Vascular Basic Overview & Aortic Cross Clamping Flashcards

1
Q

What are the 3 layers of an artery?

A

-Tunica Intima: Smooth endothelial layer. Endothelium that lines the lumen of all vessels
-Tunica Media: Muscular middle portion. Smooth muscle cells and elastic fibers
-Tunica Adventitia: Outer layer; connective. Collagen fibers.

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2
Q

How does vascular disease occur?

A

Arterial supply of oxygen and nutrients to the tissues is compromised:
-Ischemia
-Necrosis

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3
Q

What is the most common cause of occlusive disease in the arteries of the lower extremities?

A

Atherosclerosis is the most common cause of occlusive disease in the arteries of the lower extremities.
-Occlusive disease can also be due to Embolism, aneurysm, thrombosis, or trauma

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4
Q

Describe the etiology of peripheral vascular disease

A

Hypertension, hemodynamic stresses (HF, etc), toxins in cigarette smoke, and/or increased LDL cholesterol all damage the endothelium (inner, sensitive layer of vasculature).
-End up with collagen synthesis and the formation of foam cells.
-Leads to the creation of atherosclerosis.

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5
Q

How does Atherosclerosis occur?

A

Normal homeostatic functions of the endothelium are altered.
Inflammatory response:
-Damage of the endothelium
-Chronic inflammation

Injury/damage of some kind leads to macrophages entering the Media (middle), leading to development of foam cells and plaque.

Chronic inflammation implicated in disease process:
-C-reactive protein = substance released by body’s tissues in response to inflammation

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6
Q

What are the stages of Atherosclerosis?

A

1) Healthy
2) Fatty streak (lipids & foam cell in the MIDDLE Layer)
3) Fibrofatty plaque
4) Complicated plaques (thrombus or calcification can occur, leading to occlusion)

Thrombus can lead to acute ischemia.
All of these things can lead to a weakening of the arterial wall, causing aneurysm formation.

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7
Q

Where can atherosclerosis occur?

A

In basically any artery.
-Femoral, tibial, etc.
-Coronary, cerebral, or renal arteries

Mortality r/t PVD is usually due to adverse cardiac events (MI)

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8
Q

What are risk factors for development of Atherosclerosis?

A

-Smoking
-HTN
-Insulin resistance
-DM
-Ischemic Heart Disease
-Altered serum lipids
-Obesity
-Family history (genetic predisposition)
-Sedentary lifestyle
-Advancing age
-Co-Existing CAD

Non-modifiable:
-Genetics
-Gender (Male > Female)
-Menopause

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9
Q

What are S/Sx of Peripheral Vascular Disease (PVD)?

A

-5 ‘Ps’: Pain, pulselessness, paralysis, paresthesia, pallor
-Skin ulcerations
-Gangrene
-Intermittent claudication (Calf pain, usually due to Superficial femoral artery occlusion)
-Subcutaneous atrophy
-Hair loss
-Cool, dusky extremities
-Sexual dysfunction

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10
Q

How do you diagnose PVD?

A

1) Doppler ultrasound:
-Finds stenotic lesions w/in arteries
2) Duplex ultrasound scan:
-Finds plaque and abnormal blood flow (measures FLOW)
3) Transcutaneous oximetry:
-Transcutaneous oxygen tension decreases in ischemic limbs (will see less O2 sat on ischemic limbs)

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11
Q

What are the treatment goals for PVD?

A

-Restoration of normal perfusion to the affected limb or organ
-Improved functional status
-Prevent death and disability

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12
Q

What is involved in medical treatment for PVD?

A

1) Cessation of smoking
2) Dyslipidemia Tx: Statins and Diet
3) Anti-Platelet Therapy: to prevent them from forming a thrombus when plaque is present
4) Control of DM
5) Correct or improve poor pump function (Tx HF if they have it to stop endothelial damage from low blood flow)
6) Exercise training programs
7) Anti-hypertensive therapy
8) Anti-oxidants

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13
Q

What are the surgical treatments for PVD?

