Vascular II Flashcards
1
Q
What is a pro/con to direct reconstruction (anatomic reconstruction)?
What is a pro/con to extra-anatomic reconstruction?
A
- Aorta-iliac bypass
- Normal anatomy (left)
- Percutaneous revascularization (top right)
- Surgical revascularization (bottom right)
-
Direct reconstruction
- Higher morbidity (more complications)
- Better long-term patency
- Aorto-Fem; Fem-Pop; Fem-Tib; etc
-
Extra-anatomic reconstruction (reconstruction does not mimic normal anatomy?)
- Reduced morbidity
- Long term patency inferior to direct reconstruction
- Fem-Fem; Ax-Fem
-
Direct reconstruction
Extra-anatomic bypass is typically reserved for patients deemed particularly high risk for direct surgical reconstruction such as previous graft or stent complication, infection, or previous intra-abdominal surgery with resultant abdominal adhesions. Open revascularization of infrainguinal disease depends on the level of the lesion(s), and may involve the femoral, popliteal, or infrapopliteal vessels.
2
Q
Risk factors for PAD?
Indications for surgery?
first symptom PAD?
A
Lower Extremity PAD
- The same risk factors that lead to PAD also cause:
- CAD (50% concurrence)
- CVD
- Aortic vascular disease
-
Indications for surgery for PAD:
- gangrene, ischemic ulceration, & intermittent claudication/ischemic rest pain
- PAD patients are at high risk for adverse CV events
- Previous graft/stent complications, abdominal adhesions
-
Intermittent claudication often first symptom
- Slow, progressive decline in function
Risk factors for PAD
- Nonwhite
- Male
- Age > 50 yo
- Smoking
- DM
- HTN
- HLD
- Chronic renal insufficiency
- Hyperviscous/hypercoaguable states
- Hyperhomocysteinemia
- Elevated inflammatory markers
- Vulnerable to stoke, MI, death
- Tx: Antiplt, anticoagulation medications → when stopped, high risk for periop event
- Vulnerable to stoke, MI, death
3
Q
Outcomes of patients with PAD?
A
- Individuals with atherosclerotic lower extremity PAD may be
- asymptomatic (without identified ischemic leg symptoms, albeit with a functional impairment)
- OR have leg symptoms (classic claudication or typical leg symptoms)
- OR present with critical limb ischemia ( CLI ).
- All individuals with PAD face a risk for
- progressive limb ischemic symptoms
- high short-term cardiovascular ischemic event rate
- increased mortality.
- These events rates are most clearly defined for individuals with claudication or CLI and less well-defined for individuals with asymptomatic PAD.
FROM PIC- doubtful we need to know specifics. overall takeaway is these are sick patients with very high moribidty/mortality
4
Q
What are indications for peripheral revascularization for acute ischemia?
A
- Acute ischemia patho:
- emboli
- thrombus
- pseudoaneurysm postop from femoral arterial line
- Irreversible ischemic damage:
- occurs 4-6 hours
- Urgent thrombolytic therapy and or angioplasty
- Arteriography → assess flow
- Surgical intervention (emergency case → with full stomach?)
5
Q
What are indications for peripheral revascularization with chronic ischemia?
A
- Chronic limb ischemia: demand > supply
- s/s: Rest pain, ulceration, gangrene
- Often present with multi-segmental occlusion
- Patho:
- atherosclerotic plaques progressively narrowing vessel → claudication w/ eventual thrombosis of vessel
- Surgery indicated when:
- severe disabling claudication
- unable to establish METs → will need CV testing (cant walk w/o severe pain)
- critical limb ischemia (limb salvage)
- ankle-brachial index (ABI) is clinical standard for documenting severity of PVD
- severe disabling claudication
- Semi-elective sx (time to optimize)
6
Q
What is the ankle brahcial index?
