Exam 1 Plus Some Peds :/ Flashcards

1
Q

Where are smooth muscle (involuntary) found?

A

within the walls of organs and structures such as:
-esophagus
-stomach
-intestines
-bronchi
-uterus
-urethra
-bladder
-blood vessels
-arrector pili in skin

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2
Q

Cardiac and skeletal muscles are ___________.

A

striated

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3
Q

Where do cardiac muscles connect?

A

at branching, irregular angles–> intercalated discs

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4
Q

What do cardiac and skeletal muscles contain?

A

sarcomeres and are packed into highly regular, repeating arrangements of bundles

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5
Q

How are skeletal muscles arranged?

A

in regular, parallel bundles

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6
Q

What is the difference between striated vs. smooth muscle contraction?

A

striated muscle contracts and relaxes in short, intense bursts, whereas smooth muscle sustains longer or even near permanent contractions

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7
Q

Cardiac muscle is ______ muscle but more akin in structure to skeletal muscle and only found in the heart.

A

involuntary

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8
Q

Neuromuscular junction contains:

A
  1. presynaptic motor neuron
  2. synaptic cleft (contains acetylcholinesterase (AChase)
  3. Highly folded postsynaptic muscle fiber
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9
Q

Nerve stimulation

A

-depolarization reaches nerve terminal and voltage-gated calcium channels open
-storage vesicles (presynaptic) releases Ach into the cleft
-Ach diffuses across the synaptic cleft and binds to the nicotinic cholinergic receptor (postsynaptic)

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10
Q

What 5 subunits do fetal receptors contain?

A

2 alpha
1 beta
1 delta
1 gamma

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11
Q

What 5 subunits do mature receptors contain?

A

2 alpha
1 beta
1 delta
1 epsilon

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12
Q

What does the influx of calcium cause?

A

-Ach vesicles fuse with the nerve plasma membrane and then expel their content into the synaptic cleft

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13
Q

The amount of Ach released is influenced by what?

A

the amount of calcium that enters the nerve terminal during stimulation

-increased calcium that enters the nerve terminal–>increased amount of Ach released

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14
Q

What causes upregulation?

A

When frequency of stimulation of NMJ decreases over days due to:
-severe burns
-immobilization
-infection
-sepsis
-prolonged use of NMBAs in ICU, CVAs
-number of immature nAChrs increases (upregulation) within 24-48 hours

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15
Q

The number of immature nAChRs will have increased sensitivity to ________.

A

Ach and Sch (massive release of potassium if Sch given in patient with burn 24 hours after)

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16
Q

The number of immature nAChRs will have decreased sensitivity to __________.

A

nondepolarizers

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17
Q

What is Multiple Sclerosis characterized by?

A

-inflammation
-demyelination
-immune dysfunction
-failure of cell repair in the CNS

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18
Q

Downregulation is caused by _________________.

A

chronic neostigmine use (too much Ach around) decreases sensitivity of receptors to Ach

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19
Q

Multiple Sclerosis is a demyelinating disease of _______ & __________.

A

brain & spinal cord

causing:
-muscle weakness
-cognitive dysfunction
-memory loss
-personality disorders

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20
Q

What is the pathophysiology of MS?

A

autoimmune disease characterized by T-cell mediated autoantibodies against myelin (converts T-cells into inflammatory cells)
-peripheral nerves not affected

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21
Q

MS is 8x higher in ____________.

A

females

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22
Q

Symptoms of MS

A

-Depends on sites of demyelination

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23
Q

Brainstem symptoms of MS

A

DAAAN

-diplopia
-ataxia
-autonomic dysfunction
-altered ventilation
-nystagmus

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24
Q

Spinal cord symptoms of MS

A

-weakness and paresthesia (Legs > arms)

