Vascular Disease PDF

VASCULAR DISEASE PATHOPHYSIOLOGY A generalized inflammatory disorder of the arterial tree with associated endothelial dysfunction – Probable causes Endothelial damage due to hemodynamic shear stress Inflammation from chronic infection Hypercoagulability leading to thrombosis Destructive effects of o...

VASCULAR DISEASE PATHOPHYSIOLOGY A generalized inflammatory disorder of the arterial tree with associated endothelial dysfunction – Probable causes Endothelial damage due to hemodynamic shear stress Inflammation from chronic infection Hypercoagulability leading to thrombosis Destructive effects of oxidized LDLs PROGRESSION OF ATHEROSCLEROSIS Occurs in 3 stages: – Fatty streak, the initial lesion of atherosclerosis, begins in childhood forming beneath the normal endothelium – Progression of fatty streak to a fibrous plaque (covered with smooth muscle cells, size could impede flow) – Progression of the fibrous plaque with an expanded lipid-rich core, accumulation of calcium, and disruption of endothelial integrity PREDISPOSING RISK FACTORS FOR ATHEROSCLEROSIS Predisposing Risk Factors – Abdominal obesity – Atherogenic dyslipidemia – Hypertension – Insulin resistance – Proinflammatory state – Prothrombotic state Major Risk Factors – Cigarette smoking – Increased LDL / Decreased HDL – Family hx. Of premature CAD – Aging DISTRIBUTION OF ATHEROSCLEROTIC LESIONS Typically develop at branch points and along the outer surfaces of arterial curves Most Common Sites: – Coronary arteries – Carotid bifurcation – Abdominal aorta – Iliac and femoral arteries CONCURRENT DISEASE Atherosclerosis is a systemic disease and patients requiring vascular surgery may have atherosclerotic lesions at multiple locations Coronary Artery Disease (5% Aortic surgery Peripheral vascular surgery (generally sick people, be aware) Intermediate Risk – Estimated risk of MI or cardiac-related death 1-5% Carotid endarterectomy Most endovascular procedures MEDICAL THERAPY PERIOPERATIVE BETABLOCKADE ~BACKGROUND Background – 1996 Mangano “Administration of Atenolol for 7 days before and after non-cardiac surgery in patients at risk for coronary disease may decrease mortality and the incidence of cardiovascular complications for as long as 2 years following surgery”. – 2000s DECREASE Studies – Poldermans??? Perioperative bisoprolol significantly reduced short- and long-term cardiac death and MI – 2008 POISE Significant cardiac protection, but Increase in all-cause mortality, disabling stroke, and hypotension 2 PERIOPERATIVE BETABLOCKADE 2009 Guidelines – Continue long-term treatment with beta-blockers – Avoid high dose beta-blockade – Consider introducing beta-blockade in: Known CAD Reversible ischemia on stress test At risk for CAD undergoing high-risk surgery, especially vascular surgery – If possible, start at least 7 days, and preferably 30 days, prior to surgery – Titrate to effect HR 60-80 beats/min Systolic BP >100 mmHg prior to next dose Recent meta-analysis – Excluding data from DECREASE Studies 27% reduction in non-fatal MI 27% increase in all-cause mortality 73% increase in non-fatal stroke 51% increase in hypotension Which beta-blocker is preferred? Benefit seen with all except those with intrinsic sympathomimetic activity (ISA) Bisoprolol > atenolol > metoprolol (probably not best choice) ~ 2009 GUIDELINES PERIOPERATIVE BETABLOCKADE ~ META ANALYSIS ~ BB PREFERENCE PERIOPERATIVE BETABLOCKADE Beta-blockade with Anemia – Marked increase in MACE, mortality and MOSF in beta-blocked patients when hemoglobin decreases to ~60% of baseline. – May consider a higher transfusion threshold in patients who are beta-blocked. Maintain current beta-blockade Initiate new beta-blockade in high risk patients undergoing high risk surgery – Particularly if beta-blockade is independently indicated based on medical condition Titration of new initiation dosing is important Preferably initiated and titrated over >7 days – Same day initiation may be appropriate