Anesthesia for Vascular Surgery Flashcards by Julianne Fitzgerald

Major Co-existing diseases of PVD

Coronary artery disease
May require preoperative coronary revascularization
COPD
Hypertension
Renal insufficiency
Uncontrolled Diabetes
Liver disease

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____________ remains the single most important cause of morbidity following vascular surgery

Myocardial dysfunction

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Goals of Vascular Anesthesia

Minimize patient morbidity and maximize surgical benefit
Considerations: CNS – Renal – Liver – Gut

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Predictors of M&M after vascular surgery

Low serum albumin levels
ASA status (comorbid conditions)

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Perioperative Monitoring Goals
for vascular surgery patients

Detect myocardial ischemia
Identify abnormalities
Preload -afterload -ventricular function

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Pharmacologic Interventions for Vascular Surgery

** beta-blockers** (metoprolol -atenolol –esmolol)
alpha-2 agonists (pretreatment with clonidine 300 mcg 90min before surgery)
Calcium channel blockers (diltiazem – Clevidipine)
**Nitroglycerin **(used to treat arterial hypertension, elevated cardiac filling pressures and vasospasm)

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Patho of the chornic inflammation in vascular disease

Adhesion molecules
Leukocytes: Lipid accretion & vasculitis
Markers of inflammation
High-sensitivity C-reactive protein (hs-CRP)

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Major risk factors for chronic inflammation in vascular disease

Metabolic syndromes - insulin resistance - DM – pro-inflammatory state - HTN - Abd. Obesity
**Cigarette smoking **(vaping, marijuana ect.)
**Elevated LDL-C **(low-density lipoprotein-cholesterol: “bad” chol. )
Small LDL particles increase CAD risk
Penetrate endothelial barrier 2X more than large particles
Associated with high triglycerides, Low HDL, metabolic syndromes
**Low HDL ** (high-density lipoprotein: “good” chol. )
Absorbs and transports to the liver
High levels are best
Genetics
Aging

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Pathophysiology of Atherosclerosis

Generalized inflammatory disorder
Endothelial dysfunction
Vaso-protective effects - Nitric Oxide
Formation of intimal plaques
Oxidative lipids -inflammatory cells -smooth muscle cells -connective tissue fibers -calcium deposits
Endothelial damage
Inflammation
Hypercoagulability
Low-density lipoproteins
Vasoactive influences

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Medical Management of Atherosclerosis

Antihypertensives
beta-blockers - ACE inhibitors
Statin drugs
Antiplatelet
ASA - Plavix - glycoprotein Iib/IIIa inhibitors
Cessation of smoking

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Normal Cerebral Vascular System and its disease state

Cerebral Blood Flow & Metabolism
* Primarily responsible for the Delivery of O2 and glucose
Cerebral circulation (CBF)
* Internal carotids arteries give 80% of flow to the head
* Vertebral arteries give 20% of flow to the head
* Collateral channels come off of these

Auto-regulated: CBF/CMRO2 coupling they match each other. They are in balance and go up and down together.
* To match cerebral metabolic rate of oxygen CMRO2
3 ml O2 to every 100Gm brain flow per min
* Coupled: increased and decreased together
* In which situations are they Uncoupled? (pathology/medications)

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Carotid Disease

Bilateral in about 1/2 of all cases
Atherosclerotic plaque - Lateral aspect of the bifurcation and extends into the internal and external arteries
Primarily a problem of embolization
May manifest as asymptomatic bruit or Amaurosis fugax (monocular transient blindness)
TIA vs RIND (resolution 24 vs > 24hrs)

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Carotid Disease

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TIA =

Transient ischemic attack
Can last 2-15 minutes or up to 24 hours

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RIND =

Reversible Ischemic Neurologic Deficit
Can last up to 7 days

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Stroke in evolution AKA ___

Progressive Stroke
(stroke with neurological deficits that continue to worsen for hours or days after onset)

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Completed stroke

Established neurological deficit that is irreversible or only partly reversible

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Anesthetic Goals for Carotid Endartarectomy

Prevention and prompt detection of cerebral and myocardial ischemia
Maintenance of hemodynamic stability
Rapid recovery from anesthetic drug effects for prompt evaluation of neurologic function

Clinical Focal Neurological Signs

Presentation – contralateral
Weakness and numbness
Dysphasia, dyspraxia, and confusion (dominant hemisphere), transient
Blurring of vision or blindness
(Ipsilateral eye), homonymous visual field loss; ipsilateral headache

Appropriate Candidates for Carotid Endartarectomy

Symptomatic 70-99% stenosis
TIAs or non-disabling stroke
Surgically accessible stenosis
Stable medical condition

Inappropriate Candidates for Carotid Endartarectomy

Asymptomatic <60% stenosis
Symptomatic or asymptomatic with
Intracranial stenosis more severe than the extracranial stenosis
Uncontrolled DM, HTN, CHF, Unstable Angina
A major neurologic deficit or decreased LOC

Uncertain candidates for a CEA (carotid endartarectomy)

Symptomatic <70% stenosis
TIAs or nondisabling stroke
Surgically accessible stenosis
Stable medical and neurologic condition
Asymptomatic >60% stenosis
Surgically accessible stenosis
Stable medical condition

Pre-anesthetic assessment for CEA

State of health
History, physical exam and chart review
Coexisting diseases
CAD, HTN, PVD, COPD, CRI, and DM
Adverse affects from hyperglycemia
Cardiac complications
CHF and MI
Cerebral Angiogram
Contralateral carotid disease or poor collaterals
Risk stratification scheme

Formula for CBF

Cerebral Blood Flow
CPP/CVR (Cerebral Vascular Resistance)

Formula for CPP

Cerebral Perfusion Pressure MAP minus ICP **or** CVP (whichever value is greater)

What are determinants of CVR?

