14 09 13

Prof. A. K.
SethisEORCAPS-2013
1
Prof.A. K. SethisEORCAPS-2013
Management Of
The Di abet i c
Pat i ent
Dr. Ranj u Si ngh
Case 1 Case 1
60 yr old, 60 kg female, with Ca head of pancreas
scheduled for Whipples Procedure
Known diabetic
What would you want to find out from history,
examination & investigations?
What Fac t or s Af f ec t t he What Fac t or s Af f ec t t he
Per i oper at i ve Anest het i c Per i oper at i ve Anest het i c
Management of DM? Management of DM?
Type, duration of DM
Medication
Level of glycemic control
End-organ damage, particularly autonomic dysfunction
Nature of surgery - major
- minor
Urgency of surgery
Cl assi f i c at i on of Di abet es Cl assi f i c at i on of Di abet es
Type Cause Insulin Acute
complication
Type I Destruction of pancreatic
cells
Absolute
deficiency
DKA
Type II Peripheral insulin resistance,
often coupled with a failure
t t i li
Deficiency of
cells &
i t t
NKHC
to secrete insulin resistance to
insulin
Type III Wide range of sp type of DM
MODY
Endocrinopathies
Acromegaly, Cushings
Drugs - steroids, -agonists
Gestational
DM
Deficiency of
insulin
Cr i t er i a f or Cr i t er i a f or Di agnosi s of Di agnosi s of DM DM
Test Normo-
glycemia
Impaired
Fasting
Glycemia
Impaired
Glucose
Tolerance
High
Risk
Diabetes
PG, fasting
(mg/dL)
<100 100-125 126
PG, 2-hour <140 140-199 200 PG, 2 hour
(mg/dL)
OGTT
140 140 199 200
HbA
1C
(%) About 5 5.7-6.4 6.5
PG, casual
(mg/dL)
>200 mg/dl
plus
symptoms of
diabetes
Adapted from American Diabetes Association 2013
Di agnosi s Of Di abet es & Di agnosi s Of Di abet es &
Pr edi abet es Pr edi abet es
Prof. A. K. SethisEORCAPS-2013
2
Rel at i on Bet ween Whol e Bl ood Rel at i on Bet ween Whol e Bl ood
& Pl asma Gl uc ose ?? & Pl asma Gl uc ose ??
Levelofglucoseinwholeblood<<Plasmalevel
Wholebloodglucose+15%=Plasmaglucose
1mmol=18.0mgglucose
1mmol/L=18mg/dL
Relationshipbetweenarterial/capillary/venousblood
Arterialblood=Capillaryblood=7%>thanvenousblood
Cl asses of Ant i di abet i c Agent s Cl asses of Ant i di abet i c Agent s
Secretagogues (sulfonylureas,meglinides)which
insulinavailability
Biguanides (metformin)whichsuppressexcessivehepatic
glucoserelease
Thiazolidinediones (rosiglitazone,pioglitazone),which
improveinsulinsensitivity
glucosidase inhibitors(acarbose,miglitol)whichdelay
gastrointestinalglucoseabsorption
Ac t i on of Ant i di abet i c Agent s Ac t i on of Ant i di abet i c Agent s
Or al Hypogl yc emi c Agent s Or al Hypogl yc emi c Agent s
Drug Preparations Duration Mechanism of action, S/E
Sulfonylureas
1
st
generation
- Tolbutamide
- Chlorpropamide
2
nd
generation
Glibenclamide
Rastinon
Artosin
Diabinese
Diabigon
Daonil
Euglucon
6-8h
36-48h
18-24h
1. Increase pancreatic release
of insulin & also enhance
insulin-stimulated
peripheral tissue
utilization of glucose
2. Cause hypoglycemia
3. Glimepiride has stronger
extra pancreatic action
through translocation of - Glibenclamide
- Glipizide
- Gliclazide
- Glimepiride
Euglucon
Betanase
Glynase
Minidiab
Diamicron
Amaryl
Glymer
12-18h
12-24h
12-24h
through translocation of
GLUT4 to plasma
membrane & thus less
chance of hypoglycemia
interference with
myocardial ischemic
preconditioning
Biguanides
- Metformin
- Phenformin
Glyciphage
Dbi, Dbi-td
3-4 h
1. Improve insulin receptor
function, reduce hepatic
glucose production
2. Lactic acidosis (v rarely )
Meglitinides
-Repaglinide
-Nateglinide
Prandin
4-6h
Stimulate rapid insulin secretion by
closing the ATP dependent potassium
channel
-glucosidase inhibitors
- Acarbose Glucobay
Precose
Decrease digestion,& absorption of
carbohydrates
May cause diarrhea, abdominal pain
Thia olidinediones Reverse insulin resistance & enhance
Cont d.. Cont d..
Thiazolidinediones
1
st
generation
-Troglitazone
2
nd
generation
-Pioglitazone
-Rosiglitazone
-Darglitazone
Actose
Avandia
>3-4 wks
>3-4 wks
Reverse insulin resistance & enhance
insulin action in liver, adipose tissue
& skeletal muscle, possibly by raising
the number of glucose transporters,
sensitization of target cells to insulin
& inhibit hepatic gluconeogenesis
Chance of hepato-toxicity
Miscellaneous
- Guargum Diataid
Dietary fiber from Indian cluster
bean guar. Mixed with food, it slows
glucose absorption in gut
I nsul i n Pr epar at i ons I nsul i n Pr epar at i ons
3
Pr obl ems of I nsul i n Pr obl ems of I nsul i n
Repl ac ement Repl ac ement
Insulin secreted from pancreatic cells via portal system
Normal portal- peripheral insulin conc gradient
li l l l i i b/ i l f Cannot replicate complex local interaction b/w islets of
Langerhans & effects of extrapancreatic neuro-hormonal
system
S/c insulin, even if timed optimally, inevitably inadequate
peak concentrations for expected postprandial periods
Standard of BS Control
Nephropathy
Peripheral neuropathy
Retinopathy
Microvascular
complications
Ischemic heart disease, CHF & cardiomyopathy
Autonomic neuropathy
Stiff joint syndrome
Electrolyte & metabolic derangement
Macrovascular
complications
To Assess St andar d To Assess St andar d of BS of BS
Cont r ol Cont r ol
History and Examination
- Hyper/hypoglycemic episodes
Medication & compliance - Medication & compliance
Investigations
- BS (fasting, PP)
- GTT (if required)
- Glycosylated Hb (HbA
1
C)
Gl yc emi c Cont r ol Gl yc emi c Cont r ol
Control FBS PPBS HbA
lC
%
Excellent <110 <120 <6.5
Good <120 <150 6.5-7
Fair <140 <180 7-8.4
Poor >140 >180 >8.5
IDFClinicalGuidelinesTaskForce.InternationalDiabetesFederation,2005
Gl yc osyl at ed Haemogl obi n Gl yc osyl at ed Haemogl obi n
Erythrocyte haemoglobin is non - enzymatically
gylcosylated by glucose that freely crosses RBC memb.
Gives BG control in preceding60to90days
Normal range is 4%-6%
HbA
1C
>6.5% -ed risk of micro & macrovascular disease
Strict glycemic control can delay onset & slow
progression of microvascular complications
HbA
Lower i ng HbA
1c
Reduc es Ri sk of
Compl i c at i ons
Deathsrelatedto
diabetes
21%
Microvascular
complications
Myocardial
infarction
HbA
1c
37%
14%
1%
StrattonIM,etal.BMJ2000;321:405412
4
Nephropathy
Retinopathy Retinopathy
Ischemic heart disease, CHF and Cardiomyopathy
Nephr opat hy Nephr opat hy
Glomerulosclerosis, arteriosclerosis, basement memb
thickening
Microalbuminuria earliest lab manifestation of diabetic
nephropathy p p y
HT most imp factor responsible for progression of diabetic
renal disease; hyperglycemia,hypercholesterolemiaothers
ACE inhibitors: albuminuria & progression of renal
dysfunction
Renal Di sease
UTI - most common postop complication in diabetics
undergoing surgery
Renal failure - incidence 7%, most common major
complication
Greater chances of ARF in perioperative period, due to
- intrinsic renal disease
- hemodynamic impairment
- urosepsis
Adequate renal perfusion, avoidingnephrotoxins,
hemodynamic monitoring risk of postop renal dysfunction
To Assess Nephr opat hy To Assess Nephr opat hy
- H/o swelling of face and body
- H/o hypertension and its medication
Investigations
- Urine: proteins, sugar
- Microalbuminuria on a timed overnight collection
- B.urea, S.creatinine, S.electrolytes irrespective of age
Nephropathy
Retinopathy
Ischemic heart disease, CHF and Cardiomyopathy
A i h Autonomic neuropathy
To Assess Per i pher al To Assess Per i pher al
Neur opat hy Neur opat hy
- Foot ulcers
- Paresthesias, dysthesias, neuropathic pain
- Sensorimotor loss appearsintoesorfeet&
progresses
proximallyina"stockingandglove"distribution
Investigations
- Loss of light touch, propioception, pain, temperature
Diabetic ulcers - pain & temp insensitivity,
impaired perfusion, autonomic dysfunction
5
Nephropathy
Retinopathy
Ischemic heart disease, CHF and Cardiomyopathy Ischemic heart disease, CHF and Cardiomyopathy
To Assess Ret i nopat hy To Assess Ret i nopat hy
- Vision deterioration
- Changes in color vision
Investigation
- Ophthalmologic examination
Nephropathy
Hypertension, coronary artery disease, PVD, CHF,
cardiomyopathy & cerebrovascular disease
Car di ovasc ul ar Changes Car di ovasc ul ar Changes
Prematureatheromaformation
chancesofCAD(doublerisk;triplerisk)
incidenceofsilentMI(symp denervation)
HT(presentin2954%diabetics)&itssequelae
C di d t i t ith Cardiacdysautonomiamaypresentwith
suddenhypotensiononinduction
thresholdforarrhythmias
Diabeticcardiomyopathy
Suddencardiorespiratoryarrest
To Assess I schemi c Hear t To Assess I schemi c Hear t
Di sease, CHF & Car di omyopat hy Di sease, CHF & Car di omyopat hy
- Angina or MI
- Breathlessness
- Poor exercise tolerance
Ed f t l d li i d JVP b l - Edema feet, enlarged liver, raised JVP, basal
crepts, S3/S4
Investigations
- ECG
- X-ray Chest
- Echocardiography
Pr eoper at i ve Pr eoper at i ve
Car di ovasc ul ar Sc r eeni ng Car di ovasc ul ar Sc r eeni ng
Asymptomatic diabetic pt who has some or all risk
factors such as advanced age, smoking, hyperlipidemia
& HT
S i h ld b id d i i i h Stresstestingshouldbeconsideredinpatientswith
multiplecardiacriskfactors&poororindeterminate
exercisetolerance
Those with in high risk diabetics, metabolic syndrome,
undergoing major elective noncardiac surgery
6
Respi r at or y Syst em Respi r at or y Syst em
More chances of resp tract infections
ventilatory response to PaCO
2
& PaO
2
susceptibility to ventilatory depressant drugs
FVC & FEV (glycosylation of tissue proteins in
connective tissues)
2,3 DPG release of O
2
to tissues
DM affects O
2
transport by causing glucose to covalently
bind to Hb & alters allosteric interactions b/w chains
Nephropathy
Ischemic heart disease, CHF and cardiomyopathy
To To Assess Aut onomi c Assess Aut onomi c
Neur opat hy Neur opat hy (DAN) (DAN)
- Early satiety, lack of sweating
- Gastroparesis in form of nausea, vomiting, bloating,
nocturnal diarrhea, constipation, abdominal distension
- Postural syncope
- Bladder atony & urinary retention
- Impotence
- Palpitations
- Sensory discomfort of lower limbs
- Resting tachycardia
- Irregular pulse
- Poor exercise intolerance
Cont d
Investigations
- Resting tachycardia: > 100 beats/min is abnormal
- Beat-to-beat variation with deep breathing obtunded:
max HR-min HR at 6 breaths per min, < 5bpm, N >15
bpm, NormalRRinspiration/RRexpiration>1.17
- HR response to standing obtunded: ratio of longest
R-R around 30
th
beat after standing to the shortest R-R
around 15
th
beat after standing (N > 1.04)
Cont d.. Cont d..
Investigations
- HeartrateresponsetoValsalvamaneuverobtunded:
the normal ratio of longest R-R to shortest R-R > 1.21
- SBP response to standing: BP(lying) - BP(standing)
>30 mm Hg (N<10 mmHg)
- DBP response to sustained handgrip: handgrip
sustained at 30% of maximum squeeze for upto 5
minute & BP every minute, DBP just before release
initial DBP (N > 16 mmHg)
Aut onomi c Func t i on Test s Aut onomi c Func t i on Test s
Tests Normal Borderline Abnormal
Valsalva Ratio 1.21 1.11-1.20 1.10
Max-Min HR >15 11-14 <10 Max-Min HR
(BPM)
>15 11-14 <10
30
th
:15
th
Ratio >1.04 1.01-1.03 1.00
Fall in BP after
standing
(mmHg)
10 11-29 30
7
DAN Sc or i ng DAN Sc or i ng
Tests Results Scores
Sys BP decrease in upright
position (mmHg)
<10
11 29
>30
0
1
R-R intervals ratio in upright
position
>1.04
1.01 -1.03
<1 00
0
1 <1.00 1
Diastolic BP increase during
hand grip test (mmHg)
>16
11-15
<10
0
1
Respiratory dysrhythmias >15
11-14
<10
0
1
Valsalva quotient >1.21
<1.10
0
1
DAN Sc or i ng DAN Sc or i ng
Autonomic Nervous
System
Scoring
Normal 0 - 0.5
Early Change 1 - 1.5
Definitive Modification 2 - 3.5
Severe Impairment 4 - 5
BellavereFetal.BrMedJ(ClinResEd)1983;287:61
Nephropathy
Retinopathy
I h i h t di CHF d di th Ischemic heart disease, CHF and cardiomyopathy
To To Assess St i f f Joi nt Syndr ome Assess St i f f Joi nt Syndr ome
- Stiffness in hand joints
- Prayer Sign- inability to approximate the palmar
surfaces of phalangeal joints despite max effort
Palmprinttest Degreeofinterphalangealjoint
involvementassessedbyscoringtheinkimpression
madebypalmofdominanthand
- Non-familial short stature
- Tight-waxy skin
Investigations
- X-ray CS to delineate limited atlanto-axial extension
PalmPrintTest
Grade0 Allphalangeal
areasvisible
Grade1 Deficiencyinthe
interphalangealareasof4
th
&/or 5
th
digit
Apositive"prayersign"
&/or5
th
digit
Grade2 Deficiencyinthe
interphalangealareasof2
nd
to5
th
digit
Grade3 Onlytipsofdigits
seen
Nephropathy
Retinopathy
I h i h di CHF d C di h Ischemic heart disease, CHF and Cardiomyopathy
Electrolyte & metabolic derangements
8
To Assess El ec t r ol yt e & To Assess El ec t r ol yt e &
Met abol i c Der angement s Met abol i c Der angement s
- Non-compliance of drug
- Severe infection or starvation
P t l i th t f d / k - Poor control in the past few days/weeks
- S/S of hypoglycemia or ketoacidosis
Investigations
- ABG &electrolytes
Cl i ni c al Si gni f i c anc e Cl i ni c al Si gni f i c anc e
Poorglycemiccontrol impairshostresponsetoinfection,
adecreaseintensilewoundstrength,proinflammatory
responseasepcprecauons
Postoperative complications
- wound complications
- impaired anastomotic healing
Trophiculcers,worsensneurologicaloutcome,postop
cardiaceventsaggravated,edthromogenic
complications
Ac ut e Ac ut e Adver se Ef f ec t s of
Hyper gl yc emi a
Acute complications
Dehydration - osmotic diuretic effect of glycosuria
Acidemia - accumulation of lactic &/or ketoacids Acidemia accumulation of lactic &/or ketoacids
Hyperviscositywiththrombogenesis
Coma
Permissive Hyperglycemia Permissive Hyperglycemia
Unacceptable Unacceptable
DecreasedmobilityinTM&cervicalspinejoints
restrictedneckmovements&difficultairway
Proliferativeretinopathy vitreousHge onL&I
IHD - myocardial ischemia
Hypertension - pressor response to L&I, poor
intraoperative BP control, cerebrovascular infarction
Autonomicneuropathy
compensatorycardiovascularresponse IPPV,bld loss,
positionchange,drugs
Bluntedresponsetoatropine
Fullstomach riskofaspiration,longerpreopfasting,RSI
Impairedventilatoryresponses
Increasedriskofdysrhythmias
Urinarystasis unnecessarybladdercatheterization
Lossofsignsofhypoglycemia
Hypothermia increasedriskintraoperatively
Suddencardiacdeath
Neuropathy&vascularcompromise:
riskforischemiainpressurepointswhile
shifting&positioning
incidenceofnerveinjury&ischemia
implicationsforRA
Renaldisease impaireddrugexcretion, renal ischemia,
more likely to develop postoperative renal failure
Associatedcomplications DKA/NKHC
hypoglycemia
9
Di abet es & Ac c el er at ed Di abet es & Ac c el er at ed
Physi ol ogi c Agi ng Physi ol ogi c Agi ng
Adverseperioperativeoutcomesrepeatedly&substantially
correlatedwithageofpatient
Type1diabeticwithpoorcontrolofBSagesapprox1.75
yrs physiologically for every chronologic yr of disease 1 25 yrsphysiologicallyforeverychronologicyrofdisease,1.25
yearsifBShasbeencontrolledtightly
Type2diabeticagesabout1.5yrsforeverychronologicyr
ofdisease,1.06yrswithtightcontrolofBS&BP
Diabeticsphysiologicage(RealAge)considerably
higherthancalendaragejustbyvirtueofhavingdisease
DM & Sur ger y
Increased morbidity & mortality in
all diabetics undergoing surgery
Intensivemonitoring
Per i oper at i ve Pr obl ems i n
Di abet i c Pat i ent
Surgical induction of stress response with catabolic
hormone secretion antiinsulin effect insulin
requirements in this period unpredictable
Surgery associated with a reduction in insulin sensitivity
Interruption of food intake, esp after GI procedures
Altered consciousness, which masks sx of hypoglycemia
Circulatory disturbances associated with anaesthesia &
surgery, which alters absorption of subcutaneous insulin
Anaest het i c Techni que & t he
Di abet i c Pat i ent
Anaesthetic techniques (GA/RA or N blockade) may
modulate secretion of catabolic hormones & any residual
insulin secretion
Perioperative increase in epinephrine & cortisol conc in
pts under GA is blocked by EA much less disruption
of glucose metabolism
Induction agents affect glucose homeostasis
perioperatively clinically not significant
Anaest het i c Agent s & DM
Etomidate blocks adrenal steroidogenesis cortisol syn
hyperglycemic response to surgery by approx 1mmol/L
Benzodiazepines in high doses
-secretion of ACTH production of cortisol
th ti ti l ti i l i - sympathetic stimulationin glycemic response
Highdose opiate techniques block SNS & hypothalamic-
pituitary axis abolish hyperglycemia
Halothane, enflurane, isoflurane inhibit insulin response to
glucose in a reversible & dosedependent manner
Anaest het i c Management Goal s Anaest het i c Management Goal s
Tomaintainglycemiccontrol
Toavoidfurtherdeteriorationofpreexistingend
organdamage
Toshiftpatientsoononpreoperativeglycemiccontrol
drugsASAP
10
Case 1 Case 1
60 year old, 60 kg female; with Ca. head of pancreas
scheduled for Whipples Procedure
Known diabetic on Metformin and Glibenclimide, BD dose
Hypertension, CAD under check
BG: (F) = 120, (PP) = 170 mg.dl
-1
Switch over to insulin pre-op?