for clear indications Consider increasing threshold for transfusion in beta-blocked patient ~ANEMIA PERIOPERATIVE BETABLOCKADE PERIOPERATIVE BETABLOCKADE ~TYPICAL REGIMEN ALPHA2 AGONISTS Typical regimen – 7-30 days preoperatively treatment initiated with: Atenolol 25 -100 mg/day Bisoprolol 5 -10 mg/day – Intraop and postop continuation of IV drug Atenolol 5 -10 mg/day Metoprolol 5 -10 mg/day Esmolol 100 -500mcg/kg bolus followed by infusion of 50 -300mcg/kg/min, titrated to heart rate Clonidine: – Reduced intraoperative myocardial ischemia – Reduced catecholamine levels on POD 1 – Recent meta-analysis looking at vascular surgery patients showed reduction in: o Cardiac morbidity o Death 3 STATIN THERAPY ACE INHIBITORS TIMING OF VASCULAR SURGERY CARP TRIAL Perioperative statin therapy associated with a significant reduction in mortality following vascular surgery (useful) Benefits presumably explained by the pleiotropic (not primary reason, bonus effects) effects of statins – Improvement of endothelial function – Reduction in vascular inflammation – Stabilization of atherosclerotic plaques No evidence of independent reduction in perioperative cardiac events, but: Have shown potential benefits in: – Decreased stroke rate – Decreased ventricular remodeling following STEMI – Decreased mortality following infrainguinal bypass – Stabilization of atherosclerotic plaques Recommendations – Continue if already taking ACE inhibitors – Be aware of potential for hypotension in combination with general anesthesia (use vasopressor if unresponsive to other pressors) Following MI – Incidence of perioperative reinfarction decreases with time until about 6 months when risk stabilizes Following CABG – 4-6 weeks Following Angioplasty – 2 weeks Following Stent Placement – Bare metal (Velocity, Express) DAPT 30 days Surgery after 6 weeks – Drug eluting 1st generation (Cypher, Taxus) – DAPT 12 months to forever – Surgery p 12 months 2nd generation (Xience V) – May consider d/c of clopidogrel after 6 months – Surgery 7 days after clopidogrel discontinuation – Exception to this is a patient who was stented following an acute coronary event who should remain on DAPT for a full 12 months Coronary Artery Revascularization Prophylaxis – Randomized patients with CAD to coronary revascularization or medical management prior to elective vascular surgery – Characteristics of both groups identical o > 80% on beta-blockers o > 70% on ASA o > 50% on statins – Found no benefit to coronary revascularization (over medical management Finding – Coronary revascularization prior to vascular surgery is not indicated unless independently indicated for acute coronary syndrome 4 AORTIC DISEASE THORACIC THORACIC AORTIC DISSECTION AORTIC DISSECTION ETIOLOGY An intimal tear allows blood to enter the media layer As dissection through the media layer occurs a false lumen is created (can steal blood flow from branch arteries) Blood flow to arterial branches arising from the aorta may be compromised, as may the aortic valve Hypertension Iatrogenic (after surgery or something) Deceleration injury or other trauma (usually at ligament arteriosum where artery attaches to the thorax) Genetic predisposition – Involve changes in matrix proteins which produce structural weakness in the aorta o Marfan’s syndrome o Ehlers-Danlos syndrome o Bicuspid aortic valve o Non-syndromic familial aortic dissection CLASSIFICATION OF AORTIC DISSECTION AORTIC DISSECTION – SIGNS AND SYMPTOMS Acute onset of severe, sharp pain in the anterior chest, neck, or between the shoulder blades Otherwise related to occlusion of aortic branch arteries – Coronary arteries – Renal artery – Carotids – GI ischemia – Decreased or absent distal pulses – May present as neurologic injury due to inadequate perfusion to brain, spinal cord, distal extremities AORTIC DISSECTION Preoperative Preparation – Focus on systems responsible for the bulk of morbidity and mortality in these patients (if they are stable)(things most likely