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25
Other symptoms of MS
-bowel retention and urinary incontinence -central neuropathic pain -trigeminal neuralgia -spasticity -tonic seizures
26
Pregnancy is associated with a __________ risk of MS exacerbations.
reduced
27
In MS patients, the postpartum period may have an ____________ risk of relapse.
increased
28
Symptoms of MS appear between what ages
20-40 years
29
Clinical criteria for diagnosis of MS
s/s of CNS white matter disease -2 or more attacks separated by a month or more -involvement of 2 or more noncontiguous anatomic areas -elevated levels of IgG and albumin in the CSF is abnormal -MRI: demyelinated plaques in the CNS
30
White matter symptoms of MS
-memory problems -slow walking -balance issues or frequent falls -difficult performing two or more activities at once, such as walking and talking at the same time -mood changes, such as depression -urinary incontinence
31
Goal in the Tx of MS
modulate the immunologic and inflammatory responses that damage the CNS
32
Medication Tx of MS
Disease-modifying agents->interferon beta (SE=flu like symptoms, elevated liver enzymes and neutropenia) Immunosuppressants (azathioprine) Corticosteroids IV immunoglobulins Symptomatic treatments for spasticity, depression and neuropathic pain (gabapentin, baclofen, and SSRIs)
33
Assessment of a MS Patient**
1. Last neurologist appointment 2. last time they had exacerbation of the disease 3. bulbar or respiratory symptoms (post op ventilation) 4. What medications are they taking? 5. Lhermitte sign: neck flexion induces an "electrical sensation" 6. visual disturbances due to optic neuritis 7. Unthoff sign: worsening symptoms by increased body temperature (Exercise, hot temps); more remission in colder environments 8. depression
34
Perioperative risks of a MS patient
-exacerbation of symptoms with hyperthermia, stress, surgery, infection, emotional and physical trauma, postpartum -versed in preop -consider stress steroids -spinal anesthesia may exacerbate symptoms due to potential neurotoxicity -epidural and peripheral blocks ok because staying out of CNS -Avoid SUXX due to occurrence of hyperkalemia -NMDR careful use (avoid if you can) -post op respiratory support
35
What is the cause of Alzheimer's disease?
-amyloid-beta protein -this protein begins a cascade of events ending with deposits of: - amyloid plaques -neurofibrillary tangles -neuronal apoptosis -these cause a loss of cholinergic activity and loss of glutamatergic neurons
36
What is alzheimer's disease characterized by?
-loss of cognition -poor decision-making -language and gait issues -seizures -agitation -psychosis
37
Tx of Alzheimer's disease
acetylcholinesterase inhibitors and a NMDA inhibitor
38
Anesthesia considerations for Alzheimer's disease?
1. postoperative cognitive dysfuction, careful with sedative premeds (i.e. versed) 2. use glycopyrrolate (will not cross BBB) 3. patients already receiving cholinesterase inhibitors to increase Ach, may have prolonged Sux response because they will have massive amount of Ach in system do not want to use scopolamine or atropine because they can cross BBB and decrease Ach levels in brain
39
What is Parkinson's disease caused by?
-degenerative CNS disease caused by loss of dopaminergic cells in the basal ganglia (Lewy Bodies) -diminished inhibition of the extrapyramidal motor system due to dopamine deficiency
40
S/s of Parkinson's
-resting tremor -cogwheel rigidity of the upper extremities -bradykinesia -shuffling gait -stooped posture -facial immobility (frozen face)
41
Treatment of Parkinsons
Levodopa (multiple other drugs available) Deep Brain stimulatorys
42
Anesthesia considerations of Parkinson's disease
-1/2 life of Levodopa is short, interruption of therapy for more than 6-12 hours can result in severe skeletal muscle rigidity and ventilation issues -avoid dopamine antagonists (Reglan, Phenergan) -dopamine antagonists-phenothiazines, droperidol and metoclopramide should be avoided -increased risk of neuroleptic syndrome with dopamine agonists -autonomic dysfunction, upper airway dysfunction, postoperative confusion and hallucinations -problems with swallowing and secretions -alfentanil and fentanyl may produce dystonic reactions when administered rapidly
43
Deep Brain Stimulator (DBS)
2 part surgery: stimulator and generator placement -most effective in people who suffer severe tremors -suffer wearing-off spells or medication induced dyskinesia (uncontrolled shakes) -not thought to improve speech or swallowing issues or thinking problems -doesnt slow down disease process -if doing sedline or bis monitoring will pick up stimulation so readings may not be accurate
44
Motor neuron disorders
upper, lower or mixed neuron involvement of the cerebral cortex, brainstem and spinal cord ALS (Lou Gehrig's disease):mixed Kennedy's Disease (spinobulbar muscular atrophy) Friedreich's Ataxia: mixed Spinal muscular atrophy: lower motor neurons
45
What is Amyotrophic Lateral Sclerosis (ALS)?
-selective and progressive motor neuronal death -progressive degeneration of the upper and lower motor neurons causing: 1. amyotrophy (muscle wasting) 2. lateral sclerosis autonomic dysfunction
46
What gender and age is more affected with ALS?
Males>females -40-60 years onset
47
Diagnosis of ALS
EMG and neuro exam that demonstrates early spastic weakness of the upper and lower extremities, subcutaneous muscle fasciculations and bulbar involvement affecting pharyngeal function, speech and facial muscles
48
Treatment of ALS
non curative -tx symptomatically
49
Anesthetic considerations for ALS
-bulbar involvement: aspiration risk and pulmonary complications (highest) -increased sensitivity to respiratory depressant effects of sedatives and hypnotics (avoid opioids and benzos) -sympathetic hyperactivity and autonomic failure -avoid Sux (risk of hyperkalemia due to denervation and immobilization) -nondepolarizers may be prolonged and pronounced -regional OK -use short-acting anesthetics -prone to atelectasis
50
Hyperkalemia periodic paralysis
sodium channel defect causes prolonged depolarization and flaccid paralysis K>5.5mEq/L during symptoms -skeletal muscle weakness may be localized to tongue and eyelids
51
Skeletal muscle channelopathies (myotonias)
-hyperkalemic periodic paralysis -hypokalemic periodic paralysis -sodium channel myotonia -thyrotoxic periodic paralysis -myotonia congenita -paramyotonia congenita -andersen-tawil syndrome
52
Precipitating factors of Hyperkalemic periodic paralysis
-rest after excercise -potassium infusions -metabolic acidosis -cold exposure (OR hypothermia)
53
Hypokalemic periodic paralysis
calcium or sodium channel defect K level <3 mEq/L during symptoms -chronic myopathy with aging (70+)
54
Precipitating factors of hypokalemic periodic paralysis
-high glucose meals -strenuous exercise -glucose-insulin infusions -stress -hypothermia
55
Anesthetic management of hypo/hyperkalemic paralysis
-preoperative electrolytes and abnormalities corrected before surgery -keep normothermic -careful with medications that cause changes in potassium (insulin, diuretics) that can cause weakness or paralysis -avoid anectine -constant monitoring for potassium-related dysrythmias -may be sensitive to nondepolarizing muscle relaxants due to chronic myopathy
56
What is Guillain-Barre Syndrome (polyradiculoneuritis)
-autoimmune disorder characterized by: -onset of ascending skeletal muscle weakness or paralysis of the legs usually due to viral or bacterial infection -group of disorders known as the inflammatory neuropathies -autonomic dysfunction with wide fluctuations in HR/BP -physical stimulation can precipitate HTN, tachycardia and cardiac dysrhthmias -respiratory muscle weakness
57
Treatment of GB
based on symptoms plasma exchange immunoglobulin mechanical ventilation
58
Anesthetic considerations of Gullain Barre
-avoid rapid movement of patient (autonomics) -aspiration (reglan, pepcid) -maintain temperature -airway respiratory failure -maintain preload and afterload -careful with PPV (may cause autonomic instability) can trigger ganglia along spinal cord by pressure to cause autonomic dysfunction -muscle relaxants (avoid Sux), increased sensitivity to NMDR; do not want to cause K release from cells because they will be upregulated
59
What is Myasthenia gravis caused by?
a decrease in the number of functional postsynaptic, Ach receptors in the neuromuscular junction available for Ach binding -abnormal thymus tissue frequently involved
60
What is the hallmark sign of MG?
fatigability which improves with rest
61
Who does MG affect most?
bimodal disease: -young women 30-40 yo -older men >50 yo
62
Pathophysiology of MG
1. major antigen in MG is acetylcholine receptor on the muscle membrane 2. some patients without AChR antibodies have autoantibodies against Muscle Specific Kinase (MuSK) -protein that allows AchR clustering at the NMJ 3. less commonly there are low-density lipoprotein receptor-related protein 4 (LRP4) in MG patients without MuSK or AChR -receptor for neural agrin that relays the signal to MuSK to initiate AChR clustering -patient without detectable antibodies against any of these 3 antigens are referred to as seronegative
63
Clinical hallmark of MG
skeletal muscle weakness that is aggravated by repetitive muscle use and improves with rest
64
First notable sign of MG
-"weakness of extra-ocular muscles" -diplopia (double vision) common presenting complaint (cranial nerves)
65
Other s/s of MG
-muscles of facial expression, muscles of talking, chewing and swallowing especially affected -weakness of arms/legs, bulbar symptoms or weakness of muscles of respiration -environmental, physical, and emotional factors can affect the disease (surgery, pregnancy) -myocarditis in patients with thymomas-will usually see cardiac defects (decreased EF)
66
Diagnosis of MG
Clinical tests of fatigability: 1. maintaining upward gaze 2. holding out an affected limb 3. respiratory function test Electrophysiologic (EMG or supramaximal stimulation of peripheral nerve at 2 Hz) Pharmacologic (Edrophonium/Tensilon test) immunologic (anti-Achr antibody titer) -85% have anti-AChR antibodies -5% have no detectable antibodies -10% may have antibodies against MuSK or LRP4
67
75-90% of MG patients have:
-thymoma -thymic hyperplasia -thymic atrophy higher incidence of heart disease
68
What is the most common anterior mediastinal mass occurring in adults?
thymus hyperplasia
69
Myasthenic crisis is characterized by:
-progression of severe muscle weakness -respiratory failure -bundle branch blocks and A-fib
70
MG and pregnancy
pregnancy exacerbates symptoms of MG in 33% -some pregnant women experience remission or no change
71
Causes of myasthenic crisis
-poor control of MG, underdosing of meds -emotional stress -hyperthermia -pulmonary infection (severe PNA or bronchitis)
72
Exacerbations of MG in pregnancy are most likely to occur during:
1st trimester or 6 weeks post-partum Anti-AchR antibodies cross the placenta Magnesium should be avoided (for tocolysis and preeclampsia)?
73
The newborn of a mother with MG can suffer from _______________
transient neonatal myasthenia
74
Transient neonatal myasthenia may present with:
-difficulty feeding -ptosis -facial weakness -respiratory distress at birth
75
Transient Neonatal myasthenia
-in newborns of women with active MG -can begin 12-48 hours after birth and last for weeks -spontaneous remission at 2-4 weeks when maternal antibodies clear circulation -edrophonium testing (tension test): improvement in strength==positive result -serologic testing -tx of symptom management and immunomodulation
76
What conditions are associated with MG
