administered to Healthy Volunteers - Fig
4-12 The Substitution of Nitrous Oxide for a Portion of Isoflurane Produces Less Decrease in Blood Pressure Than the Same Dose of Volatile Anesthetic Alone - Fig
4-13 The Effects of Increasing Concentrations (MAC) of Halothane, Isoflurane, Desflurane, and Sevoflurane on Heart Rate (Beats/Minute) When Administered to Healthy Volunteers - Fig
4-14 The Effects of Increasing Concentrations (MAC) of Halothane, Isoflurane, Desflurane, and Sevoflurane on Cardiac Index (L/Min) When Administered to Healthy Volunteers - Fig
4-15 The Effects of Increasing Concentrations (MAC) of Halothane, Isoflurane, Desflurane, and Sevoflurane on Systemic Vascular Resistance (Dynes/Second/Cm5) When Administered to Healthy Volunteers - Fig
4-16 Comparison of Circulatory Effects of Halothane During Spontaneous Breathing (Sr) and Controlled Ventilation of the Lungs (Cr) after 1 and 5 Hours of Administration of Halothane - Fig
4-17 Comparison of Circulatory Effects of Enflurane after 1 Hour (Solid Line) and 6 Hours (Broken Line) of Administration During Controlled Ventilation of the Lungs to Maintain Normocapnia Cv, Cardiovascular - Fig
4-18 Percentage of Patients Developing Ventricular Cardiac Dysrhythmias (Three or More Premature Ventricular Contractions [pvcs]) With Increasing Doses of Submucosal Epinephrine Injected During Administration of 125 MAC of Halothane, Isoflurane, or Enflurane - Fig
4-19 Responses to Submucosally Injected Epinephrine in Patients Receiving Desflurane (DES) or Isoflurane (ISO) Anesthesia Pvcs, Premature Ventricular Contractions - Fig
4-2 Inhaled Anesthetics - Fig
4-2. Factors Determining Partial Pressure Gradients Necessary for Establishment of Anesthesia - Table
4-20 Responses to Submucosally Injected Epinephrine in Patients Receiving Sevoflurane (SEVO) or Isoflurane (ISO) Anesthesia - Fig
4-21 Inhaled Anesthetics Produce Drug-Specific and Dose-Dependent Increases in Paco2 - Fig
4-22 Impact of Surgical Stimulation on the Resting Paco2 (Mm Hg) During Administration of Isoflurane or Halothane - Fig
4-23 Changes in Respiratory System Resistance As a Percentage of the Thiopental Baseline Recorded after Tracheal Intubation but Before the Addition of Sevoflurane or Desflurane to the Inhaled Gases or Beginning the Infusion of Thiopental Airway Resistance Responses to Sevoflurane Were Significantly Different from Desflurane and Thiopental - Fig
4-24 Administration of Desflurane to Dogs Does Not Significantly Alter Hepatic Perfusion - Fig
4-25 Plasma Alanine Aminotransferase (ALT) - Fig
4-26 Hepatic Damage May Occur in the Rat Model after Administration of Inhaled or Injected Drugs When the Inhaled Oxygen Concentration is 10% Conversely, Hepatic Damage Occurs after Administration of Halothane, but Not Enflurane or Isoflurane, When the Inhaled Concentration of Oxygen is 12% or 14% - Fig
4-27 Impact of Volatile Anesthetics on Contractility of Uterine Smooth Muscle Strips Studied in Vitro *p > - Fig
4-28 Fraction of Halothane Removed During Passage through the Liver at Progressively Decreasing Alveolar Concentrations - Fig
4-3 The Pharmacokinetics of Inhaled Anesthetics During the Induction of Anesthesia is Defined As the Ratio of the End-Tidal Anesthetic Concentration (Fa) to the Inspired Anesthetic Concentration (Fi) Consistent With Their Relative Blood:gas Partition Coefficients, the Fa/Fi of Poorly Soluble Anesthetics (Nitrous Oxide, Desflurane, Sevoflurane) Increases More Rapidly Than that of Anesthetics With Greater Solubility in Blood - Fig
4-3. Comparative Solubilities of Inhaled Anesthetics - Table
4-4 The Impact of the Inhaled Concentration of an Anesthetic on the Rate at Which the Alveolar Concentration Increases Toward the Inspired (Fe/Fi) is Known As the Concentration Effect - Fig
4-4. Body Tissue Composition - Table
4-5 The Second Gas Effect is the Accelerated Increase in the Alveolar Concentration of aSecond Gas, Halothane (Haloth), Toward the Inspired (Fa/Fi) in the Presence of a High Inhaled Concentration of the First Gas (N2o) - Fig
4-5. Impact of Physiologic and Pharmacologic Factors on Minimum Alveolar Concentration - Table
4-6 Effect of the Mode of Ventilation on the Rate of Increase of the Alveolar Concentration (Fa) of Halothane Toward the Inspired Concentration (Fi) As Determined in an Animal Model Negative-Feedback Inhibition of Spontaneous Ventilation Limits the Fa/Fi to 0 - Fig
4-6. Variables that Influence Pharmacologic Effects of Inhaled Anesthetics - Table
4-7 Inhalation of 75% Nitrous Oxide Rapidly Increases the Volume of a Pneumothorax (Open Symbols) - Fig
4-7. Metabolism of Volatile Anesthetics as Assessed by Metabolite Recovery versus Mass Balance Studies - Table
4-8 Elimination of Inhaled Anesthetics is Defined As the Ratio of the End-Tidal Anesthetic Concentration (Fa) to the Fa Immediately Before the Beginning of Elimination (Fao) The Rate of Decrease (Awakening from Anesthesia) in the Fa/Fao is Most Rapid With the Anesthetics that are Least Soluble in Blood (Nitrous Oxide, Desflurane, Sevoflurane) - Fig
4-9 Decerebration Does Not Change the Minimum Alveolar Anesthetic Concentration of Isoflurane in Rats Confirming that the Effects of Volatile Anesthetics on the Spinal Cord Determine MAC - Fig
Comparative Pharmacology of Gaseous Anesthetic Drugs
Current Clinically Useful Inhaled Anesthetics
History
Inhaled Anesthetics for the Present and Future
Metabolism of Inhaled Anesthetics is Very Small but Intermediary Metabolites
Pharmacokinetics of inhaled anesthetics
Pharmacokinetics of Inhaled Anesthetics
5. Intravenous Sedatives and Hypnotics
