This document discusses various induction agents used in general anesthesia. It begins by defining general anesthesia and its key features. It then covers general principles of pharmacology relevant to induction agents, including their action on receptors, plasma protein binding, crossing the blood-brain barrier, and distribution to other tissues. The document classifies common intravenous induction agents and discusses in detail the properties, mechanisms, uses, and adverse effects of thiopental sodium, propofol, and etomidate.
This document provides information on various anesthetic agents used in ophthalmic procedures, including general anesthetics (GA), regional anesthetics (RA), local anesthetics (LA), and topical anesthetics. It describes the types, mechanisms of action, common drugs, dosages, administration routes, indications, and side effects of different anesthetic classes. Key anesthetic agents discussed include nitrous oxide, halothane, ketamine, propofol, lidocaine, bupivacaine, and tetracaine.
This document discusses various intravenous anaesthetic agents. It describes the classification of IV induction agents as barbiturates like thiopentone and methohexitone, or non-barbiturates like propofol, etomidate, ketamine and benzodiazepines. It provides details on the properties, uses, advantages and side effects of specific agents like thiopentone, propofol and etomidate. Ketamine is discussed as an agent that produces dissociative anaesthesia and has strong analgesic effects.
General anesthetics act by modifying the electrical activity of neurons at a molecular level through effects on ion channels. The most widely accepted theory is that they bind directly to ion channels or disrupt proteins that maintain channel function. Common intravenous anesthetics like propofol and benzodiazepines enhance the effects of the inhibitory neurotransmitter GABA. They produce dose-dependent decreases in heart rate, blood pressure and respiratory function.
Anesthesia affects multiple organ systems and induces a reversible state of unconsciousness. It progresses through stages from induction to maintenance. Common types include intravenous agents like propofol and barbiturates, inhalational gases, and regional techniques. Special populations like diabetics and elderly patients require careful consideration due to altered drug metabolism and responses. The brain remains highly active under anesthesia through synchronized neural firing rather than ceasing activity.
Thiopental is an ultra short-acting barbiturate that is commonly used for induction of anesthesia. It works by facilitating the inhibitory neurotransmitter GABA at GABAA receptors in the brain, causing sedation, hypnosis and general anesthesia. Thiopental has a rapid onset within 10-20 seconds after intravenous injection and its effects wear off within 5-15 minutes. It is highly soluble in water and stable in solution. Common uses include induction of anesthesia, treatment of increased intracranial pressure, and cerebral protection during certain surgeries. Side effects include respiratory depression, emergence delirium and prolonged recovery.
Local anesthetics work by blocking sodium channels and inhibiting nerve impulse conduction. The document discusses the mechanism of action, classification of nerve fibers, pharmacokinetics, pharmacodynamics, effects on organ systems, clinical profiles of various local anesthetics, and additives that are commonly used. Toxicity can occur if maximum doses are exceeded, if there is inadvertent intravascular injection, or in susceptible patients.
The document provides information on various intravenous and inhalational drugs used in anaesthesia.
It discusses IV induction drugs like propofol, sodium thiopentone and etomidate. Propofol causes the most marked fall in blood pressure but is ideal for LMA. Sodium thiopentone directly depresses the heart but airway reflexes are better preserved than propofol. Etomidate causes the least cardiovascular depression but inhibition of adrenal function is a concern.
It also discusses the inhalational agent ketamine which provides dissociative anaesthesia and cardiovascular stability but unpleasant emergence reactions are common. The uptake and release of inhalational agents depends on alveolar gas concentration
General anesthetics are drugs that induce reversible loss of consciousness and sensations during surgery. They work by depressing the central nervous system in stages, starting with cortical centers and ending with the medulla. There are two main types - inhalational gases administered through masks or intravenous drugs given through injections. A balanced anesthesia approach uses multiple drugs to induce unconsciousness, amnesia, analgesia, and muscle relaxation. Precise drug combinations and dosages are tailored for each patient and procedure type. The goal is to smoothly induce and rapidly recover from anesthesia with minimized risks and side effects.
This document provides information on various anesthetic agents used in ophthalmic procedures, including general anesthetics (GA), regional anesthetics (RA), local anesthetics (LA), and topical anesthetics. It describes the types, mechanisms of action, common drugs, dosages, administration routes, indications, and side effects of different anesthetic classes. Key anesthetic agents discussed include nitrous oxide, halothane, ketamine, propofol, lidocaine, bupivacaine, and tetracaine.
This document discusses various intravenous anaesthetic agents. It describes the classification of IV induction agents as barbiturates like thiopentone and methohexitone, or non-barbiturates like propofol, etomidate, ketamine and benzodiazepines. It provides details on the properties, uses, advantages and side effects of specific agents like thiopentone, propofol and etomidate. Ketamine is discussed as an agent that produces dissociative anaesthesia and has strong analgesic effects.
General anesthetics act by modifying the electrical activity of neurons at a molecular level through effects on ion channels. The most widely accepted theory is that they bind directly to ion channels or disrupt proteins that maintain channel function. Common intravenous anesthetics like propofol and benzodiazepines enhance the effects of the inhibitory neurotransmitter GABA. They produce dose-dependent decreases in heart rate, blood pressure and respiratory function.
Anesthesia affects multiple organ systems and induces a reversible state of unconsciousness. It progresses through stages from induction to maintenance. Common types include intravenous agents like propofol and barbiturates, inhalational gases, and regional techniques. Special populations like diabetics and elderly patients require careful consideration due to altered drug metabolism and responses. The brain remains highly active under anesthesia through synchronized neural firing rather than ceasing activity.
Thiopental is an ultra short-acting barbiturate that is commonly used for induction of anesthesia. It works by facilitating the inhibitory neurotransmitter GABA at GABAA receptors in the brain, causing sedation, hypnosis and general anesthesia. Thiopental has a rapid onset within 10-20 seconds after intravenous injection and its effects wear off within 5-15 minutes. It is highly soluble in water and stable in solution. Common uses include induction of anesthesia, treatment of increased intracranial pressure, and cerebral protection during certain surgeries. Side effects include respiratory depression, emergence delirium and prolonged recovery.