A
- ABI <0.9= PAD diagnosis
- Performed by taking systolic pressure in arms and in legs. Patient should rest supine in warm from for 10 minutes prior to testing
- highest average ankle pressure/highest average arm pressure
- each side done separately
7
Q
What is the traditional surgical approach for peripheral occlusions?
A
- Unobstructed blood flow source (donor) artery exposed. Ex:
- common femoral
- superficial femoral
- deep femoral
- Target distal artery (recipient) is exposed at or below the knee. Ex:
- dorsalis pedis artery
- posterior tibial artery
- If saphenous vein used →
- vein dissected all branches ligated → divided and excised (reversed - permits blood flow in direction of valves).
- Proximal anastomosis first with clamping, then can unclamp and move distal
- Bypass area with graft that has reduced flow
8
Q
Summary of Fem-Pop bypasS?
A
Anatomic Bypass: ex. Fem-Pop
- After donor and recipient arteries are exposed a tunnel is created and graft is passed
- Graft may be saphenous vein or prosthesis
- Femoral cross clamping is required
- Fewer hemodynamic changes than with AoX
- Heparin IV given
- Anastomosis constructed
- Arteriogram to confirm adequate flow
- Heparin not likely to be reversed
9
Q
Summary of aorto-fem bpyass?
A
Anatomic Bypass: Aorto-Fem
- Aortic cross-clamping (Aox) and uncross-clamping is required
- better tolerated than for aneurysmal disease
- more distal clamp location (why its more tolerated)
- likelihood of extensive collateralization related to chronic atherosclerotic disease → tolerate crossclamp better w/ collaterals
- Note: with aneurysms this collateral flow is not present
- better tolerated than for aneurysmal disease
10
Q
What type of patient is more likely to undergo an extra-anatomic bypass (ie ax-fem/fem-fem bypass)?
Considerations for the procedure?
Do they need to cross clamp during the procedure?
A
Extra-Anatomic Bypass:
Ax-Fem/ Fem-Fem
- Reserved for high risk patients → examples:
- previous graft or stent complication
- infection
- adhesions from previous abdominal surgery
- No need for Aox and uncross-clamping
- Frequent site:
- axillary artery to ipsilateral femoral artery
- with +/- fem-fem
-
Considerations:
- Less durable → 5 year patency
- Art-line must be on opposite side of Ax-fem site
- → Axillary artery clamping
-
Tunneling (mid-axillary)
-
*key point in the surgery à MOST STIMULATING PART
- Deepen anesthetic!
-
*key point in the surgery à MOST STIMULATING PART
11
Q
Preop management of LE Revascularization procedures?
A
- Preop – beta-blockers and/or other chronic medication
-
A-line*
- (plan for very difficult insertion- US recommended)
- Adequate vascular access –>min EBL though
- Continuous EKG monitoring + ST analysis
- Monitor volume status
- Foley catheter
- +/- CVP or PA catheter/ TEE (more likely needed for Aorto-fem with Aox
- Non-invasive/ minimally invasive hemodynamic monitoring
- I stat/ Hemochron to follow labs (coag status)
-
For emergency surgery: carefully watch →
- K+ levels
- acidosis
- Myoglobinemia
- Coagulation status
- ECG ischemia
- fasciotomy may be required (compartment syndrome)
12
Q
Regional vs general for LE revascularization procedures?
A
Regional vs. General
- Assess for coagulopathy or anticoagulation therapy
- Spinal may be best to avoid hematoma
- Most studies have shown no difference between RA and GA in terms of cardiopulmonary complications**
-
**Significant difference (5X) in complication rate in terms of graft occlusion with regional being superior
- Perfusion to limbs (Regional > GA)
- Studies regarding efficacy of post-op pain mgt. w/ epidural vs. opioids are poorly designed
13
Q
What is graft occlusion higher with GA versus RA?
