Circle of Willis

 

Common carotid origin

☛ Rt common carotid from Rt brachiocepholic trunk
☛ Lt common carotid from Arch of aorta
☛ In neck they travel in carotid sheath
☛ At level of thyroid cartilage they divide into external & internal carotid A.
☛ Internal carotid A passes through neck to enter middle cranial fossa without branching

 

 Supplies

☛  hypophysis cerebri,orbit & major portion of supratentorial region.
☛ Cerebral arteries derived from ICA & vertebral arteries
☛ Two ant. cerebral arteries (braanch of ICA).
☛ Anteriorly forms circle of Willis with two ant. communicating Arteries.
☛ Two vertebral Arteries forms – basilar Artery which gives two post cerebral arteries which form posterior circle of  Willis with two post. communicating arteries.
☛ Middle cerebral A supplies Lateral  surface of each cerebral hemisphere
☛ Ant & post cerebral  Arteries supplies medial & inferior surfaces of cerebral hemisphere

☛ Normal cerebral blood flow – 50ml/100ml/mm
☛ 4 time ↑ in gray matter then white water 80 & 20 ml/100gm/mm respectively.
☛ Metabolic requirement of oxygen in brain tissues 3 – 5 ml / 100gm/mm.
☛ Cerebral infarction depends on the degree & duration of ischemia.

Penumbra-neurons that are non-functional but that will recover fully with restoration of adequate flows are said to be penumbra

☛ If blood blow <10ml/100gm/mm- normal destruction occurs.

Cerebral auto regulation

☛ 50 to 150 mm of Hg
☛ If pr. above 150mofg vasoconstriction
☛ If pr. <50-vasodilation to maintain CBF in HTN patient limits are increased

☛Hypercarbia – cerebral vasodilation
☛Hypocarbia -vasoconstriction
☛Each mm Hg in PCO2 changes CBF 4%

Determinants

• Nerve call activity
• Cerebral perfusion pressure
• PaCO2
• pH
• PaO₂
• neurogenic influences

Luxury perfusion blood flow in excess of metabolic need

Intracerebral steal response to hypercarbia decreases blood flow to ischemia area.

Inverse steal or Robin Hood syndrome
☛ Effect of hypocapnea vasocastriction ↑ blood flow to ischemic region of brain.
☛Vasoconstriction in adjacent normal arterioles causing  local ↑in perfusion pr & augmenting collateral flow to ischemic,unreactive,maximally vasodilated area of brain.

CABG & Carotid Endarterectomy

• Combined lesion in one pt. If only CABG done 1^st then 14% risk of stroke
• If only CEA done then 20% MI risk

Bernhard et al 1972 combined approach to carotid end arterectomy  & CABG.
Frequency of stroke with cardiac sx 2 to 6%

CPB

• Embolic neurologic injury.
• An aortic cannulation.
• Plaque rupture duringg aortic cannulation.
• Release of aortic x clamp.
• Condiac manipulation according to transcraial Doppler USG.

Preop risk facters for stroke in pt  undergoing  CABG ON CPB.

1. Carotid stenosis > 80%
2. Carotid occlusion.
3. Prior stroke or travsient ischemic attack.
4. Peripheral vascular disease.
5. Post infarction angina.
6. Prolonged duration of CPB.

☛ Incidence of haemodyanamic  significant carotid stenosis in pts needing  CABG Varies between 2% & 16%
☛ Carotid bruit may be audible with minimal Carotid stenosis & silent with carotid lumen 1 -2 mm in diameter.
☛ USG with pulse Doppler & duplex scan are appropriate___ tests to assess need for carotid angiography – gold     standared for evalution carotid stenosis.
☛ Hemipheic stroke – severe carotid disease can occure in CABG Pt with CPB.
☛ Stroke rate of combined operation is twice than each opevation alone.
☛ 5.5% stroke rate in  unoperated carotid disease in CABG pt .
☛ 3.1% stroke rate who underwnt combined approach.
☛ Age > 70years have more stroke rate 40% carotid stenosis pts have CAD.
☛ Carotid Endarterectomy  pt with severe symptomatic CAD has associated with 17% & 20% incidence of MI & mortality

No Myocardial Infarction  in Combined approach CAD & CEA

• Shwarting et all – no difference  in outcom  when CEA was perfomed immediately before intiation of CPB or during hypo henic CPB
• Combined approach also decreasesa hospital stay & cost as well (Daily et all)

Anaesthetic considerations

Goals – maintain MAP without acceptable safe limit for brain as well as myocardial  perfusion (middle to upper normal range without increases HR & after load)

• Normocapnia.
• Cerebral protection.
• Neuoro monitoring.
• Early extubation for neuro assessment outnight factors –hypothermia bleeding & haemodyananic instability.

 aim for

1. Protection of heart & brain
2. Control of heart rate & BP
3. ablation of sx pain & stress response
4. Awake pt at the end of sx for purpose of neurological examination.

