VASCULAR DISEASES

NAGELHOUT CH. 26: ANESTHESIA FOR VASCULAR SURGERY

Peripheral Vascular Disease:
Atherosclerosis
The most common cause of occlusive disease in arteries of lower extremities.  Degerenative process involves formation of atheromatous plaques that obstruct vessel lumen and cause reduction in distal blood flow.
Pathophysiologic process:

1. plaque formation, which obstructs the lumen (stenosis)
2. thrombosis, which results in acute ischemia
3. embolism from microthrombi or atheromatous debris which decreases distal blood flow
4. weakening of arterial wall with aneurysm formation

Most common risk factors:

• Hypercholesterolemia
• Elevated triglycerides
• Cigarette smoking**
• HTN
• Diabetes  mellitus**
• Obesity
• Genetic predisposition
• Sex (M>F)
• Impaired long-term glucose regulation
• Homocysteine
• C-reactive protein

Typical symptoms of peripheral occlusive disease include claudication, skin ulcerations, gangrene, impotence.  The extent of disability is primarily influenced by the development of collateral blood flow.  Initially, collateral blood flow sufficiently meets tissue oxygen demands.  As the disease progresses, supply is unable to meet demand, and limb ischemia becomes symptomatic, requiring therapeutic intervention.

Mortality rates a/w PVD are 30% at 5 years and 70% at 10 years.

Interest in relationship between inflammation and the development of atherosclerosis.  Platelet interaction with leukocytes and other cells that modulate the immune response play a major role in the development of atherosclerosis. 

Treatment:
Pharmacologic therapy or surgery.
Surgical therapy includes transluminal angioplasty, endarterectomy, thrombectomies, endovascular stenting and arterial bypass procedures.  Some common surgical maneuvers used for bypassing occlusive lesions are aortofemoral, axillofemoral, femorofemoral, and femoropopliteal bypass techniques.  Bypass techniques may be classified as inflow or outflow procedures, depending on levelo of obstruction, with the dividing axis being at the level of the groin.

Preoperative Evaluation:
Atherosclerotic process should also be expected to be present in coronary, cerebral and renal arteries.  More than half the mortality a/w PVD results from adverse cardiac events.  Cardiac pathology must be managed aggressively to optimize cardiac functioning and decrease morbidity and mortality from cardiac causes.

Advantages to B-blockade on factors that affect myocardial oxygen supply and demand - their use is recommended in pts at high risk for myocardial ischemia and MI.  10-fold decrease in cardiac morbidity in AAA surgery.  B-blockade should be instituted days to weeks before surgery and titrated to HR 50-60.  Vascular surgery patients with limited HR variability after B-blockade therapy exhibit less cardiac ischemia and troponin values postop and have decreased mortality from all causes 2 years postop.

Monitoring:
Extent of periop monitoring should be based on presence of coexisting disease processes.  The detection of myocardial ischemia should be the primary objective in patients with vascular disease. Routine use of PACs are not warranted.  Transesophageal echocardiography may be used.

D/t global nature of atherosclerotic disease, the anesthetist should assume some degree of systemic CV disease in patients with PVD.  Patients with HTN and angiopathology rely on increased MAP to perfuse their vital organs.  Thus cerebral and coronary autoregulation occurs at a higher than normal pressures.  Direct intraarterial blood pressure monitoring allows for near-real-time determination of blood pressure values and is warranted bc of dramatic fluctuations that can occur during anesthesia.

Anesthetic Selection:
Depends ont he types of surgery performed and presence of co-existing disease.  Regional anesthesia for surgery on lower extremities may decrease the overal morbidity and mortality a/w this population - although some studies showed higher frequency of CV complications.  Research still pending; no conclusive evidence suggesting superior anesthetic technique.

Benefits of Epidural Technique in Vascular Surgery:

• Endocrine:
• inhibits surgical stress response
• inhibits adrenaline and cortisol release
• inhibits hyperglycemia
• inhibits lymphopenia and granulocytosis
• causes nitrogen sparing
• blocks sympathetic tone
• Cardiovascular
• decreases myocardial O2 demand and afterload
• decreases myocardial infarct size
• increases endocardial perfusion at ischemic zone
• causes fewer sympathetic blood pressure swings
• causes less blood loss
• requires less general anesthesia depressant medication
• redistribures blood to lower extremities
• Pulmonary
• decreases FVC, FEV1, PEFR (peak expiratory flow rate)
• requires less shunting O2 consumption
• improves atrioventricular O2 differentiation
• causes fewer pulmonary infections
• causes fewer thromboembolisms
• Renal
• increases blood flow in the renal cortex
• causes less renovascular constriction
• Geriatric
• causes less cardiorespiratory trespass
• improves postop mental status
• Misc
• allows earlier extubation, ambulation, discharge
• achieves greater postop pain control

Postoperative Considerations:
Postop admin of narcotics provides patient comfort and contributes to cardiac stability.  Use of epidural opioid and local anesthetics in patients recovering from vascular surgery is an important component of postoperative case because pain can greatly enhance sympathetic nervous system stimulation.


