Barbiturates are a class of drugs that act as central nervous system depressants and were one of the first intravenous anesthetic agents used clinically, with thiopental and methohexital being two examples that are ultra short-acting and can be used for anesthetic induction. Barbiturates work by enhancing the effects of the inhibitory neurotransmitter GABA in the brain and have a variety of clinical uses but also potential adverse effects like respiratory depression if overdosed.
An overview of muscarinic receptor agonists and antagonists. This presentation was delivered to 2nd year pharmacy students enrolled in a pharmacology & toxicology class and accompanies Goodman & Gilman's (12e) chapter 9.
It is a anti- hypertensive drug. It is non-selective beta blocker drug. Hence it is beta blocker drug so it has many side effect.Not only Propranolol but also Timolol,Atenolol are beta blocker drugs.
cholinergic receptors definetion and classifcation to 1-nicotinic and 2-muscarinic ...and their subtybes ..... then the sites and the mechanism ... and last the drugs effect
An overview of muscarinic receptor agonists and antagonists. This presentation was delivered to 2nd year pharmacy students enrolled in a pharmacology & toxicology class and accompanies Goodman & Gilman's (12e) chapter 9.
It is a anti- hypertensive drug. It is non-selective beta blocker drug. Hence it is beta blocker drug so it has many side effect.Not only Propranolol but also Timolol,Atenolol are beta blocker drugs.
cholinergic receptors definetion and classifcation to 1-nicotinic and 2-muscarinic ...and their subtybes ..... then the sites and the mechanism ... and last the drugs effect
Everything you need to know about Local Anesthetics. Dose, mechanism of action, toxicity, management. How to use, where to use. It also contains receptors which are involved. Which factors prolongs and makes the drug work quicker.
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.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
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Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
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).
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
2. INTRODUCTION
IV Anesthetic induction agent
1st IV anesthetic agent used in clinical practice
Deriatives of barbituric acids(2,4,6-
trioxohexahydropyrimidine)
Water soluble salts, alkaline in nature
Can be used as hypnotics, sedatives, anticonvulsants
and anesthetics
Depressant for all excitable cells,CNS most sensitive
Three clinically important drugs in anesthesia
thiopentone, thiamylal and methohexitone
3. HISTORY
First created in 1864 by a German scientist named
Adolf von Baeyer. It was a combination of urea from
animals and malonic acid from apples.
used to put dogs to sleep
Also popular and abused in pop culture because of
their alcohol like effects
Introduced clinically by Water and Lundy in 1934
Interesting facts:-
• Caused the death of many celebrities such as Jimi
Hendrix and Marilyn Monroe
• Used by the Nazis during WWII for euthanasia
4. CLASSIFICATION
A.Ultrashort acting:- C.Intermediate acting:-
(acts within seconds and (effects last 3-5hrs)
duration of action -Amobarbitone
30min)
-Methohexital -Butabarbitone
sodium
-Thiamylal sodium
-Thiopental D.Long acting:-(effects
sodium lasts 6hrs)
B.Short acting:-(acts -Phenobarbitone
within minutes and -mephobarbitone
duration of action 2hrs)
#only ultra short acting are
-Hexobarbitone useful as anesthetic agent
6. STRUCTURE ACTIVITY
RELATIONSHIP
Keto-enol tautomerization(enol form active and allow
solubility)
Either oxygen or sulphur at position 2
Sulphur at position 2 produces more lipid
solublity,rapid onset,greater hypnotic potency but
shorter duration of action eg;thiopentone
Phenyl group at position 5 produces anticonvulsant
property eg;phenobarbitone
Increase in length of side chain atC5 increases
hypnotic potency eg;pentobarbital
Addition of methyl group at C1 produces rapid onset
of action, but excitatory side effects eg;methohexital
7. PHYSICOCHEMICAL
PROPERTIES
Prepared commercially as sodium salts readily
soluble in water or saline
Decrease in alkalinity of solution precipitation
Incompatible for mixture with acidic solution
-ringer lactate
-drugs pancuronium, vecuronium, atracurium,
alfentanil, sufentanil and midazolam.
Bacteriostatic property due to alkaline pH
Mixed with 6%anhydrous sodium carbonate to
prevent precipitation of insoluble acid form of
barbiturate by atmospheric CO2.
