Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
73 Cards in this Set
- Front
- Back
|
7 types of emboli |
1. venous 2. paradoxical (arterial usually via PFO) 3. thrombus 4. C02 5. fat 6. foreign body 7. amniotic fluid (very high mortality rate)
|
|
|
CMR02 in healthy adult |
3-3.5 mL of 02/100 gm brain tissue/minute |
|
|
CMR02 in healthy child |
5-6 mL of 02/100 gm brain tissue/minute |
|
|
Glucose consumption in brain tissue/minute |
5 mg/100 gm brain tissue/min approx 1/4 total body glucose consumption used by brain |
|
|
cerebral blood flow per minute |
50 mL/100 gm/min OR approx 750 mL/minute (20% of C.O.) |
|
|
CBF amount in flatline EEG |
15-20mL/100gm/min Less than 10 mL/100gm/min=irreversible damage |
|
|
PaC02 and it's relationship with CBF |
CBF is directly proportional to PaC02 from 20-80 mmHg An increase in PaC02 from 40 to 80 mmHg will double CBF PaC02 from 40 to 20 mmHg will decrease CBF 50% *If Pa02 is below 50 it will then decrease CBF |
|
|
Cerebral Perfusion Presure |
MAP-ICP (or CVP). Normal is 70-100 Autoregulated between 50-150 mmHg but impaired in trauma, hypoxia. Curve shifted to the right in chronic hypertensives |
|
|
Temperature and CBF |
changes 5-7% per 1 degree Celcius outside of normal (decrease temp=decrease CBF=decrease CMR02) Febrile prevention is key |
|
|
Cerebral Spinal Fluid amounts and replacement |
-CSF 100-150 mL total at one time, 100 mL in ventricles, 50 mL in subarachnoid space. -Replaced 4 times/day at a rate of 0.3-0.4 mL/minute (about 600-750 mL made per day)
|
|
|
What makes up CSF? Where is it made and where is it absorbed? |
Made by Na, Cl-, Bicarb Formed in choroid plexus (cooked in the choroid) Absorbed in Arachnoid Villi (absorbed in the arachnoid) Thanks Diana :-)
|
|
|
carotid arteries |
provide 85% of the anterior circulation of Circle of Willis, become the Anterior, Middle, and Posterior cerebral arteries |
|
|
Major Inhibiting Neurotransmitters (CNS) |
open chloride channels=hyperpolarize 1. GABA (Meds: benzos, barbiturates) 2. Dopamine (inhibiting in CNS) 3. Glycine (counteracts glutamate) 4. Ach in brain |
|
|
Huntington's Chorea |
loss of GABA (receptors?) |
|
|
Major Excitatory NT in CNS |
Na+ into cell=depolarization 1.Glutamate (brain) 2. (spinal cord) 3. Substance P 4. Enkephalins/Endorphins 5. NMDA 6. AMPA |
|
|
Ketamine in neurosurgery. Recommonended? |
No. It can increase CBF up to 50%, increasing ICP |
|
|
Etamidate in neurosurgery. Recommended? |
Yes. It decreases CMRO2, CBF and ICP |
|
|
Riluzole |
glutamate receptor blocker theoretically decreases the neuronal ischemic cascade |
|
|
What is "coupling" ? |
relationship between neuronal activity and cerebral blood flow. |
|
|
Michenfelder's Curve |
curve that demonstrates the relationship between CBF and PaC02 (also Pa02 and CPP) |
|
|
How long does it take after being properly medicated for a chronic hypertensive patient's autoregulation curve return back to normal? |
about 3 months of normotension |
|
|
What ion causes NT release? |
arrival of a nerve impulse triggers an influx of calcium at the presynaptic axon terminal, which then causes the release of the NT
|
|
|
Why should dextrose fluids never be used in neuro cases? |
Hyperglycemia can exacerbate global hypoxia by increasing cerebral acidosis and promotes increase in CBF and cerebral edema |
|
|
What occurs during brain hypoxia? |
1. No 02 is reserved, so unconsciousness occurs when Pa02 decreases to 30 mmHg. If not restored in less than 8 minute the ATP stores are used up and there is irreversible cellular damage. 2. In absence of 02, glucose undergoes anerobic glycolysis, resulting in lactate which greatly increases CBF with severe uncoupling as a result. Lactic acid initiates: calcium influx, release of glutamate, release of free radicals (partly why mannitol is used) and prostaglandin release=vasoconstriction |
|
|
Respiratory Centers |
1. Medulla is where the rhythmicity center is located. Has both I (inspiratory) and E (expiratory) neurons. They are reciprocal so=rhythm.