☛ Etiology  of carotid endarterctomy

       atherosclerosis.
☛ Symptons – attack of TIA amaurosis fugax – temporary Monocular blindness caused by TIA of retina .
☛ Risk of stroke – ↑ thrombosis, disruption of plaque .

Indication  of Sx-

• TIA with angiographic evidance of stenosis.
• Reversibee ischemic neurologic deficit with >70% stenosis of vessel wall or an ulcerated plaque with / without stenosis.
• Unstable neurologic status persistant  despite anticoagulation .

Pre-op evaluation-

• Freqent   BP monitoring  & target BP range should be decided.
• Continue  all long term cardiac  medications (aspirin 100).
• HTN
• DM -sugars level
• Investigations routine/specific.

Premedication mild sedation & anxiolysis  intraop – monitoring-

1.  ECG – II, V5
2. pulse oxemetry.
3. intracrtrial pressure monitoring.
4. if CVP require then – femoral  or subclarian

GA

Goals
☛Induction   mild midazolam, fentanyl , propofol + NDMR.
☛Esmolol/lignocain to obtend  largyngoscopy reflex.
☛T/t of BP changes.
☛Pnenelepinephrene  50 to 100 microgram
☛Namisropruiside 6 to 25 us for st TN
☛Administration fluids, titration of anaesthetics & T/t of hypolension  is very important.
☛Maintainance of anaesthesia  – O₂ + nitrous oxide 50%
☛isoflurane/sevoflurane
☛Haeneodyemanic fluctuations  –

1. Light plane
2. Short acting vasocostrictors  increases BP,
3. ↑ HR/BP-↑myocardial ischemia

☛ Manipulation  of carotid sinus –  bradycavdia & hypotension
☛Infillrate carotid bifurcation with 1% lidocaine (may ↑ intra & postop HTN) .
☛End of Sx – titrate inhalations awaking – reversal  of NMBA 4↑ or 100%
☛Place pt head up recumbent position/ quiten room.

Nemologic assessment
☛Period of emergence & Extubation associate with ↑ HTN & tachycardia tight hemodyanamic control is rewarding
☛Propofol group have less emergence crisis.

Regional & Local anaesthesia

1. Blocking C₂ & C₄ – superficial & deep cerical plexus block.
2. Local infillation of sx field – necessary sensing blockade.

Allows – 1. Continous  neurolgic monitoring / assessment(most sensitive  method to dectect cerebral ischemia)

2. awoidance of expensne  on neuromonitoring  & ↓ vasopressor response and greater  BP stability
3. ↓ hospital  stay & cost.
4. Grater stability of  BP

complications- loss of conciousness

seizures

• Disadvantage-   pts claustrophobic anxiety,  irritability,difficult neuromonitoring in uncooperative patients.

Relative contraindications

1. Pt refusal for LA
2. Difficult vascular anatomy
3. Short neck, high biturcation,  vigorous mandible retraction.

PH & glucose Monitoring-

• Cerebrovascular  reactivity to CO2  is disturbed & autoregulatory capacity in ischaemic zone  is lost.

Advisable – normocarbia

• M/o BSL below 200 mg/dl

Neurolgic M/M

• Stump pressure – <50 mm of Hg – hypoperfusion.
• Regional cerebral blood flow – injecting radioactive  xenon.
• EEG – processed & unprocessed 16 lead per 7.5 to 20% pt EEG changes & influenced  by contralateral  stenosis leads  to
• Shunt malfunction
• Hypotension
• Cerebral emboli

 

Limitation

• May not detect subcortical or small cortical infarcts.
• False negative results .
• Aftected by hypothermia, hypotention & anaesthetic depth.
• False positive result.

 

SSEP: based on response of sensory cortex to electrical impulscs from peripneral sensory nerve stimulation (sensory cortex – supplied by MCA at risk during carotid artery clamping).

So able to detect sensory pathway ischemia (CBF <12ml/100gm/min)

Tran cranial Doppler USG

Continuous measurement  of mean blood flow Velocity & detection of micro embolic events in middle cerebral artery.

• 90% detection with TCD.
• Provide information  regarding shunt function , embolic phenomenon.
• Post sx – emboli  can detected by TCD

Infusion of dextran can  ↓ incidence of  emboli.

• Detects hyperperfusion syndrome

Cerebral oxygenation

• Jugular bulb venous monitoring.
• Continuous  fibroptic jugular venous oximetry  catheter  available.

Near infra red spetrophotometry monitoring of reginal cerebral saturation through  scalp & skull.

Postop

• Neurologic complication- emobilisation, hypo perfusion, cerebral hyper perfusion ,intra Cerebral haemorrhage.
• Hypertension –  carotid sinus denervation.
• Cerebral hyper perfusion syndrome.
  1. Headache
  2. Seigure
  3. Focal neurologic  signs.
  4. Brain edema
  5. ICH

• Hypotension – carotid body plays role.
• Cranial and  cervical nerve injuries.
• unilateral recurrent laryngeal nerve palsy
• ipsilateral  vocal card paralysis.

Carotid body denervation- Response to hypoxia , ventilary loss.

Wound haematoma .

 

 

dr.ajita.