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Part 2 exam > Vascular > Flashcards

Vascular Flashcards

1
Q

What are the types of patients that present for carotid endarterectomy?

A

Symptomatic with TIAs/strokes (strong evidence for them if >70% stenosis)
Asymptomatic but significant carotid bifurcation disease (weaker evidence)

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2
Q

What are the clinical implications of carotid clamping?

A

Carotid clamping will result in a decrease of cerebral perfusion that should be compensated by a patent circle of willis, however if there isn’t a complete circle of willis or cerebrovascular disease elsewhere then this is risk of cerebral hypoperfusion or hypoxia

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3
Q

How can you assess cerebral perfusion during carotid endarterectomy?

A
  • Continous neurological assessment
  • EEG
  • SSEPs
  • NIRS
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4
Q

What are the complications of a carotid endartectomy?

A

A - Vocal cord palsy, local haematoma causing airway compromise
B - Altered Carotid body receptors to CO2
C - Severe bradycardia/hypotension due to carotid body traction
Haemodynamic instability (often hypertension, can be hypoxia/pain/blunting of carotid mechanism/hypercabia)
Myocardial infarction
D - Stroke
Cerebral hyperperfusion syndrome

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5
Q

What is the arterial supply to the spinal cord?

A

Two supplies. One that descends vertically from the brainstem (runs the length of the cord) and then segmental arteries at each level

  • Cephalic vertically descending : Subclavian artery –> vertebral artery -> anterior spinal artery –> anterior 2/3 of spinal cord

Vertebral artery –> two posterior spinal arteries –> supply posterior 1/3 of spinal cord

  • Segmental vessels (segmental spinal artery): the origin depends on where in the spinal cord it is

Cervical: vertebral artery, deep cervical artery
Thorax: posterior intercostal artery (from aorta)
Abdomen: Lumbar artery

Origin artery (as above) –> Segmental spinal artery –> anterior and posterior radicular artery

At some levels there is an extra supply coming from the segmental artery that joins directly to the anterior and posterior spinal artery that reinforces blood supply from the descending arteries. Most important is the artery of adamkiewicz that arises in lower thoracic/upper lumbar region and helps reinforce the blood supply to the lower third of the spinal cord

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6
Q

What are risk factors for spinal cord ischaemia?

A
  • Supra-renal EVAR
  • Long stent graft that occludes collaterals
  • Hypoperfusion
  • Thrombosis
  • Previous AAA repair
  • Long procedure, extensive manupulations of intravascular catheters (microembolism)
  • Anaemia
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7
Q

What causes spinal cord ischaemia in Aortic repairs?

A
  • Aortic cross clamp
  • Sacrifice of segmental arterial branches (due to stent covering)
  • Circulatory arrest
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8
Q

What are spinal cord protection strategies?

A
  1. Make cord more tolerant to ischaemia: hypothermia, neuroprotective agents eg steroids, thiopentone (nil evidence for these)
  2. Minimise duration of cord ischaemia (Gott shunt which shunts from proximal aorta to post cross clamp)
  3. Early detection of ischaemia: avoid using LA for neuraxial techniques to allow for early examination, intraop spinal cord monitoring
  4. Augment spinal cord perfusion: prevent hypotension (aim MAP >80), prevent anaemia, decrease CSF pressure (lumbar drain), maintain low CVP
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9
Q

What are the anaesthetic goals of EVAR?

A
  • Lie still for 1-3 hrs
  • Maintain normotension
  • Minimise contrast nephropathy and radiation
  • Management of haemorrage
  • Temperature control
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10
Q

What is the pathophysiology of peripheral vascular disease?

A

Generalised atherosclerosis
Process is dyslipidaemia, endothelial dysfunction, inflammation, oxidative stress, hypercoaguability
Causes progressive luminal reduction leading to exercise induced ischaemia or acute ischaemia due to plaque rupture and thrombosis

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11
Q

What are the common co-morbidities of vascular patients?

A
  • Diabetes
  • Hypertension
  • High cholesterol
  • Smoking
  • Cardiac disease
  • Renal impairment
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12
Q

What is the rifle criteria?