-thymus hyperplasia/thymoma -hyper/hypothroid -rheumatoid arthritis -ulcerative colitis -pernicious anemia -diabetes mellitus
77
Bulbar symptoms refer to weakness of muscles innervated by the cranial nerves::
5 7 9 10 11 12
78
Bulbar symptoms include
-difficulty swallowing (dysphagia) -difficulty chewing, choking on fluids, nasal regurgitation -slurring of speech, dysphonia, dysarthria, dysphasia -difficulty breathing -weakness of neck muscles
79
Treatment of MG
Acetylcholinesterase inhibitors (AchEI): -oral pyridostigmine, less muscarinic SE than neostigmine -onset: 15-30 min -peak: 1-2 hours -duration: 3-4 hours (60mg can last 3-6 hours) -daily dosage: 30-120mg orally in divided doses -improves muscle strength for several hours but does not affect the course of the dz increases concentration of Ach at the postsynaptic membrane -pyridostigmine: quaternary cannot cross BBB -other typical symptoms are: diaphoresis, hypersalivation, rhinorrhea, lacrimation, bronchorrhea, bronchospasm, miosis, bradycardia, hypotension
80
Cholinergic crisis
81
Other tx for MG
immunosupressants -corticosteroids (reduced AchR antibody levels) -cylclosporine -azathioprine (interferes with production of AchR antibodies) -plasma exchange patients with respiratory compromise -IV immune globulin Thymectomy (Goal is remission or reduction in dosage of medications) -indicated in patients with thymoma -thymus gland hyperplasia -drug resistant MG -transsternal (open) or video-assisted transcervical
82
Anesthetic implications for MG
pre op: medication list (steroids, pyridostigmine dose), PFT, abilities to maintain airway, CT/MRI of thymoma, EKG (bradycardia or rhythm issues) -d/c or taper pyridostigmine dose before sx -sensitive to sedative medications, aspiration risk (reglan) -avoid muscle relaxants (TIVA/inhalational and/or regional) Anectine: resistance or unpredictable (not taking MG meds)or normal/prolonged response (taking MG meds) NMDR: dramatic sensitivity (decrease in functional receptors) especially when combined with inhalationals -use of nonopioid analgesia -patients should be informed that postop ventilation may be needed -patients with MG are sensitive to NMDBs because of decreased number of postsynaptic receptors at the motor end plate extubation (safe to extubate?) reversal: cholinergic crisis, better to use sugammadex check negative inspiratory force (how well diaphragm is pulling in >30cm H20), head lift, cough, gag, reflex, ensure full return of twitch
83
Factors which anticipate postoperative mechanical ventilation for MG
-forced vital capacity (FVC) <2.7 liters -vital capacity < 4mL/kg -previous hx of myasthenic crisis -disease duration greater than 6 yrs (Nagelhout 2-6 hours) -pyridostigmine daily dose of 750mg or more -COPD -bulbar symptoms
84
Postoperative care of MG patient
-non-opioid pain meds -pulmonary toilet -avoid meds that depress respiration or delay extubation -watch for postoperative respiratory failure -cholingergic vs myasthenic crisis (edrophonium 10mg)
85
What syndrome acts like MG and what is it associated with?
Lambert-Eaton Myasthenic Snydrome is associated with small cell lung cancer and in contrast to MG, exercise may improve the muscle weakness-related symptoms
86
What is Lambert-eaton Myasthenic Syndrome (LEMS)?
autoimmune disorder, paraneoplastic (immune-mediated associated with small cell lung ca) -IgG antibodies are produced and attack pre-synaptic calcium channels (acts similar but different mechanism) -decreased release of Ach from presynaptic terminals and decreased postjunctional response (muscle weakness) -number and quality of postjunctional AchRs is unaltered-different from MG -typically 50-70 yo male complains of proximal extremity weakness (hip and shoulder) that affects gait -improvement with exercise, no improvement with anticholinesterase or steroids
87
LEMS presentation
-hip and shoulder weakness, difficulty walking and standing -autonomic dysfunction with dry mouth reduced sweating and erectile dysfunction, orthostatic hypotension -sensitive to both depolarizing and non-depolarizers (try to avoid) -patients presenting with tumor/cancer and weakness..suspect LEMS -tx with surgery for cancer and/or and 3,4 diaminoyridine -prednizone and azathioprine can help with symptomes
88
MG vs Eaton Lambert
89
Muscular Dystrophies (MD)
hereditary disorders characterized by muscle fiber necrosis and regeneration, leading to muscle degeneration and progressive weakness Muscular Dystrophies: -duchenne''s muscular dystrophy (most common and severe type of MD) 1/3500 live male births -Becker's muscular dystrophy (Rare) 1/18,000 -myotonic dystrophy -limb-girdle -congenital muscular dystrophy Congenital Myopathies -central core disease -centronuclear myopathy
90
Duchenne's muscular distrophy (DMD)
-inherited X-linked recessive disease, the muscles (incl myocardium) are gradually replaced with: fat and connective tissue -presents in childhood (between 3-5 years of age) as proximal muscle weakness and painless muscle atrophy in boys -loss of functional dystrophin proximal muscle weakness and gait issues, gradual onset of muscle wasting, contractures (kyphoscoliosis)
91
What is dystrophin?
-protein that plays a major role in: stabilization of the muscle membrane signaling between cytoskeleton and extracellular matrix
92
Duchenne Muscular Dystrophy
93
Duchenne's Cardiac considerations
-succumb to cardiopulmonary complications by middle age -cardiomyopathy, mitral regurgitation and rhythm disorders common (tx with ACE inhibitors, diuretics, Beta blockers)---avoid cardiac depressants -sensitive to myocardial depressant effects of: -inhalationals - sedatives -narcotics
94
What is consistently elevated in Duchennes muscular dystrophy?
-serum creatinine kinase levels consistently elevated (used to screen newborns. assessment of muscle degeneration) -as they age, the more the muscle trophies the CK levels begin to decrease
95
What medication is contraindicated in DMD?
succinylcholine is contraindicated due to risk of : -hyperkalemia -rhabdomyolysis
96
Anesthetic considerations of DMD
-aspiration risk (decreased laryngeal reflexes) -delayed gastric motility-delayed gastric emptying -poor respiratory function, pulmonary HTN from chronic sleep apnea, kyphoscoliosis -increased sensitivity to non-depolarizers -associated with MH-like response, avoid inhalationals if possible -recurrent PNA due to ineffective cough and inadequate secretion clearance -post-operative respiratory failure, restrictive ventilatory pattern even with recent improvements in supportive care, cardiorespiratory complications cause most of the mortality that occurs before the 4th decade of life typical EKG abn include an R;S ratio >1 in lead V1; deep Q waves in leads I, aVL, V5 and V6; right axis deviation or R BBB
97
Becker Muscular Dystrophy
-decrease in normal amounts of dystrophin -milder disease course than DMD -onset ~12 yrs -mortality: similar to DMD but usually live until 5th or 6th decade
98
Emery-Dreifuss Muscular Dystrophy
-caused by mutations in 2 proteins -typically presents with contractures of the ankles, elbows, and neck -progressive weakness of humeral and peroneal muscles -cardiomyopathy and cardiac conduction abnormalities (present around 30 yrs of age)
99
Management of Anesthesia (DMD?)
-greatest concerns: cardiac involvement respiratory muscle weakness -premedication and respiratory depression, impaired swallowing , GI dysfunction -avoid SCh and inhaled agents: risk for rhabdo and severe hyperkalemia -sensitive to nondepolarizing muscle relaxants -preop muscle weakness may require postop mechanical ventilation -local, regional better alternatives
100
Myotonia
group of hereditary skeletal muscle diseases (myotonic dytrophy, myotonia congenita, myotonia fluctuans, paramyotonia congenita common to aLL myotonias: inability of skeletal muscles to relax after chemical or physical stimulation -dysfunction of ion channels in the muscle membrane -reduced conductance of cl ions in the sarcolema and other channelopathies -progressive muscle wasting with weakness combined with multisystem involvement
101
Myotonic Dystrophy
autosomal dominant disorder (one parent has it) usually occurs in 2nd or 3rd decade of life -slow progressive deterioration of skeletal, cardiac and smooth muscle, wasting and cardiac conduction defects--death -characterized by hypoplastic, dystrophic and weak skeletal muscles and prone to persistent contraction
102
2 types of myotonic dystrophy
1 DM-1 (steinert's): congenital, childhood onset, adult onset and late onset 2. DM-2- proximal myotonic myopathy and myopathy)
103
Myotonic Dystrophy (DM-1)
most common type and subdivided by age of onset intrinsic disorder of skeletal muscle linked to: -myotonin-protein kinase gene -defect in Na and CL channel function produces electrical instability of muscle membrane -characterized by myotonia induced by voluntary or reflex contractions followed by prolonged relaxation -muscle weakness begins distally and progresses proximally -manifests as weakness of facial muscles, wasting of sternocleidomastoid muscles, ptosis, dysarthria. dysphagia and inability to relax hand grip
104
DM-1 (myotonic dystrophy) triad of
1. mental retardation (testicular atrophy in men) 2. frontal baldness 3. cataracts
105
Considerations of DM-1
-pulmonary issues from hyopotonia, decreased cough effectiveness and chronic aspiration, diminished ventilatory response to hypoxia and hypercapnia, OSA, hypersomnolence -smooth muscle atrophy, most common is cranial and distal limb muscles (hatchet face) -conduction defects (heart blocks and tachyarrhythmias) -sudden cardiac death (3rd degree AV block or ventricular dysrhthmias), respiratory failure or PNA -hypothyroidism and insulin resistance -treatment is supportive, NA channel blockers
106
Myotonic Dystrophy type 2
-similar clinical features as DM-1 -milder than that of DM-1 -AV conduction delays but sudden death less likely -less likely to have diabetes (Type 1 almost always has DM with it) -disability from chronic myopathy occurs later -more likely to have myalgia, muscle strength variation, hypertrophy of calf muscles -normal life expectancy
107
Anesthetic considerations of DM-2
=careful with pre0post op sedation (respiratory depression) -inability to secure airway (jaw muscle spasm) -avoid Sux and neostigmine? due to its potential to trigger myotonic muscle contraction (myotonic response) -increased sensitivity to NDMR (Residual block), opioids -peripheral nerve stimulation may produce myotonia that could be misinterpreted as sustained tetanus -avoid hypothermia and shivering -regional -regional and peripheral blocks -assume patient has cardiac involvement (pacer available) -pregnancy exacerbates symptoms (uterine atony, postpartum hemorrhage and retained placenta) -can use inhalational agents in this patients -risk of MH no greater than general population
108
Early signs of MH
1. Hypercarbia-unexplained rapid increase in ETCO2 2. Muscle rigidity: especially masseter muscle rigidity 3. tachycardia: elevated heart rate
109
Late signs of MH (5-10 minutes later)
1. hyperthermia: rapid rise in body temp 2. acidosis: metabolic and respiratory acidosis 3. rhabdomyolysis: muscle breakdown. leading to elevated CK levels and myoglobinuria
110
Lab findings of MH
-respiratory/metabolic acidosis -K>6, CK increase serum and urine myoglobin increase
111
Neuroleptic Malignant Syndrome
precise mechanisms unproven antipsychotic-induced dopamine blockade sudden drop in CNS dopaminergic activity nigrostrial pathway-muscle rigidity -hypothalamus-impaired heat regulation mesolimbic/mesocortical pathways-altered mental status
112
