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.

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2
Q

Crawford: Type 2 aortic aneurysm

A

All or most of the descending thoracic aorta and most of the abdominal aorta.

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3
Q

Crawford: Type 3 aortic aneurysm

A

Lower descending thoracic aorta only and most of the abdominal aorta.

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4
Q

Crawford: Type 4 aortic aneurysm

A

No part of the descending thoracic aorta and most of the abdominal aorta.

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5
Q

Aortic dissections are classified based on location using two systems:

A

Stanford and DeBakey.

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6
Q

Aortic aneurysms are classified based on region of the aorta affected using…

A

the Crawford classification system.

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7
Q

Stanford Type A dissection

A

Involves ascending aorta.

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8
Q

Stanford Type B dissection

A

Does not involve the ascending aorta.

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9
Q

DeBakey: Type 1 dissection

A

Tear in ascending aorta and dissection along entire aorta.

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10
Q

DeBakey: Type 2 dissection

A

Tear in ascending aorta and dissection only in ascending aorta.

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11
Q

DeBakey: Type 3a dissection

A

Tear in proximal descending aorta where dissection is limited to the thoracic aorta.

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12
Q

DeBakey: Type 3b dissection

A

Tear in the proximal descending aorta with dissection along thoracic and abdominal aorta.

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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.

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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).

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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.

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16
Q

How is dissection of the descending aorta managed?

A

Medically managed - surgical repair doesn’t always provide significant benefit.

Eventual surgery.

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17
Q

Incidence of abdominal aortic aneurysm in the US in patients over 50

A

3-10%.

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18
Q

Independent risk factors for AAA

A

Smoking, male gender, advanced age.

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19
Q

S/Sx of AAA

A

Generally symptomless.

Pulsatile abdominal mass detected during routine exam.

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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.

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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).

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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.

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23
Q

When is there 0% risk of AAA rupture?

A

<4cm.

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24
Q

When is there a 30-50% chance of AAA rupture?

A

When the AAA is >8cm.

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25
Q

Classic triad of AAA rupture

A

Hypotension, back pain, and pulsatile abdominal mass (only present in 50%).

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26
Q

Most AAAs rupture where? What is the most common cause of post op death?

A

Left retroperitoneum.

Rapid exsanguination usually prevented by clot formation/tamponade effect of retroperitoneum. MI most common cause post op death.

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27
Q

Physiologic response to aortic cross clamp is related to 3 factors:

A

Location of cross-clamp placement, intravascular volume status, cardiac reserve.

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28
Q

Application of aortic cross-clamp creates central hypervolemia by…

A

reducing venous capacity, shifting blood volume proximal to the clamp, and increasing venous return.

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29
Q

Removal of aortic cross-clamp creates central hypovolemia by…

A

restoring venous capacity, shifting blood volume to the lower body, capillary leak, and decreased venous return.

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30
Q

Cross-clamping results in O2 starvation of distal tissues, presenting as…

A

increased lactic acid (metabolic acidosis), increased prostaglandins, complement activation, increased myocardial depressant factors, decreased temperature.

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31
Q

Venous Return: After Clamp is placed vs After Clamp is removed

A

Placed: Increase blood volume proximal to clamp.
Removed: Central hypovolemia and capillary leak.

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32
Q

Cardiac output: After Clamp is placed vs After Clamp is removed

A

Placed: decreased or no change (depends on CV reserve).
Removed: Reduced preload/contractility.

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33
Q

MAP: After Clamp is placed vs After Clamp is removed

A

Placed: increased preload and SVR.
Removed: decreased preload/SVR.

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34
Q

After cross-clamp placement, how is SVR affected?

A

Increased due to mechanical effect of clamp, increased catecholamine release, and increased RAAS activation.

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35
Q

After cross-clamp removal, why is SVR decreased?

A

Washout of anaerobic metabolites, causing vasodilation.

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36
Q

PAOP: After Clamp is placed vs After Clamp is removed

A

Placed: increased/no change in venous return (depends on cv reserve).
Removed: Increased Lactic acidosis causes increased PVR.

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37
Q

LV wall stress: After Clamp is placed vs After Clamp is removed

A

Placed: increased preload/afterload.
Removed: decreased preload/afterload.

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38
Q

MVO2: After Clamp is placed vs After Clamp is removed

A

Placed: increased preload, wall stress, afterload.
Removed: decreased preload and afterload.