5-1 Respiratory Resistance after Tracheal Intubation is Less after Induction of Anesthesia With Propofol Than after Induction of Anesthesia With Thiopental or Etomidate The Solid Squares Represent Four Patients in Whom Audible Wheezing Was Present - Fig
5-1. Comparative Characteristics of Common Induction Drugs - Table
5-2 Comparative Changes (Expressed in % Changes [mean ± Sd]) from Control Values (C) in Systemic Vascular Resistance (SVR) in the 45 Minutes after the Administration of Thiopental, 5 mg/Kg IV (Open Circles), or Propofol, 25 mg/Kg IV (Solid Circles) - Fig
5-2. Pharmacologic Effects of Benzodiazepine - Table
5-3 Etomidate, but Not Thiopental, is Associated With Decreases in the Plasma Concentrations of Cortisol - Fig
5-3. Comparative Pharmacology of Benzodiazepines - Table
5-4 Model of the gamma-Aminobutyric Acid (GABA) Receptor Forming a Chloride Channel - Fig
5-4. Circulatory Effects of Ketamine - Table
5-5 The Principal Metabolite of Midazolam is 1-Hydroxymidazolam - Fig
5-5. Comparative Effects of Anticholinergic Drugs - Table
Aminobutyric Acid Agonists
Barbiturates
Benzodiazepines
Etomidate
Non-gamma-Aminobutyric Acid Sedatives and Hypnotics
Overview
Scopolamine
Short-Acting Nonbenzodiazepine Benzodiazepines
6. Pain Physiology
6-1 Cellular Mechanism Underlying Nociceptor Sensitization Induced by Peripheral Inflammation - Fig
6-1. Components of Pain - Table
6-2 The Projection Pathway for the Transmission of Pain Information to the Brain - Fig
6-2. Response of Nociceptors Do Different Types of Stimuli - Table
6-3 Schematic Representation of the Spinal Projections of Primary Afferent Fibers - Fig
6-4 Illustration of Gate Theory for Pain Modulation in Spinal Dorsal Horn - Fig
6-5 The Synaptic Mechanism Underlying Peripheral, Nociceptive, Stimuli-Induced, and Persistent Heterosynaptic Potentiation of Dorsal Horn Neurons Transmitters and Mediators Released from Primary Afferents and Surrounding Microglial Cells, Including Substance P, Neurotrophins, and Cytokines May Act at a Distance on Dorsal Horn Neurons to Produce Long-Lasting Heterosynaptic Potentiation of Glutamatergic Transmission - Fig
6-6 Properties of Proposed Medullary Pain-Modulating Neurons - Fig
6-7 Visceral Innervation - Fig
6-8 Surface Area of Referred Pain from Different Visceral Organs - Fig
Central Nervous System Physiology
Embryologic Origin and Localization of Pain
Introduction
Neurobiology of Pain
Peripheral Nerve Physiology of Pain
Psychobiology of Pain
Societal Impact of Pain
Some Specific Types of Pain
Transition from Acute Pain to Chronic Pain
7. Opioid Agonists and Antagonists
7-1 Chemical Structures of Opium Alkaloids - Fig
7-1. Classification of Opioid Agonists and Antagonists - Table
7-2 Synthetic Opioid Agonists - Fig
7-2. Classification of Opioid Receptors - Table
7-3 Computer Simulation-Derived Context-Sensitive Half-Times (Time Necessary for the Plasma Concentration to Decrease 50% after Discontinuation of the Infusion) As a Function of the Duration of the IV Infusion - Fig
7-3. Time Course of Opioid Withdrawal - Table
7-4 Ventilatory Response Curves from One Individual - Fig
7-4. Pharmacokinetics of Opioid Agonists - Table
7-5 Cumulative Curves for Patients Who Did Not Request an Additional Morphine Injection Following Discontinuation of Remifentanil (Dashed Line) or Desflurane (Solid Line) - Fig
7-5. Clinical Uses of Fentanyl - Table
7-6 Opioid Agonist-Antagonists - Fig
7-6. Suggested Starting Intravenous Patient-Controlled Analgesia Opioid Regimens - Table
7-7 Opioid Antagonists - Fig
7-8 Effect-Site Concentrations With Traditional Versus Patient-Controlled Opioid Dosing - Fig
Anesthetic Requirements
Chemical Structure of Opium Alkaloids
Common Opioid Side Effects
Introduction
Mechanism of Action
Neuraxial Opioids
Opioid Agonist-Antagonists
Opioid Agonists
Opioid Allergy
Opioid Antagonists
Opioid Receptors
Patient-Controlled Analgesia
8. Centrally Acting Nonopioid Analgesics
Alpha2-Adrenergic Agonists
Conclusion
Droperidol
Introduction
Ketamine
Midazolam
Neostigmine Acts by Inhibiting Acetylcholinesterase and Preventing the Breakdown of Acetylcholine
9. Peripherally Acting Analgesics
9-1 The Cyclooxygenases Pathway - Fig
9-1. Characteristics of Commonly Prescribed Nonsteroidal Antiinflammatorychr(10)Drugs - Table
9-2. Adverse Effects of Nonsteroidal Antiinflammatory Drugs - Table
9-3. Comparative Pharmacology of Endogenous and Synthetic Corticosteroids - Table
9-4. Potential Side Effects Associated with Corticosteroid Therapy - Table
Acetaminophen (Tylenol)
Acetylsalicylic acid (Aspirin)
Clonidine
Dexmedetomidineâs proanesthetic and proanalgesic effects
Introduction
Ketamine
Nonsteroidal antiinflammatory drugs
NSAIDS belong to a number of chemical families
Opioids
Steroids
Systemic Local Anesthetics
Part III: Circulatory System
14. Circulatory Physiology
14-1 Distribution of Blood Volume in the Systemic and Pulmonary Circulation - Fig
14-1. Physiologic Roles of Endothelial Function - Table
14-10 Ventricular Function Curves (Frank-Starling Curves) Depict the Volume of Forward Ventricular Ejection (Cardiac Output) at Different Atrial Filling Pressures and Varying Degrees of Myocardial Contractility - Fig
14-10. Mean Values of Pressures Acting across Capillary Membranes - Table
14-11 Pressure-Volume Loop Representing the Cardiac Cycle - Fig
14-11. Classification of Pulmonary Hypertension - Table
14-12 Anatomy of the Microcirculation - Fig
14-13 Depiction of the Thoracic Duct and Right Lymphatic Duct As They Enter the Venous System - Fig
14-14 Comparison of Intravascular Pressures in the Systemic and Pulmonary Circulations - Fig
