ITE CA-2 General Flashcards
1
Q
Dual antiplatelet therapy peri-op guidelines for DES
A
The ACC/AHA released a statement on patients who take DAPT in 2016 that adjusted the typical one-year for DES in patients having surgery. They now recommend at least three months of DAPT in cases where postponing the surgery would result in significant morbidity, preferably 6 to 12 months of DAPT should be continued in patients having elective surgery. They break down the risk into thrombotic risk versus bleeding risk.
2
Q
DAPT for BMS
A
1 month
unless post MI, then 12 months
3
Q
How manage DAPT if thrombotic risk from surgery is intermediate (regardless of bleeding risk)
A
Postpone elective surgery: if it can’t be postponed, continue ASA and discontinue clopidogrel (resume within 24-72 hours with a loading dose)
4
Q
How manage DAPT if thrombotic risk is low (regardless of bleeding risk)
A
Continue ASA and discontinue clopidogrel (resume within 24-72 hours with a loading dose)
5
Q
How manage DAPT if thrombotic risk is high and bleeding risk is intermediate or high
A
Postpone elective surgery: if it cannot be postponed, continue ASA and discontinue clopidogrel (resume within 24-72 hours with a loading dose)
6
Q
How manage DAPT if thrombotic risk is high and bleeding risk is low
A
Postpone surgery: if cannot be postponed continue DAPT
7
Q
DAPT after balloon angioplasty
A
Nope
8
Q
Deposition
A
Depositions are statements made under oath about the case, usually for clarification of the written record or to explain the reasoning or thought process behind a decision. They are part of the discovery process.
9
Q
Testimony
A
Testimony is evidence given by a witness under oath about the case. It is part of a deposition, which is part of discovery
10
Q
Summons
A
A summons is the official beginning of a lawsuit, and it is to notify the defendant that an action has been instituted against him or her, and that he or she is required to answer to it at a time and place named.
11
Q
Discovery
A
Discovery is the process at the beginning of a malpractice suit where documents are exchanged and depositions are made
12
Q
Beta blocker guidelines
A
The current 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery recommendations for BBs are as follows:
- Continue in those taking them chronically (class I)
- Manage according to clinical circumstances (class IIa)
- Begin in patients with intermediate- or high-risk myocardial ischemia noted in preoperative risk stratification tests (class IIb)
- Begin in patients with 3 or more RCRI risk factors (class IIb)
- In patients in whom beta-blocker therapy is initiated, begin more than 1 day before surgery (class IIb)
- Not start on the day of surgery (class III)
13
Q
RCRI
A
Revised Cardiac Risk Index
- History of ischemic heart disease
- History of congestive heart failure
- History of cerebrovascular disease (stroke or transient ischemic attack)
- History of diabetes requiring preoperative insulin use
- Chronic kidney disease (creatinine > 2 mg/dL)
- Undergoing suprainguinal vascular, intraperitoneal, or intrathoracic surgery
Risk for cardiac death, nonfatal myocardial infarction, and nonfatal cardiac arrest:
0 predictors = 0.4%, 1 predictor = 0.9%, 2 predictors = 6.6%, ≥3 predictors = >11%
14
Q
Bronchial blockers
A
Bronchial blockers are potentially advantageous over DLTs for selective lobar collapse, in patients with prior oral or neck surgery with challenging airways, in patients with tracheostomies, in children < 12 years old, and when postoperative mechanical ventilation is anticipated (don’t have to exchange ETT). They are not as reliable as DLTs for providing lung isolation
While bronchial blockers can achieve lung separation, they are not considered as reliable as a DLT. Bronchial blockers can migrate into the trachea causing loss of lung isolation and interference with ventilation. Conversion of a VATS to an open procedure may signal surgical difficulty in which lung isolation may become even more critical, and thus, a DLT would be preferred.
15
Q
Laryngospasm management
A
Initial treatment of laryngospasm includes administration of 100% oxygen, CPAP, removal of any offending foreign bodies or secretions, and increasing the depth of anesthesia. Succinylcholine may be used as a last resort and with caution in pediatric patients due to bradycardia and the risk of triggering MH.
16
Q
Sodium conc in albumin
A
Albumin solutions manufactured in the United States have a sodium concentration of 145 mEq/L with a maximum range +/- 15 mEq/L. A solution of 25% albumin should never be diluted with sterile water; normal saline or 5% dextrose in water are preferred diluents.
