Flashcards in UNIT 7 Neuro Deck (112):
Name 4 types of glial cells and describe the function of each
- most abundant
- regulation of metabolic environment
- repair neuron after neuronal injury
- concentrated in roof of 3rd/4th ventricles & SC
- form the choroid plexus, which produces CSF
- form the myeline sheath in the CNS
- schwann cells form the myelin sheath in the PNS
- act as macrophages and phagocytize neuronal debris
list the name and function of the 4 lobes of the cerebral cortex
frontal: contains the motor cortex
parietal: contains somatic sensory cortex
occipital: contains vision cortex
temporal: contains auditory cortex & speech centers
- Wernicke's area: understanding speech
- Broca's area: motor control of speech
Name the 12 cranial nerves
XI spinal accessory
What CNs provide motor control of the eyes? How does each nerve contribute to the eye's movement?
- up (in, out, and straight)
- down (out and straight)
- in and down
What bedside tests are used to assess the CN?
III eye movement, pupil constriction
IV eye movement
V facial sensation (+ ant 2/3 tongue sensation)
VI eye movement
VII facial movement except chewing
VIII hearing, balance
IX posterior 1/3 tongue sensation
XI shoulder shrug
XII tongue movement
Which CN resides in the CNS? What is the implication of this?
CN II is the only CN that is part of the CNS (the rest are part of the PNS). This means that CN II is the only CN that is surrounded by dura.
It is bathed in CSF. If you inject LA into the optic nerve during RA of the eye, you will have a big problem.
What is tic douloureux? What CN contributes to this problem?
causes excruciating neuropathic pain in the face
What is Bell's palsy? What CN contributes to this problem?
causes ipsilateral facial paralysis
What is the function of CSF, and where is it located?
cushions the brain, provides buoyancy, and delivers optimal conditions for neurologic function.
It is located in the:
- ventricles (lateral, 3rd, and 4th)
- cisterns around the brain
- subarachnoid space in brain & SC
What regions of the brain are NOT protected by the BBB?
BBB separates the CSF from the plasma. It has tight junctions that restrict pass of large molecules & ions.
The BBB isn't present at the chemoreceptor trigger zone, posterior pituitary gland, pineal gland, choroid plexus, and parts of the hypothalamus
What is the normal volume and specific gravity of CSF?
spec grav 1.002-1.009
Describe the production, circulation, and absorption of CSF.
CSF production: ependymal cells of the choroid plexus (of lateral ventricles), rate of 30mL/hr
circulation: lateral ventricles --> foramen of Monro--> 3rd vent --> aqueduct of Sylvius --> 4th vent --> paired foramen of Luschka/midline foramen of Magendie --> subarachnoid space --> superior sagittal sinus
absorption: arachnoid villi within the superior sagittal sinus (to the venous circulation)
What is the formula for CBF? what are the normal values for global, cortical, and subcortical flow?
CBF = CPP/CVR
(CVR = cerebral vascular resistance)
global 45-55mL/100g (or 15% of CO)
What are the 5 determinants of CBF?
What is the normal value for CMROs? What factors cause it to increase? To decrease?
CMRO2 describes how much O2 the brain consumes per minute.
3.0-3.8mL O2/100g brain tissue/min
decreased by hypothermia (7%/1C), IA, propofol, etomidate, barbs
increased by hyperthermia, ketamine, N2O
What is the formula for CPP? What is normal?
CPP = MAP - ICP (or CVP, whichever is higher)
autoregulation via vessel diameter changes to provide a constant CPP of 50-150mmHg
- i.e. MAP needs to be higher
- autoreg is influenced by products of local metabolism, myogenic mechanisms, and autonomic innervation
What are the consequences of a CPP that exceeds the limits of autoregulation (too high and too low?)
