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39 Cards in this Set
- Front
- Back
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preop |
preop |
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what is the significance of his polysomnography study results? |
the diagnosis of OSA is confirmed with a sleep study showing: 5 or more events of complete cessation of airflow for at least 10sec despite continuing resp effort against a closed glottis, in conjunction with dec arterial oxygenation of >4% |
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classifying the severity of OSA |
the apnea-hypopnea index, or the total number of apnea and hypopnea is used 5-15: mild 16-30: moderate >30 severe |
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this patients OSA and the anesthetic considerations with it |
clearly severe anesthetic concerns: 1. the presence of coexisting disease, like HTN, CAD, arrhythmias, pulm HTN, RV failure 2. the choice of anesthetic (regional if possible) 3. difficult airway in obese patients with OSA 4. the administration of CNS depressant drugs 5. maintenance of anesthesia, with preference to short acting hydrophilic drugs 6. extubation safely (awake, strong etc) 7. postop pain control 8. appropriate discharge criteria (monitor avergae 3 hrs longer than non-OSA pts and at least 7 hrs after last episode of hypoxia or obstruction) |
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what is the difference between OSA, obstructive sleep hypopnea syndrome (OSH), obesity-hypoventilation syndrome (OHS), and Pickwickian syndrome? |
OSA is defined as the complete cessation of airflow for at least 10 seconds, 5 or more times per hour, despite continued effort against a closed glottis, and associated with a 4% dec in SpO2 OSH: milder form, a 50% reduction of airflow lasting 10sec, 15 or more times per hour and associated with a 4% dec in SpO2 OHS: develops due to obesity and is a long-term consequence of OSA, defined by the combination of obesity, daytime hypercapnia (>45), nocturnal hypoxia, and polycythemia in the absence of known causes of hypoventilation Pickwickian syndrome: severe form of OHS where chronic hypoventilation leads to pulm HTN and RV failure |
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would you give anesthesia form this surgery at an outpatient surgery center? |
no i would not, he is not a good candidate as he is at significant risk of postop airway obstruction and apnea associated with airway surgery requiring GA in a patient with severe OSA who is likely to require significant postop opioids |
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what factors would you consider when determining if outpatient sx is ok for an OSA patient? |
the severity of their OSA anatomic and physiologic abnormalities coexisting diseases nature of the surgery type of anesthesia being performed the need for post-op opioids adequacy of postdischarge observation capabilities of the outpatient center |
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how would you evaluate this patients cardiac status? does he need further testing? |
given his obesity, sedentary lifestyle, dyspnea on exertion, uncontrolled HTN, and OSA i consider him to have significant risk factors for CAD and CHF i would therefore do a focused history and physical looking for: 1. symptoms or cardiac risk factors: unstable angina, previous cardiac testing, decompensated HF, arrhythmias, MI, functional capacity 2. physical exam signs such as JVD, hepatomegally, peripheral or pulmonary edema 3. i would get an EKG 4. if i was unable to assess the risk, id consider echo, a stress echo in particular would give good information about myocardial ischemia, systolic function, and diastolic filling |
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what cardiac abnormalities would you expect in someone with longstanding OSA? |
chronic hypoxia and hypercarbia and the associated increase in catecholamines will lead to: 1. pulmonary HTN, due to inc sympathetic tone and hypoxic pulmonary vasoconstriction 2. HTN due to inc sympathetic tone 3. arrhythmias 4. polycythemia 5. inc platelet aggregability 6. pul HTn eveantually leads to RVH and right heart failure (cor pulmonale), and untreated systemic HTN leads to LVH and LH failure 7. arrhythmias could lead to angina, MI in those at risk of CAD 8. polycythemia and inc platelet aggregation make these patients more susceptible to thombosis and embolic events and CVA |
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how would you evaluate this patients airway? |
1. i would start with a history looking at previous anesthetic records for difficult airway and successful intubation attempts 2. i would do an exam focusing on Malampatti, neck circ, tonsil size, tongue size, mouth opening, thyromental distance, cervical ROM, and any other abnormalities, dentition 3. since OSA predisposes to difficult airway, i would ensure difficult airway equipment in the room |
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the patient is extremely anxious and starting to hyperventilate. the nurse wants to know if she can give midazolam. what do you think? |
recognizing that even small doses of CNS depressant drugs place OSA patients at risk of airway obstruction, hypoventilation, or apnea, i would prefer to avoid it i would start by talking to the patient, identifying his concerns, answering all questions, and providing the appropriate reassurance |
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intraop |
intraop |
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which monitors would you place for this case? |
in addition to standard ASA monitors, i would: 1. Foley to monitor fluid status and end-organ perfusion 2. assuming ill use NMBs a peripheral nerve stimulator to monitor blockade and reversal 3. since his uncontrolled HTN, dyspnea on exertion, and signs of right heart failur on echo (RVH and elevated RH pressures) are signs of pulm HTN and RHF, i would use a 5lead EKG, aline, and PAC 4. i would want to aline prior to induction and intubation since his chronic uncontrolled HTN puts him at risk of unstable hemodynamics during this time |
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what is your plan for intubation? |