17
Q
Composition of commonly used IVF
A
Composition of several commonly used intravenous fluids:
——————–NS…….LR…….Alb…….Plasmalyte
Na (mEq/L)………154……130……130-160……140
Cl (mEq/L)……….154……109……130-160……98
K (mEq/L)………….0…………4………0………………5
Osmolarity (mOsm/L) 308-310 275 310 294
Lactate (mEq/L) 0…….28………0……………0
18
Q
NPO guidelines
A
The current guidelines for NPO status recommend waiting for a minimum of:
- 2 hours after ingestion of clear liquids
- 4 hours after ingestion of breastmilk
- 6 hours after ingestion of nonhuman milk, formula, or a light meal (“tea and toast”)
- 8 hours after ingestion of a full meal or fatty foods
19
Q
LMA contraindications
A
Laryngeal mask airway use is contraindicated in patients with a high risk for aspiration of gastric contents including, but not limited to: known or potential for full stomach, hiatal hernia, gastroesophageal reflux disease, intestinal obstruction, and delayed gastric emptying.
Laryngeal mask airway use is also contraindicated in patients with poor lung compliance, high airway resistance, glottic or subglottic airway obstruction, and a limited mouth opening (generally less than 1.5 cm).
20
Q
ASA difficult airway
A
The ASA Difficult Airway Algorithm dictates that in a scenario of unanticipated difficult intubation and difficult mask ventilation to then attempt placement of a supraglottic airway. If ventilation is still inadequate, immediately call for help then follow the emergency pathway.
21
Q
ASA 4
A
Constant threat to life
22
Q
3 benefites to skipping pacu (fast-tracking)
A
Fast-tracking occurs when a patient bypasses phase I care; moving straight from the operating room to phase II recovery.
The concept of fast-tracking surgery has taken hold in modern-day anesthetic care for a variety of reasons. As surgical techniques improve, more patients are going to be eligible for this type of care. There are several possible advantages including cost savings, faster time to discharge, and potentially a decreased rate of unplanned hospital admissions.
One area that has not shown any improvement in fast-tracking is a reduced workload for the nurses. In fact, fast-tracking often requires increased staffing requirements and cross-training of staff due to the need for more nurses with the ability to care for patients across the spectrum of recovery.
23
Q
3 phases of post-op recovery process and locations
A
The first phase (phase I) refers to the period of time in which the patient recovers and regains core physiologic functions – the ‘protective reflexes’ and motor functions. This occurs in the post-anesthesia care unit (PACU) where intensive nursing care often requires a nurse to patient ratio of 1:2. During the second phase (phase II), the patient regains cognitive function and the ability to be discharged home. There are various names for the locations phase II care occurs; second stage and ambulatory surgical unit (ASU). There are several scoring systems that help healthcare providers decide when these milestones have been achieved and the patient can be discharged from each stage of recovery; Aldrete and White/Song are the two most widely used in the U.S. today. The third phase (phase III) occurs in the patient’s home where full recovery occurs.
24
Q
how many Category 1 CME credits are required every MOCA cycle?
A
250 Category 1 CME credits are required every MOCA cycle
Examples of such Category 1 CME activities include:
Fellowship - 12 months of ACGME-accredited fellowship training or another Anesthesiology sub-specialty program sponsored by an ACGME program can be counted as up to 50 CME credits
Board certification - up to 60 credits applied to state board requirements (but not MOCA)
ACLS course - when offered by an ACGME sponsor, up to 16 CME credits
Test Item Writing - for American Board of Anesthesiology (ABA) or the National Board of Medical Examiners (NBME) - 10 CME credits
Medically related advanced degrees such as a Masters of Public Health - 25 CME credits
Grand Rounds - CME credits issued by the institution
Performance Improvement - structured, long-term processes that allow physicians to assess and re-evaluate their performance.
Additionally, there are requirements on the timing at which these credits are obtained. For instance, at least half of the 250 credits must be completed by the fifth year of ten-year cycles. Lastly, 20 Category 1 credits specific to patient safety must be completed.
25
What gas is useful with increased airway resistance and why
Helium is useful with increased airway resistance and turbulent flow, as is seen with decreasing airway radius, because helium has a low gas density. The low gas density decreases resistance with turbulent flow and increases the chance for development of laminar flow.
26
Turbulent flow is more likely in what conditions
To sum up turbulent flow is more likely with greater velocity, in larger diameter tubes with a dense gas of low viscosity.
27
anesthesia residents substance abuse incidence since 1975
| risk of death in those returning to anesthesia
These reporting methods have shown that since 1975 the incidence of substance abuse has increased among anesthesia trainees and the relapse rate has not decreased. Furthermore, the risk of death due to relapse is high with approximately 11% of those returning to anesthesia dying due to relapse.
28
ACGME 6 core competencies
The Accreditation Council of Graduate Medical Education (ACGME) provides six core competencies in residency training:
1) Patient care
2) Medical Knowledge
3) Interpersonal and communication skills
4) Professionalism
5) Systems-based practice
6) Practice-based learning and improvement
29
What is the main advantage of performing a peribulbar block versus a retrobulbar block for ophthalmic anesthesia?
Peribulbar blocks offer the advantage of a decreased risk of retrobulbar hemorrhage and optic nerve injury. Other benefits include a decreased risk of central spread of local anesthetic as it is not near the optic nerve. Disadvantages include a longer onset time and a lower incidence of complete akinesia.
