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SRNA3CoExisting > VASCULAR FINAL EXAM REVIEW > Flashcards

VASCULAR FINAL EXAM REVIEW Flashcards

1
Q

What is an Aneurysm?

A

An aneurysm is a balloon-like bulge in an artery

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2
Q

When does An aneurysm occur?

A

When the pressure of blood passing through part of a weakened artery forces the vessel to bulge outward, forming somewhat ofa blister

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3
Q

If bulging stretches artery too far, What happens to the vessel?

A

vessel may burst

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4
Q

What are the layers of the artery from outer to inner?

A 
Tunica Intima
Internal Elastic Lamina
Tunica Media
External Elastic Lamina
Tunica Externa
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5
Q

When does Aortic Dissection occur:

A

Aortic dissection occurs when the layers of the wall

of the aorta separate or are torn, allowing blood to flow between those layers and causing them to separate further

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6
Q

With aortic dissection, When the aortic wall separates, what occurs?

A

blood cannot flow freely, and the aortic wall may burst.

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7
Q

Anatomic types of dissecting aneurysms Type I

A

Intimal tear originates in ascending aorta

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8
Q

% of Debakey type I

A

70% of all cases

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9
Q

In type I Debakey Dissection involves (AVA)

A

Dissection involves
ascending aorta and arch
variable lengths of the descending thoracic and
abdominal aorta

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10
Q

Anatomic types of dissecting aneurysms• Debakey

Type II

A

Confined to ascending aorta

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11
Q

Anatomic types of dissecting aneurysms Type III Confined to

A

Descending thoracic aorta or extends into abdominal aorta and iliac arteries
Begins distal to the left subclavian artery

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12
Q

% of Debakey type III

A

20%

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13
Q

2 classifications of dissection

A

Stanford type A or B

Debakey Type I, II, III

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14
Q

Stanford Type A corresponds to Debakey

A

Type I and II

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15
Q

Stanford Type B corresponds to Debakey

A

Type III

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16
Q

Mechanisms for Aneurysm Formation (4 ways)

HADS

A
  • HTN
  • Atherosclerosis
  • Syphilis
  • Deceleration Injury
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17
Q

Aneurysms of the Ascending Thoracic Aorta: age affected

A

Usually middle aged

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18
Q

Signs & Symptoms

A

result of compression or stretching are a result of compression or stretching

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19
Q

Ascending Thoracic Aorta With aneurysm, compression of Trachea sx

A

Inspiratory stridor

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20
Q

Ascending Thoracic Aorta With aneurysm, compression of Esophagus sx

A

Dysphagia

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21
Q

With aneurysm, compression of • Laryngeal nerves sx

A

Hoarseness

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22
Q

Ascending Thoracic Aorta With aneurysm, compression of •Carotids sx

A

Occlusion

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23
Q

Ascending Thoracic Aorta With aneurysm, compression of •Coronary sx

A

Occlusion

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24
Q

Ascending Thoracic Aorta With aneurysm compression, can also get

A

Cardiac tamponade

Acute Aortic Regurgitation

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25
Q

Ascending Thoracic Aorta Diagnosis

A
  • CXR

* Widening of mediastinum

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26
Q

Ascending Thoracic Aorta Treatment

M-TAFS

A
  • Medical treatment
  • Tight control of BP, HLD, and smoking cessation essential
  • Avoid strenuous exercise and stimulants• Focus on ↓ expansion rate and avoiding evolution to dissection/rupture
  • Surgical intervention
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27
Q

Replacement of Ascending Aorta with Vascular Graft: anesthesia consideration PREOP

A

Right radial A-line if the clamping is DISTAL to the LEFT subclavian artery)

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28
Q

Monitoring for patient having Ascending Aorta vascular graft

A

SSEP and EEG
Carotid Dopller
TEE

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29
Q

Replacement of Ascending Aorta with Vascular Graft:

Intra-op complications

A

CVA • Myocardial Infarction • Spinal cord injury

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30
Q

Replacement of Ascending Aorta with Vascular Graft: •POST OP Prevent

A

• HTN • Tachycardia • CNS Dysfunction

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31
Q

Aneurysm of the DESCENDING THORACIC AORTA

Classification and symptom

A

Debakey Type III

usually asymptomatic

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32
Q

Causes of DESCENDING TA

A

Deceleration injury

Myocardiac contusion

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33
Q

Treatment of DESCENDING TA

A
  • Conservative medical management

* Surgical Intervention

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34
Q

Maximum thoracic aortic diameter

A

5.5 cm

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35
Q

Most Proximal part of descending aorta min and Max

A

5.5 and 6

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36
Q

Mid part of descending aorta min and max

A

3.5 and 4

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37
Q

Lower part of descending aorta min and max

A

3.5 and 9

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38
Q

Anesthesia consideration for DESCENDING : Monitoring

A

PA catheter
Right Radial A-line
Femoral A-line

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39
Q

Anesthesia consideration for DESCENDING : Monitoring

A

Induction double lumen (thoracotomy)