14-15 Cardiac Output Can Increase Nearly Fourfold Without Greatly Increasing the Pulmonary Arterial Pressure - Fig
14-16 Gas Exchange is Maximally Effective in Normal Lung Units With Optimal Ventilation to Perfusion (V/Q) Relationships - Fig
14-17 The Lung is Divided into Three Pulmonary Blood Flow Zones Reflecting the Impact of Alveolar Pressure (Pa), Pulmonary Artery Pressure (Ppa), and Pulmonary Venous Pressure (Ppv) on the Caliber of Pulmonary Blood Vessels - Fig
14-2 Systemic Blood Pressure Decreases As Blood Travels from the Aorta to Large Veins - Fig
14-2. Pathologic Processes Associated with Endothelial Dysfunction - Table
14-3 Schematic Depiction of Systemic Blood Pressure Recorded from a Large Systemic Artery - Fig
14-3. Normal Pressures in the Systemic Circulation - Table
14-4 There is Enhancement of the Pulse Pressure As the Systemic Blood Pressure is Transmitted Peripherally - Fig
14-4. Abnormalities of Jugular Venous Pressure Waveforms - Table
14-5 There May Be a Reversal of the Usual Relationship of Simultaneous Recordings of Radial and Aortic Blood Pressures (Prebypass) in the Early Period after Separation from Cardiopulmonary Bypass (Postbypass) - Fig
14-5. Tissue Blood Flow - Table
14-6 Simultaneous Recording of the Electrocardiogram (Top Tracing) and Jugular Venous Pressure Waves (Bottom Tracing) - Fig
14-6. Anatomy of the Various Types of Blood Vessels - Table
14-7 Effect of Hydrostatic Pressure on Venous Pressures Throughout the Body - Fig
14-7. Permeability of Capillary Membranes - Table
14-8 Hematocrit Greatly Influences the Viscosity of Blood - Fig
14-8. Filtration of Fluid at the Arterial Ends of Capillaries - Table
14-9 The Relationship Between Blood Flow, Pressure, and Resistance to Flow Can Be Expressed As a Variant of OhmâS Law - Fig
14-9. Reabsorption of Fluid at the Venous Ends of Capillaries - Table
Components of the Systemic Circulation
Control of Tissue Blood Flow
Determinants of Tissue Blood Flow
Endothelial Function
Lymphatics
Microcirculation is the Circulation of Blood through the Smallest Vessels of the Body-Arterioles
Physical Characteristics of the Systemic Circulation
Pulmonary Circulation is a Low-Pressure
Regulation of Cardiac Output and Venous Return
Regulation of Systemic Blood Pressure
Systemic Circulation Supplies Blood to All the Tissues of the Body Except the Lungs
15. Cardiac Physiology
15-1 The Coronary Circulation - Fig
15-1. Placement of Precordial Leads - Table
15-10 Central Venous Waveform - Fig
15-11 Determinants of Cardiac Output - Fig
15-12 A:chr(10)Pressure-Volume Loop of a Single Cardiac Cyclechr(10)chr(10)chr(10)B:chr(10)A Reduction in Ventricular Filling Pressure Causes the Loops to Shift Toward Lower End Systolic and End Diastolic Functionchr(10)chr(10)chr(10)C:chr(10)When Afterload is Increased, the Loops Get Narrower and Longer - Fig
15-13 First-Degree Av Block - Fig
15-14 Mobitz Type I (Wenckebach) - Fig
15-15 Mobitz Type II - Fig
15-16 Third-Degree Atrioventricular Heart Block Occurring at the Level of the Atrioventricular Node (QRS Complexes are Narrow) - Fig
15-17 Third-Degree Atrioventricular Heart Block Occurring at an Infranodal Level (QRS Complexes are Wide) - Fig
15-18 Atrial Fibrillation - Fig
15-19 Multifocal Premature Ventricular Contractions - Fig
15-2 Cardiac Conduction System - Fig
15-2. Hemodynamic Equations - Table
15-20 Ventricular Tachycardia - Fig
15-21 Ventricular Fibrillation - Fig
15-3 Wave of Depolarization - Fig
15-3. Normal Hemodynamic Values - Table
15-4 Standard Limb Leads of the Electrocardiogram and Typical Recordings - Fig
15-4. ACCF/AHA Stages of Heart Failure and NYHA Functional Classification - Table
15-5 Unipolar Limb Lead Circuit (VR) - Fig
15-5. Factors that Contribute to Imbalances that Predispose to Cardiac Dysrhythmias - Table
15-6 Electrical Axis of the Heart As Determined from the Standard Limb Leads of the Electrocardiogram - Fig
15-6. Diagnosis of Cardiac Dysrhythmias from the Electrocardiogram - Table
15-7 The Normal Waves and Intervals on the Electrocardiogram - Fig
15-7. Accessory Pathways and Preexcitation Syndromes - Table
15-8 Cardiac Sympathetic and Parasympathetic Nerves - Fig
15-9 Cardiac Cycle: Mechanical, Electrical, and Acoustic Events - Fig
Cardiac Anatomy
Cardiac Cycle
Cardiac Dysrhythmias
Cardiac Physiology
Clinical Electrophysiology and Electrocardiogram
Control of Cardiac Function
Introduction
Pathophysiology
Types of Dysrhythmias
16. Renal Physiology
16-1 Schematic Depiction of a Juxtamedullary Nephron - Fig
16-1. Magnitude and Site of Solute Reabsorption or Secretion in the Renal Tubules - Table
16-10 Rifle Criteria - Fig
16-11 Intraoperative Urine Output - Fig
16-2 Countercurrent Exchange of Water and Solutes in the Vasa Recta - Fig
16-2. Risk Factors for Perioperative Acute Kidney Injury - Table
16-3 Transport Maximum for Glucose - Fig
16-4 Intravascular Pressures in the Renal Circulation - Fig
16-5 Autoregulation - Fig
16-6 The Role of the Renin-Angiotensin System in the Maintenance of Effective Circulating Volume - Fig
16-7 Small Changes in the Plasma Concentrations of Potassium Evoke Large Changes in the Plasma Concentration of Aldosterone - Fig
16-8 Plasma Concentrations of Potassium Parallel Intake When Aldosterone Activity is Impaired - Fig
16-9 Classification of Acute Renal Failure - Fig
Acute kidney injury
Anesthesia and the Kidneys
Introduction
Kidney Structure and Function
Measuring Kidney Function
Plasma Concentration of Ions and Urea
Regulation of Body Fluid
Renal Blood Flow
17. Intravenous Fluids and Electrolytes
17-1 Body Fluid Compartments With Main Ion Distribution - Fig
17-1. Common Crystalloid Solutions - Table
17-2. Common Colloid Solutions - Table