to result in bad outcomes) CAD Correction of reversible airway obstruction and infection Renal dysfunction Carotid disease – Urgency of surgery Ascending and aortic arch dissection – Require cardiopulmonary bypass Descending aorta (slightly less serious) ~PREOP ~SURGERY URGENCY AORTIC CROSSCLAMPING 5 AORTIC CLAMPING ~HEMODYNAMIC Hemodynamic Consequences Increased Afterload resulting in: Increased BP proximal to clamp Decreased cardiac output Increased Preload due to: Redistribution of blood volume following collapse of venous circulation distal to clamp Significantly greater if clamp is supraceliac rather than infraceliac Left ventricular dysfunction Likely if contractility and coronary blood flow cannot be increased to compensate for increased preload and afterload (subendocardium at risk?) Problem Pharmacologic reduction in preload and afterload with vasodilators will only further compromise perfusion pressure distal to the clamp (& tissue is already reduced d/t clamp so just worsening it) Proximal descending aorta clamping results in ~ 90% reduction in: Spinal cord blood flow Renal blood flow GFR Urinary output AORTIC UNCLAMPING Gradual release of clamp preferred to: Allow slower redistribution of blood volume, minimizing hemodynamic changes Slow the washout of evil humors (from ischemic tissues distal to clamp à further vasodilation) Declamping hypotension primarily due to: Central hypovolemia due to redistribution of blood volume to previously underperfused tissue Hypoxia-mediated vasodilation in tissues distal to the clamp Release of vasoactive and cardiodepressant metabolites from previously underperfused tissues ANTERIOR SPINAL ARTERY SYNDROME Two posterior spinal arteries (sensory) One anterior spinal artery (motor) Supplemented by radicular arteries o Artery of Adamkiewicz Watershed areas exist where blood supply is at risk Perfusion compromised by: Resection of, or exclusion of Artery of Adamkiewicz by cross clamp Reduced aortic blood flow distal to the clamp Increased CSF pressure Manifestations Flaccid paralysis of LEs Bowell and bladder dysfunction Spared sensation and proprioception Techniques to avoid spinal cord ischemia Cross-clamp time < 30 minutes Partial circulatory assistance Reimplantation of critical arterial supply (take time, the picture to kind of do retrograde flow) CSF drainage (to improve perfusion of spinal cord) Maintain proximal hypertension Hypothermia (metabolic rate of tissue slows) Mannitol/ Steroids/ Ca++ channel blockers 6 THORACIC AORTIC ANEURYSM Aneurysm – Dilation of all three layers of arterial wall – Commonly defined as a 50% increase over baseline Signs and Symptoms – Usually reflect compression of adjacent structures CLASSIFICATION OF ANEURYSM MANAGEMENT OF ANESTHESIA Monitoring Blood pressure o Right arterial line o Femoral arterial line Myocardial o PA cath o TEE (best option if available to look for wall motion abnormalities) Neurologic o EEG o Somatosensory evoked potentials (doesn’t tell you about anterior cord) o Motor evoked potentials (then cant use NMB so unlikely) Induction Minimize blood pressure increases to avoid worsening dissection or aneurysmal rupture Intubation Double-lumen ETT for surgical exposure Maintenance High-dose narcotic Balanced technique with volatiles RON: Technique much less important than aggressive monitoring of distal perfusion and myocardial function (like TEE) POSTOPERATIVE MANAGEMENT Careful monitoring of 1. Cardiac 2. Pulmonary 3. Renal Hypertension is common Pain management – Neuraxial opioids and/or local anesthetics very useful 7 ABDOMINAL AORTIC ANEURYSM ABDOMINAL AORTIC ANEURYSM AAA RUPTURE MANAGEMENT OF ANESTHESIA Etiology Related to degradation of extracellular matrix proteins Signs and Symptoms Exsanguination Asymptomatic, pulsatile abdominal mass Surgery indicated at: Diameter > 5 cm 5-year rupture risk > 25% Annual expansion of > 0.6- 0.8 cm Symptoms – Classic Triad o Hypotension o Back pain o Pulsatile abdominal mass Requires