Local anesthetics work by blocking sodium channels and inhibiting nerve impulse conduction. The document discusses the mechanism of action, classification of nerve fibers, pharmacokinetics, pharmacodynamics, effects on organ systems, clinical profiles of various local anesthetics, and additives that are commonly used. Toxicity can occur if maximum doses are exceeded, if there is inadvertent intravascular injection, or in susceptible patients.
The document provides information on various intravenous and inhalational drugs used in anaesthesia.
It discusses IV induction drugs like propofol, sodium thiopentone and etomidate. Propofol causes the most marked fall in blood pressure but is ideal for LMA. Sodium thiopentone directly depresses the heart but airway reflexes are better preserved than propofol. Etomidate causes the least cardiovascular depression but inhibition of adrenal function is a concern.
It also discusses the inhalational agent ketamine which provides dissociative anaesthesia and cardiovascular stability but unpleasant emergence reactions are common. The uptake and release of inhalational agents depends on alveolar gas concentration
General anesthetics are drugs that induce reversible loss of consciousness and sensations during surgery. They work by depressing the central nervous system in stages, starting with cortical centers and ending with the medulla. There are two main types - inhalational gases administered through masks or intravenous drugs given through injections. A balanced anesthesia approach uses multiple drugs to induce unconsciousness, amnesia, analgesia, and muscle relaxation. Precise drug combinations and dosages are tailored for each patient and procedure type. The goal is to smoothly induce and rapidly recover from anesthesia with minimized risks and side effects.
This document provides information about general anesthetics used for inducing unconsciousness during surgical procedures. It discusses the stages of anesthesia and classifications of general anesthetics as inhaled agents like gases, volatile liquids, and opioids or intravenous agents like barbiturates, benzodiazepines, ketamine, opioids, propofol, and etomidate. The mechanisms of action and effects on the central nervous system, cardiovascular system, and respiratory system are described. Factors affecting the speed of induction and mechanisms of elimination are also summarized for various inhaled and intravenous anesthetic agents.
This document discusses various intravenous induction agents used in anesthesia. It begins by providing an overview of the ideal properties of IV induction drugs and then discusses the mechanisms of action, pharmacokinetics, effects on organ systems, uses, doses and complications of specific drugs - barbiturates, propofol, ketamine and etomidate. It also presents several case scenarios and asks which IV induction drug would be most appropriate in each case. The document aims to educate attendees on the properties and appropriate uses of common IV induction agents.
Intravenous anesthetic agents include barbiturates, benzodiazepines, opioids, and miscellaneous drugs. They are used for induction and maintenance of anesthesia, as well as sedation. Barbiturates like thiopental are used for induction but have cumulative effects. Benzodiazepines provide sedation and are used in regional anesthesia and intensive care. Opioids like fentanyl, alfentanil, and remifentanil provide analgesia before and after surgery. They can cause respiratory depression, nausea, and vomiting. Ketamine is used in shocked patients and where equipment is limited due to rapid onset and short duration.
General anesthetics render patients unconscious, amnesic and cause muscle relaxation. Traditional agents included alcohol, ice and blows to the head. Modern agents include intravenous barbiturates, benzodiazepines, propofol and inhalational gases like nitrous oxide, halothane and isoflurane. These work by enhancing GABA receptors and inhibiting excitatory receptors. Local anesthetics like lidocaine and bupivacaine block sodium channels to provide analgesia without unconsciousness.
Ketamine produces dissociative anesthesia and has hypnotic, analgesic, and amnesic effects. It works by binding to NMDA receptors and other sites like opioid receptors. Ketamine has a rapid onset after IV or IM administration, with effects seen within 1-5 minutes. It causes increased blood pressure and heart rate by stimulating the sympathetic nervous system. Ketamine can also increase respiratory rate and salivation, dilate pupils, and has short-term side effects like confusion and out of body experiences. It has various indications like analgesia, anesthesia induction, and improving psychiatric disorders.
Intravenous induction agents are drugs given intravenously to induce anesthesia rapidly. Ideal properties include water solubility, stability, rapid onset within one arm-brain circulation time, rapid redistribution and clearance with no active metabolites, minimal effects on vital organs, and a high therapeutic ratio. Common IV induction agents discussed are barbiturates, propofol, ketamine, etomidate, benzodiazepines, and opioids. Each drug has different effects on the cardiovascular, respiratory, and central nervous systems and potential complications.
Intravenous induction agents are drugs that cause rapid loss of consciousness when given intravenously. Some of the most commonly used agents are thiopental, propofol, etomidate, and ketamine. Thiopental was the first agent introduced in the 1930s and provided rapid induction but was unsuitable for maintenance. Propofol provides pleasant sedation and recovery but causes hypotension. Etomidate offers hemodynamic stability but can cause excitation. Ketamine produces dissociative anesthesia and analgesia with cardiorespiratory stability but may cause emergence reactions. Each agent has advantages and disadvantages depending on the surgical situation and patient characteristics.
A powerpoint explaining in detail about all the intravenous induction agents and their clinical uses, pharmacokinetics & pharmacodynamics, adverse effects and complications.
General anesthesia alters the central nervous system and causes pain relief, muscle relaxation, relaxation of reflexes, and deep sleep. It commonly used during surgery and involves five phases: preparation, induction, maintenance, emergence, and recovery.
General anesthesia can be delivered via inhalation of gases like nitrous oxide and liquids like halothane, or intravenously with analgesics, atropine, and anti-emetics. Local anesthetics are also used to block nerve conduction in specific body areas and prevent pain sensation. They come in topical, spinal, epidural, infiltration and nerve block forms.
properties, classification and principle of action of intravenous induction agent.
pharmacokinetics
comparison between properties of various agent
summary of ketamine, propofol, thiopenton etomidate , bzd and opioids.