A
  • Objective criteria to identify renal impairment
    R: Risk = Increased creat x 1.5, UO < 0.5ml/kg/hr x 6hrs
    I: Injury = Increased creat x 2, UO <0.5 for 12 hrs
    F: Failure = Increased creat x 3, UO < 0.3 for 24hrs or anuric for 12hrs
    L: Loss = Persistent ARF for > 4 weeks
    E: End stage renal disease
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13
Q

What are the implications for patients having surgery for peripheral arterial occlusive disease?

A

Patient:
Often significant co-morbidities
May have further embolic events from uncontained source

Surgical:
Open vs endovascular clot retrieval
Remote environment
Radiation safety
Reperfusion syndrome

Anaesthetic:
Likely emergency surgery = unfasted patient
may be obtunded from pain relief
Could be anticoagulated = nil regional

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14
Q

What are the implications for patients having surgery for carotid stenosis?

A

Patient:
Recent strokes?
Co-morbidities

Surgical:
Shunt vs no shunt

Anaesthetic:
GA vs local -> allows for awake monitoring vs cerebral monitoring
Maintain adequate BP for cerebral perfusion

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15
Q

What are the implications for patients having surgery for haemodialysis?

A

Patient:
Aeitology of renal disease
Stability of renal disease
Recent dialysis
Urine production
Fluid restrictions

Surgical:
Emergency vs elective procedure
Type of access device inserted

Anaesthetic:
Regional vs GA, usually regional (supraclavicular or axillary block

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16
Q

What are the implications for patients having surgery for thoracoscopic sympathectomy?

A
  • Usually ASA1 patient young with hyperhidrosis but can be ASA 4 with refractory angina
  • GA with DLT, art line and large IV
  • Lateral positioning
  • Risk of post op pneumothorax
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17
Q

What are risks of regional technqiues in vascular surgery?

A
  • Failure
  • Haematoma
  • Nerve injury
  • Prolonged motor blockade
  • Prolonged altered sensation
18
Q

How do patients with ruptured AAA present?

A

Haemodynamically stable (contained rupture)
Haemodynamically unstable (uncontained rupture) - require immediate surgical control by clamping the aorta

19
Q

What pre-op planning is required for a ruptured AAA?

A
  • Communicate and alert staff
  • Have a theatre available
  • Have equipment eg Cell saver, art line, central line, rapid infusor eg Belmont
  • Have blood available
  • Prepare drugs
20
Q

What is the intra-op set up for ruptured AAA?

A
  • Large i.e 14g access
  • CVC
  • Art line
  • IDC
  • Vasoactive drugs eg GTN and noradrenaline
  • Induction is high risk as relaxation of abdo muscles can release tamponade and cause arrest thus do when surgeon is ready and patient prepped and draped
  • Judicious use of anaesthetic agents but also minmising hypertension from laryngoscopy i.e midaz, ket and rocuronium
  • Monitor temp (hypothermia will worsen coagulopathy)
  • Fluid management is crystalloids 5-7mls/kg/hr + colloids if needed and cell salvage
21
Q

What is the post op path for ruptured AAA?

A
  • Remain intubated + sedated and taken to ICU
  • Due to hypothermia, acidemia, large fluid shifts and transfusion
22
Q

What are the classifications for aortic dissection?

A

DeBakey:
1 = Begins in ascending aorta and extends to aortic arch or beyond
2 = Involves ascending aorta only
3 = Begins in descending aorta (often distal to left subclavian)

Stanford:
A = Involves ascending aorta (will require surgery)
B = does not involve ascending aorta (may not require surgery)

23
Q

What are risk factors for aortic dissection?

A

HTN (75%)
Genetic disorders
Cocaine use
Heavy lifting
Inflammatory conditions eg giant cell arteritis
Pregnancy

24
Q

What physical exam findings might you get with aortic dissection?

A

Pulse deficits
AR regurg
Syncope
Acute neurological issues paraplegia etc

25
Q

What is the medical management of aortic dissection?

A
  • Manage BP eg esmolol or labetalol infusions
  • Analgesia
26
Q

What is important for descending thoracic aorta aneurysm repairs?

A

Will be a left lateral thoracotomy possibly with cross clamp proximal to left subclavian artery therefore need right radial arterial line

27
Q

What are the effects of aortic cross clamping?

