2. THe answer to your second question first
TACY PHYLAXIS or ACUTE TOLERANCE is when the same dose of drug fails to produce the same effect seen earlier
or
to produce the same earlier effect,  you need to give more drug

So if you want to produce the same response as first,  you have to increase the dose of drug

Lets say you gave a spinal, and BP fell from 120 systolic to 90 and you gave ephedrine 6 mg and the BP went upto 118 mm

But again the bp fell to 90 systolic,  and if you repeat 6 mg and tacypylaxis is on,  the BP will go upto only say 100 mm. If you need to go upto 120 mm probably you will have to give 9-12 mg ephedrine.

Just need to remember that not all patients develop tachyphylaxis with the same severity and speed. So you will find a huge amount of variation in patient response.
IF you have a patient crashing BP after spinal and no good response to ephedrine bolus, you have to quickly think of tahyphylaxis and go with a higher dose, failing which patient may become significantly hypotensive for a long period.
This is more of significance,  if you are worried about maintaining uteroplacental blood flow and also in patients who have autonomic neuropathy in whom fluid preloading and small dose vasopressors may not be enough to compensate the sympathetic block.

1. Half life got very complicated these days.
If I recall right we have 3 kinds of half life
t1/2 alpha - or the distribution half life
t1/2 beta - or the elimination half life
context sensitive half life - time taken to reach t1/2 beta after cessation of a prolonged infusion of a drug.

HALF LIFE is the time taken for the serum concentration of a drug to be reduced by 50% from the intial peak concentration. It does not define the process how this decrease in concentration occurs


You give 2 mg/kg (100 mg) of propofol for induction. It acheives a serum concentration of 2.2 microg/dl at its peak effect.

Half life is when the total body concentration of Propofol gets to 50 % ie 50 mg


t1/2 alpha
You give 2 mg/kg (100 mg) of propofol for induction. It acheives a serum concentration of 2.2 microg/dl at its peak effect. Patient will wake up say if the concentration goes down below 1 microg/dl. Patient usually wakes up in 5 minutes but Propofol is still in the body as kidney has not yet eliminated it. Then the concentration in serum decereased because the propofol was redistributed to other tissues in the body

t1/2 beta
the kidney has eliminated 50% of the propofol dose given so that the body propofol concentration is reduced to 50 mg

context sensitive half life
you give propofol 2mg/kg and follow it with an infusion of 8 mg/kg/hour for 4 hours.
In such a situation the redistribution sites get saturated with propofol.
Now on stopping infusion, the time taken for patient to wake up and the time taken for serum concentration of propofol to be reduced by 50%  takes a much longer time. T

regs

1.   Equipment dead space in circle system is upto the Y piece and (marginally  beyond it on both limbs)  in a circle system.
If both the Undirectional valves(UDV) are fully functional as they should be
Then the functional analysis of the closed system is as follows

When the patient expires, the inspiratory UDV is closed, so expired air cannot travel into the inspiratory limb.  The expiratory UDV is open and expired air travels only down the expiratory limb towards the soda lime canister.

The reverse happens during inspiration and hence the entire inspired air comes from the inspiratory limb consisting of FGF and gas coming out of the circle absorber. No air is drawn in from the expiratory limb.

So theoretically if both the UDV are working well. Patient cannot expire into the inspiratory limb and he cannot inspire any gas from  the expiratory limb.

So that leaves the only place where the inspired and expired gases mix before going into separate limbs and that is the Y piece near the patient end. That then is the dead space , the only gas which can enter during the next inspiration that can possibly contain some expired air mixed into it.


2.   The breathing tubes have compliance and can stretch and collapse. This definitely contributes to wasted ventilation thereby reducing the delivered tidal volume due to wasting in the circuit expansion.

It will however not contribute to dead space. Dead space must entail rebreathing of expired gases and this does not happen in compliant breathing tubes.

Just need to remember that compliant breathing tubes may decrease TV enough to decrease minute ventilation over time and lead to slow development of hyper carbia.

3.   With an anaesthetic ventilator,  the FGF delivered in compliant tubing will be less than set value. This can be detected with a respirometer at the patient end. In modern machines this is built into the machine as delivered tidal volume.

Modern machines have tried to over come this problem using various methods including AUTOMATIC TUBE COMPENSATION ( ATC) or FRESH GAS DECOUPLING (FGD)

These features overcome wasted ventilation due to  compliant tubing and ensure that the set TV is delivered to the patient



THAT DOCTOR are very relevant questions. No need to be apologetic about asking them. It took me a very long time to understand these concepts too.

