This document provides information about conscious sedation including:
- Definitions of conscious sedation and levels of sedation from light to general anesthesia.
- Guidelines for patient selection, monitoring, equipment, medications and discharge criteria for conscious sedation.
- Risks and complications of conscious sedation like respiratory depression and how to minimize risks through careful medication selection and titration by an anesthesiologist.
- Common sedatives and analgesics used for conscious sedation like midazolam, propofol, ketamine and considerations for each.
INTRODUCTION
What is Conscious Sedation
Objectives of Conscious sedation
Indications
Routes used for conscious sedation
Drugs used for conscious sedation
Monitoring
Nitrous Oxide and phases of its administration
Fasting Guidelines
Contraindications
Adverse Effects
INTRODUCTION
What is Conscious Sedation
Objectives of Conscious sedation
Indications
Routes used for conscious sedation
Drugs used for conscious sedation
Monitoring
Nitrous Oxide and phases of its administration
Fasting Guidelines
Contraindications
Adverse Effects
Preoperative sedation and premedication in pediatrics Nida fatima
Sedation and premedication
Why? --Aims of premedication!
When?
How?
Drugs for premedication!
Routes for administration!
Side effects & complications!
Parental Anxiety
SEPARATION ANXIETY
Kids not small adults
Sedative -omitted for neonates and sick infants.
child's age, body weight, drug history, allergic status and medical or surgical conditions
Avoid needles!!
Oral premedication ≠ risk of aspiration pneumonia
Allay Anxiety & fear.
Reduce saliva and airway secretions.
Enhance the hypnotic effects of general anaesthesia.
Reduce postoperative nausea & vomiting.
Prof. Mridul M. Panditrao has added another of his very important, useful and in vogue topic to his collection. This is his well acclaimed andwell received faculty lecture at recently concluded International conference on Pain... ISSPCON 2014, at Mumbai/ Bombay from 6th to 9th Feb. 2014.
Preoperative sedation and premedication in pediatrics Nida fatima
Sedation and premedication
Why? --Aims of premedication!
When?
How?
Drugs for premedication!
Routes for administration!
Side effects & complications!
Parental Anxiety
SEPARATION ANXIETY
Kids not small adults
Sedative -omitted for neonates and sick infants.
child's age, body weight, drug history, allergic status and medical or surgical conditions
Avoid needles!!
Oral premedication ≠ risk of aspiration pneumonia
Allay Anxiety & fear.
Reduce saliva and airway secretions.
Enhance the hypnotic effects of general anaesthesia.
Reduce postoperative nausea & vomiting.
Prof. Mridul M. Panditrao has added another of his very important, useful and in vogue topic to his collection. This is his well acclaimed andwell received faculty lecture at recently concluded International conference on Pain... ISSPCON 2014, at Mumbai/ Bombay from 6th to 9th Feb. 2014.
The practice of anesthesia and sedation continues to expand beyond the operating room and now includes the gastroenterology suite, magnetic resonance imaging suites, and the cardiac catheterization laboratory. Non-anesthesiologists frequently administer sedation, in part because of a lack of available anesthesiologists and economic aspect, which emphasizes the safety of sedation. The Joint Commission International (JCI) set a standard responding to this issue indicating that qualified individuals who have drug and monitoring knowledge as well as airway management skills can only administer sedating agents.
This slides contains all you need to know about "Status Epilepticus" in a nutshell. It includes definition, investigation, emergency management of status epilepticus. This educational material is suitable for med students, paramedics, nurses & neurology residents.
Status epilepticus (SE) is a medical emergency that starts when a seizure hits the 5-minute mark (or if there’s more than one seizure within 5 minutes).
Convulsive Status epilepticus-
The convulsive type is more common and more dangerous.
It involves tonic- clonic seizures (grand mal seizures)
In the tonic phase ( lasts less than 1 minute), body becomes stiff and person lose consciousness. Eyes roll back into head, muscles contract, back arches, and trouble breathing.
As the clonic phase starts, body spasms and jerks occur. Neck and limbs flex and relax rapidly but slow down over a few minutes.
Once the clonic phase ends, patient might stay unconscious for a few more minutes. This is the postictal period.Non-convulsive Status epilepticus-
Patient lose consciousness but is in an “epileptic twilight” state.
There might not able any shaking or seizing at all, so it can be very hard for someone observing patient to figure out what’s happening.
A non-convulsive seizure can turn into a convulsive episode.
Poorly controlled epilepsy
Low blood sugar
Stroke
Kidney failure
Liver failure
Encephalitis
HIV
Alcohol or drug abuse
Genetic diseases such as Fragile X syndrome and Angelman syndrome
Head injuries
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stock
Telegram: bmksupplier
signal: +85264872720
threema: TUD4A6YC
You can contact me on Telegram or Threema
Communicate promptly and reply
Free of customs clearance, Double Clearance 100% pass delivery to USA, Canada, Spain, Germany, Netherland, Poland, Italy, Sweden, UK, Czech Republic, Australia, Mexico, Russia, Ukraine, Kazakhstan.Door to door service
Hot Selling Organic intermediates
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
1. What we need to know about
Conscious Sedation
BY
Rizk Elazhary
MD, Anesthesiology
Benha University
2. Introduction and definition
Conscious Sedation: A drug induced depression of the patient’s
level of consciousness such that the patient responds appropriately to
physical and verbal commands and maintains airway protective
reflexes, that is intended to facilitate the successful performance of
the diagnostic or therapeutic procedure while providing patient
comfort and cooperation.