- vessels are maximally dilated
- CBF becomes pressure dependent
- risk of cerebral hypoperfusion
- vessels are maximally constricted
- CBF becomes pressure dependent
- risk of cerebral edema & hemorrhage
list 4 conditions that reduce CPP as a function of increased venous pressure.
a high venous pressure decreased cerebral venous drainage & increases cerebral volume --> backpressure is created to the brain that reduces the arterial/venous pressure gradient (MAP-CVP)
conditions that impair drainage:
- jugular compression d/t head position
- increased intrathoracic pressure d/t cough, PEEP
- vena cava thrombosis
- vena cava syndrome
What is the relationship b/n PaCO2 and CBF? What physiologic mechanism is responsible for this?
- pH of the CSF around the arterioles controls the cerebral vascular resistance
- at a PaCO2 of 40mmHg, CBF is 50mL/100g tissue/min
At what PaCO2 does maximal cerebral vasodilation occur? How about maximal cerebral vasoconstriction?
for every 1mmHg change in PaCO2, CBF will change by 1-2mL/100g tissue/min
max vasodilation occurs at PaCO2 of 80-100mmhg
max vasoconstriction occurs at PaCO2 of 25mmHg
What is the relationship b/n CMRO2 and CBF?
as a general rule
- things that increase the amount of O2 the brain uses (CMRO2) tend to cause cerebral vasodilation (increased CBF) --> hyperthermia, ketamine
- things that decrease CMRO2 tend to cause cerebral vasoconstriction (decreased CBF) --> hypothermia, propofol, TPL
halogenated anesthetics are an exception; they decouple the relationship: reduce CMRO2, but also cause cerebral vasodilation
- this is why TIVA is a better choice w/ intracranial hypertension
How do acidosis & alkalosis affect CBF?
resp acidosis = increased CBF
resp alkalosis = decreased CBF
met acidosis/alkalosis don't directly affect CBF. This is because H+ doesn't pass through the BBB. A compensatory change in MV can, however, affect CBF.
How does PaO2 affect CBF?
PaO2 <50-60mmHg causes cerebral vasodilation & increases CBF
When PaO2 is >60mmHg, it doesn't affect CBF.
What is the normal ICP? What values are considered abnormal?
ICP is the supratentorial CSF pressure
normal = 5-15mmHg
cerebral HTN > 20mmHg
When is ICP measurement indicated? What is the gold standard for measurement?
when GCS <7
intraventricular catheter is the gold standard
- subdural bolt
- catheter placed over the convexity of the cerebral cortex
List the s/s of intracranial HTN
papilledema (swelling of the optic nerve)
focal neurologic deficit
discuss the monroe-kellie hypothesis
brain lives in a rigid, bony box containing brain, blood, and CSF
- if one component increases in volume, another component must decrease in order to maintain constant pressure
- remember intracranial compliance curve
What is Cushing's triad? What is the clinical relevance of this reflex?
indicates intracranial HTN
- irregular respirations
increased ICP --> decreased CPP w/ compensatory HTN
--> baroreceptor reflex activation
compression of medulla --> irregular respirations
name 4 areas where brain herniation can occur.
1. of the cingulate gyrus under the falx
3. cerebellar tonsils via the foramen magnum
4. via a site of surgery or trauma
How does hyperventilation affect CBF? What is the ideal PaCO2 to achieve this effect?
CO2 dilates vessels --> decreased CVR --> increased CBF --> increased ICP
hyperventilation --> decreased ICP in this manner
lowering PaCO2 <30 increases the risk of cerebral ischemia d/t vasoconstriction & L shift of the oxyHgb dissociation curve
How do NTG & SNP affect ICP?
cerebral vasodilators --> increases CBF --> increase ICP
How does head position affect ICP?
head elevation >30 degrees facilitates venous drainage away from the brain
neck flexion or extension can compress the jugular veins, reduce venous outflow, increase CBV, and increase ICP
head down positions increase CBV & ICP
How does mannitol reduce ICP? What problems can arise when mannitol is used in this way?