A
Hypercoagulable state with GA as opposed to RA
Reasons:
- With GA →
- Decreased Fibrinolysis → fibrinogen not broken down and clots form
- Increased Epi, NE, and cortisol release (compared to RA)
- Patency of graft maintained with RA secondary to increased blood flow with sympathectomy
14
Q
Anesthetic maintenance with LE revascularization?
A
- AVOID Vasopressors
- Keep warm
-
GA –> balanced anesthetic with opioids, inhalation agent, nitrous oxide, neuromuscular blocker
- Minimal opioids to facilitate extubation
- Do have postop pain
- Deepen anesthetic level during the tunneling phase
- Example: 3-5 mcg/kg fentanyl
- Avoid hemodynamic extremes – short acting β blockers intraop often necessary
- Minimal opioids to facilitate extubation
-
RA –> L1-L4 dermatomes (T10 level adequate)
- Epidural dosing usually - 9-12 ml including test dose
- Remember elderly patients require decreased dosing!
- Epidural dosing usually - 9-12 ml including test dose
15
Q
Postop managmeent for LE revascularization procedures?
A
- Control Pain and anxiety
- High risk for MI in this period - stress reduction essential!
- Epidural catheter is beneficial for postop pain control but must consider use of anticoagulants
- Avoid Anemia
- Control HR and BP
- Frequent checks of peripheral pulses (doppler)
- Continuous EKG monitoring + ST analysis
16
Q
Review of abdominal aorta branches?
What is critical during abdominal aorta surgery?
A
*Higher clamp → more complications pt will have*
Review and be prepared to discuss branches and levels.
- abdominal branches
- inferior phrenic
- middle suprarenal
- celiac
- first lumbar
- Superior mesenteric artery
- renal
- gonadal
- second lumbar
- inferior mesenteric artery
- third lumbar
- fourth lumbar
Ex: higher clamping in thoracic or abdominal aorta → anticipate more complications
Surgical Procedures Overview
- Surgeon-anesthesia communication critical
- All open procedures have a degree of ischemia-reperfusion
- Reconstruction for aneurysmal
- Reconstruction for aortic dissection
- Endovascular aortic surgery
- ~60-70% of patients requiring infrarenal repair
- Trials ongoing for juxtarenal, suprarenal and thoracoabdominal repair
17
Q
What is an aneurysm?
Most frequent location of aneurysms?
A
-
> 50% dilation of normal expected arterial diameter
- abdominal aortic diameter > 3.0 cm
-
Abdominal aorta: most frequent location of arterial aneurysm
- 9x more common than thoracic
-
Statistics:
-
Thoracic:
- ascending (40%)
- descending (35%)
- aortic arch (15%)
-
Thoracic:
-
AAAs: classified as:
- Infrarenal (85%)
- Juxtarenal
- Suprarenal
- Must know level of aneurysm: location of Aox is critical
18
Q
What is the pathophysiology behind an aneurysma?
A
- Distinct patho from atherosclerotic disease
-
Degenerative process
- degradation of aortic wall connective tissue
- primarily, the medial and adventitial layers (muscular layer)
- Turbulent BF causes →
- inflammation and immune responses
- biomechanical wall stress
- Size of aneurysm = single most important predictor of subsequent rupture and mortality
19
Q
What is a anuerysm rupture vs dissection?