I hope these explanations have been lucid. If not,  you will find all you need in DORSCH & DORSCH edition 5 chapter I think on breathing circuits

Or try the APSF website that has explanations on the anaesthesia machine which will explain these concepts to you

regs

26 year old healthy adult presents for hernioraphy. History is normal, claims to be a slightly anxious personality and occasional palpitation when stressed. Effort tolerance is greater than 8 METS.
Clinical examination reveals no other problem except a resting heart rate of 145 bpm. Examined on several occasions and found to be consistently above 140 bpm
patient has  normal CVS finding, ECG shows narrow complexed tachycardia, Xray is normal. All biochem including Thyroid function is within normal limits.
ECHO shows normal study exxcept for the tachycardia noticed during study.
Patient was initially started on Alprazolam 0.5 mg HS.
No improvement lead to additon of Tab. Propronalol 20 mg intitally OD and subsequently BD.
Propronalol, and not cardioselective beat blocker choosen for the complimentary CNS anti-stress effect of the drug
After 1 week rates continue to fluctutate between 130 and 140 bpm.

Do we proceed with this rate. or do we further need to stabilize his rate,

regs

Apart form  microemboli, methyl acrylate releases vasoactive mediators of inflammation which produce vasodilatation and decrease in SVR. So BP  falls leading to hypotension. The blood volume gets held up in the peripheries, so Preload drops, and heart tries to compensate the CO decreases by increasing heart rate, hence tachycardia. Although these vasoactive amines by themselves can produce tachycardia.

Till a few years ago, 200 mg of Hydrocortisone was being given prior to placement of cement claiming that it decreased the inflammatory material release. Recent evidence proves that this practice is unscientific and hence has been dropped, although quite a few anaesthetists still continue this practice.
I have have totally stopped with steroids.


what is recommended now

Before placing cement give adequate fluids and make sure hypotension is corrected and preload is optimal.
Doses of vasopressors like phenylephrine and ephedrine may be used to prevent hypotension.
True anaphlaxis is rare but possible, must be recognized and treated appropriately
Also remember the cement is placed immediately after reaming of bone hence blood loss and hypotension may already be present and this may further compound the problem

regs

I always make 2 anaesthesia charts in private practice and 1 goes to patient records and the other I have filed at home and is till have them with me
As per medicolegal rules you have to preserve all patient records for 7 years.
I started this practice about 11 years ago and I have found the energy and the perseverance to keep going on with it.
Initially it was difficult, people ridiculed, but I stuck it out and today it is almost a habit.
I am a slightly defensive human being and so is my anaesthetic practice. So i decided that in these days of litigation I be prepared with adequate records.
I use 2 type of charts. A printed one which is modelled as a compilation of 2 or 3 charts I used in my early practice.
If the hospital has no chart I follow a written format.

I will scan and post it if you so want.

Maybe at gasbag we can collect charts of many people and come up with the best combination

regs

Pain stimulates the autonomic nervous system, both sympathetic and parasympathetic. Normally in adults, sympathetic stimulation dominates, hence, we commonly encounter tachycardia and hypertension in response to pain
In paediatric age group or in adults with autonomic dysfunction, catecholamine depleted state or vagal hyperactivity, the same stimulus may produce a response that is dominated by parasympathetic stimulation and hence may lead to symptoms of parasympathetic stimulation like bradycardia, asystole, bronchospasm and laryngospasm.
Typical examples of this parasympathetic activation includes some common reflexes encountered during anaesthesia like the Brewer-Luckardt reflex, Bezold-Jarisch reflex and the ventricular mass reflexes that produce cardiac arrest in oterwise healthy young adults during spinal anaesthesia

Regs

Burn victims definitely deserve adequate pain relief at all times including during dressing change
They are grossly under-dosed in clinical practice
I don't have too much of experience dealing with burn victims. But my thoughts on this topic would include

Anaesthetics do pose serious issues in burns patients. To name a few

Altered drug distribution – pharmacokinetics and pharmacodynamics
Prone for hypothermia
Electrolyte disturbance
Airway problem
Difficult IV access
Prone to infection & Septiciemia
Difficult to fix monitoring devices
Altered fluid distribution
Hypoproteinemia
Difficulty in transportation