The rhythmic center is under the control of the Pons. Apneustic center promotes inspiration Pneumotaxic center inhibits inspiration (expiration) *The vagus nerve effects the expiratory component by inhibiting the apneustic center |
|
|
Meds to decrease CSF production |
1. Lasix. Will inhibit Na and Cl- Dose: 1mg/kg to decrease ICP
2. Diamox/Acetazolamide: decreases bicarb by inhibiting carbonic anhydrase in kidneys.
|
|
|
Monroe-Kellie Doctrine |
Components that make up ICP Brain Tissue Volume + blood volume + CSF=ICP
BTV=80% BV=12% CSF=8% If one volume increases, another must decrease |
|
|
ICP What is Intracranial Pressure? |
Pressure inside cranial vault. Normal is 10-15 mmHg mimics intraocular pressure changes throughout the day: highest in the morning |
|
|
Pressure-Volume Compliance Curve |
ICP remains relatively stable until a point/volume is reached where further increase in volume results in large increases in ICP
|
|
|
Cushing's Reflex |
reflex of direct CNS sympathetic stimulation in response to ICP causing cerebral ischemia. Increased HR and Increased contractility (increased BP) help to maintain CPP CPP=MAP-ICP
|
|
|
Cushing's Triad |
1. Hypertension baroreceptor activity in carotid and aortic arches sense increase in BP which then results in: 2. Bradycardia 3. agonal respirations
*ALWAYS DECREASE ICP FIRST (barbs) as the CV compensatory mechanisms should reverse with decrease ICP |
|
|
Define "Luxury Perfusion" |
-relative hyperemia where blood flow exceeds metabolic requirements through tissue acidosis -effects of vasomotor paralysis, as the vessels dont respond to the effects of PaC02 -tumors can enable this |
|
|
Define "Steal Effect: |
"intracerebral steal phenomenon (ISP)" is a paradoxical vasodilatory response that reduces the cerebral blood flow to the impaired perfusion area. Due to increasing overall PaC02 in system (hypoventilation). Rationale used for hyperventilating patients with areas of brain ischemia. |
|
|
Define "Robin Hood" aka "Inverse Steal" Effect |
As PaC02 decreases (usually d/t hyperventilation) blood flow will increase to the ischemia areas. Logic used for treating cerebral ischemia by keeping ET PaC02 lower. "steal from the rich, give to the poor" |
|
|
Which muscle relaxants would be best in patients with head injuries/ischemic injuries? |
Try to stick with the aminosteroids as they do not promote the release of histamine and histamine results in dilation and increased CBF. Benzolisoquinolones tend to release histamine. (although cisatricurium MUCH LESS than atricurium) |
|
|
5 Types of Skull Fractures |
1. Linear: usually no tx required. Exception: temporal area involving the middle meningeal artery can cause an epidural bleed 2. Comminuted: depressed= greater than 5 mm and may require sx and seizure prophylaxis 3. Compound: dirty. needs cleaning, risk of infection 4. Diastisis: involves widening cranial sutures. large amount blood loss, usually seen in children 5. Basilar: difficult to dx. need CT/Xray. s/s: Battle's sign, raccoon eyes, CSF leak, history of Coup-contracoup injry |
|
|
Epidural Cranial Hemorrhage |
85% arterial in origin Classic: initial LOC, then period of lucidity followed by rapid neurological decline |
|
|
Subdural Cranial Hemorrhage |
bleed into subdural space. predisposing factors: elderly, ETOH abuse, anticoagulant therapy, bleeding disorders. high morbidity/mortality burrholes/hematoma evacuation |
|
|
Glasgow Coma Scale: how to rate and how to treat based on numbers. |
Scale of 3-15 Less than 8=ventilate!
