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

Revascularization Procedures CEA Stenting Coiling EC/IC bypass

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

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

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.

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

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

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

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

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.

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

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

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

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;1060-67

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

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 ;

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

Treatment Adequate lowering of BP Treatment of cerebral edema Anticonvulsant therapy

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

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

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

Hemodynamic instabilities are postulated to be related to baro receptor reflex dysfunction Bove EL, Fry Wj,Gross WS,et al;Surgery,85:633-637 Nouraei SA, Al-rawi PG,Sigaudo-Roussel D et al ,J Vasc Surgery 41;631-637,2005

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;465-472;1982 GottliebA,Satariano HaydenP,Schoenwald P.et al : J Cardio Th Vsc Anesthesia11:67 -71,1997

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,85:633-637)

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

Complication Stroke MI CHS Death

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

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

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

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.