ITS PRESENTATION DONE BY MYSELF ON POST ANAESTHESIA CARE UNIT I WILL MAKE FEW CHANGES AND UPLOAD THE BEST ONES

1. POST ANAESTHESIA CARE
UNIT

2. Introduction
During SECOND world war
Intrest in anaesthesiology
JOHN LUNDY IN 1943.ADV
POST OPERATIVE PATIENTS- ((a) OPA
* specific area for observation, recognise surgical medical and anaesthetical
complications
Post operative nausea and vomiting -11%
Hypotension #%
Arrhythmias <!%
Hepertension 1%
Altered sensorium <1% upper airway obstruction
Major cardiac complications

3. Smooth – in most of patients
Small number – life threatening
Best managed by prompt interaction of skilled nursing and medical
intervention
* GA – 150 YEARS
PACU – 40YEARS
1863 – FLORENCE NIGHTNGLE
1923 –JOHN HOPKINS
1930 – PACU USA
1943- ANAESTHESIA STUDY COMMISSION
1944 -HALF OF DEATHS IN FIRST 24 HOURS ,.13 RD DEATHS BY POST
OPERATIVE NURSING CARE
1945 PACU is short term GCU
1988- ASA – GUIDELINES REGARDING PACU

4. • MEMBER OF ANAESTHESIA TEAM
• *
• *
• * WAIT TILL THE NURESE TAKE OVER
• DISCHARGE CRITERIA AND APPROVED
•
• ACDROCF SGRG PIC
• DESIGN AND STAFFING
• close to ot , LAB XRAY GCS
• 1.5 BED OT 2 BEDS FOR PROCEDURE in 24
hours
• Isolation room
• Paediatric picu

5. LARGE DOORS , ADEQUATE LIGHTENING, BED SPACE ,ENVIRONMENTAL CONTROL
ELECTRICAL, PUMBING FACILITIES ,CONTROL NURSING STATION
PHYSICIAN STATION ,SCAVENGER UTILITY AREA ,CONTROL OXYGEN, AIR ,VACCUM
NIBP , MANUAL BP, IV SUPPORTS – BGO SPO2, PACU CHARTS, SUCTION
CATHETERS, NEEDLES, SYRINGES, GLOVES, O2 MASKS,
ECG- ONE FOR 2 TO 3 BEDS ,IBP, CRASH CHART DEFIBRILLATOR ,PACE
MAKER, COMPUTER

6. NURSE : PAC
1:3
CAN BE 2:1
1:2
INCHARGE NURSE
TEAM
PHYSICIAN? WARD CLERK
ROUTINE RECOVERY
TIME OF RECOVERY – SOLUBILITY OF ANAESTHESIA AGENT AND ALV
VOLUME

7. Patient on side stretcher- side racings
( airway obstruction) massive aspiration of gastric contents from vomitings
REPORT to PACU nurse- patient name, surgery, age, details of
anaesthesia , medical problems fluid blood, intra operative
complications.
CARE;- O2 inhalation , major surgery , nursing of vitals , once in 15
minutes for 1hours ,
ENCOURAGE –deep breathing , movement of patient if possible.

8. GENERAL ANAESTHESIA
Arousable, oriented , stable vital signs for one hour prior
to discharge.
Reasonabl e comfortable
recovery from narcotics – observe for 30 minutes ,
spo2 at room air, ABG to call nurse for HOCA SOS
REGIONAL ANAESTHESIA – VITALS STABLE , AWAKE.
ROC nurse with handover to ward nurse.

9. RESPIRATORY primary cause of life threatening morbidity in
PACU is of respiratory origin.
* CAUSE;-
ANAESTHETICS- response
Narcotics- oxygenation impaired decreased FRC
Relaxants;- pulmonary atelectasis , altered mucosal clearance.
Impaired hypoxic pulmonary vasoconstriction.
1. AIRWAY OBSTRUCTION – pharyngeal obstruction in unconscious and
semiconscious patients due to tongue flapping.
2. PARTIAL OBSTRUCTION ;- LOUD / NOISY RESPIRATION, snoring , gurgling,
stridor. May lead to hypoxia and hypercapnia.
3. Total obstruction ;-no air entry, flaring nostrils, incresed respiratory
efforts , accessory muscles , agitation.

10. Rx.- BACKWARD TILT OF HEAD amr displacement of mandible
Cricothyroidotomy
Tracheostomy.
patient breathing spontaneously , altered / neck anatomy, { diffuse oedema
expnding haematoma blood reserve.
Intubation using much relaxant should not be attempted, unless fairy curtain the
airway can be secured.

11. Norm, than exception
routing 35-40% o2 face mask n. common
mechanism - hypoventillation v/q mismatch ,
right to left shunt incresed pulmonary shunting ,low fio2 decresed co,
diffusional hypoxia,
RX- 100% O2 5 TO 10 LITRES AFTER DISCONTINUATION OF ANAESTHESIA
SECRETIONS PAIN
DECRESED DIAPHRGMATIC FUNCTION – DECREASED VC, ATELECTASIS
leads to hypoxaemia .
pulmanory pathology , age , obesity.
atelectasis- deep inspiration ( 5 to 15 ) minutes CPAP.