A
AAA Rupture
- Catastrophic
- Many don’t even make it to the OR
- 50% mortality for repair of ruptured AAA
- 85%-90% mortality rate
- Many don’t even make it to the OR
- Goal: balance risk of surgery with risk of rupture
- Current recommendations:
- serial monitoring of known aneurysms
-
Elective Surgical repair indication: (decrease risk of rupture)
- AAAs = > 5.5 cm
- Descending thoracic aortic aneurysm = > 6.5 cm
Aortic Dissection
- Tear in the intimal layer of the arterial wall that creates a false lumen
- propagated by pulsatile blood flow
- Acute = < 14 days
- Chronic = >2 weeks symptom duration
- propagated by pulsatile blood flow
- Approximately ½ of aortic dissections originate from the ascending aorta
-
Ascending Aorta Dissection
- Surgical emergency
-
Leads to:
- acute aortic regurgitation
- pericardial tamponad
- myocardial ischemia
-
Acute descending aortic dissection:
- → end-organ compromise due to malperfusion of the visceral vessels → death
20
Q
Open abdominal aortic aneurysam repair overview of procedure
A
- Challenging Intraoperative Management
- Aortic cross clamping
- hemodynamic changes/metabolic changes
- renal impairment
- spinal cord damage
- bowel ischemia
- Unclamping
- hemodynamic changes/metabolic changes
- effect anesthesia management
- Aortic cross clamping
Pic:
- left top and bottom
- clamps are placed across aorta and common iliac arteries
- anerysm is opened
- clot is removed
- inimtal lining is repaired
- right top and bottom
- a graft is sutured between upper and lower ends of aorta
- preserved wall is wrapped around the graft
- the clamps are removed to allow blood flow
21
Q
What determines the effect of aortic cross clamp?
What are some effects of cross clamping?
A
Pathophysiology depends on:
- 1. Level & duration of clamp
-
2. Volume status of patient
- 2 most important predictors of outcomes while clamping*
- extent of CAD
- myocardial function
- degree of arterial collateralization (chronic pts w/ collateral flow → do better!)
- anesthetic agents used
- vasodilators used
- body temperature
- neuroendocrine activation
Clamping effects
- Little to no effect on HR
- Effects:
- Catecholamine surge
- ↑ SVR and MAP as a result of the sudden impedance to aortic flow
- Extent depends on cross clamp level applied
- Ex:
- infrarenal cross-clamping → ↑ BP 2%-10%
- Supraceliac clamp → ↑ MAP up to 50%
- Ex:
- ↑ or ↓ in cardiac preload, central filling pressures, and CO → depends on where clamp located
- Catecholamine surge
- BV redistribution occurs proximal to clamp placement
- Lower clamping →
- BV shift into compliant splanchnic vasculature –> all redistributes to gut (wont really see change)
- like a reservoir for majority of autotransfusion
- splanchnic organs hold 25% total BV
- > 800 ml can be autotx to systemic circ in seconds
- like a reservoir for majority of autotransfusion
- Increases in plasma epinephrine & norepinephrine = venoconstriction of splanchnic capacitance vessels – translocates blood to central circulation. Infraceliac cross-clamping is relatively well tolerated compared with supraceliac crossclamping.
- BV shift into compliant splanchnic vasculature –> all redistributes to gut (wont really see change)
-
Supraceliac cross-clamp → don’t have ability to shift BV to splanchnic vasculature (not going to compliant gut) →
- ↑ VR
- ↑ central filling pressures
-
↑ CO
- ↑ myocardial workload – large 90% develop new LV wall motion abnormalities d/t acute ↑ in BV –> HARD on already sick heart (especially those with CAD or decreased EF)
- Lower clamping →
Supraceliac has most significant impact on MAP, PAP and EF
22
Q
What si the systemic hemodynamic response to aortic crossclamping?
A
- Passive recoil distal to clamp → ↑ preload
-
↑ Catecholamines (and other vasoconstrictor) →
- Active venoconstriction proximal and distal to clamp →
- leading to ↑ preload
- Active venoconstriction proximal and distal to clamp →
-
↑ Ao flow impedance
-
→ ↑ afterload
-
Overall:
- ↑ Preload
- ↑ Coronary flow
- ↑ Afterload
-
↑ contractility → ↑ CO
- But if no ↑ in coronary flow or contractility → ↓ CO
-
Overall:
-
→ ↑ afterload
- Systemic hemodynamic response to aortic crossclamping (AoX).
- Preload does not necessarily increase.
- Most dramatic and consistent effect →
- ↑ SVR and MAP (result of sudden aortic flow).