0.25-1g/kg increases serum osm & "pulls" water across the BBB towards the bloodstream for excretion
- if BBB is disrupted, mannitol enters the brain & promotes cerebral edema
- mannitol transiently increases blood volume, which can increase ICP & stress the failing heart
describe anterior & posterior circulation of the brain. Where do these pathways converge?
converge at the circle of willis
ICA enter skull via foramen lacerum
aorta --> carotid --> ICA --> circle of willis --> cerebral hemispheres
vertebral a enter skull via foramen magnum
aorta --> SC --> vertebral --> basilar --> posterior fossa structures & cervical SC
describe the anatomy of the circle of willis.
primary function of the circle of willis is to provide redundancy of blood flow in the brain. If one side of the circle becomes occluded, the other side should theoretically be able to perfuse the affected areas of the brain
Which population of stroke patients should receive a thrombolytic agent?
CVA d/t thrombosis
diagnosis must be made by emergent head CT prior to administration
if tx can begin <3hrs after onset of symptoms, the pt should receive tPA
- aspirin is acceptable if tPA cannot be administered
What is the relationship b/n hyperglycemia & cerebral hypoxia?
During cerebral hypoxia, glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue & is associated w/ worse outcomes
monitor serum glucose, treat hyperglycemia, be careful administering dextrose containing IVF
in the context of cerebral aneurysm, how is transmural pressure calculated?
an increased transmural pressure predisposes the aneurysm to rupture.
transmural pressure = MAP - ICP
MAP = pressure pushing outward against the aneurysmal sac
ICP = counterpressure that pushes against it.
--> creates a tamponade effect
risk of rupture is increased by HTN and/or acute reduction in ICP
What is the most common clinical finding in a patient w/ SAH? What are the other s/s?
WHOL (worst HA of life)
- LOC (50%)
- neurologic deficits
What is the most significant source of M&M in the patient w/ SAH?
cerebral vasospasm (delayed contraction of the cerebral arteries); can lead to cerebral infarction
free Hgb that is in contact w/ the outer surface of the cerebral arteries increases the risk --> +correlation b/n amount of blood observed on CT & vasospasm incidence
What is the incidence of cerebral vasospasm? When is it most likely to occur?
25% of patients
most likely 4-9days after SAH
What is the treatment for cerebral vasospasm?
triple H therapy (hypervolemia, HTN, permissive hemodilution to Hct 27-32%)
nimodipine (CCB) reduces M&M associated w/ vasospasm --> doesn't actual reduce the spasm, but increases the collateral blood flow
during endovascular coil placement for a cerebral aneurysm, the aneurysm ruptures. What is the best treatment at this time?
protamine 1mg/100U heparin
+/- adenosine to temporarily arrest the heart
be able to calculate the Glascow coma scale
How do you treat the patient w/ an ICH who is on warfarin?
FFP, prothrombin complex concentrate, and/or recombinant factor VIIa to reverse the warfarin
vitamin K isn't the best option for acute warfarin reversal
How do you treat the patient w/ an ICH who is on clopidogrel?
platelet transfusion (aspirin can be reversed this way too)
there is also evidence of reversal w/ recombinant factor VIIa
What are two common ways of reducing ICP that should specifically be avoided in the patient w/ a TBI?
hyperventilation (can worsen cerebral ischemia + it's only indicated as a temp measure)
steroids (worsen neurologic outcome)
Is N2O safe in the pt w/ TBI?
other injuries, such as pneumothorax, may only become evident after anesthetic induction & PPV
compare and contrast the 5 types of seizures.
- generalized tonic/clonic activity
- respiratory arrest --> hypoxia
- tx: propofol, diazepam, TPL
- surgical: vagal nerve stim or rsxn of foci
- localized to a particular cortical region
- can be motor or sensory
- usually no LOC
absence (petit mal)
- temporary loss of awareness
- more common in children
- temp LOC & postural tone (can result in fall & TBI)
- more common in children
- seizure activity >30min or 2 grand mal w/out regaining consciousness in between
- resp arrest --> hypoxia
- tx: phenobarb, phenytoin, benzos, propofol, and even GA
What is the relationship b/n etomidate and seizures
etomidate commonly causes myoclonus. This is not associated w/ increased EEG activity in those that do not have epilepsy.