30
afferent limb of oculocardiac reflex
Both the peribulbar and retrobulbar blocks attenuate the oculocardiac reflex by blocking the ophthalmic branch of the trigeminal nerve, which is the afferent limb of the reflex.
31
what do you do if you suspect VAE
Even the slightest suspicion of a VAE should be acted on immediately. Treatment includes increasing FiO2, notifying the surgeons so that they can flood the field, and considering a position change to left lateral decubitus. If hemodynamic instability is present, inotropic support is typically indicated (e.g. dobutamine, epinephrine).
Hyperbaric oxygen works too but takes a while
CPR and right heart air aspiration also work.
32
how much air as VAE for what effects
As little as 100 mL of air entrained into the circulation can cause an airlock in the right ventricle, disrupt forward blood flow, and have devastating consequences for the patient including stroke, myocardial infarction, cardiac arrest, and/or death. Cardiovascular collapse typically occurs with 300 mL of entrained air. The fatal dose is around 300-500 mL of air, or 3-5 mL/kg. As an example, a 14 g IV with 5 cm H2O of pressure gradient would entrain 100 mL per second.
33
General neurotransmitters is PNS vs SNS
For generalization, the terminals in the PNS postganglionic fibers release ACh, in the SNS, NE is the principle transmitter released (except for sweat glands which use ACh).
34
Nicotinic vs muscarinic
Nicotinic receptors are ligand-gated channels typically found at the neuromuscular junction of skeletal muscle. Muscarinic receptors are G protein-coupled and found mostly in the peripheral visceral organs. Five different types of muscarinic receptor exist (M1 through M5) and they have diverse signal transduction mechanisms.
35
Best measure of adequate reversal
the train-of-four ratio (TOFR) of at least 0.9 is best associated with a return of physiologic neuromuscular parameters
36
Myotonic dystrophy inheritance pattern
Myotonic dystrophy is an autosomal dominant inherited disorder of the neuromuscular junction characterized by progressive muscle weakness and wasting which is most prominent in the cranial and distal limb musculature. Cranial muscle weakness presents in the facial, temporalis, masseter, sternocleidomastoid muscles, and possibly the vocal cord apparatus. These patients are at increased risk for myotonia, which is a prolonged contraction with delay of relaxation of the musculature. Myotonic dystrophy is also associated with cardiac conduction disorders, progressive myopathy, insulin resistance, neuropsychiatric impairment, and cataracts. In the perioperative period, myotonic dystrophy patients are more likely to suffer from pulmonary related complications especially when severe disease is present or they are undergoing upper abdominal procedures.
37
Myotonic dystrophy most prominent in what musculature
Myotonic dystrophy is an autosomal dominant inherited disorder of the neuromuscular junction characterized by progressive muscle weakness and wasting which is most prominent in the cranial and distal limb musculature. Cranial muscle weakness presents in the facial, temporalis, masseter, sternocleidomastoid muscles, and possibly the vocal cord apparatus. These patients are at increased risk for myotonia, which is a prolonged contraction with delay of relaxation of the musculature. Myotonic dystrophy is also associated with cardiac conduction disorders, progressive myopathy, insulin resistance, neuropsychiatric impairment, and cataracts. In the perioperative period, myotonic dystrophy patients are more likely to suffer from pulmonary related complications especially when severe disease is present or they are undergoing upper abdominal procedures.
38
Other systems affected
Myotonic dystrophy is an autosomal dominant inherited disorder of the neuromuscular junction characterized by progressive muscle weakness and wasting which is most prominent in the cranial and distal limb musculature. Cranial muscle weakness presents in the facial, temporalis, masseter, sternocleidomastoid muscles, and possibly the vocal cord apparatus. These patients are at increased risk for myotonia, which is a prolonged contraction with delay of relaxation of the musculature. Myotonic dystrophy is also associated with cardiac conduction disorders, progressive myopathy, insulin resistance, neuropsychiatric impairment, and cataracts. In the perioperative period, myotonic dystrophy patients are more likely to suffer from pulmonary related complications especially when severe disease is present or they are undergoing upper abdominal procedures.
39
Potential perioperative complications myotonic dystrophy and what to do
In the perioperative period, myotonic dystrophy patients are more likely to suffer from pulmonary related complications especially when severe disease is present or they are undergoing upper abdominal procedures.
Preoperative evaluation of these patients must include thorough examination of the pulmonary and cardiac systems.
Preoperative testing should include an electrocardiogram and echocardiography (A, B). If any conduction abnormality is present on electrocardiogram, a cardiology consultation should be obtained as these patients often have unpredictable and rapid progression of AV conduction disease. Pacemaker placement may be considered even if only first degree heart block is present (C). If second or third degree heart block is present, pacemaker implantation is warranted. Because of the elevated risk of cardiomyopathy and cardiac conduction defects, these patients need to have careful perioperative cardiac monitoring with the capability to provide external pacing should it be required. In addition, a chest radiograph may be obtained if the patient has acute symptoms of pulmonary disease.
