1. Hemodynamic goals after Intra-Cranial revascularization
Dr Rafi Avitsian,MD
Rakhi Pal

2. Revascularization Procedures
CEA
Stenting
Coiling
EC/IC bypass

3. Significant predictors of adverse events in CEA
Age
Symptom status
Severe HT (Pre-op DBP> 110 mmHg)
H/o angina
Evidence of ICA thrombus
ICA stenosis near carotid siphon
Predicting complications of coronary end arterectomy ; McCroy DC ,Stroke 1993,24:1285

4. Excessive lowering of BP –focal ischemia.
Post op HT and transient neurological deficits are more frequent with poor preoperative BP control (BP>170/95)
Excessive lowering of BP –focal ischemia.
Asiddao CB,et al ;Factors associated with perioperative complications during CEA ,Anesthesia Analgesia ;61:631

5. Intraop Art line During cross clamping maintenance of CPP is critical.
Goal of induction – to maintain stable cardiovascular parameters such that cerebral and myocardial blood flows are maintained.
Careful fluid replacement in minimizing BP liability.

6. Avoid marked increase in BP
Incidence of MI is higher in pts who received phenylephrine than those who had light anesthesia .
Smith JS et al;Does anesthetic technique make a difference ?Augmentation of SBP during CEA :effects of phenylephrine versus light anesthesia and Isoflurane versus Halothane on the incidence of MI

7. During cross clamping –BP should be kept 15-20% above its normal range
After removing cross clamp-BP should be
maintained in low normal range
As it lowers Myocardial O2 consumption
Decreases work by Heart
Decreases stress on suture line in Carotid art
Minimizes possibility of reperfusion injury

8. Esmolol- to blunt sympathetic response during ETT
Laryngoscopy of short duration without rough airway manipulation.
Critical CBF below which majority of patients developed ischemic changes within 3 mins of carotid occlusion ,was lower for Iso than Halothane or enflurane
Michenfelder JD et all –Isoflurane when compared to enflurane and Halothane decreaeses the frequency of cerebral ischemia during CEA

9. Post op HT is associated with increased risk of neurological deficits.
Pre op HT is a a major risk factor post op HT
Ref-Hans SS ,Glover JL :The relationship of cardiac and neurological complication to BP changes following CEA,AM surg 61;356
Towne JB,Bernhard VM;the relationship of post op HT to complications following CEA. Surgery 88:575

10. Cerebral Hyperperfusion Syndrome
Def > 100 % increase in CBF compared to pre- op baseline.
Procedures- CEA,CA/VA stenting & angioplasties, EC/IC bypass, Clipping of ICA aneurysm
9-14 % (0-3 %after CEA)
Onset (0 to months ,mean 5 days)
Symptoms seen with increase in CBF (30-50% above baseline)
Risk of developing CHS is 10 times with hyper perfusion than without.

11. Post –end arterectomy Hyper perfusion syndrome
I/L headache -62%
Focal seizure activity
Focal neurological deficit(cortical- hemiplegia,hemianopia,aphasia,neglect)
Features of raised ICP
If not treated cerebral edema ,intracerebral hemorrhage and SAH and death.
Imaging- Intra-cerebral edema or hemorrhage

12. Risk factors for CHS HT High grade stenosis Decreased CVR
Increased peak flow velocity
C/L carotid occlusion
Recent C/L CEA
Intraop ischemia
Intraop distal carotid pressure <40 mmHg

13. Pathophysiology Impaired Cerebral auto-regulation HT
Ischemia –reperfusion injury
O2 derived free radicals
Baroreceptor dysfunction
Intra-op ischemia

14. Prevention of CHS
Timing
Type and dose of anesthesia
Treatment of HT
Pre-treatment with free radical scavanger edaravone
Ref –ogasawara K,Inoue T,Kobayashi M,Endo H,fukuda T, Ogawa A,neurosurgery 2004:55;

15. Time of surgery
Within 3-4 wks after cerebral infarction-risk of hemorrage is more.
Benefit from CEA in neurologically stable patient is greatest if procedure is done within 2 weeks of patients last ischemic events
Rothwell PM,Eliasziw M,Gutnikov SA,Warlow CP,Barnett HJ,CEA for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery

16. High doses of volatile halogenated hydrocarbon anesthetics may lead to CHS
Ref- Skydell JL,Machleder HI,baker JD,Busutti RW,Moore WS;incidence and mechanism of post carotid endarterectomy Ht ,Arch surg 1987 ;

17. Edaravone inhibts lipid peroxidation vascular endothelial cell injury
ameliorates brain edemae and tissue injury.

18. Treatment Adequate lowering of BP Treatment of cerebral edema
Anticonvulsant therapy

19. Treatment Cerebral vasodilators are C.I (Nitroprusside or GTN or CCB)
B1 blockers- little effect on ICP
Labetolol(mixed )
no direct effect on CBF and decreases CPP and MAP by 30%.
Clonidine
vasorelaxation with decreases of art BP,HR and CO. It also decreases CBF
Labetolol and Clonidine DOC

20. Post op hemodynamic instability
HypoT-10%. HT- 50% in Post CEA
Ref-O’Connor CJ,Tuman Kj: Anesthetic consideration for carotid A surgery.

21. Carotid sinus N sparing CEA –higher incidence of HypoT d/t exposure of Carotid sinus to higher Art pressure following removal of plaque.
Decrease SVR- treated with IVF +_ Phenylephrine

22. Hemodynamic instabilities are postulated to be related to baro receptor reflex dysfunction
Bove EL, Fry Wj,Gross WS,et al;Surgery,85:
Nouraei SA, Al-rawi PG,Sigaudo-Roussel D et al ,J Vasc Surgery 41; ,2005

23. Intra operative LA blockade of the carotid sinus nerve has advocated to prevent ,or attenuate ,hypoT after CEA , but the effective ness of this treatment is still contrversial.
Ref :Cafferata HT, Merchant RF, DePalma RG: Ann surg 196; ;1982
GottliebA,Satariano HaydenP,Schoenwald P.et al : J Cardio Th Vsc Anesthesia11:67 -71,1997

24. Post op HT
More commonly ass. with Carotid N denervation (surgical division or LA blockade)
HT after Carotid sinus n sparing CEA- d/t temporary dysfunction baro receptor or N d/t intra op trauma.
(Ref:Bove EL, Fry Wj,Gross WS,et al;Surgery,85: )

25. Other MI Dysrhythmia - AF Hypoxia, Hypercarbia Pneumothorax, Pain
Confusion
Stroke
Distension of bladder

26. Complication
Stroke MI
CHS
Death

27. Post Op Stroke
Due to technical factors rather than hemodynamic factors
1/3 rd of stroke d/t Intraop- emboli
Few -intraop hemodynamic origin

28. Rockman and colleagues –J of Vascular Surgery32;1062-1070
Within the first 24 hrs of CEA
13% of stroke to be related to carotid ischemia
63% -Thrombo emboli
In addition Intra cerebral Hge contributed to 13 % peri op stroke
11 % -no relationship to operative art –may be emboli of cardiac origin

29. Cochrane systematic review of more than 15,000 patients
Post op MI -2.2 %
Post op stroke -3.3%
MI-Major cause of morbidity and mortality

30. Gold standard
AHA guidelines for CEA recommend that combined risk for death or stroke associated with CEA should not exceed 3 % for asymptomatic patients and 5 % symptomatic patients.