Intravenous Anaesthetics are a group of fast-acting
compounds that are used to induce a state of impaired
awareness of complete sedation.
These are drugs that, when given intravenously in an
appropriate dose, cause a rapid loss of consciousness.
General and local anaesthesia are reversible conditions used before, during, and after surgical procedures. General anaesthesia renders the patient unaware through drugs like inhaled gases or intravenous injections, allowing for major surgery. Local anaesthesia uses drugs like lidocaine to reversibly block nerve conduction in a restricted area without loss of consciousness, making it suitable for minor procedures. The choice of anaesthesia depends on factors like the health of the patient, type of surgery, and ability to cooperate.
General anesthetics are agents that produce controlled, reversible loss of consciousness, pain sensation, and muscle relaxation to safely perform surgical procedures. They work by depressing the central nervous system. Inhalational general anesthetics like nitrous oxide, halogenated agents, and intravenous agents are used. The ideal general anesthetic has rapid, smooth induction and recovery without complications. Inhalational agents are absorbed via lungs and eliminated primarily through exhalation. They cause various effects on cardiovascular, respiratory, neurological and other organ systems. Adverse effects include hepatitis, nephrotoxicity and malignant hyperthermia. Proper precautions must be taken in high risk patients.
This document discusses drugs that act on the central nervous system (CNS). It outlines two main types of CNS drugs - stimulants and depressants. CNS stimulants enhance excitatory neurotransmission and inhibit inhibitory neurotransmission, causing increased motor and sensory activity. Examples include analeptics and psychomotor stimulants. CNS depressants have opposite effects, potentiating inhibitory neurotransmission, inhibiting excitatory neurotransmission, and decreasing motor and sensory activity. Examples of CNS depressants include sedatives, hypnotics, general anesthetics, anticonvulsants, and opioid analgesics.
This document provides information on general anaesthetics. It discusses what general anaesthetics are and how they work on the central nervous system. It describes the four stages of general anaesthesia: analgesia, delirium, surgical anaesthesia (which has four planes), and respiratory paralysis. Common volatile and non-volatile general anaesthetic agents are identified and some of their properties and uses are mentioned, including diethyl ether, chloroform, halothane, nitrous oxide, and thiopentone. The document also discusses ideal properties of anaesthetic agents and pre-anaesthetic medication.
A General Anaesthetic is a drug that produces a reversible state of unconscious with absence of pain sensation over the entire body; such agents have been described as drugs that remove the most precious human attributes ---- Conscious.
Ketamine
Brand name: KETALAR
Phencyclidine derivative
Shorting acting
Mainly used in children and elderly adults for short procedures such as burns dressing.
ABUSIVE DRUG
Is a dissociative anaesthetic as it produces a cataleptic state in which the patient appears to be awake but is detached from the environment and is unresponsive to pain.
Please also refer to other reference books for clarity.
General anesthesia results in reversible depression of the central nervous system, causing loss of response to external stimuli. It provides benefits like sedation, lack of awareness, muscle relaxation, suppression of reflexes, and analgesia. No single agent provides all benefits, so several drugs are used in combination for optimal anesthesia. Factors like organ function and concurrent medications must be considered when choosing anesthetic drugs to safely induce, maintain, and recover the patient from anesthesia.
The document discusses the history and current use of spinal, epidural, and caudal anesthesia. It provides details on:
1) The key developments in these techniques from 1885 to present day and their current role in veterinary and human anesthesia.
2) The indications, contraindications, and complications of these regional anesthesia techniques.
3) The local anesthetics, opioids, and other agents used and their mechanisms of action, dosages, durations, and side effects.
4) Techniques for administering spinal, epidural, and caudal anesthesia including needle selection, injection procedures, and postoperative care.
This document provides information about general anesthetics used for inducing unconsciousness during surgical procedures. It discusses the stages of anesthesia and classifications of general anesthetics as inhaled agents like gases, volatile liquids, and opioids or intravenous agents like barbiturates, benzodiazepines, ketamine, opioids, propofol, and etomidate. The mechanisms of action and effects on the central nervous system, cardiovascular system, and respiratory system are described. Factors affecting the speed of induction and mechanisms of elimination are also summarized for various inhaled and intravenous anesthetic agents.
This document discusses various intravenous induction agents used in anesthesia. It begins by providing an overview of the ideal properties of IV induction drugs and then discusses the mechanisms of action, pharmacokinetics, effects on organ systems, uses, doses and complications of specific drugs - barbiturates, propofol, ketamine and etomidate. It also presents several case scenarios and asks which IV induction drug would be most appropriate in each case. The document aims to educate attendees on the properties and appropriate uses of common IV induction agents.
Intravenous anesthetic agents include barbiturates, benzodiazepines, opioids, and miscellaneous drugs. They are used for induction and maintenance of anesthesia, as well as sedation. Barbiturates like thiopental are used for induction but have cumulative effects. Benzodiazepines provide sedation and are used in regional anesthesia and intensive care. Opioids like fentanyl, alfentanil, and remifentanil provide analgesia before and after surgery. They can cause respiratory depression, nausea, and vomiting. Ketamine is used in shocked patients and where equipment is limited due to rapid onset and short duration.
General anesthetics render patients unconscious, amnesic and cause muscle relaxation. Traditional agents included alcohol, ice and blows to the head. Modern agents include intravenous barbiturates, benzodiazepines, propofol and inhalational gases like nitrous oxide, halothane and isoflurane. These work by enhancing GABA receptors and inhibiting excitatory receptors. Local anesthetics like lidocaine and bupivacaine block sodium channels to provide analgesia without unconsciousness.
Ketamine produces dissociative anesthesia and has hypnotic, analgesic, and amnesic effects. It works by binding to NMDA receptors and other sites like opioid receptors. Ketamine has a rapid onset after IV or IM administration, with effects seen within 1-5 minutes. It causes increased blood pressure and heart rate by stimulating the sympathetic nervous system. Ketamine can also increase respiratory rate and salivation, dilate pupils, and has short-term side effects like confusion and out of body experiences. It has various indications like analgesia, anesthesia induction, and improving psychiatric disorders.
