OUTLINE
vCSF SPACES
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vCSF FORMATION ? CIRCULATION ? REABSORPTION
vMETHODS OF DETERMINING Vf AND Ra
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vEFFECTS OF DRUGSvALTERATION IN CSF DYNAMICS IN PATHOLOGY
ANATOMY OF CSF SPACES
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CSF is clear, colourless liquid that is formed in brain and circulatesthrough macroscopic & microscopic spaces that are in continuity.
Macroscopic spaces (140-150ml):
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? Two lateral ventricles? Third ventricle
? Aqueduct of sylvius
? Fourth ventricle
? Central canal of spinal cord
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Microscopic spaces:? Brain and spinal cord ECF space (300-350 ml)
THREE DIMENSIONAL SHAPE OF THE VENTRICULAR
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SYSTEMPROPERTIES OF CSF
COMPOSITION
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? Na content peaks at 8:00 am & 6:00 pm? Relationship between Na concentration and migraine has been proposed as
peaks correspond to migraine attacks
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.. Harrington MG,Salomon RM, et al. Cerebrospinal fluid sodium rhythms.
Cerebrospinal fluid Res 2010
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COMPOSITION
? Varies according to sampling site
? Altered during neuroendoscopy
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Na,Cl,Mg
Glucose, Protiens, AA, K ,
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HCO3, Ca, Phosphate, Uric acid--- Content provided by FirstRanker.com ---
FORMATION OF CSF3 Sites:
? Choroid plexus ( 50 ? 70 %)
? Ependymal surfaces of ventricles
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? Perivascular spaces? Rate ( Vf ) 0.35-0.40 ml/min
500-600 ml/day
? Turnover time- 5-7 hrs (4 times/day)
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? 40%-70% enters macroscopic spaces via CP? 30%-60% enters across ependyma and pia
? Recent studies ? Bidirectional fluid exchange at BBB far exceeds CP csf formation
- Brinker T.,et al. A new look at cerebrospinal fluid circulation. Fluids Barriers
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CNS. 2014;11:10-15
Choroid plexus
It is a cauliflower like
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growth of blood vesselscovered by a thin layer of
epithelial cells.
It is made of 3 layers:
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? fenestrated capillaryendothelium
? extra cellular matrix
? epithelial cells
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Choroid plexus projects into:? Temporal horn of
lateral ventricle
? Post. Part of 3rd ventricle
? Roof of 4th ventricle
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Blood supply: ant. & post choroidal
artery (lateral & 3rd ventricle) and supr
cerebeller and PICA (temporal horn & 4th
ventricle)
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Nerve supply : branches of Vagus,Glossopharyngeal & Sympathetic N.
CSF FORMATION AT CHOROID PLEXUS
Blood entering CP capillaries filtered form
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protein rich fluid similar to ISF in CP stroma
Hydrostatic pressure & bulk flow enter cleft
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between epithelial cellsstromal fluid transported across CP epithelium-
Ultrafiltration & secretion
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ATP dependent membrane pump transport Na across luminal surface tomacroscopic spaces in exchange for K & H.
Water moves from stroma into CSF by conc gradient by ionic pump.
CSF FORMATION AT EXTRA CHOROIDAL SITES
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vDerived from ECF & cerebral capillaries across BBB
vOxidation of glucose (into H2O & CO2) by brain [60%].
vUltrafiltration from cerebral capillaries[40%]
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TIGHT JUNCTIONS
In blood-ECF interface
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Pass
Glucose /electrolyte/water/AA/lipid soluble material
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Large polar/proteinStop
Glucose rich and protein poor fluid diffuse through ECF space toward macroscopic spaces
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? Water and other constituent ofplasma crosses Blood brain
Barrier into the brain ECF space
by diffusion or transport.
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? Water and cellular metabolites
added to the ECF from neurons
and glial cells.
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MOVEMENT OF GLUCOSE & PROTEIN
? CSF glucose conc. is approx. 60% of that in blood
? Ratio remains constant till 270 -360mg/dl blood glucose
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? Glucose enters CSF -Facilitated transport & follows saturable kinetics (i.e ratedepends on serum glucose conc.)
? Protein entry in CSF limited ? conc. is 0.5% or less of serum conc.
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? Protein in CSF transported with CSF & cleared from csf space to dural venoussinuses by
? "Sink effect" ? flowing CSF keeps CSF & brain protein conc. Low.