Abdominal Aortic Aneurysms
Incidence increasing.  Increase may be results of detection of asymptomatic aneurysms by noninvasive diagnostic modalities (CT, MRI, ultrasound). M> F, white>black.  Occurence of AAAs increased d/t increased age of general population and vascular changes that occur as a result of aging.

Risk Factors:

• Atherosclerosis thought to be primary cause of AAA in over 90% of patients. 
• Other theories: aneurysmal development may result from proteolysis of elastin and collagen within a vessel wall and that atherosclerosis may be an incidental finding in the pathogenesis of aneurysm development.
• HTN is present in 60% of patients with aneurysmal lesions.
• Cigarette Smokers the incidence of AAA increases eightfold.  (Correlation but aneurysms are also observed in normotensive nonsmokers)
• Genetics may also contribute to the predisposition for aneurysmal development.
• obesity (not an independent risk factor) may mask S&S of AAA until complications arise

Mortality:
Decreased for elective AAA surgery. 5%
Advanced detection capabilities, earlier surgical intervention, extensive preop preparation, refined surgical techniques, better hemodynamic monitoring, improved anesthetic techniques, aggressive postop management have contributed to improvement in surgical outcomes. The risk for rupture is very low for AAA less than 4 cm, but risk dramatically increases for AAA with diameter of 5 cm or greater.   Surgical intervention is recommended for AAA 5.5 cm or greater.  Mortality for ruptured AAA vary from 35-94%.  5 year mortality rate for individuals with untreated AAA is 81%, and 10 year mortality rate is 100%.  Early detection and elective surgical intervention can be lifesaving.

Diagnosis:
Asymptomatic aneurysms are detected incidentally during routine exam or abdominal radiography.  Smaller aneurysms are often unetected on routine physical examination. Diagnostic techniques such as u/s, CT scan and MRI may identify vascular abnormalities in these patients. Digital subtraction angiography is the best method of evaluating suprarenal aneurysms because it provides superior definition of the aneurysmal relationship to the renal arteries.

Abdominal Aortic Reconstruction
Patient Selection:
Mortality a/w elective repair of AAAs is fairly low compared with nonsurgical management.  Most pts w abdominal aneurysms are considered surgical candidates.  Age is not a contraindication for elective aneurysmectomy.  Mortality rate for elective aortic reconstruction is 5% for those < 75 years old and 11% for those > 75 years old.  Physiologic age is more indicative of increased surgical risk than chronologic age. 

CI to elective repair include intractable angina pectoris, recent MI, severe pulmonary dysfunction, and chronic renal insufficiency.  Patients with stable CAD and coronary artery stenosis of greater than 70% who require nonemergent AAA repair do not benefit from revascularization if B-blockade has been established.  In most cases the presence of an AAA warrants surgical intervention.

Criteria for High risk patients in AAA repair:

• >85 years old
• Home O2, PaO2 < 50 mmHg, FEV1 < 1 L/s
• serum Creatinine > 3 mg/dL
• Class III-IV angina
• Resting LVEF < 30%
• Recent CHF
• complex ventricular ectopy
• Large L ventricular aneurysm
• severe valvular disease
• recurrent congestive failure or angina after CABG
• severe, noncorrectable CAD

The dimensions of an aneurysm can change over time.  AAAs grow approximately 4 mm/year.  Aneurysmal vessel dimensions correspond to the Law of Laplace. (T = P x r)    T = wall tension,  P = transmural pressure, r = vessel radius

As the radius of the vessel increases, the wall tension increases.  Therefore, the larger the aneurysm, the more likely the risk of spontaneous rupture.  Aneurysms measuring more than 4-5 cm in diameter generally require surgical intervention, but aneurysms measuring less than 4-5 cm should not be considered benign.  An aneurysm has the potentila to rupture regardless of size.

Patient Preparation
Preop fluid loading and restoration of intravascular volume are the most important techniques used to enhance cardiac function during AAA surgery.  Reliable venous access must be secured if volume replacement is to be accomplished.  Large bore IV lines and central lines can be used to infuse fluids or blood.  Massive hemorrhage is a threat so availability of blood and blood products should be ensured. Provisions for rapid transfusion and intraop blood salvage should be confirmed.