All these probably lead the patient to undergo dressing changes in the ward itself.
Administering anaesthetics to these high risk patients in "out of theatre" situation may be extremely dangerous.
I think this  is the reason why burn patients do not get what they actually deserve.
I think all burn wards must have a minor OT attached to it, fully equipped with all anaesthetic devices and monitors for safe and effective care of patients.
As regard to pain relief techniques I think potent narcotics can be combined with O2 with sevoflurane may be good.
Supraglottic devices may be good options
Propofol- Ketamine combination may work
Newer sedatives like Dexmedetomidine may have a role

regs

Dear doc
Literature does not support the use of multiple doses of succinylcholine due to problems like  phase 2 block, desensitization block and brady-asystolic arrhythmias due to ganglion stimulation.
I am sure you have enough experience with multiple dosing.
A dose of Suxa has a duration of action ranging from 5 to 15 minutes.
So 3 doses may produce relaxation for about 30 minutes.
You could have achieved the same with a single dose of intermediate duration of action NDP relaxant. The choices would include Atracurium, Cisatracurium, Vecuronium and Rocuronium.
I think this would be a better accepted practice from medicolegal point of view.
In olden days even suxa infusions have been used. Those days of medical practice without evidence are over.
I do agree that complications with suxa are extremely rare.
However in view of available evidence even if 1 person has adverse outcome due to multiple suxa dosing, it will completely be unacceptable.
We do not use multiple suxa doses.
Infact we don't use suxa at all. We prefer direct NDP even for intubation unless there is a very strong indication for use of Suxa

regs

Dr. Bhatt
I have the greatest regard for your knowledge and technical skill.
Above all I appreciate your quest for constantly trying to learn and iron out any thing that is not in tune with current evidence of good anaesthetic practice.
Hope we can continue to learn on this site and inspire youngsters to go beyond what we have achieved.

Now to the problem
Epidural catheters should be inserted only 3 to 6 cms into space.

Less than 3 cms – in 3 lateral eyed epidural catheters, we commonly use, the 3 eyes may not completely lie in the epidural space and hence we may have a patchy distribution of what is known as the "Multi-compartment block". I believe this can be avoided by using a single terminal orifice epidural catheter.

More than 6 cms insertion  - 2 things can commonly happen. First the catheter exits the epidural space along with the emerging nerve roots via the intervertebral foramina and comes to lie in the paravertebral gutter. Hence block may be unilateral and/or  patchy.
Secondly more than 6 cm insertion has been found to increase the incidences of catheters double folding on themselves. Greater lengths of inserted catheters also increase the risk of inadvertent Intravascular and subarachnoid placement of catheters.

So in the first instance a 13 cm insertion probably took the catheter to the paravertebral gutter. Pulling it out did the trick. I wonder why the second dose had poor action.

Epidural catheters greater than 6 cm insertion has been used in paediatric patients via the caudal space. But positioning of catheter in these scenarios is done under C-Arm guidance.
regs

My understanding of the subject

All materials absorb gases in varying concentrations

So Nitrous Oxide has been found to permeate across the thin PVC sheet that forms the cuff. That explains that N2O can move around
In fact various rubber and plastic tubings can absorb varying quantities of inhalational agents as gases
This uptake by circuit needs to be factored in when practising low flow anaesthesia techniques
These taken up gases by circuit may be relaesed later and can theorotically delay recovery
SO N2O can move across the thin PVC cuff

If there is a semipermeable membrane gas molecules move across it based on concentration gradient from high to low concentration. That simply explains how CO2 is given into lungs and O2 taken up at lungs. Lungs have less CO2 and more O2 compared to venous blood. The vice versa happens at the tissue level
Obviously the cuff is filled with air ( no N2O) while the inspired gas has 66% of N2O so obviously N2O will move in according to the concentration gradient. and it will continue to move until equilibrium is acheived across the membrane . Meaning inside the ETT cuff too there must be 66% N2O to prevent further movement.
There is another additinal problem. N2O is almost 30 times more diffusible than other gases. So in the time taken for 1 air molecule to move out nearly 30 N2O molecules can move in . So N2O fills in faster than air moves out( SIMILAR OCCURENCE DURING FINK EFFECT / DIFFUSION HYPOXIA). If this change occurs in a compliant space like air in intestines, then the intestines bloat as during laprotomy.
IF N2O moves into non-compliant spaes like middle ear or ETT cuff the volume cannot expand much so the pressure increases producing the damages

In ETT cuff N2O moves in faster than air moves out leads to increase in presure above the safe  allowed 18 mm Hg and can compromise tracheal mucosal blood flow
So you need to check pressure if you use N2O and deflate and make adjustments in volume as necessary

ALTERNATIVES
Fill cuff with saline or any liquid
Use Inspiratory gas mixture( 66% N2O and 33% O2) to fill cuff
Use manometer to measure and adjust pressure
Use self regulating ETT cuff systems like Lanz system or Mcginnis cuff balloon system