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40
Q

Anesthesia consideration for DESCENDING : POST OP

A

Neurologic Deficits

Artery of Adamkiewicz

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41
Q

Vessels supplying the spinal cord are

A

Adamkiewicz artery
Intercostal lumbar artery
Aorta

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42
Q

Radiculomedullary artery of Adamkiewicz

A

C3-C8
T3-T4
T11-T12 (Artery of Adamkiewicz)

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43
Q

Aortic blood supply to other organs

A 
Basilar artery
Vertebral Artery
Ascending Cervical Artery
Posterior spinal artery
Subclavian artery
Deep Certivcal artery 
Medial Sacral artery
Radicular lumbosacral arteries
Right lateral sacral artery
Rignt internal iliac artery
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44
Q

Anterior Spinal Artery Syndrome: What causes

A

Cross-clamping thoracic aorta can result in ischemic

damage to spinal cord

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45
Q

Anterior Spinal Artery Syndrome: Frequency

A

40% in acute aortic dissection/rupture involving descending aorta
8% in elective thoracic aortic aneurysm repair
0.2% after elective infrarenal AAA repair

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46
Q

Anterior Spinal Artery Syndrome: Manifestations:

A

Flaccid paralysis LE, bowel/bladder dysfunction

• Sensation and proprioception spared!

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47
Q

Abdominal Aortic Aneurysms usually due to

A

• Usually due to atherosclerosis

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48
Q

Abdominal Aortic Aneurysms: Most common

A

Most common = infrarenal

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49
Q

AAA usually age and gender and family

A
  • Usually male > 60 yrs old

* Familial tendency

50
Q

AAA Signs & Symptoms

A
  • Painless
  • Pulsating abdominal mass
  • Size dictates intervention
51
Q

Size dictates intervention < 5cm

A

5% incidence of spont rupture

52
Q

Size dictates intervention > 5cm

A

70% incidence of spont rupture

53
Q

Ruptured AAA Classic triad (50%) BPH

A
  • Hypotension
  • Back pain
  • Pulsatile abdominal mass
54
Q

Most AAA rupture into

A

left retroperitoneum

55
Q

AAA Anesthesia consideration : Requires consideration of monitoring of hemodynamic management that will be needed to control

A

hypertension during the period of aortic crossclamping:

56
Q

AAA what is more important? •

A

Proper monitoring is more important than selection of anesthetic drugs in these patients.

57
Q

Monitoring during procedures

A

• Systemic blood pressure
• Neurologic function
• Intravascular volume and planning the pharmacologic
interventions.

58
Q

Thoracic Aortic Cross Clamping

• Cross clamping

A
  • Severe hemodynamic + homeostatic disturbances

* Affects virtually all organ systems

59
Q

Hemodynamics of cross clamping

A

• Hemodynamics: • ↑ systemic BP + SVR; no change in HR; Net ↓CO

60
Q

With cross clamping what do you see with BP

A

Either ↓BF distal to clamp, ↑BF above level of occlusion

61
Q

AAA cross clamping, Pharmacological interventions

• Vasodilators and what they do

A

Nicardipine
Nitroprusside
Nitroglycerin
ften reduce the clamp-induced decrease in cardiac output and ejection fraction

62
Q

AAA, what happens to the Perfusion pressure distal to cross clamp

A

Perfusion pressure distal to cross clamp is ↓ and directly depends on proximal aortic pressure (pressure above the level of aortic clamping)

63
Q

AAA What happens to blood flow to tissues distal to aortic occlusion

A

(kidneys, liver, spinal cord) occurs through collateral vessels or through a shunt

64
Q

Aortic cross-clamping associated with

A

formation and release of hormonal factors (activation of SNS and RAAS)
and other mediators (prostaglandins, oxygen free
radicals, complement cascade).

65
Q

Mediators release with cross clamping

A

These mediators may aggravate or blunt the harmful

effects of aortic cross-clamping and unclamping.

66
Q

With cross clamping, injury to the spinal cord….

A

Injury to the spinal cord, lungs, kidneys, and abdominal
viscera is principally due to ischemia and subsequent
reperfusion injury caused by the aortic cross-clamp (localeffects) and/or the release of mediators from ischemic and reperfused tissues (distant effects).