40
Myotonic dystrophy anesthetic considerations
Succinylcholine use may result in contractions that last several minutes, making ventilation and intubation challenging. These contractions are not antagonized by prophylactic administration of a nondepolarizing muscle relaxant, thus succinylcholine should be avoided and short acting nondepolarizing agents, or no muscle relaxants at all, should be used. These patients can be quite sensitive to anesthetic agents thus careful titration of short-acting anesthetics is recommended. Additionally, several medications (methohexital, etomidate, propofol, neostigmine), hypothermia, shivering and mechanical or electrical stimulation may induce myotonic reactions. Because of the elevated risk of cardiomyopathy and cardiac conduction defects, these patients need to have careful perioperative cardiac monitoring with the capability to provide external pacing should it be required. Also, one-third of these patients who develop AV block will not respond to atropine.
41
Charcot-Marie-Tooth disease
CMT is a demyelinating disorder of peripheral nerves.
42
Charcot Marie tooth inheritance
Although some of the subtypes of CMT can be inherited through X-linked recessive, the most common type (CMT1) exhibits autosomal dominant inheritance.
43
Charcot Marie tooth symptoms
Patients with CMT typically experience slow and progressive distal muscle weakness and wasting along with diminished reflexes. Early complaints may include frequently sprained ankles caused by the distal muscle weakness or difficulty keeping up with peers. Onset generally occurs by 20 years of age. Although the disorder does not compromise lifespan, it can cause significant physical disability.
44
Charcot Marie tooth anesthesia
The anesthesia experience in patients with CMT is limited because of the small number of cases. Management of anesthesia in patients with CMT introduces challenges for protection of the involved nerve against further entrapment or trauma associated with positioning.
Autonomic neuropathy may be associated with exaggerated hemodynamic response to the anesthetic as a result of involvement of the circulatory reflexes.
There is conflicting reports regarding response to neuromuscular blockers; some report increased sensitivity to vecuronium while cisatracurium and mivacurium have been used with no evidence of prolongation of neuromuscular blockade.
Because of the demyelination that occurs in the distal extremities, monitoring the neuromuscular blockade should preferentially occur at the facial rather than the ulnar nerve.
Although succinylcholine has been successfully used in these patients, clinicians are cautioned against its routine use, considering the risk of an exaggerated hyperkalemic response.
An increased sensitivity to hypnotic anesthetics has also been suggested, but intravenous and volatile anesthetics have been used in patients with CMT with no reported complications.
Nevertheless, multiple reports of worsening CMT symptoms have been recounted in patients exposed to nitrous oxide, such that this agent should be avoided when possible.
Regional anesthesia has been used in patients with CMT without clear evidence of associated complications. Because of the concern for exacerbating the neurologic symptoms, however, regional anesthesia techniques are often avoided in these patients.
45
Eval for delayed emergence
Initial evaluation includes confirmation that all anesthetic agents are discontinued, evaluation of any medications used, and timing of each. Medication errors can be considered based on the patient’s clinical status. Residual muscular paralysis can be evaluated for with a train of four monitor and reversal agents administered if needed. If there is evidence of opioid overdose with hypoventilation, reversal can be considered using naloxone. Benzodiazepine reversal with flumazenil can also be considered. At this point, laboratory testing such as arterial blood gas analysis, capillary blood glucose, and serum electrolytes should be checked and treated. Confirmation and maintenance of normothermia is also recommended. If these fail, a neurologic evaluation of pupillary response, motor function, and gag or cough reflex should also be obtained, with a STAT computed tomography (CT) of the head, and a neurosurgery or neurology consultations as needed based on the findings
Of note, though anticholinergic medications can cause delayed emergence, anticholinesterase medications do not.
46
Paramyotonia Congenita (PC)
Inheritance
What is it
Paramyotonia Congenita (PC) is a rare autosomal dominant disorder involving a defective sodium channel on skeletal muscles. This defect results in extended, slow inactivation of normally fast sodium channels, leading to a prolonged depolarization and myotonia. The myotonic episodes of stiffening can be triggered by cold, and rewarmed muscles can be temporarily flaccid. Like central core disease, hyperkalemic periodic paralysis, and hypokalemic periodic paralysis, PC is associated with malignant hyperthermia (MH) and succinylcholine should be avoided in these patients. Similar to myotonia congenita (MC), succinylcholine can lead to generalized muscle stiffness. Despite this association, some case reports have documented safe use of volatile anesthetics in pediatric and elderly populations. Additionally, regional and neuraxial anesthesia have been safely administered. It has been proposed that anticholinesterases should be avoided to avoid triggering a myotonic reaction.