17-3. Black Box Warnings on Use of Hydroxyethyl Starch Solutions - Table
Assessing Fluid Responsiveness
Important Fluid Constituents
Intravenous Fluid Types
Introduction
Total Body Fluid Composition
18. Sympathomimetic Drugs
18-1 Sympathomimetics are Derived from -Phenylethylamine, With a Catecholamine Being Any Compound that Has Hydroxyl Groups on the 3 and 4 Carbon Positions of the Benzene Ring The Naturally Occurring Catecholamines are Epinephrine, Norepinephrine, and Dopamine - Fig
18-1. Classification and Comparative Pharmacology of Sympathomimetics - Table
18-2 Selective 2-Adrenergic Agonist Effects of Epinephrine are Responsible for Stimulating the Movement of Potassium Ions (K+) into Cells, With a Resulting Decrease in the Serum Potassium Concentration - Fig
18-2. Comparative Pharmacology of Selective Ã2-Adrenergic Agonist Bronchodilators - Table
18-3 Individual and Mean (± Sd) Plasma Potassium (K-) Concentrations Determined 1 to 3 Days Preoperatively and Immediately Before the Induction (Preinduction) of Anesthesia - Fig
18-4 Synthetic Noncatecholamine Sympathomimetics - Fig
18-5 Hemodynamic Response to Rapid Intravenous Injection of Phenylephrine in a Single Patient - Fig
18-6 Plasma Potassium (K+) Concentrations During the Infusion of Potassium Chloride (Kcl) Increase More in Patients Also Receiving Phenylephrine - Fig
18-7 Selective Ã2-Adrenergic Agonists - Fig
18-8 Cardiac Glycosides - Fig
18-9 Selective Inhibitors of Phosphodiesterase Subtype III, Amrinone and Milrinone - Fig
Calcium is Present in the Body in Greater Amounts Than Any Other Mineral
Cardiac Glycosides
Naturally Occurring Catecholamines
Selective 2-Adrenergic Agonists Relax Bronchiole and Uterine Smooth Muscle but
Selective Phosphodiesterase Inhibitors
Synthetic Catecholamines
Synthetic Noncatecholamines
19. Sympatholytics
19-1 -Adrenergic Antagonists - Fig
19-1. Comparative Characteristics of Ã-Adrenergic Receptor Antagonists - Table
19-2 Heparin Administration - Fig
19-2. Comparative Characteristics of Ã-Adrenergic Receptor Antagonists Effective in the Treatment of Congestive Heart Failure - Table
19-3 Maximum Percent Increases in Heart Rate (HR) - Fig
19-3. Comparative Characteristics of Ã-Adrenergic Receptor Antagonists Effective in the Treatment of Congestive Heart Failure - Table
19-4 Calcium Ion Entry and Exit from a Vascular Smooth Muscle Cell - Fig
19-4. Possible Explanations for Cardioprotective Effects Produced by Perioperative Ã-Adrenergic Receptor Blockade - Table
19-5 Mechanism of Action of the Three Classes of Calcium Channel Blockers - Fig
19-5. Classification of Calcium Channel Blockers - Table
19-6. Comparative Pharmacologic Effects of Calcium Channel Blockers - Table
19-7. Pharmacokinetics of Calcium Channel Blockers - Table
19-8. Effect of Chronic Antianginal Therapy on Perioperative Heart Rate (beats per minute) and P-R Interval (ms) - Table
Alpha- and Ã-Adrenergic receptor antagonists
Alpha-Adrenergic receptor antagonists bind selectively to Ã-adrenergic receptors
Beta-Adrenergic receptor antagonists
Calcium channel blockers
Combined α- and Ã-Adrenergic Receptor Antagonists
20. Vasodilators
20-1 Schematic Depiction of Effects that are Mediated by 2-Adrenergic Receptors The Site for Sedation is the Locus Ceruleus of the Brainstem, Whereas the Principal Site of Analgesia is Most Likely the Spinal Cord - Fig
20-1. Intravenous Antihypertensive Drugs Commonly Used in the Perioperative Setting - Table
20-2 Inhalation of Nitric Oxide - Fig
Introduction
Nitric Oxide and Nitrovasodilators
Specific Antihypertensive Drugs and Anesthesia
Systemic Hypertension is Estimated to Affect 30% of Adults in the United States and is Defined As 150 to 159/90 to 99 Mm Hg (Stage 1) or Greater Than or Equal to 160/100 Mm Hg (Stage 2)
21. Antiarrhythmic Drugs
21-1 The Physiologic Basis of the Cardiac Action Potential - Fig
21-1. Classification of Cardiac Antiarrhythmic Drugs - Table
21-2 After Discontinuation of Amiodarone, the Plasma Concentration Decreases Slowly, Resulting in a Prolonged Elimination Half-Time - Fig
21-2. Electrophysiologic and Electrocardiographic Effects of Cardiac Antiarrhythmic Drugs - Table
21-3. Pharmacokinetics of Cardiac Antiarrhythmic Drugs - Table
21-4. Efficacy of Cardiac Antiarrhythmic Drugs - Table
Antiarrhythmic Drug Pharmacology
Classification
Decision to Treat Cardiac Arrhythmias
Efficacy and Results of Treatment With Cardiac Antiarrhythmic Drugs
Introduction
Mechanism of Action
Other Cardiac Antiarrhythmic Drugs
Proarrhythmic Effects Describe Bradyarrhythmias or Tachyarrhythmias that Represent New Cardiac Arrhythmias Associated With Antiarrhythmic Drug Treatment
Prophylactic Antiarrhythmic Drug Therapy
22. Diuretics
22-1 The Sites of Action of the Different Diuretics - Fig
22-1. Diuretics and Their Sites of Action - Table
22-2. Side Effects of Thiazide Diuretics - Table
Aldosterone Antagonists
Aquaporin Modulators
Carbonic Anhydrase Inhibitors
Dopamine receptor agonists
Introduction
Loop Diuretics are First-Line Therapy in Patients With Fluid Retention Resulting from Heart Failure
Natriuretic Peptides
Neprilysin Antagonists
Osmotic diuretics
Potassium-Sparing Diuretics
Thiazide Diuretics are Most Often Administered for Long-Term Treatment of Essential Hypertension in Which the Combination of Diuresis
Vasopressin Receptor Antagonists
23. Lipid-Lowering Drugs
23-1 A Diagrammatic Representation of Lipid Metabolism - Fig
23-1. Classification of Lipoproteins - Table
23-2. Statin Benefit Groups - Table
23-3. Drugs for Treatment of Hyperlipidemia - Table
23-4. Statin Myotoxicity Risk Factors - Table
Drugs for Treatment of Hyperlipidemia.