3. Purpose of the lecture
Dissemination of medical knowledge
Fulfill requirements for conscious sedation understanding
and privileges
Differentiate conscious sedation from light sedation, deep
sedation and general anesthesia.
Describe the desired outcomes of conscious sedation.
4. Purpose of the lecture (continue)
Record the normal dosage, rate of administration, onset
and duration of action and adverse effects of specific
pharmacologic agents used in conscious sedation.
Describe the correct technique for administering reversal
agents.
Identify potential complications related to conscious
sedation
5. Target Audience
Attending staff who wish to be credited in
conscious sedation.
Anyone who cares conscious sedation also
requires current ACLS certification.
6. Indications
Any procedure where the patient will be
unable to cooperate, and that procedure may
cause the patient significant pain
7. Clinical Areas Administering Sedation
OR and ICU : for GIT endoscopies & ECT.
Emergency Room.
Delivery Room.
Radiology Department.
Uro-surgery, ESWEL unite.
Others: Orthopedic , Cardio-Thoracic
8. Levels of Sedation
Light Sedation
The administration of
medication in dosages
causing the sedation and
allowing the patient to
sleep and rest.
Moderate Sedation
A medically controlled
state of depressed
consciousness that allows
the patient to
independently maintain a
patent airway and respond
to verbal stimuli.
Deep Sedation
A medically controlled state
of depressed consciousness
from which the patient is not
easily aroused, is unable to
maintain a patent airway
independently, and is unable
to respond purposefully to
physical stimulation or verbal
command.
General Anesthesia
A medically controlled state
of unconsciousness which
includes loss of protective
reflexes and inability to
respond to stimuli.
9. Goals of Sedation
To titrate the medication such that the
smallest amount of medication is administered
to achieve the desired depression of
consciousness while minimizing the potential
complications.
Desired Effects:
Depressed consciousness
Amnesia
Maintaining the patient vital signs
10. Eligible Patients
Patients with the following indications
Stable vital signs
NPO
No medical contraindications to the medications that
will be given
ASA 1 & ASA 2
Malampati I or II
11. Fasting Recommendations
Ingested Material minimum fasting hours
Clear Liquids 2 h
Breast milk 4 h
Infant formula 6 h
Non-human milk 6 h
Light meal 6 h
Heavy meal ≥ 8 h
14. Classifications (continued)
ASA 3 --- Severe systemic disease that results
in functional limitation (e.g. poorly controlled
hypertension, diabetes mellitus with vascular
complications, angina pectoris, prior
myocardial infarction, pulmonary disease that
limits activity.
ASA 4 --- Severe systemic disease that is a
constant threat to life (e.g. congestive heart
failure, unstable angina pectoris, renal or
hepatic dysfunction)
15. Classifications (continued)
ASA 5 --- Moribund patient not expected to
survive without the operation (e.g. ruptured
abdominal aneurysm, pulmonary embolism, head
injury with increased intracranial pressure)
ASA 6 --- A declared dead patient whose organs
are being removed for donation.
16. Mallampati Classification
Class 1: Full visibility of tonsils, uvula and soft palate
Class 2: Visibility of hard and soft palate, upper portion of tonsils and
uvula
Class 3: Soft and hard palate and base of the uvula are visible
Class 4: Only hard palate is visible
The Mallampati classification is
used to predict the ease of
intubation.
A high Mallampati score (class 3 or
4) is associated with more difficult
intubation as well as a higher
incidence of sleep apnea.
17. “At Risk” Patients for Sedation or Analgesia
The ASA physical status risk classification of 3 or greater
Critical care patients
Extremes in age (<1 or >70 years of age)
Patients with chronic respiratory disease, chronic
obstructive pulmonary disease, emphysema
History of sleep apnea
Mentally and neurologically handicapped patients
Patients at risk for aspiration (i.e. hiatal hernia with
regurgitation, diabetes with gastroparesis
Altered mental status
18. Technique of conscious sedation
The procedure begins once oxygen is given via nasal
cannula, the intravenous (IV) access established,
skin sensitivity test for local anesthetic done,
cardiopulmonary and other required monitors
connected.
