Flashcards in sleep apnea Deck (34):
pt undergoes polysomnography, which reveals 280 episodes of apnea lasting greater than 10 secs in an 8-hour period. what does this mean?
sleep study meets the criteria for sleep apnea. criteria are 5 or more episodes of airflow cessation despite respiratory effort against a closed glottis for 10 secs or more in conjunction with arterial oxygen saturation decrease of 4$ or greater.
the apnea-hypopnea index, consisting of the total number of apneas and hypopneas (50% reduction in airflow) per hour is used to classify severity of disease. this patient had 280 over 8 hours, so roughly 35 times an hour. severity is as follows:
what are some symptoms of OSA?
nocturnal apnea, sleep disruption, daytime somnolence
what anesthetic considerations do you have for this patient?
1. presence of coexisting disease
2. choice of anesthetic (regional may be preferable)
3. airway management (possibly difficult, difficulty in 13-24% of obese patients with OSAHS)
4. sensitivity to CNS depressants (narcotics)
5. maintenance of anesthesia (hydrophillic and short-acting preferable)
6. extubation (preferably awake, semi-upright, full reversal of NDNMB, intact airway reflexes)
7. multi-modal pain control with decreased narcotics if possible
8. appropriate discharge criteria (ASA guidelines recommending monitoring for 3 hours longer than non-OSA patients and for at least 7 hours since last airway obstruction/hypoxemia)
what is the difference in OSA, obstructive sleep hypopnea syndrome, obesity-hypoventilation syndrome, and pickwickian syndrome?
OSA - complete cessation of airflow for more than 10 seconds, occuring 5 or more times per hour of sleep, despite continued respiratory effort against a closed glottis with a >4% decrease in SpO2
OSH - milder form of the disease with 50% reduction in airflow for more than 10 seconds, occuring 15 or more times per hour of sleep, associated with 4% decrease in SpO2
OHS - develops secondary to obesity or as a long-term consequence of OSA. obesity (BMI >30), daytime arterial hypercapnia (PaCO2 >45 mmHg), nocturnal hypoxia, polycythemia. this must occur in the absence of known causes of hypoventilation (pulm dz)
pickwickian syndrome - severe form of OHS where chronic hypoventilation leads to pulm htn and RV failure
could this be done at a surgery center?
i would recommend against performing this surgery at an outpatient center due to significant risk of airway obstruction and apnea a/w airway surgery requiring GETA in this patient with severe OSA. additionally, the patient will likely require significant postop narcotics.
what factors would you consider in determining whether a an OSA patient is a good candidate for outpatient surgery?
severity of OSA, anatomical/physiologic abnormalities, coexisting dz, type of surgery and anesthesia, need for postop opioids, adequacy of postdischarge observation, and the capabilities of the surgery center
the patient has DOE and uncontrolled htn. how would you evaluate his cardiac status? does he need more testing?
given his history of obesity, sedentary lifestyle, DOE, uncontrolled htn, and OSA, i would consider him to have significant RFs for CAD/CHF.
i would perform a focused history and physical, focusing on signs/symptoms of cardiac disease.
symptoms: stable/unstable angina, prior cardiac testing, decompensated heart failure, arrhythmias, MI, and functional capacity
signs: JVD, hepatomegaly, peripheral edema, pulm edema
if i were unable to adequately assess his risk, i would consider additional testing, such as CXR, ECG, ABG, PFTs or echo. a stress echo in particular would provide valuable information regarding ischemia, systolic function, and diastolic filling.
what cardiac abnormalities would you expect in someone with longstanding OSA
chronic arterial hypoxemia/hypercarbia and increased serum catecholamines lead to:
1. pulm htn secondary to increased sympathetic tone and hypoxic pulm vasoconstriction
2. nocturnal and diurnal systemic hypertension secondary to sympathetic tone
3. cardiac arrhythmia
5. increased platelet aggregability
pulm htn eventually leads to cor pulmonale (RVH, RVF) while systemic htn leads to LVH/LVF. cardiac arrhythmias may lead to angina, MI. polycythemia and increased platelet aggregability make these patient's more susceptible to DVT and PE.