A
  • Dependent on the level of clamping, more proximal = bigger effect

Haemodynamic:
Increased afterload
Increased venous return
Increased contractility (due to larger LVEDV)
Increased myocardial work -> risk of ischaemia
Decreased renal blood flow (even if infra-renal)
Decreased spinal blood flow (due to loss of segmental supply especially to distal spinal cord)
Reduced bowel blood supply (espc Inferior mesenteric artery which is descending colon)

Neurohumeral:
Activation of RAAS
Sympathetic activation and increased catecholamines

28
Q

How can you mitigate the effects of aortic cross clamping?

A
  • Minimise cross clamp time
  • Minimal fluid load prior to cross clamping
  • Vasodilators i.e GTN
  • Nil warming of lower limb
  • Spinal cord monitoring
  • Spinal drain
  • Distal clamp as possible (less likely to get artery of adamkiewicz)
29
Q

What is the management of severe intraoperative haemorrhage

A
  • Call for help
  • Confirm there is surgical effort to control bleeding
  • 100% oxygen
  • Warm fluids, warm patient, warm theatre
  • Use vasopressors only as absolutely neccessary
  • Insert 2 x 14g cannulae, consider an 8.5F PA sheath
  • Use rapid infuser and cell saver
  • Consider TXA
  • Monitor acidosis, Ca, fibrinogen
30
Q

What is the management of intraoperative myocardial ischaemia?

A
  • 100% oxygen
  • Confirm there is adequate ventilation, anaesthesia, analgesia
  • Control the heart rate (introduce beta blockers)
  • GTN infusion
  • Maintain BP
  • Consider anticoagulation/PCI/cardiology input
31
Q

What is the difference between stump pain and phantom limb pain?

A

Stump pain is localised to the site of amputation
Phantom limb pain is noxious sensory phenomenon in the missing limb

32
Q

What increases the risk of phantom limb pain?

A
  • severe pre amputation pain
  • Poorly controlled postoperative stump pain
  • Chemotherapy
33
Q

What can prevent post amputation pain?

A
  • nil good evidence but usually regional either epidural or nerve sheath catheters
  • Ketamine started prior to skin incision and continued as an infusion for 72 hrs may reduce the incidence of severe phantom limb pain
34
Q

What is the treatment of established phantom limb pain?

A
  • Calcitonin infusion for 48hrs
  • Ketamine (short term)
  • Opioids and gabapentin
  • Lignocaine helps with stump pain but nil effect on phantom pain
35
Q

How do you perform a superficial cervical plexus block?

A
  • Landmarks are the mastoid process, clavicular head of SCM and midpoint of the posteiror border of SCM (imagine its a straight line from collarbone to mastoid behind ear on posterior border of SCM)
  • Needle is inserted along the posterior border (around the midpoint between the clavicle and mastoid) of the SCM and 3 injections of 5ml LA in a fan fashion (cephalad, caudad and perpendicularly)
36
Q

What nerves does a superficial cervical plexus block anaesthetise?

A

C2-4 which supplies four cutaneous branches to the neck

Greater auricular
Lesser occipital
Transverse cervical
Supraclavicular

37
Q

What are the implications of the location of IR service?

A

-Isolated/remote environment: unfamiliar environment+staff+equipement
- Limited access to patient due to IR equipment
- Radiation exposure

38
Q

What are implications of patients having endovascular embolisations?

A
  • Usually for vascular malformations, tumours and haemorrhage
  • Procedures that are superficial, involve AV malformations and use of alcohol are very painful = need GA
39
Q

What are pre op considerations for an elective EVAR?

A
  • Pre op assessment for cardioresp disease, renal disease, diabetes and stroke
  • Review medicaitions and optomise
  • Consideration of preop spinal drain
40
Q

What are some of the considerations intraop for an elective EVAR?

A
  • GAs including breath holds so ETT and paralysis
  • Long IV lines and monitoring cables as limited access to patient
  • Use of heparin
  • Risk of radiation
  • Large IV access, arterial line +/- CVC
41
Q

What is the use of EVAR for emergency ruptured AAAs?

A
  • As long as amnedable to EVAR the IMPROVE trial showed improved mortality at 3 years and improved QOL, nil difference at 7 years

Part 2 exam (15 decks)

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