23
Q
What is the blood volume redistribution following aortic cross clamp placement?
A
- Passive venous recoil distal the aortic cross-clamp →
- Result: shift BV from distal to aortic occlusion to proximal to the occlusion.
- 1. Aorta occluded above celiac axis level → splanchnic reserve redistributed to organs and tissues proximal to the clamp.
-
2. Infraceliac cross-clamp placed →
- BV shift into splanchnic system
- Shift into other organs proximal to clamp
- The ability to shift into or out of the splanchnic vasculature accounts for variability in preload augmentation.
- Result: shift BV from distal to aortic occlusion to proximal to the occlusion.
26
Q
What determines pathophys during aortic unclamping?
Hemodynamic changes during unclamping?
Metabolic changes during unclamping?
A
Aortic Unclamping
- Pathophysiology depends on:
- Level of clamp
- Duration of clamp time
- Use of diverting support
- Intravascular volume
Aortic Unclamping: Hemodynamic Changes
- Drop in SVR up to 80% *
- ↓ Myocardial contractility
- ↓ CO
- ↑ PAP
- Release of inflammatory mediators →
- increase pulmonary vascular resistance
- Pulmonary edema
- ↓ Arterial blood pressure
- ↓ Central venous pressure
- ↓ Venous return
- ↓ LV pressure
- Relative central hypovolemia develops as blood pools in tissues distal to crossclamp
Aortic Unclamping: Metabolic Changes
- ↑ Total-body oxygen consumption
- ↑ Lactate
- ↓ Mixed venous oxygen saturation
- ↑ Prostaglandins
- ↑ Activated complement
- ↑ Myocardial depressant factor(s)
- ↓ Temperature
- Metabolic acidosis**
PIC: A complex cascade of events, including release of inflammatory mediators, distal vasodilation, increased vascular permeability, and decreased myocardial contractility results in a relative central hypovolemia, decreased cardiac output/VR, and systemic hypotension.
35
Q
Describe the perfusion to the spinal cord and the role of radicular artery distrubiton in maintaining spinal cord perfusion.
A
- The spinal cord is supplied primarily by the single anterior and paired posterior spinal arteries, arising from the posterior circulation.
- Posterior spinal arteries supply approximately 25% of spinal cord blood flow and supply the sensory tracts of the posterior columns.
-
Anterior spinal artery supplies anterolateral cord
-
Includes: motor tracts
- supplies 75% of SC flow.
-
Includes: motor tracts
-
Anterior spinal artery is fed by a series of radicular arteries
- arising from the aorta, although collateralization is variable.
- This leaves areas of the spinal cord vulnerable to watershed ischemia, particularly with aortic occlusion or prolonged hypotension.
- Most important radicular artery supplying the thoracolumbar cord is derived from the artery of Adamkiewicz.
- The artery of Adamkiewicz originates between T8 and T12 in 75% of cases and at the level of L1 or L2 in an additional 10% of cases.
Artery of Adamkiewicz- presence at T11-12
Radicular arteries present throughout thoracic and abdominal aorta
36
Q
What can we do to prevent spinal cord damage during aortic cross clamp?
A
- *Short cross clamp time & total surgical time
- Optimization of cardiac function
-
CSF lumbar drainage (most common in thoracic repairs)
- Goal = CSF pressure < 12 mmHg
- Rationale: SC pp can be augmented by →
- Increasing forward driving pressure (MAP)
- w/ Aneurysmal dx & vascular reconstruction→ best not augment MAP
-
Relieving any obstructing pressure (CSF)
- Autoregulatory mech w/ AoX → increase CSF (lowers SC pp)
- → CSF drainage improves SC perfusion
- Autoregulatory mech w/ AoX → increase CSF (lowers SC pp)
- Increasing forward driving pressure (MAP)
- Rationale: SC pp can be augmented by →
- Goal = CSF pressure < 12 mmHg
- Hypothermia: prolongs the safe ischemic time for the SC
PIC: Relationship between spinal cord injury and length of aortic occlusion
41
Q
What is the crawford classification of TAA?
