Foundations

Arterial anatomy, head to toe Memorize

You will be asked to name vessels in order, in the operating room, while holding a retractor. Learn the path of blood from the aorta to the toes and from the arch to the fingertips, then the neck and the gut, because those are the beds the service operates on.

The aorta and the arch

The aortic root gives the coronary arteries, and the ascending aorta then becomes the arch, which gives three branches before it descends. The classic arch order, right to left, is the brachiocephalic (innominate) trunk, the left common carotid, and the left subclavian. The brachiocephalic then splits into the right common carotid and right subclavian. Each subclavian gives a vertebral artery, which climbs through the cervical transverse foramina (usually entering at C6) and joins its partner to form the basilar artery.

Arch variants worth knowing

Bovine arch common origin

The brachiocephalic trunk and left common carotid share a single origin, or the left common carotid arises from the brachiocephalic trunk itself. It is the most common variant, seen in roughly 10 to 25 percent of people depending on the series. The name is a misnomer (cattle have a different arrangement) but everyone uses it. It changes how the left carotid is catheterized for angiography or stenting.

Left vertebral from the arch

The left vertebral arises directly from the arch between the left common carotid and left subclavian in about 5 percent of people. It matters for catheter selection and for thoracic stent-graft planning near the left subclavian.

Aberrant right subclavian arteria lusoria

Arises as the last arch branch, beyond the left subclavian, and usually crosses behind the esophagus (about 1 percent of people). It can cause dysphagia, may arise from an aneurysmal Kommerell diverticulum, and comes with a non-recurrent right laryngeal nerve that is at risk in neck surgery.

Arch type I to III

Describes how far below the top of the arch the great vessels arise. In a type I arch they come off the top; in a type III arch the innominate origin sits well below it. Steeper, elongated arches are more common with age and hypertension and make transfemoral carotid work harder.

The carotid bifurcation

The common carotid normally gives no branches in the neck. It divides, usually at about the upper border of the thyroid cartilage (roughly C3 to C4), into the internal and external carotid arteries. The level varies, and a high bifurcation near the angle of the mandible makes distal exposure harder, so look for it on the preoperative imaging. The origin of the internal carotid is dilated as the carotid bulb, home of the carotid sinus baroreceptors and the carotid body. That is why handling the bifurcation can drop the heart rate and blood pressure.

The internal carotid (ICA) has no branches in the neck; its first branch, the ophthalmic artery, arises inside the skull. At its origin the ICA usually lies posterolateral to the external carotid. The external carotid (ECA) supplies the face, scalp and neck through eight branches, and it becomes an important collateral to the brain when the ICA is occluded.

Structures met during carotid endarterectomy

Through an incision along the anterior border of the sternocleidomastoid, roughly in the order you meet them:

Great auricular nerve

Crosses the top of the incision toward the earlobe. Injury leaves a numb earlobe.

Facial vein common facial vein

Crosses the field to drain into the internal jugular vein and reliably overlies the carotid bifurcation, so it is the landmark. It is ligated and divided, and the internal jugular is retracted laterally.

Carotid sheath

Common carotid medially, internal jugular vein laterally, vagus nerve posteriorly between them.

Ansa cervicalis

A nerve loop on the front of the sheath, descending from the hypoglossal to the strap muscles. It can be divided to free the hypoglossal with little consequence.

Vagus nerve (X)

Usually posterior in the sheath but occasionally anterior, so it must be seen before clamps go on. Injury, including clamp injury, paralyzes the ipsilateral vocal cord (hoarseness, weak cough) because the recurrent laryngeal fibers travel within it.

Hypoglossal nerve (XII)

Crosses superficial to the ICA and ECA a short distance above the bifurcation, beneath the posterior belly of the digastric, tethered by the sternocleidomastoid branch of the occipital artery. Injury makes the tongue deviate toward the injured side. This is the classic carotid nerve injury.

Superior laryngeal nerve

Runs deep (medial) to the ICA and ECA near the bifurcation; its external branch travels with the superior thyroid artery. Injury causes voice fatigue and loss of high pitch, which matters a great deal to a singer.

Marginal mandibular nerve branch of VII

Runs just below the angle of the mandible and is stretched by retraction at the top of the incision. Injury droops the lower lip on that side. Curving the upper incision back toward the mastoid helps protect it.

Glossopharyngeal nerve (IX)

Met only with very high exposure toward the skull base. Injury causes dysphagia and aspiration risk.