emergent surgery – Typically rupture into the left retroperitoneum (good b/c it’s a confined space & can help tamponade) – May tamponade the aneurysm and limit bleeding – Fluid resuscitation sometimes deferred until the aorta is controlled Elective AAA Repair Monitoring Arterial line PA catheter (Ideally TEE) Anesthetic technique Balanced technique with volatile and opioids common Combined general anesthetic with epidural analgesia – No evidence of reduced M&M compared to GETA alone – May improve postoperative course Aortic cross clamping As previously discussed, but less hemodynamic derangement due to more distal aortic clamp Postoperative care Risk of cardiac, pulmonary, renal dysfunction as discussed Usefulness of neuraxial analgesia 8 PERIPHERAL ARTERIAL DISEASE PERIPHERAL ARTERIAL DISEASE PAD RISK FACTORS & PROGNOSIS Intermittent Claudication Metabolic demands exceed oxygen delivery during exercise Ankle-brachial index < 0.9 Rest Pain Inadequate tissue blood supply even at rest Ankle-brachial index < 0.4 Ischemic ulceration/ impending gangrene Minor trauma results in non-healing skin lesions Ankle-brachial index < 0.25 Risk Factors Similar to CAD 1. Diabetes mellitis 2. Hypertension 3. Smoking 4. Dyslipidemia 5. Hyperhomocysteinemia 6. Family history of PAD Prognosis Atherosclerosis being a systemic disease, survival is primarily related to cardiovascular and cebrovascular ischemic events (heart & head) PAD SIGNS & SYMPTOMS Signs and Symptoms Decreased or absent pulses Subcutaneous atrophy Hair loss Coolness to touch Pallor Cyanosis Dependent rubor PAD TREATMENT Medical Surgical PAD SURGERY Exercise Smoking cessation Management of diabetes Lipid lowering drugs (statins, can also slow progression of the dx) Treatment of hypertension Thromboembolectomy (good for clot but not for atherogenic emboli b/c they break into many small pieces) Be aware this could always end up converting to an open procedure Surgical reconstruction Endovascular procedures Indications for surgery Disabling claudication Ischemic rest pain Impending loss of limb Surgical prognosis depends on: Extent of arterial disease Acuity of ischemia Time required to restore circulation Operative Risk Due primarily to associated atherosclerotic disease (heart & head) 9 PAD MANAGEMENT OF ANESTHESIA PAD POSTOPERATIVE MANAGEMENT Primary risk is ischemic heart disease Most cardiac events occur at emergence and postoperatively RAYNAUDS PHENOMENON RAYNAUD’S PHENOMENON MANAGEMENT OF ANESTHESIA Episodic vasospastic ischemia of the digits Signs and Symptoms Blanching Cyanosis Rubor following cold exposure and rewarming Primary Raynaud’s disease Typically, bilateral (both hands) Secondary Typically, due to autoimmune disease, such as cleroderma or SLE Often unilateral Warm the operating room Active warming of the patient Forced air warming Avoid arterial cannulation for BP monitoring unless absolutely required Reduce frequency of BP cuff cycle if BP stable Avoid use of epinephrine or other vasoconstrictor in peripheral blocks, if possible 10 CAROTID ARTERY DISEASE CAROTID DISEASE Etiology Primarily an embolic problem Rarely due to occlusion or insufficiency Signs and Symptoms Asymptomatic carotid bruit TIAs Evidence of impending ischemic stroke Sudden onset of vascular-related focal neurologic deficit that resolves within 24 hours – Paresthesias – Amaurosis fugax (blindness from embo of retinol artery) – Speech problems – Clumsiness of the extremities ACUTE ISCHEMIC STROKE CAROTIC ENDARTERECTOMY CAROTID ENDARTERECTOMY Correlates of surgical outcome Age Diabetes Smoking TIAs History of stroke Creatinine > 1.5 mg/dl Hypoalbuminemia Long operative time ~CORRELATES OF SURGICAL OUTCOME CAROTID ENDARTERECTOMY ~COMPOSITE #1 Cause of disability in U.S. #3 Cause of death in U.S. Risk Factors 1. Systemic hypertension 2. Cigarette smoking 3. Hyperlipidemia 4. Diabetes mellitis 5. Alcohol > 6/day 6. Hyperhomocysteinemia Extremely effective in reducing stroke in symptomatic patients