Sulphur is hygroscopis so,Vaccum is created in vial
with removal of oxygen
9. MECHANISM OF ACTION
Preferentially affect the function of nerve synapses rather
than axons
1.Enhance action of inhibitory neurotransmitters
2.Suppress action of excitatory neurotransmitters
Interact with GABAA receptors → Decrease rate of
dissociation of GABA → Increase duration of GABA activated
opening of Chloride channels → depresses RAS → decrease
wakefulness
Interferes with transmitter release (presynaptic) and
stereoselectively interacting with receptors (postsynaptic)
Barbiturates also targets other receptors – Adenosine
recptors and n Ach receptors
10. GABA creates a negative change in the
transmembrane potential(hyperpolarization).
This makes it an Inhibitory neurotransmitter
GABA binding site
Barbiturate binding site
11. At low conc.-GABA-facilitator
At high conc.- GABA-mimetic(barbiturate
anesthesia)
Block AMPA receptor which is sensitive to
glutamate,excitatory neurotransmitter
12. PHAMACOKINETICS
Absorption
Protien binding
Distribution
Ionization
Metabolism
Renal excretion
USUAL DOSE-First order kinetics
HIGH DOSE-Zero order kinetics
13. PROTEIN BINDING
Depends on lipid solubility
Thiopentone is highly lipid soluble barbiturate
Most avidly PP BOUND
Decreased protein binding in uremia &cirrhosis of liver
In cirrhosis of liver due to hypoalbuminemia PP binding
decreases but clearance rate not altered because
adequate protein present still at advanced stage
In neonate pp binding half of adult -reason for
increased sensitivity to thiopentone. In stressful
delivery (fetal acidosis ) unbound fraction further
increases.
14. DISTRIBUTION
FACTORS AFFECTING
PP binding:Low PP binding more free form
Lipid solubility:High lipid solubility readily crooss BBB
Degree of ionization:Low ionization readily cross BBB
Dose and Rate of administration
Tissue blood flow:in hypovolemia exaggerated cerebral
and cardiac depression
Volume of disribution-larger in females and pregnancy
-smaller in elderly and hypovolemia
15. Compartment model
Induction dose
rapid mixing of drug with central blood volume
quick distribution to highly perfused,low voume tissues(i.e.,brain)in 30sec
slower redistribution of drug to lean tissue(muscle)
termination of effect of induction dose(rapid recovery)in 5-10 mins
Continuous infusion
slower process of uptake into adipose tissue after 30sec
elimination clearance through hepatic metabolism
delay of recovery
16. IONIZATION
Thiopentone has pk 7.6 that is near blood ph
Acidosis thus favour non ionised drugs
Acidosis increase the intensity of barbiturate
effect
More effected by metabolism induced
alteration in pH
17. METABOLISM
A.Thiobarbiturate –Hepatic & Extrahepatic(kidney and CNS)
B.Oxybarbiturates-Hepatic
BIOTRANSFORMATION
1.Oxidation of alkyl,aryl, or phenyl moiety at C5(most imp)
2.N-dealkylation
3.Desulfuration of thiobarbiturate at C2
4.Destruction of barbituric acid ring
Metabolites-polar alcohols,ketones,phenols,carboxylic acids
-inactive,water soluble and readily excreted in urine
-glucuronide conjugation in bile
Drugs that induce oxidative microsome enhance metabolism
Long term administration induce enzymes
18. EXCRETION:-
Renal excretion is limited to water-soluble end products
of hepatic biotransformation
<1% of administered thiopental or methohexital is
excreted unchanged in the urine
Renal excretion is important in the elimination of
phenobarbital only
Alkalinization of urine with bicarbonate enhance renal
excretion of phenobarbital
19. COMPARATIVE PHARMACOKINETICS
Thiopentone Methohexitol
Rapid COMPARATIVE
distribution 8.5 5.6
T½(min)
PHARMACOKINETIC
Slow distribution 62.7 58.3
T½(min.)
