Import from anki test (patho for exam 2) Flashcards
1
Q
Crawford: Type 1 aortic aneurysm
A
All or most of the descending thoracic aorta and upper abdominal aorta.
2
Q
Crawford: Type 2 aortic aneurysm
A
All or most of the descending thoracic aorta and most of the abdominal aorta.
3
Q
Crawford: Type 3 aortic aneurysm
A
Lower descending thoracic aorta only and most of the abdominal aorta.
4
Q
Crawford: Type 4 aortic aneurysm
A
No part of the descending thoracic aorta and most of the abdominal aorta.
5
Q
Aortic dissections are classified based on location using two systems:
A
Stanford and DeBakey.
6
Q
Aortic aneurysms are classified based on region of the aorta affected using…
A
the Crawford classification system.
7
Q
Stanford Type A dissection
A
Involves ascending aorta.
8
Q
Stanford Type B dissection
A
Does not involve the ascending aorta.
9
Q
DeBakey: Type 1 dissection
A
Tear in ascending aorta and dissection along entire aorta.
10
Q
DeBakey: Type 2 dissection
A
Tear in ascending aorta and dissection only in ascending aorta.
11
Q
DeBakey: Type 3a dissection
A
Tear in proximal descending aorta where dissection is limited to the thoracic aorta.
12
Q
DeBakey: Type 3b dissection
A
Tear in the proximal descending aorta with dissection along thoracic and abdominal aorta.
13
Q
Which type of aortic aneurysms are most difficult to repair?
A
Crawford type II and III, because they involve the thoracic and abdominal aorta.
14
Q
Which type of aortic aneurysms present the most significant perioperative risk for paraplegia and/or renal failure?
A
Crawford type II.
Mandatory period of stopping flow to the renal arteries and some radicular arteries that perfuse the spinal cord (artery of Adamkiewicz).
15
Q
Which types of dissections are surgical emergencies? Which valve may be affected?
A
DeBakey I or II or Stanford A.
Dissection involving the ascending aorta. Aortic valve often affected - consider AI in anesthetic plan.
16
Q
How is dissection of the descending aorta managed?
A
Medically managed - surgical repair doesn’t always provide significant benefit.
Eventual surgery.
17
Q
Incidence of abdominal aortic aneurysm in the US in patients over 50
A
3-10%.
18
Q
Independent risk factors for AAA
A
Smoking, male gender, advanced age.
19
Q
S/Sx of AAA
A
Generally symptomless.
Pulsatile abdominal mass detected during routine exam.
20
Q
Primary mechanism for development of AAA
A
Destruction of elastin and collagen that form the matrix of the vessel wall.
Atherosclerosis, inflammation, endothelial dysfunction, and platelet activation may contribute.
21
Q
Which law predicts rupture of an AAA?
A
LaPlace.
Wall tension = Transmural pressure x Vessel radius (increased diameter → increased transmural pressure → increased wall stress).
22
Q
Surgical correction of an AAA is indicated when…
A
the aneurysm exceeds 5.5cm or if it grows more than 0.6-0.8cm/year.
23
Q
When is there 0% risk of AAA rupture?
A
<4cm.
24
Q
When is there a 30-50% chance of AAA rupture?
A
When the AAA is >8cm.
25
Classic triad of AAA rupture
Hypotension, back pain, and pulsatile abdominal mass (only present in 50%).
26
Most AAAs rupture where? What is the most common cause of post op death?
Left retroperitoneum.
## Footnote
Rapid exsanguination usually prevented by clot formation/tamponade effect of retroperitoneum. MI most common cause post op death.
27
Physiologic response to aortic cross clamp is related to 3 factors:
Location of cross-clamp placement, intravascular volume status, cardiac reserve.
28
Application of aortic cross-clamp creates central hypervolemia by...
reducing venous capacity, shifting blood volume proximal to the clamp, and increasing venous return.
29
Removal of aortic cross-clamp creates central hypovolemia by...
restoring venous capacity, shifting blood volume to the lower body, capillary leak, and decreased venous return.
30
Cross-clamping results in O2 starvation of distal tissues, presenting as...
increased lactic acid (metabolic acidosis), increased prostaglandins, complement activation, increased myocardial depressant factors, decreased temperature.
31
Venous Return: After Clamp is placed vs After Clamp is removed
Placed: Increase blood volume proximal to clamp.
Removed: Central hypovolemia and capillary leak.
32
Cardiac output: After Clamp is placed vs After Clamp is removed
Placed: decreased or no change (depends on CV reserve).
Removed: Reduced preload/contractility.
33
MAP: After Clamp is placed vs After Clamp is removed
Placed: increased preload and SVR.
Removed: decreased preload/SVR.
34
After cross-clamp placement, how is SVR affected?
Increased due to mechanical effect of clamp, increased catecholamine release, and increased RAAS activation.
35
After cross-clamp removal, why is SVR decreased?