Pre-op orders?
Cl assi f i c at i on of Sur ger i es
Classification Duration Effect Examples
Minor
(onlyskin,mucus
membranes&
connectivetissue
resected)
<30mins Unlikelyto
interferewith
DMtreatment&
diet
Cystoscopy
Intermediate 30 min 3 hrs Might interfere Laminectomy Intermediate 30min3hrs Mightinterfere
withtreatmenton
dayofsurgery
Laminectomy,
Cholecystectomy,
internalfixationof
fractures
Major
(bodycavity
entered,organsare
removed,ornormal
anatomyaltered)
>3hrs Longer
interferencewith
management&
diet
Bowelresection
Shi f t To I nsul i n Shi f t To I nsul i n ??
Wellcontrolledtype2DM(onOHA),minorsurgery,donot
requireinsulin
Poorlycontrolledtype2DM,alltype1DMhavingminor
surgeryrequireinsulin
All diabetics having major surgery need insulin Alldiabeticshavingmajorsurgeryneedinsulin
Formajorsurgery,ifPG>270mg/dLpreoperatively,surgery
delayed&rapidcontrolachievedwithIVinsulin
IfPG>400mg/dL,surgerypostponed&metabolicstate
stabilized
Ai ms of Per i -oper at i ve
Gl uc ose Management
Avoid hypoglycaemia (intraop BG 120-180mg/dl)
Minimize hyperglycemia
Avoid loss of electrolytes (potassium, magnesium &
phosphate)
Prevent lipolysis &proteolysis
H. J. Robertshaw1, G. M. Hall. Anaesthesia 2006;61:11871190
Pr eoper at i ve Or der s Pr eoper at i ve Or der s
1
st
on list
If taking a long acting insulin, convert to short/
intermediate acting several days prior & stabilize
Stop long acting sulfonylureas (chlorpropamide) p g g y ( p p )
OHA/ insulin to continue one day prior to surgery
On morning of surgery, omitoralhypoglycemic/normalSC
insulin
InvestigationsFBS,serumelectrolytesmorningofsurgery
Pr eoper at i ve Or der s Pr eoper at i ve Or der s
NPOfor12hrspreop
Gastricprokineticagent+H
2
blocker
Sedation&anxiolysis,othermedications(anti
h t i ' ) ti d hypertensive's)continued
Insulin&IVfluidsonmorningofsurgery accordingto
regimen
Toarrangefordextrostix,insulin,glucometeretc
11
I nt r aoper at i ve Management
Intraoperativeserumglucoselevelsshouldbemaintained
between120and180mg/dl
1unitinsulinlowersBG2530mg/dl
I iti l h l t f ti i li i f i t t l d il Initialhrlyrateforcontinuousinsulininfusion=totaldaily
insulinreqm/24
Typicalrate0.02U/kg/hror1.4U/hrin70kgpt
Insulininfusionpreparedbymixing100Uregularinsulin
in100mLNS(1U/mL)
Cont d..
Insulininfusionaccompaniedbyaninfusionof5%D
inhalfNSwith20mEqKClat100150mL/hr
Insulininfusionrequirementshigherfor
CABGsurgery
solidorgantransplant
ptsreceivingsteroids
ptswithsevereinfection
ptsreceivinghyperalimentation
ptsonvasopressorinfusions
Algorithm1:Startformostpatients
I npat i ent I nsul i n Al gor i t hm
Stoelting'sAnesthesiaAndCoexistingDisease
Cont d..
Algorithm2:Startifptrequireshigherinsulinor
receiving >80U/dinsulinasoutpatient
Movingup:algorithmfailuredefinedasBGoutsidegoal
rangefor2hrs&leveldoesnotchangebyatleast60
mg/dLwithin1hr
Movingdown:WhenBGis< 70mg/dLfortwochecksORif
BGdecreasesby> 100mg/dLinanhour
Ptmonitoring:CheckBGeveryhruntilitiswithingoal
rangefor4hr,thenevery2hrfor4hr,&ifitremainsat
goal,maytoevery4hr
The Vel l or e Regi men The Vel l or e Regi men
Ondayofsurgery,OHA&insulinomitted,allptshadBG
measuredat6 AM
Insulin5Uin500mLD5Wstartedinwardat8 AMusing
measuredvolumeset,@100mL/hruntiltimeof
operation
Intraoperative BG control with 1 U of insulin for every 1
50 mg of BG value more than 100 mg/dL added to 100 mL
of 5% dextrose in a measured volume set
Hourly monitoring of BG, BGmeasurementsfollowed
onlyuntilptsleavePACU
Simple & effective method , combines advantages of
combined glucose insulin & variable rate insulin infusion
* MiriamAetal.AnesthAnalg2004;99:598602
Mostoperativeptscanbemaintainedin120180mg/dL
range
withinsulininfusionrate1 2U/h
Serumpotassiummeasuredduringmajorabdominalsurgery,
supplementationgiveniflevels<3.5mEq/L
12
Post oper at i vel y Post oper at i vel y
RecommenceOHA 1/2dosewithfirstmeal
fulldosenextday
RecommencenormalSCinsulinwithfirstmeal
Majorsurgery continueinsulininfusion
regularinsulinonceptstartsorally
Adequatepainreliefdecreasescatabolichormone
secretion
Ti ght Cont r ol Regi men Ti ght Cont r ol Regi men
Indications ??
Pregnancy, CPB, neurological surgeries, reqr postop ICU
Advantages ??
Improve wound healing
Prevent wound infection
Improves neurological outcome Improves neurological outcome
Disadvantages?
No monitoring of K
+
More chances of hypoglycemia
Difficult in ward settings
Meticulous frequent monitoring
Mi chael Mi chael Roi zens Regi men Roi zens Regi men
Aim : To keep BS between 79-120mg/dl
Night before surgery do preprandial glucose
Start 5% D @ 50ml/hr (in 70 kg bw)
Piggyback infusion of regular insulin (50U insulin in
250ml of 0.9% NS) to dextrose
To saturates insulin binding sites of tubing-flush line with
60 ml of infusion mixture & discard flushing solution
Mi chael Mi chael Roi zens Regi men Roi zens Regi men
Insulin infusion rate (U/h) = Plasma Glucose/150 or
If on steroids/sepsis/obesity = Plasma Glucose/100
Intraoperatively monitor plasma glucose every 1-2 hrly
IVfluids nondextrosecontainingsolutions
If hypoglycemia <50mg/dL, give 15ml 50% dextrose IV
This regimen accomplishes its goals except in brittle
diabetics given high doses of steroids
Al ber t i s Al ber t i s Regi men Regi men
Omit morning dose of insulin
Start GKI (10, 10, 10) after checking BS and K
+
levels
@ 100-125ml/hr on morning of surgery
2-3 hrly blood sugar level charting 2 3 hrly blood sugar level charting
Advantages - simple, inherent safety
Disadvantages -fixedinsulinconc,necessarychangebag
eachtime,waterload,hyponatremia,hyperglycemia
Not Currently Recommended
Al ber t i s Regi men
Blood sugar
<5mmol/L ( 90mg/dl)
5-10mmol/L (90-180mg/dl)
Infusion
10%D+5U Insulin+10 mEq K
+
+
10-20mmol/L (180-
360mg/dL)
>20mmol/L (>360mg/dL)
+
+
IfplasmaK
+
>4mEq/L,thenstopKC1,ifplasmaK
+
is
<4mEq/L,to2gper500mlbottle
13
Hi r schs Var i abl e Rat e Regi men Hi r schs Var i abl e Rat e Regi men
To maintain BG b/w 120-180mg/dL
Mix 50U insulin in 500ml NS (10ml=1U;
1U/hr=10ml/hr), infuse @ 0.5-1.0 U/hr
Not
Check BS hourly during surgery
Blood sugar level
<80 mg/dL
80-120 mg/dL
120-180 mg/dL
180-240 mg/dL
>240 mg/dL
Infusion rate
Turn off infusion, give 25ml
of 50% D, recheck in30 min
insulin infusion by 0.3U/hr
No change in infusion
infusion by 0.3U/hr
infusion by 0.5U/hr
Not
Commonly
Used
Adsor pt i on of I nsul i n Adsor pt i on of I nsul i n
Significantamountsofinsulinadsorbedontogivingsets:
highvolume,lowinsulinconcregimenused
Reducinginitialratesofinsulindelivery
Insolwithconcofinsulinof10U/L,effectisminimal
Strategiestominimize useconcentratedsolutions
usesmallercontainers
useshortertubings
primetubingwithinsulinizedsol
addwholeblood/humanalbumin
Fl ui d & Vol ume Repl ac ement Fl ui d & Vol ume Repl ac ement
Ringers lactate? Bank blood?
Lactate is a gluconeogenic substrate, RL = 28 mEq/L
Bank blood = variable amounts (anaerobic metabolism
during storage)
Hepatic conversion to glucose aggravation of stress-
induced hyperglycemia
RL/blood NOT contraindicated but inappropriate as
these can confound calculation of glucose load &
insulin requirements somewhat
Hypogl yc emi a
Plasma glucose level less than 70mg/dL (4mmol/L)
Exacerbated by simultaneous administration of alcohol,
OHA, ACE inhibitors, MAO inhibitors, nonselective
blockers, in poorly controlled pts, liver disease, fasting,
sepsis, equipment failure seps s, equ p e t a u e
Adrenergic symptoms: sweating, tachycardia,
palpitations, restlessness, pallor
Neuroglycopenic: fatigue, confusion, headache,
somnolence, convulsions, coma
Hypogl yc emi a Hypogl yc emi a
Awake patient - profuse sweating, tachycardia, pallor,
light-headedness, confusion & incomprehensible speech
UnderGA initiallysxofsympatheticstimulation:
sweating,tachycardia,hypertension,&/ordilatedpupils
Treatment - if conscious oral glucose (sugar cube, juice)
- if unconscious
25ml of 50%D IV (BGlevel100mg/dl)
glucagon 0.5-1.0 mg IV/IM/SC
Case 1 Case 1
60 year old, 60 kg female, with Ca. head of pancreas
scheduled for Whipples procedure
Known diabetic on Metformin & Glibenclimide, BD dose
Hypertension, CAD under check
Shifted & stabilized on regular insulin
Epidural + GA planned;
Considerations during CN Blockade?
14
CNB & Ner ve Bl ock s CNB & Ner ve Bl ock s
LA requirements lower
Risks of nerve injury higher
Risk of infection greater
Combination of LA with epinephrine may pose greater
risk of ischemic or edematous nerve injury (or both) in
diabetic patients
Use of ultrasound recommended, avoid PNS - higher
stimulating current reqd*
*Reg Anesth Pain Med;2003:28:479-82
CNB & Ner ve Bl ock s CNB & Ner ve Bl ock s
Document peripheral neuropathy
Relative contraindication
Keeps patients & relatives informed
Avoids medico-legal issues later on
Pt with autonomic neuropathy - profound hypotension may
occur with deleterious consequences in a pt with
coexisting CAD, cerebrovascular or renovascular disease
Use of continuous techniques DOES NOT predispose pt to
persistent neuropathy after surgery*
* Anesth Analg 2003; 96:247-52
Advant ages of Advant ages of RA i n RA i n D Di abet i c s i abet i c s
Awake pt, early recognition of intraop hypoglycemia
risk of difficult intubation, aspiration, PONV
Rapid return to diet & insulin/OHA
risk of thromboembolism, phantomlimbpain?
Metabolic effects of anaesthetic agents avoided
Insulin response to hyperglycemia
high thoracic (T1-T6) blockade inhibited
low blockade (T9 - T12) no effect
EA blocks catecholamine release irrespective of segmental
level, but prevents in BG only if block height T6/T8
Case 2 Case 2
40 yr, 45kg lady, known diabetic on OHAs
High grade fever x1wk, vomiting x 2d, altered sensorium x 12h
P=180 bpm, BP=70/40 mmHg, BG=470 mgdl
-1
DKA
Blood ketones (+++), pH=6.8, Na
+
-116 mEq/L, K
+
- 3.4 mEq/L,
HCO
3
-10 mEq/L, PCO
2
- 34 mmHg, PO
2
- 78 mmHg
Emergency laparotomy
Yes/No? How quickly? What till then?
DM & Emer gency Sur ger y
Littletimeavailableforstabilizationofpatients
23hrsufficientforcorrectionoflifethreateningfluid&
electrolyteimbalance
FutiletodelaysurgerytoeliminateKA completelyif
d l d l/ f h b l d underlyingconditionl/tfurthermetabolicdeterioration
LikelihoodofI/Ocardiacarrhythmia&hypotensionif
volumedepletion&hypokalemiaatleastpartiallytreated
Monitormoreoften
Ti l l Then Ti l l Then
Start aggressive treatment of DKA
Aims: - Rehydration (water and salt) reestablish U/O
- Lower blood sugar
- Correction of potassium depletion
Partial correction of hyperglycemia, metabolic acidosis
& ketosis
Start treatment of infectious process, if present
Definite Trend Towards Metabolic Improvement
15
Tr eat ment of DKA
Volume resuscitation-start an IV infusion of 0.9 % NS as
-1 litre over 30 min
- then 1 litre over 1 hr
- then 1 litre over 2 hrs
Continue 2-4 hourly until BG below 250mg/dL, then add
>100
ml/kg
5% D to IV fluids, then 0.45% NS @ 250ml/hr
Use BP, HR, CVP, conscious level to judge fluid amount
Insulin - 50Uin50ml0.9%NS,atafixedr/o0.1U/kg/hr,
i.e.7ml/hrin70kgpt calledfixedrateIVII
Maxr/oinBGfairlyconstant75to100mg/dL/hr
Tr eat ment of DKA
K
+
deficitsrangefrom3to10mEq/kgbwt
High blood K
+
initially, falls as BG level , measure hrly
Put 10mEqK
+
in 1
st
litre of NS, then 10-40 mEq per litre
subsequently, depending on K
+
level (<5.5mEq/L) q y p g ( q )
If K
+
measurements unavailable, put 10mEq KCl in each
litre of fluid, if low K+ levels initially, delay insulin
Other measures -100 % O
2
, consider HCO
3
if pH<7.0,
bicarb conc < 10 mEq/L, hypotension unresponsive to IV
fluids
Intra-operative Management?
Post-operative Management? Post-operative Management?
What do persistent ketosis with S. bicarb
< 20 mEq/L & normal BG indicate?
Cont d.. Cont d..
Continue management started for DKA, monitor more often
Achiever/ofallofketonesofatleast0.5mmol/L/hr,HCO
3
shouldby3mmol/L/hr,BGshouldby3mmol/L/hr
Usually be a rapid in insulin requirements after surgery
metabolic control regained
need for careful & frequent monitoring of BS &
metabolic parameters
Persistent ketosis with S. bicarb < 20 mEq/L & normal
BG indicate need for intracellular glucose & insulin for
reversal of lipolysis
Resol ved !!! Resol ved !!!
TheguidelinesfromAmericanDiabetesAssociation
(ADA)considerDKAresolvedwhen
Bloodglucose<200mg/dl
Bicarbonateis18mEq/L
VenouspHis>7.3
Calculatedaniongap12mEq/L
ThecriteriaforresolutionofHHSinclude
Improvementofmentalstatus
Bloodglucose<300mg/dL
Serumosmolalityof<320mOsm/kg
Ar eas of Cont r over sy Ar eas of Cont r over sy
CanyoumeasurevenousratherthanarterialHCO
3
&pH
differencebetweenvenous&arterialpHis0.020.15pH
units&b/wHCO
3
is1.88mmol/L
Notnecessarytousearterialbloodtomeasureacidbase
status
Bestpracticeinmonitoringresponsetotreatment
KetonemiahallmarkofDKA bloodketonesmeasurement
Isfluidresuscitationwithcolloidbettermore
physiologicaltoreplaceelectrolytelosswithcrystalloids*
*Perel 2007
16
Cont d..
Isaprimingdose(bolus)ofinsulinreqd notnecessary
providedinsulininfusionstartedpromptlyatadoseofatleast
0.1U/kg/hour
KitabchiAEetal.DiabetesCare2009;32:1335
Isintravenousphosphatereqd phosphatedeficitsinDKA
substantial,averaging1mmol/kg
Noevidenceofbenefitofphosphatereplacement&routinely
notrecommended
Ifrespiratory&skeletalmsweakness,orlevelbelow1.0
mg/dL,phosphatemeasurement&replacementshdbe
considered LiuPetal.JChinMedAssoc2004;76:355359
DM Wi t h Unc ont r ol l ed BS DM Wi t h Unc ont r ol l ed BS For For
Semi Semi --em em Tomor r ow Tomor r ow
Most of the poorly controlled diabetics can be controlled
in about 12 hrs
Start insulin infusion
Give sufficient glucose & potassium
Check blood gases & blood glucose hourly
Hemodynamic stability
Diabetic Ketoacidosis (DKA) vs.