Hope this explanation is decipherable and
Hope to God this is the correct explanation for this oft ignored phenomenon

regs

I have also been trained to identify the epidural space by LORT – AIR technique and am quite  happy with it and the results have mostly been good

There are certain definite advantages of LORT-SALINE technique
1.   The flowing saline pushes the dura away and hence the chances of accidental dural puncture are minimized
2.   Even a small amount of air injected into the space if it  accidentally enters the epidural vein it can precipitate air embolism. This is particularly relevant in paediatric age group. Remember that 30% of all normal people have a probe patent foramen ovale.
3.   A small amount of air in the epidural space may form a small bubble around one of the nerve roots. Subsequent LA solution will be prevented by this bubble from accessing the nerve root leading to patchy block or root sparing

The reason why we persist with LORT- AIR is because if we use saline to identify the space
Then thread the catheter in
And then find some liquid in the catheter then we are in a dilemma
Is this liquid the saline we instilled or CSF due to catheter entering the sub-arachnoid space
To evaluate this doubt we could use
1.   Temperature of the returning liquid
2.   Precipitation with freshly prepared Thiopentone solution
3.   Use of Glucose strips

I think it is this doubt that makes us persist with a technique we are so well used to – LORT – AIR

Given the scientific evidence I think the youngsters must be encouraged to switch to LORT- SALINE
right from the beginning of their anaesthetic careers

regs

Checking vocal cords after thyroid surgery was a routine
Its usefulness and validity are under question now

Cord injuries seen immediately after sugery may be transient neuropraxia due to edema around nerve during surgery. These can change dramatically
Also the same edema induced neuropraxia related cord dysfunction have been known to occur as late as 24 hours after checking them post-surgically and finding them to be normal

The more important factor seems to be that laryngoscopy during recovery may produce 2 things

1. Hypertension due to sympathetic stimulation that can increase reactionary and secondary haemorrhage and hence risk of post-op heamatoma and airway compromise
2. Layrngoscopy may induce laryngospasm in a patient not fully recovered from the residual effect of anesthetics


So what is recommended instead

Ensure adequate recovery
Adequately suction oropharynx
Deflate cuff
Demonstrate " Breathing around the ETT
Extubate over AEC
IF stridor is seen reintubate and leave ETT in situ

If no stridor seen after extubation
Ask patient to phonate
If phonation is OK patient should do OK
If phonation is absent no need to reintubate but oral feeding not to be started until ENT clearance

All cases of suspected cord problem can be referred to ENT for adequate evaluation using videolaryngoscopy and further management

with regs

a 22 year old woman is posted for encirclage for cervial incompetence. Procedure is likely to last 10 to 15 minutes only

She is a known case of Mitral stenosis of Rheumatic etiology
Her effort tolerance is 4 METS
she has a history of Dyspnoea on Exertion NYHA class 2
Her last Echo shows a MVO size of 1 cm2. She has mild PHT and her LV function is good
She is in sinus rhythm and on regular anti- CCF therapy


our plan
Debated about short duration day care procedure and role of Spinal anesthesia
Also debated about potential for full stomach scenario and aspiration risk
Wondered about the utility of blocks like pudendal and paracervical and dropped them due to lack of experience and confidence
IV ranitidine and IV MEtoclopramide 10 mg given 30 min before surgery
Routine monitors including ETCO2 and IV line started. Fetal heart rate monitoring started
Patient received Glycopyrrolate 0.2 mg + Fentanyl 2 mcg /kg
SC Terbutaline was used as tocolytic as only that was available
Induced with Propofol 2.5 mg / kg mixed with Lignocaine 1 mg /kg
Once under, size 3 PLMA inserted Positioning confirmed
N2o + O2 + Isoflurane intial IPPV followed by Spontaneous assisted ventilation
Ryle's tube inserted
Procedure in lithotomy lasted 17 minutes
Recovered in supine and extubated fully awake

Is this technique good enough or are there any holes to punch into it
Was it OK to overcome our intial urge to be safe and just go with a spinal since we hoped to return patient home as early as possible

Thanks for your inputs

the truth is that all of use either intermediate flow or high flow
very few people use low flow
because
it needs good machine
good monitoring
good understanding of concepts

is low flow then necessary?
newer Inhalationals will be more better,  but more costly
if you use low flow you can use better agents at a more economical rate


atmosphere needs to be protected
like cars and industries have stingent emission standards anaesthetists will alos have to follow it sooner or later

So it is inevitable that slowly but surely anaesthesia will move towards low flow

regs

Hyponatremia may present similarly in the post-operative period of elderly
Electrolyte check and appropriate correction helps.
How does methcobalamin help

regs