The "paramyotonia" designation comes from its "paradoxical myotonia" since, unlike MC, it is not triggered by rest after exercise, but is triggered by exercise itself. Other triggers include hyperkalemia, pregnancy, hypothyroidism, and starvation.
47
paramyotonia congenita Similarities to myotonia congenita
```
Similarities to MC:
Often diagnosed in early childhood.
Hypertrophied appearance of the muscles.
Similar treatment, including phenytoin, mexiletine, quinine therapy.
Avoid succinylcholine.
```
48
paramyotonia congenita differences to myotonia congenita
paramyotonia congenita Differences to myotonia congenita
Differences from MC:
Stiffness is exacerbated by exercise, not rest. In MC, sustained exercise improves the myotonia.
Triggered also by hyperkalemia, leading some to believe it is a phenotyping variant of hyperkalemic periodic paralysis (HPP) especially since both are genetically associated to malignant hyperthermia.
Can be differentiated from MC by electromyogram (EMG).
49
paramyotonia congenita
| Perioperative management:
paramyotonia congenita
Perioperative management:
Avoidance of triggers such as hyperkalemia, acidosis, hypothermia, rapid changes in temperature, anticholinesterase, succinylcholine, and MH triggers such as volatile anesthetics.
Anticipation of airway difficulties from muscle contractions.
Anticipation of respiratory muscle weakness. Hence, short-acting anesthetics and judicious use of nondepolarizing neuromuscular blockade should be employed.
Maintenance of normothermia perioperatively: warm ambient temperature, forced-air warming devices, warmed intravenous fluids, blankets should be employed. Shivering should be treated proactively.
Maintenance of normokalemia.
50
Stage II of anesthesia
Stage II is the stage of delirium and excitement according to Guedel's classification in assessing depth of anesthesia. It may be characterized by agitation, excitation, confusion, irregular breathing, and breath holding. Patients in stage II may respond to noxious stimuli with vomiting, hypertension, laryngospasm, tachycardia, and reflexive or uncontrolled movements. The purpose of premedication with drugs like benzodiazepines and opioids is to synergize with the induction agent to progress through stage II to stage III as quickly as possible.
51
Stage I
Stage I of general anesthesia is a state of amnesia/analgesia. This stage starts at induction of anesthesia, and ends with loss of consciousness. Patient's in stage I may still be alert and speaking with regular breathing. The patient's pain perception threshold is not significantly lowered.
52
Stage III
Stage III is surgical anesthesia. This phase is characterized by fixed and dilated pupils, loss of corneal and laryngeal reflexes, shallow yet regular respirations, and skeletal muscle relaxation. Note that pupil dilation occurs in Stage II as well. Painful stimulation generally should not issue an autonomic response or somatic reflexes, but extremely invasive stimuli may require an increased depth of anesthesia.
53
Stage IV
Stage IV is medullary paralysis. It is often caused by an anesthetic overdose. It causes respiratory and circulatory depression, and is lethal if the patient is not treated with both ventilatory and pharmacological support in a timely manner.
54
Hypocalcemia clinical picture
Hypocalcemia can result in myriad clinical manifestations including neuromuscular (e.g. peripheral numbness and tingling, weakness, fatigue, spasms, seizures), respiratory (e.g. laryngeal or bronchospasm, respiratory failure), psychiatric (e.g. depression, anxiety, psychosis), and smooth muscle effects (e.g. abdominal cramps, urinary frequency).
Cardiac manifestations include ECG changes, arrhythmias, hypotension, and heart failure. Hypocalcemia classically causes prolongation of the QT interval by slowing ventricular repolarization. In severe cases, this can result in heart block and also predispose to torsades de pointes.
55
Hypothermia has several pathological effects:
Hypothermia has several pathological effects:
Impairment of platelet function, thromboxane generation, and local hemostatic vasoconstriction. This leads to bleeding that may be irreversible. The degree of coagulopathy may not be adequately captured by laboratory tests since they are rewarmed to 37 degrees Celsius
Even mild hypothermia can increase the risk of postoperative wound infection, leading to sepsis in these already critically ill patients.
Hypothermia leads to local vasoconstriction, low oxygen tension, impaired chemotaxis, and increased bacterial growth
Impaired anesthetic medication clearance via hepatic and renal pathways
Impaired central nervous system, with obtundation, excess sedation, poor response to hypoxemia and hypercarbia
Cold-induced vasoconstriction leads to high catecholamine concentration with increased myocardial ischemia
Severe hypothermia (under 33 degrees Celsius) leads to multiple organ damage and failure
56
Hypothermia effect on post-resuscitation myocardial ischemia
Hypothermia exacerbates, not protects against, post-resuscitation myocardial ischemia by leading to increased catecholamine release.
57
Core temp locations
Those standard locations are nasopharyngeal, tympanic, esophageal, and pulmonary artery.