The visceral aorta

Below the diaphragm the abdominal aorta gives, in descending order, the celiac trunk (roughly T12), the superior mesenteric artery (L1), the paired renal arteries (L1 to L2), the inferior mesenteric artery (L3), and finally bifurcates into the common iliac arteries at about L4, near the level of the umbilicus. Paired lumbar arteries leave its back wall along the way.

One venous relationship matters in every open aortic exposure. The left renal vein crosses in front of the aorta just below the origin of the superior mesenteric artery. In a few percent of people it runs behind the aorta (retroaortic) or splits around it (circumaortic), where an unsuspecting clamp can tear it. Look for it on the CTA before the operation.

The lower extremity, in order

This is the single most asked sequence in the field. Trace it until it is automatic.

• The common iliac splits into the internal iliac (hypogastric), supplying the pelvis, and the external iliac.
• The external iliac passes under the inguinal ligament and becomes the common femoral artery.
• The common femoral bifurcates into the profunda femoris (deep femoral), the key collateral vessel of the thigh, and the superficial femoral artery.
• The superficial femoral travels down the thigh through the adductor (Hunter's) canal and, at the adductor hiatus, becomes the popliteal artery.
• Below the knee the popliteal gives the anterior tibial artery (which becomes the dorsalis pedis on the foot) and then the tibioperoneal trunk, which splits into the posterior tibial (passing behind the medial malleolus) and the peroneal (fibular) artery.

The upper extremity, in order

The subclavian passes over the first rib, behind the clavicle, and becomes the axillary at the lateral border of the first rib. Past the lower border of teres major it becomes the brachial, which bifurcates just below the elbow into the radial and ulnar arteries. These join in the hand as the superficial and deep palmar arches. This dual supply is what makes the Allen test meaningful and what lets a radiocephalic fistula work.

Venous anatomy

Veins are divided into a deep system (paired with the named arteries, carrying roughly 85 to 90 percent of return), a superficial system, and the perforators that connect them. Naming them correctly is not pedantry: whether a clot is in a deep or a superficial vein decides whether the patient is anticoagulated.

Deep veins by name

Below the knee the deep veins are paired companions (venae comitantes) of the anterior tibial, posterior tibial and peroneal arteries, plus the muscular gastrocnemius and soleal veins, where many calf DVTs begin. They join to form the popliteal vein, which becomes the femoral vein at the adductor hiatus. The femoral vein joins the deep femoral (profunda) vein to form the common femoral vein, which receives the great saphenous vein at the saphenofemoral junction and becomes the external iliac vein under the inguinal ligament. The external and internal iliac veins form the common iliac veins, which join at about L5, to the right of the aorta, to form the inferior vena cava.

In the arm, paired radial, ulnar and brachial veins drain to the axillary vein, which becomes the subclavian vein at the first rib and joins the internal jugular to form the brachiocephalic vein. The superficial cephalic vein (lateral, ending in the axillary vein through the deltopectoral groove) and basilic vein (medial, diving deep in the mid-arm to join the brachial veins) are the dialysis access veins; see Open operations.

Superficial veins and their nerves

The great saphenous vein begins in front of the medial malleolus and runs up the medial leg and thigh to join the common femoral vein at the saphenofemoral junction, just below and lateral to the pubic tubercle. The small saphenous vein begins behind the lateral malleolus and runs up the posterior calf to join the popliteal vein in the popliteal fossa, at a level that varies. Each runs with a sensory nerve that is at risk during vein harvest, stripping or thermal ablation.

Superficial vein thrombosis is usually treated less aggressively than DVT, with one exception worth remembering: thrombus in the great saphenous vein within about 3 cm of the saphenofemoral junction is generally managed like a DVT, because it is a step away from the common femoral vein.

Perforators

Perforating veins pierce the deep fascia and connect the superficial and deep systems. Their valves normally direct flow from superficial to deep, so the calf muscle pump can empty the leg. When they fail, high pressure from the deep system is transmitted to the skin. The medial lower-leg perforators (historically called Cockett perforators, now posterior tibial perforators) drain the gaiter area above the medial malleolus, which is exactly where venous ulcers cluster. Others sit just below the knee (Boyd) and in the thigh (Dodd). A perforator is usually considered pathologic, and worth treating, when it shows outward flow of 500 milliseconds or more, a diameter of about 3.5 mm or more, and lies beneath a healed or open ulcer.