A

1) Revascularization: (uses a graft to bypass atherosclerosis plaque)
-Endovascular procedures (Percutaneous angioplasty or stent placement)
-Thrombectomy
-Embolectomy
-Surgical reconstruction
-Bypass (ex: Fem-Pop bypass)
2) Amputation (Worst case scenario if unable to revascularize and tissue is gangrenous)

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14
Q

What is Percutaneous Transluminal Angioplasty (PTA)?

A

-The most common treatment for PVD
-Endovascular procedure
-A catheter with a balloon is placed in the occluded area.
-Balloon is inflated to open up the blood vessel by smushing away the foam cells, fatty deposits, etc.
-Restores blood flow
-Stent is often placed.

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15
Q

Describe anesthetic management of an Endovascular procedure for PVD.

A

-Role of Percutaneous Technique (Fluoro and contrast are used). Not as stimulating (femoral stick)
-Regional is beneficial due to significant comorbidities in these patients. High risk for MI or stroke if atherosclerosis is also in coronary or cerebral vessels.
-General is used for larger cases or if going into the abdomen for aortic work
-Need plenty of IV access (lots of fluid/blood replacement)
-Arterial line (comorbidities)
-Will give heparin to prevent thrombosis of catheter and reverse with protamine
-Emergence -> PACU

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16
Q

Describe an Open Surgical thrombectomy/embolectomy

A

May have to do Open instead of endovascular if the disease is very severe.
-Incision is made
-Heparin is given
-Artery is isolated and arteriotomy is performed.
-Clamp artery, remove debris
-Balloon is used to ensure clog is cleared
-Once blood shoots out, obstruction is cleared.

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17
Q

Where can you perform bypass procedures?

A

Can do a bypass pretty much anywhere.
-Lower extremities: Aorta-bifemoral, Aorto-iliac, Fem-popliteal, etc.
-Upper extremities: Axillo-bifemoral bypass

Named by proximal to distal
-Most proximal thing you’ll ever bypass to is the Aorta. Larger surgeries.

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18
Q

What is an Aorto-Bifemoral Bypass?

A

Bypassing from the aorta to bilateral femoral arteries.
-A larger surgery. Have to open abdomen
-Both a vascular and an abdominal case
-Evaporative losses more of an issue. Requires arterial line
-Cross clamp will be applied
-ICU post-op

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19
Q

Describe the pre-op evaluation of a patient with PVD.

A

-History
-Physical exam
-EKG
-CXR
-Labs
-Exercise tolerance
-Invasive testing

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20
Q

Why do patients with PVD always need a Cardiac Consult pre-op?

A

Myocardial dysfunction is the single most important cause of morbidity following vascular surgery!!!!!
-Whether they know it or not, they have underlying CAD
-Myocardial dysfunction occurs intra-op and post-op.

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21
Q

What are the different options for Anesthesia for the patient with PVD?

A

-GA
-Epidural or RA (good for smaller or peripheral cases)
-GA + RA: Good for larger cases that you have to paralyze. Can do thoracic epidural for post-op pain control.

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22
Q

What are advantages to Epidural Anesthesia for PVD?

A

-Excellent surgical exposure
-Excellent muscle relaxation
-Potential for decrease in myocardial ischemia (by avoiding GA)
-Great post-op pain control
-Decreased blood loss
-Vaso-dilated extremity

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23
Q

What are disadvantages associated with Epidural Anesthesia for PVD?

A

-Use of heparin and risk of epidural hematoma
-Inability to evaluate patient’s sensory and motor function post-op
-Hypotension
-As the block “wears off”, the patient may not receive adequate pain control, which may trigger myocardial ischemia

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24
Q

What are advantages to using GA for a patient with PVD?

A

-Removes any controversy over using regional anesthesia in a patient with drug induced anticoagulation.
-Control of the airway, and the patient, for what may be a long case.

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25
Q

When would you need invasive monitoring for a patient with PVD?

A

-The patient’s pre-op condition and evaluation will determine the extent of invasive monitoring
-The location of the surgery, and the need to place an aortic cross clamp, will further determine the extent of invasive monitoring (Anytime you’re doing stuff to the aorta will need a central line and invasive monitoring)
-Always do arterial line due to frequency of labs being drawn

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26
Q

What is an aneurysm?