58
ALS anesthetic considerations
When anesthesia is planned, certain medications predispose to increased risk. No specific medication regimen has proven to be better for patients with ALS. These patients are at elevated risk of forming extrajunctional acetylcholine receptors and can mount an exaggerated hyperkalemic response to succinylcholine. These patients often show a prolonged response to nondepolarizing muscle relaxants; thus careful titration is recommended.
Neuraxial anesthesia is commonly avoided in patients with neuromuscular disease, and it is relatively contraindicated in patients with amyotrophic lateral sclerosis for fear of exacerbating the disease. The mechanism behind disease exacerbation is unknown.
59
minimal sedation
normal response to verbal stimulation, airway remains unaffected, spontaneous ventilation maintained, and cardiovascular function unaffected.
60
moderate sedation
("Conscious Sedation"): purposeful response to verbal or tactile stimulation, no intervention required to maintain patent airway, adequate spontaneous ventilation, and cardiovascular function usually maintained.
61
deep sedation
purposeful response following repeated or painful stimulation, airway intervention may be required, spontaneous ventilation may be inadequate, and cardiovascular function usually maintained.
62
general anesthesia
unarousable even with painful stimulation, intervention on the airway often required, spontaneous ventilation is inadequate, and cardiovascular function may be impaired.
63
myasthenia gravis
Myasthenia gravis is an autoimmune disorder with antibodies against postsynaptic acetylcholine receptors. Ninety percent of patients with myasthenia gravis have thymus gland abnormalities. The clinical presentation of myasthenia gravis is progressive weakness with activity. Vision, speech, and swallowing may be affected along with global muscle weakness.
It worsens with exercise, muscle pain is uncommon, deep tendon reflexes are normal, and autonomic instability is not a feature. Most commonly it starts as ocular or bulbar weakness although when it progresses it can involve the limbs (mostly arms).
64
myasthenia gravis staging
Staging is based on type and extent of weakness. Important clinical markers suggesting the need for postoperative mechanical ventilation are as follows:
- Duration of myasthenia gravis > 6 years
- Chronic respiratory disease
- Pyridostigmine dose greater than or equal to 750 mg/day
- Vital capacity less than or equal to 2.9 L
65
maintenance therapy for myasthenia gravis
Maintenance therapy for myasthenia gravis includes anticholinesterases, most commonly pyridostigmine. It is also important to realize that weakness can be caused by a dose that is too high and weakness can remain if the dose is too low.
66
myasthenia response to sux and nondepolarizing agents
These patients are resistant to depolarizing neuromuscular blockade and exquisitely sensitive to nondepolarizing agents. Small doses of nondepolarizing agents can cause profound weakness and anticholinesterase agents are often ineffective secondary to chronic therapy with pyridostigmine. Sugammadex is being investigated as an alternative reversal agent for patients with myasthenia gravis.
67
myasthenia crisis
Myasthenic crisis may be precipitated by poor disease control, stress, hyperthermia, or pulmonary infections. Clinically these patients report severe weakness and subsequently develop respiratory failure. Treatment includes cholinesterase inhibitors, corticosteroids, immunosuppressant agents, intravenous immunoglobulin (IVIG), and plasmapheresis.
68
Lambert-Eaton
Lambert-Eaton myasthenic syndrome (LEMS) is caused by antibodies against P/Q-type voltage-gated calcium channels. It improves with exercise, muscle pain is common, has decreased deep tendon reflexes, and autonomic dysfunction. Most commonly it starts as weakness in proximal legs, although it can sometimes involve bulbar muscles (and rarely ocular muscles).
69
Lambert-Eaton rxn to sux and NDMBDs
Patients are very sensitive to both non-depolarizing neuromuscular blocking agents and succinylcholine. Mnemonic: lambs are sensitive animals.
70
Pulmonary hypertension is defined as
Pulmonary hypertension is defined as mean pulmonary artery pressure over 25 mm Hg at rest or 30 mm Hg with exercise.
71
Preservation of Total hepatic blood flow amongst volatile anesthetics at 1 MAC, from greatest to least
Preservation of THBF amongst volatile anesthetics at 1 MAC, from greatest to least, is sevoflurane > isoflurane > halothane.
72
SpO2 measurement in methemoglobinemia
Conventional pulse oximetry can neither detect MetHgb nor accurately measure SpO2 in the presence of elevated MetHgb levels. The standard two-wavelength pulse oximeters generally give measurements approaching 85% in the presence of high methemoglobin levels. In the setting of suspected methemoglobinemia, multi-wavelength co-oximetry should be used.
73
Treatment methemoglobinemia
Methylene blue (1-2 mg/kg) is the primary pharmacologic treatment of methemoglobinemia. However, methylene blue can cause hemolysis in patients with G6PD-deficiency. Therefore ascorbic acid (vitamin C) is the treatment of choice of methemoglobinemia in the setting of G6PD-deficiency.