given his obesity, OSA, short neck, micrognathia, MIII, he is at risk of difficult ventilation and intubation, so i would plan for an awake intubation (recognizing its harder given his anxiety), but given his high risk airway and the sensitivity of severe OSA patients to sedatives, i would avoid sedation if possible my plan is: 1. give aspiration prophylaxis and glycopyrrolate to dry the upper airway 2. place the appropriate monitors including aline and PAC 3. ensure presence of difficult airway equipment 4. adequately anesthetize the airway with topical lidocaine and a superior laryngeal nerve block 5. place in 30degree reverse Tberg 6. perform a fiberoptic intubation and confirm placement of the ETT 7. proceed with induction |
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the patient, who would rather be asleep with intubation, tells you he was successfully intubated 2 years ago under GA, without any problems. what would you tell him? |
i would say that while a successful intubation is somewhat reassuring, it does not diminish my concerns about a difficult airway today, since he has experienced significant weight gain since then and has had progressively worsening symptoms of airway obstruction since then, and i would tlel him that an awake intubation with minimal sedation remains the safest way to secure his airway today, and reassure him i will do everything i can to make him comfortable |
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what if he refused an awake intubation without sedation, or did not tolerate the procedure? |
i would cautiously sedate with precedex, with the goal of improved patient cooperation while maintaining spontaneous ventilation and intact airway reflexes other options would be to slowly titrate benzos or opioids whatever is chosen i would do so carefully titrating and ensure presence of reversal agents (naloxone, flumazenil, etc) |
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what type of ETT would you place? what does UPPP surgery involve? |
i would discuss the procedure details, positioning, and preference with the surgeon, and generally place a standard or oral rae OVC ETT if the surgeon planned to use laser i would place a laser ETT |
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after successful awake intubation the surgery begins. how would you maintain anesthesia for this case? |
given his obesity and severe OSA, ideal maintenance anesthesia would include short-acting drugs without active metabolites, with minimal depression of ventilation, and with allowance for rapid return of airway reflexes i would therefore do a balanced technique with desflurane (fastest wakeup and return of airway reflexes), remifentanil (rapid onset/offset), and cisatracurium (Hoffman eliminate since obese patients often have some liver dysfunction) |
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assuming the surgeon is planning to use a laser for the procedure, would you use an oxygen/nitrous mix? |
while i would want to dilute the oxygen with another gas, and while nitrous does have some advantages like a short duration of action and low blood/gas solubility coeffient, i would avoid it in this case due to the patients pulm HTN instead i would reduce the FiO2 with air as much as possible during lasering, in doing so balancing the risks of airway fire with the risk of hypoxia in the obese patient with inc oxygen demand and signs of right heart failure |
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does the dosing of IV anesthetics need to be adjusted due to the patients obesity? |
theoretically lipohillic drugs will have a higher volume of distribution in obese patients, and so the initial dose should be increased, but by the same token the large VOD increases clearance time of the drugs, so maintenance doses should be decreased, while hydrophilic drugs (NMBD) should not be affected and should be doses based on ideal body weight in practice though the theoretical affects of obesity are more complicated and do not mirror theory, so i would calculate my initial dose based on ideal body weight and titrate additional doses to clinical effect |
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what weight to use for specific drugs |
PIC |
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suddenly the airway pressure alarm goes off and the bellows do not fill in between breathes. what do you think is going on? |
low pressure alarm and insufficient gas flow to fill the bellows is consistent with a circuit leak the most likely places for a leak include the circle system, Y piece, ETT connection, or ETT cuff, but i would also consider the gas flow meters, CO2 absorber, scavenging system, and ventilation bellows |
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so what would you do? |
while attempting to locate the leak, i would switch to hand ventilation, switch to 100% oxygen, and increase fresh gas flows if hand ventilation was not adequate and i was unable to quickly identify the leak, i would switch to an ambu bag with 100% oxygen |
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what if ventilation remained inadequate with the ambu bag? |
i would consider a ruptured ETT cuff and prepare for replacement of the damaged ETT over a tube exchanger |
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the surgeon reports that he has accidentally cut a hole in the ETT and there is a large leak in the oropharynx. what would you do? |
immediately call for help, inc fresh gas flows, ensure 100% oxygen, and hand ventilate if hand ventilation proved inadequate in terms of oxygenation OR ventilation despite high fresh gas flows, i would advance the ETT under a fiberoptic scope so the leak is past the vocal cords, if still inadequate, i would ask the surgeon to prep for an emergency trach, have the neck prepped and draped, and attempt to exchange the ETT over an exchange catheter adapted for oxygen insufflation |
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after a brief episode of hypoxia, you successfully exchange the ETT over an exchange catheter. the hypoxia resolves, but the blood pressure in now 66/31. what is your differential? |
the timing being right after a hypoxic episode would indicate myocardial ischemia, infarction, arrhythmia or failure could also be: anesthetics tension pneumo (central line was placed) anaphylaxis |
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so how would you address this? |