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EFFECT OF INCREASED ICP ON CSF FORMATIONRelation between Vf and ICP/CPP
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? ICP
? CPP
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? Vf? Vf
?As long as CPP remain > 70mm of Hg, increase of ICP[upto 20mm of Hg] has
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no major impact on Vf (rate of CSF formation).?When CPP is significantly lowered <70 mmHgCBF and CPBF , Vf
CIRCULATION OF CSF
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? Hydrostatic pressure of CSF formation15 cmH20 produce CSF flow.
? Cilia of ependymal cell generate current to propel CSF toward 4th ventricle & its
foramina into subarachnoid space.
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? Respiration variations Additional CSF movement
? Vascular pulsation of cerebral arteries , CP
? 15cm H20 CSF pressure of formation
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6 cm of
pressure
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?gradient across
arachnoid villi
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? 9 cm H20 superior sagittal sinus pressure
Suction pump effect
Reabsorption ? arachnoid villi (SSS) & spinal dural sinusoids in dorsal nerve
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roots.REABSORPTION
? CSF pass from Subarachnoid spaces via Arachnoid villi & granulation
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into venous blood.? Arachnoid villi or granulations are protrusion of the arachnoid cells from
subarachnoid space into & through wall of venous sinuses
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? Arachnoid villi are located:
? Intracranial- Superior Sagittal sinus (85-90% reabsorbed)
? Spinal - dural sinusoids on dorsal nerve root (10-15%)
DETERMINANTS OF REABSORPTION
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? Normal intracranial pressure:
? Endothelium covering the villus acts as a CSF- blood barrier
? Rate of pass of CSF? 1.Trans villus hydrostatic pressure gradient
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(CSF pressure ? venous sinus pressure)2.Pressure sensitive resistance to CSF outflow at arachnoid villi
CSF passes through endothelium via: 1. Pinocytotic vesicles
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2. Transcellular openingsDETERMINANTS OF REABSORPTION
? Increased intracranial pressure:
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? Rate of reabsorption of CSF (Va) if pressure gradient across villus
? Resistance to reabsorption of CSF(Ra) remains normal upto a CSF
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pressure of 30 cm of H20; above this it is decreased.FUNCTION OF CSF
? Protection, Support, Nutrition
? The low Specific gravity of CSF (1.007) relative to that of the
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brain (1.040) reduces the effective mass of a 1400g brain to only
47 g.
? Stable supply of nutrients, primarily glucose(active transport); also
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vitamins/ eicosanoids/monosaccharides/neutral & basic amino
acids/monocarboxylic acid (specialized pump mechanism).
CONTROL OF CHEMICAL ENVIRONMENT
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? Exchange between neural tissue & CSF occurs readily by diffusion
? (because distance b/w CSF and any brain area is max 15 mm & ISF
spaces of brain and spinal cord is continuous with macroscopic CSF
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spaces.)? Acid-base characteristics of CSF influence:-
? Respiration
? CBF, CBF-AR
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? Cerebral metabolismCONTROL OF CHEMICAL ENVIRONMENT
HR
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EmotionalBP
CSF
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Ca/K/Mg/bicarb
Muscle tone
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VasomotorRespiration
CONTROL OF CHEMICAL ENVIRONMENT
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Primary pumps
? K/HCO3
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(active transport) ? Ca/MgSecondary pumps ? H+
(passive
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? Cl-
transport)
EXCRETION
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? Removes metabolic products, unwanted drugs
? BBB excludes out toxic, large , polar and lipid insoluble drug,
humoral agents etc.
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INTRACEREBRAL TRANSPORT
MEDIAN
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EMINENCECSF
ECF
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Neuron
Neurohormonal releasing factor formed in hypothalamus
METHODS OF DETERMINING CSF
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FORMATION RATE & RESISTANCE TO
CSF ABSORPTION
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?Ventriculocisternal perfusion?Manometric infusion
?Volume injection or withdrawal
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VENTRICULOCISTERNAL PERFUSION
? EXPERIMENTAL ANIMALS:
? 1st described in 1960 by Heisey and Pappenheimer.
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? Cannula is placed in one/ both lateral ventricles & in cisterna magna.? Labelled mock CSF infused into the ventricle & mixed sample of labelled and native
CSF collected from cisterna magna.
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? Conc. Of labelled CSF in outflow sample is measured & time of sample collectionnoted.
? Vf, Va, Ra is measured using formulas.
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IN HUMANS:? Outflow catheter is placed in lumbar subarachnoid(SA) space and ventricular
& spinal CSF pressure closely monitored.