23. Monitoring of Patients
Personnel
*Nurse or *physician other than the physician
performing the procedure
Team member able to establish an airway, provide
positive pressure ventilation (Ambu bag)
Mechanism for additional personnel with Advanced
Life Support capability
*ACLS required for physicians and nurses
24. Monitoring of Patients (continued)
Record:
Blood pressure
ECG
Pulse oximetry
Respiratory rate & depth of respiration
Supplemental oxygen throughout procedure
Level of consciousness—ask simple questions
Medications – dose & times
25. Monitoring of Patients (continued)
Record
Supplemental oxygen throughout procedure
Level of consciousness—ask simple questions
Medications – dose & times
26. Ramsey Sedation Scale
Level of Sedation Clinical Description
1 – Anxious, bordering
2 – Cooperative, oriented, tranquil
3 – Responds only to verbal commands
4 – Asleep with brisk response to light stimulation or
physical stimuli
5 – Asleep with sluggish response to stimulation
6 – Asleep with no response to stimulation
**Levels 2, 3 and 4 are desired range of levels during moderate sedation
34. Narcotic Analgesics
Morphine Meperidine Fentanyl
Initial Dosage 5-10 mg IV 0.5-1 mg/kg 0.51.5 mcg/kg
Incremental
Dosage
0.02-0.1 mg/kg/5-10
minute intervals
0.5 mg/kg/5
minute intervals
0.50 mcg per dose at
2-3 minute intervals
Pediatric
Dosage
0.1 mg/kg oral
0.03 -0.05 mg/kg IV
0.5-1 mg/kg 1 mcg/kg followed by
0.25-1.5 mcg/kg at
2-3 minute intervals
Onset 2-5 minutes 1-5 minutes 1-2 minutes
35. Narcotic Analgesics (continued)
Morphine Meperidine Fentanyl
Duration 2-6 hrs 2 hrs 20-30 minutes
Side Effects ↓ HR / ↑BP
Respiratory
depression
↓ HR / ↓ BP
Respiratory
depression
↓ BP
Respiratory
depression
Anaphylaxis
Muscular rigidity
Contraindications &
Comments
Head injury Head injury Use with caution in
patients with reactive
airway disease
Reversal Agents Naloxone 0.4 mg IV Naloxone 0.4 mg IV Naloxone 0.4 mg IV
36. Midazolam
A short-acting, water-soluble benzodiazepine,
an ideal agent for its amnestic and anxiolytic
properties.
Midazolam, with a half-life of 2 hours, has limited
cardiovascular effects, allows for quick recovery and
has no postoperative sequelae such as nausea and
vomiting.
Dose: 0.05 mg/kg bolus IV.
37. Propofol
A rapidly-acting sedative and hypnotic agent having a
quick recovery property.
Can be used in bolus and infusion dose along with
local anesthetic injection.
Slow administration maintains hemodynamics.
Does not cause postoperative nausea or vomiting .
May cause postoperative shivering.
Dose: Bolus - 0.5-1 mg/kg; infusion - 25 µg/kg/min
38. Ketamine
Agent of choice as an analgesic in conscious sedation.
Produces dissociated anesthesia.
Psychotic reactions such as hallucination, serious
cardiovascular adverse effects, seizures and
postoperative shivering have been reported.
Dose: 2 mg/kg IV or 6-10 mg/kg IM.
39. Dexmedetomidine
Has both sedative and analgesic properties.
Does not cause respiratory depression, though
hemodynamic parameters need to be closely
monitored.
Has a high incidence of postoperative dry mouth.
Dose: 1 μg/kg IV.
40. The disadvantages of conscious sedation
Mainly are the lack of airway control and the risk of
airway obstruction or aspiration.
Thus to minimize the disadvantage, the medication
should be selected and titrated by the
anesthesiologist
41. Discharge Criteria
Patient awake and alert to pre-sedation levels
Stable vital signs
Aldrete Score equal to or greater than 8 or equal to
baseline
Patient able to walk unassisted
Discharge to a responsible adult
42. Points to Remember
When appropriately administered, moderate sedation
should make the patient’s procedures tolerable to
pain and reduce anxiety.
Moderate sedation is the responsibility of the
anesthesiologist.
Give drugs “slowly”.
Let “routine” be your friend.
44. Conscious sedation in pregnancy
Consider the physiological changes in pregnancy.
Propofol is taken as a safe agent.
The American College of Obstetricians and
Gynecologists (ACOG) has recommended that
intermittent or continuous fetal monitoring during
conscious sedation is a more sensitive and important
indicator of placental perfusion and fetal oxygenation
than observations of maternal hemodynamic stability.
45. References
• Longnecker DE, Tinker JH, Morgan Jr., GE.
• Principles and Practice of Anesthesiology 1998; Vol. 1:(12) 227-228 and Vol. 2:
(86) 2268.
• Mallampati S, Gatt S, Gugino L, Desai S, Waraksa B, Freiberger D, Liu P
(1985).
• “A clinical sign to predict difficult tracheal intubation; a prospective study”.
• Can Anaesth Soc J 32 (4): 429-34.
• Nuckton TJ, Gledden DV, Browner WS, Claman DM (Jul 1, 2006).
• “Physical examination: Mallampati score as an independent predictor of
obstructive sleep apnea”. Sleep 29 (7); 903-8.
• http://sedationconsulting.blogspot.com/2008/09/guidelines-for-conscious-moder
• JAYASHREE SEN*, BITAN SEN: “Conscious Sedation: An Observation”,
Indian Journal of Clinical Practice, Vol. 24, No. 10, March 2014