May-Thurner anatomy

The right common iliac artery crosses in front of the left common iliac vein and compresses it against the fifth lumbar vertebra. Chronic pulsatile compression can leave webs and spurs inside the vein. The result is a predisposition to left iliofemoral DVT, classically in younger women. Some degree of this compression is common on imaging in people with no symptoms, so the anatomy alone is not the diagnosis; intravascular ultrasound at venography is the usual way to judge it. An extensive, symptomatic left iliofemoral DVT may be treated with thrombus removal and stenting of the compressed segment in selected patients. See Presentations.

Collateral pathways High yield

Collaterals explain why a patient can occlude a major vessel and still keep a viable limb, brain or gut. Named collateral routes are favorite teaching material.

Circle of Willis

Anastomotic ring at the base of the brain linking the anterior (carotid) and posterior (vertebrobasilar) circulations. It explains why some patients tolerate carotid occlusion or clamping and others stroke. It is complete in only a minority of people.

External to internal carotid

When the ICA is occluded, ECA branches around the face and orbit can fill the ophthalmic artery backward and supply the intracranial ICA. One reason the ECA is worth preserving.

Vertebral reversal subclavian steal

With a proximal subclavian occlusion, blood flows up one vertebral artery and down the other into the arm. Arm exercise can then steal from the brainstem. Suspect it when the arm pressures differ by more than about 15 to 20 mmHg.

Pancreaticoduodenal arcades

Link the celiac (through the gastroduodenal artery) to the superior mesenteric artery. They keep the liver and foregut alive when the celiac origin is stenosed, and can become aneurysmal under the extra flow.

Marginal artery of Drummond

Continuous arcade along the mesenteric border of the colon connecting the SMA and IMA territories.

Arc of Riolan meandering mesenteric artery

A shorter, more central SMA to IMA connection that enlarges dramatically when one mesenteric vessel occludes chronically.

Aortoiliac collaterals

In Leriche-type occlusion, flow reaches the legs through lumbar to iliolumbar routes and through the IMA to superior rectal to middle and inferior rectal (internal iliac) routes.

Internal thoracic to epigastric Winslow pathway

Internal thoracic (mammary) to superior epigastric to inferior epigastric to external iliac. In aortoiliac occlusion it can carry much of the leg's flow, so it should not be divided carelessly.

Profunda femoris and the geniculates

The main collateral around an occluded superficial femoral artery; geniculate branches reconstitute the popliteal. A good profunda can carry a limb despite a dead SFA.

Hemodynamics and physiology

A handful of physical principles get asked again and again because they explain disease. See also the teaching questions on physiology.

Poiseuille's law

Flow is proportional to the fourth power of the radius and inversely proportional to length and viscosity. The punchline is that small changes in lumen diameter cause large changes in flow, which is why a focal stenosis can be so hemodynamically costly, and why a slightly larger conduit dramatically improves flow.

Critical stenosis

A stenosis generally becomes hemodynamically significant once it narrows the diameter by about 50 percent (roughly 75 percent of cross-sectional area), at which point a measurable pressure and flow gradient appears across it. This is the threshold that duplex velocity criteria are designed to detect.

Because the same volume of blood must pass through a smaller opening, velocity rises within a stenosis (flow equals area times velocity). That jump in velocity is what duplex ultrasound measures, which is why reports grade stenoses by peak systolic velocity and by the ratio of velocity in the stenosis to velocity just upstream.

Why disease shows up with exercise

At rest, collaterals around a stenosis or occlusion may carry enough flow for resting muscle. Exercise dilates the muscle bed and multiplies demand, but the collaterals have a fixed, high resistance, so pressure beyond them falls and the muscle becomes ischemic. That is claudication, and it is why an exercise ABI can reveal disease that a resting ABI misses.

Laplace's law and aneurysms

Wall tension rises with both pressure and radius. As an aneurysm enlarges, wall tension climbs, which raises rupture risk and accelerates further dilation, a self-reinforcing loop that is the entire rationale for size-based repair thresholds.

The vascular history and physical exam

The exam is where you earn credibility. Do it the same way every time. Documentation templates for the exam are on History, exam and charting.

History: localizing claudication

The level of arterial disease predicts where the patient hurts when walking, because the pain occurs one level below the occlusion. Buttock and hip claudication points to aortoiliac disease, thigh claudication to the common femoral or iliac level, and the most common pattern, calf claudication, to the superficial femoral and popliteal segment. The full presentations are on Presentations.

