Exam 9 - O2 Monitoring & Brain Protection Flashcards
Health depend’s on bodies ability to:
- deliver appropriate amount of O2 to each cell
- for each cell to uptake and consume oxygen
Normal oxygen consumption
200-250 ml O2/min
70 kg adult consumes:
10 quintillion molecules of O2 per second
10,000,000,000,000,000,000
Final cause of death
- always ends up being tissue hypoxia
Aerobic
- 1 mole glucose = 36 ATP
- glucose -> 2 pyruvate -> acetyl CoA
Anaerobic
- 1 mole glucose = 2 net ATP
- 97% reduction in energy plus lactic acid waste build up
- lactic acid later sent to liver for conversion
C3H6O3
Lactic acid
C3H5O3 + H
Lactate
CaO2
- Oxygen content of venous and arterial
- 2% dissolved in plasma
- 98% carried by hemoglobin
Arterial O2 content
17-20 ml/100ml blood
Venous O2 content
12-15 ml/100 ml blood
A-V O2 difference
4-6 ml O2/100 ml blood
Biggest factor of O2 content
Hemoglobin
DO2
- oxygen delivery
- available oxygen x delivery rate
- arterial content x CO
Normal O2 delivery
950-1150 ml O2/min
Index: 550-650 ml O2/min/m2
VO2
- Oxygen consumption
- CO x (Ca-Cv)
Ca = arterial O2 content Cv = venous O2 content
Normal O2 consumption
200-250 ml O2/min
Index: 120-160 ml O2/min/m2
RO2
- oxygen reserve
- O2 left AFTER consumption
- built in buffer in time of need
- what is in venous blood
Normal O2 reserve
700-800 ml O2/min
Index: 450 ml O2/min/m2
Anaerobic respiration kicks in at:
< 32% O2
Factors increasing O2 consumption
- Patient conditions
~surgery/fever/agitation/fast breathing/infection/trauma
~biggest are shivering and sepsis….50-100% increase - Medications
~NE/Dopamine/Dobutamine/Epi - Procedures
~dressing change/exam/visitors/turning/nasal intubation/trach suction
Factors decreasing O2 consumption
- Hypothermia (up to 50% at 7 degrees)
- Morphine IV
- Anesthesia
- Assist/control ventilation
- Neuromuscular blocking agents
Conditions that compromise tissue O2
- ischemic hypoxia
- hypoperfusion / peripheral vascular disease / thrombosis - hypoxemic hypoxia
- bad O2 transfer in lungs / CO poison / methemoglobinemia - anemic hypoxia
- less Hgb molecules - toxic hypoxia
- body cells can’t uptake or use O2 / sepsis / cyanide / ethanol - excessive tissue requirements
- demand > supply / fever / SIRS / hypermetabolism / thyroid - impaired O2 unloading
- at cap level / alkalemia / hypocarbia / excessive bank blood
Compensatory mechanism for low O2
- Increase CO - primary
- can get to 15-25 L/min - draw on venous reserve
- extract more O2 - Polycythemia
- increase amount of Hgb and RBC mass….takes weeks
Arterial and mixed venous gases from central lab
- lag time between sample and results
- intermittent
- cannot detect acute/severe hypoxemia
POC blood gas analyzers
Pros: been around/measures a lot/portable/small volume required/self calibrating/disposable cartridges
Cons: expensive and labor intensive quality control
- like the i-STAT
Non-invasive pulse oximetry
- 2 LEDs w/ red and infrared light
- Saturated Hb absorbs infrared
- Desaturated Hb absorbs red
- placed on finger / toe / earlobe / nose bridge
- +/- 4% (need above 50% O2 and less reliable below 70%)
- Does NOT guarantee O2 is being delivered
Factors causing underestimation w/ pulse oximetry
- nail polish
- dark skin
- IV dyes
- Lipid infusions
- Anemia
- Venous pulses
- movement
Factors overestimating pulse oximetry
- elevated carboxyhemoglbin (CO poisoning)
- elevated methemoglobin
- intense surgical light
SpO2 ranges
Normal: 96-99%
Mild hypoxia: 85-90%
Hypoxia: 75-85%
Normal SvO2
60-80%
-cells extract about 25%
Invasive mixed venous saturation
- fiber optic pulmonary artery catheter
- uses reflectance spectrophotometry
- read manufactures guides
- calibration required
- do not bend or kink
- away from wall of artery
- old accuracy 4%….now higher
- Cannot tell difference between carboxy/methem from oxy
Continuous in dwelling arterial and venous gases
- CDI 500
- needs gas calibration
Transcutaneous measurement of local tissue saturation
- NIRS
- can measure at specific depths
Causes of brain injury
- Ischemia - biggest factor
- hypoxia
