Anesthesia &
Peripheral Vascular
Disease
Justin Scott Fulkerson
ACNP-BC, sRNA
Outline
• Anatomy Review
• Peripheral Arterial Diseases (major)
• Peripheral Venous Diseases (secondary)
• Systemic Vasculitis (time permitting)
ANATOMY REVIEW
QuickReminders
• Arteries
Large
Medium
Small
• Arterioles
Higher muscle ratio and
can completely occlude
lumen
2/3 of total systemic
resistance
• Capillaries
One-cell thick
Highest cross-sectional
area
Exchange nutrients
• Venules
Collect blood
• Veins
Blood reservoir (64%)
8x more distensible
Low pressure
Thin walls (less muscle)
BloodVessels
Tunica intima (Endothelium, basement membrane); tunica media; tunica externa
PERIPHERAL ARTERIAL DISEASE
Bottom Line Up Front
• Also known as peripheral artery disease, peripheral arterial disease,
peripheral vascular disease, peripheral arterial insufficiency, chronic
arterial insufficiency, PAD, PVD
• Miller: Aneurysmal or occlusive arterial disease of the extremities,
visceral organs, head, neck, and brain
• Defined as compromised blood flow to the extremities
• Ankle brachial index < 0.9
• Peripheral disease imparts a three to five times higher rate of
cardiovascular ischemic events
• 91.5% of vascular surgery patients have abnormal coronary arteries
• More than 60% have advanced (>70% stenosis) CAD
• 20% PAD patients have >70% carotid artery stenosis
• Claudication usually masks ischemic heart disease (functional decline)
• Primary anesthesia goal is to preserve cardiac and vital organ
function
Risk Factors
• Male
• Older age
• Family history
• Marfan syndrome
• Ehler’s Danlos
• Low high-density lipoproteins
• Smoking (doubles risk and causes progression)
• Diabetes mellitus
• Hypertension
• Obesity
• Dyslipidemia
• Homocysteine, fibrinogen, lipoprotein(a), apolipoproteins B
and A-I, C-reactive protein levels
LesionLocations
• Most commonly from
atherosclerosis in
large to medium
vessels, at sites of
turbulent flow
• Peripheral disease
mirrors that of the
aorta, coronary
arteries, and
extracranial cerebral
arteries.
EndothelialCellInjury
Damage causes monocyte adhesion
InflammatoryCellMigration
Monocytes migrate to the tunica intima, becoming macrophages and engulf lipoproteins (LDL).
T-cells also implicated
LipidsAccumulateandSmoothMuscleProliferates
Macrophages oxidize and phagocytize the LDL , becoming foam cells. They also release growth
factors
PlaqueForms
Fibrofattyplaqueofatherosclerosis
Signs and Symptoms
• Intermittent claudication
• Rest pain
• Nonhealing skin lesions
• Decreases to absent arterial pulses
• Bruits
• Subcutaneous atrophy
• Alopecia
• Coolness
• Pallor
• Cyanosis
• Dependent redness
• Relief from hanging affected extremity dependently
Diagnosis
• Ankle-Brachial Index
• 1.0-1.1: Normal
• <0.9: Intermittent claudication (other texts say < 0.5)
• <0.4: Rest pain
• <0.25: ischemic ulceration & gangrene (other texts say < 0.2)
• Indicates disease proximal to measurement
• Transcutaneous oximetry
• Normal in the resting foot: 60 mm Hg
• <40 mm Hg: ischemic ulceration
• MRI and contrast angiography
• Used to guide surgical intervention
Treatment
• Exercise programs
• Modifying risk factors
• Smoking cessation
• Lipid-lowering therapy
• Glucose control
• Pharmacologic
• Antiplatelet drugs (ASA, clopidogrel)
• Statins
• Lumbar sympathectomy for persistent vasospasm
• Revascularization (Endovascular and Surgical)
• For severe claudication, rest pain, non-healing wound, acute
occlusive event
Treatment (Endovascular)
• Highest success with percutaneous transluminal angioplasty
(PTA) of the iliac arteries
• Femoral & popliteal artery PTA less successful
• Intraarterial thrombolytic therapy
• Balloon catheter embolectomy
• Stents
• Stent placement has improved both approaches
• Restenosis still a large problem
Treatment (Surgical)
• Depends on location and severity
• Endarterectomy
• Bypass grafting
• Saphenous (reversed) > umbilical vein and
polytetrafluoroethylene
• Aortobifemoral bypass for aortoiliac disease
• Aortoiliac reconstruction
• Axillobifemoral bypass (circumvents the abdominal aorta)