Intravenous induction agents are drugs given intravenously to induce anesthesia rapidly. Ideal properties include water solubility, stability, rapid onset within one arm-brain circulation time, rapid redistribution and clearance with no active metabolites, minimal effects on vital organs, and a high therapeutic ratio. Common IV induction agents discussed are barbiturates, propofol, ketamine, etomidate, benzodiazepines, and opioids. Each drug has different effects on the cardiovascular, respiratory, and central nervous systems and potential complications.
Intravenous induction agents are drugs that cause rapid loss of consciousness when given intravenously. Some of the most commonly used agents are thiopental, propofol, etomidate, and ketamine. Thiopental was the first agent introduced in the 1930s and provided rapid induction but was unsuitable for maintenance. Propofol provides pleasant sedation and recovery but causes hypotension. Etomidate offers hemodynamic stability but can cause excitation. Ketamine produces dissociative anesthesia and analgesia with cardiorespiratory stability but may cause emergence reactions. Each agent has advantages and disadvantages depending on the surgical situation and patient characteristics.
A powerpoint explaining in detail about all the intravenous induction agents and their clinical uses, pharmacokinetics & pharmacodynamics, adverse effects and complications.
General anesthesia alters the central nervous system and causes pain relief, muscle relaxation, relaxation of reflexes, and deep sleep. It commonly used during surgery and involves five phases: preparation, induction, maintenance, emergence, and recovery.
General anesthesia can be delivered via inhalation of gases like nitrous oxide and liquids like halothane, or intravenously with analgesics, atropine, and anti-emetics. Local anesthetics are also used to block nerve conduction in specific body areas and prevent pain sensation. They come in topical, spinal, epidural, infiltration and nerve block forms.
properties, classification and principle of action of intravenous induction agent.
pharmacokinetics
comparison between properties of various agent
summary of ketamine, propofol, thiopenton etomidate , bzd and opioids.
Intravenous Anaesthetics are a group of fast-acting
compounds that are used to induce a state of impaired
awareness of complete sedation.
These are drugs that, when given intravenously in an
appropriate dose, cause a rapid loss of consciousness.
General and local anaesthesia are reversible conditions used before, during, and after surgical procedures. General anaesthesia renders the patient unaware through drugs like inhaled gases or intravenous injections, allowing for major surgery. Local anaesthesia uses drugs like lidocaine to reversibly block nerve conduction in a restricted area without loss of consciousness, making it suitable for minor procedures. The choice of anaesthesia depends on factors like the health of the patient, type of surgery, and ability to cooperate.
General anesthetics are agents that produce controlled, reversible loss of consciousness, pain sensation, and muscle relaxation to safely perform surgical procedures. They work by depressing the central nervous system. Inhalational general anesthetics like nitrous oxide, halogenated agents, and intravenous agents are used. The ideal general anesthetic has rapid, smooth induction and recovery without complications. Inhalational agents are absorbed via lungs and eliminated primarily through exhalation. They cause various effects on cardiovascular, respiratory, neurological and other organ systems. Adverse effects include hepatitis, nephrotoxicity and malignant hyperthermia. Proper precautions must be taken in high risk patients.
This document discusses drugs that act on the central nervous system (CNS). It outlines two main types of CNS drugs - stimulants and depressants. CNS stimulants enhance excitatory neurotransmission and inhibit inhibitory neurotransmission, causing increased motor and sensory activity. Examples include analeptics and psychomotor stimulants. CNS depressants have opposite effects, potentiating inhibitory neurotransmission, inhibiting excitatory neurotransmission, and decreasing motor and sensory activity. Examples of CNS depressants include sedatives, hypnotics, general anesthetics, anticonvulsants, and opioid analgesics.
This document provides information on general anaesthetics. It discusses what general anaesthetics are and how they work on the central nervous system. It describes the four stages of general anaesthesia: analgesia, delirium, surgical anaesthesia (which has four planes), and respiratory paralysis. Common volatile and non-volatile general anaesthetic agents are identified and some of their properties and uses are mentioned, including diethyl ether, chloroform, halothane, nitrous oxide, and thiopentone. The document also discusses ideal properties of anaesthetic agents and pre-anaesthetic medication.
A General Anaesthetic is a drug that produces a reversible state of unconscious with absence of pain sensation over the entire body; such agents have been described as drugs that remove the most precious human attributes ---- Conscious.
Ketamine
Brand name: KETALAR
Phencyclidine derivative
Shorting acting
Mainly used in children and elderly adults for short procedures such as burns dressing.
ABUSIVE DRUG
Is a dissociative anaesthetic as it produces a cataleptic state in which the patient appears to be awake but is detached from the environment and is unresponsive to pain.
Please also refer to other reference books for clarity.
General anesthesia results in reversible depression of the central nervous system, causing loss of response to external stimuli. It provides benefits like sedation, lack of awareness, muscle relaxation, suppression of reflexes, and analgesia. No single agent provides all benefits, so several drugs are used in combination for optimal anesthesia. Factors like organ function and concurrent medications must be considered when choosing anesthetic drugs to safely induce, maintain, and recover the patient from anesthesia.
The document discusses the history and current use of spinal, epidural, and caudal anesthesia. It provides details on:
1) The key developments in these techniques from 1885 to present day and their current role in veterinary and human anesthesia.
2) The indications, contraindications, and complications of these regional anesthesia techniques.
3) The local anesthetics, opioids, and other agents used and their mechanisms of action, dosages, durations, and side effects.
4) Techniques for administering spinal, epidural, and caudal anesthesia including needle selection, injection procedures, and postoperative care.