A
- Type I - Aneurysm involving descending thoracic and upper abdominal aorta
-
Type II –
-
Descending thoracic and most abdominal aorta
-
Greatest risk:
- Paraplegia
-
Renal failure
- d/t ischemia during crossclamp even w/ extracorporal circulatory support
-
Greatest risk:
-
Descending thoracic and most abdominal aorta
-
Type III –
-
Lower thoracic aorta and most abdominal aorta
-
Type II & III → most difficult to repair
- à involves the thoracic and abdominal segments of the aorta
-
Type II & III → most difficult to repair
-
Lower thoracic aorta and most abdominal aorta
- Type IV - most or all abdominal aorta
42
Q
What ist he DeBakey classification of dissecting aortic aneurysms?
A
- Type I - ascending aortic tear with dissection down entire aorta
- Type II - tear in ascending aorta with dissection limited to ascending aorta
- Type III - tear in proximal descending thoracic aorta with dissection from thoracic aorta to abdominal aorta
45
Q
What is the effect of aortic cross clamping during thoracic repairs?
A
- AoX (Thoracic) → BV shift to brain → increase ICP
- → decrease SC pp and flow
- Ao distal pressure decrease
- Ao proximal pressure increase
- Spinal cord blood flow and perfusion pressure during thoracic aortic occlusion, with or without sodium nitroprusside (SNP) infusion.
- The changes (arrows) represent the response to aortic cross-clamping per se.
- SNP+ - SNP aggravates the effect of cross-clamping;
- SNP- = SNP counteracts the effect of cross-clamping
- AoX - aortic cross-clamping; Ao = aortic; ICP = intracranial pressure; [arrow up] and [arrow down] increase and decrease, respectively.
47
Q
How do we manage risks durign TAA REPAIR?
A
- TAA surgery not often performed without extracorporeal support (bypass):
- When no bypass used clamp time < 30 min are associated with 0-10% paraplegia
- Clamp time 30-60 min → paraplegia incidence 10-90%
-
Reduce risk:
- Epidural cooling
- Regional hypothermia (renal protection)
- In-line mesenteric shunting
- Best → reduce clamp time < 30 min
- When no bypass used clamp time < 30 min are associated with 0-10% paraplegia
PIC: Gott shunt is heparinized and placed between ascending & descending thoracic aorta
48
Q
What is partial bypass’ role in TAA repair?
A
- Approaches to protect the brain, spinal cord & kidneys
- Include: (Examples of partial bypass)
- LV, pulmonary vein, or ascending aorta to descending aorta shunt
- LA to femoral artery bypass
- Femoral-femoral cardiopulmonary bypass
- Axillofemoral bypass graft
- Deep Hypothermic Circulatory Arrest
54
Q
What is the technique for endovascular stent grafting?
A
- Pre-op aortic anatomy studied extensively via radiological exam
- high IV contrast load – may need diuretics, mannitol
- Bilateral groin incisions
- used for access to femoral or iliac arteries
- Occasional extensive retroperitoneal surgical incisions required for vascular access with unusual anatomy- small femoral and iliac arteries, etc.
- Supine position – arterial sheaths introduced 16-27F
- Expandable stent is deployed
57
Q
What are the different classifications of endo leaks?
A
- Type I- high flow leak adjacent to a stent that is not sealing the sac from the systemic circulation (requires immediate intervention).
- Type II—low flow leak due to arterial branches that have been excluded by the stent (can be treated with embolization).
- Type III—failure with the stent itself or at its junction with another stent (requires immediate recognition and treatment).
- Type IV—porosity in the stent (often resolves with reversal of anticoagulation).
- Type V (endotension)—persistent or recurrent pressurization of the aneurysm sac despite no detectable endoleak.