Hyperglycemic Nonketotic Coma
(HNKC) (HNKC)
Profound dehydration in an elderly comatose without
Kussumauls respiration !!
Hyperglycemia osmotic diuresis plasma volume
contracts renal insufficiency (B urea > 100 mg/dl) y ( g )
inability to excrete glucose more hyperglycemia
(BG >500mg/dl) severe hyperosmolarity
Severe hyperosmolarity lethargy, confusion
intake of fluids, also polyuria coma
Essent i al s Of Di agnosi s Essent i al s Of Di agnosi s
DKA
BG > 250 mg/dl
pHa < 7.3
HCO
3
< 15mEq/L
NKHC
BG > 600 mg/dl
pHa > 7.3
HCO
3
> 15mEq/L
Anion gap > 12
Moderate/severe ketonemia
Moderate/severe ketonuria
S.osmolarity <310 mOsm/L
Normal anion gap
Absent/minimal ketonemia
Urinary ketones -/minimal
Osmolality > 320 mOsm/kg
S.osmolarity >350 mOsm/L
Tr eat ment - NKHC
More than 10 liters of fluid deficit; 6-8 liters corrected over
first 12 h with 0.9% NS
5% glucose with 0.45% saline- when BG <300mg/dl
Insulin infusion @ 0.1U/kg/hr
If BG does not fall by 50mg/dl in 1
st
hr, double insulin dose
K+ replacement - as in DKA, if level<3.5 mEq/L, withhold
insulin, give 40mEq/kg/hr
17
Why Avoi d Pr ec i pi t ous Fal l s i n
Bl ood Gl uc ose ??
Extreme hyperglycemia - brain accumulates idiogenic
osmoles (glucose, polyols, free amino acids) to prevent
cerebral osmotic dehydration
As the movement of these osmoles across BBB is very
slow relative to water, hence
Rapid reduction in BG leaves brain hyperosmolar relative
to plasma development of osmotic cerebral edema
Case3
25 year, pregnant lady, diagnosed as diabetic, for
LSCS
WhatisGestationalDM? at s Gestat o a ?
Timeofoccurrence?
Relevance?
Di agnosi s of GDM Di agnosi s of GDM
Perform a 75-g OGTT, at 24-28 weeks gestation in
women not previously diagnosed with overt DM
OGTT performed in morning after an overnight fast of at
least 8 h &afteratleast3dofunrestricteddiet(150g
carbohydrate/day)&unlimitedphysicalactivity
PG measurement - fasting, at 1 & 2 hrs
Diagnosis of GDM made when 2ormorevaluesmet
PG values: Fasting 92 mg/dL (5.1 mmol/L)
1 h 180 mg/dL (10.0 mmol/L)
2 h 153 mg/dL (8.5 mmol/L)
Gest at i onal DM
Glucose intolerance which has its onset in, or is first
diagnosed during, pregnancy
Typically occurs in latter half - AFTER organogenesis &
thus not a cause for congenital anomalies
Associatedwithinriskof fetalmacrosomia
morbidity
IUD duringthelast48weeksofgestation
edfrequencyofmaternalhypertensive
disorders
Relevanceofpreexistingdiabetesinpregnancy?
Gest at i onal DM
Establishedassociationb/welevatedmaternalBGduring
embryogenesis&highrateofspontaneousabortions &
majormalformations innewborns
Neonatalhypoglycemia,jaundice,polycythemia&
hypocalcemia as well hypocalcemiaaswell
Maternal hyperglycemia crosses placenta fetal cell
hypertrophy ed insulin sev neonatal hypoglycemia
Evidence that tight control of BG might be of benefit for
pregnant diabetic & her future offspring
Importantconsiderationsifpregnant
diabeticundergoesLSCS?
A i l ti i th Anyspecialprecautionsinthe
neonate?
18
GestationalDM
Insulinreqmesduringlaterhalfofpregnancy,plateauat
36wks
End-organs may be involved, watch out for DAN
I id f id i ti b DKA Incidence of acid aspiration may be more
Airway management may be more difficult
Glycosylation of Hb es RBC O
2
transport in pregnant pts
Monitor BS level of neonate
DKA
Gl yc emi c Cont r ol & Out c ome Gl yc emi c Cont r ol & Out c ome
i n I CU i n I CU
Insulinresistancedevelopsincriticalillness
Previouslytightlycontrolledbetween80110mg/dL
Nobenefitsintermsofmortalityorhospitalstaybutcan
increase risk of hypoglycemia expensive labour intensive increaseriskofhypoglycemia,expensive,labourintensive
Noevidencetosupportthatbenefitsofintensiveinsulin
therapyoutweighitsharms
*AmJMedQuality 2013:DOI:10.1177/1062860613489339
Moremoderaterecommendationtotargeta
BGconcbetween144 180mg/dL
Newer I nsul i n I nnovat i ons Newer I nsul i n I nnovat i ons
InhaledInsulin(pulm aerosoltherapy) Exubera/
Afrezza,fastactingformulation,inhaledbeforemeals
Insulinpatchtransdermaldeliverysystem
Oralspray,inwhichliquidinsulinisdeliveredviaan
aerosol spray device & absorbed through buccal mucosa & aerosolspraydevice&absorbedthroughbuccal mucosa&
oropharynxregion
Continuoussubcutaneousinsulininfusiondevice(CSII)
MedicationssuchasINGAPpeptidemaycauseregrowth
ofnormallyfunctioningisletcells(without
transplantation)
1
Interpretation of ABG Reports
Dr. A. K. Sethi
ABG = Arterial Blood Gases
Gases Gases in the Blood
(O
2
,CO
2
, CO, He, Kr, N
2
)
All Blood Gas machines
Measure pH, PaCO
2
, PaO
2
Calculate HCO
3
-
+
Interpreting ABG Reports
Calculate HCO
3
ABG 2 sets of Tests

Gases + Acid Base Status
Co-oximetry True values
Hb, SaO
2
, %COHb,
%MetHb, CaO
2
Why is it important to know about
Arterial Blood Gases ?
Blood Gases
Direct information about lung function
Why is it important to know about

Acid Base Status ?
Adequacy of Oxygenation in the arterial blood
Adequacy of CO
2
excretion
H
+
andHCO
3
concentration(pH)inPlasma
mustberegulated precisely
&constantlymaintainedatnormal levels
Acid Base Homeostasis
Enzyme activity Tissue Oxygenation Enzyme activity
Chemical reactions within cells
Force of Cardiac contraction
Hb Saturation with O2
O2 delivery
Tissue Oxygenation
Neurological & Muscular functioning
Vascular Response to Catecholamines
Response to effects of Medications
and,
many more activities . . . . . .
Blood pH < 6.8 and > 7.8 - Not Compatible with life
(Irreversible cell damage, Death)
Hb, HCT, FiO
2
, PaO
2
, PaCO
2
, pH, Na
+
, K
+
, SaO
2
(%)
RQ CO
2
produced:O
2
consumed, Set value, Can be fed
HCO
3
A
(Actual)
Parameter for non-respiratory component of acid-base balance
HCO
3
S
(Standard)
Parameter for non-respiratory component of acid-base balance
but reported after standardising at PCO
2
at 40 mm Hg,
Temperature 37C, SO
2
100%
Base Difference between normal quantity of Total Buffer Base (BB)
The Terminology ......
ase
excess or
deficit
q y ( )
and the BB calculated from Blood Sample. (+) or (-).
Calculated from entered (actual) Hb value, measured pH &
PCO
2
values.
Standard
Base
excess
Difference between normal quantity of Total Buffer Base (BB)
and the BB calculated from Blood Sample. (+) or (-).
Calculated from a standard Hb value of 6 gm%, pH of 7.4 &
PCO
2
of 40 mmHg.
BB (Buffer
bases)
Sum of all buffer anions in blood
(Hb, HCO
3
, Protein, Phosphate)
TCO
2
Content (SerumCO
2
) HCO
3
conc. + dissolved CO
2
in plasma
O
2
CT, CaO
2
, O
2
content Hb bound O
2
+ Plasma dissolved O
2
A-aDO
2
Difference between PO
2
(Alv) and PO
2
(art)
P50
Semisaturation pressure = Partial pressure of
O
2
at which Hb is 50% saturated
The Terminology ......
2
LAC Lactate concentration
GLU Glucose concentration
Ca Calcium ion concentration
Li Lithium ion concentration
+ + . .
2
Know Normal & Reference Values for Interpretation
K
+
3.5 5.1
Ca
+
1.12 1.32
Cl
-
97 100
Base excess (mEq/L) 0 2
TCO
2
Content (mEq/L) 27
Hb (gm%) Measured,
Calculated or Fed
(HCT/3)
HCT (%) Measured or
Calculated (3xHb)
FiO
2
Fed
TCO
2
Content (mEq/L) 27
BB (mEq/L) 48
O
2
Sat (%) >95%
O
2
CT (ml/dL) 16 22
P50 mmHg 27
A-aDO
2
(mmHg) 5 15,25,100
RQ 0.85
PaO
2
(mmHg) 80 100
PaCO
2
(mmHg) 35 45
pH 7.35 7.45
HCO
3
A (mEq/L) 22 26
Na
+
135 145
Arterial, Venous or Mixed
Arterial Venous
Askthepersonwho
aspiratedthesample
Bloodpulsates Blooddoesnot pulsate
Syringeplungermay
riseonitsown
Syringeplungernever
risesonitsown
PO
2
PO
2
>40mmHg PO
2
<40
(often < 30 mmHg).
Sometimes, there is no way to know if the sample is arterial or venous !
(often<30mmHg).
O
2
saturationvalues SaO
2
>75% SvO
2
<75%
No.ofattempts Single
orMultiplepunctures
Singlepuncture,
rapidfilling
Multiple,LowerPO
2
duetovenousmixture
pH Abnormalornormal,
Notdiagnostic
Abnormalornormal,
Notdiagnostic
PCO
2
Abnormalornormal,
Notdiagnostic
Abnormalornormal,
Notdiagnostic
Venousadmixture(CHD) LowerPaO
2
values Venousadmixture.
Basic Precautions (Sampling)
1. Ensure a Steady State of Oxygenation & Ventilation (3,20,30 min)
2. Precautions for arterial blood sampling Site, Puncture, Cannula,
Heparin, Syringe
3 Do not keep the sample exposed to air - Air bubble in Syringe 3. Do not keep the sample exposed to air - Air bubble in Syringe
4. Do not delay the processing (O
2
, CO
2
, pH, Ca
++
) Otherwise, keep
sample in Ice. (never beyond 10-15 min) (Icing K
+
)
5. Analyze Step-by-Stepand completely
Ensure Steadystateofoxygenationandventilation
To reach to a Steady State
3minforhealthylungs
20 min in COPD lungs
Basics
20mininCOPDlungs
Before you withdraw a sample for ABG
Allow 20min,afteranychangesFiO
2
Allow 30min,afteranychangesinventilatoryparameters
Basics
Too much & Too little Heparin in Syringe can alter results
ExcessiveHeparin PaCO
2
drops,pHrises
(LiberalFlushing, Samplingfromindwellingarteriallinewith
continuousflush)
Heparinisation of syringes
)
PredictionsonthepHchangenotpossible
Effectvariable HeparinalreadyAcidic
ToolittleHeparin
Clotformation
Blockadeinsamplinglineofmachine
What should be done ?
Type of Heparin Remarks
Liquid,NaorLiHeparin OnlyWettheinside Discardtherest.
Leavenovisibleheparininthesyringe.
Samplevolume=24ml
Dry,BalancedLithium,
Preheparinised, Preset
Syringes,Prescribed
i (23 50
Samplevolume=0.51,12, 3or5ml
concentrations(23,50,
80U)
3
1. Airbubbleinthesample
2. Leavingsampleexposedopentoair
Basics
AtmosphericAir
PO
2
160mmHg,PCO
2
almostZero
Patients PaO
2
Resulting Effect Remarks
<160mmHg PO
2
insamplewillrise Degreeofrise&fall
dependsuponinitialPaO
2
&durationofexposure
>160mmHg PO
2
insamplewillfall
PaCO
2
ResultingPaCO
2
ofanyairexposedsamplecanfall&thepHrise
Airbubbleinthesample
Basics
Air Bubble in Blood Gas Machine
- Erroneous readings, False very high PaO2
- Machine may not give any results
Basics
Do not delay the processing (O
2
, CO
2
, pH, Ca
++
)
- Process as early as possible, within 10-15 minutes
Otherwise keep it in ice-slurry (Icing K
+
)
If processing gets delayed & sample not kept in ice
PaO
2
fallsveryfast,PaCO2rises
Bloodcellskeepmetabolising,keepusingO2
atnormalorhightemperatures
Metabolismverylessatnear0C
IcedSamplesstablefor 1hr(?3hr)
UsualTurnaroundtime=1015min
Reading the Report Step-by-Step
Step 1
Check if the required parameters have been correctly fed ?
Barometricpressure
Patientstemperature
Haemoglobin
(ifmachinedoesnotmeasure,doesnotcalculate)
FiO
2
Results in the report are bound to
change, get incorrect and misleading
if the above values are not correctly fed
AaDO
2
value[PAO
2
PaO
2
]ifP
B
&FiO
2
(PiO
2
)notfedcorrectly.
Alveolargasequation:PAO
2
=PiO
2
1.2(PaCO
2
)[PiO
2
=FiO
2
(P
B
47)]
OxygenationImpairment(Assess.) WrongifFiO
2
notfedcorrectly
Machinesalwaysanalysebloodat37 C
SampleofHyperthermic Patient=>37 C,GayLussacsLaw
MeasuredvalueofPaO
2
andPaCO
2
willbelessthanactual
SampleofHypothermicPatient=<37 C,GayLussacsLaw
Effects of Wrong Feedings
MeasuredvalueofPaO
2
andPaCO
2
willbemorethanactual
TemperatureChange ShiftingofODC CalculatedSO
2
,ODC@37C
Increase Right Higherthanactual
Decrease Left Lower thanactual
TrueassessmentofadequacyofO
2
inarterialblood(CaO
2
)can
onlybemadeifHb valuesareentered.SaO
2
&PaO
2
donot.
Hb affectsBufferBasevalues(Baseexcessordeficit)
4
Total O
2
attached
to Hb Content +
Total Dissolved O
2
carried by Plasma
Hb content (gm%)
O
2
carried by 1 gm Hb (ml)
Saturation Hb (SaO2)
PaO
2
Solubility Coefficient
15 x 1 34 x 100 (say) = 20 10 100 x 0 003 = 0 30
+
15 x 1.34 x 100 (say) = 20.10 100 x 0.003 = 0.30
+
= 20.40 ml / dL
15 x 1.34 x 85 (say) = 17.09 50 (say) x 0.003 = 0.15
+
= 17.24 ml / dL
8 x 1.34 x 100 (say) = 10.72 100 x 0.003 = 0.30
+
= 10.75 ml / dL
Most common mistake
FiO
2
notenteredwhilethesample
isfedinthemachine
%FiO
2
writtenonthereportlater
onmanually
Hb alsonotenteredatthetimeof
FiO
2
feedingsamplebuttoldlateron
Interpretation of PO
2
affected adversely
A-aDO
2
values are wrongly calculated
(PAO
2
calculated from PiO
2
)
Interpretation of adequacy of Oxygenation
affected adversely if Hb not fed properly.
If FiO
2
not fed properly
Step - 2
Analyse the Adequacy of Oxygenation
(i) Look at PaO
2
and SaO
2
first
PaO
2
(mmHg) SaO
2
(%)
Normalvalues(onair) >80 >95
Mildhypoxemia 6079 9094
HealthyAdult SeaLevel,RoomAir,AaO
2
=5mmHg,PAO2=101
Moderatehypoxemia 4059 7589
Severehypoxemia <40 <75
PaO
2
, SaO
2
- Important
Low PaO
2
, Low SaO
2
= Surely something wrong in terms of Oxygenation
Low PaO
2
= degree of hypoxemia
Saturation of Hb (SaO
2
) is dependent upon PaO
2
Never rely totally on PaO
2
& SaO
2
Look at CaO
2
also
(ii) Relate PaO
2
with FiO
2
Classify Hypoxemia
O
2
% x 5 = PaO
2
Uncorrected
Hypoxemia
<60,onO
2
Refractory
PaO
2
Inspired O
2
% PaO
2
mmHg
30 > 150
40 > 200
50 > 250
80 > 400
100 > 500
Excessively
Corrected
Corrected 60100,<predicted
>100,<predicted
Responsive
100%Oxygen,Flow
Rate
FiO2achieved
1L/min 0.24
Predicting FiO2 with Low Flow Devices
2L/min 0.28
3L/min 0.32
4L/min 0.36
5L/min 0.40
6L/min 0.44
4%
100%Oxygen,FlowRate FiO2achieved
5 6 L/ i 0 40
5 6L/min 0.40
6 7L/min 0.50
7 8L/min 0.60
10%
5
100%Oxygen,FlowRate FiO2achieved
6L/min 0.60
7L/min 0.70
8L/min 0.80
9L/min 0.80
10L/min 0.80
10%
Predicting FiO2 with High Flow Devices Venturi
Fairly accurate
(iii) Find if Oxygenation is adequate or not CaO
2
PaO
2
and SO
2
may not give true estimate.
Low PaO
2
but Oxygen Content still adequate . (V/Q mismatch)
Normal PaO
2
, still profound hypoxemia. (Anaemia, Altered affinity of Hb for O
2
)
Calculated SaO
2
may mislead & show false normal results. (CO, MetHb )
Total Oxygen Content
CaO
2
measured directly or calculated by O
2
content equation.
CaO
2
= Hb(gm%) x 1.34 x SaO
2
+ 0.003 x PaO
2
(mmHg).
(If no Co-oximeter in the machine, SaO
2
is calculated from PaO
2
, ODC)
PaO
2
= 89.2 mmHg : OK
SaO
2
= 97.3 % : OK
Correlate FiO2 of 60% with PaO
2
.
PaO
2
of 89.2 - very less than predicted (300).
Oxygenation impaired.