- seizures
- hypoglycemia
- hyperglycemia
- improperly calculating CaCl2 dose
Neurological injury
Combo of patient at risk with surgical stresses for which vascular system cannot compensate
Pathophysiology of cerebral ischemia
- buildup of ADP and lactate
- K buildup causes vasospasms
- buildup of Ca causes lipolysis / proteolysis / high consumption
- Platelet activation and vascular obstruction
- free radical build up
- receptor dysfunction
- Apoptosis
Type I Neuro outcome
- cerebral death
- non-fatal strokes
- New TIAs (no permanent damage from TIA)
- Predictors: Age (biggest factor)…. >70 is 4-9% risk
Aortic atherosclerosis
History of neuro events
Carotid stenosis
# of GMEs
Type II Neuro outcome
- New intellectual deterioration
- New seizures upon discharge
-Predictors: Low CO / hypotensive
GME
Atrial arrhythmias
Hypertension
Diabetes
Pulmonary disease
Alcoholism
Post op delirium
- If LOS longer…..more effects (20-25 vs <10)
- 10-60%
Neuro impairment
- 6.1%
- strokes / coma / poor intellectual function / seizure / memory
Incidence of neurological dysfunction
- almost always with CV surgery
- Permanent complications: 1.6-23%
Most surgical stress happens when:
- Short filling of beating heart
- bubbles on tissue of heart flow to brain - any filling of heart
Surgical techniques to prevent GME
- Epiaortic ultrasound
- single XC
- no touch technique
- pay attention
How perfusionists contribute to injury
- Focal:
- Embolisms
- Hypoperfusion
- Inflamation
- Global:
- Complete cardiac arrest
- Complete DHCA
- Incomplete hypotension
- Inadequate CPB flow
RSO2
Regional SO2….uses on brain….NIRS
EEG
- electroencephalogram
- activity on surface of brain only
- electrodes cover 2.5 cm2
Alpha and Beta waves
- patient awake waves
- normal waves
- Alpha = relaxed
- beta = alert
Theta and delta waves
- patient asleep
- Theta = sleeping
- delta = coma / deep sleep / anesthesia / cerebral ischemia
- 15% of pop may show evidence of old brain injury
- if seen during awake
EEG uses
- EPILEPSY / brain tumors / stroke
- diagnosis of coma / brain death
- monitor depth of perfusion
EEG disadvantages
- complex analysis
- large equipment
- distracting
- electrically sensitive
BIS
- Bispectral index
- one number and graph tells us how alert
- non-invasive
- continuous / direct / real time
- refresh every 10-15 seconds
- 1-100 (100 is fully awake)
BIS based on
- degree of high frequency activation
- degree of low frequency synchronization
- degree of nearly suppressed periods of EEG
- degree of fully suppressed periods of EEG
- uses algorithm plus above and turns into one number
BIS ranges
- 100 = awake
- 80 = light/moderate sedation
- 60 = general anesthesia
- 40 = deep hypotonic state
- 20 = burst suppression
- 10 = flat line EEG
> 70….patient will remember
BIS benefits
- reduction in anesthesia use
- decrease in patient awakening
- reduction in LOC and recovery
- improved satisfaction
- ONE part of the big picture to help monitor hemodynamics
BIS disadvantages
- trending device
- can’t treat level of sedation
- often monitor only faces anesthesia
INVOS system
- most primitive NIRS
- most widely used
NIRS benefits
- non-invasive
- continuos
- real time
- site specific
- EARLY warnings of ischemia
- not pulse / pressure / temp dependent
NIRS facts
- must baseline patient first
- gives us rSO2
- can aid in decision making
- drops MOM from 13 to 3%
NIRS applications
- OR
- Neuro
- ER
- any surgery
- Peds (ECMO / surgery / neuro)
Adequacy of cerebral perfusion
- head position
- O2 delivery
- cerebral vascular resistance
- cerebral O2 demand
- venous drainage
Cerebral inflow issues
- head position
- heart position
- arterial obstruction
- cannula malposition
- NIRS can help detect inflow supply issues and prescriptive perfusion
RSO2 target and thresholds
- Normal: 47-83
- Intervention threshold: <50 or 20% drop from baseline
- Critical: <40 or 25% drop from baseline
What can we do to protect brain
- medical history
- monitor
- filters on machines
- controlled temp
- maintain correct pressures and flow
- drugs
- brain hypothermia
