Neurologic Complications Flashcards

0
Q

Percent of patients that have neurological dysfunction

A

25-80%

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1
Q

Percent of patients that have a stroke

A

1-5%

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2
Q

6 examples of neurological deficits

A
Psychomotor speed
Attention
Concentration
New learning ability
Short term memory
Peds: seizures, movement disorders, development delays
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3
Q

Characteristics of a transient ischemic attack (TIA)

A

Localized event
Rapid onset and recovery (min-hrs)
Severity depends on collateral flow

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4
Q

Difference between TIA and reversible ischemic neurological deficit

A

RIND lasts longer (24-72hrs)

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5
Q

Lacunar brain infarct (stroke)

A

Specific focal deficit from cerebral artery occlusion
Much more severe, doesn’t resolve
Hemiparesis, aphasia, sensory

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6
Q

Global ischemia

A

Results from long periods of hypoperfusion or massive embolic load
More than 50% are brain dead and never wake

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7
Q

Risk factors for neurological dysfunction

A
Advanced age
Atherosclerosis
History of previous neurological incident
Intracardiac operation
Hypertension and diabetes 
Carotid stenosis
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8
Q

Age ranges and their incidence of stroke

A

75: 8%

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9
Q

Percent of patients with stroke that show multiple infarcts

A

75%
Average of 6 zones
Indicative of embolic origins

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10
Q

3 causes of atherosclerosis/thromboembolic debris

A

Aortic plaques
Platelet-fibrin and leukocyte aggregates
Bubbles from CPB circuit

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11
Q

Surgical event causing the largest surge in embolic events

A

XC removal/Filling of beating heart

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12
Q

Percent of patients that have history of neurological events, and risk associated

A

13%

3x greater risk of new deficit or exacerbation of previous deficit

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13
Q

Riss associated with Intracardiac operation

A

Valves, ASD/VSD, myxomas
Increased risk of air emboli
Risk (5-13%) is 2X higher than CABG alone

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14
Q

Risks associated with HTN and diabetes

A

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)

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15
Q

Stroke rates with differing severity of carotid stenosis

A

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

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16
Q

Greater than 50% of strokes occur during what period?

A

Immediately Postop

no evidence that higher MAP on CPB is beneficial

17
Q

List of “other” risk factors for neurological dysfunction

A
PVD
Alcohol abuse
IABP
Prolonged hypotension
Arrhythmias
CHF
Gender
Decreased CO
18
Q

Cerebral metabolic requirement of oxygen (CMRO2)

A

40-50mlO2/min

Index: 3-3.5 mlO2/100g/min

19
Q

Cerebral blood flow

A

750ml/min
Index: 50-50ml/100g/min
15% of CO

20
Q

Average brain weight

A

1400g

21
Q

Average CBF:CMRO2

A

10-15:1

So get more cerebral blood flow than metabolically required

22
Q

4 factors influencing CBF

A

CMRO2
PaCO2
HCT
MAP

23
Q

Auto regulation range in awake patients

A

50-150mmHg

24
Q

Auto regulation range for anesthetized patients at moderate hypothermia

A

Preserved auto regulation down to 28mmHg

Deeper hypothermia: down to 20mmHG

25
Q

Primary determinant of CBF

A

Temperature

26
Q

CMRO2-Temp (flow-metabolism) coupling

A

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)

27
Q

CO2 effects on CBF

A

Increased pCO2 = increased CBF

Effects are regardless of temp, MAP, HCT, pO2

28
Q

Blood stat management good for pediatric patients

A

pH stat

Adults toners lose auto regulation, causing luxury flow

29
Q

Effects of oxygen tension on CBF

A

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

30
Q

MAP affect on CBF for alpha stat and pH stat

A

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

31
Q

Neurologic events on CPB vs off pump cases

A

3 months Postop: 21% off, 29% on
1 year Postop: 31% off, 34% on
CPB has no significant effect

32
Q

7 Surgical techniques to attenuate neurological injury

A
  1. Attention to aorta: Use epiaortic ultrasound for cannulation, XC, and proximal anastamosis sites vs. just feeling
  2. Use devices to deflect/trap emboli
  3. Do preop carotid studies in older pt, pt with hx of TIA, stroke, carotid disease
  4. Minimize aortic manipulations
  5. Flood chest cavity with CO2
  6. Carefully decannulate
  7. Use TEE to ensure deairing prior to XC removal
33
Q

3 Anesthesia methods to attenuate neurological injury

A

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

34
Q

6 Perfusion methods to attenuate neurologic injury

A
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
35
Q

Intra operative methods to attenuate neurological injury

A

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

36
Q

Characteristics of NIRS

A

Noninvasive transcutaneous assessment of regional brain oxygenation
Sensitive to temp, pCO2, HCT, and CPB flow
Hgb sat does not indicate tissue utilization

37
Q

Characteristics of transcranial Doppler

A

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

38
Q

Flow path for antegrade cerebral perfusion

A

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

39
Q

Flow for antegrade cerebral perfusion

A

10mL/kg/min

40
Q

Flow for retrograde cerebral perfusion

A

Up SVC–>circle of Willis–>down carotid arteries

Useful for deairing

41
Q

Flow and SVC pressure for retrograde cerebral perfusion

A

Flow: <25mmHg