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.

2. General Anesthesia and
its Complications

3. Contents
• Introduction
• Mechanism of GA
• Stages of anaesthesia
• Properties of ideal GA
• Classification
• Inhalation Anaesthetics
• Intravenous Anaesthetics
• Slower acting drugs
• Conscious sedation
• Complications of GA
• Preanaesthetic medications
• Reversal Agents
• Conclusion
• References

4. Introduction
• General Anaesthesia refers to the reversible loss of all sensation and
consciousness
• This is achieved by a combination of inhaled and IV drugs
• Early use of general anaesthesia dates back to 1844 – use of nitrous oxide by
Horace Wells
• Modern era of GA began in 1956 with the discovery of Halothane

5. Cardinal Features
• Loss of all sensation
• Sleep(unconsciousness) and amnesia
• Immobility and muscle relaxation
• Abolition of somatic and autonomic reflexes

6. Mechanism of GA
• The exact mechanism of GA is not precisely known
• Minimal Alveolar Concentration (MAC) is the factor used to estimate the potency
of inhalation Gas
• MAC refers to the lowest concentration of the anaesthetic in pulmonary alveoli
needed to produce immobility in response to a painful stimulus in 50% individuals

7. Mechanism of GA (contd.)
• Recent studies have revealed the various centres that Gas act upon which
produce the desired results –
Unconsciousness – Thalamus or the reticular activating system
Amnesia – Hippocampus
Immobility – Spinal Cord

8. Mechanism of GA (contd.)
Ligand Gated
Ion Channels
• Most important – GABAA receptor gated Cl- channel
• Barbiturates, Benzodiazepines, many inhalation anaesthetics
NMDA type
of glutamate
receptor
• Gates CA2+ selective cation channels in neurones
• Ketamine and N2O

10. Stages of Anaesthesia
• Stage of analgesia
• Stage of delirium
• Surgical anaesthesia
• Medullary paralysis

11. Surgical anaesthesia
• Plane 1 – roving eyeballs
• Plane 2 – loss of corneal and laryngeal reflexes
• Plane 3 – pupil starts dilating and light reflex is lost
• Plane 4 – intercostal paralysis, shallow abdominal respiration, dilated pupil

13. Properties of an ideal anaesthetic
Pleasant, non-irritating, should
not cause nausea or vomitting
Adequate analgesia, immobility,
muscle relaxation, non
inflammable, non explosive
Administration should be easy,
controllable, versatile
Margin of safety should be wide
Rapid adjustments in depth of
anaesthesia

14. Classification
Inhalation
Gas
Nitrous Oxide
Volatile Liquids
Ether
Holathane
Sevoflurane
Intravenous
Inducing agents
Thiopentone sodium
Propofol
Slower acting drugs
Diazapam
Midazolam
Ketamine
Fentanyl

15. Inhalation
Anaesthetics

16. Techniques of inhalation
• Open drop method
• Anaesthetic Machines –
• Open system
• Closed system
• Semi closed system

17. Nitrous Oxide (N2O)
• Non irritating but low potency anaesthetic
• MAC = 105%
• Combination used – 70% N2O + 30% O2
• Poor muscle relaxant need for neuromuscular blockers

18. Nitrous Oxide (N2O)
• Onset and recovery are rapid due to poor blood solubility
• Second gas effect and diffusion hypoxia occur
• Elimination is same as entry pathway Alveoli of lungs

19. Second gas effect

20. Halothane
• Potent anaesthetic – 2-4% induction ; 0.5-1% maintenance
• Potentiates competitive neuromuscular blockers
• Direct depression of myocardial contractility by reducing intracellular Ca2+
concentration
• Cardiac output is reduced with deepening anaesthesia
• BP falls parallel to depth

21. Halothane
• Heart rate reduced by
• Vagal stimulation
• Direct stimulation of SA nodal automaticity
• Lack of baroreceptor activation
• Sensitizes the heart to arrhythmogenic action of adrenaline –tachyarrhythmia
• Pharyngeal and laryngeal reflexes are abolished along with suppression of
coughing preferred in asthmatics

22. Sevoflurane
• Fairly soluble in blood and tissues
• Induction and emergence from anaesthesia fast
• Rapid changes in depth can be achieved
• Recovery is smooth – orientation, cognitive and motor functions

23. Sevoflurane
• Does not cause sympathetic stimulation and airway irritation
• Approx. 3% of absorbed sevoflurane is metabolised but amount of fluorine
liberated is safe for kidney and liver
• High cost and need for high flow open system

24. Comparison between inhalation anaesthetics

25. Intravenous
Anaesthetics

26. Propofol
• Applied as an emulsion
• Onset of action – 15-45 seconds
• Duration of action – 5-10 minutes
• Elimination t1/2 – 100 minutes

27. Propofol
• Intermittent injection or continuous infusion
• No airway irritancy, residual impairment is very low
• Fall in BP due to vasodilation with less marked cardiac depression
• Pain during injection frequent and minimized by combining with lidocaine