67
Q

Thoracic Aortic Unclamping: RESP

PVR, and cap membrane

A

Pulmonary damage 2° ↑PVR, ↑pulm cap
membrane permeability, development of pulmonary
edema

68
Q

Thoracic Aortic unclamping MOA

A

may include pulmonary hypervolemia and the effects of various vasoactive mediators

69
Q

Thoracic Aortic Unclamping:Hemodynamics:

SVR, BP, CO , LVEDP , myocardial BF

A

↓SVR + systemic BP
CO can ↑↓ or no ∆
↓ LVEDP, ↑myocardial BF

70
Q

Causes of unclamping hypotension:

Volume and hypoxia

A
  • Central hypovolemia caused by pooling of blood in reperfused tissues
  • Hypoxia-mediated vasodilation, which causes an ↑ in vascular capacitance in tissues below the level of aortic clamping
71
Q

Causes of unclamping hypotension: Vasodilation and hypotension may be further

A

aggravated by the transient increase in carbon dioxide release and oxygen consumption in these tissues following unclamping.

72
Q

Cause of unclamping hypotension: vasoactive substances

A

Accumulation of vasoactive and myocardial depressant metabolites in these tissues

73
Q

Unclamping and hypotension

A

Correction of metabolic acidosis does not significantly
influence the degree of hypotension following aortic
unclamping

74
Q

Peripheral Vascular Diseases
• Chronic peripheral arterial occlusive disease
(atherosclerosis)

A
  • Distal abdominal aorta or iliac arteries
  • Femoral arteries
  • Subclavian steal syndrome
  • Coronary-subclavian steal syndrome
75
Q

PVD acute

A

Acute peripheral arterial occlusive disease (embolism)

76
Q

What are the systemic vasculitis? (TTT WSP)

A
  • Takayasu’s arteritis
  • Thromboangiitis obliterans
  • Temporal arteritis
  • Wegener’s granulomatosis
  • Systemic vasculitis
  • Polyarteritis nodosa
77
Q

Other vascular syndromes

A
  • Raynaud’s phenomenon

* Kawasaki disease

78
Q

Peripheral Arterial Occlusive Disease (PAOD) aka

A

(atherosclerosis)

79
Q

Peripheral Arterial Occlusive Disease (PAOD) risk factors

FOSDDOH

A 
Risk factors same as ischemic heart disease:
Family Hx 
Older age
Smoking (doubled)
DM
Dyslipidemia
Obesity
HTN
80
Q

• S/S of PAOD

Most reliable.

A

Intermittent claudication, pain at rest,

↓/absent arterial pulses = most reliable physical finding associated with PAD

81
Q

Management of Anesthesia for Surgical
Revascularization
• Principal risk and how to prevent it ? who’s at increased risk

• Choice of anesthetic
• GETA if regional contraindicated (blood thinners, dementia, long surgical time)
• Inhalation agent-induced cardiac preconditioning might help
• Benefits of regional: ↑ graft BF, postoperative analgesia, ↓ activation of
coagulation system, and fewer postoperative respiratory complications
• Intraoperative heparinization is not a contraindication for epidural anesthesia
• Risk of bleeding ↑if on multiple blood thinners

A

myocardial ischemia
• Perioperative HR control c/BB ↓incidence
• ↑incidence CAD in pt population

82
Q

Management of Anesthesia for Surgical
Revascularization
• Principal risk and how to prevent it ? who’s at increased risk

A

myocardial ischemia
• Perioperative HR control c/BB ↓incidence
• ↑incidence CAD in pt population

83
Q

Management of Anesthesia for Surgical Revascularization: Do this test->

A

• Pharmacological stress test

84
Q

Management of Anesthesia for Surgical Revascularization Choice of anesthetic
• GETA if regional contraindicated (examples)
• Intraoperative heparinization is not a contraindication for epidural anesthesia
• Risk of bleeding ↑if on multiple blood thinners

A

(blood thinners, dementia, long surgical time)

85
Q

Management of Anesthesia for Surgical Revascularization Choice of anesthetic
• GETA if regional contraindicated (examples)

A

(blood thinners, dementia, long surgical time)

86
Q

Management of Anesthesia for Surgical Revascularization: Benefits of regional

A

↑ graft BF
postoperative analgesia
↓ activation of coagulation system
Fewer postoperative respiratory complications

87
Q

Management of Anesthesia for Surgical Revascularization: Benefits of regional

A

↑ graft BF
postoperative analgesia
↓ activation of coagulation system
Fewer postoperative respiratory complications

88
Q

Management of Anesthesia for Surgical Revascularization: RISK OF BLEEDING

A

• Risk of bleeding ↑if on multiple blood thinners

89
Q

Subclavian Steal Syndrome

•

A

Occlusion of innominate artery proximal to the origin of the vertebral artery ➔reversal of flow through the ipsilateral vertebral artery into distal subclavian artery
• Reversal of flow diverts blood flow from brain to supply the arm (subclavian steal syndrome)

90
Q

Subclavian Steal Syndrome: EXPLAIN

ORR

A

Occlusion of innominate artery proximal to the origin of the vertebral artery ➔
Reversal of flow through the ipsilateral vertebral artery into distal subclavian artery➔
Reversal of flow diverts blood flow from brain to supply the arm (subclavian steal syndrome)

91
Q

Subclavian Steal Syndrome: Symptoms

A
  • Vertigo
  • Ataxia
  • Hemiplegia
  • Syncope
92
Q

Coronary-Subclavian Steal Syndrome

• Requires surgical bypass grafting

A

Rare complication of using the internal

mammary artery for coronary revascularization

93
Q

Coronary-Subclavian Steal Syndrome : when does it occur?