12. ↓ ACV VENTILLATION →↑PACO2
POOR respiratory muscle function
↑co2 production ( lung dysfunction
Dnags – respiratory depression ( narcotics)
ASPIRATION ; emesis , regurgitation aspiration
Patients with excessive sedation , coma stupour , GCP
FULL STOMACH PRIOR TO GENERAL ANAESTHESIA
Anxiety

13. 0.4 ml / kg if ph< 2.5
chracter of material
sepsis , dgach
INVESTIGATION – CHEST XRAY ABG
RX supportive;- suctioning , maintaining airway , o2 ventillation
cpap antibiotics . Steroids? Fluids
CARDIOVASCULAR COMPLICATIONS;-
HYPERTENSION , ;-
Causes - p. pin, excitement shivering mild hypothyroidism
hypervolaemia hypoxaemia.

14. hypertension patients;,- ↑ b.p → increase left ventricular wall tension ↑svr and
myocardium work leads o myocardial infarction.
IN CCF PATIENTS ;IMPAIRED VENTRICULAR FUNCTION ↑SVR,
IMPEDENCE to outflow of blood from left ventricle leads to decreased cardiac
output leads to pulmonary oedama.
s average hypertension leads to mi , arrhythmias ARF, CCF, SAH, CVV
RX- analgesics
warming observation anti hypertensive drugs
SNP, NTG, LABETALOL, HYDRALAZINE CCB , BETA BLOCKERS, ACEI, ARBS,
DIURETICS.
HYPOTENSION- MOST common
Causes- hypovolaemia →decreased returning blood volume →→↓venous return
→↓preload →↓ventricukar filling →↓stroke volume→↓cardiac output- pump
failure→myocardial dysfunction.
sequale = MI, STROKE, AKI.
LOW PAOP , ↓co hypovolaeeia → RX→ fluids , blood.
↑PAOP , LOW CO,→↓ MYO CONTROL → RX → IONOTROPHIC SUPPORT.

15. ↓Svr → paop ± co →sepsis likely.
RX.-
MECHANISM →DISORDER IN IMPULSE FORMATION
disorder in impulse conduction.
Major complications of arrhythmias - ↓ myo o2 supply ↓ CO
COMMON DISTURBANCES ‘- SINUS BARDYCARDIA sinus tachycardia VPS , SVT, VT.
;- 1. CAUSE EVALUATED
2. PHARTMACOLOGICAL
3. PACEMAKER
4. SYN. CARDIOVASCULAR.
5. DEFIBRILLATOR.

16. COMMON – MI, OTHERS PULMONARY PNEUMOTHORAX,
MYOCARDIAL o2demand.
Not a common problem
incidence;- o.4 to 13.0 %
frequency – tonsillectomy , thyroid surgery , circumcision, hysterectomy,
Causes- hypoxia , hypercarbia , pain urinary bladder , anticholinergics,
drug interactions axiety alcohol depression.
TREATMENT;- DETERMINE ETIOLOGY
RULE OUT HYPOXIA ( SPO2 MONITORING VITALS.)
ELECTROLYTE IMBALANCE
PHYSOSTIGMINE (SCOPOLmine)
Analgesics ( pain) benzodiazepines ,(anxiety)
Psychiatry consultancy

17. Described – 1950, after GA incidence 22 to 50 %
halothane, isoflurane sevoflurane narcotic + n2o amides regional
attributed too intra operative hypothermia
( loss of blood, large fluid administration ) according to OR
SHIVERING _ INVOLUNTARY tremors in homeotherms
induced by cocaine , effect of which is provocation of heat.
Undesirable side effects ( ↑o2 consumption , ↑co2 production )
MI, WOUND DEHISCENCE, DENTAL DAMAGE ↑GAP.
MECHANISM;- ADR SUPRESSION,
↓SYMPATHETIC ACTIVITY.
TREATMENT;- HUMIDIFIER ( anaesthesia circuit)
Surface warming
forced air warmer, ↑temp 1.5celsiushr pethidine 12.50mg iv

18. ETIOLOGY-*PROLONGED ACTION OF ANAESTHETIC DRUGS
* METABOLIC CAUSES
hypothermia
neurological injury
prolonged sedation
premedication
hypoglycemia(DM)
electrolyte disturbance
unsuspected CVA
fat embolism
monitor spo2, ABG etco2.

19. ETIOLOGY ; MAINTAIN ADEQUATE VENTILLATION
NALOXANE, FLUMANEZIL, WARMING
electrolytes ( Na,Mg, Ca, correction.)
neurological - diagnosis of exclusion
neurological consultancy.