Classic Tetrad of clinical signs of NMS
1. muscle rigidity (first sign) 2. fever 3. altered mental status (drowsiness, agitation, confusion, severe delirium and coma) 4. autonomic dysfunction (labile BP, tachypnea, tachycardia, diaphoresis, flushing skin, incontinence)
113
Cause of NMS
-adverse rxn to meds with dopamine-receptor antagonist properties -MOA: dopamine receptor blockade in the CNS (hypothalamus) leading to dysregulation of temperature and muscle control -rapid withdrawal of dopaminergic meds
114
Tx of NMS
-stop offending agent -supportive measures, benzo or dantrolene
115
Porphyria
-enzymatic deficiencies in the heme synthesis pathway -accumulation of neurotoxic porphyrin precursors (porphobilinogen PBG) and aminolevulinic acid (ALA) -an acute porphyria should be suspected if a patient presents with neurovisceral signs and symptoms and an initial evaluation excludes more common causes -most important first-line screening test is measurement of urinary porphobilinohen (PBG) PBG is expected to be substantially increased in all patients during acute porphyria attacks but not in other medical conditions -PBG test is both sensitive and specific for dx of acute porphyria under most circumstances an exception is ADP in which ALA and porphyrins but not PBG are elevated
116
Acute intermittent Porphyria (AIP) Clinical features
-fever, tachycardia, nausea, emesis, severe abd pain, weakness, seizures, confusion and hallucinations -respiratory failure -hyponatremia secondary to inappropriate secretion of ADH young adults and usually women attacks can last for 2 weeks
117
What is AIP triggered by?
-hormone changes during menstrual cycle -fasting -infection -exposure to triggering agents (barbiturates, etomidate) AIP may be considered in patients with unexpected delayed emergency from anesthesia or postop muscle weakness
118
The circle of Willis connects the ______ and _______ as a major intracranial arterial system.
anterior (carotid) posterior (vertebrobasilar)
119
The circle of willis acts to _______________.
provide collateral blood flow between the anterior and posterior circulations of the brain, protecting against ischemia in the event of vessel disease or damage in one or more areas.
120
Venous drainage to the brain leads to _________.
the internal jugular veins
121
The cerebral ventricular system is made up of:
4 ventricles that include 2 lateral ventricles (1 in each cerebral hemisphere) 3rd ventricle in the diencephalon 4th ventricle in the hindbrain inferiorly it is continuous with the central canal of the spinal cord
122
Role of CSF
protects and maintains the central nervous system by absorbing shock, supplying nutrients , maintaining intracranial pressure, removing waste, controlling temperature, and containing immune cells. -The fluid-filled ventricles also help keep the brain buoyant and cushioned
123
CSF is produced by _______________.
ependymal cells in the choroid plexus of the lateral 3rd and 4th ventricles
124
in adults about ______________ mL of CSF is produced every day.
400-600mL
125
there is about ______ of CSF at any given time.
150cc
126
Circulation of CSF
lateral ventricles-->interventricular foramina-->3rd ventricle-->cerebral aqueduct--->4th ventricle-->subarachnoid space via 4 openings in the 4th ventricle
127
What is CSF reabsorbed by?
arachnoid granulations and drained into the dural venous sinuses of the arachnoid mater into the sinuses with one-way valves
128
The spinal cord begins at ______________________.
Foramen magnum as a continuation of the medulla oblongata at the base of the skull. It is located within the vertebral or spinal canal.
129
In men the spinal cord extends up to ________.
45cm
130
In women, the spinal cord extends up to ___________.
43cm
131
What is the spinal cord composed of?
longitudinal columns of nuclei (Gray matter) surrounded by ascending and descending tracts (white matter)
132
The gray matter is butterfly or H-shaped and divided into:
anterior (ventral) posterior (Dorsal) lateral (intermediate) horns
133
Where do somatic and visceral afferent (Sensory) fibers enter the spinal cord?
posterior horns
134
The gray matter horns divide into:
the white matter into posterior (Dorsal), lateral, and anterior (ventral) columns
135
The white matter columns include both:
ascending and descending tracts
136
Ascending neural tracts convey information from _______ to _______.
periphery to brain
137
Descending tracts convey information from _______ to __________.
brain to periphery
138
Major ascending tracts include:
1. dorsal column (posterior area): conveys tactile sensation, vibration, and proprioception 2. spinothalamic tract (anterior): conveys pain, temp and crude touch.
139
Major descending tracts include:
corticospinal tract: controls find motor movement. Crosses midline at the upper part of midbrain
140
Where does the anterior spinal artery originate from?
vertebral artery
141
What does the anterior spinal artery supply?
anterior 2/3 of the spinal cord and medulla
142
What is the largest radicular artery and the major blood supply to the lower 2/3 of the spinal cord?
Artery of Adamkiewicz (great radicular artery)
143
Where is the Artery of Adamkiewicz located??
left side between T9-T12.
144
Where do the 2 posterior spinal arteries originate from?
inferior cerebellar artery, as well as, the segmental spinal arteries (originating from the intercostal and lumbar arteries) supply the posterior 1/3 of spinal cord
145
Which areas of the spinal cord are more prone to ischemia?
anterior and deep portions of the SC due to fewer anterior medullary feeder vessels than the posterior region and can lead to anterior spinal artery syndrome
146
What is anterior spinal artery syndrome characterized by?
ischemia of the b/l corticospinal and spinothalamic tracts This causes loss of motor function and loss of pain and temperature sensation below the level of the lesion
147
Common etiologies of anterior spinal artery syndrome
aortic dissection emboli covering large segments of the thoracoabdominal aorta with endovascular stents surgical dissection during thoracoabdominal aortic aneurysm repair
148
What is the main substance used for energy production in the brain?
glucose
149
Overall metabolic rate for the brain for a young adult is_________.
3.5mL O2/min/100g brain tissue or 5.5 mg glucose/min/100g skeletal muscle=0.29 ml O2/min/100g
150
Brain receives ______% CO yet makes up only _____of total body weight.
15% 2% this disproportionately large blood flow is a result of high metabolic rate of the brain
151
no anaerobic metabolism, ATP levels zero out around _______.
5 min= cell death
152
Cerebral perfusion pressure=
CPP=MAP -ICP (CVP substituted fro ICP if higher than ICP)
153
Decrease in MAP or increase in ICP will ________ CPP.
decrease
154
What is the Monro-Kellie Doctrine?
describes the relationship between the contents of the cranium and ICP
155
In non-pathological states, 3 components exist in equilibrium to maintain normal ICP:
-brain tissue -blood -CSF
156
Normal ICP
7-15mmHg
157
ICP >20mmHg =
substantial redistribution of CSF
158
at 40-50 mmHg ICP_______________.
vascular structures collapse
159
ICP >50mmHg =
high risk for herniation
160
Common presenting symptoms of intracranial HTN include:
-nausea -vomiting -headache -downcast eyes -papilledema -altered mental status and/or -acute focal neuro deficit
161
What is the concern with acute Intracranial HTN?
progression to brain herniation
162
What does the cushings triad include?
1. HTN 2. Irregular Respirations 3. Bradycardia -reflects severe, increased ICP
163
What is cerebral autoregulation?
ability of the body to maintain constant CBF despite changes in CPP. -protects the brain from hypo-or hypoperfusion secondary to decrease or increase in CPP, respectively.
164
CBF is expected in healthy adults, assuming normal ICP of 10mmHg to be within a MAP of _______ or CPP of _______.
MAP 60-160mmHg CPP 50-150mmHg
165
Normally out PaCO@ is ~40mmHg. As this drops, the vasculature _____ dropping CBF by _______________.
constricts dropping CBF by 1-2cc/100g/min for every 1mmHg drop in PaCO2. very low PaCO2 will significantly drop CBF. This can be useful in extenuating circumstances (ie. impending brain herniation) but also places the brain at a real risk for ischemia-related damage.
166
Does PaO2 affect CBF?
really doesnt affect CBF in hyper-oxia. As patient becomes more hypoxemic, CBF will increase once the PaO2 drops below ~40-50mmHg to deliver more blood (and therefore oxygen content ) to the brain
167
When does PaCo2 correlate with CBF?
when PaCO2 is within the range of 25-70mmHg, it correlates with CBF. 1 mmHg increase in PaCO2 will result in 1-2 mL/100g/min (or 4%) increase in CBF.
168
The effect of PaCO2 changes in CBF is attenuated after ______.
6 hours. Prolonged hyperventilation should be avoided secondary to the risk of cerebral ischemia
169
How does Hypothermia affect CMRO2?
hypothermia results in a dose-dependent reduction in CMRO2
170
How does hyperthermia affect CMRO2?
hyperthermia increases CMRO2, increased uptake of glucose: severe hypoglycemia (blood glucose <2mmol/L or 36mg/dL) results in increased CBF.
171
How does TBI affect cerebral autoregulation?
cerebral autoregulation is impaired or absent in severe TBI. In these patients, decreases in CPP result in decreases in CBF that may reach ischemic levels and lead to secondary brain injury.
172
How do cerebral tumors affect cerebral autoregulation?
cerebral tumors are frequently associated with disruption of the BBB, leading to the development of vasogenic edema and increase in ICP. Cerebral autoregulation in peritumurol areas is impaired and these areas are more
173
How does chronic hypertension affect cerebral autoregulation?
with HTN, cerebral autoregulation curve shifts to the right, BP management should aim to keep MAP within 20-25% of baseline if not monitoring autoregulation specifically
174
How does preeclampsia affect auto regulation?
endothelial dysfunction, alterations in cerebral blood flow and impaired autoregulation are some of the mechanisms of cerebral edema in preeclampsia.
175
Aim of Intraoperative neurophysiologic monitoring (IONM)
aims to protect the integrity of the peripheral and CNS during surgical manipulation
176
SSEPs are sensitive to _________________.
all inhalational agents and nitrous oxide
177
SSEPs less affected by ________.
IV agents.
178
__________&___________ increases SSEP amplitude.
Ketamine and etomidate
179
What do SSEPs monitor?
sensory pathway (through the dorsal root ganglia and posterior column) by electrical stimulation of a peripheral nerve distal to surgery and recording the potential at different landmarks as it propogates along the pathway from the peripheral nerves, through the spinal cord, subcortical and cortical regions
180
What do MEP's monitor?
-monitor the motor pathway (including the motor cortex, corticospinal tract, nerve root and peripheral nerve) by transcranial electric stimulation of the motor cortex and recording the elicited muscle contractions by recording electrodes
181
MEPs are more sensitive to:
the effects of anesthetic agents than SSEPs and MEP changes precede changes in SSEP, allowing time to react
182
MEPs affected by _______ more than ___________.
affected by inhalational more than IV agents
183
_______________ can weaken or eliminate MEPs making them unsuitable for use during MEP monitoring.
NMBDs
184
What do EEG's monitor?
-cortical electrical activity with surface scalp electrodes or brain surface electrodes to detect cortical ischemia and seizure activity -can be used to monitor depth of anesthesia
185
What is the effect of anesthetics on EEG?