• Femorofemoral bypass for unilateral iliac artery disease
• Infrainguinal bypass
• Femoropopliteal
• Tibioperoneal
• Amputation
Anesthesia for PAD (Preop)
• Risk factor modification more important than anesthetic
approach
• Patient’s usually can’t perform ETT, so they receive MPS with
TTE
• May require PCI for ischemic heart disease first (ACC/AHA
guidelines)
• Statin therapy
• β-blocker therapy (but not initiated day of surgery). At least 7-
10 days prior
Anesthesia for PAD (Intraop)
• Principle risk is myocardial ischemia
• “Tight” hemodynamics
• Avoid hypervolemia, tachycardia (HR <85), anemia (HgB >9.0g/dL)
• Virtually all patients require intra-arterial monitoring
• Allen test is pretty much useless
• Radial artery preferred (collateral circulation)
• Regional (neuraxial) vs. general
• Inconclusive as to one benefiting over the other
• GA: Hypercoaguable state, higher cortisol
• RA: attenuates clotting, stress response, better pain control
• Intraoperative heparinization (at least 1 hour after epidural placement)
• Often on clopidogrel
• Delayed 12-24 hours after last dose of LMWH
• Aortoiliac/Aortofemoral surgery
• Infrarenal aortic cross-clamping vs. aortic cross-clamping
• Heparin prior to clamping
• Spinal cord damage unlikely and special monitors not normally used
Anesthesia for PAD (Postop)
• Analgesia
• Anxiety
• ST-segment analysis
• Frequent peripheral pulse checks
• Fluid and electrolyte derangements
• Ready for urgent re-stenosis management
Acute Arterial Occlusion
• Thrombotic
• More common at 6:1
• Embolism
• Atrial fibrillation, AMI >
• Valve lesions, prosthetic
valves, infective
endocarditis, patent
foramen ovale, plaque
rupture, hypercoagulable
disease
• Usually lodge at arterial
bifurcations
• Aortic dissection
• Trauma
• Signs and Symptoms
• Pistol shot
• Pain
• Paresthesia (late)
• Paralysis (late)
• Pulseless (early)
• Pallor/cyanosis (early)
• Treatment
• Surgical embolectomy
• Heparin
• Intraarterial thrombolysis
Raynaud’s Phenomenon
• Episodic vasospastic
ischemia of the digits
followed by vasodilation and
hyperemia
• Women > men
• Associated to cold exposure
& sympathetic activation
(stress)
• Primary: Raynaud’s disease
• Secondary: Scleroderma and
systemic lupus
erythematosus, beta-
blockers, TCA, ergot
alkaloids, amphetamines
implicated
• Diagnosis: history and
physical, with inflammatory
markers sent to diagnose
secondary causes
• Treatment: Protect from
cold, CCB, alpha blockers,
surgical sympathectomy
• Anesthesia: Keep room
warm, NIBP, regional
anesthesia (without
epinephrine)
Peripheral Venous Disease
Conditions
• Superficial
thrombophlebitis
• Deep vein thrombosis
• Chronic venous
insufficiency
Risk Factors
• Virchow’s triad
• Venous stasis
• Surgery
• Trauma
• Immobility
• Pregnancy
• Low cardiac output
• Stroke
• Hypercoagulability
• Surgery
• Estrogen therapy
• Cancer
• ATIII, protein C, protein S deficiency
• Stress
• Inflammatory bowel disease
• Vessel wall abnormality
• Varicose veins
• Drug-induced
• History of thromboembolism
• Morbid obesity
• Advanced age
Venous Thromboembolism
Prevention
• Early ambulation
• Compression stockings
• Procedure < 1 hour
• Subcutaneous heparin 5000
units BID – TID
• Intermittent external
pneumatic compression
devices
• Use of regional anesthesia
• 20-40% reduction after total
hip or knee surgery
(vasodilation)
• Allows for earlier ambulation
(analgesia)
Treatment
• Heparin (LMWH or
unfractionated)
• Warfarin (INR 2-3)
• Inferior vena cava filter
• Thrombophilia workup
• Factor V Leiden
• Antithrombin III deficiency
• Protein C deficiency
• Protein S deficiency
• Plasminogen
• Increased antiphospholipid
antibodies
SYSTEMIC VASCULITIS
Key Points to Vasculitis
• “Angiitis, arteritis”
• Signs/Symptoms: fever, myalgias, arthralgia, malaise
• Understand what vessels are affected
• Large vessels: aorta and main branches
• Medium vessels: coronary arteries
• Small vessels: arterioles, venules, and capillaries. Type III
immune complex reactions. Serum antineutrophil cytoplasmic
antibodies (ANCA) correlate to disease severity.