Corrected Hypoxaemia
CaO
2
= 4.2 ml/dl : Very low (16-20)
Oxygenation grossly inadequate
CaO
2
= 4.2 ml/dl : Very low (16-20)
Oxygenation grossly inadequate
Reading the Report Step-by-Step
id B Acid Base Status
Terminology for Acid Base Homeostasis
Acidemia : Blood pH < 7.35
Acidosis :
A primary physiologic process that,
occurring alone, tends to cause acidemia
(e.g., respiratory acidosis from hypoventilation
or metabolic acidosis from decreased perfusion or shock) p )
Alkalemia : Blood pH > 7.45
Alkalosis :
A primary physiologic process that,
occurring alone, tends to cause alkalemia
(e.g., respiratory alkalosis from acute hyperventilation
or metabolic alkalosis from excessive diuretic therapy)
6
Terminology
Primary acid-base disorders
Respiratory Acidosis, Respiratory Alkalosis, Metabolic Acidosis, Metabolic Alkalosis
manifestasinitialchangesinPaCO
2
orHCO
3
First
Change
Disorder Change Primary
disorder
Effect pH
Rises Respiratory Acidemia Falls
PaCO
2
Respiratory
Rises Respiratory
acidosis
Acidemia Falls
Falls Respiratory
alkalosis
Alkalemia Rises
HCO
3
Metabolic
Rises Metabolic
alkalosis
Alkalemia Rises
Falls Metabolic
acidosis
Acidemia Falls
SecondarychangesinHCO
3
orPaCO
2
occur inresponsetotheprimaryevent
Compensation
when the acid-base imbalance exists over a period of time
Terminology
tonormalizepH
Donebytheorgansystemwhichisnotprimarilyaffected
Respiratorycompensationformetabolicdisorders
Metaboliccompensationforrespiratorydisorders
Step 3 : Analyse pH (First Impression)
pH Analysis
7.35 7.45
(7.4)
Normal No acid-base disorder
Or, Compensated disorder
(Mixed disorder)
7.34 Acidemia Uncompensated Acidosis
Or, Partially compensated
7.46 Alkalemia Uncompensated Alkalosis
Or, Partially compensated
Acidemia (pH 7.34) Alkalemia (pH 7.46)
Mild 7.30 7.34 7.46 7.50
Moderate 7.20 7.29 7.51 7.54
Severe < 7.2 > 7.55
Incompatible with life < 6.8 > 7.8
Step 4 Know the Primary disorder
- Respiratory or Metabolic ?
Respiratory
Change Disorder PaCO
2
pH Primarydisorder
>45 Respiratoryacidosis
PaCO
2
Respiratory
<35 Respiratoryalkalosis
If pH & PaCO
2
move in opposite directions
Primary defect is Respiratory.
If pH is not moving in opposite direction to PaCO
2
Primary defect is Not Respiratory (Metabolic).
Change Disorder HCO
3
pH Primarydisorder
HCO
3
Metabolic
>26 Metabolicalkalosis
......Step 4
Analyse the Primary disorder
- Respiratory or Metabolic ?
Metabolic
HCO
3
(base)
Metabolic
<22 Metabolic acidosis
If pH moves in same direction as HCO
3
Primary defect is Metabolic

If pH moves in opposite direction to HCO
3
Primary defect is not Metabolic (Respiratory)
Step 5 : Analyse if Compensation ? See pH
Compensation - Body tries to bring pH towards normal, with time
Lungs and kidneys are primary buffer response systems
pH outside normal range Uncompensated or Partially compensated
pH in normal range Fully compensated, or Mixed disorder,
(or no acid base disturbance)
7
Step 6 : Calculate the Expected Compensation
- Match it with actual report
Compensations Base for Acid
(Formula for every 10 mmHg change in PaCO
2
)
Change in PaCO
2
Disorder Compensation (Kidney)
10 mmHg Acute rise
Respiratory acidosis
1 mEq/L rise in HCO
3
10 mmHg Chronic rise 4 mEq/L rise in HCO
3
10 mmHg Acute fall
Respiratory alkalosis
2 mEq/L fall in HCO
3
10 mmHg Chronic fall 4 mEq/L fall in HCO 10 mmHg Chronic fall 4 mEq/L fall in HCO
3
Compensations Acid for Base
(Formula for every 1 mEq/L change in HCO
3
)
Change in HCO
3
Disorder Compensation (Lungs)
1 mEq/L fall Metabolic acidosis 1.25 mmHg fall in PaCO
2
1 mEq/L rise Metabolic alkalosis 0.75 mmHg rise in PaCO
2
Match the Calculated Compensation with the Actual (Report)
Step 7 : Find out if the Disorder is Mixed ?
(1) Check relative movement of both pairs
pH PaCO
2
and pH HCO
3
If both pairs are moving & in correct directions
Mixed disorder
(2) pH = 7.4 , PaCO
2
or HCO
3
not normal Mixed disorder
(3) Presume the Primary disorder to be Respiratory or
Metabolic. Then analyse compensation
If analysis supports no compensation Mixed disorder
If values are < or > than expected values Mixed disorder
Step 8 : Unmask Hidden Metabolic Disorders
Use concept of Serum Electrolytes
Do not interpret any ABG data without Serum Electrolytes
(Na
+
, K
+
, Cl
-
, CO
2
)
3 Parameters need to be determined
1. Anion Gap and its change from normal ( AG)
2. Venous CO
2
and its change from normal ( CO
2
)
3. Bicarbonate Gap (BG)
Anion Gap and its change over normal
AG = (Routinely measured Cations Routinely measured Anions)
AG = (Na
+
+ K
+
) (Cl
-
+ HCO
3
)
Normal AG = 16 4 mEq/L
AG = (Na
+
) (Cl
-
+ CO
2
)
Normal AG = 12 4 mEq/L
Hidden Metabolic Disorders
Change in AG from normal ( AG) = Measured AG 12
Positive (+) or Elevated AG (> 16)
Metabolic Acidosis
Negative (-) or Low AG
Reduction in unmeasured Anions (Hypoprotienemia)
Excess unmeasured Cations (Lithium Toxicity)
Excess abnormal +vely charged proteins (Multiple Myeloma)
Halide ion measured as Chloride (Bromism, Cough syrups)
Venous CO
2
(Serum CO
2
) and its change from normal
Index of Plasma HCO
3
Total CO
2
= Plasma HCO
3
+ Dissolved CO
2
in Plasma
Normal = 24 30 mEq/L (27 mEq/L)
(Out of Range = An acid base disorder ALWAYS)
Change in Venous CO
2
from normal
( CO
2
) = 27 measured CO
2
Bicarbonate Gap
Unmasks the co-existence of 2 metabolic disorders
BG = AG - CO
2
BG = (Measured AG 12) (27 Measured CO
2
)
(Normal range of BG not agreed upon)
Positive (+) or Elevated BG = > + 6 mEq/L
Metabolic Alkalosis
Bicarbonate retention as compensation for Respiratory Acidosis
Negative (-) or Low BG = < 6 mEq/L
Metabolic Acidosis
Bicarbonate excretion as compensation for Respiratory Alkalosis
8
Shortcut to calculating BG
BG = AG - CO
2
= (Measured AG 12) (27 Measured CO
2
)
= [(Na
+
) (Cl
-
+ CO
2
) 12] [27 CO
2
]
= [(Na
+
Cl
-
CO
2
) 12] [27 CO
2
]
= Na
+
Cl
-
CO
2
12 27 + CO
2
]
= Na
+
Cl
-
39
Steps (Summary)
Step 1 : Check if the required parameters have been correctly fed?
Step 2 : Analyse the Adequacy of Oxygenation.
Step 3 : Analyse pH Acidemia or Alkalemia?
Step 4 : Analyse the Primary disorder - Respiratory or Metabolic ?
Step 5 : Find if Compensation ?
Step 6 : Calculate the Expected Compensation. Match it with actual.
Step 7 : Find out if the Disorder is Mixed ?
Step 8 : Unmask Hidden Metabolic Disorders.
1
J.S Haldane-1917
Father of modern O
2
Therapy
O
2
lack not only stops the machine,
but totally ruins the supposed machinery
2
Hb
3
Hb 7 gm%
4
Hb 7 gm%, SpO2
5
Hb 7 gm%, SpO2 normal, PaO2 -
6
Hb 7 gm%, SpO2 normal, PaO2 normal
7
Oxygen content
8
Oxygen content 100 ml of blood
Hb x 1.39 x SpO2 + dissolved O2
PO
2
SPO
2
O
2
content
Normal 97mm Art. blood 14g x 1.39 x 100% + 0.3 = 20 ml
40mm Ven. blood 14g x 1.39 x 75% + 0.1 = 15ml
Tissue extraction 25% = 5ml
9
PO
2
SPO
2
O
2
content
Anaemic Art. blood 7g x 1.39 x 100% + 0.3= 10 ml
Ven. blood 7g x 1.39 x 50% + 0.1 = 5ml
10
PO
2
SPO
2
O
2
content
Ven. blood 7g x 1.39 x 50% + 0.1 = 5ml
?
11
Oxygen flux
DO
2
12
Oxygen flux = [Hb x 1.39 x SpO2 + dissolved O2] x C.O.
DO
2
= 20 x 50 = 1000 ml
13
DO
2
= 20 x 50 = 1000 ml
Oxygen consumption = 250 ml per minute
Cardio Pulm. ARREST
Hypoxia time = 4 min vs 3 min
14
DO
2
= 20 x 50 = 1000 ml
Cardio Pulm. ARREST
?
15
A B
Hb 14gm (normal) 7gm (Anaemic)
C.O. 5 L (normal) 3.5 L (Low)
SPO
2
30 % 90 %
O
2
Flux 300ml 300ml
Which patient is better placed ?
16
28 % @ 4 L P M
%age of O2 if flow is doubled (8 LPM) ?
%age of O2 if flow is halved ( 2 LPM) ?
17
Oxygen Therapy &
O
2
Delivery Systems
Dr. J. S Dali
MAMC
18
Aim of O
2
Therapy
To restore tissue O
2
towards normal
19
O
2
Cascade
Air
mitochondria
20
O
2
Cascade
Atm. Air
(dry)
Lower
Resp. Tract
(moist 37
o
c)
159mm Hg
(21 % of 760)
149mm Hg
(21 % of 713)
?
21
O
2
Cascade
Atm. Air
(dry)
Lower
Resp. Tract
(moist 37
o
c)
159mm Hg
(21 % of 760)
149mm Hg
(21 % of 713)
Humidification
6 Vol % (47mm Hg)
22
O
2
Cascade
149mm Hg
(21 % of 713)
?
Lower
Resp. Tract
(moist 37
o
c)
?
Alveolar
air
101mm Hg
23
O
2
Cascade
149mm Hg
(21 % of 713)
Lower
Resp. Tract
(moist 37
o
c)
Alv. ventilation
Alveolar
air
101mm Hg
(15 % of 673)
673 = 760 47 40
?
24
O
2
Cascade
149mm Hg
(21 % of 713)
O
2
consumption
Lower
Resp. Tract
(moist 37
o
c)
Alv. ventilation
Alveolar
air
101mm Hg
(15 % of 673)
673 = 760 47 40
25
O
2
Cascade
?
P
A
O
2
= 101mm Hg
(15 % of 673)
673 = 760 47 40
Alveolar
air
Arterial
blood
P
a
O
2
= 97mm Hg
P
a
O
2
= 100 0.3 x age (years) mm Hg
(A a) D O2 = 4 25 mmHg
26
O
2
Cascade
Venous admixture
P
A
O
2
= 101mm Hg
(15 % of 673)
673 = 760 47 40
Alveolar
air
Arterial
blood
P
a
O
2
= 97mm Hg
P
a
O
2
= 100 0.3 x age (years) mm Hg
(A a) D O2 = 4 25 mmHg
27
Venous admixture
(physiological shunt)
O
2
Cascade
Low VA/Q Normal True shunt
(normal anatomical shunt)
28
Venous admixture
O
2
Cascade
Pulmonary
(Bronchial veins)
Extra Pulm.
(Thebesian veins)
29
Venous admixture
O
2
Cascade
Pulmonary
(Bronchial veins)
Extra Pulm.
(Thebesian veins)
Normal = upto 5 % of cardiac output
30
O
2
Cascade
Utilization by tissue
Arterial
blood
P
a
O
2
= 97mm Hg
(Sat. > 95 %)
Mixed
Venous
blood
P
V
O
2
= 40mm Hg
Sat. 75%
Cell
Mitochondria
PO
2
7 37 mmHg
31
O
2
Cascade
Arterial
blood
P
a
O
2
= 97mm Hg
(Sat. > 95 %)
Mixed
Venous
blood
P
V
O
2
= 40mm Hg
Sat. 75%
Cell
Mitochondria
PO
2
7 37 mmHg
The critical level for aerobic metab. to continue
32
O
2
Cascade
Arterial
blood
P
a
O
2
= 97mm Hg
(Sat. > 95 %)
Mixed
Venous
blood
P
V
O
2
= 40mm Hg
Sat. 75%
Cell
Mitochondria
PO
2
7 37 mmHg
Pasteur point The critical level for aerobic metab. to continue
(PO
2
1-2 mmHg in mitochondria, 22mmHg in capillary)
33
Minimum gradient for O2 transfer
from capillary to cell.
Approx. 20 mm Hg
34
O
2
Cascade
Arterial
blood
P
a
O
2
= 97mm Hg
(Sat. > 95 %)
Mixed
Venous
blood
P
V
O
2
= 40mm Hg
Sat. 75%
Cell
Mitochondria
PO
2
7 37 mmHg
Pasteur point The critical level for aerobic metab. to continue
(PO
2
1-2 mmHg in mitochondria, 22mmHg in capillary)
35
Organ PvO2 (mm Hg)
Heart 23
Brain 33
Muscle 34
Liver 43
Kidney 56
Skin 60
_____________________________
Mixed venous 40
36
A B
SPO
2
30 % 90 %
O
2
Flux 300ml 300ml
37
A B
SPO
2
30 % 90 %
P
a
O
2
23 mm 60 mm
O
2
Flux 300ml 300ml
Min. gradient for O
2
transfer from cap. to cell (app. 20 mm Hg)
= sat. 20 30% = 200 300ml O
2
flux
Critical Level for O
2
delivery / critical O
2
flux 38
DO
2
= 20 x 50 = 1000 ml
?
39
PO
2
SPO
2
O
2
content
Ven. blood 7g x 1.39 x 50% + 0.1 = 5ml
?
40
PO
2
SPO
2
O
2
content
Anaemic 97mm Art. blood 7g x 1.39 x 100% + 0.3= 10 ml
41
Adequacy of tissue oxygenation
Mitochondrial PO
2
--- not practical
Mixed venous PO
2
--- practical basis
Mixed Venous sat. (SVO
2
)
V/s
Central Venous sat. (ScV0
2
)
Balance b/w oxygen delivery & consumption
42
Oxygen Therapy
Indications
43
Oxygen Therapy Indications
F
I
O
2
Barometric Pressure
P
I
O
2
44
F
I
O
2
- F
I
O
2
during anaes.
- Rebreathing
Barometric Pressure
- High altitude
P
I
O
2
45
F
I
O
2
- F
I
O
2
during anaes.
- Rebreathing
Barometric Pressure
- High altitude
P
I
O
2
P
A
O
2
O
2
Consumption Alveolar Ventilation
46
F
I
O
2
- F
I
O
2
during anaes.
- Rebreathing
Barometric Pressure
- High altitude
P
I
O
2
P
A
O
2
O
2
Consumption Alveolar Ventilation
-resp. depression
-Resp. muscle paresis
- resp.effort (trauma)
-airway obstruction
47
F
I
O
2
- F
I
O
2
during anaes.
- Rebreathing
Barometric Pressure
- High altitude
P
I
O
2
P
A
O
2
O
2
Consumption
-convulsions
-thyrotoxicosis
-shivering
-pyrexia
Alveolar Ventilation
-resp. depression
-airway obstruction
48
F
I
O
2
- F
I
O
2
during anaes.
- Rebreathing
Barometric Pressure
- High altitude
P
I
O
2
P
A
O
2
O
2
Consumption
-convulsions
-thyrotoxicosis
-shivering
-pyrexia
(7 % /
o
C)
Alveolar Ventilation
-resp. depression
-airway obstruction
49
Abn. Pulmonary shunt
- pneumonia
-lobar atelectasis
-ARDS
Abn.extra Pulm. Shunt
cong. heart disease
(R L )
PaO
2
50
- pneumonia
-lobar atelectasis
-ARDS
cong. heart disease
(R L )
PaO
2
Hypoxic hypoxia
51
52
Hypoxia due to hypoventilation
Slight increase in O
2
conc.
(Thus the importance of ventimask)
Higher O
2
conc.
Simple Rule
53
Hypoxia due to hypoventilation
Slight increase in O
2
conc.
(Thus the importance of ventimask)
Higher O
2
conc.
hypercapnoea
absence of cynosis
Simple Rule
54
55
- pneumonia
-lobar atelectasis
-ARDS
cong. heart disease
(R L )
PaO
2
Cell
PO
2
Hb concentration
-Anaemia
-CO poisoning
Perfusion
local - PVD, thrombosis
gen shock, Hypovol.,
card. Failure
cardiac arrest
Hypoxic hypoxia
Stagnant hypoxia
Anemic hypoxia
56
Benefit of O
2
therapy in Hypoxia
Hypoxic hypoxia (gas phase) + + +
Anaemic hypoxia (fluid phase const.) +
Stagnant hypoxia (fluid phase flow) +
Histotoxic hypoxia (tissue phase) -
57
Benefit of O
2
therapy in Hypoxia
Hypoxic hypoxia (gas phase) + + +
Anaemic hypoxia (fluid phase const.) +
Stagnant hypoxia (fluid phase flow) +
Histotoxic hypoxia (tissue phase) -
Normal Person (breathing 100% O
2
)
14gm x 1.34ml = 18.7ml + 1.8ml = 20.5ml (1.8 is 9%20.5)
Anaemic patient (breathing 100% O
2
)
4gm x 1.34ml = 5.4ml + 1.8ml = 7.2 ml (1.8 is 25%of 7.2)
58
Dissolved O
2
in plasma
0.003ml / mm PO
2
/ 100ml of blood
Breathing Air (P
a
O
2
100mm Hg)
0.3ml / 100ml of blood
59
Dissolved O
2
in plasma
0.003ml / 100ml of blood / mm PO
2
Breathing Air (P
a
O
2
100mm Hg)
Breathing 100% O
2
60
Dissolved O
2
in plasma
2
Breathing Air (P
a
O
2
100mm Hg)
Breathing 100% O
2
(P
a
O
2
600mm Hg)
61
Dissolved O
2
in plasma
2
Breathing Air (P
a
O
2
100mm Hg)
Breathing 100% O
2
(P
a
O
2
600mm Hg)
Breathing 100% O2 at 3 Atm. Pressure
62
Dissolved O
2
in plasma
2
Breathing Air (P
a
O
2
100mm Hg)
Breathing 100% O
2
(P
a
O
2
600mm Hg)
63
Dissolved O
2
in plasma
2
Breathing Air (P
a
O
2
100mm Hg)
Breathing 100% O
2
(P
a
O
2
600mm Hg)
Basis of Hyperbaric O
2
therapy
64
Physical effects of O
2
65
2
Air in the body where it should not be
66
2
Air in the body where it should not be
Surgical emphysema
Pneumothorax
Air embolism
Bowel decompression
67
mmHg
Art. blood Ven. blood
Breathing air
PO
2
100 40
PCo
2
40 46
P
N
2
570 570
Breathing 100% O
2
PO
2
600 ?