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MANOMETRIC INFUSION? IN EXPERIMENTAL ANIMAL :
? Described by Maffeo and Mann in 1970.
? A manometric infusion device inserted into spinal or supracortical SA space.
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? Mock CSF infused into SA space, CSF pressure is measured at same site ofinfusion.
? IN HUMANS:
? No. of infusion is reduced & infusion rate are limited to 0.01 - 0.1ml/sec.
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? Infusion is restricted to 20-60 secs.? Infusion discontinued at CSF pressure of 60-70 cm H2O or rapid rise of CSF
pressure.
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VOLUME INFUSION OR WITHDRAWAL? IN EXPERIMENTAL ANIMALS
? Described by Marmarou and Miller in mid 1970.
? Ventricular/spinal SA catheter inserted to permit injection or withdrawal of
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CSF & measurement of CSF pressure change that accompanies injection or
withdrawal.
IN HUMANS:
? Previous two methods are less commonly used due to hazards associated with
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prolonged infusion of mock CSF.
? Advantages:
? In case of raised ICP- withdrawal of CSF is therapeutic
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? Calculate Vf, Ra, compliance (C)? Risk of infection is minimum(closed system)
? Test can be use for repeated testing.
? anaesthetic and drug induced changes in csf
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formation rate (Vf) and resistance to csf
absorption (ra)
INHALED ANESTHETICS
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ENFLURANE
Vf
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RaICP
LOW[0.9%-1.8%]
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0
+
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+HIGH[2.65& 3.5
+ (40%)
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0
+
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end expired]ENFLURANE INCREASES METABOLISM
INHALED ANESTHETICS
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HALOTHANEVf
Ra
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ICP
1 MAC
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--+
+
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INCREASES GLUCOSE TRANSPORT INTO BRAIN
INCREASES Na/Cl/H2O/ALBUMIN TRANSPORT INTO CSF
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HALOTHANE INDUCED STIMULATION OF VASOPRESSIN RECEPTORSDECREASEVf
INHALED ANESTHETICS
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ISOFLURANE
Vf
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RaICP
LOW[0.6]
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0
0
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0[1.1%]
0
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+
+
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HIGH[1.7-2.2]0
--
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--
INHALED ANESTHETICS
SEVOFLURANE
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Vf
Ra
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ICP1 MAC
--
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+
?
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INHALED ANESTHETICSDESFLURANE
Vf
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Ra
ICP
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HYPOCAPNIA &0
+
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+
CSF PRESSURE (0.5
& 1 MAC)
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OTHER SITUATI0NS
0
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00
INHALED ANESTHETICS
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NITROUS OXIDEVf
Ra
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ICP
66%
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00
0
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DECREASES BRAIN GLUCOSE INFLUX AND EFFLUX
I.V. ANESTHETICS
KETAMINE
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Vf
Ra
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ICP40mg/kg/hr
0
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+
+
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I.V. ANESTHETICSETOMIDATE
Vf
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Ra
ICP
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Low dose .86mg/kg 00
0
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High dose
--
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----
I.V. ANESTHETICS
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PROPOFOLVf
Ra
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ICP
6mg/kg
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00
0
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12,24, &
48 mg/kg/hr
PENTOBARBITAL
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Vf
Ra
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ICP40mg/kg
0
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0
0
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I.V. ANESTHETICSTHIOPENTAL
Vf
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Ra
ICP
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LOW (6mg/kg F/B 0+/0
+/0
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6-12mg/kg/hr)
HIGH (18-
--
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--
--
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24mg/kg/hr)I.V. ANESTHETICS (SEDATIVES
&HYPNOTICS)
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MIDAZOLAMVf
Ra
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ICP
LOW (1.6mg/kg fb 0
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++
0.5mg/kg/hr)
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INTERMEDIATE (1-0
0
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0
1.5 mg/kg/hr)
HIGH (2mg/kg/hr)
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--
+
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--/?FLUMAZENIL
Vf
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Ra
ICP
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LOW (0.00250
0
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0
mg/kg)
HIGH (0.16 mg/kg) 0
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--
I.V. ANESTHETICS (OPIOIDS)
FENTANYL
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Vf
Ra
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ICPLOW DOSE
0
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--
--
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HIGH DOSE--
0/+
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--/?
