Vascular Flashcards
What are the indications for AAA repair?
What are the risk factors?
How are they classified
OPEN Vs EVAR
surigcal intervention (size and growth) >5.5cm AP diametre , or symptomatic which is clinically rather than radiological.
Male (4-8%), Age (65-80), Family History, Smoking (also increases rate of growth)
Relationship to renal arteries
Most occur between renal and IMA
Only 5% involve renal and visceral arteries
40% associated with illiac artery aneurysm.
Push towards EVAR over past decade
better short term survival BUT no survivaldifference at 5 years.
EVAR associated with increased risk of complications, reinterventions and cost.
Certainly has a reduced LOS ~2 vs 8 days
How do we risk stratify AAA candidates?
MDT
Risk Scores such as the British Aneurysm Repair score
Scoring systems can be used to supplement clinical judgement of experienced surgeons and anaesthetists
Current risk models are subjective with variations in the definition of diagnosis,
They rarely reflect the severity or duration that an individual has been exposed to the disease.
Consideration can be given to CPET - low/sub thershold values associated with reduced life expectancy post EVAR
Biochemical markers such as NTproBNP is a valuable predictor, becoming more widely used,
How do we preop evaluate and optimise for AAA repair
Stratifying risk
Counselling patient
TIMING
CVS - evidence of IHD? should be on aspirin and statin, continue Bblockers if already on.
? dobutamine stress test.
Resp - evidence of COPD - manage. Otherwise optimise. If steriod responsive consider short course of steroids.
Anaesthetic Technique for Elective AAA
Preop
Risk stratifying, optimisation, counselling
Group and Hold
Intra Op
Analgesia
- thoracic epidural
Monitoring
5 lead ECG
IAL
CVC
Airway
ETT
Blood
Monitor blood loss
POCT
Cell saver
Cross clamping
Post op
ICU
Aim to extubate
May stay intubated profound metabolic acidosis, refractory hypotermia, resp failure, high pressor support.
Watch for myocardial ischaemia/infarction. resp failure, atelectasis, VTE, AKI
Essential Equipment of ruptured AAA
Rapid Infusion Device
Cell Salvage
POC testing
White board to record losses
What are the factors affecting haemodynamic chages with cross clamping
Level of cross clamp Duration of cross clamp Blood Volume distribution LV function Presence of CAD Extent of co lateral circuulation Type of disease AAA vs aorto-occlusive Intravascular volume statu anaesthesia
What are the changes with cross clamping?
Clamp on!
Prior give dose heparin (elective 100IU/kg)
Perfusion below cross clamp entirely dependant upon collateral circulation and sudden increase in arterial pressure proximal to clamp
Increase in afterload and LV wall tension of the heart.
increase in myocardial workload and oxygen demand.
In normal circumstanes CBF and o2 supply increase - however in bad CAD this wont happen - and can cause myocardial ischaemia and impaired cardiac output.
Requires vasodilation!
UNCLAMPING
Peripherl vascualr resistance decreases by 75% resulting in profound hypotension
Decrease in arterial pressure may be compounded by blood sequestration in the lower half of the body
Ischaemia reperfusion injury and release of anaerobic metabolites.
SEVERITY OF HYPOTENSION IS PROPORTIONAL TO CROSS CLAMP TIME>
suggested to have a haemostatic pause - get everything in order! volume resuscitation, CVS stability, correct acid base, electrolytes and temperature.
Graduated release of cross clamps can reduce degree of hypotension.
If its refractory may need to replace cross clamp.