A

Occurs when proximal stenosis in the left subclavian artery produces reversal of blood flow through the patent internal mammary artery graft

94
Q

Coronary-Subclavian Steal Syndrome Symptoms

A

• Symptoms
• Angina pectoris
• Signs of central nervous system ischemia
• 20-mm Hg or more decrease in systolic blood
pressure in the ipsilateral arm

95
Q

Coronary-Subclavian Steal Syndrome : Requires

A

• Requires surgical bypass grafting

96
Q

Thromboangiitis Obliterans: what is it?

A

Inflammatory and occlusive disease of the arteries and veins

97
Q

Thromboangiitis Obliterans: men vs women

A

• Greatest incidence in men

98
Q

Thromboangiitis Obliterans• worsens condition

99
Q

Thromboangiitis Obliterans• Exacerbated by

A

cold and trauma

100
Q

Thromboangiitis Obliterans: S/S

A
  • Migratory thrombophlebitis

* Intermittent claudication

101
Q

Thromboangiitis Obliterans Treatment:

A
  • Stop smoking
  • Avoid trauma
  • Avoid cold
102
Q

Thromboangiitis Obliterans Anesthesia Considerations

A
  • Positioning
  • Temperature
  • No Aline
  • Increase FiO2
  • General
  • Regional
103
Q

Thromboangiitis Obliterans Anesthesia Considerations: NO _____

104
Q

Thromboangiitis Obliterans Avoid this vasopressor

A

• Avoid epinephrine

105
Q

Wegeners Granulomatosis

A

Formation of granulomas in the vicinity of inflammed

vessels-> This leads to infiltration bynecrotizing granulomas

106
Q

Wegeners Granulomatosis Respiratory tract

A
  • Nose

* Sinusitis

107
Q

Wegeners Granulomatosis Respiratory tract• Larynx

A
  • Narrowing of the glottic opening

* Destructive lesions of the epiglottis common

108
Q

Wegeners Granulomatosis Respiratory tract• ALSO AFFECTS

A

Maxillary sinus

Hard palate

109
Q

Wegeners Granulomatosis Pulmonary vessels

A

Lead to occlusion with V/Q mismatch

110
Q

Wegeners Granulomatosis Upper trachea

A
  • Pneumonia

* Hemoptysis

111
Q

Wegeners Granulomatosis Signs & Symptoms

CV system

A

• Infarction of tips of digits

112
Q

Wegeners Granulomatosis Signs & Symptoms• Nervous system

A
  • CVA
  • Peripheral neuropathy
  • Skeletal muscle wasting
113
Q

Wegeners Granulomatosis Kidneys

CHAP

A

Complete destruction of the renal glomeruli
• Hematuria
• Azotemia
• Progressive renal failure = mostcommon cause of death

114
Q

Wegeners Granulomatosis Kidneys most common cause of death

A

Progressive renal Failure

115
Q

Treatment of Wegeners Granulomatosis : Medication

A

Cyclophosphamide

Corticosteroids

116
Q

Reaction to Cyclophosphamide (LHD)

A
  • Leukopenia
  • Hemolytic anemia
  • Decreases activity of plasma cholinesterase
117
Q

Wegeners Granulomatosis and Succ

A

Variable responses to Succinylcholine

118
Q

PE Manifestations PANTA RTFH

A 
Pleuritic Chest pain
Accentuation of Pulmonary Valve closure sound (P2) 
Nonproductive Cough
Tachypnea
Acute dyspnea

Rales
Tachycardia
Fever
Hemoptysis

119
Q

Pathophysiology of PE (BID PATARAA)

A 
Bronchospasm
Increase in alveolar dead space
Decrease in surfactant
Pulmonary Compliance decreases
Atelectasis
Tissue Necrosis
Acute increase in PVR 
RV failure occur
Arterial hypoxemia
Airway resistance increases
120
Q

PE ECG manifestations

A

S1
Q3
T3
Deep, Precordial T-wave inversions

121
Q

PE signs during Anesthesia HATBD

A 
Hypotension
Arterial Hypoxemia
Tachycardia
Bronchospasm
Decrease in ETCO2

SRNA3CoExisting (16 decks)

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