In those w/ sz disorders, etomidate (or methohexital or alfentanil) increases EEG activity and can be used to help determine location of seizure foci during cortical mapping
Describe the patho of Alzheimer's disease
diffuse beta amyloid rich plaques and neurofibrillary tangles in the brain
- dysfunctional synaptic transmission (most notable at nACh neurons)
- apoptosis (programmed cell death)
What class of drugs is used to treat Alzheimer's disease?How do they interact w/ succinylcholine?
tx is palliative & aims to restore the [ACh]; cholinesterase inhibitors (tacrine, donepezil, rivastigmine, galantamine)
cholinesterase inhibitors increase the DOA of succ, although the clinical significance is debatable
Describe the patho of Parkinson's disease.
dopaminergic neurons in the basal ganglia are destroyed ---> imbalance of DA & ACh (relative ACh increase)
this leads to suppression of corticospinal motor system + overactivity of extrapyramidal motor system
What drugs increase the risk of extrapyramidal s/s in the pt w/ Parkinson's disease?
butyrophenones (haldol, droperidol)
What is the most common eye complication in the perioperative period? What is the most common cause of vision loss?
ischemic optic neuropathy = most common cause of vision loss
Describe the patho of ischemic optic neuropathy.
ischemia of the optic nerve. Most likely explanation is that venous congestion in the optic canal reduces perfusion pressure
ocular PP = MAP - intraocular pressure
central retinal & posterior ciliary arteries are at highest risk b/c they are "watershed" areas -- they lack anastomoses w/ other arteries
What surgical procedure presents the most significant risk of ION? What are other procedure & patient risk factors?
spinal surgery in the prone position = most significant risk
- use of Wilson frame
- long duration of anesthesia
- large EBL
- low colloid:crystalloid resus
- old age
discuss the blood flow to the SC
SC is perfused by:
1 anterior spinal artery (anterior 2/3 of SC)
2 posterior spinal arteries (posterior 1/3 of SC)
6-8 radicular arteries
What is the most important radicular artery? Which spinal segment does it typically enter the SC?
artery of Adamkiewicz
along w/ the anterior spinal artery, the artery of adamkiewicz supplies the anterior cord in the thoracolumbar region. Most commonly originates b/n T11-T12
Envision the anatomy of the SC & spinal nerve in cross section.
sensory neurons from the periphery via the dorsal nerve root
motor & autonomic neurons exit via the ventral nerve root
describe the organization of the 3 neuron pathway common to the spinal tracts.
each pathway consists of three neurons:
1. first order: peripheral nerve to SC or brainstem
2. second order: SC or brainstem to subcortical structure
3. third order: subcortical structure to the cerebral cortex.
compare the structure & function of the dorsal column with the spinothalamic tract.
dorsal column (medial lemniscal system)
- transmits mechanoreceptor sensations (fine touch, proprioception, vibration, pressure)
- capable of 2 point discrimination (high degree of localization)
- large, myelinated, rapidly conducting fibers
- faster transmission than anterolateral system
- a "more evolved" system
anterolateral system (spinothalamic tract)
- transmits pain, temp, crude touch, tickle, itch, sexual sensation
- no 2 point discrimination
- smaller, myelinated, slower conducting fibers
- more "primitive" system
What bedside exam can assess the integrity of the corticospinal tract? How can you interpret it?
most important motor pathway (often referred to as the pyramidal tract, all others are collectively the extrapyramidal tract)
Babinski test (firm stimulus to underside of foot) yields:
- normal: downward motion of all the toes
- upper motor neuron injury: upward extension of big toe + fanning of the others
- lower motor neuron injury: no response
contrast the presentation of upper vs. lower motor neuron injury
upper motor neurons begin in the cerebral cortex & end in the ventral horn of the SC, while the lower motor neurons begin in the ventral horn & end at the NMJ
upper motor neuron injury presents w/ hyperreflexia & spastic paralysis
lower motor neuron injury presents w/ impaired reflexes & flaccid paralysis
discuss the patho of neurogenic shock.
impairment of cardioaccelerator fibers (T1-T4) --> unopposed cardiac vagal tone --> bradycardia & decreased inotropy
decreased SNS tone --> vasodilation --> venous pooling --> decreased CO & BP
impairment of sympathetic pathways from hypothalamus to blood vessels --> inability to vasoconstrict or shiver --> hypothermia
how can you differentiate neurogenic shock from hypovolemic shock?
neurogenic: bradycardia, hypotension, hypothermia w/ pink, warm extremities d/t cutaneous vasodilation
hypovolemia: tachycardia, hypotension, cool, clammy extremities.