why is platelet aggregability increased?
possibly due to increased circulating catecholamines
what is hypoxic pulm vasoconstriction
pulmonary artery constriction in the presence of hypoxia without hypercapnia. this redirects blood flow to alveoli with higher O2 content.
how would you evaluate this patients airway?
history and review of medical records, specifically looking for any information on difficulties encountered with previous intubations.
physical exam to assess Mallampati score, nasopharyngeal characteristics, neck circumference, tonsil size, tongue volume, mouth opening, thyromental distance, cervical range of motion.
the patient becomes very anxious and begins to hyperventilate. the nurse wants to know if she can give midazolam. what do you think?
even small doses of CNS depressants can cause airway obstruction, hypoventilation, or apnea so i would prefer to avoid midazolam administration. i would go talk to the patient and address any concerns or questions and provide reassurance.
chest auscultation reveals loud P2 and decreased bilateral breath sounds. patient's ECG shows R axis deviation. ECHO shows RVH, RVSP >40 mmHg. what monitors would you like for this case.
Foley catheter (monitor end-organ perfusion/fluid status)
PNS (monitor neuromuscular function)
arterial line (HD status in this patient with possible RVF)
PAC (pulm htn, RVF)
all prior to induction given his uncontrolled htn if possible
airway exam revealed short neck, MP III, micrognathia, an full cervical ROM. what is your plan for intubation?
given the risk of difficult ventilation/intubation a/w his obesity, severe OSA, short neck, micrognathia and MP III, i would plan to perform awake FOI, however recognizing that this may prove difficult in this extremely anxious patient. considering his high-risk airway and the sensitivity of OSA patients to CNS depressants, i would ideally perform this without sedation. if this was not possible, i would slowly and carefully titrate dexmedetomidine to sedate and keep the patient spontaneously breathing. my plan:
1. metoclopramide and glycopyrrolate to facilitate gastric emptying and dry upper airway secretions
2. place appropriate monitors, including arterial line and PAC if possible
3. check difficult airway equipment
4. provide adequate airway anesthesia, including viscous lidocaine, progressively moving backward down the oropharynx, nebulized lidocaine, and blockade of superior laryngeal, lingual and recurrent laryngeal nerves.
5. place patient on ramp and 30 degree reverse trendelenberg
6. perform fiberoptic intubation and confirm placement with ETCO2
7. proceed with induction
what nerves need to be blocked for AFOI?
glossopharyngeal - can be done peristyloid
superior laryngeal - inject at cornu of hyoid bone
recurrent laryngeal - transtracheal block through cricothyroid membrane
what is the toxic dose of LA?
chloroprocaine 12 mg/kg
lidocaine 5 mg/kg
lido + epi 7 mg/kg
bupivacaine 3 mg/kg
the patient was successfully intubated under general anesthesia a few years ago and would like to be put to sleep. what do you say?
although his history of successful intubation is somewhat reassuring, he has had significant weight gain since that time and worsening symptoms of airway obstruction since 2 years ago. i would tell him that awake intubation without sedation still remains the safest option to secure his airway.
if he refused awake FOI or did not tolerate the procedure, i would cautiously sedate him using dexmedetomidine, with the goal of maintaining patient cooperation, spent vent, and intact airway reflexes.
what type of endotracheal tube would you place? what does UPPP surgery involve?
i would discuss the planned procedure, positioning, and tube preference with the surgeon. usually a standard or oral are polyvinyl chloride endotracheal tube is utilized. however, if the surgeon was planning a laser assisted UPPP, i would consider using a laser resistant tube.
awake FOI is performed. how would you maintain anesthesia for this case?