The pulse exam

Palpate and grade every pulse, comparing sides. A common scale is 0 absent, 1+ diminished, 2+ normal, 3+ bounding (some services add a fourth grade, so use the one your team uses). Document the sites: radial, brachial, carotid, femoral, popliteal, dorsalis pedis, and posterior tibial. If you cannot feel a distal pulse, reach for the handheld Doppler and describe the signal.

A 2020 consensus from the Society for Vascular Medicine and the Society for Vascular Ultrasound recommends describing waveforms as multiphasic or monophasic, with descriptors such as high or low resistance, rather than counting phases. You will still hear triphasic, biphasic and monophasic at the bedside every day.

Provocative and inspection findings

• Buerger's test. Elevation causes pallor in an ischemic limb, and dependency causes a dusky dependent rubor. The angle at which pallor appears tracks severity.
• Signs of chronic ischemia. Capillary refill beyond 2 to 3 seconds, along with loss of hair, shiny atrophic skin, and thickened nails.
• Allen test. Before radial access or radial-artery harvest, confirms that the ulnar artery and palmar arch can supply the hand alone. A Doppler or pulse-oximetry version is more objective than watching the palm color.
• Bruits. Auscultate over the carotids, abdomen, and femorals; a bruit signals turbulent flow across a stenosis.

Noninvasive testing and the ABI Core skill

The ankle-brachial index is the bedside number that quantifies perfusion. Measure the higher of the two ankle systolic pressures (dorsalis pedis or posterior tibial) in each leg and divide by the higher of the two brachial pressures.

How to measure an ABI

1. Rest the patient. Supine and still for 5 to 10 minutes, legs at heart level. Measurements taken right after a walk from the waiting room run low.
2. Choose the right cuff. Cuff width should be at least 40 percent of the limb circumference. The ankle cuff goes just above the malleoli, with the lower edge about 2 to 3 cm above them.
3. Measure both brachial pressures. Cuff on the upper arm, Doppler probe over the brachial artery. A difference of more than about 15 mmHg suggests subclavian stenosis on the lower side.
4. Measure both ankle pressures in each leg. Probe at about 45 to 60 degrees over the dorsalis pedis, then the posterior tibial. Inflate about 20 mmHg past the point where the signal disappears, deflate slowly, and record the pressure at which the signal returns.
5. Calculate each leg separately. The higher of that leg's two ankle pressures divided by the higher brachial pressure. Some labs also report the lower ankle pressure, which is more sensitive for disease.
6. Document the raw pressures as well as the ratio. If an ABI is above 1.40 or does not fit the foot in front of you, move on to toe pressures.

The rest of the noninvasive toolbox

• Segmental limb pressures and pulse-volume recordings. Cuffs at the thigh, calf, and ankle localize the level of disease by where the pressure drops or the waveform flattens.
• Exercise ABI. A normal resting ABI that falls after treadmill walking reveals significant disease and confirms that leg symptoms are vascular. A fall in ankle pressure of more than 30 mmHg, or in the ABI of more than 20 percent, is generally considered diagnostic.
• Arterial duplex ultrasound. Combines B-mode imaging with Doppler velocities, and a rise in peak systolic velocity across a segment grades the stenosis. This is the first-line tool for surveillance.
• Venous duplex. DVT is diagnosed mainly by a vein that will not compress under the probe. Reflux is generally defined as reversed flow lasting more than 0.5 seconds in superficial veins and more than 1 second in the femoral and popliteal veins; thresholds vary slightly between guidelines.

Duplex criteria you will hear quoted

Peak systolic velocity and the visible plaque are the primary criteria; the ratio and end-diastolic velocity help when the picture is mixed. A tight stenosis or occlusion on the other side can raise velocities on this side and overcall it. Percentages refer to the NASCET method of measurement, which is what the trials and repair thresholds use. The clinical side is on Presentations.

Native arteries and bypass grafts

In native leg arteries, a peak systolic velocity ratio of about 2 or more (velocity in the stenosis divided by velocity in the normal segment just upstream) suggests a stenosis of 50 percent or more. Vein grafts are surveilled with duplex because a stenosis found and fixed before the graft clots has far better results than a graft that has already failed.

Uniformly low velocities throughout a graft (under about 45 cm/s) with no focal stenosis also mark a graft at risk, usually from inflow or outflow disease. A drop in ABI of more than about 0.15 between visits should prompt a duplex. Many labs require both the velocity and the ratio criterion; surveillance intervals follow SVS follow-up guidance and local protocol, most intensively in the first year.