Discuss the use of succinylcholine in the patient w/ SC injury.
avoid if >24hrs post injury
do not use for at least 6months thereafter, some books say 1yr
When does a pt w/ SC injury become at risk for autonomic hyperreflexia? What factor (other than time) contributes to this risk?
After the neurogenic shock phase ends (1-3 weeks), the body begins to mend itself in a pathologic and disorganized way, putting the pt at risk for autonomic hyperreflexia.
up to 85% of patients w/ injury >T6 will develop, very unlikely to occur in those w/ injury
List 6 situations that can precipitate autonomic hyperreflexia
sitmulation of the hollow organs (bladder, bowel, or uterus)
surgery (esp cysto, CLN)
Discuss the presentation & pathophysiology of autonomic hyperreflexia.
classic presentation = HTN & bradycardia.
stimulation below the level of SCI triggers sympathetic reflex arc that creates a profound degree of vasoconstriction below the level of injury --> baroreceptor activation in carotid bodies (bradycardia) --> body attempts to reduce afterload w/ vasodilation above the level of the injury.
- reflex vasodilation above level of SC injury --> nasal stuffiness
- HTN --> HA/blurred vision
- malignant HTN --> CVA, sz, LV failure, dysrhythmias, pulmonary edema, and/or MI
detail the anesthetic management of the patient w/ autonomic hyperreflexia.
prevent stimulation to the area below level of injury to prevent AH!
- GA or spinal = best
- epidural not as good for laboring mother b/c doesn't inhibit sacral nerve roots as much
- tx HTN w/ removal of stim, deepen IA, + rapid vasodilator (SNP)
- tx bradycardia w/ atropine/glyco
- avoid meds that increase HR & vasoconstrict
- avoid sux x6months
- monitor for AH closely in the immediate post-op period, when anesthesia is wearing off.
Discuss the patho of amyotrophic lateral sclerosis.
causes progressive degeneration of motor neurons in the corticospinal tract. Astrocytic gliosis replaces the affected motor neurons. Both the upper & the lower motor neurons are affected.
Etiology is unknown
Detail the anesthetic management of ALS
- no clear evidence that supports one technique over another
- avoid sux (hyperK+)
- increased sensitivity to NDMR
- bulbar m dysfunction increases risk of aspiration
- chest weakness decreases VC & MMV
- consider post-op mechanical ventilation
describe the patho of myasthenia gravis
IgG Ab destroy post-junctional nAChR at the NMJ. (ACh is present in sufficient quantity, the receptors just aren't there)
--> skeletal m weakness.
Key feature is skeletal m weakness that becomes worse later in the day or that develops w/ exercise & can recover some w/ rest.
What surgical procedure can reduce symptoms in the patient w/ myasthenia gravis?
the thymus gland plays a key role in MG, and thymectomy brings symptom relief to many patients
- it reduces circulating anti-AChR IgG in most patients
- surgical approach may be via median sternotomy or by the transcervical approach
How does myasthenia gravis affect the pregnant mother & the fetus?
in 1/3 of women, pregnancy intensifies the symptoms of MG.
Anti-AChR IgG Ab cross the placenta and cause weakness in 15-20% of neonates. This can persist x2-4 weeks, which is consistent w/ the half-life of these antibioties in the neonates circulation
- they may require airway management.
How can you tell the difference b/n cholinergic crisis and myasthenic crisis?
Pryidostigmine (anticholinesterase) is the first line tx for MG. An OD can cause cholinergic crisis, which can include skeletal m weakness (makes differentiation difficult)
diagnosis is made by administering 1-2mg IV edrophonium ("Tensilon test")
- if weakness is made worse, then the pt has cholinergic crisis (tx = anticholinergic)
- if weakness improves, then it was an MG exacerbation (tx = anticholinesterase, immunosuppression, plasmapheresis)
How do patients with myasthenia gravis respond to NMB?
bc there is a reduction in the number of m-nAChR at the NMJ, those w/ MG have an increased sensitivity to NDMR and a resistance to succinylchline.