PCo
2
40 46
P
N
2
0 0
Gas Tensions
68
mmHg
Art. blood Ven. blood
Breathing air
PO
2
100 40
PCo
2
40 46
P
N
2
570 570
Breathing 100% O
2
PO
2
600 50
PCo
2
40 46
P
N
2
0 0
Gas Tensions
69
Tissue requirement per 100ml = 5ml
Dissolved Fraction = 1.8 ml
Balance = 3.2 ml
1% fall in saturation = 0.2 ml
16%fall in saturation= 3.2ml
84% saturation = PO
2
50mm Hg
70
Pre oxygenation / ?
71
Pre oxygenation / denitrogenation
To the O
2
reserve in the body ?
72
O
2
stores in the body
Breathing
air
Breathing
100% O
2
Lungs (FRC) 450 ml 3000 ml
Blood 1000 ml 1090 ml
Tissue fluids / myoglobin + +
73
Oxygen Therapy
Partial Pr of O
2
in insp. gas
(P
i
o
2
)
74
Oxygen Therapy
Conc. of O
2
(Fi o
2
)
(Orthobaric)
Total Pressure
(Hyperbaric)
Partial Pr of O
2
in insp. gas
(P
i
o
2
)
75
O
2
Delivery systems
76
O
2
Delivery systems
Ambient pressure
Variable performance devices
Fixed performance devices
77
O
2
Delivery systems
Ambient pressure
Positive pressure ventilation
Non invasive (BIPAP, CPAP)
Invasive
78
O
2
Delivery systems
Ambient pressure
Positive pressure ventilation
Non invasive (BIPAP, CPAP)
Invasive
ECMO
79
O
2
Delivery systems
Ambient pressure
Variable performance devices (Pt. dependent) low flow
No capacity system no rebreathing
nasal catheter / cannulae
Capacity system chance of rebreathing
Small (mass shell only)
Large (with reservoir bag)
Fixed performance devices (Pt. independent) high flow
HAFOE ventimask / Nebuliser
Anaesthesia circuits
80
High flow system
The gas flow is sufficient to meet all inspiratory
requirement
Low flow system
The gas flow is insufficient to meet all inspiratory
requirement.
Part of tidal volume is provided by room air.
81
Variables
O
2
flow rate
Patient factors
Device factors
82
Variables
O
2
flow rate
Patient factors
Inspiratory flow rate
Expiratory time (active exp. flow + exp. pause)
Device factors
83
Variables
O
2
flow rate
Patient factors
Inspiratory flow rate
Expiratory time (active exp. flow + exp. pause)
Device factors
Physical volume (capacity)
Vent resistance (tight fit)
84
Variable
+ =
=
No cap.
Devices
Capacity devices
FIO2 F
I
O
2
F
I
CO
2
O
2
flow rate +
Patient
Factors
Insp.
Flow rate
+
Exp.
time
+
Device
Factors
Physical
volume
+
Vent
resistance
+
85
Variable
+ =
=
No cap.
Devices
Capacity devices
FIO2 F
I
O
2
F
I
CO
2
O
2
flow rate +
Patient
Factors
Insp.
Flow rate
+
Exp.
time
+
Device
Factors
Physical
volume
+
Vent
resistance
+
86
Variable
+ =
=
No cap.
Devices
Capacity devices
FIO2 F
I
O
2
F
I
CO
2
O
2
flow rate +
Patient
Factors
Insp.
Flow rate
+
Exp.
time
+
Device
Factors
Physical
volume
+
Vent
resistance
+
87
Variable
+ =
=
No cap.
Devices
Capacity devices
FIO2 F
I
O
2
F
I
CO
2
O
2
flow rate +
Patient
Factors
Insp.
Flow rate
+
Exp.
time
+
Device
Factors
Physical
volume
+
Vent
resistance
+
88
89
90
91
Nasal Catheter
O
2
Flowrate (L/min)
1
2
3
4
5
6
Fi O
2
0.24
0.28
0.32
0.36
0.40
0.44
92
Normal Anatomic Reservoir
(50ml)
3 Ltr/min
= 50 ml/Sec
93
Nasal Catheter
Merits
Easy to fix
Keeps hands free
Not much interference with further airway care
Useful in both spont. breathing and apnoeic
94
95
96
97
98
Nasal Catheter
Merits
Easy to fix
Keeps hands free
Not much interference with further airway care
Useful in both spont. breathing and apnoeic
Small but definite rise in FiO
2
(dose not critical)
Demerits
Mucosal irritation (uncomfortable)
Gastric dilatation (especially with high flows)
99
100
101
For higher O
2
Concentration
gadgets with storage capacity (reservoir)
problem of re-breathing
minimized / avoided by higher flows
102
Simple face mask
Simple Face Mask ?
103
Simple face mask
NO YES
Simple Face Mask
104
Simple face mask
O
2
Flowrate (L/min)
5-6
6-7
7-8
Fi O
2
0.40
0.50
0.60
105
Partial Rebreathing mask (polymask) 106
107
Partial Rebreathing mask
(polymask)
O
2
Flowrate (L/min)
6
7
8
Fi O
2
0.60
0.70
0.80
108
Non Rebreathing mask
Non Rebreathing Mask
109
110
10 15 Ltr/min flow rate 50-100 O
2
conc.
111
Face Masks
Merits
Higher Oxygen Conc.
Demerits
Air dilution (if not fitting properly)
Rebreathing (if O
2
flow is inadequate)
Interfere with further airway care
Uncomfortable (sweating, spitting)
112
Bag Valve Mask assembly
(Ambu Resuscitator)
(Ambu Resuscitator)
113
114
(Ambu Resuscitator)
Delivers O
2
during BOTH spont. & artf. Vent
115
(Ambu Resuscitator)
Delivers O
2
during BOTH spont. & artf. Vent
O
2
concentration
30 50% (without reservoir)
80 100% (with reservoir)
To deliver 100% O
2
Reservoir as large as bag vol
O
2
flow rate > minute volume (10 l/m)
Drawback keeps rescuers hands engaged
116
117
Pocket Mask
Delivers O
2
in BOTH spont. & aponeic
Allows use of both hands for maintaining airway
Upto 4 ltr reserve vol. (rescuers vital capacity)
O
2
Flowrate (L/min)
5
10
15
Fi O
2
0.40
0.50
0.80 (Spont.)
0.54 (M - mask)
118
Incubator
Small infants not on ventilator
Works on venturi principle
Complete air change 10 times / hour
Control of humidity & temperature
O
2
conc. falls rapidly when access ports are open
119
O
2
tents
For children not tolerating mask / catheter
Large capacity system
Upto 50% O
2
concentration
Large tent cap. and leak port limited CO
2
build up.
Disadvantage
Limited access
Risk of fire
Conflict in O
2
therapy / nursing care
120
Fixed Performance Device
X
Room
App. Dead Space
Rebreathing
An. Circuit
with collasible reservoir
Inspiratory flow waveform
Known, fixed & selectable
HAFOE
Venturi
Continous flow > PIFR
Constant Inspiratory mixture
121
Ventimask
Air + O2 > PIFR(35-40 l/ min)
122
Ventimask
123
Simple face mask
NO YES
Simple Face Mask
124
28 % @ 4 L P M
%age of O2 if flow is doubled (8 LPM) ?
%age of O2 if flow is halved ( 2 LPM) ?
125
Works on principle of constant pressure jet mixture.
O
2
jet entrains air as per entrain. ratio.
Total flow > PIFR (30 35 L/min)
Eliminates the problem of dead space & leak free connection.
Upper limit is 60 %.
Humidification of O
2
supply is not sensible.
126
127
Nebulizer
FiO
2
> 0.4 with high flow system
Max. gas flow 14 16 L / min
To meet the ventilatory demand
128
Nebulizer
FiO
2
> 0.4 with high flow system
Max. gas flow 14 16 L / min
To meet the ventilatory demand
2 nebulizers to feed a single mask
129
If conc. of O
2
which a patient is getting
is not known
then the situation is similar to
a drug being administered
without knowing the dose
which can do harm if given more
or provide insufficient effect if given less
130
100% - not more than 12hrs
O
2
Toxicity
131
Humidifiers
132
Rest
(read it yourself)
133
J.S Haldane-1917
Father of modern O
2
Therapy
O
2
lack not only stops the machine,
but totally ruins the supposed machinery
134
It must be remembered that patients dont die from
failure to maintain airway or intubate
but
from failure to oxygenate
Prys Robert & Brown.
P.2/108/13
135
136
137
A B
Anaemic patient Patient with Hb 14gm%
Hb = 7gm % Normal Hb 7gm%
Hb Co 7gm%
138
A B
Hb Co 7gm%
2,3 DPG
Shift to R Shift to L
unloading of O
2
unloading of O
2
(blood tissue) (blood tissue)
P
V
O
2
? P
V
O
2
?
139
A B
Hb Co 7gm%
2,3 DPG
unloading of O
2
unloading of O
2
P
V
O
2
27 mm Hg P
V
O
2
?
140
A B
Hb Co 7gm%
2,3 DPG
unloading of O
2
unloading of O
2
P
V
O
2
27 mm Hg P
V
O
2
14mmHg
141
Hypoxia in co poisoning
is out of proportion
to degree of anemia
142
A B
Hb Co 7gm%
2,3 DPG
unloading of O
2
unloading of O
2
P
V
O
2
27 mm Hg P
V
O
2
14mmHg
Cardiac Output
143
1
RAYNAUDSDISEASE
BUERGERSDISEASE
DR.A.R.GOGIA
RAYNAUDSDISEASE
HISTORY
KAVITA28Yrs.F,HOUSEWIFE
BLUISHDISCOLOURATIONOFFINGERSOF
O S O OS O CO S C BOTHHANDSONEXPOSURETOCOLDSINCE
3Yrs
PINS&NEEDLESENSATIONS.
EPISODESLASTINGFOR15Min.
CHANGEINCOLOUROFFINGERSTORED.
RAYNAUDSDISEASE
HISTORYCONTD..
NoH/OJOINTPAINS
No H/O DRUG INTAKE NoH/ODRUGINTAKE
NoH/ODIABETES,H.T.
NoH/OSMOKINGORTOBACCOCHEWING.
NoH/OPERTAININGTOCVS,CNS,RESP
SYSTEMINVOLVEMENT.
RAYNAUDSDISEASE
EXAMINATION
AVERAGEBUILT.
56Kg.160CmHeight.
PULSE84/MinBP.110/80mmHg
CVS
CNSNAD
NOTROPHICCHANGESINFINGERS
NOLOSSOFHAIRS
NOULCERATIONS
RAYNAUDSDISEASE
WHATISRAYNAUDS
DISEASE?
RAYNAUDSDISEASE
DISEASEOFIDIOPATHICORIGIN.
WOMENAREAFFECTEDMORETHANMEN
(5:1).
AGEGROUP2040YEARS.
BILATERALINVOLVEMENT.
SYMPTOMSOFATLEAST2YEARS
DURATION.
SPASMOFARTERIOLESUSUALLYOFDIGITS
,OCCASIONALLYNOSE&TONGUE.
2
RAYNAUDPHENOMENON
WHATISRAYNAUDSPHENOMENON?
RAYNAUDPHENOMENON
EPISODICDIGITALISCHEMIA
COLOURCHANGESMAYBEBIPHASIC(CYANOSIS&
REDNESS).
TRIPHASIC(PALLOR,CYANOSIS, REDNESS). TRIPHASIC(PALLOR,CYANOSIS,REDNESS).
DONOTOCCURABOVEMETACARPOPHALANGEAL
JOINTS.
MOSTLYUNILATERAL.
ASSOCIATEDWITHSOMEUNDERLYINGORGANIC
CAUSE.
RAYNAUDPHENOMENON
pathophysiology
INCREASEDSENSITIVITYTOCIRCULATING
CATECHOLAMINES
INCREASEDNO.OFalpha2RECEPTORS
C S S O SO C INCREASEDLEVELSOFVASOACTIVE
SUBSTANCES
DECREASEDSYSTEMICPRESSURES
RAYNAUDPHENOMENON
WHATARETHEIMPORTANTCAUSESOF
RAYNAUDSPHENOMENON?
RAYNAUDPHENOMENON
(A)CONNECTIVETISSUEDISORDERSE.g.:
SCLERODERMA,SLE,RHEUMATOIDARTHRITIS,
DERMATOMYOSITIS.
(B) ARTERIAL OCCLUSIVE DISEASES (B)ARTERIALOCCLUSIVEDISEASES
ATHEROSCLEROSIS,BUERGERSDISEASE,
THORACICOUTLETSYNDROME,CERVICALRIB.
Cont.
3
RAYNAUDPHENOMENON
(C)NEUROLOGICSYNDROMES
CARPALTUNNELSYNDROME
REFLEXSYMPATHETICDYSTROPHY
SYRINGOMYELIA
(D)BLOODDYSCRASIAS
MYELO&PROLIFERATIVEDISORDERS
CRYOGLOBINEMIA.
Cont..
RAYNAUDPHENOMENON
(E)TRAUMA
VIBRATIONINJURY
FROSTBITE
ELECTRICSHOCK
TYPING,PIANO
(F)DRUGS
ERGOTDERIVATIVES
B BLOCKERS
METHYSERGIDE
ANTICANCERAGENTe.g.
BLEOMYCIN,CISPLATIN
TRICYCLICANTI
DEPRESSANTS
RAYNAUDSDISEASE
WHATARETHETREATMENTMODALITIESOFFEREDTOTHESEPATIENTS?
TREATMENTOFUNDERLYINGCAUSE
PROTECTINGTHEHANDS&FEETFORMEXPOSURETOCOLD
DRUGS
ALPHA BLOCKERS
CaCHANNELBLOCKERS
ORALVASODILATORS
PROSTAGLANDINS PROSTAGLANDINS
PENTOXYPHYLLINE
REPEATEDSYMPATHETICBLOCKS
SURGICAL SURGICALSYAMPATHECTOMIES
MICROSINGLEINCISION
ENDOSCOPICTHORACICSYMPATHECTOMY
RAYNAUDSDISEASE
WHATAREGOALSOFANAESTHETICMANAGEMENT
OFTHEPATIENTSUNDERGOINGUPPERLIMB
SYMPATHECTOMY?
RAYNAUDSDISEASE
1.MAINTENANCEOFAMBIENTOT.TEMPERATURE&BODY
TEMPERATURE.
2.INFUSIONOFWARMI/VFLUIDS.
3.PROPERPADDINGOFPRESSUREPOINTS.
4.HUMIDIFIEDGASESANDINPOSTOPERATIVEPERIODHUMIDIFIED
OXYGEN OXYGEN.
5.NOIBPRECORDING.
6.COMPLETEAVOIDENCEOFDRUGS LIKEBBLOCKERS,CLONIDINE,
ERGOTS.
7.REGIONALANAESTHESIAISACCEPTABLEFORPERIPHERALOPERATIONS
BUTAVOIDEPINEPHRINEWITHLOCALANAESTHETICS.
8.KEEPINMINDINTERACTIONOFDRUGSWITHANAESTHETICAGENTS.
RAYNAUDSDISEASE
WHATISTHESYMPATHETICINNERVATIONOFUPPER
LIMB?
4
RAYNAUDSDISEASE
PREGANGLIONICSYMPATHETICOUTFLOWTOUPPER
EXTREMITYISDERIVEDFROMT2 T7.
FIBRESFORMTHESESEGMENTSSYNAPSEINSTELLATE
GANGION,MIDDLECERVICAL,THORACIC2nd&3rd.GANGLIA.
SOME FIBRE FROM SECOND & THIRD THORACIC GANGLION SOMEFIBREFROMSECOND&THIRDTHORACICGANGLION
GODIRECTLYTOARMTHROUGHSEGMENTALNERVES.
STELLATEGANGLION
RAYNAUDSDISEASE
WHATARETHESIGNSOFSUCCESSFULSTELLATE
GANGLIONBLOCK?
STELLATEGANGLIONBLOCK
STELLATEGANGLIONBLOCK
EYE:PTOSIS,MEIOSIS,ENOPTHALMOS,
CONJUNCTIVALINJECTION,
LACRIMATION.
FACE:ANHYDROSIS,ELEVATEDLOCALTEMPERATURE,
NASAL STUFFINESS NASALSTUFFINESS.
ARM:INCREASEDTEMPERATURE,
PLETHYSMOGRAPHICEVIDENCEOFIMPROVED
CUTANEOUSBLOODFLOW
TYMPANICMEMBRANE:INJECTIONOFEARDRUM.
RAYNAUDS
DISEASE
5
BUERGERSDISEASE
HISTORY
KISHORE34Yrs.OLD,MANUALLABOURER
PAININTHELIMBSONWALKING 3MONTHS
TINGLINGSENSATIONINFINGERS&TOES 2MONTHS
PAINFULULCERIN(RT)BIGTOE 2MONTHS
BLUISHDISCOLARATIONOFTHESKIN ONEXPOSURETO
COLD.
CHRONICBIDISMOKERFORLAST 20Yrs.