A

Intimal damage secondary to disease, congenital defect, or physical damage that causes weakening of the media of the arterial wall.
-Arterial wall expands, forming a sac
-Organs and tissue distal to the aneurysm are compromised due to clotting and decreased blood flow.

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27
Q

What is a Pseudoaneurysm?

A

Injury to vessel wall leads to leakage of blood into a sac.
-Sac can clot off or may become problematic
-May need to be clipped. Not as urgent/emergent
-Damage to intima or vessel wall

28
Q

What is the cause of Abdominal Aortic Aneurysms (AAA)?

A

-Most commonly due to Atherosclerosis of the Aorta
-Can be due to degeneration of the arterial media (traumatic, genetic, etc)
-Smoking + HTN = markedly increased risk
-Frequently are painless (until rupture), pulsating masses found co-incidentally on physical exam
-Occur predominantly in white males

29
Q

What is the Law of LaPlace?

A

T = P x r

Where T = wall tension, P = transmural pressure, and r = vessel radius.

30
Q

How does the Law of LaPlace affect aneurysms?

A

As the radius of a damaged vessel increases, the wall tension increases, increasing risk of rupture.
-The larger the aneurysm, the higher the likelihood of spontaneous rupture.

31
Q

At what cm in radius do surgeons typically operate on a AAA?

A

Usually operate at 5 cm.
-At 5 cm radius: 5% chance of spontaneous rupture
-At 7 cm radius: 70% chance of spontaneous rupture

32
Q

What do you have to consider when planning anesthesia for a AAA repair?

A

-Co-Existing Diseases
-Supra vs Infra renal
-Open vs Endograft
-Schedule vs Emergent

33
Q

What co-existing diseases commonly occur with AAA?

A

-HTN
-CAD
-COPD
-DM
-Renal Impairment
-Carotid Artery Disease

Patients tend to be sick.

34
Q

Why does it matter if the AAA is Supra or Infra Renal?

A

Supra renal is worse (the more proximal, the worse it is).
-Have to cross clamp aorta above and below aneurysm.
-If aneurysm is supra renal, the renal arteries do not get perfusion during the time the clamp is on (bad).
-With infrarenal, the renal arteries maintain perfusion so not a problem

35
Q

Why does it matter if the AAA is repaired Open vs Endovascularly?

A

-Endovascular is more common. Enter via femoral artery and place a stent & graft. Better outcomes for patient.
-Open is a huge abdominal case, but allows for direct visualization. Has to be done if vascular is so damaged that the catheter can’t pass through (severe disease)

36
Q

What is the difference between Schedule vs Emergent AAA repair?

A

Scheduled:
-Possibly found on routine exam
-Small aneurysms monitored q 6 mos that grow
-Lower mortality rate

Emergent: ruptured aneurysm.
-S/Sx: Hypotension, back pain, pulsatile abdominal mass
-EMERGENCY!
-High mortality rate (>90%)
-Treat this patient as a controlled trauma
-Need lots of volume/blood products resuscitation
-Can be done endovascularly.

37
Q

What is the setup for AAA repair?

A

Standard monitors plus:
-Arterial line (always)
-CVP vs Swan (open repairs)
-Foley (always)
-TEE (sometimes)

Adequate venous access is mandatory!! Need large CVC (cordis) and several large bore IVs.
-Blood warmer set up, ready to go

38
Q

How do they perform a AAA repair?

A

-Locate the aneurysm
-Clamp above and below (may have to double clamp lower if at bifurcation)
-Excise aneurysm and place graft
-Close

39
Q

What are the hemodynamic effects associated with Aortic Cross Clamping?

A

-Hypertension proximal to cross clamp (Back pressure in the heart because blood has nowhere to go).
-Hypotension distal to cross clamp (blood flow has ceased distal to clamp)
The more proximal the clamp, the greater the hemodynamic response.
-Infrarenal aortic occlusion minimally increases afterload (more room for blood to go)

40
Q

Describe what occurs to the area distal to the Cross Clamp

A

Tissue distal to the clamp is hypoperfused, ischemic, cold, and has a buildup of lactic acid and metabolites.
-Blood flow distal to the clamp is via collaterals, and is dependent on proximal systemic pressures

41
Q

Describe the hemodynamic effects that occur with Aortic Cross Clamping

A

1) Passive recoil distal to the clamp (distal to clamp is constricting, trying to get blood from somewhere). This increases Preload, worsening pressure in the heart.
2) Catecholamines and other vasoconstrictors are released proximally and distally to clamp. This increases AL further.
3) Increased impedance to aortic flow (LV can’t push out blood due to high back pressure from clamp). This increases AL, Contractility, and may increase CO. Or, could get into HF situation due to increased AL and heart can’t pump against that high pressure and can fail.
-Risk of myocardial ischemia due to pressure.