74
Common acquired causes of methemoglobinemia include:
Common acquired causes of methemoglobinemia include: prilocaine, benzocaine, metoclopramide, nitrites (including nitric oxide and nitroglycerin), aniline dyes, benzene, chloroquine, dapsone, and sulfonamides. Congenital methemoglobinemia is either a deficiency in MetHgb reductase or a deficiency in NADPH production (G6PD-deficiency). When methemoglobinemia is associated with prilocaine use it is a dose-dependent (>500 mg) phenomenon, while methemoglobinemia associated with benzocaine is not dose-dependent.
75
Methylene blue on pulse ox
Methylene blue transiently decreases the observed pulse oximetry reading in a dose dependent manner. Pulse oximetry reading approach 65% for roughly 10 minutes.
76
ESRD when dialyze
For ESRD patients on a stable hemodialysis regimen, dialysis is ideally timed for the day prior to elective surgery. This provides the best balance between the risks of hypervolemia and electrolyte abnormalities if dialysis is too distant from surgery and hypovolemia if dialysis is too close to surgery.
77
Sulfhemoglobinemia
Shifts curve right or left
What meds cause it
Sulfhemoglobin shifts the oxyhemoglobin dissociation curve to the right.
Sulfhemoglobinemia is a rare condition believed to be caused by irreversible binding of a sulfur atom to the porphyrin ring of the heme moiety of hemoglobin. Agents reported to cause sulfhemoglobinemia as a side effect include sulfonamides, dapsone, metoclopramide, sumatriptan, and some industrial chemicals.
78
Differences between methemoglobinemia and sulfhemoglobinemia
Methemoglobinemia and sulfhemoglobinemia can be confused because they have a similar clinical presentation (cyanosis and falsely low SpO2) and are caused by some of the same drugs. However they are important differences between the two. First, methemoglobinemia shifts the hemoglobin dissociation curve to the left while sulfhemoglobinemia shifts it to the right; this makes sulfhemoglobinemia much better tolerated (and probably frequently missed) compared to methemoglobinemia. Second, there is a specific treatment for methemoglobinemia (methylene blue), whereas sulfhemoglobinemia does not have an antidote and will only resolve when the sulfhemoglobin is eventually replaced by newly synthesized hemoglobin (or exchange transfusion in an extreme case). Third, methemoglobin is classically described as conferring a chocolate-brown color to blood, while sulfhemoglobin has been described as dark greenish-black blood.
79
Other things that shift the hemoglobin dissociation curve to the left include
things that shift the hemoglobin dissociation curve to the left include fetal hemoglobin, carboxyhemoglobin, cold temperature, alkalosis, decreased 2-3 DPG (e.g. PRBC transfusion, septic shock, hypophosphatemia), sulfhemoglobinemia and hypocarbia.
Things that shift the hemoglobin dissociation curve to the right include sickle hemoglobin, pregnancy, hyperthermia, acidosis, increased 2-3 DPG (e.g. chronic anemia, CHF), and hypercarbia (the right-shift in the hemoglobin dissociation curve caused by CO2 is otherwise known as the Bohr effect).
80
Things that shift the hemoglobin dissociation curve to the right include
Other things that shift the hemoglobin dissociation curve to the left include fetal hemoglobin, carboxyhemoglobin, cold temperature, alkalosis, decreased 2-3 DPG (e.g. PRBC transfusion, septic shock, hypophosphatemia), and hypocarbia.
Things that shift the hemoglobin dissociation curve to the right include sickle hemoglobin, pregnancy, hyperthermia, acidosis, increased 2-3 DPG (e.g. chronic anemia, CHF), and hypercarbia (the right-shift in the hemoglobin dissociation curve caused by CO2 is otherwise known as the Bohr effect).
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Nephron segment for most of sodium reabsorption
Of the nephrons tubular segments, the proximal tubule accounts for 65-75 percent reabsorption of ultrafiltrate formed by the Bowman capsule.
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What products cause TRALI
Plasma is typically considered the most common blood product associated with TRALI. However, in some areas platelets carry a higher risk of TRALI. This is due to the use of male-only plasma by certain centers, such as the American Red Cross
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Most common cause adult jaundice in US
Patients with Gilbert syndrome have approximately 1/3 normal bilirubin glucuronyltransferase activity. This enzyme is required for hepatocyte uptake of unconjugated bilirubin. Blood transfusion increases serum bilirubin levels approximately 250 mg per unit transfused. Patients with Gilbert syndrome are at a higher risk for development of jaundice after multiple PRBC transfusions
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How avoid exacerbation of acute intermittent porphyria
Certain things increase the risk of an acute exacerbation in patients with acute intermittent porphyria. These include stressful situations, prolonged fasting times, and certain medications. Trying to avoid or decrease the extent of these will help decrease the risk of exacerbation. This includes adequate hydration to decrease the risk of dehydration and supplementation with glucose to avoid starvation states. Additionally, avoidance of medications that are known to precipitate an exacerbation can help (in the perioperative period this includes barbiturates, sulfonamides, ethyl alcohol, and ergotamine).