BUERGERSDISEASE
EXAMINATION
52Kg,168CmTALLMALEOFAVERAGEBUILT
PULSERATE76/Min,BP130/70MmHg
(RT.)DORSALISPEDISA..NOTPALPABLE
HAIRLOSSON(RT)FOOT
COLDTOTOUCH
ULCERON(RT)BIGTOE2x2Cm,HARDCRENATED
MARGINS,COVEREDWITHWHITISH
DISCHARGE,VERYTENDER
CNS,CVSAREUNREMARKABLE
BUERGERSDISEASE
WHATIS
BUERGERSDISEASE?
WHODESCRIBEDIT
FIRST? FIRST?
BUERGERSDISEASE
BUERGERSDISEASEISNONATHEROSCLEROTIC,
SEGMENTAL,INFLAMMATORY,VASOOCCLUSIVEDISEASE
THATAFFECTSTHESMALLSIZEDARTERIESANDVEINSOF S S S S S O
THEUPPER&LOWEREXTREMITIES.ITISALSOKNOWNAS
THROMBOANGIITISOBLITERANS.LEOBUERGER
DESCRIBEDTHISDISEASEIN1908.HECALLEDIT
SPONTANEOUSGANGRENE.
BUERGERSDISEASE
WHATARETHEOTHERVESSELSWHICHMAYGET
INVOLVEDINBUERGERSDISEASE?
BUERGERSDISEASE
BESIDESSMALL&MEDIUMSIZEDARTERIESAND
VEINSOFTHEEXTREMITIESOTHERVESSELSLIKE
AORTA, CEREBRAL VESSELS, CORONARIES, ILIAC, AORTA,CEREBRALVESSELS,CORONARIES,ILIAC,
MESENTERIC,PULMONARY&RENALVESSELS
CANBEINVOLVED.
6
Buerger Buergerss Disease Disease
Thromboangitis
obliterans
Relativelyuncommon
occlusivediseaselimited
tothemediumandsmall
arteriesandveins
Distalupperandlower
limbsarethemost
frequentlyaffected
Typicallyidentifiedin
youngadultmenwho
smoke
ClinicalFeatures
ClassificationSystems
MajorCriteria
Onsetofdistalextremityischemicsymptomspriortoaqe45
Tobaccoabuse
Undiseasedarteriesproximaltobrachial&popliteal
Objectivedocumentationofdistalocclusivediseaseby
plethysmography plethysmography
Exclusionofproximalembolicsource,trauma,autoimmune
disease,hypercoagulablestate,atherosclerosis
MinorCriteria
Migratorysuperficialphlebitis
Raynaudssyndrome
Upperextremityinvolvement
Instepclaudication
Notypicallababnormalities
BUERGERSDISEASE
WHATINVESTIGATIONSCANHELPCONFIRMTHE
DIAGNOSISOFBUERGERSDISEASE?
AnkleBrachialIndex
Comparisonofanklepressureto
brachialSBP
Reproducible,usefulforlong
term surveillance termsurveillance
Normal0.851.2
Claudicants0.50.7
Criticalischemia<0.4
Maybefalselyelevatedin
calcifiedvessels(DM)
BUERGERSDISEASE
(A)ANGIOGRAPHY
NONATHEROSCLEROTIC,OCCLUSIVELESIONSOF
SMALL&MEDIUMSIZEDVESSELSWITHFORMATION
OF DISTINCTIVE SMALL VESSEL COLLATERALS OFDISTINCTIVESMALLVESSELCOLLATERALS
KNOWNASCORKSCREWCOLLATERALS.
Cont..
BUERGERSDISEASE
7
BUERGERSDISEASE
(B)EXCISIONALBIOPSY&HISTOPATHOLOGY
ACUTEPHASE INFLAMMATORY,SEGEMENTAL,OCCLUSIVETHROMBIIN
WALLSOFAFFECTEDVESSELS.
SUBACUTE PHASE SUBACUTEPHASE INTRALUMINALTHROMBUSINPROCESSOF
ORGANISATION.
ENDSTAGEPHASE MATURETHROMBUSWITHVASCULARFIBROSIS.
INTEGRITYOFINTERNALELASTICLAMINAISMAINTAINEDINALLSTAGES.
BUERGERSDISEASE
WHATARETHEAVAILABLEMODALITIESOF
TREATMENTFORPATIENTSOFBUERGERSDISEASE?
BUERGERSDISEASE
CONSERVATIVE
COMPLETEABSTINENCEFROMTOBACCO
AVOIDEXPOSURETOCOLD
USEOFWELLFITTINGPROTECTIVEFOOTWEAR
AVOIDENCE OF DRUGS THAT LEAD TO VASO CONSTRICTION AVOIDENCEOFDRUGSTHATLEADTOVASOCONSTRICTION
USEOFVASODILATORS&CORTICOSTEROIDS,PLATELET
INHIBITORS,ANTICOAGULANTS,THROMBOLYTICSISNOT
ESTABLISHED.
ILOPROSTPROSTAGLANDINI2,ANTIPLATELETWITH
VASODILATORACTIVITY,MOREEFFECTIVEBYINTRAARTERIAL
ROUTETHANI/V
,Cont.
BUERGERSDISEASE
SURGICALTREATMENT
LOCALDEBRIDEMENT
AMPUTATIONOFAFFECTEDPARTS
ARTERIALBYEPASSOFLARGEVESSELS
SYMPATHECTOMYSEGMENTALSUPPLYT10L2
P.G.FIBRESLEAVESYM.CHAINATORBELOWL2
OMENTOPAXYFORREVASCULARISATION
ACUPUNCTURE VERYBENEFICIALININITIAL
STAGES.
BUERGERSDISEASE
WHATARETHEINVESTIGATIONSREQUIREDFORA
PATIENTUNDERGOINGLUMBARSYMPATHECTOMYON
ONE SIDE ? ONESIDE?
BUERGERSDISEASE
COMPLETEHAEMOGRAM
URINE RE
ME ME
BLOODUREA
BLOODSUGAR
XRAYCHEST PAVIEW
ECG
8
BUERGERSDISEASE
WHATANAESTHETICTECHNIQUEYOUWILL
SELECTFORPATIENTUNDERGOINGLUMBAR
SYMPATHECTOMY?
BUERGERSDISEASE
CANBEDONEUNDERREGIONALORGA
CONSIDERATIONARE:
POSITIONOFPATIENT
PADDINGPRESSUREPOINTS
AMBIENTTEMP.OFO.T.
USEOFWARM&HUMIDIFIEDINSPIREDGASES
NONINVASIVEMONITORINGOFSYSTEMICPRESSURE
POSSIBLEINTERACTIONOFANAESTHETICDRUGSWITHPERIPHERAL
VASODILATORS
NEEDFORSUPPLEMENTALCORTICOSTEROIDS
BUERGERSDISEASE
WHATANAESTHESIAONECANCHOOSEFOR
AMPUTATIONOFBIGTOE?
BUERGERSDISEASE
REGIONALANAESTHESIA ANKLE
BLOCK
OMITVASOPRESSORSFROM
LOCALANAESTHETICSOLUTION
DEEPPERONEAL,SUPERFICIAL
PERONEAL TIBIAL NERVE TO BE PERONEAL,TIBIALNERVETOBE
BLOCKED
CANBEDONEUNDERG.A.OR
REGIONALBLOCK
1
Vaporizers
Dr Rakesh Garg
What is a Vaporizer ?
Instrument designed to facilitate the
change of a liquid anesthetic into its vapor
And add a
Controlled amount
of this vapor to the flow of gases.
Functions of Vaporizers
Produce vaporisation of volatile agent
Mix vapour with fresh gas flow
Control the mixture despite variables
-- to deliver safe and accurate concentrations of inhalational
anaesthetic agents to the patient.
Related Physics
Critical temperature: It is that temperature, above which no amount of pressure
will convert a gas to a liquid.
O2 = -118.4 C; N2O = 36.5 C; CO2 = 31 C
Vapor: is the gaseous phase of an agent which is normally a liquid at room
temperature and atmospheric pressure.
Gas: is a substance which exists only in gaseous state at room temperature and
atmospheric pressure.
Vapor pressure:
When enclosed in a container, molecules of a volatile liquid break
away to form vapor.
Vapor pressure is the pressure with which they bombard the walls of
Related Physics
the container.
Vapor pressure depends only on the temperature and nature of liquid.
Vapor pressure of an agent determines how much of vapor will be
formed from 1 ml of the liquid.
Since different anaesthestic agents have different vapor pressures so
need separate vaporizers.
Saturated Vapor Pressure: is the Maximum Vapor
pressure at a particular temperature.
The SVP of most inhalation agents is MUCH more than is
required to produce anaesthesia i.e. 32% vs 0.75 or 243 mmHg
vs 5.7 mmHg for halothane.
Related Physics
g
Need to dilute this vapor with the carrier gas and deliver a
controlled amount of this vapor to the patient.
2
Related Physics
Boiling point: of a liquid is that temperature at which the
Vapor pressure is equal to the atmospheric pressure.
The lower the atmospheric pressure, the lower the boiling point
Heat of Vaporization:
It is the number of calories needed to convert 1g or1ml of
liquid to vapor.
Specific Heat:
Quantity of heat required to raise the temperature of 1g or1
ml of the substance by 1C.
Thermal Conductivity:
Related Physics
Thermal Conductivity:
A measure of speed with which heat flows through a
substance. Amount of heat that flows through unit area of a
plate of unit thickness in unit time per degree of
temperature gradient
Thermal Capacity:
Amount of heat stored in the vaporizer body.
Specific Heat X Mass.
Clinical significance:
Liquid anesthetics with low specific heat vaporize easier.
Higher the thermal conductivity, better a substance conducts
heat.
Related Physics
Construct vaporizers of materials with high thermal conductivity and
specific heat Eg-Copper, bronze to minimise tempertaure changes when
in use.
Thermostabilization:
Methods:
Vaporizer constructed of metal with high thermal conductivity
Heavy metal parts act as a heat reservoir
Wicks to be in contact with the metal part so that heat loss due to
i i i i kl l d
Related Physics
vaporisation is quickly replaced
Immerse vaporizer chamber in a large mass of water
Thermocompensation:
Some means to maintain the vaporizer output constant
despite any temperature changes
Methods:
Alteration in the splitting ratio (automatic compensation)
Eg. Bimetallic strip in tec vaporizers, ether filled bellows in
Related Physics
Eg. Bimetallic strip in tec vaporizers, ether filled bellows in
penlon vaporizers, EMO
Computer control - electronic vaporizers.
Manually adjust flow - measured flow, drager Vapor.
Supplied heat - tec 6 (electrically heated)
Properties of commonly used
Anaesthetic agents
Volatile agent SVP
(mmHg) at
20C
BP (C) at
760 mmHg
Ether 440 36.5
Trilene 57 87.5
Halothane 243 51
Enflurane 175 56
Isoflurane 238 48
Sevoflurane 157 58
Desflurane 669 23
3
Concentration of Gases is Expressed as
- Partial Pressure
Related Physics
- Volumes Percent
Concentration of Gases
Partial Pressure (P.P):
The part of the total pressure due to any one gas in the mixture.
Depends on
Nature of liquid
Temperature Temperature
Clinical Significance
Patient uptake and Anaesthetic depth are directly related to Partial
pressure
Volumes Percent (Vol %):
The number of units of volume of a gas in relationship to a total of 100
units for the total gas mixture.
Concentration of Gases
Clinical Significance
Gas and Vapor concentration delivered by a vaporizer are
expressed in Vol %
MAC (Minimum Alveolar Concentration)
The MAC of an inhaled
anaesthetic is the alveolar
concentraion that prevents
movement in 50% of
patients in response to a
Agent MAC in O2
(%)
Halothane 0.75
Isoflurane 1.15
patients in response to a
standardized stimulus (eg.
Surgical incision)
Vol % of alveolar gas at 1
atm.
Enflurane 1.68
Desflurane 6.4
Sevoflurane 2.0
Minimum alveolar partial pressure
(MAPP)
Expresses MAC in terms of pp (Pmac1)
MAC of halothane is 0.75
pp of halothane for 1 MAC is
0.75/100 x 760 = 5.7 mm Hg
Pmac1 of desflurane for 1 MAC is
6/100 x 760 = 45.6 mm Hg
Terminology for Vaporizers
Plenum:
FGF is pushed into the vaporizer, high resistance.
Drawover:
Gas is pulled into the vaporizer by the patients own inspiratory effort,
low resistance e.g. Goldman, EMO, OMV, BSIU ow es sta ce e.g. Go d a , O, O V, S U
Inhaler:
A drawover vaporizer in which the carrier gas is air
4
CLASSIFICATION OF
VAPORIZERS
Oldest Classification of Vaporizers
A. Method of regulating Output Concentration
1. Variable Bypass
2. Measured Flow
B. Method of Vaporization
1. Flow Over
2. Bubble Through
3 Flow over or Bubble Through 3. Flow over or Bubble Through
C. Location
1. Outside the Breathing System
2. Inside the Breathing System
D. Temperature Compensation
1. None
2. By Supplied Heat
3. By Flow Alteration
E. Specificity
1. Agent Specific
2. Multiple Agent
Older Classification
1. Variable Bypass
2. Measured Flow
1. Flow Over
2 Bubble Through 2. Bubble Through
3. Injection
C. Resistance
1. Plenum
2. Low Resistance
1. Thermocompensation
2. Supplied Heat.
E. Specificity
1. Agent Specific
2. Multiple Agent
New Classification of Vaporizers
1. Variable Bypass
2. Electronic
1 Flow Over 1. Flow Over
2. Injection
C. Temperature Compensation
1. Mechanical
2. Supplied Heat
3. Computerized
A. Method of regulating Output
Concentration
1. Variable Bypass
2. Measured Flow
1. Flow Over
2. Bubble Through
3. Flow over or Bubble Through
C. Location
1 Outside the Breathing System
Concentration
1. Variable Bypass
2. Measured Flow
1. Flow Over
2. Bubble Through
3. Injection
C. Resistance
1 Plenum
Concentration
1. Variable Bypass
2. Electronic
1. Flow Over
2. Injection
Evolution of Classification of Vaporizers
1. Outside the Breathing System
2. Inside the Breathing System
1. None
2. By Supplied Heat
3. By Flow Alteration
E. Specificity
1. Agent Specific
2. Multiple Agent
1. Plenum
2. Low Resistance
1. Thermocompensation
2. Supplied Heat.
E. Specificity
1. Agent Specific
2. Multiple Agent
C. Temperature Compensation
1. Mechanical
2. Supplied Heat
3. Computerized
Method of Regulating Output
Concentration
5
Variable Bypass (Direct Reading, Concentration
Calibrated, Dial Controlled, Automatic Plenum)
Fresh gas flow (FGF) enters the inlet of the vaporiser and splits into
Carrier gas (20%)
Bypass gas( 80%)
At the outlet, the Bypass gas meets the Carrier gas (fully saturated with vapor)
Flowmeter
Patient
VARIABLE BYPASS
Flowmeter
Patient
Flowmeter
Patient
SPLITTINGRATIO
The ratio of the bypass gas to the gas going to
the vaporizing chamber is called the
SPLITTING RATIO. Splitting ratio depends on:
The resistance of the two pathways, which
inturn depends on the variable orifice of the p
inlet/outlet.
Temperature of the liquid/carrier gas.
Flow rate of gases
IFWEDIALAHIGH
CONCENTRATION
IFWEDIALALOW
CONCENTRATION
6
Measured Flow Vaporizer
Uses a measured flow of carrier
gas to pick up agent.
Consists of:
(1) Vaporizer
(2) Flowmeter assembly
(3) Vaporizer Circuit Control Valve
Limitations:
Cumbersome calculations
If the bypass flowmeter is turned
off, it is possible to supply gas
fully saturated with anesthetic to
the patient.
Measured Flow Vaporizer
Operator has to set the flow to the vaporizer and bypass
with separate flowmeters
This means that respective flows have to be calculated
for each agent for a given temp and vapour output
To calculate the vaporizer output one must know the To calculate the vaporizer output, one must know the
Vapor pressure of the agent
The atmospheric pressure
The total flow of gases
The flow of the vaporizer
Calculations for output in measured
flow vaporisers
Set 100ml/min flow of carrier gas (oxygen) from dedicated
flowmeter
SVP of halothane in vap. chamber is 243 mmHg
Halothane forms 243/760 x100= 32%of gas mixture
Carrier gas will occupy the rest of the vol i.e. 100-32= 68%
This 68% is occupied by 100 ml/min carrier gas
And 32% hal will be = 100/68 x32 = 47 ml
Gas exiting is 147ml with 47 ml hal vapor
To get a mixture containing 1% hal this 47 ml should be diluted
in 4700ml.
Required carrier gas is 4700-147= 4553 ml
If set 100ml measured flow to vaporiser, usually set 5 L/min
flow of carrier gas to get 1% halothane
Ratio of gas through vaporiser:main gas flow is 100:4600=1:46.
% concentration of agent = 100 x vaporizer output of
anaesthetic/total flow
Method of Vaporization
Method of Vaporization
The Pathway followed by the carrier gas as it travels through the
vaporizing chamber.
Flow Over
Bubble through Bubble through
Injection
Method of Vaporization...
Flow over : a stream of gas passes over liquid surface
Efficiency depends on
Gas-liquid interface e.g. baffles, spiral tracks, wicks
V l it f i fl Velocity of carrier gas flow;
Height of gas flow
7
Bubble through: Bubble the gas through the liquid
Efficiency depends on
- Size; Depth of the liquid; Velocity
Eg. sintered diffuser, cowl in Boyles Bottle
Injection :
Injecting a known amount of liquid anesthetic from a reservoir
in the vaporizer /an agent bottle into a known volume of gas.
Eg. TEC 6 desflurane vaporizer (it is more ideally classified as a
gas-vapor blender)
1 ml of halothane = ? ml hal vapor at 20 C
Density of halo is 1.86 so 1 ml weighs 1.86 gm
Avogadros law- Equal volumes of gas at the same temperature and pressure
contain equal number of molecules; One gram-MW (mole) of gas occupies 22.4
litres STP (760mm Hg and 0
0
C).
1 GMW(197 g) of halothane occupies 22.4 l at STP (0C/273 K)
How much liquid agent does a vaporiser use per hour?
At 20 C (293 K)
Using Charles Law- V1/T1 = V2/T2
= 22.4/273 = V2 /293 = 24 L
197 gm(1 GMW) occupies 24 L at 20C
1.86 g( 1 ml) will generate 24/197 x 1.86 = 0.227 L = 227 ml
If FGF is 4000 ml/min for a 1% conc need 40 ml vapor/min
How much liquid agent does a vaporiser use per hour?
