Vascular Disease Student Notes PDF

VASCULAR DISEASE NRAN 80413 SPRING 2024 RON ANDERSON, M.D. 1 OUTLINE GENERAL AORTIC DISEASE Thoracic Dissection Aneurysm Abdominal Aneurysm PERIPHERAL ARTERIAL DISEASE RAYNAUD’S CAROTID DISEASE 2 PATHOPHYSIOLOGY A generalized inflammatory disorder of the arterial tree with associated endothelial dys...

VASCULAR DISEASE NRAN 80413 SPRING 2024 RON ANDERSON, M.D. 1 OUTLINE GENERAL AORTIC DISEASE Thoracic Dissection Aneurysm Abdominal Aneurysm PERIPHERAL ARTERIAL DISEASE RAYNAUD’S CAROTID DISEASE 2 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 3 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 Progression of the fibrous plaque with an expanded lipid-rich core, accumulation of calcium, and disruption of endothelial integrity 4 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 5 OVERLAP OF VASCULAR DISEASE BARASH 6 DISTRIBUTION OF ATHEROSCLEROTIC LESIONS Typically develop at branch points and along the outer surfaces of arterial curves Most Common Sites: MILLER Coronary arteries Carotid bifurcation Abdominal aorta Iliac and femoral arteries 7 CONCURRENT DISEASE Atherosclerosis is a systemic disease and patients requiring vascular surgery may have atherosclerotic lesions at multiple locations Coronary Artery Disease Cerebrovascular Disease Peripheral Vascular Disease – – – – Diabetes mellitis Renal Insufficiency Hypertension Pulmonary Disease 8 PREDICTORS OF PERIOPERATIVE CARDIOVASCULAR EVENTS Major Acute MI ( 70 years Abnormal ECG Rythym other than sinus Uncontrolled systemic HTN 10 SURGICAL RISK High Risk – Estimated risk of MI or cardiac-related death >5% Aortic surgery Peripheral vascular surgery Intermediate Risk – Estimated risk of MI or cardiac-related death 1-5% Carotid endarterectomy Most endovascular procedures 11 12 BARASH MEDICAL THERAPY INTERVENTION COMMENTS RECOMMENDATION Perioperative beta-blockade Oral therapy initiated at least 30 days preop and IV therapy intraop and postop α2 - agonists Oral clonidine at least 90 min preop and oral/transdermal/IV for 72 hours postop Class IIa Statin therapy Initiated at least 45 days preop and extended-release form day of surgery. Reumed postop Class IIa ACE inhibitors Class I Class IIb Ca++ channel blockers Decreased SVT following non-cardiac surgery. Limited evidence for use in vascular surgery Class IIb Nitroglycerin Not indicated for prophylaxis or initial treatment of myocardial ischemia Class III 13 PERIOPERATIVE BETA-BLOCKADE Background – 1996 Mangano “Administration of Atenolol for 7 days before and after noncardiac 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 PERIOPERATIVE BETA-BLOCKADE 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 PERIOPERATIVE BETA-BLOCKADE 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 PERIOPERATIVE BETA-BLOCKADE 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. PERIOPERATIVE BETA-BLOCKADE 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 PERIOPERATIVE BETA-BLOCKADE 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 19 ALPHA2 AGONISTS Clonidine: Reduced intraoperative myocardial ischemia Reduced catecholamine levels on POD 1 Recent meta-analysis looking at vascular surgery patients showed reduction in: – Cardiac morbidity – Death 20 STATIN THERAPY Perioperative statin therapy associated with a significant reduction in mortality following vascular surgery Benefits presumably explained by the pleiotropic effects of statins Improvement of endothelial function Reduction in vascular inflammation Stabilization of atherosclerotic plaques 21 STATIN THERAPY 22 ACE INHIBITORS 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 23 TIMING OF VASCULAR SURGERY 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 nd – 2 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 24 25 BARASH CARP TRIAL Coronary Artery Revascularization Prophylaxis Randomized patients with CAD to coronary revascularization or medical management prior to elective vascular surgery Characteristics of both groups identical – > 80% on beta-blockers – > 70% on ASA – > 50% on statins Found no benefit to coronary revascularization Finding Coronary revascularization prior to vascular surgery is not indicated unless independently indicated for acute coronary syndrome 26 CARP TRIAL MILLER 27 BARASH 28 AORTIC DISEASE