NEUROLOGIC COMPLICATIONS Flashcards

1
Q

amount of cardiac surgical procedures are carried out worldwide

A

1.4 million world wide

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2
Q

Overt stroke occurs in ______ of all patients

A

1-5%

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3
Q

Neurologic dysfunction may be present in _____

of pts.

A

25-80%

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4
Q

Annual cost for treating these pts. with neuro deficits exceeds

A

$2 billion/ yr

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5
Q

Neurologic Deficits Include:

A

 Psychomotor speed  Attention  Concentration
 New Learning Ability
 Short term memory

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6
Q

neuro deficits for peds include

A

Seizures, Movement disorders, developmental delays`

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7
Q

Transient Ischemic Attack (TIA)

A

Localized event Rapid onset and recovery (minutes to hours) Severity depends on collateral flow

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8
Q

Reversible Ischemic Neurologic Deficit (RIND)

A

Similar to TIA but lasts longer (24-72hrs)

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9
Q

Lacunar Brain Infarct (stroke)

A

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

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10
Q

Global Ischemia

A

Results from long periods of hypoperfusion or massive embolic load
Poor recovery. >50% are brain dead and never wake.
Symptoms often overlap and share causative mechanism with others

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11
Q

Risk Factors for neuro injuries

A
  1. Advanced Age 2. Atherosclerosis 3. History of previous neurologic incident 4. Intracardiac operation 5. Hypertension and Diabetes 6. Carotid Stenosis 7. Other
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12
Q

<45 years old

A

0.2% incidence of stroke

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13
Q

<60 years old

A

1% incidence of stroke

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14
Q

60-70 years old

A

3.0% incidence of stroke

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15
Q

> 75 years old

A

8.0% incidence of stroke

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16
Q

At MGH, average age was _____ in______ and up to ____ in______

A

56 in 1980 up to 67 in 1994.

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17
Q
Atherosclerosis/ Thromboembolic debris
• •
•
• •
75% of pts with stroke show
A

multiple infarcts, with an average of 6 zones

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18
Q

normal aorta prevalence of stroke

A

5%

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19
Q

stroke rate with large intraluminal plaques

A

45%

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20
Q

Atherosclerosis/ Thromboembolic debris

 Embolic events related to:

A

 Aortic Plaques  Platelet-fibrin and leukocyte aggregates  Bubbles from CPB circuit
 Often associated with specific surgical events

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21
Q

______of cardiac patients have a history of TIA/Stroke

A

13%

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22
Q

______greater risk of new deficit or exacerbation of previous deficit

A

3x

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23
Q

types of intracardiac ops that increase risk for neuro injury

A

Valves, ASD/VSD, Myxomas, etc. • Increased risk of air emboli

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24
Q

risk for neuro injury Valves, ASD/VSD, Myxomas, etc. compared to CABG alone

A

Risk (5-13%) is 2X higher than CABG alone

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25
Q

percent of cardiac patients that have hypertension

A

55%

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26
Q

percent of cardiac patients with diabetes

A

25%

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27
Q

how diabetes may increase neuro injury

A

May be due to changes in cerebral autoregulation Narrows arteries penetrating the brain Decrease in collateral blood flow Decrease ischemic tolerance

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28
Q

PERCENT OF PATIENTS WITH MORE THAN 50% carotid stenosis

A

15%

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29
Q

stroke rate in asymptomatic patients with carotid disease

A

9.2%

30
Q

stroke rate in patients with no carotid disease

A

1.3%

31
Q

stroke rate with >75% Carotid Stenosis

A

14%

32
Q

> 75% Carotid Stenosis before carotid endarterectomy had strokes.

A

0 of 19 pts.

33
Q

Carotid Stenosis,

 Mechanism is unclear, whether

A

embolic or ↓Q, but >50% of strokes occur in immediate postoperative period

34
Q

No studies prove higher CPB

A

MAP is beneficial

35
Q

Risk Factors

Other

A

PVD
Alcohol abuse IABP- balloon or preexisting condition?? MI Prolonged hypotension Arrhythmias
CHF Gender Decreased Cardiac Output

36
Q

Cerebral Metabolic Requirement of Oxygen (CMRO2)

A

CMRO2 ~40-50mL of O2/min  Indexed at 3.0-3.5 mL of O2/100g/min

37
Q

Cerebral Blood Flow (CBF)

A

CBF~ 750mL/min  Indexed at 50-60mL/100g/min (about 15% CO)

38
Q

Average brain weighs about

A

1400 grams

39
Q

CBF:CMRO2 is typically

A

10-15

40
Q

CBF is influenced by:

A

CMRO2, PaCO2, Hct, MAP

 All may increase or decrease cerebral blood flow

41
Q

Without bypass:

 Cerebral delivery of oxygen (CDO2) normally

A

exceeds the oxygen demand

42
Q

When delivery decreases, CMRO2 is maintained by

A

increasing oxygen extraction

Further decrease in delivery will result in ischemia

43
Q

Autoregulation tries to maintain a constant

A

CBF over a wide range of pressures.