• Treatments usually include glucocorticoids (adrenal
suppression), underlying pathology, and immunosuppression
agents
Systemic Vasculitis Types
Large Artery
• Takayasu’s arteritis
• Temporal (giant cell)
arteritis
Small & Medium Artery
• Kawasaki’s disease
• Thromboangiitis obliterans
• Wegener’s granulomatosis
• Polyarteritis nodosa
Takayasu’s Arteritis
• Many names
• Pulseless disease
• Occlusive thromboaortopathy
• Aortic arch syndrome
• Large-vessels
• Aorta and it’s branches
• Carotid arteries
• Subclavian arteries
• Pulmonary arteries
• Renal arteries
• Treatment:
• Glucocorticoids
• Methotrexate
• Azathioprine
• Anticoagulants/antiplatelets
• Percutaneous/surgical
intervention
• Anesthesia
• Adrenocortical suppression?
• Head positioning implications on
cerebral function?
• Avoid hyperventilation (cerebral
vasculature already stenotic)
• EEG monitoring?
• NIBP vs. IBP monitoring?
Temporal (Giant Cell) Arteritis
• Head & Neck Large
Arteries
• Ophthalmic artery
• Diagnosis
• Persons >50yo with
unilateral headache,
jaw claudication,
ischmic optic neuritis,
unilateral blindess
• Treatment:
• Glucocorticoids
• Anesthesia…
Kawasaki’s Disease
• “Mucocutaneous lymph
node syndrome”
• Signs and Symptoms
• Children
• Fever
• Conjunctivitis
• Inflamed mucous membranes
(“Strawberry tongue”)
• Swollen hands/feet
• Truncal rash
• Cervical lymphadenopathy
• Medium-sized vessels
• Coronary arteries
• Treatment
• Gamma globulin
• Aspirin
• Anesthesia
• Intraoperative MI
• Sympathectomy potentially
good
Thromboanglitis Obliterans
• “Buerger’s disease”
• Associations
• Men <45 yo
• Tobacco use
• Raynaud’s
• Small-Medium arteries
and veins of the
extremities
• Treatment
• Stop smoking
• No established drug
therapy
• Anesthesia
• Avoid triggers
• Warm room
• Warmed and humidified
gas (maintain body temp)
• Meticulous padding of
pressure points
• NIBP
• Avoid epinephrine if using
regional anesthesia
Wegener’s Granulomatosis
• Necrotizing
gramulomas in vessels
• CNS
• Airways
• Lungs
• Cardiovascular
• Kidneys
• Treatment
• Glucocorticoids
• Methotrexate
• Rituximab
• Maintenance with
azathioprine or
methotrexate
• Anesthesia
• Sinusitis may be present
• Renal failure may be
present
• Laryngeal mucosa
replaced by granulation
tissue (narrowed, stiff)
Churg-Strauss Syndrome
• Small-medium vessels
• Respiratory system
• Rhinitis
• Asthma
• Eosinophilia
• Treatment
• Glucocorticoid
• Immunosuppression
• Anesthesia
• Often come in for nasal
polypectomy &
myringotomy tubes
• Reactive airway
Polyarteritis Nodosa
• Associated
• HIV, HBV, HCV, hairy
cell leukemia
• Males
• Small to medium
vessels
• Treatment
• Glucocorticoids
• Cyclophosphamide
• Treat underlying
disease
• Anesthesia
• Likely renal disease
• Likely cardiac disease
• Systemic hypetension
Key References
1. Hall JE. Guyton and Hall Textbook of Medical Physiology. Elsevier
Health Sciences; 2016.