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39
Q

Coronary Blood Q: After Clamp is placed vs After Clamp is removed

A

Placed: Increased aortic DBP.
Removed: decreased AoDBP.

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40
Q

Renal Blood Q: After Clamp is placed vs After Clamp is removed

A

Placed: >30min increased risk AFR.
Removed: decreased/no change depends on MAP.

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41
Q

Total Body VO2: After Clamp is placed vs After Clamp is removed

A

Placed: Anaerobic metabolism.
Removed: aerobic metabolism.

42
Q

SVO2: After Clamp is placed vs After Clamp is removed

A

Placed: increased; d/t decreased TB VO2 (less O2 consumed more left over).
Removed: decreased; increased TBVO2 (more O2 consumed less left over).

43
Q

Spinal cord circulation consists of…

A

2 posterior spinal arteries, 1 anterior spinal artery, 6-8 radicular arteries.

44
Q

Circulation sequence to posterior spinal arteries

A

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
Q

What do the posterior spinal arteries perfuse?

A

Posterior 1/3 of the spinal cord.

46
Q

Circulation sequence to anterior spinal artery

A

Aorta - subclavian artery - vertebral artery - anterior spinal artery.
Aorta - segmental artery - anterior radicular artery - anterior spinal artery (perfuses anterior 2/3 spinal cord).

47
Q

What does the anterior spinal artery perfuse?

A

Anterior 2/3 of spinal cord.

48
Q

What perfuses the anterior spinal cord in the thoracolumbar region?

A

Artery of Adamkiewicz - most important.

49
Q

The artery of Adamkiewicz most commonly originates…

A

on the left side between T11-T12.

In 75%, originates T8-12, in 10% at L1-L2.

50
Q

Watershed areas of the spinal cord

A

Areas where there is only a single blood supply.

Vulnerable to ischemia.

51
Q

____ spinal artery syndrome is also called Beck’s syndrome

52
Q

What can cause anterior spinal artery syndrome?

A

Aortic cross-clamp above the artery of Adamkiewicz, resulting in ischemia to the lower portion of the anterior spinal cord.

53
Q

S/Sx of anterior spinal artery syndrome

A

Flaccid paralysis of lower extremities, bowel and bladder dysfunction, loss of temperature and pain sensation.

54
Q

What type of sensation is preserved with anterior spinal artery syndrome?

A

Touch and proprioception.

55
Q

The corticospinal tract is perfused by…

A

the anterior blood supply.

why patient presents with flaccid paralysis of lower extremities.

56
Q

Autonomic motor fibers are perfused by…

A

the anterior blood supply.

why patients experiences bowel/bladder dysfunction.

57
Q

The spinothalamic tract is perfused by…

A

the anterior blood supply.

why patient loses pain and temp sensation.

58
Q

The dorsal column is perfused by…

A

the posterior blood supply.

why touch and proprioception are spared.

59
Q

Thoracic clamp times of how long pose significant risk for cord ischemia?

A

> 30 minutes.

60
Q

Spinal cord protection strategies

A
  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
Q

Amaurosis fugax

A

Blindness in one eye.

Sign of impending stroke. Emboli travel from internal carotid artery to ophthalmic artery.

62
Q

Amaurosis fugax occurs in ______% patients with high grade carotid stenosis

63
Q

Regional anesthesia for CEA includes…

A

Local infiltration, superficial cervical plexus block (C2-C4), deep cervical plexus block (C2-C4).

64
Q

Best method to assess cerebral perfusion and neurologic integrity during CEA

A

Awake patient.

65
Q

What will an EEG not detect during CEA?

A

Subcortical problems.

66
Q

What on an EEG indicates risk of cerebral hypoperfusion?

A

Loss of amplitude, decreased beta wave activity, and/or appearance of slow wave activity.

67
Q

Possible causes of increased frequency on EEG

A

Mild hypercarbia, early hypoxia, seizure activity, ketamine, N2O, light anesthesia.

68
Q

Possible causes of decreased frequency on EEG

A

Extreme hypercarbia, hypoxia, cerebral ischemia, hypothermia, anesthetic overdose, opioids.

69
Q

What do you use to monitor cerebral oximetry?

A

Near-infrared spectroscopy (NIRS) to monitor o2 sat in frontal lobe.

70
Q

When is cerebral perfusion considered at risk when monitoring cerebral oximetry?

A

When rSO2 is reduced >25% from baseline.

71
Q

What does a transcranial doppler do?

A

Assesses continuous blood flow velocity in the middle cerebral artery, where most emboli lodge.

