Nitous Oxide Cylinder.. pressure gaudge..

The picture is self explanatory One Nitrous Oxide cylinder when connected to anaesthesia machine showed the pressure to be 100kPa, where as the other cilder fitted to the other port showed 50kPa. When the cylinders were interchanged the pressure  in the gauge also changed.
So it was presumed this cylinder is mixed with some other gas which is exerting this additional pressure.
As there was noscope to examine this gas. , the gases from the cylinder was discharged to open atmosphere slowly  in an open space.
So all are cautioned that  a very high pressure in N2O cylinder should be looked at. There were some discussion that there is no need for Pressure gaudge in N20 side as the pressure is always  the same as long as  the last  drop of liquid N2O is present. But here is a scenario where the pressure gaudge  could help us to avoid a possible critical incident in Anaesthesia.

50 Joules for successful defibrillation

Introduction:

            Definite protocol for resuscitation after Cardiac arrest  exists and practiced all over the world. But the success lies in early detection and early defibrillation .

It is also seen  after 10 mins of resuscitation if the activity does not return  there it is likely that the patient has residual neurological deficit because of ischaemic encephalopathy.

            We describe here with 1 cases of Cardiac arrest  lasting 21 minutes  and 28  minutes, which was successfully revived with no neurological deficit

Case 1.  A middle aged patient of 48 years undergoing open  Cholicystectomy. The patient  was of ASA- ! with no known abonormality of any parameter. The patient was premedicated with Midazolam 2mg , Pentazocine 30 mg and  induced with Thiopentone 200 mg and intubated with Vecuronium 6mg . The anaesthesia was maintained with Oxygen 33%N2O 66%  , Halothane 0.5- 0.7 % and IPPV Manually. About 45 mins after induction of Anaesthesia the operation was over there was no undue Hemodynamic changes  intraoperatively.  After the end of surgery about 40- 45 mins from the start, limited bagging was done so that  respiratory activity can be noticed , some CO2 accumulation was allowed so as to stimulate the respiration.. Within a short time respiratory activity appeared and the  the patient was allowed to breath spontaneously with 100 % Oxygen  with intermittent support..Then Injection of Neostigmine  and atropine mixture was given slow IV over 3 minutes. Before completion of  all the prostigmine  there was alarm in monitor with bizarre waves, thinking that the lead has come off, it was readjusted and  the same pattern continued, When the radial pulse was examined , there was no pulse. Immidiately it was  thought that the patient has gone  to Ventricular fibrillation which was confirmed with another monitor. Immidiately a defibrillator was called for, Artificial ventilation continued with 100 % Oxygen and external Cardiac massage  commenced . There was  panic in OR ,I started a good and forceful cardiac massage and  the assistants were encouraged to do the same  where pulsatile plethysmographic waves were detected in Pulse Oxymeter  with Saturation of 60 – 75 %. When a BPL defibrillator arrived it did not start because the battery was almost totally discharged The  failed to charge 200 joules even when connected to electricity supply.  The BPL supplier was contacted who advised  to  charge the battery before  charging the defibrillator. With no other option  the external Cardiac massage continued  with full  vigor.   When somebody was fiddling with the defibrillator , it changed to  the Pediatric mode.  By this time more than 18 mins had elapsed  . With the pediatric mode the defibrillator was charged with 50 joules, that was the upper limit  in pediatric setting . Initially it also failed. Again after 3 mins it clicked. With intruption of External cardia c massage. 50 joules were delivered.

Alash ! It worked The rythm was convereted to sinus  witha HR of 60 which increased to 90. The peripheral pulse was plabale and the NIBP recorded was 105/60 mmHg. and SpO2 99-100 %. There was no facility to do an ABG analysis or adminster any Sodi bicarb. The patient was hyperventilated for next 15 mins when ts respiratory effort returned and was vey normal. Consciousness returned too. Post op recovery was totally uneventful. When we checked with the monitor trend graph we found  that the period of fibrillation was around 21 mins. 

Discussion: what could be the cause ?

24 Hrs after surgery with no damage, no memory of any incident

Critical Anasthesia Incident: Rapid & severe hypotension

Critical Anasthesia Incident: Rapid & severe hypotension: "A look at these photographs from the trend graph shows the following. When there is a slipped arterial blood vessel the result is devastatting..."

Rapid & severe hypotension

A look at these photographs from the trend graph shows  the following. When there is a slipped arterial blood vessel the result is devastatting.....
Pic1 : Time 13 :07 
 HR 111, BP:  125/74

Pic 2 shows : Time 13:08 
HR ...   BP : 54 / 39 ( Mean BP - 45 )

Pic 3 shows Time 13.09

HR  110 , BP 26/ 19 ( Mean 22 )

PIC : 4  Time  13.10

HR 71 , BP 20 / 13 ( Mean 13 )

PIC : 5  Time 13.11

HR 52 , BP 28/ 13 ( Mean 15 )

PIC 5  shows Time 13.12
HR 55 , BP 55/39

 PIC 6  shows Time 13.13
HR 93 BP 28/ 19

What you have to do is push and push the blood  through the canula by a 20 ml syringe , push and push & push

Theere was no use of ionotrops, no ephedrine, no mephenteramine.......
And after



PIC 7 : Time 13.49

HR 108 BP 72 / 47 ( Mean 58 )

The patient had a remarkable recovery after another 6 hours of  continued surgery under epidural anaesthesia, sedation, 10. 5 Lits of I/V fluid  including 6 Inits of blood transfusion, 2 units of Hesta starch, and an Injection of Lasix.  As the graph shows the Blood pressure  next few hours were around 80 mmhg systolic  and 45 -50 mm Diastolic

Post operatively ,there was no renal shutdown or dysfunction.

This was possible because the hypotension was of short duration ........ and  the mean blood pressure was around 50~60 mmHg.  intraoperatively .



Anaesthesia in an unconscious patient

Das 25 years , Unconscious since 23 days following road traffic accident, GCS 8-9, CT scan does not show any definite pathology like blood, midline shift, Clinically patient is stable vitals, spontaneouly breathing , On ryles tube feeding, Neurologically the patient had increased muscle tone in  limb muscles like UMN disease.No convulsion. Needed opeartion for # shaft of femur and Tibial head. A spinal anaesthesia was adminstered at L-3-4 interspace  with sensorcaine 3 ml and appropriate positioning for minimal fall in BP
The spinal fluid was discolored  some what deep straw colored but no increased pressure.
Intra operatively a small dose of thiopentone was given to reduce the muscle tone and Oxygen by mak

The intra operative period was uneventful ..