Routine Monitoring
Standard monitoring methods:
EKG (II for dysrhythmias and precordial V5 for analysis of ischemic ST segment changes)
Pulse Ox
ETCO2
Foley for continuous measurement of UOP and renal function
Neuromuscular function may also be monitored

Invasive Monitoring
Maintaining cardiac function is crucial for successful surgical outcome; cardiac function should be closely monitored during AAA reconstruction. 
A-line: Permits beat-to-beat analysis of BP, immediate ID of hemodynamic alterations r/t aortic clamping, and access for blood sampling.
PAWP: can be used for monitoring of Left sided filling pressures as a guide for fluid replacement. low sensitivity and low specificity in detecting MI when compared with EKG and TEE. No difference in cardiac morbidity with PAC vs. CVP monitoring.
TEE: provides a sensitive method for assessing regional myocardial perfusion  by detecting changes in ventricular wall motion.  Wall motion abnormalities also occur much sooner than EKG changes during periods of reduced coronary blood flow.  MI poses the greatest risk of mortality after AAA reconstruction.

Aortic Cross-Clamping
The most dramatic physiologic change occurs with the application of an aortic cross-clamp.  Temporary aortic occlusion produces various hemodynamic and metabolic alterations.

Hemodynamic alterations:

• Hemodynamic effects of aortic cross-clamping depend on the application site along the aorta, the patients preoperative cardiac reserve, and the patients intravascular volume
• The most common site for cross-clamping is infrarenal, because most aneurysms appear below the level of the renal arteries. 
• Less common sites of aneurysm development are the juxtarenal and suprarenal areas
• During aortic cross-clamping, hypertension occurs above the cross-clamp, and hypotension occurs below the cross-clamp.
• Organs proximal to the aortic occlusion may experience a redistribution of blood volume
• There is an absence of blood flow distal to the clamp in the pelvis and lower extremities.
• Increases in afterload cause myocardial wall tension to increase
• MAP and SVR also increase
• CO may decrease or remain unchanged.
• Pulmonary artery occlusion pressure may increase or display no change
• Patients with adequate cardiac reserve commonly adjust to sudden increases in afterload without the occurrence of adverse cardiac events.  However, patients with ischemic heart disease or ventricular dysfunction are unable to fully compensate ans a results of hemodynamic alterations.  The increased wall stress attributed to aortic cross-clamp application may contribute to decreased global ventricular function and MIschemia.  Clinically, these patients experience increases in PAOP in response to aortic cross-clamping.

Metabolic Alterations:

• After application of aortic cross-clamp, the lack of blood flow to distal structures makes these tissues prone to develop hypoxia.  In response to hypoxia, metabolites such as lactate accumulate.
• The reduction in CO during aortic cross-clamping might be partly the result of metabolic alterations, such as decreased oxygen consumption
• Plasma catacholamine levels increased significantly during application of aortic cross clamp
• Epi and Norepi stimulate myocardial B1-receptors that can increase HR and myocardial O2 demand.
• Release of arachidonic acid derivatives may contribute to cardiac instability observed during aortic cross-clamping. Thromboxane A2 synthesis (accelerated by aplication of aortic cross clamp) may be responsible for the decrease in myocardial contractility and CO that occurs.  Current studies on pretreatment with NSAIDS.
• Traction on mesentery is a surgical maneuver used for exposing the aorta.  Can lead to mesenteric traction syndrome a/w this procedure.  S&S include decreases in BP and SVR, tachycardia, increased CO, and facial flushing
• cause unknown
• a/w high concentrations of 6-ketoprostaglandin F1, the stable metabolite of prostacyclin
• NSAIDS may reduce mesenteric traction syndrome
• Neuroendocrine response to major surgical stress is mediated by cytokines such as interleukin (IL)-1B, IL-6, and tumor necrosis factor as well as plasma catecholamines and cortisol.
• these mediators are thought to be responsible for triggering the inflammatory response that results in increased body temperature, leukocytosis, tachycardia, tachypnea, and fluid sequestration.

Effects on Regional Circulation:

• structures distal to the aortic clamp are underperfused during aortic cross-clamping
• renal insufficiency and renal failure have been reported to occur after abdominal aortic reconstruction.
• Suprarenal and juxtarenal cross-clamping may be a/w a higher incidence of altered renal dynamics but reductions in renal blood flow can occur with any level of clamp application
• Infrarenal aortic cross clamping is w/e 38% decrease in renal blood flow and a 75% increase in renal vascular resistance; these effects may lead to acute renal failure which is fatal in 50-90% of patients who undergo AAA repair.
• Preop evaluation of renal function is the most significant predictors of postop renal dysfunction
• Spinal cord damage is a/w aortic occlusion.  Interruption of blood flow to the greater radicular artery (artery of Adamkiewicz) in the absence of collateral blood flow has been identified as the causative factor in paraplegia.
• the incidence of neurologic complications increases as the aortic cross-clamp is positioned in a higher or more proximal area.
• SSEP monitoring has been advocated as a method of identifying spinal cord ischemia.  However, SSEP monitoring reflects dorsal (sensory) spinal cord function and does not provide information regarding the integrity of the anterior (motor) spinal cord.
• Motor evoked potential (MEP) monitoring is capable of determining anterior cord function. Can't use muscle relaxant.
• Ischemic colon injury is a well-documented complication a/w AAA resections.  Most frequently attributed to manipulation of the inferior mesenteric artery, which supplies the primary blood supplies to the L colon.
• This vessel often sacrificed during surgery and blood flow to the descending and sigmoid colon depends on the presence and adequacy of collateral vessels.  Mucosal ischemia occurs in 10% of patients.
• In less than 1% of these patients, infarction of L colon requires surgical intervention.