Intravenous induction agents like thiopentone and propofol cause rapid loss of consciousness when given in appropriate doses. They act very quickly, within one arm-brain circulation time, by enhancing GABA inhibition in the brain. Thiopentone was the first barbiturate used for intravenous anesthesia induction. Propofol is now commonly used due to its rapid onset and offset of action. Both drugs can cause hypotension due to vasodilation, so doses must be titrated slowly, especially in vulnerable patients. Their effects are short-lived due to rapid redistribution from the brain to other tissues.
Intravenous induction agents are drugs that cause rapid loss of consciousness when given intravenously in an appropriate dose. The ideal IV induction drug has rapid onset and offset, minimal cardiorespiratory depression, no excitatory effects, and is safe to use across patient populations. Common IV induction agents discussed include barbiturates, propofol, ketamine, etomidate, and benzodiazepines. Each drug has unique effects on organ systems and potential complications that must be considered when selecting an agent for induction of anesthesia.
Intravenous induction agents such as thiopental, propofol, etomidate, and methohexital cause rapid loss of consciousness when given in the appropriate intravenous dose due to their fast onset within one arm-brain circulation time. Thiopental was the first ultra-short acting barbiturate and intravenous anesthetic introduced in the 1930s, while propofol launched in 1986 is now widely used due to its favorable properties. These induction agents work by enhancing GABA inhibition in the brain and cause dose-dependent decreases in heart rate, blood pressure and respiratory function upon induction before redistributing out of the brain and allowing for rapid wake up.
General anesthesia and its complicationsAbhishek Roy
General anesthesia refers to the reversible loss of sensation and consciousness achieved through a combination of inhaled and intravenous drugs. It involves stages including analgesia, delirium, and surgical anesthesia. Complications may include respiratory depression, arrhythmias, nausea, and emergence delirium. Anesthesia is induced and maintained using inhalational agents like nitrous oxide, halothane, and sevoflurane or intravenous drugs like propofol and ketamine. Premedication, reversal agents, and conscious sedation techniques help optimize anesthesia outcomes and safety.
The document provides an overview of general anaesthesia. It discusses the aims and requirements of general anaesthesia including unconsciousness, analgesia, muscle relaxation and physiological stability. It describes the processes involved such as pre-medication, induction, maintenance of anaesthesia and muscle relaxation. Common intravenous agents for induction and maintenance like thiopental, propofol and ketamine are explained. Inhalational agents including nitrous oxide, halothane, sevoflurane and isoflurane are also discussed. Their properties, mechanisms of action, advantages and disadvantages are summarized.
IV induction drugs are used to rapidly induce anesthesia prior to other drugs being given to maintain anesthesia. The ideal IV induction drug has favorable physical, pharmacokinetic, and pharmacodynamic properties. Barbiturates like thiopental are commonly used IV induction agents that depress the central nervous system by enhancing GABA transmission. Propofol is a popular agent with a rapid onset due to high lipid solubility and redistribution, though it can cause hypotension. Ketamine is used for induction and analgesia as an NMDA receptor antagonist that produces dissociative anesthesia while maintaining respiratory drive and airway reflexes.
general anesthesia are the drug given before surgery which have reversible effect on consciousness. discussing ideal GA, stages of GA, mechanism of action of GA, classification of drugs parenteral or inhaled.
complete and detail study on the topic of general anesthetics by the collaboration of teacher and students for the student , teachers and other health care professionals to learn more on the topics
This document provides information about different types of anesthesia. It discusses local anesthesia and general anesthesia. For general anesthesia, it describes the stages and classification into inhalation and intravenous agents. Specific agents are discussed like nitrous oxide, halothane, isoflurane, ketamine and propofol. Their properties, uses, and risks are summarized. For local anesthesia, the mechanisms of action, types of administration, advantages, and adverse effects are covered at a high level.
This document provides information on general anesthesia including:
1. It defines general anesthesia as reversible blocking of pain and sensation in the whole body or parts using pharmacology or other methods.
2. It describes the parts of general anesthesia including hypnosis, analgesia, areflexia, and muscle relaxation which must be balanced.
3. It explains the different types of general anesthesia including total intravenous anesthesia, volatile induction and maintenance anesthesia.
This document discusses different types of anesthesia and anesthetic agents. It defines anesthesia as the loss of sensation and consciousness without loss of vital functions, artificially produced by administering agents that block pain impulses. General anesthesia involves stages including analgesia, excitement, surgical anesthesia, and medullary paralysis. Common general anesthetic agents administered by inhalation include cyclopropane, desflurane, enflurane, halothane, isoflurane, and nitrous oxide. Injectable general anesthetics include thiopental sodium, ketamine, methohexital sodium, and thiamylal sodium. Adjuncts to general anesthesia are also used like sedatives, analgesics, antiemetics, and ant
General Anaethetics & Pre-anaethetics.pptxManish Gautam
Pre-anaesthetic medication involves administering drugs before general anesthesia to make anesthesia safer for the patient. Common drugs used include anti-anxiety drugs like diazepam to reduce apprehension, sedatives/hypnotics like promethazine for its sedative and antiemetic effects, opioid analgesics like morphine for analgesia and sedation, and anticholinergics like atropine to reduce secretions. General anesthetics produce reversible unconsciousness, analgesia, amnesia, muscle relaxation and inhibition of reflexes. Common intravenous anesthetics used include thiopental for induction, propofol for its rapid onset and offset, and ketamine for its analgesic properties. Inhalational agents like
This document discusses sedative and hypnotic drugs, focusing on barbiturates. It classifies barbiturates and describes their mechanism of action, pharmacological effects, kinetics, therapeutic uses, adverse effects, interactions, and compares them to benzodiazepines. It also discusses non-benzodiazepine hypnotics including zopiclone, zolpidem, zaleplon, buspirone, and chloral hydrate.