72
Q

SSEP

A

Monitors sensory pathway only.

Requires light GA (volatiles decrease amplitude/increases latency - looks like ischemia).

73
Q

Rotation, flexion, extension of the head can:

A

Compress carotid/vertebral arteries (reducing cerebral perfusion).

74
Q

Hyperglycemia day of surgery is associated with:

A

(POCT >200) increased risk stroke/death.

75
Q

Normocapnia or mild hypocapnia should be______- cerebral vessels distal to point of stenosis may be_______.

A

Maintained; max dilated.

76
Q

Hypercarbia _____ all cerebral vessels and create a ______ phenomena by shunting blood away from ________ tissue

A

dilates; steal; hypoperfused cerebral.

77
Q

After the carotid artery is cross-clamped, ipsilateral cerebral perfusion relies on…

A

collateral flow from the circle of Willis.

78
Q

Cerebral Perfusion pressure equation

A

CPP = MAP - CVP (or use ICP - whichever is higher).

79
Q

Anesthetic technique during carotid cross-clamping for CEA

A

Give Phenylephrine, reduce anesthetic depth.

Normal or slightly high BP (the ischemic regions of the brain are max dilated and lose autoregulation & become pressure dependent).

80
Q

Anesthetic technique after carotid cross-clamping for CEA

A

Reduce BP to <145 mmHg to prevent reperfusion injury and cerebral edema.

81
Q

What is the anesthetic technique after carotid cross-clamping for CEA?

A

Reduce BP to <145 mmHg to prevent reperfusion injury and cerebral edema.

Give vasodilators or labetalol.

82
Q

What does stump pressure monitor?

A

Perfusion pressure in the carotid artery on the operative side.

83
Q

What is the risk of cerebral hypoperfusion if stump pressure is below what value?

84
Q

Where should a shunt be placed if needed during CEA?

A

Distal to the carotid cross-clamp.

Increases risk of embolic stroke.

85
Q

What is a possible complication of CEA that is considered an airway emergency?

A

Hematoma can compromise airway; cric or trach may be required.

Surgeon not available - remove sutures and decompress wound.

86
Q

Which nerve may be damaged during CEA and what are the signs and symptoms?

A

Ipsilateral RLN.

Paralyzed ipsilateral vocal cord, resulting in hoarseness and inspiratory stridor.

87
Q

What is the usual cause of postoperative stroke following a CEA?

A

Embolic phenomena (NOT hypotension/hyperperfusion).

88
Q

What happens when baroreceptors are exposed?

A

Alters their sensitivity.

89
Q

Is hypertension or hypotension more likely to occur after CEA?

A

Hypertension - subsides in 24 hours.

90
Q

What can hypertension lead to after CEA?

A
  1. Reperfusion injury, cerebral edema, hematoma.
  2. Reduction in CPP.
91
Q

What may occur with carotid body denervation during CEA?

A

Reduction of the ventilatory response to hypoxia.

92
Q

What does Carotid Artery Angioplasty Stenting (CAS) use?

A

Percutaneous transvascular access to pass stent into carotid artery.

93
Q

How much heparin do you give for carotid artery angioplasty stenting and what should the ACT be?

A

50-100 units/kg.

Maintain ACT >250-300.

94
Q

What may occur with balloon inflation during carotid artery angioplasty stenting?

A

Baroreceptor response leads to bradycardia and hypotension.

Can pretreat with atropine or glycopyrrolate.

95
Q

What is the most common complication from carotid artery angioplasty stenting?

A

Thromboembolic stroke.

Distal protection filter placed beyond angioplasty balloon will catch most debris. Embolic stroke treatment with TPA.

96
Q

What is subclavian steal syndrome?

A

Occurs when there is an occlusion of the subclavian or innominate artery proximal to the origin of the ipsilateral vertebral artery.

Usually occurs on the left side.

97
Q

On which side does subclavian occlusion usually occur?

98
Q

What does subclavian steal syndrome result in?

A

Reversal of blood flow, where vertebral blood follows a pressure gradient toward the ipsilateral subclavian artery.

Blood is ‘stolen’ from the posterior cerebral circulation where it’s diverted to the ipsilateral arm.

99
Q

What are the signs and symptoms of subclavian steal syndrome?

A

Syncope, vertigo, ataxia, hemiplegia, arm ischemia, weak pulse, BP much lower in ipsilateral arm.

100
Q

What is the treatment of subclavian steal syndrome?

A

Subclavian endarterectomy.