Washout of anaerobic metabolites, causing vasodilation.
36
PAOP: After Clamp is placed vs After Clamp is removed
Placed: increased/no change in venous return (depends on cv reserve).
Removed: Increased Lactic acidosis causes increased PVR.
37
LV wall stress: After Clamp is placed vs After Clamp is removed
Placed: increased preload/afterload.
Removed: decreased preload/afterload.
38
MVO2: After Clamp is placed vs After Clamp is removed
Placed: increased preload, wall stress, afterload.
Removed: decreased preload and afterload.
39
Coronary Blood Q: After Clamp is placed vs After Clamp is removed
Placed: Increased aortic DBP.
Removed: decreased AoDBP.
40
Renal Blood Q: After Clamp is placed vs After Clamp is removed
Placed: >30min increased risk AFR.
Removed: decreased/no change depends on MAP.
41
Total Body VO2: After Clamp is placed vs After Clamp is removed
Placed: Anaerobic metabolism.
Removed: aerobic metabolism.
42
SVO2: After Clamp is placed vs After Clamp is removed
Placed: increased; d/t decreased TB VO2 (less O2 consumed more left over).
Removed: decreased; increased TBVO2 (more O2 consumed less left over).
43
Spinal cord circulation consists of...
2 posterior spinal arteries, 1 anterior spinal artery, 6-8 radicular arteries.
44
Circulation sequence to posterior spinal arteries
Aorta - subclavian artery - vertebral artery - posterior spinal artery.
Aorta - segmental artery - posterior radicular artery - posterior spinal artery (perfuses posterior 1/3 of spinal cord).
45
What do the posterior spinal arteries perfuse?
Posterior 1/3 of the spinal cord.
46
Circulation sequence to anterior spinal artery
Aorta - subclavian artery - vertebral artery - anterior spinal artery.
Aorta - segmental artery - anterior radicular artery - anterior spinal artery (perfuses anterior 2/3 spinal cord).
47
What does the anterior spinal artery perfuse?
Anterior 2/3 of spinal cord.
48
What perfuses the anterior spinal cord in the thoracolumbar region?
Artery of Adamkiewicz - most important.
49
The artery of Adamkiewicz most commonly originates...
on the left side between T11-T12.
## Footnote
In 75%, originates T8-12, in 10% at L1-L2.
50
Watershed areas of the spinal cord
Areas where there is only a single blood supply.
## Footnote
Vulnerable to ischemia.
51
____ spinal artery syndrome is also called Beck's syndrome
Anterior.
52
What can cause anterior spinal artery syndrome?
Aortic cross-clamp above the artery of Adamkiewicz, resulting in ischemia to the lower portion of the anterior spinal cord.
53
S/Sx of anterior spinal artery syndrome
Flaccid paralysis of lower extremities, bowel and bladder dysfunction, loss of temperature and pain sensation.
54
What type of sensation is preserved with anterior spinal artery syndrome?
Touch and proprioception.
55
The corticospinal tract is perfused by...
the anterior blood supply.
## Footnote
why patient presents with flaccid paralysis of lower extremities.
56
Autonomic motor fibers are perfused by...
the anterior blood supply.
## Footnote
why patients experiences bowel/bladder dysfunction.
57
The spinothalamic tract is perfused by...
the anterior blood supply.
## Footnote
why patient loses pain and temp sensation.
58
The dorsal column is perfused by...
the posterior blood supply.
## Footnote
why touch and proprioception are spared.
59
Thoracic clamp times of how long pose significant risk for cord ischemia?
>30 minutes.
60
Spinal cord protection strategies
1. Moderate hypothermia to 30-32 degrees - to reduce cord O2 consumption.
2. CSF drainage - perfusion depends on pressure gradient of anterior spinal artery to CSF (draining CSF increases gradient).
3. Proximal HTN during cross-clamping (MAP ~100 mmHg).
4. Avoid hyperglycemia.
5. SSEP/MEPs (SSEP only monitors posterior cord).
6. Partial CPB.
7. Corticosteroids, CCBs, mannitol.
61
Amaurosis fugax
Blindness in one eye.
## Footnote
Sign of impending stroke. Emboli travel from internal carotid artery to ophthalmic artery.
62
Amaurosis fugax occurs in ______% patients with high grade carotid stenosis
25%.
63
Regional anesthesia for CEA includes...
Local infiltration, superficial cervical plexus block (C2-C4), deep cervical plexus block (C2-C4).
64
Best method to assess cerebral perfusion and neurologic integrity during CEA
Awake patient.
65
What will an EEG not detect during CEA?
Subcortical problems.
66
What on an EEG indicates risk of cerebral hypoperfusion?
Loss of amplitude, decreased beta wave activity, and/or appearance of slow wave activity.
67
Possible causes of increased frequency on EEG
Mild hypercarbia, early hypoxia, seizure activity, ketamine, N2O, light anesthesia.
