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Aorto-occlusive disease Major Vascular Surgery Peripheral Arterial Disease Carotidendarterectomy
Aorto-occlusive disease is characterized by pathophysiologic, atherosclerotic changes within the aorta that extends into the iliac and/or femoral arteries and results in inadequate perfusion of vital organs and the lower extremities
Myocardial dysfunction remains the single most important cause of morbidity following vascular surgery
A mortality rate of about 5% is associated with elective abdominal aortic aneurysm (AAA) repair (j
Patients presenting for surgery with poorly controlled CHF have a 20% mortality with a AAA repair
The majority of these patients present in their fifth decade or older
Coronary artery disease is present in 25-65% of this population
Additional comorbidities include: Angina pectoris Hypertension H/O myocardial infarction Congestive heart failure Pulmonary disease Diabetes mellitus Renal insufficiency Cerebrovascular disease
PreOp evaluation of the ECG is more often abnormal than not in elderly patients and does not appear to be independently associated with adverse events
Patients who have survived recent coronary revascularization (CABG < 5 years, PTCA < 2 years) have fewer cardiac complications after vascular surgery
Perioperative MI may occur from rupture of atherosclerotic plaque (50%) or due to a prolonged imbalance between myocardial oxygen supply and demand in the setting of CAD
Myocardial oxygen supply may be diminished by anemia or hypotension, whereas oxygen demand may be increased by tachycardia and hypertension
Studies have consistently identified CHF, previous MI, advanced age, severely limited exercise tolerance, chronic renal insufficiency, and diabetes as risk factors for the development of perioperative cardiac morbidity.› The presence of three or more of these risk factors makes an
individual patient a “high risk” for surgery
Age Gender (male) Smoking Diabetes mellitus Hypertension Hyperlipidemia Obesity Physical inactivity
The strongest association is with smoking and diabetes
The goals of perioperative cardiac monitoring are to detect myocardial ischemia and to identify abnormalities of preload, afterload, and ventricular function
ECG monitoring The mainstay of perioperative detection of myocardial ischemia Evidence of ST segment depression is a more common indicator of
myocardial ischemia than ST elevation during vascular surgery Pulmonary capillary wedge pressure
Has low sensitivity and specificity for detecting ischemia PCWP elevations tend to be associated with tachycardia and hypertension
(suggestive of inadequate anesthesia) PCWP remained normal in 80% of patients who developed wall motion
abnormalities on TEE Transesophageal Echocardiography (TEE)
When myocardial ischemia is produced, mechanical dysfunction precedes surface ECG changes
Though regional wall motion abnormalities are more sensitive than ST segment changes in detecting intraoperative ischemia, TEE during noncardiac surgery appears to have little incremental clinical value
Carotid atherosclerosis is the leading cause of extracranial vascular cerebral events
The disease is primarily a problem of embolization and rarely occlusion or insufficiency
Plaque rupture or embolization can lead to Transient ischemic attack (TIA) or cerebrovascular accident (CVA)
Carotid disease may manifest itself as an asymptomatic bruit, or as transient attacks of monocular blindness› Amaurosis fugax (from the Greek "amaurosis," meaning dark,
and the Latin "fugax," meaning fleeting) Anesthetic management attempts to optimize cerebral
perfusion in patients with a high prevalence of Coronary artery disease
The two main goals of intraoperative management are to protect the brain and to protect the heart; these two goals often conflict
Increasing arterial blood pressure to augment cerebral blood flow can increase afterload or myocardial contractility, thus increasing myocardial oxygen demand
A high-normal blood pressure may be best to balance these two goals
Normocarbia or moderate hypocarbia Hypercarbia dilates cerebral vessels and
thus increases cerebral blood flow, but may cause a diversion of blood flow from hypoperfused brain regions to normally perfused regions (“steal phenomenon”)
Normoglycemia Moderate hyperglycemia may worsen
ischemic brain injury
Monitors ASA standard monitors,+ A-line, 2 large bore IVs
Induction These patients tend to be hypovolemic; they may present
hypertensive, but are prone to hypotension on induction Thiopental decreases cerebral metabolic oxygen requirements to
about 50% of baseline Maintenance
Inhalational agents reduce cerebral oxygen requirements Avoid administering more than 10 mL/kg of crystalloid because fluid
overload may contribute to postOp hypertension Emergence
Deep extubation is best if no contraindications exist; this aids in the prevention of hypertension and tachycardia during emergence
PostOp Both acute tachycardia and hypertension can precipitate
myocardial ischemia, and hypertension may lead to cerebral edema and hemorrhage
Aneurysmal Disease Mortality from aneurysm rupture may be as high as
85%, and even patients who receive emergent surgery have mortality rates one-half that
Risk factors for aneurysm Advanced age Smoking > 40 years Hypertension Low serum HDL High level of plasma fibrinogen Low blood platelet count
Rupture of the AAA is related to the absolute diameter of the aortic aneurysm sac; the risk of rupture increases once the aneurysm is greater than 4.5 to 5 cm in diameter