SUFENTANYL
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VfRa
ICP
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LOW DOSE
0
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----
HIGH DOSE
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0
+/0
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+/0AlFENTANYL
Vf
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Ra
ICP
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LOW DOSE0
--
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--
HIGH DOSE
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00
0
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I.V. ANESTHETICSLIDOCAINE
Vf
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Ra
ICP
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0.5mg/kg--
0
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0/+
1?g/kg/min
CRUX OF VF AND RA
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?
? Ra increases
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Vf increases?
? Halothane ( 1MAC)
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High dose Enflurane
? DES( hypocapnia + increase csf pressure)
? Low dose enflurane
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? Sevo ( 1 MAC )? Midazolam(low dose)
? Ketamine
Both Vf & Ra Fentanyl , Etomidate
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I.V DRUGS
? IV acetaminophen moves readily and attains peak conc. in an hour in CSF
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rapid central analgesia and antipyretic effect? Ibuprofen : peak at 30-40 min
DIURETICS
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VfMECHANISM
ACETAZOLAMIDE
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-- BY 50%
INHIBITION OF CA
INDIRECT ACTION ON ION
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TRANSPORT(VIA HCO3)CONSTRICTS CP ARTERIOLES
& DECREASE CPBF
METHAZOLAMIDE
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ACETAZOLAMIDE +OUABAIN Vf BY 95%= ADDITIVE
DIURETICS
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Vf MECHANISMFUROSEMIDE
--
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DECREASE Na+ OR Cl-
TRANSPORT
MANNITOL
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--
DECREASE CP OUTPUT
AND ECF FLOW FROM
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BRAIN TO CSFCOMPARTMENT
OTHERS
DRUG
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Vf
MECHANISM
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DIGOXIN,OUABAIN--
INHIBIT NA-K PUMP OF CP
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THEOPHYLLIN
+
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PHOSPHODIESTERASEINHIBITOR
CAMPSTIMULATE
CP NA-K PUMP
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VASSOPRESSIN--
CONSTRICTS CP BLOOD
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VESSELS3% HYPER TONIC SALINE
--
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OSMOLALITY GRADIENT FOR
MOVEMENT OF FLUID
PLASMACP OR BRAIN
TISSUE OR CSF
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DINITROPHENOL
--
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UNCOUPLE OXIDATIVEPHOSPHORYLATION
ANP
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--CGMP
MUSCLE RELAXANT
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RELAXANTV
Vf
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RaSCOLINE, VECURONIUM
0
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0
INFUSION
STEROIDS
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? Decrese Ra
? MethylPrednisolone/prednisolone/cortisone/dexamethasone
? Probable mechanism :
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? Improved CSF flow in SA spaces/ A.villi? Reversal of metabolically induced changes in structure of villi, action at CP
? Dexamethasone Vf by 50%(inhibition of Na-K ATPase)
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ALTERATION IN VARIOUS PATHOLOGY? Intracranial volume changes
? Volume of intracranial blood/gas/tissue CSF volume
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?Mechanism: Translocation into spinal spaces? increased reabsorption
? Volume of intracranial blood/gas/tissue CSF volume
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?Mechanism: Cephalad translocation
? Decreased reabsorption
ACUTE SAH
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? Increases ICP
? Intrathecal injection: Whole blood, plasma, diasylate of plasma, serum &
saline--- Va & Ra values measured by Manometric method
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? Whole blood and plasma raised ICP and caused a 3 to 10 fold rise in Ra
respectively
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? Fibrin deposits within villiCHRONIC CHANGES AFTER SAH
? Extensive fibrosis of villi leptomeningeal scarring functional
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narrowing or blockage of CSF outflow tracts [ Ra isincreased]hydrocephalus
BACTERIAL MENINGITIS
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? Animal study with S.pnemoniae, E coli
? ICP & Ra increased in both
? Even with antibiotic Ra remained high for 2 weeks post Rx
? Methyl prednisolone ed Ra to a value that was intermediate between control
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and infected.
PSEUDOTUMOR CEREBRI
? Increased ICP Increased 1.Ra, 2.Vf, 3. greater water
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movement into brain 4 . CBF & CBV, 5 glial or cellular edema .
? Impaired reabsorption is the principal cause
? Prednisone decreases Ra
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HEAD INJURY
Ra increased and Vf within normal limits in 75% patients.
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20% of the raised ICP derived from changes in Ra /Vf.IN SUMMARY
? CSF plays a key role in brain well being
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? Vf changes : changes ICP? Ra changes: Changes ICP, alters pressure buffering capacity of brain
? In raised ICP, Anesthetics induced changes in Vf & Ra significantly alter the
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effectiveness of treatments employed to reduce ICP.