Decerebrate=injury to brainstem Decorticate=injury higher than brainstem |
|
|
Cerebral blood flow formula |
CPP/SVR |
|
|
Frontal lobe functions |
reason, will, intellect, personality. Separated from parietal lobe by central sulcus Harbors Broca's Area, if damaged results in expressive aphasia (inability to speak) |
|
|
Parietal lobe functions |
verbal articulation, speech comprehension. Interprets textures/shapes of objects |
|
|
Alpha Waves |
apparent in awake state |
|
|
Delta Waves |
Common during sleep, emitted from cerebral cortex |
|
|
Function of Caudate Nucleus |
controls unconscious contractions of skeletal muscles during awake state. Damaged in ALS, Parkinson's Disease=tremors |
|
|
Temporal Lobe functions |
contains auditory centers, interprets sensory experiences and stores memories, and comprehension harbors Wernicke's Area. If damaged can not understand language and causes receptive aphasia (word salad) |
|
|
Pituitary Gland location |
covered by dura mater in sella turcica of sphenoid bone |
|
|
What is the Pons and its major function? |
bulge on underside of brain between that connects cerebellum and medulla. Cranial Nerves V, VI, VII, and VIII have nuclei within the pons. Harbors the apneustic and pneumotaxic areas |
|
|
Cerebellum primary functions |
coordination of skeletal muscles. Maintains posture and muscle tone. Disease of cerebellum: cerebral palsy |
|
|
Reticular Activating System |
Reticular formation (complex nuclei and nerves within brain stem) that arouses the cerebrum. Principle function to keep cerebrum alert and conscious.
|
|
|
List layers of spinal cord and surrounding structures. |
X |
|
|
Where does brain herniation occur? |
Foramen of Madendie (cisterna magna). Basilar cerebral artery is compressed and S/S: headache, dizziness, coma, flaccidity, pinpoint pupils, hyperreflexia |
|
|
What characteristics allow a substance to easily pass through the BBB? |
1. lipid solubility. Example: ETOH, induction agents. 2. Mediated transport. Ex: glucose 3. Simple diffusion (depends on molecular size and polarity)
|
|
|
Where does Dural Sac end in adults? peds? |
adults: S2 Peds: S3 |
|
|
Where does spinal cord end in adult? child over 1 yr? infant? |
adult: L1 child: L2 infant: L3 |
|
|
What is Cauda Equina Syndrome? Causes and symptomology |
damage to cauda equina causes acute loss of function of the lumbar plexus. Is a lower motor neuron lesion. S/S: back pain, bowel/bladder dysfuntion, sciatic pain, weakness in legs, loss of ankle reflex, gait disturbances |
|
|
Circle of Willis blood supply |
Two Internal Carotids Two vertebral arteries (arise from subclavian, enter through foramen magnum, form the basilar artery) |
|
|
Management of Carotid Endarderectomy |
1. maintain adequate cerebral perfusion. 2. monitor adequacy of CBF during cross-clamping (if awake=follow commands, if anesthetized= "appropriate" stump pressure of greater than 60 mmHg. 3. Regional vs. General: deep cervical plexus block at C3/4 plus superficial block. Or Isoflurane offers most cerebral protection. 4. Minimize stress response, CV instability. Use benzos and narcotics. 5. Major Complications: Identify Carotid Sinus Syndrome, Postoperative airway compression from hematoma, 5% incidence of post op stroke d/t emboli
|
|
|
Carotid Sinus Syndrome |
exaggerated activity of carotid baroreceptors in response to mechanical manipulation. 80% will vagal, 10% severe hypotension d/t inhibition of SNS. Treatment: infiltration with lidocaine 3-5 mL of 1%. For other causes other than surgery: cardiac pacing and carotid sinus ablation |
|
|
Causes of seizures |
structural, brain lesion, trauma, stroke, uremia, liver failure, low blood sugar, decreased Ca++, drug toxicity, drug/ETOH withrawal |
|
|
Epileptogenic Drugs |
1. ketamine 2. brevital 3. atricurium(laudanosine byproduct) 4. demerol (normeperidine byproduct) 5. Ethrane GA gas, esp at high MAC
*remember that dilantin, barbituates, carbamazapine, smokers are enzyme inducers, so will need higher doses/increased redose of NDMB |
|
|
Autonomic Hyperreflexia Pathophysiology |
Usually occurs in pts with SCI above T4 (88%) The reflex arc from sensory stimulation is not able to be inhibited by the efferent motoneurons from lateral/anterior corticospinal tracts. This results in generalized and persistent vasoconstriction below damage to spinal cord. Baroreceptors in aortic arch and carotid sinus are activated and results in bradycardia (2/2 severe hypertension) and the parasympathetics take over in areas above the lesion vasodilate. All of these result in: profuse sweating upper body and flushing, nasal stuffiness, nausea/vomiting, visual field defects, cold skin and pallor on lower region, pulmonary edema 2/2 increased afterload and LV failure, dysrhythmias. |
|
|
Ideal Anesthesia for pts with known Autonomic Hyperreflexia |
1. spinal anesthesia for lower surgeries but difficult to assess the effectiveness of the block 2. general anesthesia--MAC BAR will blunt sympathetic responses.