2. Stoelting RK, Hines RL, Marschall KE. Stoelting's anesthesia and co-
existing disease. 6th ed. Philadelphia: Saunders/Elsevier; 2012.
3. Miller RD. Miller's anesthesia. 8th ed. Philadelphia, PA:
Elsevier/Saunders; 2015.
4. Yao FSF, Fontes ML, Malhotra V. Yao and Artusio’s Anesthesiology:
Problem-Oriented Patient Management. Wolters Kluwer Health;
2012.
5. Horlocker TT, Wedel DJ, Rowlingson JC, et al. Regional Anesthesia
in the Patient Receiving Antithrombotic or Thrombolytic Therapy:
American Society of Regional Anesthesia and Pain Medicine
Evidence-Based Guidelines (Third Edition). Regional Anesthesia
and Pain Medicine. 2010;35(1):64-101.

CV-Peripheral Vascular Disease 2

  • 1.
  • 2.
    Outline • Anatomy Review •Peripheral Arterial Diseases (major) • Peripheral Venous Diseases (secondary) • Systemic Vasculitis (time permitting)
  • 3.
  • 4.
    QuickReminders • Arteries Large Medium Small • Arterioles Highermuscle ratio and can completely occlude lumen 2/3 of total systemic resistance • Capillaries One-cell thick Highest cross-sectional area Exchange nutrients • Venules Collect blood • Veins Blood reservoir (64%) 8x more distensible Low pressure Thin walls (less muscle)
  • 5.
    BloodVessels Tunica intima (Endothelium,basement membrane); tunica media; tunica externa
  • 6.
  • 7.
    Bottom Line UpFront • Also known as peripheral artery disease, peripheral arterial disease, peripheral vascular disease, peripheral arterial insufficiency, chronic arterial insufficiency, PAD, PVD • Miller: Aneurysmal or occlusive arterial disease of the extremities, visceral organs, head, neck, and brain • Defined as compromised blood flow to the extremities • Ankle brachial index < 0.9 • Peripheral disease imparts a three to five times higher rate of cardiovascular ischemic events • 91.5% of vascular surgery patients have abnormal coronary arteries • More than 60% have advanced (>70% stenosis) CAD • 20% PAD patients have >70% carotid artery stenosis • Claudication usually masks ischemic heart disease (functional decline) • Primary anesthesia goal is to preserve cardiac and vital organ function
  • 8.
    Risk Factors • Male •Older age • Family history • Marfan syndrome • Ehler’s Danlos • Low high-density lipoproteins • Smoking (doubles risk and causes progression) • Diabetes mellitus • Hypertension • Obesity • Dyslipidemia • Homocysteine, fibrinogen, lipoprotein(a), apolipoproteins B and A-I, C-reactive protein levels
  • 9.
    LesionLocations • Most commonlyfrom atherosclerosis in large to medium vessels, at sites of turbulent flow • Peripheral disease mirrors that of the aorta, coronary arteries, and extracranial cerebral arteries.
  • 10.
  • 11.
    InflammatoryCellMigration Monocytes migrate tothe tunica intima, becoming macrophages and engulf lipoproteins (LDL). T-cells also implicated
  • 12.
    LipidsAccumulateandSmoothMuscleProliferates Macrophages oxidize andphagocytize the LDL , becoming foam cells. They also release growth factors
  • 13.
  • 14.
  • 15.
    Signs and Symptoms •Intermittent claudication • Rest pain • Nonhealing skin lesions • Decreases to absent arterial pulses • Bruits • Subcutaneous atrophy • Alopecia • Coolness • Pallor • Cyanosis • Dependent redness • Relief from hanging affected extremity dependently
  • 16.