I
T½ Elimination (Hrs.) 11.6 3.9
CL (ml/kg/min.) 3.4 10.9
Vd(L/kg) 2.5 2.2
Distribution t½ , protein binding &Vd of both drug is similar
Elimination T½ & Cl differ
20. Earlier awakening In pediatric due to rapid
total clearance
Delayed awakening in elderly due to
increased CNS sensitivity,altered metabolism
and decreased Vd
IMP. Points about PK of methohexitol
Lesser lipid soluble
More metabolized
Rapid hepatic clearance &
recovery rapid than thiopentone
21. CLINICAL CONSIDERATIONS
Prompt awakening in 5-10min after a single dose of
thiopental or methohexital reflects redistribution of
these drugs from brain to inactive tissues
Elimination from the body depends almost entirely on
metabolism So abnormal skills for 8hrs and residual
CNS impairment for about 1 day
22. EFFECTS ON ORGAN SYSTEMS
Cerebral metabolism:
Decreases CBF and ICP but CPP preserved
CMRO2 and ATP consumption decreased
Metabolic activity concerned with neuronal signaling
and impulse traffic reduced by barbiturates but not
metabolic function
CNS:
progressive cns depression
EEG changes-Low-voltage fast activity- small dose
-High-voltage slow activity- large dose
Potent hypnotic and anticonvulsant
poor analgesic(at low dose antianalgesic- threshold)
23. Cardiovascular:
-CV depression by both central and peripheral effects
-Peripheral vasodilation and fall in BP
-Decreased myocardial contractility and CO
-increase in HR(baroreceptor mediated sympth reflex)
-CV effects vary markedly depending on volume status,
baseline autonomic tone and preexisting CV ds
Respiratory:
Depression of medullary and pontine ventilatory centres
Decreased response to hypercapnia and hypoxia
Leads to upper airway obstruction and double apnea
Laryngeal reflex and cough reflex are not depressed
Laryngospasm and bronchospasm
24. Hepatic:
Hepatic blood flow is modestly decreased
Induction doses do not alter postoperative LFTs
Enzyme induction
Renal:
Reduce RBF and GFR in proportion to fall in BP
Liberation of ADH and decrease urine output
Skeletal muscle
-Tone is reduced at high dose
-When used as sole anesth agent poor muscle relaxation
Eye
-IOP reduced approx. 40%
25. Immunologic:
Thiopentone inhibit nuclear transcription factor κB
Impair neutrophil function
Anaphylactic and anaphylactoid reactions are rare
Some evoke mast cell histamine release
Uterus:
contractions suppressed at high dose
Placenta:
Maternal doses of thiopental up to 4 mg/Kg IV
probably do not result in excessive concentrations
of barbiturates in fetal brain
Other:
Antithyroid(d/t thio-urea group) and Hypokalemia
26. CLINICAL INDICATIONS
1. Principal clinical uses of barbiturates:
Induction and maintenance of anesthesia
Treatment of increased intracranial pressure
1. Preanesthetic medication (replaced by BZDs)
2. Status epilepticus and treatment of grand mal seizures,
but benzodiazepines are probably superior
3. Cardioversion
4. ECT
5. Narcoanalysis,Narcotherapy or truth spells
6. Cerebroprotective agent in trauma patients and focal
cerebral ischemia
7. T/t of hyperbilirubinemia & kernicterus
28. 6. Severely anemic and Acidotic patients
7.Jaundice, severe hepatic or renal disease
8. Previous hypersensitivity reactions
9.Dystrophia myotonica, FPP
10.Hypothyroid and myxoedema pt.
11.Without proper iv or airway equipment
12.H/o convulsion for methohexitol
29. ADVERSE EFFECTS
A.COMPLICATIONS
1.On injection-garlic or onion taste
2.Perivenous and Intramuscular injections-Local tissue
irritation tissue necrosis ulceration(more with thiopentone)
mechanism-crystal precipitation in alkaline pH
t/t-10ml of 1%lignocaine with 100unit of hyalase inj
3.Pain on injection and phlebitis (more with methohexital)
4.Allergic rkn-Urticarial rash on head,neck and trunk,lasts a
few mins;sometime severe reactions- facial edema, hives,
bronchospasm and anaphylaxis (T/t- symptomatic,
epinephrine and fluid replacement)
5.Excitatory symptoms-cough,hiccough,tremors,twitching
(5times more with methohexital)
30. 6. Intraarterial Inj.-Degree of injury related to conc. of drug
s/s: pt.complains of intense burning pain down to the inj
site followed by pallor,cyanosis,edema and finally necrosis
1st symptom-pain
1st sign-white hand with cyanosis of nail
Mechanism-release norad locally so vasoconstriction
-pptation in arterial pH→crystal formation →embolization in
arteriole→occlusion → Ischemia → gangrene
-inflammation and endothelial cell destruction
Prev:-give inj at dorsum of hand in adult;scalp vein in infants
-avoid inj at antecubital fossa
-always use 2.5%soln.