*Succ NOT advised d/t upregulation of extrajunctional receptors in paralyzed limbs after 72 hours of injury. |
|
|
pharmacologic treatments for Autonomic Hyperreflexia |
ganglionic blockers, trimethiphan (Ach at N2 blocker so blocks all ANS), alpha blockers (prazosin, terazosin, phentalamine/regitine), nipride
*always remove stimulus first! |
|
|
A.Which levels of SCI would cause permanent ventilatory support? B. Quadripelegia? C. Paraplegia? D. High incidence of AHR? E. Most common sites of SCI? |
A. C3, C4, C5 (diaphragm innervation) but anything above T7 has high respiratory dysfunction so increased risk pneumonia B. Above T1 C. Above L4 D. T4 and above E. C 5-6 from MVA and T12-L1 |
|
|
What is Ondine's Curse? |
having to consciously breath 2/2 SCI to anterolateral portion of C2-4
Fun/Not so Fun Fact: dolphins always have to consciously breath and when are kept in captivity and become depressed, often commit suicide by consciously deciding to not breath. Flipper from the infamous TV show did this |
|
|
Describe the effects of upper SCI on ventilation |
1. If intercostals are paralyzed, 60% of TV is lost d/t inability for rib cage expansion. Also, cough mechanism is decreased so both put pt at high risk for atelectasis/pneumonias. 2. Respiratory acidosis 2/2 decreased alveolar ventilation |
|
|
What is Spinal Shock and its pathophysiology |
Loss of vascular tone, vasopressor reflex, and somatic sensory loss immediately after a SCI and can last hours to 6 weeks. Loss of sympathetic tone causes vasodilation to predominate and results in pooling of blood and hypotension. Bradycardia d/t loss of cardiac accelerators in T1-T4. Poikliothermic d/t loss of sympathetic tone via hypothalamus so keep pts warm!!!
(Although, injuries C7 and greater can cause an increase in temp as pts unable to sweat--also can result in hypoxemia as increased temp will increase 02 consumption and limited ventilatory drive can not compensate.) |
|
|
How does Spinal Shock increase the risk of Malignant Hyperthermia? (with succ) |
Increased Ca++ d/t decreased muscle activity occurs 10 days post injury and can last 3 months. |
|
|
Effects of Halogenated gases on SSEP monitoring (latency and amplitude) |
amplitude=decreased latency=increased |
|
|
Risks of sitting position on a craniotomy patient |
1. VAE 2. Cervical cord infarction 3. Pneumocephalus
4. cerebral hypotension |
|
|
Pathophysiology of VAE and S/S in anesthetized pt. |
Transvenous pressure in a noncompressible vessel is less than atmospheric pressure so air is sucked inwards. Air emboli reaches R heart and causes massive air "lock", which results in severe decrease in venous return and cardiac output/ BP. If large amount of air enters PA to lungs, can increase alveolar dead space, pronounced V/Q mismatch and hypoxemia and hypercarbia which will significantly increase PVR. This can result in R sided Heart failure/cor pulmonale. S/S: May attempt to cough if not paralyzed, Decrease ETC02 but high PaC02. hypotension, hypoxemia and cardiac dysrhythmias are late signs. |
|
|
How to monitor and diagnose VAE |
1. TEE--sensitive to both volume and rate of air. 2. ET N2. Nitrogen is 33Xs more diffusable than 02 and air from the emboli is absorbed into alveoli. 3. Doppler ultrasound is very sensitive to air (not volume). Listen over 3rd ICS right of sternum. Listen for "mill wheel murmur" |