This document summarizes several IV anaesthetic agents including thiopentone, propofol, etomidate, and ketamine. It describes the chemical name, mechanism of action, effects on major body systems, clinical uses, and side effects for each agent. Thiopentone is an alkaline powder that acts as a GABA receptor agonist. Propofol is a white oil suspension that facilitates GABA transmission. Etomidate causes adrenocortical suppression. Ketamine acts as an NMDA receptor antagonist and has analgesic and psychomimetic effects but can increase intracranial pressure. All of these agents are used for induction of general anesthesia and have varying effects on the CNS, CVS,
This document provides an overview of intravenous anaesthetic agents. It discusses the uses of general anaesthesia including induction and maintenance. It describes the properties of ideal intravenous anaesthetics such as rapid onset and recovery, minimal side effects, and solubility. The document then covers the pharmacokinetics, metabolism, and effects of specific intravenous agents - barbiturates like thiopental, propofol, and ketamine. It provides details on their mechanisms of action, pharmacology, uses, and side effects.
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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4. GENERAL ANESTHESIA
General anesthesia is a reversible state of unconsciousness from which a person cannot be
aroused by an external stimulus. There is a complete or partial loss of protective reflexes
including the ability to maintain airway independently.
General Anesthetics are drugs which produce reversible loss of all sensation and consciousness.
5. CARDINAL FEATURES OF GENERAL ANESTHESIA
• Loss of all sensation (analgesia)
• Sleep (unconsciousness) & amnesia
• Immobility & muscle relaxation
• Abolition of somatic & autonomic reflexes
7. ACTION ON RECEPTORS
• A receptor is a complex structure on the cell membrane which can bind selectively with endogenous
compounds or drugs resulting in changes within the cell which can modify its function.
These include changes in GABA receptors, cGMP receptors, NMDA receptors.
PLASMA PROTEIN BINDING
• Many drugs are bound to plasma and only unbound drug is free to cross the BBB.
• Protein binding may be reduced by low plasma protein concentration or displacement by drugs
resulting in higher concentration of free drug leading to exaggerated anesthetic effect.
• Protein binding is also affected by changes in blood pH.
8. THE BLOOD BRAIN BARRIER
• The brain is protected from most potentially toxic agents by tightly overlapping endothelial cells
which surround the capillaries & interfere with passive diffusion.
Many drugs used in the anesthetic procedure must cross the BBB to reach their site of action
• Highly ionized drugs (e.g., muscle relaxants, glycopyronium) do not cross the BBB
• Reduced cerebral blood flow results in reduced delivery of drug to the brain. E.g., carotid artery
stenosis
If the CBF is low because low cardiac output, the initial blood concentrations are higher than normal
after IV anesthetic administration, therefore, the anesthetic effect is delayed but enhanced.
9. SOLUBILITY OF DRUG IN LIPIDS
• Highly lipid soluble drug enhances transfer into the brain.
SPEED OF INJECTION
Rapid IV administration results in high initial concentration of the drug
Decreased protein binding
There is increased intensity of side effects (cardiovascular & respiratory side effects)
10. DISTRIBUTION TO OTHER TISSUES
• Anesthetic effect of all IV anesthetics is terminated by distribution to other tissues.
• A large proportion of the drug is distributed initially into well perfused organs (brain, liver,
kidneys).
• Distribution into muscle is slower because of low lipid content but important because of its
good blood supply & large mass.
• Distribution to fat is slower because of its poor blood supply but contains large proportions of
injected dose. It could remain in the body for up to 24 hours.
11. PROPERTIES OF IDEAL IV ANESTHETIC AGENT
• Rapid onset: achieved by an agent which is mainly unionized at blood pH & which is highly
soluble in lipids
• Rapid recovery: early recovery of consciousness is usually produced by rapid redistribution of
the drug into other tissues. The quality of late recovery is related to the rate of metabolism of
the drug. Decreased recovery = prolonged “hangover” effect
• Analgesia at subanesthetic concentrations.
• Minimal cardiovascular & respiratory depression.
• No emetic effects
12. PROPERTIES OF IDEAL IV ANESTHETIC AGENT
• No excitatory phenomena on induction (e.g., coughing, hiccup, involuntary movements)
• No emergence phenomena (e.g., nightmares)
• No interaction with neuromuscular blocking drugs.
• No venous sequalae
• Safe if inadvertently injected into an artery.
• No toxic effect on other drugs
• No release of histamine
• Water soluble formulation
• No stimulation of porphyria
13. CLASSIFICATION OF IV ANESTHETICS
RAPIDLY ACTING AGENTS [PRIMARY INDUCTION]
Barbiturates
methohextal
thiobarbiturates: thiopental, thiamylal
Imidazole compounds
etomidate
Sterically hindered alkyl phenol
propofol
Steroids (none currently available)
eltomolone, althesin, minaxolone
Eugenols (none currently available)
propanidid
16. THIOPENTAL SODIUM
• It is an ultra short acting barbiturate
• Pale yellow colour.
• Stored in Nitrogen to prevent chemical reaction with atmospheric CO2
• Onset of action: One arm brain circulation 15 – 20 seconds
• Duration of action : α Half life - 10 minutes
β Half life - 45 minutes
γ Half life - 6-20 hours
Dosage: 1-2mL of 2.5% solution for adults
4mg/Kg for adults
6mg/Kg for children
• Clearance : 3.4 ml/Kg/min
17. Metabolism
• It follows zero order kinetics i.e. constant amount
of drug is eliminated per unit time irrespective of
plasma concentration.
Mechanism of action
• Activation of GABAA which increases transmembrane Chloride channels
• This results in Hyperpolarization of post synaptic neurons
• causing “FUNCTIONAL INHIBITION OF POST-SYNAPTIC NEURONS”
18. Central Nervous System
Produces anesthesia within 30 minutes
Potent hypnotic action
Analgesic effect is poor
At subanesthetic doses (i.e. low dose or during recovery), it can decrease pain threshold
resulting in restlessness during post op period.
