Vascular Flashcards
(41 cards)
What are the types of patients that present for carotid endarterectomy?
Symptomatic with TIAs/strokes (strong evidence for them if >70% stenosis)
Asymptomatic but significant carotid bifurcation disease (weaker evidence)
What are the clinical implications of carotid clamping?
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
How can you assess cerebral perfusion during carotid endarterectomy?
- Continous neurological assessment
- EEG
- SSEPs
- NIRS
What are the complications of a carotid endartectomy?
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
What is the arterial supply to the spinal cord?
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
What are risk factors for spinal cord ischaemia?
- Supra-renal EVAR
- Long stent graft that occludes collaterals
- Hypoperfusion
- Thrombosis
- Previous AAA repair
- Long procedure, extensive manupulations of intravascular catheters (microembolism)
- Anaemia
What causes spinal cord ischaemia in Aortic repairs?
- Aortic cross clamp
- Sacrifice of segmental arterial branches (due to stent covering)
- Circulatory arrest
What are spinal cord protection strategies?
- Make cord more tolerant to ischaemia: hypothermia, neuroprotective agents eg steroids, thiopentone (nil evidence for these)
- Minimise duration of cord ischaemia (Gott shunt which shunts from proximal aorta to post cross clamp)
- Early detection of ischaemia: avoid using LA for neuraxial techniques to allow for early examination, intraop spinal cord monitoring
- Augment spinal cord perfusion: prevent hypotension (aim MAP >80), prevent anaemia, decrease CSF pressure (lumbar drain), maintain low CVP
What are the anaesthetic goals of EVAR?
- Lie still for 1-3 hrs
- Maintain normotension
- Minimise contrast nephropathy and radiation
- Management of haemorrage
- Temperature control
What is the pathophysiology of peripheral vascular disease?
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
What are the common co-morbidities of vascular patients?
- Diabetes
- Hypertension
- High cholesterol
- Smoking
- Cardiac disease
- Renal impairment
What is the rifle criteria?
- 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
What are the implications for patients having surgery for peripheral arterial occlusive disease?
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
What are the implications for patients having surgery for carotid stenosis?
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
What are the implications for patients having surgery for haemodialysis?
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
What are the implications for patients having surgery for thoracoscopic sympathectomy?
- 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
What are risks of regional technqiues in vascular surgery?
- Failure
- Haematoma
- Nerve injury
- Prolonged motor blockade
- Prolonged altered sensation
How do patients with ruptured AAA present?
Haemodynamically stable (contained rupture)
Haemodynamically unstable (uncontained rupture) - require immediate surgical control by clamping the aorta
What pre-op planning is required for a ruptured AAA?
- 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
What is the intra-op set up for ruptured AAA?
- 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
What is the post op path for ruptured AAA?
- Remain intubated + sedated and taken to ICU
- Due to hypothermia, acidemia, large fluid shifts and transfusion
What are the classifications for aortic dissection?
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)
What are risk factors for aortic dissection?
HTN (75%)
Genetic disorders
Cocaine use
Heavy lifting
Inflammatory conditions eg giant cell arteritis
Pregnancy
What physical exam findings might you get with aortic dissection?
Pulse deficits
AR regurg
Syncope
Acute neurological issues paraplegia etc