IA cause skeletal m relaxation by acting in the ventral horn of the SC - in many cases this eliminates the need for NMB.
WHy are patients w/ myasthenia gravis prone to aspiration?
bulbar m weakness (mouth and throat) manifests as difficulty handling oral secretions --> increased risk of aspiration
describe the patho of Eaton Lambert syndrome
IgG mediated destruction of the presynaptic v-gated Ca++ channel at the presynaptic nerve terminal.
When the AP depolarizes the nerve terminal, Ca++ entry into the presynaptic neuron is limited, thereby reducing the amount of ACh that is released into the synaptic cleft.
Postsynaptic nAChR is normal
compare and contrast myasthenic gravis to eaton-lambert syndrome in terms of patho, common comorbidities, and response to NMB
- v-gated Ca++ channels
- decreased ACh release
- presynaptic neuron of NMJ
- comorb: small cell lung CA
- sensitive to NMB (both)
- AChE inhibitors doesn't improve symptoms
- Nm receptor (post)
- decreased ACh response
- postsynaptic motor endplate
- comorb: thymoma
- resistant to sux, sensitive to NDMR
- AChE inhibitors improve symptoms
describe the patho of Guillain-Barre syndrome.
characterized by an immunologic assault on the myelin in the peripheral nerves. The AP can't be conducted --> the motor endplate never receives the incoming signal
usually persists for approx 2 weeks and ends w/ full recovery in approx 4 weeks.
discuss the presentation of guillian-barre
flu-like illness usually precedes paralysis by 1-3 weeks
- flaccid paralysis begins in the distal extremities and ascends bilat toward proximal extremities, trunk, face
- intercostal m weakness impairs ventilation
- facial, pharyngeal weakness causes dysphagia
- sensory deficits: paresthesias, numbness, +/- pain
- autonomic dysfunction is common: HR, BP, sweating abnormalities, orthostatic hypotension
What is familial periodic paralysis and how can the 2 variants of this disease be distinguished from each other?
two distinct disease processes that are characterized by acute episodes of skeletal m weakness that is accompanied by hypo or hyperkalemia
hypokalemia: diagnosed if skeletal m weakness follows a glucose-insulin infusion
hyperkalemia: diagnosed if skeletal m weakness follows oral K+ administration
What drugs should be avoided in the patient w/ each type of familial period paralysis? How about temperature?
- glucose containing slns
- K+ wasting diuretics
- B2 agonists
- K+ containing slns (LR)
acetazolamide is the tx for both forms bc it creates a nonanion gap acidosis, which protects against hypokalemia. It also facilitates renal K+ excretion which guards against hyperkalemia
avoid hypothermia for both types.
detail the functions of the following receptors in skeletal m:
which is dysfunctional in the patient w/ MH?
when T-tubule is depolarized, extracellular Ca++ enters the myocyte via the dihydropyridine receptor at the T-tubule
this activates the ryanodine receptor (RYR1), which instructs the SR to release massive Ca++ into the cell. In the case of MH, it releases WAY TOO MUCH
(consumes ATP, O2, produces CO2)
cell attempts to return some Ca++ into the SR via the SERCA2 pump (in MH, this pump becomes overworked)
(consumes ATP, O2, produces CO2)
when the skeletal m consumes all of its ATP, cell membrane integrity is no longer maintained & intracellular components (myoglobin & K+) are released into the systemic circulation I
list 8 consequences of too much Ca++ inside of the skeletal myocyte
- sustained muscular contraction
- accelerated metabolic rate & rapid ATP depletion
- increased O2 consumption
- increased CO2 & heat production
- mixed respiratory and lactic acidosis
- sarcolemma breaks down
- K+ & myoglobin leak into the systemic circulation
- rigidity from sustained contraction
identify 3 conditions that are definitively linked to MH
1. King-Denborough syndrome
2. central core disease
3. multiminicore disease
some texts list that Evans myopathy is also definitively linked to MH (not according to the MHAUS website)
list 6 conditions that are NOT definitively linked to MH
- Duchenne muscular dystrophy
- Becker muscular dystrophy
- neuroleptic malignant syndrome
- myotonia congenita or dystrophy
- osteogenesis imperfecta
what is the most sensitive indicator of MH? What is the time course of the other s/s?