Surgical anesthesia is difficult to achieve unless large doses are used
Sympathetic nervous system is depressed resulting in bradycardia
followed by tachycardia (due to baroreceptor inhibition caused by modest hypotension
& partly because of loss of vagal tone)
19. Cardiovascular System
Myocardial contractility is depressed & peripheral vasodilatation occurs when large doses are
administered or injected rapidly.
Arterial pressure decreases & hypotension may occur
Heart rate may decrease, but there is often reflex tachycardia
Respiratory System
Ventilatory drive [product of TV x RR i.e. 6L/min, rate and strength of contraction of
respiratory muscles] is decreased
When spontaneous ventilation is resumed, ventilatory rate & TV are usually lower than
normal but they increase in response to surgical stimulation.
Skeletal Muscle
There is poor muscle relaxation & movement in response to surgical stimulation
20. Eye
Intraocular pressure is reduced by approximately 40 %
Corneal, conjunctival, eyelash & eyelid reflexes are abolished.
Hepatorenal Function
Hepatic microsomal enzymes are induced and this may increase the metabolism &
elimination of other drugs.
21. ADVERSE EFFECTS
• Contraindicated in porphyrias
• Abdominal pain
• Psychiatric symptoms like hysteria
• CNS symptoms like seizures, cortical blindness & coma
• Local tissue necrosis
• Inadvertent intra – arterial injection causes intense pain
Management
a) Stop further injection
b) Inject saline into canula & flush
c) Inject preservative free lignocaine Papaverine 40 – 80 mg (vasodilation) Heparin
d) Stellate ganglion nerve block or brachial plexus nerve block to achieve sympatholysis if pain is intense & tissue
perfusion is in jeopardy.
23. PROPOFOL
• 2,6 Di isopropyl phenol
• Highly lipid soluble
• Contains 10% Soybean oil,
1.2% Egg Lecithin and
2.25% Glycerol (osmotic agent)
• Propofol causes pain on injection
PROPOFOL LIPURO – preparation of propofol containing both long & medium chain triglycerides
in 1:1 ratio. It reduces pain on injection
FOSPROPOFOL- A water soluble methylphopshorylated prodrug of propofol, no Pain on injection
but slow onset of action.
24. PHARMACOKINETICS
• Volume of distribution – 4.6 L/Kg
• Clearance – 25 ml/Kg/min
• Protein binding - 98%
• Water solubility – No
• pH: 7.0 – 8.5
• Onset of action – One arm brain circulation time ( 15 -20 seconds)
• Duration of action – 3 to 5 minutes when given I.V.
• Half life: α half life – 3-5 min
β half life – 20-50 min
γ half life – 200-500 min
25. MECAHNISM OF ACTION
• Activates chloride channels of GABA receptors inhibitory synaptic transmission.
• It also inhibits NMDA subtype of glutamate receptors
DOSES
• Induction: 2 – 2.5 mg/Kg in adults ; 2.5 – 3 mg/Kg in children
• Maintenance: At a dose of 50-150 μg/Kg/min
• Conscious sedation: @ 50-75 μg/Kg/min
ELIMINATION
• Propofol is metabolized by conjugation to glucuronide & sulfate by liver.
• Propofol also undergoes extrahepatic metabolism in kidney and lungs (30%)
26. Central Nervous System
• Reduces Cerebral metabolic rate
• Reduces Cerebral blood flow through auto-regulation Reduces Intracranial pressure
• Can cause some involuntary movements during induction
• Dose dependent depression of CNS
Loss of response to verbal commands end point of induction
Cardiovascular System
• Causes hypotension due to peripheral vasodilatation which can be minimized by slow injection.
Respiratory system
• Causes transient apnea
• Obtunds airway reflexes.
GIT
Propofol has low anti emetic properties
27. USES
• Useful in day care anaesthesia and surgery
• Useful in patients susceptible to Malignant hyperthermia
• Can be used as an anticonvulsant
• Can be used as anti-puritic & anti emetic
• Safe in patients with porphyria
28. PROPOFOL VERSUS THIOPENTONE
• Residual impairment is less & short lasting, hence, patient is ambulatory early.
• Incidence of post operative nausea & vomiting is low.
• Patient acceptability is very good
• Does not cause bronchospasm, hence can be used in asthamatics.
29. ADVERSE EFFECTS
• Hypotension
• Allergic reactions to egg protein
• Pain on injection ( can be reduced with lignocaine 20 mg)
• Susceptible to growth of microorganisms (emulsions must be discarded after 12 hours)
• Can cause involuntary epileptiform movements.
30. PROPOFOL INFUSION SYNDROME
• Occurs in children & infants
• Due to prolonged infusion
• Occurs when used in excess of 4mg/kg/hour for more than 48 hours.
Causes:
Metabolic acidosis, hyperkalemia, rhabdomyolysis, renal failure, hepatomegaly, cardiac failure,
hyperlipidemia
Management:
Cardiorespiratory support
Hemodialysis
33. ETOMIDATE
• Carboxylated Imidazole ester.
• Weak Base & poorly water soluble
• Available as lipid emulsion at a concentration of 2mg/mL
• MECAHNISM OF ACTION
Activates chloride channels of GABA Inhibitory synaptic transmission
• Onset of action: One arm-brain circulation time 15-20 seconds
• Duration: 3-5 minutes when given I.V.
Dosage: 0.3mg/Kg IV
34. Central Nervous System
• Dose dependent depression of CNS
• Can produce involuntary movements during induction.
• Recovery is rapid due to redistribution.
Cardiovascular System
• Least cardiovascular depression
• Used in shock and cardiovascularly compromised patients.
Respiratory system
• Can cause cough or hiccups.
• Transient apnea occurs with induction doses
GIT
• Increased incidence of Nausea & Vomiting
35. ADVERSE EFFECTS
• Pain on injection & Thrombophlebitis
• Recovery is frequently unpleasant and accompanied by nausea and vomiting
• Continuous infusion of etomidate for sedation in critically ill patients has been shown to increase mortality.