31. T/t :-1.Leave the needle at site;dilution of drug by saline
4p’s-2. 5-10ml of plain xylocaine1%(old drug-procaine)
-3.Papaverine 40-80mg in 10-20ml saline for
vasodilatation
-4.Tolazoline(priscol)5ml- alpha blocking agent or
phenoxybenzamine 0.5mg-ganglion blocking agent
-5.Inject 500units of heparin to prevent thrombosis
-6.Sympathectomy by stellate ganglion block or brachial
plexus block relieve vasoconstriction and pain
-7.Urokinase to improve blood flow
-8.Oral anticoagulants for 7-10 days
-9.Elective surgery cancelled only emergency Sx done
32. B.SYSTEMIC ADVERSE EFFECTS
1.CVS -mild decrease SBP d/t vasodilation
-profound hypotension d/t nonimmunologically
mediated histamine release
m/m-Consider slow rate of injection and adequate
preoperative hydration
2.RESP-Transient apnea(t/t:no m/m but if >20sec IPPV)
-Laryngospasm & Bronchospasm
3.CNS –continuous infusion of thiopentone 4mgkg causes
Isoelectric EEG
4.KIDNEY –Decrease in urine output
33. 5.LIVER- Enzyme induction so
a.accelerate metabolism of drug e.g;oral anticoagulants,
phenytoin and TCAs
b.accelerate metabolism of endogenous substances as,
corticosteroids, bile salts and vit.k
c.stimulate ALA synthatase and exacerbate porphyria
d. tolerance by inducing own metabolism
6.TOLERANCE AND PHYSICAL DEPENDENCE
7.IMMUNOSUPPRESION-
-increased incidence of nosocomial infection
-bone marrow suppression and leucopenia
34. RECOMMENDED DOSES
DRUG INDUCTION ONSET(sec) IV
DOSE(mg/kg) MAINTENANCE
INFUSION
THIOPENTAL 3-4 10-30 50-100mg every
(2.5%) 10-12 min
METHOHEXITAL 1-1.5 10-30 20-40mg every 4-
(1%) 7 min
Adult and pediatric dose are roughly same
Methohexital can be given rectally in pediatric patients
as 20-25 mg/kg/dose
Thiopentone in 5% or 10% solution may be used in
children basal narcosis
35. PREPARATIONS
0.5gm is diluted with 20cc of distilled water to
make 2.5% concentration
1gm preparation is also available
37. INCREASED DOSE REQUIREMENT
A.urbans people
B. chronic alcoholics
C. Children >1yr after thermal injury
38. MEDICATION INTERACTIONS
Contrast media, sulfonamides,
aspirin,coumarin anticoagulants and other
drugs that occupy the same protein-binding
sites as thiopental will increase the amount of
free drug available
Alcohol, narcotics, antihistamines, and other
CNS depressants potentiate the sedative
effects of barbiturates
Chronic alcohol abuse
39. COMPARISON
THIOPENTONE PROPOFOL
A.PROPERTIES
1.Ultra short acting barbiturate 1.Short acting propyl phenol
2.Available as yellow powder 2.Available as white emulsion
3.Soluble in water 3.Insoluble in water
4.Stable,sterile at r.t. 6days 4.Discard in 6hrs
5.Bacteriostatic 5.Good bacterial culture
6 pH=10.5 6 pH=7
7.2.5%soln 7.1%soln
8.Contain Na2CO3 8.Contain Na edatate/metabisulphite
B.PHARMACOKINETIC
OA:15sec OA:15sec
DOA:8-10min DOA:2-8min
Elimination:10hr Elimination:3-4hrs
Recovery:delayed Recovery:rapid and smooth
40. THIOPENTONE PROPOFOL
C.ACTIONS
1.Sedation,hypnosis,antianalgesia 1.hypnosis, amnesia,noanalgesia
2.CNS:Maintain CPP 2.CNS:Decrease CPP
3.CVS:BP both central and peripheral 3.CVS:BP only peripheral
4.Resp:bronchospasm/laryngospasm 4.Resp:bronchodilation,apnea
5.GIT: risk of aspiration 5.GIT: vomiting
6.Pregnancy:safe upto 4mg/kg 6.preg:neonatal depression
7.Muscle:localise spasm 7.Muscle:no effect
8.Antioxidant:no 8.Antioxidant effect
9.Stress response:no effect 9.Stress response:block
D.SIDE EFFECT
1.More hangover 1.Less
2. More vascular compromise 2.Less
3.Tissue necrosis 3.No tissue necrosis