Lipid Disorders
Lipoprotein Metabolism
Part IV: Pulmonary System
24. Gas Exchange
24-1 Diagram of the Larynx from the Base of the Tongue to below the Thyroid Cartilage As Viewed from its Posterior Aspect - Fig
24-1. Lung Volumes and Capacities - Table
24-10 The Distribution of Pulmonary Blood Flow in the Upright Position - Fig
24-11 A Simplified Three-Compartment Model of the Lung With A Representing Shunt; B an Ideal Gas Unit; and C Alveolar Dead Space (Vdalv) Physiologic Dead Space (Vdphys) is Filled With Air Containing No Co2, Shown As the White Area - Fig
24-12 The Heavy Line Indicated All Possible Values of Alveolar O2 (Pao2) and Co2 (Paco2) With Ventilation Perfusion (V/Q) Ratios Ranging from Zero (to the Left, Lung Base) to Infinity (to the Right, Lung Apex) for a Person Breathing Air Mixed Expired Gas is a Mixture of Ideal Alveolar Gas and Dead Space - Fig
24-13 A Simplified Diagram of the Effects of a Decrease in Mixed Venous Oxygen Saturation (v) on Arterial Oxygenation (a) - Fig
24-14 The Relationship Between Hypoxic Pulmonary Vasoconstriction (HPV) (Vertical Axis) and Time in Hours (H) (Horizontal Axis) in Humans Exposed to Isocapnic Hypoxia (Approximate Inspired Po2 60 Mmhg), Beginning at 0h With a Return to Normoxia at 8h HPV Response Was Measured As the Increase in Echocardiographic Right Ventricular Systolic Pressure - Fig
24-15 Dissociation Curves of Normal Adult (Hba) and Fetal (Hbf) Hemoglobin - Fig
24-16 Carbon Dioxide (Co2) Enters the Plasma in Molecular Form from the Tissues - Fig
24-17 A Diagram of the Connections Between Individual Components of the Chemical and Neural Portions of the Physiologic Control of Respiration (See Text for Details) - Fig
24-18 Factors Affecting the Distribution of Pulmonary Blood Flow During One-Lung Ventilation (OLV) - Fig
24-2 Diagram of the Glottis As Seen from above Using a Laryngoscope or Fiberoptic Bronchoscope - Fig
24-3 The Average Length from the Incisors to the Vocal Cords is Approximately 15 Cm, and the Distance from the Vocal Cords to the Tracheal Carina is 12 Cm - Fig
24-4 Diagram of the Trachea, Lobar, and Segmental Bronchi Showing Median Lengths and Diameters for a 170 Cm Height Patient - Fig
24-5 Complete Pulmonary Function Testing Will Provide Data on Lung Volumes and Capacities to Differentiate Obstructive from Restrictive Lung Diseases - Fig
24-6 An Example of a Portable Handheld Spirometer that Can Be Easily Used in the Preoperative Assessment Clinic or at the Bedside to Measure the Majority of the Clinically Important Lung Volumes and Capacities - Fig
24-7 A Simple Spirogram - Fig
24-8 The Relationship Between Pulmonary Vascular Resistance (PVR) and Lung Volume - Fig
24-9 Distribution of Blood Flow (Perfusion) and Alveolar Ventilation and the Ventilation-to-Perfusion Ratio (Va/Q) As a Function of the Distance from the Base of the Lung (to the Left in the Figure) to the Apex (to the Right) - Fig
Abnormal Breathing Patterns
Altered Physiologic Conditions
Carbon Dioxide Transport
Chronic Respiratory Disease is Divided into Obstructive and Restrictive
Distribution of Ventilation
Functional Anatomy
Introduction
One-Lung Ventilation (OLV) is Performed During Thoracic Surgery to Facilitate the Surgical Exposure in the Chest
Oxygen Transport
Pulmonary Circulation
Respiratory Control
Respiratory Mechanical Function
Thorax and Muscles of Respiration
25. Respiratory Pharmacology
25-1. Pharmacologic Influence on the Autonomic Nervous System - Table
25-2. Pharmacologic Influence on Inflammation - Table
25-3. Anesthetics with a Favorable Influence on Bronchomotor Tone - Table
Hypoxic Pulmonary Vasoconstriction
Influence of Anesthetics on the Airways
Influence of Inflammation on the Airway
Intrinsic Pharmacologic Effects of the Lungs
Pharmacology of the Airways
Pharmacology of the Pulmonary Circulation
26. Acid-Base Disorders
26-1 Buffering Systems Present in the Body - Fig
26-1. Basic Definitions - Table
26-2 Hydration of Carbon Dioxide Results in Carbonic Acid (H2co3), Which Can Subsequently Dissociate into Bicarbonate and Hydrogen Ions - Fig
26-2. Intracellular Functions Affected by Local pH - Table
26-3 The Henderson-Hasselbalch Equation Can Be Used to Calculate the pH of a Solution from the Concentration of Bicarbonate and the Pco2 - Fig
26-3. Distinguishing Respiratory and Metabolic Acidosis versus Alkalosis - Table
26-4 Schematic Depiction of the Renal Tubular Secretion of Hydrogen Ions, Which are Formed from the Dissociation of Carbonic Acid in Renal Tubular Epithelial Cells - Fig
26-4. Electrolytes in Plasma and Commonly Available Crystalloid Solutions - Table
26-5 Ammonia Formed in Renal Tubular Epithelial Cells Combines With Hydrogen Ions in the Renal Tubules to Form Ammonium - Fig
26-5. Causes of Metabolic Acidosis - Table
26-6. Alpha-Stat versus pH-Stat Management during Hypothermia - Table
Classification of Acid-Base Disturbances
Compensation for Acid-Base Disturbances
Effects of Temperature on Acid-Base Status
Intracellular pH Regulation
Introduction
Mechanisms for Regulation of Hydrogen Ion Concentration
Part V: Blood and Hemostasis
27. Physiology of Blood and Hemostasis
27-1 Initiation, Amplification, Propagation, and Stabilization of Hemostasis and Clot Formation - Fig
27-1. Plasma Levels, Half-lives of Coagulation Factors - Table
27-2 Procoagulant Forces (Red) and Natural Anticoagulant/Fibrinolytic Forces (Green) and Diagrammed Dashed Lines Indicated an Inhibitory Effect - Fig
27-2. Endothelial Proteins and Mediators of Hemostasis - Table
27-3 Fibrinogen is Converted to Fibrin that Polymerizes by the Action of Thrombin The Electron Micrograph Shows a Fibrin Clot With Red Blood Cells Trapped - Fig
Coagulation Testing
Hemostasis and History
Hemostatic Therapy
Inflammation and Coagulation: An Important Link
Introduction
Perioperative Changes in Coagulation
28. Blood Products and Blood Components
28-1 Transfusion-Related Acute Lung Injury (TRALI) - Fig
28-1. Predictors of Postoperative Bleeding: Cardiothoracic Surgery - Table
28-2. Evidence-Based Indications for Transfusing Red Blood Cells, Platelets, Fresh Frozen Plasma, and Cryoprecipitate in Perioperative Settings Guidelines - Table
