Neurologic Complications Flashcards
Percent of patients that have neurological dysfunction
25-80%
Percent of patients that have a stroke
1-5%
6 examples of neurological deficits
Psychomotor speed Attention Concentration New learning ability Short term memory Peds: seizures, movement disorders, development delays
Characteristics of a transient ischemic attack (TIA)
Localized event
Rapid onset and recovery (min-hrs)
Severity depends on collateral flow
Difference between TIA and reversible ischemic neurological deficit
RIND lasts longer (24-72hrs)
Lacunar brain infarct (stroke)
Specific focal deficit from cerebral artery occlusion
Much more severe, doesn’t resolve
Hemiparesis, aphasia, sensory
Global ischemia
Results from long periods of hypoperfusion or massive embolic load
More than 50% are brain dead and never wake
Risk factors for neurological dysfunction
Advanced age Atherosclerosis History of previous neurological incident Intracardiac operation Hypertension and diabetes Carotid stenosis
Age ranges and their incidence of stroke
75: 8%
Percent of patients with stroke that show multiple infarcts
75%
Average of 6 zones
Indicative of embolic origins
3 causes of atherosclerosis/thromboembolic debris
Aortic plaques
Platelet-fibrin and leukocyte aggregates
Bubbles from CPB circuit
Surgical event causing the largest surge in embolic events
XC removal/Filling of beating heart
Percent of patients that have history of neurological events, and risk associated
13%
3x greater risk of new deficit or exacerbation of previous deficit
Riss associated with Intracardiac operation
Valves, ASD/VSD, myxomas
Increased risk of air emboli
Risk (5-13%) is 2X higher than CABG alone
Risks associated with HTN and diabetes
HTN: 55% of patients
Diabetes: 25% patients
May be due to changes in cerebral autoregulation (narrows arteries penetrating brain, decreased collateral BF, decreased ischemic tolerance)
Stroke rates with differing severity of carotid stenosis
15% of pts have >50% carotid stenosis
9.2% stroke rate in asymptomatic pts with carotid disease
1.3% in pts with no cardiac disease
14% with >75% stenosis
Greater than 50% of strokes occur during what period?
Immediately Postop
no evidence that higher MAP on CPB is beneficial
List of “other” risk factors for neurological dysfunction
PVD Alcohol abuse IABP Prolonged hypotension Arrhythmias CHF Gender Decreased CO
Cerebral metabolic requirement of oxygen (CMRO2)
40-50mlO2/min
Index: 3-3.5 mlO2/100g/min
Cerebral blood flow
750ml/min
Index: 50-50ml/100g/min
15% of CO
Average brain weight
1400g
Average CBF:CMRO2
10-15:1
So get more cerebral blood flow than metabolically required
4 factors influencing CBF
CMRO2
PaCO2
HCT
MAP
Auto regulation range in awake patients
50-150mmHg
Auto regulation range for anesthetized patients at moderate hypothermia
Preserved auto regulation down to 28mmHg
Deeper hypothermia: down to 20mmHG
Primary determinant of CBF
Temperature
CMRO2-Temp (flow-metabolism) coupling
Brain regulates flow in response to its O2 demand
Maintained in auto regulatory state
CBF is adjusted according to CMRO2
Loses coupling <22C (CBF exceeds CMRO2)
CO2 effects on CBF
Increased pCO2 = increased CBF
Effects are regardless of temp, MAP, HCT, pO2
Blood stat management good for pediatric patients
pH stat
Adults toners lose auto regulation, causing luxury flow
Effects of oxygen tension on CBF
Normal cerebral tissue pO2: 35-40mmHg
If pO2 <30: immediate reduction in cerebral vascular resistance, yields an increase in CBF
Hyperoxia: increased cerebral vascular resistance
15% reduction in CBF when PaO2 increased from 125 to 300mmHg
MAP affect on CBF for alpha stat and pH stat
Alpha stat: CBF constant over varying MAP, safety margin narrows <50mmHg
PH stat: CBF dependent on MAP, high pressure yields excessive flow, low pressure yields hypoperfusion
Neurologic events on CPB vs off pump cases
3 months Postop: 21% off, 29% on
1 year Postop: 31% off, 34% on
CPB has no significant effect
7 Surgical techniques to attenuate neurological injury
- Attention to aorta: Use epiaortic ultrasound for cannulation, XC, and proximal anastamosis sites vs. just feeling
- Use devices to deflect/trap emboli
- Do preop carotid studies in older pt, pt with hx of TIA, stroke, carotid disease
- Minimize aortic manipulations
- Flood chest cavity with CO2
- Carefully decannulate
- Use TEE to ensure deairing prior to XC removal
3 Anesthesia methods to attenuate neurological injury
Pharmacological agents that reduce CMRO2: Thiopental and Propofol
Ensure air removed from IVs and arterial lines
Apply manual compression on carotid arteries during XC removal
6 Perfusion methods to attenuate neurologic injury
Use ALF and cardiotomy filters Ensure proper deairing of circuit Maintain adequate anticoagulation Monitor warming/cooling gradients Communicate with surgeon and understand sequence of events Alpha stat management
Intra operative methods to attenuate neurological injury
Check arterial line post CPB prior to transfusion of volume
Avoid hyperglycemia (increases CMRO2, aggravates neurologic ischemic injury)
Discuss venous drainage problems
Decrease CO2 during embolic periods
Avoid excessive pO2
Characteristics of NIRS
Noninvasive transcutaneous assessment of regional brain oxygenation
Sensitive to temp, pCO2, HCT, and CPB flow
Hgb sat does not indicate tissue utilization
Characteristics of transcranial Doppler
Measures blood velocity in middle cerebral artery
Sensitive to temp, MAP, pump flow, pCO2, HCT
Reliable velocity requires constant vessel diameter (so better as a trending device)
Peds: more useful, easier to obtain temporal window
Adults: better at emboli detection than indicating CBF
Flow path for antegrade cerebral perfusion
Patient is in Trendelburg position
Flow up Axillary artery–>innominate artery–>head via right common carotid artery–>circle of Willis–>down jugular veins–>SVC
Must leave venous lime open to drain heart!
Can also use direct cannulation of head vessels
Flow for antegrade cerebral perfusion
10mL/kg/min
Flow for retrograde cerebral perfusion
Up SVC–>circle of Willis–>down carotid arteries
Useful for deairing
Flow and SVC pressure for retrograde cerebral perfusion
Flow: <25mmHg