Blood viscosity Diameter of resistance vessels

How do we optimize CBF during CEA?

Arterial BP control Arterial CO2 tension

Strategies to mitigate cerebral and myocardial Ischemia

**Hyperventilation** Creates an Inverse steal aka Robinhood effect Decreased Co2->vasodilation to focal ischemia areas *** Carotid shunt** **Blood Pressure** Consider baseline Essential HTN *Temperature * Neuroprotective vs myocardial ischemia

With preexisting chronic hypertension, the autoregulation curve is _____.

shifted

During carotid cross-clamp CBF response to PaCO2 is _____.

impaired and dependent on CPP

BP goals during CEA

BP within normal preoperative range (170/90?) Some clinicians prefer 10 – 20% above baseline

Superficial cervical plexus block

Subcutaneous local in posterior border of sternocleidomastoid (lateral neck) Cutaneous branches of the plexus fan out to innervate the skin

Deep cervical plexus block

Paravertebral block of C2-4 nerve root Intravascular compilations

PEARLs for regional anesthesia

**Intraoperative monitors** Basic monitoring **Arterial line** +/- Cerebral oximeter **Supplemental O2 ** mask or nasal cannula (risks) **Sedation for block** Fentanyl and midazolam **Sedation for case: Consider assessment** Dexmedetomidine Propofol (after CNS assessment) Be prepared for conversion to GA

Advantages of Regional Anesthesia with vascular surgery

Superior neurologic monitoring while awake Technically a simple block Intubation not required Potential to minimize interventions (shunt) Less expensive Blunts catecholamine responses Reports of more rapid recovery and shorter hospitalization Provides postoperative analgesia

Disadvantages of regional anesthesia during vascular surgery

Patience and gentle technique Reinforcement of block **Lack of airway and ventilatory control** Complication Stroke – TIAs – cross clamp intolerance – seizure – airway obstruction – confusion – hypoventilation – agitation – angina **LA toxicity** Subarachnoid injection Vertebral artery injection **Phrenic nerve injury Recurrent laryngeal nerve injury** **Horner’s Syndrome (30-45 min after block)** Ipsilateral Ptosis (lid), myosis (pupil)

Monitors and Meds to use during vascular durgery with GA

**Intraoperative Monitors** Arterial catheter ECG Pulse oximetry and capnography CVP or PCWP (high risk) Cerebral oximeter Multimodality monitoring Maintenance of hemodynamic stability ETCO2: Normocapnia **Pharmacologic** +/- Midazolam – Propofol – Etomidate - Dexmedetomidine Opioids Nondepolarizing NMB (avoid Sch) Volatile anesthetic (nitrous oxide is controversial)

Advantages of GA with vascular surgery

Potentially more comfortable Controlled ventilation Management of complications X-clamp intolerance and transient ischemia Reduces the need for expedience Cerebral protection???

Disadvantages of GA with vascular surgery

Need for an alternative method for monitoring cerebral function Hemodynamic instability Difficult to detect neuronal damage Prolonged emergence Confused postoperative assessment More expensive

Step before carotid cross clamping and type of monitoring

Prior To Clamp give (75 – 100 Units/Kg) Heparin Increased BP above the clamp and decreased below the clamp **Neurologic Monitoring happens during this time** * Awake Patient * EEG * Stump Pressures * Cerebral Oximeter * TCD (transcranial doppler)

Interventions In Response To Evidence Of Cerebral Ischemia

Increasing CPP (Vasopressor) Suppress CMRO2 (Controlling Anesthesia for a nice calm state - Etomidate…) Restore Internal Carotid Artery Blood Flow **Shunt may be needed**- the rate of shunting is decreased with regional anesthesia

Emergence from GA after CEA and postop management

Avoid excessive coughing or straining and increased BP **Hematoma risk**: Assess and document yourself Heparin reversal controversial (surgeon to surgeon- have the conversation) Awake and extubated for neurologic examination before you move the patient Close monitoring of ventilatory status Hemodynamic stability

Potential Complications of CEA

MI Dysrhythmia – AF Hypoxia and Hypercarbia Pneumothorax Pain Distension of Bladder

Perioperative complications by order of incidence for vascular surgery

Hypertension Hypotension Crnaial nerve injury Stroke Wound hematoma MI

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Anesthesia for Vascular Surgery Flashcards

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