Asymptomatic patients Should only be operated on if the overall complication rate by that surgeon, in that institution is < 3%, because: – Stroke risk reduction is small – Perioperative complication rate is relatively high – NNT = 20-40 Composite incidence of stroke, death, or cardiac event = 4.0% Composite incidence of stroke, death = 3.4% 18% of these cases were done with regional anesthesia which, compared to general anesthesia, resulted in: – 17% reduction in stroke – 24% reduction in death – 33% reduction in cardiac event – Composite risk reduction = 31% 11 CAROTID ENDARTERECTOMY CAD OPERATIVE CONSIDERATIONS CEREBRAL ISCHEMIA MONITORS CAD MANAGEMENT OF ANESTHESIA ~GOALS, MONITORS Preoperative Assessment – Atherosclerosis is a systemic disease – CAD – Renal dysfunction Additional assessment beyond routine – Determine normal blood pressure and heart rate range o Over a period of time, if possible § Hospital records § Doctor’s visits § Day surgery – Assess patient for neurologic changes related to extremes of head position (and then avoids those positions) Blood pressure o Stable, high-normal Ventilation / ETCO2 o Normocarbia Blood sugar o Tight control Brain protection o Decreased CMRO2 § Volatile agents § Barbiturates § Etomidate § Propofol Temperature control o Hypothermia o Normothermia Reason Determination of need for shunting Modalities EEG SSEP Stump pressure (needle into occluded side above clamp will reflect flow coming from the other side) Transcranial doppler Cerebral oximetry (regional to middle cerebral artery not global cerebral perfusion) Direct xenon cerebral blood flow measurement Awake patient (regional anesthetic) – gold standard per Ron Two Primary Anesthetic Goals – Hemodynamic stability Adequate blood pressure for collateral perfusion following cross-clamp of carotid Diseased vessels exhibit failure of autoregulation (become pressure dependent (why we maintain a high normal BP) Surgical manipulation of the carotid sinus can produce large changes in HR and BP (some surgeons may inject local to minimize but may have post-op HTN d/t blunted barorectors) – Rapid emergence To allow for neurologic assessment in the operating room Monitors – Arterial line – ST-T segment analysis in leads II and V5 – TEE or central line unnecessary unless severe cardiac comorbidities 12 CAD MANAGEMENT OF ANESTHESIA ~ INDUCTION, MAITENANCE, EMERGENCE Induction – As appropriate for cardiac status keeping in mind the desire for prompt awakening and neuro assessment – Avoidance of hyperdynamic response to laryngoscopy and intubation Maintenance – Maintain a “light” level of anesthesia o Aids in monitoring of cerebral ischemia with EEG, SSEP o Maintains a high-normal blood pressure – Avoid excessive use of longer-acting narcotics o Interference with postop neuro exam – Choice of maintenance drug not really critical o Volatiles o Propofol infusion o Combination of above Emergence – Consider deep extubation if appropriate to avoid hypertensive response (a lot of these patients are smokers, if its appropriate for this patient they won’t buck the tube & disrupt their repair) CAD POSTOPERATIVE MANAGEMENT CAROTID ANGIOPLASTY AND STENTING Primary Concerns Cardiac events New neurologic deficits Airway management Hematoma Denervation of carotid bodies Blood pressure control Can be extremely labile Hypertension Needs to be addressed promptly Increases incidence of new neurologic deficits by 2-3x Increases potential for bleeding Seen more frequently in patients who are hypertensive preoperatively Injection of local anesthetic may be more hypertensive Usually peaks 2-3 hours postop, may last up to 24 hours May be due to altered activity or denervation of carotid sinus Hypotension Presumed due to removal of plaque and better exposure of baroreceptors to pressure, creating a period of hyperresponsiveness “Resets” within 12-24 hours Major complication is microembolization When done with an emboli protection device, results are equivalent to CEA 13