dose-dependent and similar to their effect on cortical evoked potentials. EEGs moderately sensitivity to inhalational agents and insensitive to NMBA
186
What does EMG monitor?
-monitor nerve roots and peripheral nerves by detecting muscle activity (EMG) or nerve action potentials (NCS) -spontaneous or free-run EMG provides continuous monitoring and detection of neuronal structures during surgical dissection around nerve roots, cranial and peripheral nerves -triggered EMG is used to identify and map nerve roots and nerved by delivering stimulation intermittently. It can be used for assessment of pedicle breech during pedicle screw placement.
187
Do anesthetic agents have effects on EMG?
no except for NMBas
188
What do BAEPs monitor?
auditory nerve and auditory pathway through the brainstem by acoustic stimulation of the auditory nerve and scalp surface electrode recording -mostly used during base of skull surgery
189
What are BAEPs affected by?
hypothermia
190
How do anesthetic agents, IH agents and NMBAs affect BAEPs?
little effect
191
IV agents have _____ effect on monitoring than inhalationals.
lesser
192
SSEPs effect of latency and amplitude from propofol and high dose barbs
increased latency decreased amplitude
193
Ketamine and etomidate effects on SSEPs
increased amplitude
194
Opioid and benzo's effect on SSEPs
little effect
195
Propofol, barbs, dexmedetomidine (high dose) and lidocaine effects on MEPs
increased latency decreased amplitude
196
Opioids, ketamine, and etomidate effect on MEPs
little to no effect
197
How do neuromuscular blocking agents affect neuromonitoring?
Affects EMG and MEP no effect on SSEP, BAEP and EEG
198
All volatile agents produce a dose-dependent reduction of _______________.
CMRO2 however, due to their intrinsic vasodilatory properties, volatile agents uncouple CMRO2 and CBF. Their overall effect on CBF will result in a balance between CMRO2 related to CBF reduction and intrinsic vasodilatory-related increase in CBF.
199
At 0.5 MAC, CBF is ________.
reduced
200
At 1 MAC, CBF level is _____________.
at baseline
201
above 1.0 MAC, CBF is ____________.
increased
202
How does nitrous oxide affect neuroprocedures?
classically avoided -administration results in increased CMRO2 and CBF. Its effect on CBF is attenuated when administered with volatile agents and is minimal when administered with propofol.
203
Barbs_______________ CMR and CBF.
decrease a major problem with barbs is that they can substantially reduce MAP which if not controlled can reduce CPP. Barbs are also effective in reducing elevated ICP and controlling epileptiform activity Methohexital is an exception with regard to epileptiform activity; it can activate some seizure foci
204
Propofol ______________ CMR and CBF
reduces it reduces the CMR similar to sevoflurane but since it does not increase CBF it is able to reduce ICP.
205
What drug can be used to achieve burst suppression of EEG?
propofol
206
Etomidate _______________ CMR and CBF.
reduces in addition to the indirect effect of reduced cerebral metabolism on blood flow, etomidate is also a direct vasoconstrictor even before metabolism is suppressed. EEG effects include initially increased alpha amplitude followed by progressive decrease in activity. These effects are though to lengthen seizure duration, making etomidate a useful agent for ECT
207
Ketamine effect on CBF and CMR
-dissociative anesthetic, activated certain areas in the brain and can increase CBF and CMR -great for spines, avoid for brains -increases ICP by increasing CBF. CMRO2 rises and is mirrored by increase in CBF. Has traditionally been avoided in the setting of increased ICP.
208
Does ketamine lower the seizure threshold?
no- it is thought to possess anticonvulsant activity
209
Ketamine _______the cortical amplitude of somatosensory evoked potentials but ______________auditory and visual evoked potentials.
increases decreases
210
Benzos effect on CMR and CBF
reduce CMR and CBF but effect not as pronounced as that with the barbs -blood flow reduction by benzos is thought to be secondary to a reduction in CMR -benzos may reduce ICP owing to their effect on CBF.
211
Effect of opioids on CMR and CBF
opioid anesthetics, morphine and fentanyl, cause either a minor reduction or no effect on CBF and CMR -remifentanil had similar effects to fentanyl on CBF aside from difference in recovery time. -controversy with effects of sufentanil-some has reduction in CBF whereas others had increase in BF and ICP.
212
How does succinylcholine affect ICP?
-mild transient increase in ICP -not contraindicated in patients with an intracranial mass or increased ICP -no significant effect on CBF
213
GCS score of mild injury
13-15
214
GCS of moderate injury
9-12
215
GCS severe injury
<8 intubate!
216
common induction choices for neurosurgical procedures
-lidocaine -propofol -opioid (fentanyl or remi) -neuromuscular blockade --sux? -vasopressors and/or short acting antihypertensives
217
fluids and electrolytes with neurosurgical procedures
-avoidance of hypo-osmolar Fluids -correction of electrolyte abnormalities due to diuretics -sodium control -glycemic control
218
How does hypothermia affect brain?
reduces ICP by decreasing brain metabolism, CBF, cerebral volume and CSF production. intraop, a modest degree of hypothermia, 34C, has been recommended as a way to confer neuronal protection during focal ischemia
219
How does hyperthermia affect brain?
particularly dangerous in neurosurgical patients because it increases brain metabolism, CBF and propensity for cerebral edema
220
Are glucose solutions used in neurosurgical patients?
avoid glucose solutions since these solutions exacerbate ischemic damage and cerebral edema -hyperglycemia augments ischemic damage by promoting neuronal lactate production, which worsens cellular injury -moderate glucose control 80-140mg/dl recommended
221
seizures increase:
-CMRO2 -CBF-lactate production -contribute to neuronal death
222
additional agents given during intracranial sx that lowers seizure threshold
Levetiracetam (Keppra)-500-1000mg IV Phenytoin-15-20mg/kg IV Fosphenytoin-20 PE/kg IV at a rate of <150 PE/min
223
hyperventilation's effectiveness for lowering ICP may be as short as __________.
4-6 hours
224
target of PaCO2 is______.
30-35mmHg. in some pathologic conditions, PaCO2 less than 25-30 mmHg may be associated with ischemia caused by extreme cerebral vasoconstriction.
225
How does hyperventilation affect brain volume?
hyperventilation reduces brain volume by decreasing CBF through cerebral vasoconstriction elevate head: increased venous drainage keep MAC <0.5 for most volatiles
226
Dose of mannitol
0.25-1.0 g/kg
227
How does mannitol work?
osmotic diuretic rapid brain dehydration and ICP reduction by increasing the osmolality of blood relative to brain, mannitol pulls water across the BBB from brain to blood to restore the osmolar balance caution in CHF
228
How does furosemide work?
-reduces ICP by inducing a systemic diuresis, decreasing CSF production and resolving cerebral edema by improving cellular water transport -not as effective as mannitol in reducing ICP. Can be given alone as a large initial dose (0.5-1mg/kg) or as a lower dose with mannitol (0.15-0.30mg/kg)
229
Additional factors for ICP control:
-avoidance of hypoxia, hypercarbia, fever - avoidance of hypo-osmolar fluids glucose containing -avoid excessive PEEP -treat and avoid seizures -decrease CMRO
230
What is venous gas embolism?
abnormal collection of gas that forms a bubble in the systemic venous circulation. This bubble can act as an embolus, affecting blood flow
231
Venous air embolism may occur whenever the operative field is elevated ______________.
5cm or more above the right atrial level
232
How much air is needed to produce severe symptoms?
1-5ml/kg
233
some of the highest incidence of venous air embolism in:
-sitting position intracranial surgeries and/or posterior fossa surgeries
234
Pathophysiology of venous air embolism
1. air lock phenomenon-right ventricular outflow obstruction 2. severe increase in pulmonary vascular resistance-vasoconstriction of the pulmonary circulation, which results in ventilation/perfusion mismatch, interstitial pulmonary edema and reduced CO as pulmonary vascular resistance increases
235
s/s of venous air embolism
-mill-wheel murmur, loud and machinery-like -tachy or brady arrythmias -elevation in jugular venous pressure -hypotension -MI -tachypnea -rales, wheezing -cyanosis, hypoxia -AMS -seizures -Coma -transient focal neuro deficits
236
Detection of venous air embolism most to least sensitive
TEE (most sensitive) doppler (l or r parasternal, between 2nd and 3rd rib, mill wheel murmur PA pressure ETCO2 ETN2 (ET nitrogen)
237
treatment of venous air embolism
-notify surgeon to flood/pack surgical field -jugular compression -lower head -aspirate RA-cath -100% Fio2 -Epi/ACLS durant's position -trendelenburg left lateral decubitus
238
Causes of delayed awakening
-preop decreased LOC -large intracranial tumor -residual anesthetics -metabolic or electrolyte disturbances -residual hypothermia -surgical complications-seizures cerebral edema -hematoma -pneumocephalus -vessel occlusion/ischemia
239
Neurogenic shock
-hypotension, bradycardia and hypothermia resulting from acute SCI -occurs with injury above T6 level -seen in 14% of isolated SCI -up to 8% major traumas -unopposed vagal tone on heart can lead to refractory bradycardia, bradyarrythmias and heart block -map goal 85-90 for first week -fluid resuscitation -pressors/inotropes -chronotropes: atropine, glyco, isoproterenol -steroids-controversal, not recommended at this time
240
If ECoG is required ______ should not be given on induction because they suppress EEG activity.
Benzos Propofol/Remi TIVA common, LONG IV lines needed, intraop MRI -high paralytic requirement due to P450 activation by AEDs
241
intraoperative electrocorticography (ECoG)
short period of invasive EEG monitoring. EEG electrodes places directly on cortical surface and epileptiform activity identified and this can guide the extent of a resection.
242
Anesthetic goals for cerebral aneurysm surgery/AVM
-avoid aneurysm rupture -maintain CPP -maintain transmural aneurysm pressure -provide "slack" brain -"hypotensive induction -typical craniotomy monitoring -dynamic BP management in the case of rupture, induced burst suppression (give propofol to decrease CMRO2)
243
Common features of Achondroplasia
-decreased limb length with rhizomelia -prominent forehead -flattened midfaace -depressed nasal brdige
244
Anesthetic considerations of achondroplasia
-proper positioning of extremities-lack of full elbow extension -difficult IV access and insertion-lots of redundant soft tissue -predisposition to obesity -OSA -decreased chest wall compliance -kyphosis -foramen magnum stenosis -upper airway obstruction and hyptonia of airway musculature =absense of motion/articulation at atlantooccipital level -compression of medulla and upper cervical cord because foramen magnum constricted
245
true/false: majority of cases of achondroplasia are born to parents of average height
true
246
Other names for Andersen's syndrome
andersen-tawil long Q-T 7
247
What is Anderson's syndrome?
triad of : 1. potassium sensitive periodic paralysis 2. ventricular dysrhythmias 3. dysmorphic features
248
How does Anderson's snydrome affect the heart?
-episodes of muscle weakness (periodic paralysis) -changes in heart rhythm-arrythmia -most common changes affecting the heart are ventricular arrhythmias and long QT syndrome
249
Anderson's snydrome effects on face and back
severe midface hypoplasia: low-set eats and widely spaced eyes Kyphoscoliosis -restrictive lung disease -decreased pulmonary function
250