Ehrenworth and Eisenkraft (1993) gave formula:
3 x FGF (L/min) x vol % = ml liquid used / hr
Another formula:
Amount of vapor used/min= FGF x time x concentration setting
e.g. to deliver 1% isoflurane at FGF of 2 litres per min for 60 mins.
One would need 1/100 x 2000 ml x 60 min = 1200 ml of
isoflurane vapor. This would correspond to 1200/180 = 6.7 ml of
liquid isoflurane
Location
In-System Vaporizers (VIC):
Should have standard male and female 22-mm fittings or
standard screw threaded fittings; inlet and outlet ports should
have arrows;
Should have low resistance;
Location
Vaporiser concentration and output vary
Easy to wash and clean
Drawover vaporizer Gas is pulled into the vaporizer by
the patients own inspiratory effort eg. Goldman, EMO,
OMV.
8
Location
Out of System Vaporizers (VOC):
Usually on back bar - between flowmeters and FGF outlet
Most Variable Bypass Vaporizers and All measured flow
vaporisers are VOC and the vaporiser output is connected just
upstream of CGO
If connected after the CGO, vaporiser should not tip;
resistance of vaporiser may lead to activation of low pressure resistance of vaporiser may lead to activation of low pressure
relief valve especially with oxygen flush.
Location
Out of System
(VOC)
In-System
(VIC)
Resistance High Low
Determinants of
Vapour Output
Vapour Output =
Vapour
Concentration
Vapour Output >
Vapour
Concentration
Temperature Compensation
To maintain a constant output from the vaporizer, mechanisms
to compensate for the fluctuations in temperature are to be
employed.
Methods:
Automatic -Alteration in the splitting ratio (Bimetallic strip in
tec vaporizers, ether filled bellows in penlon vaporizers, EMO)
Supplied heat -tec 6 (electrically heated)
Computer control electronic vaporizers
TemperatureCompensation
Most variable bypass vaporizers compensate for
changes in vapor pressure by altering the splitting
ratio.
Done by using a thermosensitive element (Bimettalic
Strip) incorporated in the vaporizing chamber or
bypass chamber.
So, the splitting of gas is controlled by 2 valves:
(1) the dial we set (splitting valve)
(2) the temperature compensating valve.
9
In a bimetallic strip, two metals with very
different coefficients of thermal expansion
are fixed together.
When the temp. of the vaporizing chamber drops,
the bimetallic strip bends and moves away. This
reduces the resistance to flow and thus more flow
occurs into the vaporizing chamber
Resistance
Resistance
PLENUM ( Latin = fullness):
Vaporizers with high resistance which depend on compressed
gas driven under pressure are called plenum vaporizers.
E B l b l k l TEC i Eg. Boyle bottle, copper kettle, TEC vaporizers
Resistance
DRAW OVER:
Carrier gas is drawn through the vaporizer either by the
patients own respiratory efforts, or by a self-inflating bag
or manual bellows
D t t t l th t bi t Drawover systems operate at less than, or at ambient
pressure
Flow through the system is intermittent, varying with
different phases of inspiration, and ceasing in expiration.
Resistance
DRAWOVER:
Have a low internal resistance to gas flow
So that they may be used within the breathing
circuit, the gas flow being driven through them by circuit, the gas flow being driven through them by
the patients breathing.
TheymaybeusedinanonrebreathingDROWOVER
APPARTUS, orasINCIRCUITVAPORZERSinaCIRCLE
ABSORBERSYSTEM.
Eg.Goldmanbottle,EMO
10
Factors Affecting Vaporizer
Performance in Basic Design
1. Flow rate of fresh gas.
2. Extremes of temperature.
3. Pumping Effect/ Pressurizing Effect
4. Barometric pressure
5. Anaesthetic agent
1. Problem of High Flow
At high flows, the vaporizer delivers less anesthetic
concentration than is set on the dial.
Problems of the Basic Design
Problem solving:
Increase the surface area of contact between the fresh gas and
anesthetic agent .
Wicks
Problem solving:
Bubbling through a sintered disc
e.g. "Copper Kettle"
2. Problem of Temperature
As anesthetic molecules escape temperature decreasesmore
difficult for the remaining molecules to escape Less
Vaporisation .
Thus at lower temperatures, there is less vaporization.
Problem solving:
Giving Heat
Giving Flow
Problem solving:
Giving Heat:
Vaporizer material
oGood conductor (high thermal conductivity)
oActs as a Heat reservoir (High Specific heat)
Supplied heat (tec 6 - electrically heated).
pp ( y )
11
Problem solving:
Giving Flow:
(Thermocompensation) by alteration in splitting ratio
Mechanical. Eg-Bimetallic strip in Tec Series
Computer controlled
Effects of Back Pressure on Vaporizer:
Pumping effect (Hill and Lowe effect)
Pressurizing Effect (Cole effect)
3. The Pumping Effect
(Hill and Lowe effect)
The effect of changing pressure during IPPV increasing the
output of the vaporizer is called the "pumping effect".
During positive pressure ventilation, pressure transmitted back
results in compression of gas.
Since the vaporizing chamber volume is much larger than the 'by
pass' channel volume more fresh gas gets compressed into it.
This extra fresh gas that enters the vaporizing chamber collects
anesthetic vapor .
Some of the rapidly expanding gas (containing vapor) enter the
inlet of the vaporizer and cross over into the 'bypass' channel .
12
The addition of the 'bypass' vapor to the VC vapor raises the
final concentration of anesthetic delivered.
The 'pumping effect' increases the delivered concentration of
anaesthetic agent.
Modifications to reduce the
'pumping effect'
Bypass Channel made larger
Inlet Tube made longer
Exclude wicks from the inlet
Increased Resistance
A high internal resistance to "resist" changes to flow
One Way Valve:
Also called unidirectional valve can be put between the
vaporizer outlet and the ventilator / breathing system
Mechanism of Pressurising effect
(Cole Effect) - output of anesthetic agent
An in pressure (p) causes an in pressure - p inside the vaporizer. The
carrier gas is compressed but the vapor pressure of the volatile anaesthetic is
unaffected.
Net result- in concentration of anaesthetic delivered
13
Changes in vapor output
Pumping effect > Pressurizing effect.
Factors Affecting Delivery
Increasing temperature causes an increase in SVP.
Temperature tends to fall in chamber due to latent heat of
vaporisation, which is more marked at higher flows.
In spite of methods of thermostabilisation and
thermocompensation there are still limitations as
Temperature
thermocompensation, there are still limitations as
the function of all the temperature compensating devices
vary linearly with temperature while SVPs of volatile
agents vary nonlinearly with temperature.
With rise in temperature - decrease viscosity of
fluids and increase viscosity of gases
Carrier Gas Composition
Most vaporisers are calibrated using 100% O
2
Addition of air little change
Compostion of carrier gas affects output in many (vaporiser
aberrance)
If add N
2
O If add N
2
O
Temporary effect decreased output (25% less with 100%
N20) due to solubility of N
2
O in agent (about 4.5 ml in
1ml). As N
2
O dissolves in liquid anaesthetic, flow of gases
exiting vaporiser decreases
Once saturated with N
2
O, output gradually increases but is
less than before (10% less with 100% N
2
O)
FGF Rate
At high dial concentrations and high flow rates, output may
be less
due to high flows, saturation may be incomplete.
also due to high demand, may cause a fall in temperature
and hence vaporization rate and hence vaporization rate
incomplete mixing in vaporizing chamber.
At low flow rates (<250 ml/min) output less due to inability of
FGF to push heavy vapor
Effect of Barometric pressure
Vaporizers are calibrated at standard atmospheric pressure (at
sea level).
Low boling point, high SVP anaesthetic volatile agents more
susceptible to influence by barometric pressure. p y p
VP of agents is independent of barometric pressure
Anaesthetic potency depends on partial pressure.
Required dial setting = dial setting x 760/ambient pressure
14
Effect of Low atmospheric Pressure:
Conc Calibrated Vaporizers-
Deliver Higher concentration if measured in
Volume% BUT deliver same partial pressure.
Clinical effect unchanged.
Small deviations in performance due to altered
splitting ratio (less gas density so increased flow
through the vaporizing chamber)
Measured Flow Vaporizers-
Deliver Higher concentration both when measured
in Volume% or partial pressure.
Effect of High atmospheric Pressure:
Conc Calibrated Vaporizers-
Increased density of gas increased resistance
through VC decreased vapour output both in
partial press re and ol me% partial pressure and volume%.
Measured Flow Vaporizers-
Deliver decreased conc both when measured in
Volume% or partial pressure.
Specific vaporizers
Early Methods
Open Drop Method - Inhalation anesthesia by vaporization
of a liquid anesthetic placed drop by drop on a gauze mask
covering the mouth and nose
Devices: Schimmelbusch mask
Other modifications Yankauer, Bellamy Gardner
Semiopen - A frame added to keep the ether in in an
enclosed area permitted some degree of rebreathing.
Eg. Ogston inhaler, Junkers chloroform apparatus, Flaggs can
Schimmelbusch Mask
Early Devices - Open Drop method
Bellamy Gardner wire mask with dropper
Yankaeur mask
Early Devices - Open Drop method
15
Early Devices - SemiOpen Drop method
Ogston mask with schimmelbusch frame
Flaggs can
EVOLUTION OF VAPORIZERS
MORTONS ETHER INHALER
1846, OCT 16
Open Ether Administration
Technique:
-Volatile anesthetic dripped onto a gauze :
Ether -16 layers gauze over mask.
Chloroform/ethyl chloride -12 layers of
gauze/1 layer lint (chloroform dropped over
half the area)
- Gradually increased no. of drops/ min.
-During inspiration: air passed through the gauze
and vaporized the liquid anesthetic into high
concentration
Open drop Ether
Bellamy Gardner
amber coloured
control on pouring
capacity -90 ml ether
INDUCTION
Ether
Rate of Drops
1
ST
min = 12 drops = 1 %
2
nd
3
rd
4
th
min = 100 drops = 10-12 %
Ethyl Chloride- 3 to 5 ml - 3 to 5 %
Rate of drops
1
st
min = 30 drops
2
nd
min = 60 drops
3
rd
min = 90 drops
Maintenence
Concentration for maintenance with ether is 6 -8 %
Heat loss = 200-300 cal/min
Temp. above and below mask = 2-3 degrees < room temp.
Temp. at mask = 0 1 degrees C
Gas composition under mask p
0% ether = 80% N2 + 20% O2
5% ether = 76% N2 + 18% O2
10% ether = 72% N2 + 16% O2
16
Advantages
Easy to administer; No specialized apparatus required
Low Dead Space 40-60 ml
Low Resistance
Wid M i f S f t Wide Margin of Safety
Relatively Cheap
Disadvantages of Open drop anesthesia
Significant rebreathing
Hypoxic mixtures may occur
Poor control of inspired gas concentrations
Inability to assist or control ventilation
No conservation of heat or humidity
Difficult airway management especially during head
and neck procedures
Pollution of the operating room
Hazardous especially with flammable agents
In-System Vaporizers (VIC)
There are two ways that gas flows through a
vaporizer
- Push Through Push Through
- Drawover
Drawover Anaesthesia
Drawover system:
Provide anaesthesia without a supply of compressed
gases.
Atmospheric air - main carrier gas
- drawn by the patient's inspiratory effort
- volatile agent (ether or halothane) added
to vaporizer.
Inhaled by the patient via a non - rebreathing valve.
Principle of the draw-over vaporizer
Drawover Anaesthesia
The components of a drawover circuit
17
EMO Vaporizer
Inlet for air
Temperature
Control lever
(Epstein Macintosh Oxford Vaporizer-1952)
Ether Level
Indicator
Outlet for ether
and air
Filler
Temperature
indicator
EMO
Classifictaion:
Concentration calibrated
Flow over with wick
In System (Inhaler)
T i b li d h & fl Temperature compensation by supplied heat & flow
alteration
Agent specific (diethyl ether, halothane, chloroform,
trilene, ether-halothane azeotrope)
EMO vaporizer - can be a part of a Drawover
system or used as a plenum vaporizer
Wt- 5.5 kg ; ht 24 cm ; diameter 23cm.
Outlet(male) inlet(female)
CONTROL lever 0 to 20%; In TRANSIT
position control lever seals ether chamber.
Inlet to Outlet- R to L
LEVEL INDICATOR- moves only after 150 ml
dd 300 l f f ll
Inlet
Control lever
Outlet
; add 300ml for full
FILLER - depress to fill ether (control lever
should be at 0-not transit- for air to escape)
springs back automatically.
Ether Level
Indicator
EMO-Physical characteristics
Temperature
Indicator
Filler
Temperature Indicator - rod with black & red bands & metal top
- At 20-25 C-black line with metal top visible
- At > 32 C - red band also visible- temp above working range
TAP for filling /draining water chamber at bottom
EMO
Surrounding V.C Water reservoir-1250cc (Heat reservoir)
(Al in Mark I, stainless steel in Mark II, III)
At outlet of V.C
- Thermocompensation mechanism at outlet of vc.
Metal bellows with liquid Ether[ether capsule]
connected to plunger
Working temp. range 15-29 C
Tropical climates may require precooling.
Water jacket serves as heat reservoir
EMO..
Care
Mark I--empty Al water jacket every 3 months, Mark II & III-
yearly water check
Evaluation
Calibration of EMO is accurate only for intermittent gas
flows; maintains output at 5 13L/min flows Highest conc flows; maintains output at 5-13L/min flows. Highest conc.
delivered 16%. If use as plenum i.e. blow air into it increase
output
Splashing during transit if in ON position.
Sticking of rotor-PTFE coating in Mk4 (Stetson)
Advantage- compact, low cost, portable, mass casualties, no
effect of altitude, easy maintenance, no need for sterilisation
18
Oxford inflating bellows
Self inflating bellows used with
spontaneous / controlled
ventilation.
Bellows sit vertically; internal
volume maintained by a spring;
6 bellows -150 ml each
2 unidirectional flap valves p
Ramaraos modification (for O2)
Magnet to inactivate distal
unidirectional valve.
EPSTEINMACINTOSHOXFORDVAPORIZER
1952(EMO)
Spontaneous ventilation
To facilitate gas flow through the OIB there are two one way
valves in the form of metal discs on circular seats.(A& B)
This arrangement works well for SV
Less satisfactory for IPPV as constant adjustment of the
Heidbrink valve required.
Assisted ventilation
1. Non-rebreathing valves (e.g.
Laerdal, Ambu) used to
facilitate IPPV with OIB.
2. Disable the downstream
valve with the magnet (hold
i i i i ) id it in open position) to avoid
jam.
3. If the OIB jams the patient
cannot exhale as an air lock
develops. The patient must
be disconnected from the
circuit to allow exhalation.
4. More common with IPPV
OMV
(Oxford Miniature Vaporizer)
1966 (Macintosh and Epstein of Oxford)
OMV
The OMV is a small thermally buffered vaporizer
- originally produced to be used with the EMO
- to speed the induction of anaesthesia
CLASSIFICATION
Concentration calibrated Concentration calibrated
Flow over with wick
Temp compensation by supplied heat
Low resistance
Can operate as Plenum vaporizer
Multiple agent (halothane, Trilene, Methoxyflurane)
19
OMV
Versatile, most portable drawover vaporizer
13.5 cm high,1060 gms with full water jacket.
Original models contained 20 ml, modern ones 50 ml .
Body stainless steel/Metal mesh wicks
Arrow indicates direction of flow
- With EMO flow is R to L
- With continuous flow machine indicates flow L to R
Suitable for multiple agents - halothane, isoflurane, chloroform,
methoxyflurane;
Different dial with calibrated scales is attached for each agent
[halo (0-4%),tri (0-1.5%), methoxy (0-0.6%)]
OMV
Thermal compensation (reservoir of glycol within a
metal heat-sink -water jacket at base with 25% glycol)
Designed for continuous flow rates of 3-8L/min or drawover rates
of 4-10 L/min; ambient temperature18 to 28C.
Special filler with 2 springs p p g
light pressure-air relief
more pressure-opens filler
Funnel around filler has capacity of 10 ml, covers 1/8th of level
indicator. A second 10ml can be added
Plugged into outlet of EMO - performance unaffected by IPPV-
can place on patient side of bellows.
OMV
Do not use in Circle system can produce very high
concentration.
Cleaning:
- Drain by tipping after pressing filler lever. y pp g p g
- Wash out with alcohol or Ether.
Disadvantages
- Holds only 20 ml ; cannot mount on backbar.
Goldman Vaporizer
Low resistance vaporizers
Goldman, Mckesson
Classification
Flow over without wick
No temperature compensation No temperature compensation
Multiple agents- Halothane , Trilene
In or out of system
Goldman Vaporizer
Small glass bowl
Capacity 20 cc
Bowl attached to a head, which divides gas between
bypass and vaporizing chamber
Control lever at top; max conc delivered at 3
rd
mark of Control lever at top; max. conc delivered at 3 mark of
2.21%
Young modification -Added a wick (increase to 4%).
Halls modification - 2 in series
20
Goldman Vaporizer
Mark I Mark II Mark III
Locking Self locks in
Off
Click stops No locking
Off
Divisions Off-1-2-3-on Off-1-2-3-on Off-1-2-on
Max. Concn. At 3 At 3 At on
Output from Goldman Vaporiser
Halothane 2l 8l 30l
1 0.03 0.03 0.03
2 0.41 0.74 0.92
3 0.73 2.21 1.31
On 0.74 2.08 1.21
Trilene
1 0.01 nil 0.01
2 0.16 0.44 0.35
3 0.47 0.68 0.52
On 0.45 0.70 0.45
Boyles Bottle
BOYLES BOTTLE
Classification
1. Concentration calibrated
2. Flow over or bubble through
3. No temp. compensation
4. Multiple agent (ether, halothane, trilene)
5. Out of system
Prof.A. K. SethisEORCAPS-2013 Prof.A. K. SethisEORCAPS-2013
P - Plunger
C Cowl/hood
Propotionating
valve
U - U/inlet tube
O - Outlet
Boyles Bottle
Control
lever
21
Boyle Bottles
Ether Bottle
Larger VC - 300 ml filled fully
Inlet tube & hood - Cu
Has 4 lines between off & on-begins to operate at
2
nd
mark
Trilene bottle -100ml
Chrome plated U tube & hood; cowl adjusted by
stainless steel plunger
Delivers 0.5-2 %
Boyle Bottles
Halothane bottle
Uses only control lever no plunger/hood
Inlet tube plugged at end, side hole 1 cm above 100 cc
mark.