6 year incidence of rupture < 4.0 cm is 1% 4.0-4.9 cm is 2% >5.0 cm is 20%
Patients with AAAs that do not undergo operation have an 80% 5-year mortality, predominantly because of rupture
It is recommended that in good-risk patients with aneurysms greater than 4.5-5 cm surgical repair should be considered
Surgery for ruptured AAA is still associated with a mortality approaching 50%
Aortic cross-clamping increases mean arterial pressure and systemic vascular resistance up to 50%
During the cross-clamp period even relative hypotension should be avoided
Unclamping of the aorta can result in severe arterial hypotension unless aggressive therapy is undertaken prior to unclamping
Even with an infrarenal aortic clamping, renal blood flow is 45% lower during cross-clamping
Renal vascular resistance increases by as much as 70%; this may persist for 30 minutes or more after release of the clamp and return to baseline hemodynamics
Renal protection methods center on improving renal blood flow or glomerular flow
Diuretics such as mannitol and lasix are often used but outcomes have not been shown to improve with use
One of the most important factors for preventing postOp renal failure is good hydration
Monitoring ASA standard monitors + A-line Central Venous Access Consider a PAC in patients with a H/O CHF or poor left ventricular
function, though improvements in outcome have not been demonstrated, may also use TEE
Induction Slow and Easy Consider Regional techniques, high dose narcotics
Maintenance Volatile agents, Air / Oxygen N20 increases afterload and myocardial work, and depresses
myocardial inotropic performance and output; as well as Inc. bowel gasses
Emergence Deep extubation unless contraindicated to reduce stress of
emergence PostOp
Postoperative pain control is key to minimizing tachycardia and hypertension associated with postOp pain
Prehydration minimizes variations in blood pressure associated with induction
Hemodynamic variables within 20% of baseline (PCWP < 15 mmHg, HR < 80-90)
Mannitol prophylaxis is generally used, but time of initiation varies with the surgeon (most after clamping)
Patient should be kept relatively hypovolemic prior to cross-clamp, vasodilators should be initiated with cross-clamping as tolerated, and vasodilators should be stopped prior to the release of the clamp (allowing for increases in blood pressure and filling volumes)
PAP and CVP may increase during reperfusion because of release of lactic acid and other mediators which cause pulmonary vasoconstriction and cardiac depression
Unlike the elective AAA in which preserving myocardial function is the primary goal, the crucial factor for patient survival is control of blood loss, reversal of hypotension, and then preservation of myocardial function
Rapid control of the proximal portion of the aorta is more important than optimizing the patient
Volume resuscitation with crystalloid, colloid, and blood products is essential
Current trend with minimally invasive technique› Both femoral arteries are accessed by cut down to
“float” a gortex graft into place in the aneurysmal sac.
Graft will provide the lumen for blood flow and the sac will shrink over time
Potential for “leaking” is ~14% › May need to return to the OR for further repair
Must be prepared to convert to an open AAA Not as painful nor as long as a recovery period Not all patients are a candidate for this
procedure
The incidence of cardiac morbidity after infrainguinal procedures may exceed that associated with abdominal aortic procedures because patients for distal procedures often have more preoperative risk factors
Patients undergoing lower-extremity revascularization may receive less attentive care; “it is just a spinal case”
These procedures are often done utilizing regional technique which can lead to hypotension
Patients are most often hydrated, and sometimes over hydrated in response to the venodilatation caused by the spinal sympathectomy
As the sympathetic effect wears off, an “autotransfusion” can lead to CHF in a susceptible patient
Length of surgical time varies and use caution with a single shot RA technique
Usually patient is typical “vasculopath” and has prior vascular associated procedures
Acts as an anticoagulant, preventing the formation of clots and extension of existing clots within the blood› While heparin does not break down clots that have
already formed (unlike tissue plasminogen activator), it allows the body's natural clot lysis mechanisms to work normally to break down clots that have not yet formed
Provided in “units” with varying concentrations - ***must use caution***
Given either IV or SC ½ life is ~60 min Dosing varies with goal (50-150 units/kg) Results measured with aPTT or ACT
Reversal of Heparin Highly cationic molecule Forms inactive complex with heparin Can cause a massive histamine release
if administered quickly (hypotension, bronchoconstriction, tachycardia)
1mg of protamine to reverse 100units of heparin
Lab test to determine the effectiveness of heparin dose or reversal
Blood sample drawn 2 min after heparin administered or 5 minutes after protamine
Specimen requirement is 2 mL of whole blood collected in a celite activated glass vacutainer tube, mixed, and immediately inserted into the instrument
Sheath pull› <150 to <250
Extracorporeal circulation› 180 to 220
Catheterization/ vascular surgery› >180 to >200
Angioplasty without ReoPro› >300 to >350
Angioplasty with ReoPro› 200 to 300
CABG› >400
CABG with aprotinin› >480 to >600
Reference range is 99 - 130 seconds