Airway issues associated with Anderson snydrome
-midface hypoplasia -mandibular problems -small lower jaw (micrognathia) -dental abnormalities -curving of the fingers or toes (clinodactyly)
251
Which syndrome is a deletion of chromosome 15q11-13 and an example of an "imprinting disorder"
angelman's snydrome
252
what is angelman's syndrome characterized by?
-ataxia -hand-flapping -seizure disorder -subtle dysmorphic features -mental retardation -happy disposition with uncontrollable laughter
253
when angelman's snydrome most commonly diagnosed when?
after age 2 when characteristic behaviors become most evident
254
Arnold Chiari Malformation anesthesia considerations
-aspiration precautions -potentially difficult airway -vocal cord paralysis -potential ventilation issues -latex precautions
255
What is arnold chiari malformation?
congenital defect in the area of the back of the head where the brain and spinal cord connect
256
symptoms of arnold chiari malformation
-headaches -stiffness or pain in neck or back of head area -poor feeding or swallowing -decreased strength in arms -decreased sensation in arms and legs -rapid back and forth eye movement -developmental delays -weak cry -breathing problems
257
Type 1 arnold chiari malformation
-most common -commonly goes unnoticed until problems arise in adolescent or adult years -base of skull and upper spinal area not formed properly
258
Type II Arnold Chiari Malformation
-part of the back of the brain shifts downward through the bottom of the skull area -typically seen in infants born with spinal bifida -can be associated with hydrocephalus
259
Type III Arnold chiari malformation
-back of brain protrudes out of an opening in the back of the skull area
260
Type IV Arnold chiari malformation
-back of brain fails to develop normally
261
Beckwith-Wiedmann snydrome
-50% born prematurely -weight >4000gm -macrosomia (LGA) -macroglossia -microcephaly -exopthalmos -ompahlocele -medullary renal dysplasia -neonatal hypoglycemia -polycythemia -umbilical hernia -potentially difficult airway -glucose issues -impaired renal drug excretion -pre-op cardiac eval
262
Carpenter Syndrome
-short neck -hypoplastic mandible -omphalocele -CHD -premature closure of cranial sutures -elevated ICP -psychomotor retardation -potentially difficult airway -preop cardiac eval -management of ICP
263
Charcot-Marie Tooth Disease
-chronic peripheral neuropathy -distal muscle weakness and wasting -sympathetic nervous system impairment -difficult to control body temperature -ANS hypersensitivity -impaired thermoregulation -potential post-op respiratory dysfunction -sensitive to muscle relaxants -risk of hyperkalemia with Sux
264
CHARGE Synndrome
Colomboma ("curtailed or missing a structure (eyes)) Heart defects Atresia choanae (nasal obstruction) Retardation (Mental) Genital Hypoplasia Ear Deformations (with or without hearing loss)
265
Choanal Atresia (incomplete or complete)
-congenital disorder where back of nasal passage (choanae) is blocked usually by abnormal bony or soft tissue (membranous) due to failed recanalization of the nasal fossae during fetal development
266
Crouzon Syndrome
-wide skull -proptosis -maxillary hypoplasia -coronal suture synostosis -nystsagmus, strabismus -cleft palate -elevated ICP -difficult airway -strabismus and MH -exopthalmos
267
Dandy-Walker Snydrome
-hydrocephalus Associated CNS Malformations -Meningomyelocele -developmental delay -microglossia -micrognathia -ICP/VP shunts -latex precautions -postop laryngeal incompetence and vocal cord paralysis
268
DiGeorge Snydrome
-first described in the 1960s -Dr. DiGeorge observed a combo of a lack of thymus gland and lack of parathyroid glands (low calcium levels in blood) -high percentage of these patients have certain forms of congenital heart disease
269
Genetics of DiGeorge Snydrome
-chromosome 22q11 deletion -defect of 3rd/4th brachial arches -PTH deficiency leading to hypocalcemia, tetany and cardiac failure
270
Anesthesia concerns for Digeorge snydrome
-micrognathia -tracheomalacia -choanal atresia -airway issues? -calcium monitoring -exaggerated response to NDMR -prevent graft-versus-host reaction
271
down syndrome/trisomy 21 common features
-brachycephaly -flat occiput -dysplastic ears -epicanthal folds -upslanting palpebral fissures -enlarged tongue midface hypoplasia -skeletal and visceral anomalies -resp problems -cardiac anomalies (40%)
272
Anesthetic considerations for down syndrome
-difficult airway management -spinal cord compression secondary to occipital-atlatoaxial instability -possible endocarditis prophylaxis -bradycardia during induction -difficult vascular access -possible OSA
273
Dwarfism-osteochondrodystrophies
-odontoid hypoplasia/atlantoaxial instability -micrognathia -cleft palate -tracheal stenosis -small chest cavity -kyphoscoliosis -CHD -restrictive lung disease -preop C-spine -potential for difficult airway -pulmonary function -care in OR positioning
274
Ehlers-danlos
-10_+ types of connective tissue disorders due to abnormal production of collagen
275
What is Ehlers-Danlos characterized by
joint hypermobility -skin hyper-elasticity -bruising -scarring -muscular discomfort -GI, uterus and vascular complications -mitral regurg and cardiac conduction abnormalities
276
Anesthetic management of Ehlers-Danlos
-evaluation of CV manifestation -caution with instrumentation of nose, airway, esophagus, vascular structures -extravasation of fluids may go unnoticed because of skin laxity -must have low airway pressures during mechanical ventilation to decrease incidence of pneumo -propensity to blood -regional anesthesia not recommended
277
Fetal alcohol syndrome
-growth restriction -craniofacial abnormalities -Cardiac defects (VSD) -renal abnormalities -inguinal hernia intellectual impairment +/- airway issues +/- CHF
278
Goldenhar syndrome patho
-possible vascular accident occuring during fetal development leading to defects of first and second branchial arches
279
Features of Goldenhar Snydrome
-preauricular appendages -fistulas -epibulbar dermoids -vertebral anomalies -upper eyelid colobomas -ear anomalies -hearing loss -hemifacial macrosomia -micrognathia -high arched palate -CHD -renal abnormalities
280
Anesthestic considerations of Goldenhar syndrome
-preparation for difficult airway -difficult mask because of facial asymmetry -preop radiographs recommended of mandible because predict difficult laryngoscopy -absent ramus, condyle and TMJ -airway abnormalities can predispose to obstructive sleep apnea
281
Marfan syndrome a result of
-autosomal dominant connective tissue disorder characterized by tall stature, arm span > ht, high arched palate, pectus exxcavatum, joint hyperextensibility
282
Marfan syndrome has early development of
pulmonary emphysema high incidence of spontaneous pneumo -ocular changes -kyphoscoliosis
283
Preop evaluation for MArdan snydrome
-cardiopulmonary abnormalities (echo) avoidance of TMJ dislocation -avoidance of sustained increase in SBP
284
Cardiac issues with Marfan
-defective connective tissue in aorta and heart valves lead to aortic dilation, dissection, rupture/prolapse of cardiac valves -mitral regurgitation common -cardiac conduction abnormalities (BBB) -CV abnormalities responsible for premature death
285
Klippel-Feil syndrome
-scoliosis -CHD -Sprengel deformity -congenital snostosis of cervical vertebrae -renal dysfunction -VSD -care in neck manipulation for intubation -impaired renal drug excretion -assessment of CHD -progressive airway obstruction
286
Meckel's Syndrome
-occipital encephalocele -microcephaly -micrognathia -cleft epiglottis, lip, palate -polycystic kidney -CHD -polydactlyl -cataracts -airway -renal function -cardiac evval -prophylacitc abx
287
Does fascioscapulohumeral muscular dystrophy have cardiac involvement?
no
288
Nemaline Rod Muscular dystrophy
-delayed motor development -hypotonia -intelligence normal -dysmorphic features -micrognathia -kyphoscoliosis and pectus-->restrictive lung disease, dilated cardiomyopathy, possible difficult intubation
289
IS MH reported in Nemaline Rod Muscular dystrophy patients?
no
290
Initial symptoms of muscular dystrophies
-waddling gait -frequent falling -difficulty climbing -fatty infiltration of affected muscles
291
Concern with muscular dystrophies
-degeneration of cardiac muscle -poss mitral regurg due to papillary muscle dysfunction with diminished contractility -chronic weakness of respiratory muscles, decreased ability to cough, and kyphoscoliiosis predisposes to URIs, restrictive lung disease, possible pulmonary HTN
292
Anesthetic considerations of Muscular dystrophies
-contraindication of sux -availablility of MH cart/ dantrolene for Duchenne's patients-mimics MH) -postop need for chest physiotherapy =hypomotility of GIT, delayed gastric emptying and weak laryngeal reflexes increase risk of aspiration -risk of rhabdomyolysis, hyperkalemic cardiac arrest or v-fib
293
Do muscular dystrophy patients benefit from regional?
yes
294
Noonan syndrome
-shield-shaped chest, short stature, kyphoscoliosis -webbed neck -micrognathia -renal function -hypoplastic kidneys -mild retardation -platelet dysfunction -airway -CHD, ASD. PS =hypertrophic cardiomyopathy -C-spine x-ray to exclude atlantoaxial instability -aortic coarcation -dissection aortic aneurysym
295
Anesthetic considerations of Noonan syndrome
-difficult intubation and IV access -decreased FRC -possible bleeding diathesis or altered metabolism of drugs
296
is there a relationship between Noonan syndrome and MH?
unclear
297
Neurofibromatosis-von REcklinghausen syndrome
-cNS neurofibroas -Cafe-au-lait spots -increased incidence of pheochromocytoma -kyphoscoliosis -honeycomb cystic lung changes -renal artery dysplasia and HTN -tumors may involve larynx -prolonged paralysis with NMDR difficult airway especially if tumor -preop screening for Pheo -renal and lung function
298
Which syndrome has -increased incidence of pheochromocytoma?
neurofibromatosis-von Recklinghausen syndrome
299
Classic triad of Osteogenesis imperfecta
1. blue sclera 2. multiple fractures 3. deafness
300
Cause of osteogenesis imperfecta
-defect in synthesis of collagen and associated dysfunction of platelet aggregation
301
features of osteogenesis imperfecta
-small mandible -midface hypoplasia -short limbs and trunk
302
What is a rare, autosomal dominant inherited disease of connective tissue that affects bones, sclera and inner ear?
osteogenesis imperfecta
303
is osteogenesis imperfecta more common in males or females?
females very smart and intellect intact
304
Classic presentation of osteogenesis imperfecta
-blue sclera -fractures after minor trauma -kyphoscoliosis -bowing of femur and tibia -gradual deafness -impaired platelet function -increased serum thyroxine in 50% of patients
305
Anesthetic considerations of Osteogenesis imperfecta
-kyphoscoliosis and pectus may decrease vital capacity and chest wall compliance leading to arterial hypoxemia and V/Q mismatching -automated BP cuffs may be hazardous since inflation can cause fractures -present with a prolonged bleeding time despite normal platelet count -desmopressin may be effect in normalizing platelet function -may have mild hyperthermia
306
Management of anesthesia
-C-spine eval with care during tracheal intubation -avoid sux -careful positioning -PFTs if severe kyphoscoliosis and pectus -consider NIBP vs. a-line monitoring -coagulation checks and intraop monitoring of temp
307
Two forms of OI
1. congenita occurs in utero and death often in perinatal period -tarda manifests in childhood
308
Pierre-Robin syndrome may occur in isolation but is often part of underlying syndrome, most common ______________
Stickler syndrome