i would: 1. quickly look at the EKG, aline BP, PA pressure, CO, SVR, SaO2, and end-tidal CO2 2. i would discontinue volatile agents to attenuate any dec in SVR 3. place in tberg to improve preload 4. start a fluid bolus 5. consider giving an inotrope or a pressor |
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the patients EKG shows the follows **PIC** what would you do? |
its irregularly irregular with no P waves consistent with afib since this is new onset afib associated with HD instability, i would call a code, start chest compressions, and perform synchronized cardioversion using 100J and progressing to 200J, 300J, and 360J as needed to convert to NSR |
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could you administer amio for pharmacologic cardioversion? |
given his HD instability he may not tolerate amiodarone which can cause hypotension and bradycardia, but if i thought the benefits outweighed the risks i would give a 150mg bolus over 10min, followed by an infusion of 1 mg/min over 6 hrs, and a 0.5 mg/min infusion for the next 18hrs but i would be prepared to quickly address any subsequent HD changes |
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postop |
postop |
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how would you manage postop pain in this patient? |
my goal is to give adequate analgesia while avoiding postop respiratory depression, and since OSA patients are extremely sensitive to the depressant effects of opioids, i would maximize nonopioid methods of analgesia, including NSAIDs, acetaminophen, local anesthetic if possible, and ice if opioids were necessary i would use small doses of short acting opioids like fentanyl, possibly in a PCA without a continuous bolus no matter what i used i would give supplemental oxygen, headup position, and use his home CPAP to reduce resp compormise |
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what are the recommendations for CPAP in OSA patients? |
recommend using it afterwards in those treatedwith it preop, equivocal in those not treated with it preop (but i would do it) |
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after successful extubation the patient is taken to PACU. how would you monitor his resp status postop and when would you consider it safe to DC home? |
in accordance with the ASA practice guidelines for OSA patients, i would: 1. place him in the nonsupine position during recovery 2. provide continuous supplemental oxygen until he shows he can maintain his baseline O2 sat on room air 3. use continuous pulse oximetry during the hospital stay 4. apply CPAP or NIPPV if he had used either of these modalities before in terms of discharge, i would not DC to an unmonitored setting until: 1. pain is controlled without narcotics 2. airway swelling has decreased 3. i no longer considered him at risk of postop resp depression, verified by him being able to maintain his baseline sat on room air in a quiet setting 4. ASA guidelines recommend these patients be monitored for a median of 3 hrs longer than nonOSA patients, and at least 7 hours following their latest episode of obstruction or hypoxemia |
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30min youre called to the PACU where you find the staff trying to mask ventilate the patient. he is hypoxic with a SaO2 of 78%. what would you do? |
1. immediately call for help, the difficult airway cart, and the ENT surgeon 2. ensure head up position, take over mask ventilation, place an oral airway, do a 2 handed jaw thrust, and attempt to mask ventilate with 100% oxygen 3. if ventilation was inadequate i would place an LMA and consider reintubation 4. i would be continuously be moniotring his HD, and ready to start chest compression at any time |
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bag mask ventilation is ineffective, intubation attempts are unsuccessful, and he has become bradycardiac. what would you do? |
i would ask the ENT to do an emergency surgical airway while i continued to try to ventilate the patient if the surgeon was unavalable i would do a cricothyroidotomy by placing a needle though the cricothyroid membrane until i could aspirate air, pass a wire through the needle, make a skin incision next to the wire, and advance an ETT (or trach tube) over the wire once the airway was in place i would confirm ventilation with auscultation of all lung fields, observed chest rise, and ETCO2 |
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after successful trach and resuscitation, the patient remains mildly hypoxic with an SaO2 of 89% while breathing 100% oxygen. what do you think is going on? |
there are several possibilities in this obese patient following an emergent surgical airway, including: 1. aspiration of blood or gastric contents 2. bronchospasm 3. pulm edema (neg pressure or fluid overload/CHF) 4. atelectasis 5. hypoventilation 6. pneumo 7. malpositioned ETT 8. PE 9. acute HF |
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so how would you address the hypoxia? |
1. auscultate the lungs to confirm proper ETT placement and ventilation 2. look at his BP, EKG, PAC numbers and CO 3. order a CXR 4. depending on the findings i may give a bronchodilator, reposition the tube, place a chest tube, optimize the HDs, or adjust the vent settings |
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PE reveals diffuse pulmonary crackles and CXR shows generalized pulmonary edema that was not present preop. What could have caused this? |
given his OSA< HTN, and recent hypoxia event, its likely either negative pressure pulmonary edema of heart failure: -the upper airway obstruction and sustained ventilatory effort against a closed glottis could have caused negative intrapleural pressure and movement of fluid from the pulm capillary bed to the alveoli -on the other hand, hypoxia could have induced ischemia, dysrhythmias, and/or HTN which could lead to L heart failure and subsequent pulm edema other potential causes: fluid overload, aspiration, anaphylaxis |
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assuming this were NPPE, how would you manage? |
recognizing the treatment is supportive, i would ensure a patent upper airway, give supplemental oxygen, and PPV if oxygenation did not improve i would add PEEP to promote alveolar expansion diuretics are sometimes used but are controversial, so i would not give unless HD data indicated hypervolemia |
