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TCI

Overview
by

ayush sinha

on 9 October 2014

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Transcript of TCI



Dr Ayush Sinha,
West Suffolk Hospital, BSE

TIVA/TCI: An overview
Outline
TIVA/TCI: Why
Drug delivery: As it happened
Drug delivery: As it happened
Basic pharmacokinetics
Pharmacokinetics of infusions and target controlled infusions
TCI: Why?
TCI: Advantages, applications, practical aspects
TCI: Accuracy, pitfalls, precautions
Global warming, work place pollution
Specific equipment, venilatory techniques, Compromised airway
Seal, bronchoscopy
Thoracic surgery
N & V, dysphoria, ICP, IOP
Autoregulation
MH
Manual controlled infusion: Not easy to control, time consuming calculations, no compensation for interrupted infusion, delayed emergence, require skill & experience



Single injection
Intermittent injection
Continuous iv drips
Syringe pumps- control rates
Drug delivery: As it happened
An infusion controlled in such a manner as to achieve a user defined drug concentration in a body compartment of interest required for a particular effect
Infusion to control the depth of anaesthesia by adjusting required target conc.
B.E.T. scheme
Context sensitive half time
Pharmacokinetic model
Mathematical model
Target
concentration
Bolus
Fill central
compartemnt
Bolus dose= CtxV1
Elimination
Compensate for metabolism & elimination
=CtxCL=CtxK10xV1
Transfer
Compensate for peripheral distribution
Decreasing infusion rate
=CtxV1(k12e(-k21t)+k13e(-k31t))
To achieve a target concentration
Context sensitive half time
TCI Propofol concentration
TCI: merits in practice
Common pitfalls
Propofol TCI: cautions, precautions
CP50 2.7-3.4 mcg/ml
loss of response to
verbal or tactile
stimuli
Cet 2-3mcg/ml
loss of eyelash reflex
Cet 4-8mcg/ml
Anaesthetic procedures
Intubation, LMA
Target conc based on
-level of stimulation
-drug interaction
-desired clinical end point
-individual variability
One lung ventilation- not inhibit
HPV

Open eye injury- decrease
IOP

Day surgery, Neuro exam- clear headed
recovery

Neurosurgery- decrease ICP, CBF


Laparoscopic Sx, Ophth, ENT, Hx of PONV- decrease emesis


No scavenging
Pharmacokinetic Models
Inadequate depth, delayed awakening-> Unfamiliarity, unsecured iv access, BIS

Awareness-> BIS

Movement-> Muscle relaxant, NM monitoring

Hypotension-> Hypovolemia
Less than 15 yr old
BW>150 kg
C/S
liver impairment
Not recommended for
Propofol related infusion syndrome
High dose infusion for >48hrs
Sudden onset bradycardia, met acidosis, lipemia
Rhabdomyolysis, renal failure
Fatty liver
Risk factor: sepsis, poor o2 delivery
Thank you
Ultimate goal
Dose

Blood concentration

Effect site concentration

Drug-receptor interaction


Clinical effect
Distribution
Metabolism
Excretion
Early pioneers
Kruger-Thiemer
: Continuous intravenous infusion and multicompartment accumulation. Eur J Pharm 1968; 4: 317-24

Vaughen Tucker
: General theory for rapidly establishing steady state drug concentrations using two consecutive constant rate intravenous infusions. Eur J Clin Pharmacol. 1975; 9: 235-8

General derivation of the ideal i.v drug input required to achieve and maintain a constant plasma drug concentration. Theoretical application to lignocaine therapy. Eur J Clin Pharmacol 1976; 10: 433-40
Diprifusor: First commercially available TCI system
Components of TCI
Delivery of steady state blood
concentrations
Early pioneers
Each model- no of comp
volume
rate of drug elimination
rate of transfer
Accuracy of TCI system
Conc displayed on user interface is only an estimate
Divergence
MDPE
MDAPE
Wobble
Divergence
Pharmacology
Pharmacokinetic/Pharmacodynamic variability
Dose
Response
Pk variability 25%
Pd variability 200%
Exponential decay
Concentration
Time
C(0) at time = 0
C(t)=C(0).e-kt
Value for C at any point in time, t, is an
exponential function of the starting value, C(0) at t = 0
Precautions
Dedicated cannula

One way valve

Withdraw residual drug, flush lines

Administration sets

No mixing of two drugs in one syringe

Drug concentration
Manual infusion regimens
TCI for novice
TCI opioids
Practical aspects
Quick attainment of SS blood conc....but....