309
What is stickler syndrome?
group of hereditary conditions characterized by distinctive facial features, eye abnormalities, hearing loss and joint abn
310
How does Pierre-robin occur?
not known usually in utero round 14 weeks gestation, during stage of formation of bones of fetus-fixed fetal position that inhibits mandibular growth -may have swallowing difficulties from abnormalities in brainstem dysfunctionW
311
What is Pierre Robin characterized by?
Micrognathia Cleft Palate Glossoptosis
312
Main concern in PRS is?
difficult airway
313
Neonates with PRS may require:
-prone positioning -nasopharyngeal airway -suturing of tongue to lip -tracheostomy to preserve an airway
314
Prader willi snydrome due to
deletion in chromosome 15 -proposed autosomal recessive mode of inheritance
315
What does Prader Willi syndrome manifest as?
hypotonia at birth but progresses to hyperphagia and obesity with endocrine abnormalities between 1-6 years
316
Prader Willi syndrome physical characteristics
short stature mental retardation severe dental carries common related to chronic regurg of gastric contents
317
Anesthetic considerations for Prader Willi syndrome
-hypotonia altered metabolism of carbs and fats -possible difficult mask ventilation and intubation -IV access -thermoregulation -sleep apenea -evaluation for cor pulmonale -intraop monitoring of glucose necessary and they may actually need exogenous glucose administration because these patients use circulating glucose to make fat instead of meet basal energy needs endocrine abn include hypogonadism and DM -they hide their food
318
Progeria (Hutchinson-Gilford syndrome)
-premature aging -start 6 month to 3 years -cardiac disease-HTN, ischemia, cardiomegaly -Alopecia -micrognathia -joint stiffness -small stature -careful padding and positioning -potential difficular airway -monitor and treat for myocardial ischemia
319
Turner's syndrome characterized by
short-webbed neck broad shield like chest maxillary and mandibular hypoplasia shorter trachea length possible coarcation of aorta or bicuspid aortic valve ovarian failure
320
preop considerations for turner syndrome
-difficult airway -thorough cardiac eval -optimization of medical comorbidities
321
Is intelligence normal in turner syndrome
-may be normal or slightly diminished
322
Treacher Collins Syndrome
-facial and pharyngeal hypoplasia -aplastic zygomatic arches -micrognathia -microstomia -choanal atresia -CHD -marked narrowing of airway above larynx extreme difficult intubation -cardiac problems
323
Xeroderma Pigmentosum (XP)
"children of the night" keratosis, telangiectasia, hyperpigmentation and neoplasia in areas exposed to sunlight
324
Genetics of XP
autosomal recessive genetic disorder of DNA repair, hypersensitivity to UV radiation and progressive neurologic complications
325
Elderly account for _____% of all inpatient hospital stays.
44%
326
Over 65 yrs account for ______ the US healthcare costs.
1/2
327
Theories of aging
Killer gene-Programmed cell death Telomere shortening-every time a cell divides
328
What is a primary factor in death?
mitochondrial damage b/c we run out of energy from less effective energy production in the mitochondria.
329
Effects of aging on liver
-liver mass decreases by 20-40% -decreased liver blood flow -decreased phase-1 drug metabolism -decreased bile production
330
GFR decreases ________ >40 years.
1ml/min/yr
331
Effects of aging on renal changes
-renal mass decreases by 20-25% -1/2 of all glomeruli decreased by 80 yr -effectively reduces renal drug excretion -slower elimination of Excess H20 vs. young kideys -sensation of thirst declines with age-chronic dehydration state less conservation of Na -reduced aldosterone secretion
332
_______y.o. required a reduction in drug doses.
60 years old.
333
What happens to insulin and hormones as we age?
-decreased secretion with age -increased insulin resistance (Especially skeletal) muscle
334
Which hormone levels decrease as we age?
-Testosterone -Estrogen -Growth hormone
335
Elderly have ______ rates of infection due to excess _______.
higher circulating glucose
336
Brain mass decreases after age ______.
50 by age 80-10% mass lost
337
Neurotransmitter functions decrease:
-dopamine -serotonin -GABA -Ach system-connection to Alzheimers, loss of cholinergic neurons
338
CNS changes of aging
-slower cognition and response times -atherosclerosis in cerebral vasculature -ironially, the brain is capable of rewiring new neurons, dendritic connections and neural pathways
339
Anesthesia Care challenges with CNS changes:
-potential anesthesia interactions -post-op cognitive impairment and delirium -stress of sx effect on brain with a minimal reserve function
340
Bolus concentrations ______initially in the elderly-->contracted circulating blood volume.
higher
341
decreased muscle mass=_________drug available.
increased free drug available high concentration in circulation because less sequestered in the muscle group -increased drug absorption by the target organ (brain) and heart
342
Slower circulation times-->delayed target organ delivery and response
343
Pharmacology-metabolism in elderly
-decreased drug metabolism -decreased drug clearance -increased Vd-drug reservoir -decreased liver mass and blood flow -lower GFR-lower excretion
344
CV system effects of aging
1. Decreased Beta-receptor Stimulation 2. stiffening of myocardium, arteries and veins 3. Autonomic nervous system changes: increased SNS activity, decreased PNS activity 4. conduction system changes 5. defective ischemic preconditioning
345
Decreased Beta-receptor stimulation
-not believed to be beta receptors in the heart -defects in intracellular coupling -HR has less response to catecholamines -chronic HTN decreases baroreceptor control of HR -HR increase to exercise is altered (220-age) -decreased exertional capacity -impaired regulation of BP
346
SNS activity _______ as we age.
increase -increase SNS activity at rest -exaggerated response to stimuli -excessive changes to vascular resistance (BP Lability) during anesthesia , wild fluctuations and profound low BP after inductions
347
Vagal tone __________ with aging.
decreases -may limit responsiveness to anticholinergics
348
Ischemic Preconditioning
-effective is limited or abolished with age -defined as brief period of ischemia lessen the effect of a prolonged myocardial ischemia event -in younger adults who experienced angina within 2 weeks of an infarction had less death or heart failure -protective effect of angina is not present in older adults
349
Stiffening of chest wall causes:
-increases work of breathing -barrel-shaped chest and flattening of diaphragm -decrease muscle mechanical advantage to generate negative pressure to breathe -increase minute ventilation and fatigue by increased effort to breathe
350
Decreased elasticity of lung parencyhma causes:
-makes lung earlier to inflate but at a cost of less springiness -small airways have less stiffness and depend on tethering to stay open -greater internal lung pressure is needed to prevent airway collapse and ventilate -closing capacity of the airways will eventually exceed lung TV -less ventilated lung tissue-reduced alveolar ventilation-->decreased PaCO2
351
With aging ____decrease in response to hypercapnia.
50%
352
With aging, _____decreased response to hypoxia.
50%
353
> ______% over 65 have some degree of sleep-disordered breathing.
75%
354
Generalized loss of muscle tone of upper airway:
-hypopharyngeal muscles -genioglossal muscles -both lead to an increased risk of upper airway obstruction -aspiration risk due to inability to clear secretions
355
Cold response in elderly:
Vasoconstriction-shunt blood to core Shivering-not as profound as younger patients both are triggered by the following temps: skin temp change=1 degree C core temp change=0.2C
356
Risks of hypothermia with aging
-increased risk of MI -surgical wound infection -coagulopathy -impaired drug metabolism
357
Aging impairs the threshold for response to thermoregulation by ______.
1 degree C
358
The most common medications that cause postoperative delirium are:
1. atropine 2. opioids 3. benzodiazepines
359
Differential diagnosis of delirium
-subdural hematoma -dementia -depression -delirium tremors
360
Post-operative delirium
Delirium is a medical emergency (1/3rd preventable) Emotional changes Lint picking (obvious with central anticholinergic effect) Incoherent speech and swearing Reversal of sleep pattern Indifferent to what is going on Un-cooperative Memory loss
361
postoperative cognitive dysfunction is defined as:
deterioration in cognitive function following surgery
362
Obesity
abnormally high percent of body weight as fat
363
Overweight
increased body weight above a standard related to height
364
Obesity types:
1. android 2. gynecoid
365
Android
-distribution of body fat in the upper body (truncal) -very metabolically active -increased oxygen consumption -higher rate of CV disease -visceral fat -increased CV disease - high rates of LV dysfunction -most dangerous
366
Gynecoid
-adipose tissue mostly located in hips, buttocks and thighs -less metabolically active -to a lesser degree less associated with CV disease
367
Ideal body weight calculation
IBW (kg)=height (cm)- X Males (x=100)-result represents 80% TBW Females (x=105)-result represents 75% TBW
368
True/False: immediate preperative weight loss has not been shown to reduce perioperative morbidity or mortality.
true
369
What is the most sensitive indicator of obesity's effects on body?
ERV
370
Obese patient's maintain normal responses to:
-hypoxemia -hypercapnia
371
Respiratory system changes with obesity
-decreased chest wall and lung compliance from thorax/abdominal fat -increased pulmonary blood flow-higher circulating volume -polycythemia (more blood viscosity) from chronic hypoxia -decreased lung elasticity-reduced lung compliance -decreased FRC & ERV-most commonly reported pulmonary abnormaility -lung volumes below closing capacity (small airway closure)
372
At least ___% of obese patients have OSA
5%
373
Diagnosis of OSA
-frequent episodes of sleep apnea (>10secs and or >5/min) typically against a closed glottis (10 sec />15 sec per hour of sleep
374
OSA normal classification (number of apnea-hypopnea events/hr)
<5
375
OSA mild classification (number of apnea-hypopnea events/hr)
> or equal to 5 but <15
376
OSA moderate classification (number of apnea-hypopnea events/hr)
> or equal to 15 but <30
377
OSA severe classification (number of apnea-hypopnea events/hr)
> or equal to 30
378
S/s of OSA
-hypoxemia -hypercapnia -pulmonary/systemic vasoconstriction -secondary polycythemia -respiratory acidosis limited to sleep time
379
Complications of OSA
-Ischemia heart disease -cor pulmonale from hypoxic pulmonary vasoconstriction -cerebral vascular disease/events
380
Obesity Hypoventilation syndrome results from
(Pickwickian sydrome) -long term OSA alters breathing control (less sensitive to high PaCO2) and more reliant on hypoxic (low O2 drive) -CNS mediated apneic events -seen in 5-10% morbidly obese patients
381
combination of obesity hypoventilation syndrome
-obesity -chronic hypoventilation -leads to pulmonary HTN or cor pulmonale BMI>30 -awake Pa CO2 >45mmHg
382
Hallmark of obesity Hypoventilation (Pickwickian) syndrome
alveolar hypoventilation independent of intrinsic lung disease
383
What happens to the heart with obesity?
increased left ventricular wall stress-->obesity cardiomyopathy -hypertrophy (ultimately fails to keep up with diastolic dysfunction) -impaired LV filling (diastolic dysfunction) -elevated LV and diastolic dysfunction) end result-->bi-ventricular failure
384
Blood volume and CO changes with obesity