    Diagnosis • Ankle-Brachial Index •1.0-1.1: Normal • <0.9: Intermittent claudication (other texts say < 0.5) • <0.4: Rest pain • <0.25: ischemic ulceration & gangrene (other texts say < 0.2) • Indicates disease proximal to measurement • Transcutaneous oximetry • Normal in the resting foot: 60 mm Hg • <40 mm Hg: ischemic ulceration • MRI and contrast angiography • Used to guide surgical intervention
  • 17.
    Treatment • Exercise programs •Modifying risk factors • Smoking cessation • Lipid-lowering therapy • Glucose control • Pharmacologic • Antiplatelet drugs (ASA, clopidogrel) • Statins • Lumbar sympathectomy for persistent vasospasm • Revascularization (Endovascular and Surgical) • For severe claudication, rest pain, non-healing wound, acute occlusive event
  • 18.
    Treatment (Endovascular) • Highestsuccess with percutaneous transluminal angioplasty (PTA) of the iliac arteries • Femoral & popliteal artery PTA less successful • Intraarterial thrombolytic therapy • Balloon catheter embolectomy • Stents • Stent placement has improved both approaches • Restenosis still a large problem
  • 19.
    Treatment (Surgical) • Dependson location and severity • Endarterectomy • Bypass grafting • Saphenous (reversed) > umbilical vein and polytetrafluoroethylene • Aortobifemoral bypass for aortoiliac disease • Aortoiliac reconstruction • Axillobifemoral bypass (circumvents the abdominal aorta) • Femorofemoral bypass for unilateral iliac artery disease • Infrainguinal bypass • Femoropopliteal • Tibioperoneal • Amputation
  • 20.
    Anesthesia for PAD(Preop) • Risk factor modification more important than anesthetic approach • Patient’s usually can’t perform ETT, so they receive MPS with TTE • May require PCI for ischemic heart disease first (ACC/AHA guidelines) • Statin therapy • β-blocker therapy (but not initiated day of surgery). At least 7- 10 days prior
  • 21.
    Anesthesia for PAD(Intraop) • Principle risk is myocardial ischemia • “Tight” hemodynamics • Avoid hypervolemia, tachycardia (HR <85), anemia (HgB >9.0g/dL) • Virtually all patients require intra-arterial monitoring • Allen test is pretty much useless • Radial artery preferred (collateral circulation) • Regional (neuraxial) vs. general • Inconclusive as to one benefiting over the other • GA: Hypercoaguable state, higher cortisol • RA: attenuates clotting, stress response, better pain control • Intraoperative heparinization (at least 1 hour after epidural placement) • Often on clopidogrel • Delayed 12-24 hours after last dose of LMWH • Aortoiliac/Aortofemoral surgery • Infrarenal aortic cross-clamping vs. aortic cross-clamping • Heparin prior to clamping • Spinal cord damage unlikely and special monitors not normally used
  • 22.
    Anesthesia for PAD(Postop) • Analgesia • Anxiety • ST-segment analysis • Frequent peripheral pulse checks • Fluid and electrolyte derangements • Ready for urgent re-stenosis management
  • 23.
    Acute Arterial Occlusion •Thrombotic • More common at 6:1 • Embolism • Atrial fibrillation, AMI > • Valve lesions, prosthetic valves, infective endocarditis, patent foramen ovale, plaque rupture, hypercoagulable disease • Usually lodge at arterial bifurcations • Aortic dissection • Trauma • Signs and Symptoms • Pistol shot • Pain • Paresthesia (late) • Paralysis (late) • Pulseless (early) • Pallor/cyanosis (early) • Treatment • Surgical embolectomy • Heparin • Intraarterial thrombolysis
  • 24.
    Raynaud’s Phenomenon • Episodicvasospastic ischemia of the digits followed by vasodilation and hyperemia • Women > men • Associated to cold exposure & sympathetic activation (stress) • Primary: Raynaud’s disease • Secondary: Scleroderma and systemic lupus erythematosus, beta- blockers, TCA, ergot alkaloids, amphetamines implicated • Diagnosis: history and physical, with inflammatory markers sent to diagnose secondary causes • Treatment: Protect from cold, CCB, alpha blockers, surgical sympathectomy • Anesthesia: Keep room warm, NIBP, regional anesthesia (without epinephrine)
  • 25.