44
Q

Due to changes in CMRO2 between an awake patient and an anesthetized patient at hypothermic temperatures,

A

different CBF’s are maintained over variable MAP’s

45
Q

Awake patients  Maintain autoregulation from

A

50-150mmHg

46
Q

Anesthetized patients at moderate hypothermia  may have preserved autoregulation down to CPP of

A

28mmHg. Deeper Hypothermia – down to 20mmHg

47
Q

While intrinsic autoregulation strives to maintain a CBF:CMRO2 coupling, there are other factors that play major roles:

A
  1. Temperature

Carbon Dioxide Oxygen Tension Mean Arterial Pressure

48
Q

Primary determinant of CBF  CMRO2 ~ T

A

low-metabolism “coupling”
 Brainregulatesflowinresponsetoit’sO2demand
 is maintained in autoregulatory state
 When there is an increase or decrease in CMRO2, CBF is adjusted accordingly

49
Q

At profound levels of hypothermia (<22°C)

A

“coupling” disappears  CBF can become in excess of CMRO2

50
Q

Carbon Dioxide (alpha- stat)

A

 pCO2 is a large player in determining CBF
 ↑CBF as ↑pCO2 and vice versa
 Effects are regardless of Temperature, MAP, Hct, pO2

51
Q

pH-stat acid-base management

A

Maintain temperature corrected pH= 7.40 and pCO2 = 40mmHg  By continually adding CO2

52
Q

Alpha-stat acid-base management

A

Maintain an uncorrected value of pH = 7.40 and pCO2 = 40mmHg  Keeping the total CO2 constant

53
Q

pH-stat management good for pediatric cases

A

 Adult patients lose cerebral autoregulation  where CBF becomes dependent on CPP
 This leads to “luxuriant” cerebral blood flow and can have significant neurological side effects

54
Q

Normal cerebral tissue pO2

A

35-40mmHg

55
Q

if cerbral pO2 < 30mmHg

A

Immediate reduction in cerebral vascular resistance  Yielding an increase in CBF

56
Q

Hyperoxia causes an

A

increase cerebral vascular resistance.

57
Q

when PaO2 was increased from 125 to 300mmHg (all other parameters constant)

A

15% reduction in CBF

58
Q

With alpha-stat: map

A

CBF is relatively constant over varying MAP.

 At mild hypothermia or normothermia, the safety margin for CDO2 vs. CMRO2 starts to narrow at MAP’s < 50mmHg

59
Q

With pH-stat map

A

CBF is dependent on MAP  High pressures can yield excessive flow  Low pressures can yield hypoperfusion.

60
Q

CPB is not responsible for

A

cognitive inju

61
Q

neuro injury off pump vs on pump post 3 mo.

A

 21% off pump vs. 29% on pump

62
Q

neuro injury off pump vs on pump post 1 yr.

A

 31% off vs. 34% on pump

63
Q

Attenuation of Neurological Injury – Surgical Management

A

Attention to Aorta  Use the epiaortic ultrasound (versus “feel”) for
cannulation, cross clamp, and proximal anastamosis sites  Devices to deflect / trap emboli
 Pre-op carotid studies in older patients and those with a history of TIA/ Stroke/ Carotid Dz.
 Minimize aortic manipulations  Flood chest cavity with CO2  Use care during de/cannulation  Utilize TEE to ensure de-airing prior to XC removal

64
Q

Attenuation of Neurological Injury – Anesthesia Management

A

 Pharmacologic agents that reduce CMRO2  Thiopental  Propofol
 Ensure air removed from IV’s and arterial lines
 Apply manual compression on carotid arteries with XC removal???

65
Q

Attenuation of Neurological Injury – Perfusion Management filter/ de airing/

A

 Use of arterial line & cardiotomy filter
 Ensure proper de-airing of circuit (CO2 flush)
 Maintain adequate anticoagulation
 Monitor warming/cooling gradients  Slow rewarm is better
 Better cognitive performance 6 weeks post op  Avoid Hyperthermia
 Communicate with surgeon and understand surgical sequence of events
 Alpha-stat acid-base management

66
Q

Attenuation of Neurological Injury

A

 Check arterial line post CPB prior to transfusion of volume
 Avoid hyperglycemia (potential for ↑CMRO2)  May aggravate neurologic ischemic injury
 Discuss venous drainage problems.  If SVC is congested, CPP is diminished
 ↓pCO2 during embolic periods???  Avoid excessive pO2???

67
Q

 Near Infrared Spectroscopy

A

 Noninvasive transcutaneous assessment of regional

brain oxygenation  Sensitive to temperature, pCO2, Hct, CPB flow  Hgb sat does not indicate tissue utilization

68
Q

Transcranial Doppler

A

 Measures blood velocity in middle cerebral artery  Correlation to blood flow
 Sensitive to Temperature, MAP, pump flow, pCO2, Hct.
 Reliable velocity requires a constant vessel diameter  Not always true on bypass  Better trending device
 Pediatrics – much more useful – easier to obtain temporal window
 Adults – better at emboli detection than indicator of CBF.

69
Q

Antegrade Cerebral Perfusion

A

Patient put in Trendelenburg position
 Flow up the axillary artery to the innominate artery, to the head via the right common carotid artery. Thru the Circle of Willis and down the jugular veins to the SVC/ Atrium.
 Have to leave venous line open to drain the heart  Can also do via direct cannulation of the head
vessels  Flow: 10ml/kg/min

70
Q

Retrograde Cerebral Perfusion

A

 1st used as a method to treat massive air embolus  Flow up the SVC through the Circle of Willis and
down the carotid arteries  Many variations to do so
 Useful to deair for aortic surgeries  Flow <25mmHg