• Adreno-cortical suppression:
It inhibits 11-β-hydroxylase, an enzyme important in adrenal steroid production.
A single induction dose: blocks the normal stress induced increase in adrenal cortisol production for 4-8 hours,
and up to 24 hours in elderly and debilitated patients.
37. KETAMINE HYDROCHLORIDE
• Phencyclidine derivative
• Produces DISSOCIATIVE ANAESTHESIA
• Dissociative anaesthesia resembles a cataleptic state in which the eyes remain open with a
slow nystagmic gaze.
• Exists in two optical isomers
38. S(+) ketamine produces:
• More intense analgesia
• More rapid metabolism & thus recovery
• Less salivation
• Lower incidence of emergence reactions
39. Mechanism of action:
• Inhibits NMDA receptors
• Inhibits serotonin & muscarinic receptors
• Onset of action: 30-60 seconds I.V,
5 minutes I.M
25-45 minutes orally
• Duration of action : 10-15 min when given I.V
α half life – 10-15 minutes
γ half life – 2-3 hours
• Dosage: Induction: 2 mg/Kg
• Maintenance: 1-1.5 mg/Kg
40. Central Nervous System
• Produces “ Dissociative anaesthesia”
• Causes Functional & Electrophysiological dissociation of Thalamocortical system (depressed) from Limbic
system (stimulated).
• This produces intense analgesia & amnesia as the sensory impulses from the body do not reach the cortex.
• Increases CBF which increases the Intracranial pressure.
• Also increases the intraocular pressure.
Cardiovascular System
• Causes hypertension & tachycardia: by indirect stimulation of sympathetic system causing release of
catecholamines.
• In larger doses or patients with depressed sympathetic system, can cause hypotension due to direct
myocardial depression
41. Respiratory system
• Good bronchodilator
• But does not obtund airway reflexes well.
GIT:
• Increases secretions salivary & bronchial secretions
42. Doses
• As a sole anesthetic for short procedures .
• Can be given as infusion:
@ 15-45 μg/Kg/min with 50% Nitrous oxide
@ 30-90 μg/Kg/minutes without Nitrous oxide
43. ADVERSE EFFECTS
• EMERGENCE REACTIONS: occurs due to ketamine induced depression of
auditory & visual relay nuclei, leading to misperception or misinterpretation
of auditory & visual stimuli.
• Muscle rigidity due to increased muscle tone.
• Hypertension & Tachycardia
44. PROPOFOL VERSUS KETAMINE
• Propofol causes transient decrease in arterial blood pressure
• Propofol causes less respiratory depression.
• Time for recovery is less for propofol is less than ketamine
• Recovery agitation is less in propofol
46. MIDAZOLAM
• Water soluble Benzodiazepine with an IMIDAZOLE ring in its structure
• The solubility of midazolam is pH dependent
@ pH: 3.5, Imidazole ring is open: Water soluble
@ body pH, Imidazole ring is closed: Lipid soluble
MECHANISM OF ACTION
Activates chloride channels of GABA inhibitory synaptic transmission
Duration of action: 1 hour when given IV
47. Central Nervous System
Dose dependent depression of the CNS
Cardiovascular System
Doesn’t affect Heart rate and Blood pressure
Respiratory System
Does not produce change in respiration at usual doses
48. Doses
• Induction: 0.1 – 0.2 mg/kg IV
• Premedication: Given 0.5 mg/kg orally up to maximum dose of 10 mg
Uses
• Used to supplement regional anesthesia for sedation
• Used as anticonvulsant
• Used for sedating critically ill patients as it is cardio-stable
Adverse Effects
• In patients with hypovolemia, it may aggravate hypotension
50. FENTANYL
• It is a highly lipophilic, short acting potent opiod analgesic.
• Frequently used to supplement anesthetics in balanced anesthesia.
• It is combined with Benzodiazepines
• Induction: 2-4 µg/kg
51. Cardiovascular system
• Heart rate decreases because fentanyl stimulates the vagus nerve.
• Fall of blood pressure.
Respiratory System
• Respiratory depression is marked.
Muscles
• Masseter & chest muscles become rigid. ( a muscle relaxant is needed)
52. ADVERSE EFFECTS
• Cerebral flow and Oxygen consumption decreases.
• Nausea, vomiting and itching
• Respiratory depression
54. DEXMEDETOMIDINE
• Developed in the 1980s
• Acts on alpha 2 adrenergic receptors.
• Dose: 0.2 to 0.7ug/kg/hr
• Duration of action: 6 minutes
• Elimination: 2 hours
• Protein binding capacity: 94%
55. Central Nervous System
• It reduces the CBF
• Its effect on the ICP is not yet clear
Cardiovascular System
• Biphasic BP response: Hypertensive phase & subsequent Hypotension
Respiratory effects
• Does not depress respiration even at high doses
56. USES
• Locoregional analgesia
• Sedation in intensive care units
• Can be used for treatment of withdrawal from benzodiazipines, opiods,
alcohol, drugs, etc.
• Management of Tetanus
• Anti shivering agent
• Prevents alcohol induced neurodegeneration.
57. ADVERSE EFFECTS
• Hypotension
• Vomiting
• Bradycardia
• pleural effusion
• Atelectasis
• Hypocalcaemia
• Acidosis
• Long term use can result in sensitization
60. REFERENCES
• Essentials of medical Pharmacology, 7th Edition, KD Tripathi
• Miller’s Anesthesia, 8th Edition, Ronald D. Miller
Editor's Notes
Normally, the laryngeal & cardiovascular functions are not depressed.
In modern practice of balanced anesthesia, these modalities are achieved by using a combination
of inhaled & IV anesthetics.
None of the available agents at present meet all these requirements
First order kinetics: constant faction of drug is eliminated per unit time i.e. dependent on plasma concentration.
Zero order kinetics: Occurs when metabolic pathways lead to accumulation of active drugs & delayed recovery.
Naloxone can be used to counteract persisting respiratory depression.