Control lever scale longer Control lever scale longer
Calibrated in numbers from 0-10; starts at 3 , 1% at 4 ,
8% at 10.
Boyles Bottle
Factors affecting output:
1. Temp. of liquid
2. Plunger level
3. Control lever position
4. Level of liquid q
5. Eccentricity of hood
6. Agitation of vaporizer (Concn > 5 % for upto
15 secs)
Difficult to develop a meaningful calibration curve;
Unpredictable with potent and highly volatile
agents
Boyles Bottle
Care and Cleaning:
Empty after use/allow to dry
Unique Features:
Special grease for free rotation of drum
If Plunger loose-tighten the gland nut g g g
Replace packing in gland nut-cotton, neoprene, nylon
Bottle may chip off leading to leakage
Bottle washer may get damaged
Pressure build up in unused ether bottle
Static charges on cork-chain
Copper Kettle Vaporizer
FOREGGER COPPER KETTLE 1952
Classification
Measured flow
Bubble through
Out of system
Temperature compensation Temperature compensation
by supplied heat and manual
flow alteration
Multiple agent
choloroform, ether,
halothane.
- 2 models 400ml/ 160 ml
22
- Constructed of Copper
- High heat capacity
- High thermal
conductivity
- Gas breaks as it passes Gas breaks as it passes
through the diffuser and gets
fully saturated in its passage
through the liquid.
- High degree of accuracy.
Precision Vaporizers
Precision vaporizers deliver precise concentrations of
anesthetic.
Regulation of the vaporizer output may be fully automated or
manually controlled by the anesthetist.
A fully automated precision vaporizer will deliver the
concentration of anesthetic indicated by the vaporizer dial
even when there are changes in temperature fresh gas flow even when there are changes in temperature, fresh gas flow
rate, and circuit pressure
Automated precision vaporizers are designed for use with only
one anesthetic.
V.C has network of wicks/channels to ensure emerging gas is
fully saturated with vapor.
Include Ohmeda Tec series, Drager Vapor 900 series,
Forreger, Penlon, Ohio vaporizers.
Tec 2 Vaporizer
TEC 2 Vaporizer
Classification:
Flow over with wick
Out of system
Temp. compensation by automatic flow alteration
Agent specific (halothane or methoxyflurane)
Plenum
Spindle pulled out & rotated anticlockwise, concentration
0-4%
Internal Construction
VC round; 135 ml; concentric, circular wicks
TEC 2 Vaporizer
VC round; 135 ml; concentric, circular wicks
Filling tap at side, drain at bottom
Window on side for liquid level
Temp. Compensation-Bimetallic strip of v.c.-Ni-Cu at
outlet of V.C
TEC 2 Vaporizer
23
Very inaccurate at low flows below
4l/min.
< 1 Lpm flow & < 3% - delivers less
>3% & flows 2 Lpm delivers more
Little change in output <0 5%
TEC 2 Vaporizer
Little change in output <0.5%
Good for flow rates > 5 L/min
Addition of N2O increases vapor
output at dial set below 1%
Back pressure plays a significant role
at flows < 2 Lpm.
Care and Cleaning
Fluotec - Drain Halothane every 2 weeks & discard as
THYMOL accumulates Sticking of spindle and bimetallic
strip
H d
TEC 2 Vaporizer
Hazards
Tipping
Agitation
Reverse flow
TEC 3 Vaporizer
Classification
Concentration Calibrated
Flow over with wick
O t f t
TEC 3 Vaporizer
Out of system
Temperture compensation by automatic flow
alteration
Agent specific (Halothane, Methoxyflurane,
Enflurane, Isoflurane
Construction:
Concentration control dial is on top with +ve
catch at OFF
Calibrated from off to 5% in 0.5% gradations
Locking lever to be depressed before dial can be
TEC 3 Vaporizer
Locking lever to be depressed before dial can be
turned
Screw cap filler with drain at bottom
Optional pin safety system for filling
Sight window for liquid level on left
Internal Structure:
Completely redesigned
Has 2 sections-lower vaporizing chamber and
upper duct and valve system
2 bypass channels-one directs gas stream over
TEC 3 Vaporizer
bimetallic strip
Bimetallic strip at inlet of 2
nd
bypass
Gas exits vaporizing chamber by way of the
control channel and joins gas coming from the
bypass
Bypass is located concentrically within the
vaporizing chamber.
24
Methods to reduce the effect of intermittent back pressure.
Larger Bypass
Vaporizing chamber volume is reduced
Tube leading to VC longer
TEC 3 VAPORISER
Expansion area in the inlet tube.
Wicks excluded from area of vaporizing chamber near
the inlet.
TEC 3 Vaporizer
Hazards:
Faulty locking lever
Tipping to 180 increases concentration delivered to > 12%
Leaks small amount of vapor in off position Leaks small amount of vapor in off position
Reverse flow increases output
Comparison -Tec 2 and 3
Tec 2 Tec 3
External
Structure
Has one bypass and V.C
Side filling tap, Drain at
bottom,Side window for liquid
level
Not so
Has 2 sections-lower V.C & upper
duct and valve system
Side filling tap, Drain at
bottom,Side window for liquid level
Can be placed upright
Not so
Switching on Spindle pulled out &
rotated anticlockwise
Depress locking lever
Turn Concentration dial
Tec II Tec III
Bypass
Channel
One ; Smaller
Not so
Two; Larger
Bimetallic strip( regulates flow)
Vaporizing
Chamber
Round; Concentric wicks
Bimetallic strip at outlet
Not so
Wicks excluded from inlet
Not so
Tube leading to VC longer
Comparison -Tec 2 and 3
Tec II Tec III
Performance
data
Inaccurate at lower
flowrates (< 4L/min)
At flowrates <2L/min
- Dial settings < 2% -
delivers less
Accurate at lower
dial settings
At high dial settings
-conc at low flowrates
Accurate at high
Comparision - Tec 2 and 3
delivers less
- Dial settings > 2% -
delivers more
- Accurate at high
flowrates
TEC 4 Vaporizer
25
Classifcation - Same
Differences:
Depress release button on left of Control dial to turn on
Control dial on top - Rotate counterclockwise
Locking lever on the rear-Vaporizer can be turned on only if
locked on the manifold
TEC 4 Vaporizer
Two filling mechanisms
1. Screw cap with drain plug
2. Keyed filling Device
Helix
Bypass
Rotary valve
Inlet
Outlet
TEC 4 Vaporizer
Vaporizing
chamber
Bypass
chamber
Helix
Temperature sensitive
device
Wick
filler
Improvement over Tec III:
Output unaffected by back pressure changes under clinical
conditions
Unaffected by Tipping even upto 180.
Limitations
TEC 4 Vaporizer
a o s
Excess pressures (> 400 mmHg ) cause in output
Not so Accurate at low flow rates, low dial settings and larger
pressure fluctuations
Overfilling possible
Use of N2O decreases output
TEC 4 Vaporizer
Hazard
Leakage of agent if inadvertent loosening of drain plug
Overfilling of keyed filling vaporizer if vaporizer is in on
position or bottle adaptor is loose
TEC 5 Vaporizer
Introduced in 1989 responding to criticism of the
TEC 4
Difficulty in operation one-handed
Poor performance
Yearly service interval.
TEC 5 Vaporizer
y
26
Construction Features:
Top control dial
Locking lever and release
button.
Si h Gl B i h
TEC 5 Vaporizer
Sight Glass Bottom right
Keyed Filling device.
Features:
-Internal Baffle System
-V.C lies within the bypass
-Bypass along side of the
vaporizer
-Bimetallic strip in the base
TEC 5 Vaporizer
Bimetallic strip in the base
of bypass
-Before reaching VC
helical IPPV assembly-spiral
wick
Improved features
Bypass chamber at the base; an improved bimetallic strip.
Improved response to fluctuating back pr.
Agent capacity sed from 125 ml to 300 ml.
TEC 5 Vaporizer
One-handed dial control; more obvious 'off' position.
Improved safety interlock
Service interval now three yearly.
Improved characteristics with tubular woven cotton wicks
Evaluation
Greatest accuracy at fresh gas flow less than 5L/min and dial
settings < 3%. At higher flows and higher dial settings output
decreases.
More pumping effect than Tec 4
TEC 5 Vaporizer
Greatest accuracy between 15 to 35C
Carrier gas composition affects output.
Improved key filler
Easier mech. to switch on rotary valve and lock with one hand
Hazards:
More prone to pumping effect than tec 4
Large liquid loss if filling port is opened
Overfilling - bottle adaptor loose, vaporizer on
R fl i
TEC 5 Vaporizer
TEC VAPORIZERS
CLASIFICATION (TEC I-V)
1. Variable bypass
2. Flow over with wick
3. Out of system
4. Temp. compensated by automatic flow
alteration
5. Conc. calibrated.
6. Agent specific
27
TEC 7 Vaporizer
The TEC 7, an improved version of the TEC 5.
Introduced in July 2002
Modifications :
a) Three filling devices
- Funnel-filler
TEC 7 Vaporizer
- Quik-Fil
- "Easy-fil" filler mechanism(for sevoflurane)
b) Soldered sump assembly eliminating seals
c) Improved sight glass design
d) New ergonomics and design
e) Planned factory service free
Evaluation
Performance curves and characteristics similar to Tec 5
Hazards
TEC 7 Vaporizer
Tilting affects output
Overfilling can occur
TEC 6 Vaporizer
(Desflurane)
Classification
Injection
Thermocompensation by supplied heat
El i ll h d d l i i G /
TEC 6 Vaporizer
or Electrically heated, dual circuit Gas /
Vapor blender
Single agent-Desflurane
Desflurane is extremely volatile (Boiling Point- 22.8C)
The Tec 6 vaporizer:
- heating the desflurane liquid to above its Boiling point in a
sealed chamber and mixing pure desflurane gas with the carrier
TEC 6 Vaporizer
g p g
gas.
Tec 6 is electrically powered and electronically controlled
Since the vaporizing chamber is sealed from the atmosphere, a
special filler arrangement is required.
28
H-Heating element
O-Orifice
P-Differential Pressure
Transducer
R1-Resistor
R2 2 d R i t
TEC 6 Vaporizer
Desflurane heated to 39C in a sealed chamber, adjusts by H
Carrier gas flow restricted by O, so that pr. is proportional to flow
Pressure sensed by P-which readjusts R1 so that flow of desflurane ~
carrier gas flow
Control dial adjusts R2, and thus the output concentration
R2-2nd Resistor
Evaluation
Output almost linear at3%, 5%,7% settings. Slightly
lower output at <5L/min flow; Ideal temp 18-30C.
Tilting Resistant.
TEC 6 Vaporizer
Pumping effect insignificant.
The output decreases with Air or N2O as carrier gas.
Drager Vapor
Most accurate
Classification
Conc calibrated
Flow over with wick
Drager Vapor
Flow over with wick
Out of system
Temp. compensation by
manual flow alteration
Agent specific
Very accurate at all dial
settings over a wide
range of flow rates
Drager Vapor
Drager Vapor 2000
29
Concentration range:
Halothane 0.2 to 6%
Enflurane 0.2 to 8%
Isoflurane 0.2 to 6%
Drager Vapor 2000
Sevoflurane 0.2 to 8%
Temperature range:
Ambient and Vapor temperature during operation 10 to
40C
during shut-down (filled, control dial at T) 0 to 40C
during storage (empty, dry wick) -20 to 70C
Filling volume for anesthetic agent:
about 360 mL with dry wick
about 300 mL with moist wick
about 260 mL between minimum and maximum mark
Drager Vapor 2000
about 260 mL between minimum and maximum mark
Maximum angle of tilt:
during operation 30
Penlon Sigma Delta
Specifications:
Weight: 5 kg approx.
Capacity Volume: at MAX mark 250 mL
nominal Volume at MIN mark: 35 10 mL
Penlon Sigma Delta
nominal Volume at MIN mark: 35 10 mL
Flow Range: Operating flow range 0.2 to 15
litres/min
Temperature Range: Operating temperature range 15
to 35C
Hazards:
The Penlon Sigma Delta may malfunction if exposed
to excessively high temperatures. This may affect the
calibration. The vaporizer should be stored between -
Penlon Sigma Delta
p
20C and 50C.
This vaporizer is flow-direction sensitive.
possibility of overfilling.
Safety features
Keyed fillers
Low filling port
Penlon Sigma Delta
Low filling port
Secured vaporizers (less ability to move them about
minimizes tipping)
Interlocks
30
Aladin Cassette Vaporizer
Classification
Conc calibrated
Flowover
Automatic
thermocompensation
Cassettes containing liquid
anesthetic inserted into a port
Agent recognized & dispensed
into the stream of FGF.
Tipping resistant & maintenance
free free.
Power or battery backup &
adequate O2 (or air) pressure
mandatory
Fixed output irrespective of fresh
gas mixture
Extremely light& can be removed
with one hand.
Hazards Of Vaporizers
Hazards of Vaporizers
Incorrect agent /Misfiiling
Tipping
Foaming
Overfilling
Reversed flow
Leaks
Dual Vaporizers on
Misfilling
Vaporizers are calibrated according to the vapor
pressure of the agent
If you fill with an agent with a higher vapour pressure
-- overdose
If you fill with an agent with a lower vapour pressure
-- underdose
31
AGENT SPECIFIC FILLING
SYSTEMS
AGENT SPECIFIC FILLING SYSTEMS
A vaporizer designed for a single agent be fitted with
a permanently attached agent specific device to
prevent accidental filling with a wrong agent.
They prevent accidental filling with the wrong agent.
Reduce air pollution.
Vaporization chamber
TYPES
KEYED FILLING SYSTEM
SCREWCAPPED FILLING SYSTEM
PIN SAFETY SYSTEM
Filling Devices
Filling Systems
1. Funnel Filler
Isotec 4 vaporizer with funnel-filler
2. Keyed Filling System
Two projections -- one thick &
one thin to mate with
corresponding indentation on
bottle cap of adaptor tube
Filling Systems
Isotec 4 vaporizer with key-filler
32
BOTTLE COLLAR
Attached at the neck of the bottle.
2 projections, one thicker than the other are there.
This mates with the corresponding indentations on
the bottle adaptor
Agent Specific Filler Tube
(Bottle Adaptor)
Filler
block-
fits into
vaporizer
receptacle
Bottle cap-keyed & color coded
Prof.A. K. SethisEORCAPS-2013 Prof.A. K. SethisEORCAPS-2013
FILLING
Cap of bottle removed
Adapter screwed to the collar
FILLING
Vaporizer turned off
Plug removed
Bottle with adapter inserted such that the grooves
match; (tube bent such that bottle is below inlet)
33
DRAINING
Adapter attached to bottle filler plug removed
male adaptor inserted retaining screw
tightened bottle held below the receptacle
drain valve opened drained screw loosened
d t d fill l i t d adaptor removed filler plug inserted
PROBLEMS
1. Difficulty in filling
2. Misalignment of adaptor in filler receptacle
3. Adaptor not sealing at the bottle end
4. Leak in the bottle adaptor
5 Air bubbles 5. Air bubbles.
6. Lost bottle adaptor
7. Failure of keyed system
8. Liquid leaks
Vaporizer Mounting Systems
If >1 vaporizer can be switched on at a time the patient
exposed to a overdose of anesthetic agent.
The downstream vaporizer is contaminated.
Types of mounting system:
Selectatec back bar -A switch on the back bar may be used to
direct gas flow through only one vaporizer at a time, e.g. the
Fraser Harlake Selectatec back bar
A mechanical locking system may be used that only allows
one vaporizer to be switched on, e.g. Ohio selector manifolds
and Drger 19.3 vaporizers.
A mechanical inter-connector
Selectatec back bar
Ohmeda selectatec has
pins in manifold linked to
control dial
If one on extend to prevent If one on extend to prevent
other
Selectatec back bar
Pair of port valves for
each vaporizer
Vaporizer is mounted
and locked
When ON 2 plungers When ON 2 plungers
open the valve ports &
activate extension rods
that prevent other
vaporizers
Mechanical locking system
OHIO SWITCH
Allows lt, centre, rt to
be used
Slots in selector line up
with flanges on g
vaporizer control dial
34
Mechanical locking system
DRAGER LOCK
For Drager 19.2
has rotating bar on
manifold with teeth
that fit into a cut that fit into a cut
out on the control
dial
Vaporizer Mounting Systems
Vaporizers should be arranged in the order
- most volatile agent downstream
Less potent upstream, More potent
downstream
If equipotent: High SVP downstream
- If explosive downstream
- Trilene downstream
- Easy to clean downstream
ORDER OF VAPORIZERS
UP
STREAM
DOWNSTREAM
SEVOFLURANE ENFLURANE ISOFLURANE HALOTHANE DESFLURANE
VP- 157 175 238 243 669
Ideal Vaporiser
Deliver fixed desired concentration and equal to
concentration on dial settings.
Independent of
temperature,
flow rate and
carrier gas alterations.
No effect of back pressure.
Easy to maintain and clean.
Agent specific.
Vaporizers ASTM standards
1. Effects of variation in temperature, Pressure, tilting, back
pressure and input flow rate and gas mixture composition on
vaporizer performance should be stated.
2. Average delivered conconteration not more than 20% or
5% of the max. setting.
3. System that prevents gas from passing through the vaporizing
chamber or reservoir of one and then through another should be
provided.
4. Output of the vaporizer should be < 0.05% in the OFF or
zero position if the zero is also Off.
ASTM Standards
5. All vaporizer control knobs must open counterclockwise.
6. Either the max or min filling levels or the actual usable
volume and capacity should be displayed.
7. Cannot be overfilled in normal operating position.
8 If unsuitable for use in breathing system noninterchangeable 8. If unsuitable for use in breathing system, noninterchangeable
23 mm fittings; inlet male, outlet female, direction of gas flow
must be marked
9. If suitable for use in breathing system, standard 22 mm
fittings ; inlet female, outlet male, direction of gas flow
marked.

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