MH can occur as late as 6hrs after exposure to a triggering agent.
most sensitive: EtCO2 rises out of proportion to MV
- masseter spasm
- warm soda lime
- irregular heart rhythm
- pt warm to touch
- irregular heart rhythm
- muscle rigidity
- cola-colored urine
- irregular heart rhythm
what is the difference b/n trismus and MH? How should you proceed if the patients presents with either condition?
trismus & masseter m rigidity exist on a continuum
- trismus: jaw can still be opened
- masseter m rigidity: cannot open jaw
trismus is a normal response to succinylcholine - ok to proceed w/ surgery if occurring in isolation, but may want to avoid other triggering agents.
if the pt has masseter m rigidity, assume MH until proven otherwise
- as an aside, NMB will not help this since it's occurring distal to the NMJ
What is the definitive test for susceptibility to MH?
halothane contracture test
- it only has an 80% specificity, so there is a risk of false-negative result
How does dantrolene treat MH? What are its most common side effects?
classified as a muscle relaxant.
two mechanisms of action:
- halts Ca++ release from the RyR1 receptor
- prevents Ca++ entry into the myocyte which reduces the stimulus for calcium induced calcium release.
the most common side effects are muscle weakness & venous irritation
How is dantrolene formulated? How is it prepared?
each vial contains 20mg dantrolene + 3g mannitol & must be reconstituted w/ preservative free H2O
NaCl introduces additional solute which prolongs the time required for dantrolene to dissolve into the dilutent
enlist help early!!
How do you treat MH?
d/c triggering agent
100% FiO2 >10L/min
dantrolene 2.5mg/kg IV
- repeat Q5-10mins
correct lactic acidosis w/ bicarb
- CaCl 5-10mg IV
- insulin 0.15U/kg + D50 1mL/kg
protect against dysrhythmias
- class I agents (lido, procain)
- avoid CCB w/ dantro to avoid hyperK+
- IV hydration
- 0.25mg/kg mannitol
- 1mg/kg lasix
cool the pt until temp <38C
- cold IVF
- cold fluid lavage
- ice packs
monitor coags, avoid DIC
describe the patho of Duchenne muscular dystrophy
dystrophin is a critical structural component of the cytoskeleton of skeletal and cardiac m cells. It helps anchor actin & myosin to the cell membrane. Absence of it destabilizes the sarcolemma during muscular contraction & increases membrane permeability
extrajunctional receptors populate --> avoid succinylcholine
classic teaching suggests that DM increases the risk of MH, but more recent meta analysis refutes this claim.
How does Duchenne muscular dystrophy affect pulmonary function?
kyphoscholiosis (restrictive lung disease) --> decreased pulmonary reserve --> increased secretions & risk of PNA
respiratory muscle weakness also occurs
How does Duchenne muscular dystrophy affect cardiac function? What EKG findings might you expect?
- degeneration of cardiac m --> decreased contractility, pap m dysfunction, mitral regurg, cardiomyopathy, CHF
- signs of cardiomyopathy = resting tachycardia, JVD, S3/S4 galllop
- gold standard = echo
- ST + short PR
- scarring of posterobasal aspect of LV manifests as increased R wave amplitude in lead 1 & deep Q waves in the limb leads
What is the Cobb angle and what is its significance?
describes the magnitude of the spinal curvature
40-50degrees = indication for surgery
60 = decreased pulmonary reserve
70 = pulmonary symptoms present
100 = gas exchange significantly impaired, higher risk of post-op pulmonary complications
contrast the early & late complications of scoliosis
alters thoracic geometry, which compresses the lungs & creates a restrictive ventilatory defect. One side of the thorax becomes smaller than the other
- restrictive ventilatory defect (same lung volume, capacity decreases as any)
- decreased chest wall compliance
- VQ mismatching
- hypercarbia (sign of impending failure)
- reduced response to hypercapnia
- cor pulmonale
- cardiorespiratory failure
List 3 ways that rheumatoid arthritis affects the airway.