    Peripheral Venous Disease Conditions •Superficial thrombophlebitis • Deep vein thrombosis • Chronic venous insufficiency Risk Factors • Virchow’s triad • Venous stasis • Surgery • Trauma • Immobility • Pregnancy • Low cardiac output • Stroke • Hypercoagulability • Surgery • Estrogen therapy • Cancer • ATIII, protein C, protein S deficiency • Stress • Inflammatory bowel disease • Vessel wall abnormality • Varicose veins • Drug-induced • History of thromboembolism • Morbid obesity • Advanced age
  • 26.
    Venous Thromboembolism Prevention • Earlyambulation • Compression stockings • Procedure < 1 hour • Subcutaneous heparin 5000 units BID – TID • Intermittent external pneumatic compression devices • Use of regional anesthesia • 20-40% reduction after total hip or knee surgery (vasodilation) • Allows for earlier ambulation (analgesia) Treatment • Heparin (LMWH or unfractionated) • Warfarin (INR 2-3) • Inferior vena cava filter • Thrombophilia workup • Factor V Leiden • Antithrombin III deficiency • Protein C deficiency • Protein S deficiency • Plasminogen • Increased antiphospholipid antibodies
  • 27.
  • 28.
    Key Points toVasculitis • “Angiitis, arteritis” • Signs/Symptoms: fever, myalgias, arthralgia, malaise • Understand what vessels are affected • Large vessels: aorta and main branches • Medium vessels: coronary arteries • Small vessels: arterioles, venules, and capillaries. Type III immune complex reactions. Serum antineutrophil cytoplasmic antibodies (ANCA) correlate to disease severity. • Treatments usually include glucocorticoids (adrenal suppression), underlying pathology, and immunosuppression agents
  • 29.
    Systemic Vasculitis Types LargeArtery • Takayasu’s arteritis • Temporal (giant cell) arteritis Small & Medium Artery • Kawasaki’s disease • Thromboangiitis obliterans • Wegener’s granulomatosis • Polyarteritis nodosa
  • 30.
    Takayasu’s Arteritis • Manynames • Pulseless disease • Occlusive thromboaortopathy • Aortic arch syndrome • Large-vessels • Aorta and it’s branches • Carotid arteries • Subclavian arteries • Pulmonary arteries • Renal arteries • Treatment: • Glucocorticoids • Methotrexate • Azathioprine • Anticoagulants/antiplatelets • Percutaneous/surgical intervention • Anesthesia • Adrenocortical suppression? • Head positioning implications on cerebral function? • Avoid hyperventilation (cerebral vasculature already stenotic) • EEG monitoring? • NIBP vs. IBP monitoring?
  • 31.
    Temporal (Giant Cell)Arteritis • Head & Neck Large Arteries • Ophthalmic artery • Diagnosis • Persons >50yo with unilateral headache, jaw claudication, ischmic optic neuritis, unilateral blindess • Treatment: • Glucocorticoids • Anesthesia…
  • 32.
    Kawasaki’s Disease • “Mucocutaneouslymph node syndrome” • Signs and Symptoms • Children • Fever • Conjunctivitis • Inflamed mucous membranes (“Strawberry tongue”) • Swollen hands/feet • Truncal rash • Cervical lymphadenopathy • Medium-sized vessels • Coronary arteries • Treatment • Gamma globulin • Aspirin • Anesthesia • Intraoperative MI • Sympathectomy potentially good
  • 33.
    Thromboanglitis Obliterans • “Buerger’sdisease” • Associations • Men <45 yo • Tobacco use • Raynaud’s • Small-Medium arteries and veins of the extremities • Treatment • Stop smoking • No established drug therapy • Anesthesia • Avoid triggers • Warm room • Warmed and humidified gas (maintain body temp) • Meticulous padding of pressure points • NIBP • Avoid epinephrine if using regional anesthesia
  • 34.