-increased total body volume (goes to adipose tissue) & polycythemia -CO increased with increased weight
385
How does obesity affect atherosclerosis?
-lower mobility -increased angina/ischemic events -dyspnea on exertion at rest, they will appear asymptomatic, minimal exertion precipitates symptoms
386
Cardiac dysrhythmias/failure in obesity results from:
-fatty infiltration into the into the conduction system -CAD -electrolytes imbalances -hypoxia/hypercapnia
387
Most sensitive leads for ischemic events
Leads II and V5
388
Obese patients are high aspiration risk due to:
-delayed gastric emptying -gastric volumes >25mL -gastric fluid pH <2.5 -increased incidence of Hiatal hernia and GERD
389
Fasting guidelines for Obese patients
-no solids for 8 hours -clear liquids up to 2 hours -take their antacid/H2 blockers-as scheduled consider IV
390
In Hepatic system in obesity High incidence of:
-NAFLD -inflammation -abnormal LFTs -focal necrosis and cirrhosis
391
Degree of weight loss correlates directly with _________.
LFT improvement
392
Is there a clear connection between elevated LFTs and liver metabolism of drug ability?
no
393
Diagnosis of metabolic syndrome
-central obesity -any (2) of the following: -high Triglycerides -low HDL -HTN -high fasting glucose
394
Metabolic syndrome cluster of abnormalities:
-abdominal obesity -glucose intolerance -HTN -dyslipidemia -increased vascular events
395
Half life of endogenous GLP-1
1-2 min
396
GLP-1 and anesthesia
-high aspiration risk --long half life -very delayed gastric emptying -case reports of retained gastric contents up to 1-2 weeks after D/C -need to POCUS scan GI -treat as full stomach-RSI -actively vomiting/retching/symptoms for elective case-delay!
397
Half-life of Dulaglutide (Trulicity)
5 days
398
Half life Exenatide (Byureoun) extended releast
8-14 days
399
Half life Liraglutide (Victoza)
11-15 hours
400
Half-life Lixisenatide (Adlyzin)
3-5 hours
401
Half life of Ozempic (Wegovy)
6-7 days
402
HAlf life Rybelsus (Oral)
6-7 days
403
Emergence for obese patients
-resp rate 12-24/min (stable/regular) -neg inspiratory force >20mmHg -TV >6ml/kg -hemodynamically stable -O2 saturation >93-95% -sustained head lift >5s and strong handgrip -following commands -suction airway -ETCO2 relatively normal range -extubate elevated HOB
404
Maintenance of anesthesia for obese patients
-volatile agents ok-minimally metabolized -propofol GTT-good choice if not long case -remifentanil-quick on/off -shorter acting opioids -NMBDs-roc ok, cistricurium (organ independent elimination pathway) -reversal-sugammadex! -dexmedetomidine -sedline or BID-tailor anesthetic level -PEEP-only ventilatory parameter that consistently improves respiratory function
405
Supine positioning in obese patients
-ventilatory impairment -aortocaval compression -decreased FRC/oxygenation -induction -consider HOB up for preoxygenation - prolonged denitrogenating -face strap with tight mask seal -peep 5-10 cm H20
406
Which position for obese patients will allow better movement of the diaphragm?
-lateral
407
What is the weight limit for regular OR tables
200kg
408
What is the weight limit for obese OR table?
455kg
409
What is the number 1 indicator for problematic intubation in obese patients?
neck cirumference
410
What is the major cause of sudden death in morbidly obese?
DVT -Heparin 5000 U sq repeated q 8-12 hours until fully mobile or unfractionated heparin 40mg sq Q 12hours
411
What happens to the liver with aging?
-mass decreases by 20-40% -decreased liver blood flow -decreased phase 1 metabolism -decreased bile production -other than drug metabolism liver reserve should be more than adequate in the absence of disease
412
Renal changes with aging
-mass decreases by 20-25% -1/2 of all glomeruli decreased by 80 years old. -decrease GFR by 1 ml/min/yr >40 year -60 yr requires reduction in drug doses -effectively reduces renal drug excretpion -less conservation of Na-reduced aldosterone secretion
413
True/false: eAirway may remain hyperactive for 4-6 weeks
true
414
Most common cause of symptomatic OSA in children
adenotonsillar hypertrophy
415
What % of adult patients are unaware they have OSA prior to sx?
80-90%
416
STOP-Bang
Snoring Tired Observe Apnea Pressure (HTN) Body Mass index >35 kg/m2 Age older than 50 Neck size large >40cm/16inches Gender: Male
417
0-2 on Stop Bang
low risk
418
3-4 on stop bang
intermediate risk
419
5-8 on stop bang
high risk
420
Discharge Criteria
-return to room air o2 saturation at baseline -no hypoxic episodes or periods of airway obstruction when left alone -monitoring for a minimum of 3 hours more than non-OSA -monitoring for 7 hours following episode of airway obstruction or hypoxemia on ra /unstimulated problem with surgery center
421
Definite no for outpatient sx
-unstable asa III or IV active alcohol/substance abuse -no caregiver -poorly managed OSA, morbid obesity with comorbidities -ex-premie less than 60 weeks post-conceptual age under ET Anesthesia --active infection/sepsis -potential for uncontrolled pain relief
422
mot common reason sx cancelled in children
acute URI
423
context sensitive half time
time it takes for plasma concentration to decline by 50% after terminating infusion
424
2 most common types of patients to encounter troubles with:
1. Coronary Artery Disease 2. Congestive heart failure
425
First sign of myocardial ischemia
hypotension
426
most common sign of myocardial ischemia
tachycardia often a reaction to, not the cause of, myocardial ischemia
427
3 most common reasons for delay in patient discharge from PACU
1. drowsiness 2. N/V 3. Pain
428
hypothermia is temp below __________.
36 C
429
Hypothermia can cause:
1. prolonged recovery, drug metabolism decreases 2. physiologic instability (decreased oxygen, cardiac and rhythm changes) 3. post operative morbidity
430
high risk patients for hypothermia
-elderly -neonates -intoxicated -general anesthetics
431
Apfel's risk assessment for PDNV
-female -hx of motion sickness and/or PONV -age <50 years -use of post-op opioids -PONV in PACU
432
Modified Aldrete Scoring System (aldrete)
-frequently used to quantify readiness for discharge from PACU phase 1
433
What score is considered ready for discharge in the Aldrete and Postanesthetic discharge scoring system
9/10
434
Patient factors requiring sedation or anesthesia for Non operating room procedures
-claustrophobia, anxiety, panic disorder -cerebral palsy, developmental delay or learning difficulties -seizure disorders, movement disorders, muscular contractures -pain, related to the procedure or the positioning or unrelated pain -acute trauma with unstable CV, resp, or neurologic function increased intracranial pressure -significant comorbidity grades III and Iv -child's age especially children <10
435
Most common complications associated with NORA
airway obstruction and respiratory depression
436
Minimal sedation (anxiolysis)
-normal response to verbal stimulation airway, spontaneous ventilation and CV function unaffected
437
Moderate conscious sedation
-purposeful response to verbal or tactile stimulation -spontaneous ventilation adequate cv function usually maintained airway-no intervention required
438
Deep sedation
-purposeful response after repeated or painful stimulation -airway intervention may be required -spontaneous ventilation may be inadequate -CV system usually maintained
439
General anesthesia
unarousable even with painful stimulus airway-intervention often required -frequently inadequate spontaneous respiration -CV function may be impaired
440
Deterministic
severity of tissue damage is dose dependent, such at a cataract or infertilityS
441
Stochastic
probability of occurence is dose related, such as in cancer or genetic effect
442
Staff exposure to radiation can be minimized
-limiting the time of exposure to radiation -increasing distance from the source of radiation -using protective shielding -using radiation dose badges -radiation accumulates over time -inverse square rule-4ft distance decreases dose by 16 times
443
MOA of contrast agents for MRI
contain gadolinium-may be given IV before MRI to increase speed at which protons realign with magnetic field. The faster the protons realign, the brighter the image
444
Advantages of MRI
-no ionizing radiation like CT and Xray -can see non-bony tissues more clearly (brain, SC, nerves, muscles, ligaments, tendons_
445
Disadvantages of MRI
-more costly than CT and xray
446
Problems/contraindications associated with MRI
-AICD, cardiac pacemakers may malfunction, insulin pumps and other implantable devices, cochlear implants, Deep brain stimulators, implanted pumps -intracerebral clips might move -large area tattoos with ferromagnetic links -transdermal medication patch may cause burn -bullet fragments and shrapnel
447
Is it safe to undergo an MRI during pregnancy?
yes preferable during first trimester
448
IV contrast agents used in radiology are eliminated by
kidneys
449
Which IV contrast agents have less adverse reactions less pain on injection
nonionic
450
Immediate hypersensitivity reaction time
<1 hour
451
non-immediate hypersensitivity reaction time
>1 hour
452
Contrast-induced nephropathy is defined as
increase in serum creatinine of 0.5mg/dl or a 25% increase from baseline within 48-72 hours after iodinated contrast medium
453
Risk factors for contrast induced nephropathy
-renal disease -prior renal surgery -proteinuria -diabetes -dehydration -hypertension -advanced age -concominant use of nephrotoxic drugs and patients on metformin
454
Preventative measures of contrast induced nephropathy
-adequate hydration -maintaining good UOP -using sodium bicarb infusions to improve elimination of contrast agent
455
Most frequent immediate hypersensitivity reactions
pruritis and urticaria
456
most frequent non immediate hypersensitivity reactions
pruritis and exanthema
457
Tx of hypersensitivity reaction
-stop causative agent -oxygen -secure airway -fluids -vasopressors and inotropes -bronchodilators -pre-tx with corticosteroids and antihistamines questionable
458
Interventional neuroradiology
-tx by endovascular access for the purpose of delivering therapeutic drugs and devices -hybrid environment -occlusive or opening procedures -cerebral aneurysm, AVMs and vascular tumors -ABSOLUTE immobility
459
459
Angiography
-usually under local with MAC -General/ET (stroke, subarachnoid,hemm, increased ICP or depressed LOC) -need a motionless field -contrast dye injections into cerebral arteries can cause burning and/or pruritus around face and eyes -full bladder from IV fluid andIV contrast administration
460
TIPS (transjugular intrahepatic portosystemic shunt)
-significant hepatic dysfunction -bridge to transplant
461
Which interventional radiology procedure has radioactive concerns
Theraspheres placement (liver tumors)
462
Kyphoplasty
treats spinal compression fractures using a balloon like device to present bones from collapsing
462
What are the proposed mechanisms by which ECT is effective?
-monoamine neurotransmitter theory (increasing dopamine, serotonin, adrenergic and possible GABA and glutamine neurotransmission -neuroendocrine theory (release of pituitary or hypothalamic hormones) -neurotrophic theory (increasing signaling in the brain)
463
Durg that is gold standard for ECT
methohexital
464
Induction dose of methohexital
1-1.5mg/kg
465
What happens with methohexital at lower doses
-can paradoxically increase or activate cortical EEG seizure discharges in patients with temporal lobe epilepsy -this property makes a bolus dose of methohexital the IV anesthetic of choice for ECT therapy
466
Goal for ECT
tonic-clonic seizures that can last 60 sec or more
467
What is the most common tach