42
Q

What patients do not tolerate aortic cross clamping?

A

-Ischemic heart disease
-Left Ventricular Dysfunction

Inc AL and pressure in the top half of body increases myocardial wall tension. Risk of Myocardial ischemia due to pressure.

43
Q

How do you treat the hemodynamic effects associated with aortic cross clamping?

A

-TEE is the best way to evaluate cardiac function and filling after the clamp is placed. Evaluate cardiac filling, SVR, etc.
-Treat afterload with Sodium Nitroprusside, NTG, or Primacor

44
Q

Do you give Heparin with Aortic Cross-Clamping?

A

Yes. The surgeon will ask you to administer
-Generally 70 – 100 u/kg
-An initial ACT should be communicated to the surgeon
-ACTs should be done every 30 minutes
-Generally you will partially reverse with PROTAMINE (due to lots of suture lines)

45
Q

What are the adverse effects of Aortic Cross Clamping?

A

-hemodynamic instability
-visceral ischemia (ischemia to abdominal organs, mesentery, etc)
-spinal cord ischemia (Placement of clamp affects blood flow to spinal cord)
-renal compromise (clamp above renals affects blood flow)

46
Q

What is the response to Aortic Unclamping?

A

-Unclamping causes the release of K+, lactic acid, and other inflammatory mediators being released into systemic circulation (decreases myocardial contractility)
-“Washout” of Arachidonic acid derivatives and free radicals occurs
-Leads to increase volume of blood entering the heart and can cause pulmonary edema
-Suddenly reperfusing dry vascular beds creates a relative hypovolemia.
-Neuroendocrine response: IL, TNF, catecholamines, and cortisol are released now into system circulation

47
Q

What is anesthetic management during Aortic Unclamping?

A

-Aggressive fluid loading prior to unclamping and reperfusion (all fluid goes to lower extremities when we release)
-Increase PCWP or PAD (or CVP) to 5mm above baseline
-Communicate with surgeon, can replace clamp
-Have Neo, Bicarb, and Calcium ready and available if needed for hemodynamic stability

48
Q

Why should they slowly release the clamp?

A

-Each cross-clamp release will result in metabolic washout to the previously ischemic organs, although the subsequent quick replacement of the cross-clamp lower on the graft will mitigate some of the hemodynamic alterations.
-Can move cross clamp sequentially lower on Aorta as each anastomosis is completed to reduce side effects. Results in less severe hypotension.

49
Q

What is the post-op morbidity associated with Aortic Cross-Clamping?

A

-Pulmonary Edema and decreased myocardial contractility
-CVA (can cause cerebral ischemia due to pressure changes in the upper extremities)
-Liver failure/infarcted bowel (depends on if clamp involved Mesenteric arteries and time of clamping). Visceral ischemia
-Spinal cord ischemia leading to neurologic dysfunction or paralysis
-Renal issues

50
Q

How can aortic cross clamping cause spinal ischemia?

A

-Proximal location of clamp increases the risk of spinal ischemia
-Lots of feeder arteries to the spinal cord come off of the Aorta.
-Flow in the spinal arteries is dependent on collateralization and bi-directional flow.
-Might place spinal drain to monitor pressures during clamp to see if it increases, might have to drain CSF to avoid spinal hypertension

51
Q

What is the blood flow to the spinal cord?

A

-One anterior spinal artery provides blood supply for the anterolateral cord (75%)(motor)
-Two posterior spinal arteries (25%)
-The radicular arteries are branches of the intercostal and lumbar arteries
-Arteria Radicularis Magna (Artery of Adamkiewciez)

52
Q

What is the Arteria Radicularis Magna (Artery of Adamkiewciez)?