    Wegener’s Granulomatosis • Necrotizing gramulomasin vessels • CNS • Airways • Lungs • Cardiovascular • Kidneys • Treatment • Glucocorticoids • Methotrexate • Rituximab • Maintenance with azathioprine or methotrexate • Anesthesia • Sinusitis may be present • Renal failure may be present • Laryngeal mucosa replaced by granulation tissue (narrowed, stiff)
  • 35.
    Churg-Strauss Syndrome • Small-mediumvessels • Respiratory system • Rhinitis • Asthma • Eosinophilia • Treatment • Glucocorticoid • Immunosuppression • Anesthesia • Often come in for nasal polypectomy & myringotomy tubes • Reactive airway
  • 36.
    Polyarteritis Nodosa • Associated •HIV, HBV, HCV, hairy cell leukemia • Males • Small to medium vessels • Treatment • Glucocorticoids • Cyclophosphamide • Treat underlying disease • Anesthesia • Likely renal disease • Likely cardiac disease • Systemic hypetension
  • 37.
    Key References 1. HallJE. Guyton and Hall Textbook of Medical Physiology. Elsevier Health Sciences; 2016. 2. Stoelting RK, Hines RL, Marschall KE. Stoelting's anesthesia and co- existing disease. 6th ed. Philadelphia: Saunders/Elsevier; 2012. 3. Miller RD. Miller's anesthesia. 8th ed. Philadelphia, PA: Elsevier/Saunders; 2015. 4. Yao FSF, Fontes ML, Malhotra V. Yao and Artusio’s Anesthesiology: Problem-Oriented Patient Management. Wolters Kluwer Health; 2012. 5. Horlocker TT, Wedel DJ, Rowlingson JC, et al. Regional Anesthesia in the Patient Receiving Antithrombotic or Thrombolytic Therapy: American Society of Regional Anesthesia and Pain Medicine Evidence-Based Guidelines (Third Edition). Regional Anesthesia and Pain Medicine. 2010;35(1):64-101.

Editor's Notes

  • #5 Figure 14-1: Hall JE. Guyton and Hall Textbook of Medical Physiology. 13th ed. Elsevier Health Sciences; 2015. https://books.google.com/books?id=krLSCQAAQBAJ. Arteries are classified as large, medium, and small based on compliance. Arterioles are the site of highest systemic vascular resistance (remember in the large cross-sectional anatomy that in parallel, we can change the circuit’s resistance). Capillaries are where nutrient exchange occurs, and are only one cell thick without musculature. Venules receive blood from the capillaries and feed to the blood reserviour – the veins. Veins are more highly distensible, and the peripheral veins have valves (whereas the larger abdominal and thoracic veins do not).
  • #6 FIGURE 30.2 • Blood vessels—microanatomy of the artery, vein, and capillary beds. (From McConnell T. H., Hull K. L. (2011). Human form human function: Essentials of anatomy & physiology (p. 433, Figure 11–12). Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins.) All vessels are three layers, except capillaries. Endothelial cells form a continuous lining – the endothelium. It regulates molecule transfer, platelet adhesion, modulation of blood flow, metabolism of hormones, regulation of immune and inflammatory reactions, and produce nitric oxide and endothelins. The endothelium is a huge site of interest as a biologically active tissue. Tunica media is smooth muscle interconnected with gap junctions. Norepinephrine is released from sympathetic nerves regulating tone here (remember the SVR). Blood flow is regulated by myogenic means, production of local metabolites, and can auto-regulate between 70 – 175 mm Hg (systemic vasculature). External regulation occurs from sympathetic tone (and occasionally parasympathetic producing Nitric Oxide, as in the case of the naught—bits), and hormones.
  • #7 Just a quick reminder of a few last physiology concepts: Poiseulle’s law tells use flow is fastest away from vessel lumens. As diameter changes in vessels, the conductance is altered by a fourth power. Figure 14-8: Hall JE. Guyton and Hall Textbook of Medical Physiology. 13th ed. Elsevier Health Sciences; 2015. https://books.google.com/books?id=krLSCQAAQBAJ.
