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