A

The largest radicular artery.
-Normally joins the anterior spinal artery between T8 and T12-L2
-The Aortic Cross Clamp may cause ischemic change secondary to interruption of spinal blood flow through the radicular branches or d/t an anomalous Artery of Adamkiewciez
-Risk of paralysis post-op if affected. Supply is dependent on collaterals if it is clamped off.

53
Q

How do you protect the spinal cord during Aortic Cross Clamping?

A

-Avoid prolonged systemic hypotension
-Avoid prolonged ACC time
-Subarachnoid drain (manipulate spinal cord perfusion pressure)
-Cooling
-Avoid hyperglycemia
-No reliable method of evaluating spinal cord ischemia is currently available

54
Q

How do you calculate Spinal Cord Perfusion Pressure?

A

SCPP = MAP - CSF Pressure
-With ACC, CSF pressure increases (stress) and MAP decreases distal to the clamp.
-To avoid ischemia, can drain CSF to allow blood to flow to spaces distal to the clamp.

55
Q

What are strategies for Renal Protection with Aortic Cross Clamping?

A

-BEST Protection of the kidneys is by maintaining intravascular volume and cardiac output. AVOID HYPOTENSION AND HYPOVOLEMIA
-Osmotic Diuretics (Mannitol) and Loop Diuretics (Lasix)
-Renal Dose Dopamine (1-3 mcg/kg/min): controversial
-NaHCO3 drip (3 amps to 1 L D5W @ 1 mL/hr) to alkalinize the proximal tubule and help combat acidosis

56
Q

Why is Mannitol useful for renal protection?

A

-Osmotic diuretic
-Can be given 30 minutes prior to ACC (0.25 - 0.5 gm/kg)
-Functions as a hydroxyl free radical scavenger
-Increases total and cortical renal blood flow

57
Q

Why are Loop Diuretics (Lasix) useful for renal protection?

A

Can give lasix with aortic cross clamping
-5- 40 mg
-Increases total and cortical renal blood flow

58
Q

What is a AAA Endograft (EVAR)?

A

-Specialty case. Place catheter with stent to repair AAA
-Cardiology & Vascular surgery share case responsibility
-Requires hybrid OR with C-Arm and Fluoroscopy
-Cath Lab personnel and X-ray come to OR
-Better for the patient if able to do it.

59
Q

What are the advantages to a AAA Endograft (EVAR)?

A

-Increased hemodynamic stability
-Decreased embolic events
-Reduced stress response
-Decreased incidence of renal dysfunction
-Decreased post-op discomfort
-No external ACC (no external damage but do have an internal balloon)

60
Q

What is the most common complication associated with an AAA Endograft (EVAR)?

A

Endoleak: Blood flow between the graft and the aneurysm

61
Q

What is a Type 1 Endoleak?

A

-Related to graft itself.
-Leak where proximal (or distal) placement of graft is. Leak between suture line and aneurysm. Aneurysm continues to expand

62
Q

What is a Type 2 Endoleak?

A

-Retrograde flow from collaterals
-Feeder vessel bleeds into the aneurysm

63
Q

What is a Type 3 Endoleak?

A

-Fabric Tears, graft disconnection, disintegration
-Leaks out from some suture line inside graft

64
Q

What is a Type 4 Endoleak?

A

-Graft wall porosity.
-Leaking all over the place

65
Q

What is Endotension?

A

Persistent pressurization of sac with no evidence of endoleak.
-With EVAR, you don’t actually cut out the aneurysm. Just place a graft so it can’t expand. But, can continue to expand for unknown reason (Endotension)

66
Q

What are complications associated with with a AAA Endograft (EVAR)?

A

-Graft thrombosis, migration or rupture
-Graft infection
-Iliac artery rupture
-Lower extremity ischemia
-Open repairs are more definitive (getting a good look at aneurysm with open approach, but EVAR is less definitive)

67
Q

What is the anesthetic management of a AAA Endograft (EVAR)?

A

-Anesthetic mgmt similar to open AAA
-Less blood loss
-Generally place an arterial line
-Heparin dose 50-100u/kg
-ACTs q 30 minutes
-Regional vs GA (Most commonly doing GA)