28. Slower Acting
Drugs

29. Benzodiazepines
• Used as preanaesthetic medication as well as for conscious sedation
• Anaesthetic dose – 0.2-0.3 mg/kg IV cause unconsciousness in 5-10 mins
• Poor analgesics
• Usually given in conjunction with opioids
• Decrease muscle tone by CNS action but require neuromuscular blockers for
muscle relaxation of surgical grade

30. Benzodiazepines
• Preferred for endoscopies, cardiac catheterization, angiographies, conscious
sedation
• Reversed by Flumazenil – 0.5-2 mg IV

31. Benzodiazepines
• Diazepam – 0.2-0.5 mg/kg
• Lorazepam – 2-4 mg IV
• Midazolam – 1-2.5mg IV

32. Ketamine
• Dissociative Anaesthesia – profound analgesia, immobility, amnesia with light sleep,
feeling of dissociation from ones own body
• Primary site of action – cortex and subcortical areas
• Dose – 1.5 mg/kg IV or 5 mg/kg IM
• Recovery – 10-15 minutes ; Amnesic – 1-2 hours ; elimination t1/2 – 3-4 hours

33. Ketamine
• Respiration is not depressed, airway reflexes maintained, muscle tone
increases, limb movements may occur
• Heart rate, cardiac output and BP are elevated due to sympathetic stimulation
• Emergence delirium, hallucinations and involuntary movements occur in
50% patients during recovery
• Dangerous in hypertensives , ischaemic heart disease and patients with
increased intracranial pressure(increases cerebral blood flow)

34. Fentanyl
• Short acting opioid analgesic (30-50 min)
• Used frequently in balanced anaesthesia
• Allows use of lower anaesthetic concentrations with better haemodynamic stability
• Dose – 2-4 μg/kg

35. Fentanyl
• After application, patient remains drowsy but conscious
• Respiratory depression is marked but predictable
• Tone of chest muscle may increase with rapid injection
• Heart rate decreases due to vagal stimulation

36. Fentanyl
• Slight fall in BP, heart is not sensitized to adrenaline
• Supplemental doses needed after every 30 mins but recovery prolonged
• Naloxone is used to counteract persistent respiratory depression

37. Conscious Sedation
• It is a monitored state of altered consciousness that can be employed to
carry out diagnostic/short procedures in apprehensive patients or medically
compromised patients in place of general anaesthesia
• Drugs used –
 Diazepam – 1-2 mg IV (Midazolam – shorter acting alternative)
 Propofol
 Nitrous Oxide
 Fentanyl – 1-2 μg/kg IV every 15-30 min

38. Complications of general anaesthesia
During Anaesthesia
Respiratory depression and hypercarbia
Cardiac arrhythmias
Fall in BP
Acid pneumonitis
Laryngospasm and asphyxia
After Anaesthesia
Nausea and vomiting
Persistent sedation – impaired psychomotor
function
Pneumonia, atelectasis
Organ toxicities – liver, kidney
Emergence delirium

39. Preanaesthetic
medication

40. Sedative – Antianxiety drugs
• Benzodiazepines – Diazepam or Lorazepam (2mg iv)
• Smoothen induction
• Loss of recall of preoperative events
• Counteract CNS toxicity of LAs
• Promethazine (50 mg IM) – antihistaminic with sedative, antiemetic and
anticholinergic properties

41. Anticholinergics
• Atropine or hyoscine (0.6 mg IM/IV)
• Reduce salivary and bronchial secretions (before non irritant anaesthetics)
• Currently, prevent vagal bradycardia and hypotension and prophylaxis of
laryngospasm
• Not be used in febrile patients
• Glycopyrrolate (0.1-0.3 mg IM) – longer acting atropine substitute which has
potent antisecretory and antibradycardiac effect

42. H2 blockers
• Ranitidine (150mg) or Famotidine (20 mg) prevent gastric regurgitation and
aspiration pneumonia
• Raise pH of gastric juice and reduce its volume
• Alternative – proton pump inhibitor – omeprazole/pantoprazole

43. Antiemetics
• Metoclopramide – 10-20 mg IM
• Enhances gastric emptying and tone of lower oesophageal sphincter – reduces
effect of reflux and its aspiration
• Domperidone – better efficacy and lesser side effect
• Ondansetron (4-8 mg IV) – selective 5-HT3 blocker

44. Reversal
Agents

45. Flumazenil
reverses the effects of benzodiazepines
Naloxone
reverses the effects of opioids
Neostigmine
helps reverse the effects of non-depolarizing muscle relaxants
Sugammadex
new agent that is designed to bind Rocuronium therefore terminating its
action

46. Conclusion
• It is necessary to know about general anaesthetics for performing oral and
maxillofacial surgeries
• Knowledge regarding the correct dosage, route of administration and side
effects is vital while inside the operating theatre

47. References
• Essentials of Medical Pharmacology – K.D. Tripathi – 6th Edition
• Online sources