68
Possible causes of decreased frequency on EEG
Extreme hypercarbia, hypoxia, cerebral ischemia, hypothermia, anesthetic overdose, opioids.
69
What do you use to monitor cerebral oximetry?
Near-infrared spectroscopy (NIRS) to monitor o2 sat in frontal lobe.
70
When is cerebral perfusion considered at risk when monitoring cerebral oximetry?
When rSO2 is reduced >25% from baseline.
71
What does a transcranial doppler do?
Assesses continuous blood flow velocity in the middle cerebral artery, where most emboli lodge.
72
SSEP
Monitors sensory pathway only.
## Footnote
Requires light GA (volatiles decrease amplitude/increases latency - looks like ischemia).
73
Rotation, flexion, extension of the head can:
Compress carotid/vertebral arteries (reducing cerebral perfusion).
74
Hyperglycemia day of surgery is associated with:
(POCT >200) increased risk stroke/death.
75
Normocapnia or mild hypocapnia should be______- cerebral vessels distal to point of stenosis may be_______.
Maintained; max dilated.
76
Hypercarbia _____ all cerebral vessels and create a ______ phenomena by shunting blood away from ________ tissue
dilates; steal; hypoperfused cerebral.
77
After the carotid artery is cross-clamped, ipsilateral cerebral perfusion relies on...
collateral flow from the circle of Willis.
78
Cerebral Perfusion pressure equation
CPP = MAP - CVP (or use ICP - whichever is higher).
79
Anesthetic technique during carotid cross-clamping for CEA
Give Phenylephrine, reduce anesthetic depth.
## Footnote
Normal or slightly high BP (the ischemic regions of the brain are max dilated and lose autoregulation & become pressure dependent).
80
Anesthetic technique after carotid cross-clamping for CEA
Reduce BP to <145 mmHg to prevent reperfusion injury and cerebral edema.
81
What is the anesthetic technique after carotid cross-clamping for CEA?
Reduce BP to <145 mmHg to prevent reperfusion injury and cerebral edema.
## Footnote
Give vasodilators or labetalol.
82
What does stump pressure monitor?
Perfusion pressure in the carotid artery on the operative side.
83
What is the risk of cerebral hypoperfusion if stump pressure is below what value?
<50 mmHg.
84
Where should a shunt be placed if needed during CEA?
Distal to the carotid cross-clamp.
## Footnote
Increases risk of embolic stroke.
85
What is a possible complication of CEA that is considered an airway emergency?
Hematoma can compromise airway; cric or trach may be required.
## Footnote
Surgeon not available - remove sutures and decompress wound.
86
Which nerve may be damaged during CEA and what are the signs and symptoms?
Ipsilateral RLN.
## Footnote
Paralyzed ipsilateral vocal cord, resulting in hoarseness and inspiratory stridor.
87
What is the usual cause of postoperative stroke following a CEA?
Embolic phenomena (NOT hypotension/hyperperfusion).
88
What happens when baroreceptors are exposed?
Alters their sensitivity.
89
Is hypertension or hypotension more likely to occur after CEA?
Hypertension - subsides in 24 hours.
90
What can hypertension lead to after CEA?
1. Reperfusion injury, cerebral edema, hematoma.
2. Reduction in CPP.
91
What may occur with carotid body denervation during CEA?
Reduction of the ventilatory response to hypoxia.
92
What does Carotid Artery Angioplasty Stenting (CAS) use?
Percutaneous transvascular access to pass stent into carotid artery.
93
How much heparin do you give for carotid artery angioplasty stenting and what should the ACT be?
50-100 units/kg.
## Footnote
Maintain ACT >250-300.
94
What may occur with balloon inflation during carotid artery angioplasty stenting?
Baroreceptor response leads to bradycardia and hypotension.
## Footnote
Can pretreat with atropine or glycopyrrolate.
95
What is the most common complication from carotid artery angioplasty stenting?
Thromboembolic stroke.
## Footnote
Distal protection filter placed beyond angioplasty balloon will catch most debris. Embolic stroke treatment with TPA.
96
What is subclavian steal syndrome?
Occurs when there is an occlusion of the subclavian or innominate artery proximal to the origin of the ipsilateral vertebral artery.
## Footnote
Usually occurs on the left side.
97
On which side does subclavian occlusion usually occur?
Left.
98
What does subclavian steal syndrome result in?
Reversal of blood flow, where vertebral blood follows a pressure gradient toward the ipsilateral subclavian artery.
## Footnote
Blood is 'stolen' from the posterior cerebral circulation where it's diverted to the ipsilateral arm.
99
What are the signs and symptoms of subclavian steal syndrome?
Syncope, vertigo, ataxia, hemiplegia, arm ischemia, weak pulse, BP much lower in ipsilateral arm.
100
What is the treatment of subclavian steal syndrome?
Subclavian endarterectomy.