28-3. Plasma Transfusion Indications - Table
28-4. Presentation of Transfusion-Associated Circulatory Overload - Table
28-5. Transfusion-Related Acute Lung Injury - Table
Adverse Effects of Transfusions
Graft Versus Host Disease (GVHD) is a Potentially Fatal Complication that Occurs More Commonly after a Bone Marrow or Stem Cell Transplant
Hereditary Angioedema and C1 Esterase Inhibitor Concentrates
Indications for Platelet Transfusions and Transfusion Triggers
Introduction
Purified Protein Concentrates
Summary
Transfusion Therapy for Bleeding
29. Procoagulants
29-1 Excess Protamine Contributes to Elevations in the Activated Clotting Time (ACT), at Excesses of the Exact Dose Required to Reverse Systemic Anticoagulation Thus, Overdosage of Protamine Should Be Strictly Avoided - Fig
29-2 Thromboelastography Recordings Obtained With the Rotem Device after the Addition of Rfviia and/or Fibrinogen in the Presence of Tissue-Type Plasminogen Activator in Volunteer Plasma Tissue-Type Plasminogen Activator Was Added to Stimulate Fibrinolysis - Fig
Antifibrinolytic Agents: Aprotinin
Antifibrinolytic Agents: Lysine Analogs
Desmopressin (DDAVP) is the V2 Analog of Arginine Vasopressin that Stimulates the Release of Ultra Large Von Willebrand Factor (vWF) Multimers from Endothelial Cells
Fibrinogen is Synthesized in the Liver and a Critical Component of Effective Clot Formation
Introduction
Protamine is a Basic Protein that Inactivates the Acidic Heparin Molecule Via a Simple Acid-Base Interaction (Does Not Reverse Low-Molecular-Weight Heparin)
Recombinant Coagulation Products are Used to Manage Bleeding in Hemophilia
Summary
30. Anticoagulants
30-1 The Major Targets for Anticoagulants in the Coagulation Pathway are Directed Against Either Factor Xa or Thrombin (IIa) - Fig
30-1. Direct Thrombin Inhibitors Currently Available - Table
30-2. Current and Emerging Factor Xa Inhibitors and Vitamin K Antagonist - Table
30-3. Drugs Used for Platelet Inhibition Therapy - Table
30-4. Antiplatelet Therapy following Stent Placement (AHA/ACC Recommendations) - Table
30-5. Properties of Glycoprotein IIb/IIIa Antagonists - Table
Anticoagulants
Clinical Uses
Direct Thrombin Inhibitors: Parenteral Agents
Heparin Acts As an Anticoagulant by Binding to Antithrombin (AT)
Low-Molecular-Weight Heparins
Oral Anticoagulants
Perioperative Management of Patients on Platelet Inhibitors
Platelet Glycoprotein Iib/Iiia Antagonists
Platelet Inhibitors
Prophylaxis Against Venous Thromboembolism
Thrombolytic Drugs
31. Physiology and Management of Massive Transfusion
31-1 Massive Transfusion Protocol (MTP) Template - Fig
31-2 Suggested Criteria for Activation of Massive Transfusion Protocol (MTP) Template - Fig
Introduction
Massive Transfusion is Defined As Greater Than 10 Units of Red Blood Cells Within 24 Hours after Initiating Treatment
Monitoring Hemostasis During Massive Transfusion
Multimodal Resuscitation: Damage Control Resuscitation
Pathophysiology of Hemostatic Abnormalities Associated With Trauma
Perioperative Hemostatic Changes
Postpartum Hemorrhage is an Important Cause of Life-Threatening Hemorrhage and Continues to Be a Major Cause of Maternal Mortality
Summary
Part VI: Gastrointestinal System and Metabolism
32. Gastrointestinal Physiology
32-1 Schematic Depiction of a Hepatic Lobule With a Central Vein and Plates of Hepatic Cells Extending Radially - Fig
32-1. Functions of Hepatocytes - Table
32-2 Connections of the Ducts of the Gallbladder, Liver, and Pancreas - Fig
32-2. pH and Gastrointestinal Secretions - Table
32-3 Schematic Depiction of the Dual Afferent Blood Supply to the Liver Provided by the Portal Vein and Hepatic Artery - Fig
32-3. Site of Absorption - Table
32-4 Schematic Depiction of Bilirubin Formation and Excretion - Fig
32-5 Overall Fluid Balance in the Human Gastrointestinal Tract - Fig
32-6 Application of Cricoid Pressure Causes the Lower Esophageal Sphincter Pressure to Decrease - Fig
32-7 Anatomy of the Stomach Indicating the Site of Production of Secretions - Fig
32-8 Gastric Emptying of Liquids is Exponential, Whereas Emptying of Solids is a Linear Process - Fig
32-9 Anatomy of the Colon - Fig
Gastrointestinal Tract
Liver
33. Metabolism
33-1 Metabolism of Nutrients in Cells is Directed Toward the Ultimate Synthesis of Adenosine Triphosphate (ATP) Energy Necessary for Physiologic Processes and Chemical Reactions is Derived from the High-Energy Phosphate Bonds of ATP - Fig
33-1. Estimates of Energy Expenditure in Adults - Table
33-2 Comparison of the Composition of Body Weight to Caloric Stores - Fig
33-2. Composition of Lipids in the Plasma - Table
33-3. Types of Proteins - Table
33-4. Amino Acids - Table
33-5. Drugs Commonly Associated with Weight Gain - Table
33-6. Criteria for Diagnosis of Metabolic Syndrome (Any Three of the following Characteristics) - Table
Carbohydrate Metabolism
Effects of Stress on Metabolism
Lipid Metabolism
Metabolism of Nutrients
Obesity
Protein Metabolism
34. Antiemetics
34-1 Pharmacological Systems that Interact With the Vomiting Center - Fig
34-1. Pharmacologic Therapies for Treatment of Nausea and Vomiting - Table
Definition
Incidence
Introduction
Pathophysiology
Pharmacologic Interventions
Prophylaxis
35. Gastrointestinal Motility Drugs
35-1 Erythromycin, 200 mg Intravenously over 15 Minutes, Followed by Ingestion of a Radioactive-Labeled Meal (Scrambled Egg, Toast, and Water) Resulted in More Rapid Emptying of Solids and Liquids (IV Solids and IV Liquids) in Patients With Diabetic Gastroparesis and Patients Without Diabetes Compared With Gastric Emptying Times in the Absence of Erythromycin (Basal Solids and Basal Liquids) - Fig
35-1. Complications of Antacid Therapy - Table
35-2. Pharmacokinetics of H1-Receptor Antagonists - Table
35-3. Pharmacokinetics of H2-Receptor Antagonists - Table
35-4. Side Effects of H2-Receptor Antagonists - Table
35-5. Drug Interactions with Cimetidine - Table
35-6. Pharmacokinetics of Proton Pump Inhibitors - Table
Complications of Antacid Therapy.