Imaging modalities

Each test answers a different question. Pick the one that answers yours with the least contrast, radiation and risk.

Duplex ultrasound first-line, no contrast

Cheap, repeatable, operator-dependent. The workhorse for carotid disease, graft surveillance, aneurysm screening and follow-up, DVT, venous reflux and vein mapping.

CT angiography the anatomy roadmap

Fast and detailed, the go-to for aneurysm sizing, dissection, trauma, and operative planning. The costs are iodinated contrast and radiation, and heavy calcium in small tibial vessels can bloom and hide the lumen.

MR angiography contrast-sparing option

Good soft-tissue detail without iodinated contrast or radiation. Slower, tends to overestimate stenosis, and degraded by stents and some implants. The gadolinium concern in kidney failure (nephrogenic systemic fibrosis) is now very small with the newer agents, but follow radiology's policy for advanced kidney disease.

Digital subtraction angiography the gold standard

Catheter angiography has the highest spatial resolution and is the only modality that is also therapeutic. Invasive, so it is reserved for when intervention is likely or other imaging is equivocal. Carbon dioxide angiography can spare iodinated contrast below the diaphragm, never in the cerebral or coronary circulation.

Anticoagulation and antiplatelets Asked often

The pharmacology of clotting is asked constantly, both on the wards and in the operating room, and it changes the plan on most vascular patients most mornings.

For VTE, a weight-based heparin infusion classically starts with an 80 units per kg bolus, then is adjusted to an aPTT or anti-Xa nomogram per local protocol. The overnight version of managing a drip is on On call.

Intraoperative heparin

Before clamping any artery, the surgeon asks anesthesia to give systemic heparin, classically about 80 to 100 units per kg, and the team confirms an activated clotting time of roughly 250 seconds or more before the clamp goes on (targets vary by surgeon and procedure). At the end, heparin may be reversed with protamine.

The 4T score

A total of 0 to 3 is low probability, 4 to 5 intermediate, and 6 to 8 high. A low score makes HIT very unlikely; an intermediate or high score means stopping heparin and sending a PF4 immunoassay, with a functional test (serotonin-release assay) to confirm.

Around procedures

Whether and when to hold an anticoagulant depends on the drug, kidney function, the bleeding risk of the procedure and the patient's clotting risk. As a common pattern, warfarin is stopped about 5 days before surgery with an INR check the day before, and bridging with heparin is reserved for the highest clotting risk (for example a mechanical mitral valve or a VTE in the past 3 months). Apixaban and rivaroxaban are commonly held about 1 day before a low-bleeding-risk procedure and 2 days before a high-risk one, longer with poor kidney function or neuraxial anesthesia; dabigatran depends heavily on kidney function. Aspirin is usually continued through vascular operations.

Medical and risk-factor therapy

Revascularization treats the plumbing; medical therapy treats the disease. Every patient with PAD should be on best medical therapy regardless of whether they get an operation, and it is a fair question on rounds for any vascular patient.

• Smoking cessation. The single highest-impact intervention, slowing progression and improving graft patency more than any drug. Offer counseling and pharmacotherapy (nicotine replacement, varenicline) at every encounter.
• High-intensity statin. For every atherosclerotic patient, for plaque stabilization and cardiovascular and limb event reduction, not just lipids.
• Antiplatelet therapy. A single agent, aspirin or clopidogrel, for symptomatic PAD. Dual antiplatelet therapy after endovascular intervention is common for a period, with practice varying.
• Low-dose rivaroxaban plus aspirin. In selected patients, to reduce limb and cardiovascular events (below).
• Blood pressure and diabetes control. Plus an SGLT2 inhibitor or GLP-1 agonist where indicated for cardiovascular benefit, and daily foot inspection and podiatry care for diabetic patients.
• Supervised exercise therapy. First-line for claudication; it rivals revascularization for walking distance (below).
• Cilostazol. A phosphodiesterase-3 inhibitor that improves claudication distance, but is contraindicated in heart failure of any severity.