Propofol-Roberts regime: 3 mcg/ml, analgesia, nitrous oxide. Bolus 1 mg/kg, 10 mg/kg/hr for 10 minutes, 8 mg/kg/hr for 10 minutes, 6 mg/kg/hr

Remifentanil

Ketamine
No fixed recepies!!

Start with spontaneously breathing, non-paralysed patients
Set the initial blood concentration higher than the likely therapeutic effect-site concentration


Procedural sedation: initially 0.5mcg/ml, small (0.1mcg/ml) increments or decrements. Manual regimen- 3mg/kg/hr, 10-20 mg bolus.
Start propofol before starting the remifentanil infusion

Like hypnotics, no firm recommendations for opioids

Remifentanil: 4-6ng/ml laryngoscopy/tracheal intubation, lower conc for LMA. 6-8ng/ml for laparotomy, 10-12ng/ml for cardiac surgery

Remifentanil: post op analgesia
TCI for high risk patients
Altered Pk- higher than expected blood concentrations

More profound Pd effects

High Remi, low propofol- increased CV stability

BIS

Start with low targets, increase in small increments observing clinical effect
Pharmacoeconomics of TIVA
Compared with sevoflurane-N2O, use of propofol-N2O for office-based anaesthesia was associated with an improved recovery profile, greater patient satisfaction, and lower costs.
Target-controlled infusion/ total IV anaesthesia was associated with the largest intraoperative costs but allowed the most rapid recovery from anaesthesia, was associated with fewest postoperative side effects, and permitted earlier discharge from the postanesthesia care unit.
Quality of recovery withTIVA
In children, recovery from anaesthesia with sevoflurane results in a higher incidence of agitation compared with propofol.
Recovery from anaesthesia was significantly faster in the propofol group. There was significantly less nausea in the propofol group (15.4%) than in the isoflurane group (33.7%) in the first two postoperative hours.
Pharmacokinetics!!
Conc = C1.e-alpha.t + C2. e-beta.t + C3.e-pi.t

a1=a10+((k21*a20)+(k31*a30)+q-(e*a10))*dt; a2=a20+((k12*a10)-(k21*a20))*dt; a3=a30+((k13*a10)-(k31*a30))*dt; ct=a1/vc;...................................................

!....%........@.........&..........$............:-(
a....................................................................l

V1, V2, V3, k10, k12, k13, k21, k31 !!!
...............................................................................................
Pharmacokinetics!!
Three compartment model
Schwilden
: A general method for calculating the dosage scheme in linear pharmacokinetics. Eur J Clin Pharmacol 1981; 20: 379-86

Shafer
: Algorithms to rapidly achieve and maintain stable drug concentrations at the site of drug effect with a computer-controlled infusion pump. J Pharmacokinet Biopharm 1992; 20: 147-69

Fentanyl and other PK models
Dose
Outcome
dC/dt C
dC/dt = -kC
C= C .e-kt
Integral
calculus
Rate constant for elimination (kel)- Proportion of plasma from which the drug is removed per minute

Clearance (Cl)- Total volume of plasma cleared of drug every minute = kel x Vd

Elimination (el) = Cl x C mg/min

Single compartment- Cp (t) = Cp (0).e-kel.t
C0
C
C/2
Time constant
Half life
Half -life- Time taken for drug conc to halve from its previous value

Time constant- The time it would have taken plasma conc to fall to zero if the original rate of elimination had continued

Longer than half life
Half life= 0.693 x time constant
Half life= 0.693/ elimination rate constant (kel)
Three compartments elimination, slow and fast redistribution
Log blood concentrations
Time
Cpt= C1.e-alpha.t + C2. e-beta.t + C3.e-pi.t
Predict plasma conc.
Programme computers
BUt.........assumptions!!!
Marsh model

Schnider model

Schuttler model

Kataria model

Paedfusor model

Minto model
Target controlled infusion
Components of TCI
Full transcript