  • #9 Peripheral arterial disease is known by many names, as listed. By definition, PAD is an ankle brachial index < 0.9 (this correlates very well to angiographic-evidenced PAD). The major concern is perioperative cardiac events more than developing critical limb ischemia, as evidenced by the 91.5% association with abnormal coronary arteries. Our primary goal is preserve cardiac and vital organ perfusion. 1 Stoelting RK, Hines RL, Marschall KE. Stoelting’s Anesthesia and Co-Existing Disease. Vol 6. Saunders/Elsevier; 2012. https://books.google.com/books?id=LXPBrqZAIiEC.
  • #10 Occurs in 70% of persons over 75 years old. I bolded the modifiable risk factors (hence, the ones we can “optimize” the patient prior to surery). Claudication and PVD risk is doubled in smokers with higher rates of disease progression (leading to amputation)
  • #11 Notice that the disease primarily occurs at bifurcations. The most common sites are the aortoiliac vessels, with a close second at the coronaries. The key point is that peripheral vessels mirror central vessels.
  • #12 And with mono
  • #14 The “fatty streak” begins in childhood
  • #16 FIGURE 30.8 • Fibrofatty plaque of atherosclerosis. (A) In this fully developed fibrous plaque, the core contains lipid-filled macrophages and necrotic smooth muscle cell (SMC) debris. The “fibrous” cap is composed largely of SMCs, which produce collagen, small amounts of elastin, and glycosaminoglycans. Also shown are infiltrating macrophages and lymphocytes. Note that the endothelium over the surface of the fibrous cap frequently appears intact. (B) The aorta shows discrete raised, tan plaques. Focal plaque ulcerations are also evident. (From Rubin R., Strayer D. (Eds.). (2012). Rubin’s pathology: Clinicopathologic foundations of medicine (6th ed., p. 447–448). Philadelphia, PA: Lippincott Williams & Wilkins.) Type
  • #17 Intermittent claudication occurs when metabolic demand exceeds oxygen delivery Rest pain occurs without exertion. Usually the first sign is decrease peripheral pulses Bruits can indicate the site of the lesion. Hanging the extremity increase hydrostatic pressure in the arterioles, facilitating better oxygen delivery
  • #20 Beta blockers have been theorized to evoke peripheral cutaneous vascoconstriction, but RCTs have failed to bear this out.
  • #23 Regional: can reduce change of postoperative delirium, allows for patient to communicate myocardial ischemia symptoms, less activation of the coagulation system, fewer post operative pulmonary complications Intraoperative heparinization is not a contraindication. Surgical team should be aware that if a blood tap occurs, procedure may need to be delayed General anesthesia: for longer procedures, vein harvesting from upper extremities. Cardiac preconditioning from inhaled agetns? Infrarenal aortic cross-clamping associated with fewer hemodynamic changes than aortic cross clamping (same for unclamping).
  • #26 Occlusion of subclavian or innominate artery proximal to vertebral artery origin. The occlusion causes a reversal of flow through the ipsilateral vertebral artery into the distal subclavian artery. Diverts blood from the brain to the arm. Signs and symptoms are CNS ischemia and ipsilateral arm ischemia. Extremes of neck movements and exercise and produce symptoms. Pulses can be absent or diminished in the affected arm with SBP 20 mm Hg lower in that arm (like coarctation of the aorta). Bruit over the subclavian artery
  • #27 Occurs with proximal stenosis of the left subclaviarn artery causing reversed blood flow through a patent internal mammary artery graft. Signs and symptoms are angina pectoris and 20 mm Hg or more decrease in systolic BP in the ipsilateral arm.
  • #28 Surgical embolectomy is used for large vessel occlusion that are not atheromatous. Atheromas fragment with manipulation.
  • #30 Superficial thrombophlebitis: palpable cord-like veins, localized swelling and pain. DVT: generalized pain, unilateral limb swelling. Compression ultrasonography highly sensitive for proximal thrombus but less for calf thrombus. Can also consider venography
  • #35 Takayasu’s is rare, idiopathic, chronic, progressive occlusive vasculitis that causes narrowing, thrombossis, or large vessel (aorta) anuerysms. Mostly in Asian women < 40 years old.
  • #36 Takayasu’s is rare, idiopathic, chronic, progressive occlusive vasculitis that causes narrowing, thrombossis, or large vessel (aorta) anuerysms. Mostly in Asian women < 40 years old.