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Porphyrias
Porphyrias are a family of autosomal inherited diseases which result from a deficiency in one or more of the enzymes required for heme synthesis. This deficiency causes an accumulation of metabolites that are upstream from that specific reaction. The majority (> 75%) of hemoglobin synthesis occurs in the bone marrow through a complex set of steps.
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perioperative conditions leading to sickling:
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perioperative conditions leading to sickling:
SIX H's cause SICKling (HbS)
1. Hypothermia
2. Hyperthermia
3. Hypoxemia
4. Hypotension
5. Hypovolemia
6. H+ ions (acidosis)
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Fetal O2 requirement
The fetus uses approximately 8mL/kg/min of oxygen, which is significantly higher than the adult oxygen requirement of 3mL/kg/min.
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Adult O2 requirement
The fetus uses approximately 8mL/kg/min of oxygen, which is significantly higher than the adult oxygen requirement of 3mL/kg/min.
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Bohr effect
The Bohr effect is a physiologic effect that describes hemoglobin’s affinity for oxygen at different conditions. During alkalotic conditions oxygen has a greater affinity for hemoglobin and during acidic conditions oxygen binds to hemoglobin less avidly. Therefore, in the lung, oxygen binds to hemoglobin with a greater affinity than when it reaches the periphery or tissues like the placenta.
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Potential complications of brachial artery cannulation include
Potential complications of brachial artery cannulation include median nerve damage, distal ischemia due to lack of collateral circulation, and CRBSIs (infections)
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Signs of PRIS
Propofol infusion syndrome is a rare complication of prolonged, high-dose propofol administration. Signs may include metabolic lactic acidosis, cardiac failure, renal failure, rhabdomyolysis, hyperkalemia, hypertriglyceridemia, hepatomegaly, and pancreatitis.
TrueLearn Insight : Phenol excretion during PRIS causes green-tinged urine.
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Jet ventilation vs oscillatory regarding expiration
In HFJV exhalation is passive (depends on passive lung and chest-wall recoil) whereas in HFOV gas movement is caused by in-and-out movement of the “loudspeaker” oscillator membrane. Thus in HFOV both inspiration and expiration are actively caused by the oscillator, and passive exhalation is not allowed.
In both HFJV and HFOV, CO2 removal is inversely proportional to frequency (opposite of what we usually do in conventional ventilation modes). This is because the higher the frequency the lower the amplitude, which is the key to CO2 removal. NEITHER ALLOWS etco2 SAMPLING
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MELD components
MELD: "I Crush Several Beers Daily" for INR, creatinine, sodium, bilirubin, dialysis
Childs-Pugh: "Pour Another Beer At Eleven" for PT, Ascites, Bilirubin, Albumin, Encephalopathy
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Childs-Pugh components
MELD: "I Crush Several Beers Daily" for INR, creatinine, sodium, bilirubin, dialysis
Childs-Pugh: "Pour Another Beer At Eleven" for PT, Ascites, Bilirubin, Albumin, Encephalopathy
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Management of acute mountain sickness
Management of AMS symptoms includes hydration, supplemental oxygen, descent in altitude, hyperbaric chambers, acetazolamide, dexamethasone, and nonbenzodiazepine sleep aids. Most sedatives and hypnotics (e.g., benzodiazepines) should be avoided due to the potential for hypoventilation and exacerbation of hypoxia.
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Spinal cord stimulator contraindications
Spinal cord stimulation is relatively contraindicated in the setting of major untreated psychological disease, substance abuse, and lack of social support.
Absolute contraindications for spinal stimulation include (but are not limited to): sepsis, coagulopathy, previous surgery or trauma obliterating the spinal canal, localized infection, and spinal bifida.
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Blood volume by age
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Age Group Blood Volume
Premature infant 90-105 mL/kg
Full-term newborn 80-90 mL/kg
Infant 3-12 months 70-80 mL/kg
Child 1-12 years 70-75 mL/kg
Adult male 65-70 mL/kg
Adult female 60-65 mL/kg
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Absorption of __________ irrigation solution during TURP may lead to hyperammonemia causing neurological complications including encephalopathy and coma.
Absorption of glycine-containing irrigation solution during TURP may lead to hyperammonemia causing neurological complications including encephalopathy and coma.
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TENS device indications
TENS device use is indicated for symptomatic relief of chronic intractable pain, relief of acute post-surgical and post-traumatic pain, and relief of pain associated with arthritis.
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Contraindications for TENS therapy
Contraindications include patients with demand-type pacemakers, patients with known cardiac dysrhythmias, undiagnosed pain syndromes with unknown etiology, and mentally incompetent patients. There are differing thoughts on TENS therapy during pregnancy – some resources state it is safe following the first trimester while other sources consider it contraindicated throughout pregnancy due to the theoretical risk of premature labor. The FDA has not approved TENS use during pregnancy