Rivaroxaban 2.5 mg twice daily plus aspirin

This "vascular dose" of rivaroxaban, a quarter of the usual VTE dose and given with low-dose aspirin, is a different strategy from full anticoagulation. In COMPASS, patients with stable coronary disease or PAD had fewer major cardiovascular events and fewer major adverse limb events, including major amputation, at the cost of more major bleeding. In VOYAGER PAD, patients who had just undergone lower-extremity revascularization (open or endovascular) had fewer events in a composite of acute limb ischemia, major amputation, heart attack, stroke and cardiovascular death, driven largely by less acute limb ischemia, again with more bleeding. The 2024 ACC/AHA PAD guideline recommends it for symptomatic PAD and after revascularization in patients who are not at high bleeding risk.

Statin intensity and LDL goals

Every patient with PAD should be on a high-intensity statin, or the highest dose they tolerate. The 2026 ACC/AHA dyslipidemia guideline restored LDL goals: for patients at very high risk, which includes many with symptomatic PAD and other atherosclerotic disease, the target is an LDL below 55 mg/dL (non-HDL below 85 mg/dL), adding ezetimibe or a PCSK9 inhibitor when a maximally tolerated statin does not get there. European guidance uses the same 55 mg/dL (1.4 mmol/L) target with at least a 50 percent reduction. The 2024 ACC/AHA PAD guideline's older trigger for add-on therapy was an LDL of 70 mg/dL or more.

Supervised exercise therapy

Supervised exercise is a class 1 recommendation for claudication and the first treatment to offer. A typical program is 30 to 60 minutes of treadmill walking at least three times a week for at least 12 weeks: walk to moderate or near-maximal claudication pain, rest until it settles, and repeat. Medicare covers up to 36 sessions over 12 weeks for symptomatic PAD with a referral. When a supervised program is not available, a structured home- or community-based walking program is the alternative.

Perioperative cardiac risk

The vascular patient is a cardiac patient. Atherosclerosis rarely confines itself to one bed, and myocardial infarction is the leading cause of death both around vascular operations and in the years after. Assessing and managing cardiac risk is part of every preoperative workup on this service.

The stepwise approach

The 2024 ACC/AHA perioperative guideline follows a sequence you can apply to any elective vascular patient.

1. Is it an emergency? A ruptured aneurysm or an immediately threatened limb goes to the operating room; cardiac risk is managed around the operation, not before it.
2. Is there an active cardiac condition? Acute coronary syndrome, decompensated heart failure, a significant arrhythmia or severe valve disease needs evaluation and treatment first unless the surgery is an emergency.
3. Estimate the risk. Use a validated tool such as the RCRI or the NSQIP calculator. Two or more RCRI points, or a predicted risk of major cardiac events of 1 percent or more, is elevated risk.
4. Assess functional capacity. A patient who can do 4 METs or more (climb two flights of stairs, walk up a hill, do heavy housework) without symptoms can proceed without further testing. The guideline also accepts a Duke Activity Status Index score above 34.
5. Test only if it changes management. In an elevated-risk patient with poor or unknown functional capacity, pharmacologic stress testing is reasonable only if the result would change care: coronary revascularization indicated regardless of the operation, a different operation (endovascular rather than open), or not operating. Routine screening stress tests are not recommended.

The guideline also supports measuring BNP or NT-proBNP before surgery in selected higher-risk patients for added prognostic information, and troponin surveillance after surgery in elevated-risk patients, because myocardial injury after noncardiac surgery is common, usually painless, and carries real mortality.

The RCRI is known to underestimate risk in vascular surgery patients, which is why vascular-specific tools such as the Vascular Quality Initiative cardiac risk index exist. It remains the score you will be asked to recite.

Medications around surgery

Beta-blockers

Continue them in patients already taking them; abrupt withdrawal causes rebound tachycardia and ischemia. Do not start a beta-blocker on the day of surgery: in POISE, starting metoprolol just before surgery reduced heart attacks but increased strokes and deaths, largely through hypotension and bradycardia. If a patient needs one for another reason, it is started well ahead of surgery and titrated.

Statins

Continue them. Vascular patients who are not on a statin almost always have an indication, and guidelines support starting one before vascular surgery.

Antiplatelets

Aspirin is usually continued through vascular operations. Never stop a P2Y12 inhibitor in a patient with a recent coronary stent without talking to cardiology; elective surgery is usually deferred after a recent stent.

Anticoagulants

Held and restarted according to a written plan; see Anticoagulation.

SGLT2 inhibitors

Held for 3 days before surgery (4 days for ertugliflozin) because of the risk of euglycemic ketoacidosis.

ACE inhibitors and ARBs

Practice varies; some teams hold them the morning of surgery to reduce hypotension after induction, while continuing them in heart failure is reasonable.