Gastrointestinal Prokinetics
Histamine Receptor Antagonists
Introduction
Oral Antacids
Proton pump inhibitors
36. Nutrition
36-1 Chemical Structure of Water-Soluble Vitamins - Fig
36-1. Established Indications for Use of Nutritional Support - Table
36-2 Chemical Structure of Fat-Soluble Vitamins - Fig
36-2. Metabolic Complications of Parenteral Nutrition - Table
36-3. Vitamins. - Table
36-4. Suggested Uses, Potential Toxicities, and Drug Interactions of Dietary Supplements and Herbal Remedies - Table
36-5. Suggested Uses, Potential Toxicities, and Drug Interactions of Nonherbal Dietary Supplements - Table
Dietary Supplements
Enteral and Parenteral Nutrition
Enteral Nutrition is Almost Always Preferred over Parenteral Nutrition
Immunonutrition
Nutritional Support
Parenteral Nutrition is Indicated for Patients Who are Unable to Ingest or Digest Nutrients or to Absorb Them from the Gastrointestinal Tract
Vitamins
Part VII: Endocrine System
37. Normal Endocrine Function
37-1 Effects of Human Growth Hormone Manifesting As Direct Effects or Via Production of Somatomedins in the Liver - Fig
37-1. Hypothalamic Hormones - Table
37-2 Chemical Structure of Thyroid Hormones - Fig
37-2. Pituitary Hormones - Table
37-3 Proinsulin, Which is Converted to Insulin by Proteolytic Cleavage of Amino Acids 31, 32, 64, 65, and the Connecting Peptide - Fig
37-3. Regulation of Growth Hormone Secretion - Table
37-4 Insulin Stimulates Tissue Uptake of Glucose and Amino Acids, Whereas Release of Fatty Acids is Inhibited - Fig
37-4. Regulation of Prolactin Secretion - Table
37-5 Schematic Depiction of the Insulin Receptor Consisting of Two and Two Subunits Joined by Disulfide Bonds (-S-S-) - Fig
37-5. Regulation of Adrenocorticotrophic Hormone Secretion - Table
37-6 Glucagon Stimulates Tissue Release of Glucose, Free Fatty Acids, and Ketoacids and Hepatic Uptake of Amino Acids - Fig
37-6. Regulation of Arginine Vasopressin Secretion - Table
37-7. Physiologic Effects of Endogenous Corticosteroids (mg) - Table
37-8. Regulation of Insulin Secretion - Table
37-9. Regulation of Glucagon Secretion - Table
Adrenal Cortex
Hypothalamus and Pituitary Gland
Mechanism of Hormone Action
Normal Endocrine Function
Pancreas
Parathyroid Glands
Reproductive Glands
Thyroid Gland
38. Drugs that Alter Glucose Regulation
38-1. Etiologic Classification of Diabetes Mellitus - Table
38-2. Classification of Insulin Preparations - Table
38-3. Oral Drugs for Treatment of Type 2 Diabetes Mellitus - Table
38-4. Classification and Pharmacokinetics of Sulfonylurea Oral Hypoglycemics - Table
38-5. Comparison of Sulfonylurea Therapy with Insulin Therapy - Table
Diabetes Mellitus
Insulin
Oral Glucose Regulators
39. Drugs for the Treatment of Hypothyroidism and Hyperthyroidism
Hyperthyroidism
Hypothyroidism
40. Other Endocrine Drugs
40-1 Endogenous Corticosteroids - Fig
40-1. Comparative Pharmacology of Endogenous and Synthetic Corticosteroids. - Table
40-2 Synthetic Corticosteroids - Fig
Androgens are Administered to Males to Stimulate the Development and Maintenance of Secondary Sexual Characteristics
Clinical Uses
Corticosteroid Supplementation in the Perioperative Period
Corticosteroids
Drugs for Pituitary FunctionâAnterior Pituitary Hormones
Drugs for Reproductive Regulation-Ovarian Hormones
Drugs that Regulate Calcium
Electrolyte and Metabolic Changes and Weight Gain
Introduction
Melatonin is the Principal Substance Secreted by the Pineal Gland
Posterior Pituitary Hormones
Side Effects
Synthetic Corticosteroids
Part VIII: Miscellaneous
41. Antimicrobials, Antiseptics, Disinfectants, and Management of Perioperative Infection
41-1 Histamine Release (%) from Dispersed Human Cutaneous Mast Cells after the Administration of Vancomycin - Fig
41-1. SCIP Measures Related to Prevention of Surgical Site Infection - Table
41-2. Recommended Doses and Redosing Intervals for Commonly Used Antimicrobials for Surgical Prophylaxis - Table
41-3. Direct Drug Toxicity Associated with Administration of Antimicrobials - Table
41-4. Antimicrobials in Pregnancy - Table
Aminoglycoside Antimicrobials are Poorly Lipid-Soluble Antimicrobials (<1% of an Orally Administered Aminoglycoside is Absorbed) that are Rapidly Bactericidal for Aerobic Gram-Negative Bacteria
Antibacterial Drugs Commonly Used in the Perioperative Period
Antimicrobial Prophylaxis for Surgical Procedures
Antimicrobial Selection
Antiseptic and Disinfectant Prophylaxis for Surgical Procedures
Bacitracins are a Group of Polypeptide Antibiotics Effective Against a Variety of Gram-Positive Bacteria
Cephalosporins
Clindamycin Resembles Erythromycin in Antimicrobial Activity
Ethylene Oxide is a Readily Diffusible Gas that is Noncorrosive and Antimicrobial to All Organisms at Room Temperature
Fluoroquinolones are Broad-Spectrum Antimicrobials that are Bactericidal Against Most Enteric Gram-Negative Bacilli
Hexachlorophene (Phisohex) is a Polychlorinated Bisphenol that Exhibits Bacteriostatic Activity Against Gram-Positive but Not Gram-Negative Organisms
Introduction
Macrolides are Stable in the Presence of Acidic Gastric Fluid
Methods for Sterilization of Instruments