Thoracic Dissection Aneurysm Abdominal Aneurysm 29 THORACIC AORTIC DISSECTION An intimal tear allows blood to enter the media layer As dissection through the media layer occurs a false lumen is created Blood flow to arterial branches arising from the aorta may be compromised, as may the aortic valve 30 AORTIC DISSECTION - ETIOLOGY Hypertension Iatrogenic Deceleration injury or other trauma Genetic predisposition Involve changes in matrix proteins which produce structural weakness in the aorta – – – – Marfan’s syndrome Ehlers-Danlos syndrome Bicuspid aortic valve Non-syndromic familial aortic dissection 31 CLASSIFICATION OF AORTIC DISSECTION DeBakey Type I DeBakey Type II Stanford Type A DeBakey Type III Stanford Type B 32 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 33 AORTIC DISSECTION Preoperative Preparation Focus on systems responsible for the bulk of morbidity and mortality in these patients – – – – 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 34 AORTIC CROSSCLAMPING % CHANGE IN VARIABLE BY LEVEL OF AORTIC OCCLUSION CARDIOVASCULAR VARIABLE SUPRACELIAC SUPRARENAL INFRACELIAC INFRARENAL MAP 54 5 2 PCWP 38 10 0 (-38) (-10) (-3) Abnl. Wall Motion % of Pts. 92 33 0 New MI % of Pts. 8 0 0 EF 35 ADAPTED FROM BARASH AORTIC CLAMPING 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 36 AORTIC CLAMPING Problem Pharmacologic reduction in preload and afterload with vasodilators will only further compromise perfusion pressure distal to the clamp Proximal descending aorta clamping results in ~ 90% reduction in: Spinal cord blood flow Renal blood flow GFR Urinary output 37 AORTIC UNCLAMPING Gradual release of clamp preferred to: Allow slower redistribution of blood volume, minimizing hemodynamic changes Slow the washout of evil humors 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 38 ANTERIOR SPINAL ARTERY SYNDROME Two posterior spinal arteries One anterior spinal artery Supplemented by radicular arteries – 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 39 MILLER ANTERIOR SPINAL ARTERY SYNDROME 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 CSF drainage Maintain proximal hypertension Hypothermia Mannitol/ Steroids/ Ca++ channel blockers 40 MILLER 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 SYMPTOM STRUCTURE Hoarseness Left recurrent laryngeal nerve Stridor Trachea Dysphagia Esophagus Dyspnea Lungs Plethora, edema Superior vena cava 41 CLASSIFICATION OF ANEURYSM 42 MANAGEMENT OF ANESTHESIA Monitoring Blood pressure – Right arterial line – Femoral arterial line Goal MAP ~ 100 mmHg MAP > 50 mmHg Myocardial – PA cath – TEE Neurologic – EEG – Somatosensory evoked potentials – Motor evoked potentials 43 MANAGEMENT OF ANESTHESIA 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 Technique much less important than aggressive monitoring of distal perfusion and myocardial function 44 POSTOPERATIVE MANAGEMENT Careful monitoring of Cardiac Pulmonary Renal Hypertension is common Pain management Neuraxial opioids and/or local anesthetics very useful 45 ABDOMINAL AORTIC ANEURYSM 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 46 AAA RUPTURE Symptoms Classic Triad – Hypotension – Back pain – Pulsatile abdominal mass Requires emergent surgery Typically rupture into the left retroperitoneum May tamponade the aneurysm and limit bleeding Fluid resuscitation sometimes deferred until the aorta is controlled 47 MANAGEMENT OF ANESTHESIA Elective AAA Repair Monitoring – Arterial line – PA catheter 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 crossclamping – 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 48 PERIPHERAL ARTERIAL DISEASE 49 PERIPHERAL ARTERIAL DISEASE 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 50 PERIPHERAL ARTERIAL DISEASE Risk Factors Similar to CAD – – – – – – Diabetes mellitis Hypertension Smoking Dyslipidemia Hyperhomocysteinemia Family history of PAD Prognosis Atherosclerosis being a systemic disease, survival is primarily related to cardiovascular and cebrovascular ischemic events 51 MILLER52 PERIPHERAL ARTERIAL DISEASE Signs and Symptoms Decreased or absent pulses Subcutaneous atrophy Hair loss Coolness to touch Pallor Cyanosis Dependent rubor 53 TREATMENT OF PAD Medical Exercise Smoking cessation Management of diabetes Lipid lowering drugs Treatment of