1. TMJ: limited mouth opening
2. cricoarytenoid joints: decreased diameter of glottic opening
3. cervical spine: A-O subluxation w/ flexion + limited extension
What is the most common airway complication of rheumatoid arthritis? What's it's clinical significance?
AO subluxation is the most common airway complication of RA
This is d/t the weakening of the transverse axial ligament, which allows the odontoid to directly compress the SC at the level of the foramen magnum.
- puts the pt at risk for quadriparesis or paralysis
- side note: pts w/ Down syndrome are also at risk for AO subluxation
Discuss the pathophysiology of RA.
autoimmune disease that targets the synovial joints. There is also widespread systemic involvement d/t infiltration of immune complexes in teh small & medium arteries --> vasculitis.
cytokines (TNF & interleukin-1) play a central role in the pathogenesis.
Hallmark of RA: morning stiffness that improves w/ activity
joints are painful, swollen, and warm
- lymph node enlargement
using a systems approach, list the complications of RA.
- TMJ synovitis
- cricoarytenoid arthritis
- AO instability
- pleural effusion
- restrictive pattern d/t diffuse interstitial fibrosis + costochondral involvement that limits chest wall expansion
- pericardial effusion/tamponade
- restrictive pericarditis
- aortic regurgitation
- valvular fibrosis
- coronary artery arteritis
- platelet dysfunction d/t NSAIDs
- renal insufficiency d/t vasculitis, NSAIds
- adrenal insufficiency & infections d/t steroids
- gastric ulcerations d/t NSAIDs, steroids
- Sjogren's syndrome - risk of corneal abrasion
- peripheral neuropathy d/t nerve entrapment
describe the patho of systemic lupus erythematosus.
SLE is an autoimmune disease characterized by the proliferation of antinuclear Ab.
SLE affects nearly every organ system & most consequences are the direct result of Ab-induced vasculitis and tissue destruction
Using a systems based approach, list the complications of systemic lupus erythematosus
targets young women
most common problems are polyarthritis (generally not the spine) & dermatitis
only 33-50% develop the "butterfly rash"
- cricoarytenoiditis: hoarseness, stridor, a/w obstruction
- RLN palsy
- interstitial lung dz w/ impaired diffusing capacity
- pleural effusion
- recurrent PE
- conduction defects
- antiphospholipid Abs
renal: nephritis w/ proteinuria
what drugs can exacerbate SLE?
occurs d/t stress or drug exposure
drug induced usually persists for several weeks-months & presents w/ mild symptoms
most common offenders (PISSED CHIMP)
what is the relationship b/n SLE & antiphospholipid syndrome?
those w/ SLE are prone to developing antiphospholipid antibodies. Although aPTT is prolonged, these pts are prone to a state of hypercoagulability & thrombosis
- risk for stroke, DVT, PT
- pregnant pts are at higher risk
Discuss the patho of myotonic dystrophy.
characterized by prolonged contracture after a voluntary contraction. This is the result of dysfunctional Ca++ sequestration by the SR. Contractions can be so severe that they interfere w/ ventilation & intubation
What 3 things can increase the risk of contractures in the patient w/ myotonic dystrophy?
2. reversal of NMB w/ anticholinesterases (theoretical)
3. hypothermia (shivering --> sustained contractions)
Discuss the patho of Marfan syndrome.
autosomal dominant trait
connective tissue disorder that's associated w/ an elevated risk of aortic dissection, MV prolapse, mitral regurg, aortic regurg.
dissection of the ascending aorta can extend into the pericardium, and this increases the risk of cardiac tamponade. Becks' triad: JVG, hypotension, muffled heart tones.
as an aside, spontaneous pneumo is a common complication in these patients.