Metronidazole is Bactericidal Against Most Anaerobic Gram-Negative Bacilli and Clostridium Species
Other -Lactam Antimicrobials
Pasteurization (Hot Water Disinfection) is a Process that Destroys Microorganisms in a Liquid Medium by Application of Heat (Water Temperatures in the Range of 55°C to 75°C) Will Destroy All Vegetative Bacteria of Significance in Human Disease
Preference for Chlorhexidine or Iodine for Skin Disinfection
Quaternary Ammonium Compounds are Bactericidal in Vitro to a Wide Variety of Gram-Positive and Gram-Negative Bacteria
Silver Nitrate is Used As a Caustic
Special Patient Groups
Topical Antiseptics
Vancomycin is a Bactericidal Glycopeptide Antimicrobial that Impairs Cell Wall Synthesis of Gram-Positive Bacteria
42. Chemotherapeutic Drugs
42-1 Cell Cycle Specificity of Chemotherapy Agents - Fig
42-1. Chemotherapeutic Drugs, Therapeutic Uses, and Associated Side Effects - Table
42-2 The Probability of Developing Doxorubicin-Induced Congestive Heart Failure (CHF) Versus the Total Cumulative Dose of Doxorubicin - Fig
42-2. Side Effects of Cyclophosphamide - Table
42-3 The Relationship Between the Total Dose of Bleomycin and the Incidence of Pulmonary Toxicity - Fig
42-3. Risk Factors for Development of Chemotherapy-Induced Pulmonary Toxicity - Table
Alkylating Agents
Antimetabolites
Aromatase inhibitors block the conversion of androgens
Classification
Drug Resistance
Introduction
Monoclonal antibodies
Platinating Drugs
Signal Transduction Modulators (Hormones) that May Be Useful in the Treatment of Neoplastic Disease Include Antiestrogens
Topoisomerase Inhibitors
Toxicities
Tubulin-Binding Drugs
43. Drugs Used for Psychopharmacologic Therapy
43-1 The Two Forms of Monoamine Oxidase Enzyme (MAO-A and MAO-B) Exhibit Substrate Selectivity - Fig
43-1. Clinical Uses of Antidepressant Drugs - Table
43-2 Droperidol Produces Dose-Dependent Prolongation of the Antegrade and Retrograde Effective Refractory Period of Accessory Pathways - Fig
43-2. Comparative Pharmacology of Antidepressant Drugs - Table
43-3. Pharmacologic Treatment of Tricyclic Antidepressant Overdose - Table
43-4. Dietary Restrictions in Patients Treated with Monoamine Oxidase Inhibitors - Table
43-5. Serotonin Syndrome and Commonly Mistaken Diagnoses - Table
43-6. Drug Interactions with Lithium - Table
43-7. Signs and Symptoms of Lithium Toxicity - Table
43-8. Comparative Pharmacology of Antipsychotic (Neuroleptic) Drugs - Table
Antidepressants
Antipsychotic (neuroleptic)
Anxiolytics
Cannabis Has Been Used for Thousands of Years and is Presently the Most Commonly Used Illicit Drug in the World
Introduction
Lithium
Psychostimulants
Serotonin syndrome
Part IX: Special Populations
44. Physiology of the Newborn
44-1 Pressure Volume Curve for Neonatal and Adult Heart - Fig
44-1. Active Mechanisms Used by Neonates to Maintain Lung Volume - Table
Introduction
Neonatal Physiology
45. Maternal and Fetal Physiology and Pharmacology
45-1 Blood Volume Changes During Pregnancy - Fig
45-2 Maternal Hemodynamic Changes of Pregnancy - Fig
45-3 Changes in Maternal Pulmonary Function - Fig
45-4 Right Shift of Maternal Hemoglobin Oxygen Dissociation Curve - Fig
45-5 Diagram of the Fetal Circulation - Fig
45-6 Spinal Reflex and Pain Perception Pathways - Fig
Anesthetic Toxicity in the Fetus
Fetal Heart Rate Monitoring
Fetal Neurophysiology
Fetal Physiology
Introduction
Maternal Physiology
Pain Management
Uteroplacental Physiology
46. Physiology and Pharmacology of the Elderly
46-1 Age-Dependent Changes to Cardiovascular Tissues - Fig
46-1. Diseases Commonly Encountered in the Elderly that Are Associatedchr(10)with Diastolic Dysfunction - Table
46-2 Effect of Aging on Lung Volumes - Fig
46-2. Intrinsic and Extrinsic Events that Influence the Respiratorychr(10)System during Aging - Table
46-3 Effect of Aging on Gas Exchange - Fig
46-3. Functional Consequences of the Intrinsic and Extrinsic Eventschr(10)that Influence the Respiratory System during Aging - Table
46-4. Factors Associated with Reduced Resting Core Temperatures inchr(10)the Elderly - Table
46-5. Factors that Predispose to the Increased Incidence of Gastroesophagealchr(10)Reflux Disease in the Elderly - Table
46-6. Medications that Are Commonly Administered in the Elderly thatchr(10)Reduce Lower Esophageal Sphincter Tone and Predispose to Gastroesophagealchr(10)Reflux - Table
46-7. Factors that Are Thought to Be Responsible for the Significantchr(10)Decrease in Lean Muscle Mass that Occurs with Aging - Table
46-8. Perioperative Functional Consequences of the Loss of Skeletalchr(10)Muscle Mass that Typically Accompanies Aging - Table
Aging and the Cardiovascular System
Aging and the Respiratory System
Gastrointestinal Function in the Elderly
Introduction
Neurophysiology of Aging
Pain and Aging
Renal Function in the Elderly
Skeletal Muscle Mass and Aging
Thermoregulation in the Elderly
47. Physiology and Pharmacology of Resuscitation
47-1 Events Triggered by Hypoxia Leading to Cell Death - Fig
Cardiac Arrest
Hemorrhage
Introduction
Oxygenation/Ventilation
Pathophysiology
Pharmacology
Summary
Front Matter
Acknowledgment
Preface
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