hypertension Surgical Thromboembolectomy Surgical reconstruction Endovascular procedures 54 SURGERY FOR PAD 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 55 MANAGEMENT OF ANESTHESIA ADVANTAGE Avoids hyperdynamic response to intubation and extubation REGIONAL DISADVANTAGE Use of anticoagulants Increased cost of postop surveillance? Reduced postop respiratory and infectious complications May be poorly tolerated with severe COPD Reduced postop hypercoagualability and graft thrombosis Improved postop analgesia GENERAL Improved patient comfort? Higher graft failure rate Uncooperative patient Increased postop pneumonia Length of surgery Upper extremity vein harvest 56 POSTOPERATIVE MANAGEMENT Primary risk is ischemic heart disease Most cardiac events occur at emergence and postoperatively BARASH 57 POSTOPERATIVE MANAGEMENT MILLER 58 RAYNAUDS PHENOMENON 59 RAYNAUD’S PHENOMENON Episodic vasospastic ischemia of the digits Signs and Symptoms Blanching Cyanosis Rubor following cold exposure and rewarming Primary Raynaud’s disease Typically bilateral Secondary Typically due to autoimmune disease, such as cleroderma or SLE Often unilateral 60 MANAGEMENT OF ANESTHESIA 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 61 CAROTID ARTERY DISEASE 62 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 » Speech problems » Clumsiness of the extremities 63 ACUTE ISCHEMIC STROKE #1 Cause of disability in U.S. #3 Cause of death in U.S. Risk Factors Systemic hypertension Cigarette smoking Hyperlipidemia Diabetes mellitis Alcohol > 6/day Hyperhomocysteinemia 64 CAROTIC ENDARTERECTOMY 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 65 CAROTID ENDARTERECTOMY Correlates of surgical outcome Age Diabetes Smoking TIAs History of stroke Creatinine > 1.5 mg/dl Hypoalbuminemia Long operative time 66 CAROTID ENDARTERECTOMY 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% 67 CAROTID ENDARTERECTOMY Preoperative Assessment Atherosclerosis is a systemic disease – CAD – Renal dysfunction Additional assessment beyond routine Determine normal blood pressure and heart rate range – 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 68 OPERATIVE CONSIDERATIONS Blood pressure Stable, high-normal Ventilation / ETCO2 Normocarbia Blood sugar Tight control Brain protection Decreased CMRO2 – – – – Volatile agents Barbiturates Etomidate Propofol Temperature control Hypothermia Normothermia 69 CEREBRAL ISCHEMIA MONITORS Reason Determination of need for shunting Modalities EEG SSEP Stump pressure Transcranial doppler Cerebral oximetry Direct xenon cerebral blood flow measurement Awake patient 70 MANAGEMENT OF ANESTHESIA Two Primary Anesthetic Goals – Hemodynamic stability Adequate blood pressure for collateral perfusion following cross-clamp of carotid Diseased vessels exhibit failure of autoregulation Surgical manipulation of the carotid sinus can produce large changes in HR and BP – Rapid emergence To allow for neurologic assessment in the operating room 71 MANAGEMENT OF GENERAL ANESTHESIA Monitors Arterial line ST-T segment analysis in leads II and V5 TEE or central line unnecessary unless severe cardiac comorbidities 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 72 MANAGEMENT OF GENERAL ANESTHESIA Maintenance Maintain a “light” level of anesthesia – Aids in monitoring of cerebral ischemia with EEG, SSEP – Maintains a high-normal blood pressure Avoid excessive use of longer-acting narcotics – Interference with postop neuro exam Choice of maintenance drug not really critical – Volatiles – Propofol infusion – Combination of above Emergence Consider deep extubation if appropriate to avoid hypertensive response 73 POSTOPERATIVE MANAGEMENT Primary Concerns Cardiac events New neurologic deficits Airway management – Hematoma – Denervation of carotid bodies Blood pressure control – Can be extremely labile 74 POSTOPERATIVE MANAGEMENT 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 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 75 CAROTID ANGIOPLASTY AND STENTING Major complication is microembolization When done with an emboli protection device, results are equivalent to CEA 76 SOURCES Anesthesia and Coexisting Disease –Hines. 2022. 8th Edition Miller’s Anesthesia –Miller. 2020. 9th Edition Clinical Anesthesia –Barash. 2017. 8th Edition 77