NEUROLOGIC COMPLICATIONS Flashcards
amount of cardiac surgical procedures are carried out worldwide
1.4 million world wide
Overt stroke occurs in ______ of all patients
1-5%
Neurologic dysfunction may be present in _____
of pts.
25-80%
Annual cost for treating these pts. with neuro deficits exceeds
$2 billion/ yr
Neurologic Deficits Include:
Psychomotor speed Attention Concentration
New Learning Ability
Short term memory
neuro deficits for peds include
Seizures, Movement disorders, developmental delays`
Transient Ischemic Attack (TIA)
Localized event Rapid onset and recovery (minutes to hours) Severity depends on collateral flow
Reversible Ischemic Neurologic Deficit (RIND)
Similar to TIA but lasts longer (24-72hrs)
Lacunar Brain Infarct (stroke)
Specific focal deficit from cerebral artery occlusion. Much more severe, often doesn’t resolve Hemiparesis/aphasia/sensory
Global Ischemia
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
Risk Factors for neuro injuries
- Advanced Age 2. Atherosclerosis 3. History of previous neurologic incident 4. Intracardiac operation 5. Hypertension and Diabetes 6. Carotid Stenosis 7. Other
<45 years old
0.2% incidence of stroke
<60 years old
1% incidence of stroke
60-70 years old
3.0% incidence of stroke
> 75 years old
8.0% incidence of stroke
At MGH, average age was _____ in______ and up to ____ in______
56 in 1980 up to 67 in 1994.
Atherosclerosis/ Thromboembolic debris • • • • • 75% of pts with stroke show
multiple infarcts, with an average of 6 zones
normal aorta prevalence of stroke
5%
stroke rate with large intraluminal plaques
45%
Atherosclerosis/ Thromboembolic debris
Embolic events related to:
Aortic Plaques Platelet-fibrin and leukocyte aggregates Bubbles from CPB circuit
Often associated with specific surgical events
______of cardiac patients have a history of TIA/Stroke
13%
______greater risk of new deficit or exacerbation of previous deficit
3x
types of intracardiac ops that increase risk for neuro injury
Valves, ASD/VSD, Myxomas, etc. • Increased risk of air emboli
risk for neuro injury Valves, ASD/VSD, Myxomas, etc. compared to CABG alone
Risk (5-13%) is 2X higher than CABG alone
percent of cardiac patients that have hypertension
55%
percent of cardiac patients with diabetes
25%
how diabetes may increase neuro injury
May be due to changes in cerebral autoregulation Narrows arteries penetrating the brain Decrease in collateral blood flow Decrease ischemic tolerance
PERCENT OF PATIENTS WITH MORE THAN 50% carotid stenosis
15%
stroke rate in asymptomatic patients with carotid disease
9.2%
stroke rate in patients with no carotid disease
1.3%
stroke rate with >75% Carotid Stenosis
14%
> 75% Carotid Stenosis before carotid endarterectomy had strokes.
0 of 19 pts.
Carotid Stenosis,
Mechanism is unclear, whether
embolic or ↓Q, but >50% of strokes occur in immediate postoperative period
No studies prove higher CPB
MAP is beneficial
Risk Factors
Other
PVD
Alcohol abuse IABP- balloon or preexisting condition?? MI Prolonged hypotension Arrhythmias
CHF Gender Decreased Cardiac Output
Cerebral Metabolic Requirement of Oxygen (CMRO2)
CMRO2 ~40-50mL of O2/min Indexed at 3.0-3.5 mL of O2/100g/min
Cerebral Blood Flow (CBF)
CBF~ 750mL/min Indexed at 50-60mL/100g/min (about 15% CO)
Average brain weighs about
1400 grams
CBF:CMRO2 is typically
10-15
CBF is influenced by:
CMRO2, PaCO2, Hct, MAP
All may increase or decrease cerebral blood flow
Without bypass:
Cerebral delivery of oxygen (CDO2) normally
exceeds the oxygen demand
When delivery decreases, CMRO2 is maintained by
increasing oxygen extraction
Further decrease in delivery will result in ischemia
Autoregulation tries to maintain a constant
CBF over a wide range of pressures.
Due to changes in CMRO2 between an awake patient and an anesthetized patient at hypothermic temperatures,
different CBF’s are maintained over variable MAP’s
Awake patients Maintain autoregulation from
50-150mmHg
Anesthetized patients at moderate hypothermia may have preserved autoregulation down to CPP of
28mmHg. Deeper Hypothermia – down to 20mmHg
While intrinsic autoregulation strives to maintain a CBF:CMRO2 coupling, there are other factors that play major roles:
- Temperature
Carbon Dioxide Oxygen Tension Mean Arterial Pressure
Primary determinant of CBF CMRO2 ~ T
low-metabolism “coupling”
Brainregulatesflowinresponsetoit’sO2demand
is maintained in autoregulatory state
When there is an increase or decrease in CMRO2, CBF is adjusted accordingly
At profound levels of hypothermia (<22°C)
“coupling” disappears CBF can become in excess of CMRO2
Carbon Dioxide (alpha- stat)
pCO2 is a large player in determining CBF
↑CBF as ↑pCO2 and vice versa
Effects are regardless of Temperature, MAP, Hct, pO2
pH-stat acid-base management
Maintain temperature corrected pH= 7.40 and pCO2 = 40mmHg By continually adding CO2
Alpha-stat acid-base management
Maintain an uncorrected value of pH = 7.40 and pCO2 = 40mmHg Keeping the total CO2 constant
pH-stat management good for pediatric cases
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
Normal cerebral tissue pO2
35-40mmHg
if cerbral pO2 < 30mmHg
Immediate reduction in cerebral vascular resistance Yielding an increase in CBF
Hyperoxia causes an
increase cerebral vascular resistance.
when PaO2 was increased from 125 to 300mmHg (all other parameters constant)
15% reduction in CBF
With alpha-stat: map
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
With pH-stat map
CBF is dependent on MAP High pressures can yield excessive flow Low pressures can yield hypoperfusion.
CPB is not responsible for
cognitive inju
neuro injury off pump vs on pump post 3 mo.
21% off pump vs. 29% on pump
neuro injury off pump vs on pump post 1 yr.
31% off vs. 34% on pump
Attenuation of Neurological Injury – Surgical Management
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
Attenuation of Neurological Injury – Anesthesia Management
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???
Attenuation of Neurological Injury – Perfusion Management filter/ de airing/
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
Attenuation of Neurological Injury
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???
Near Infrared Spectroscopy
Noninvasive transcutaneous assessment of regional
brain oxygenation Sensitive to temperature, pCO2, Hct, CPB flow Hgb sat does not indicate tissue utilization
Transcranial Doppler
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.
Antegrade Cerebral Perfusion
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
Retrograde Cerebral Perfusion
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