Aortic Cross-Clamp Release:
Whilte the aorta is occluded, metabolites that are liberated as a result of anaerobic metabolism (lactate) accumulate below the aortic cross-clamp and induce vasodilation and vasomotor paralysis.  As the cross-clamp is released, SVR decreases and the blood is sequestered into previously dilated veins, which decrease venous return.  Reactive hyperemia causes transient vasodilation secondary to the presence of tissue hypoxia, release of adenine nucleotides, and liberation of an unnamed vasodepressor substance that acts as a myocardial depressant and peripheral vasodilator.  This results in decreased preload and afterload. The hemodynamic instability that may ensure after the release of an aortic cross-clamp is called declamping shock syndrome. Venous endothelin (ET)-1 may be responsible for hemodynamic alterations (has positive inotropic effect on heart and vasoconstricting/vasodilating action on vessels).

Most commonly observed hemodynamic response to aortic declamping:

• MAP decrease
• SVR decrease
• CO no change or increase
• PAOP decrease

Intravascular volume may influence the direction and magnitude of change in cardiac output.  The site and duration of cross-clamp application, as well as gradual release of the clamp, influence the magnitude of circulatory instability. Partial release of the aortic cross-clamp over time frequently results in less severe hypotension.

Surgical Approach
Transperitoneal incision - good exposure, but increased fluid losses, prolonged ileus, postop incisional pain, pulmonary complications

Retroperitoneal approach - excellent exposure (juxtarenal and suprarenal aneurysms), decreased fluid losses, less incisional pain, fewer postop pulmonary and intestinal complications.  Does not elicit mesenteric traction syndrome. Inaccessibility to distal R renal artery

Management of Fluid and Blood Loss
Evaporative losses and 3rd spacing.  Most blood loss occurs because of back bleeding from lumbar and inferior mesenteric arteries after vessels have been clamped and aneurysm is open.  Use of heparin contributes to EBL. Blood replacement is commonly administered during abdominal aortic resections.

Presence of Concurrent Disease
Preoperative Management
The presence of underlying CAD in patients with vascular disease exists in more than 50% of patients requiring AAA reconstruction and is the single most significant risk factor influencing long-term survivability.  MI is responsible for 40-70% of all fatalities that occur after aneurysm reconstruction.  Cardiac function must be optimized.
Stress test: dipyridamole thallium
HTN, COPD, DM, renal impairment and CAD is frequently observed in patients with AAA.

Intraoperative Management
Anesthetic Selection
A superior technique has not been identified. 
VAA: may depress myocardium; avoid high concentrations
Narcotics: high-dose narcotics with N2O can be used as the anesthetic for major vascular surgery.  Opioids provide CV stability.
Regional Anesthesia: epidural; may cause hypotension or hematoma formation (heparin)
Combo techniques: balanced technique of low-dose inhalation agents maintains CV hemodynamics and controls momentary autonomic responses to surgical stimulation. Epidural anesthesia combined with light general anesthesia

Fluid Management
Maintaining intravascular volume is a challenge
Crystalloids vs. Colloids
Crystalloids: may be used for replacing basal and 3rd-space losses at approximate rate of 10 ml/kg/hr
Blood losses initially can be replaced with crystalloid at ratio of 3:1.
Fluid replacement should be sufficient for the maintenance of normal cardiac filling pressures, cardiac output, and urine output of 1 ml/kg/hr
Patients with limited cardiac reserve can develop CHF if hypervolemia occurs.

Hemodynamic Alterations

Renal Preservation

Postoperative Considerations

Juxtarenal and Suprarenal Aortic Aneurysms

Ruptured AAA

Thoracic Aortic Aneurysms

Aortic Dissection

Descending Thoracic and Thoracoabdominal aneurysms

Endovascular Aortic Aneurysm Repair

Cerebrovascular Insufficiency and Carotid Endarterectomy

Carotid Artery Stenting