given obesity and severe OSA the ideal anesthetic agents will be short-acting, without active/toxic metabolites, minimal depressive effects on ventilation, and allow for rapid return of airway reflexes.
i would prefer to use desflurane as it is less-lipid soluble than iso/sevo, remifentanil (rapid onset/offset, rapid metabolism by nonspecific esterase's, inactive metabolites) and cisatracurium (hoffman degradation)
surgeon plans on using a laser for the procedure. would you use nitrous oxide?
although N2O has some advantages, given the increased risk of airway fire and its effects on pulmonary hypertension, i would avoid it. additionally, i would use as low FiO2 as possible during laser use.
does the dosing of medications needs to be adjusted based on the patient's obesity?
lipophilic drugs theoretically have a larger volume of distribution in obese patients secondary to increased deposition into body fat, making an initial loading dose based on total body weight reasonable. by the same token, a larger volume of distribution increases clearance time of lipophilic drugs so reduced dosing during maintenance is also reasonable. the volume of distribution of hydrophilic drugs, should theoretically be dosed based on ideal body weight. in clinical practice, however, the effects of obesity on anesthetic drugs and complicated and not always predictable. therefore, initial dose can be based on ideal body weight and maintenance titrated to effect.
which drugs would you dose based on TBW and IBW?
propofol: induction IBW, maintenance TBW
pentothal: induction TBW, maintenance TBW
midazolam: loading TBW, maintenance TBW
succinylcholine: induction TBW, maintenance TBW
vec/rocuronium: induction IBW, maintenance IBW
atra/cisatracurium: TBW, maintenance TBW
fentanyl/sufentanil: loading TBW, maintenance IBW
remifentanil: induction IBW, maintenance IBW
suddenly, the airway pressure alarms and the bellows will not fill. what do you think is going on?
this is consistent with a circuit leak. most likely locations include the circle system, y-piece, any connections, or the endotracheal cuff, i would also consider the gas flow meters, CO2 absorber scavenging system, and bellows.
while attempting to locate the leak, i would switch to hand ventilation with 100% FiO2 and increase gas flow. if hand ventilation via the current circuit was inadequate, i would attempt to ventilate the patient using an ambu bag with 100% oxygen. if ventilation remained inadequate, i would be concerned about ETT cuff rupture and prepare for replacement of the ETT over tube exchanger.
surgeon reports he accidentally cut a hole in the ETT cuff and there is a large leak in the oropharynx. what do you do
1. call for help
2. increase FGF
3. FiO2 100%
4. advance ETT over FOS so leak is past VCs
5. if that failed, i would ask surgeon to prepare for a possible emergency teach
6. have neck prepped and draped
7. attempt to change ETT over tube exchanger adapted for oxygen insufflation
after a brief episode of hypoxia, you successfully change the ETT over the exchange catheter. hypoxia resolves, but BP is 66/31. what is your ddx?
the timing of hypotension, immediately following hypoxia, suggests the patient is experiencing myocardial ischemia, infarction, arrhythmia, or acute failure. other possible causes: excessive anesthesia, tension ptx (CVL placed earlier), anaphylaxis.
i would quickly evaluate the ECG, art line, PA pressure, cardiac output, SVR, SaO2, and end-tidal CO2. depending on my findings, i may d/c volatile agents, place the patient in trendelenberg to improve preload, start a fluid bolus, and consider administering an inotrope or alpha-agonist.
the ECG shows atrial fib. what would you do?
this is new onset atrial fib with hemodynamic instability, so i would call a code, start chest compressions, and perform synchronized cardioversion using 100 J and progressing to 200, 300, 360 J as necessary to convert patient back to sinus.
could you administer amiodarone?
this patient has significant hemodynamic instability and may not tolerate antiarrhythmics, which can lead to bradycardia and worsening hypotension. if it were determined that the benefits of phamarcologic cardioversion outweighed the risks, i would administer a 150 mg IV bolus over 10 minutes (preferred drug with significant heart disease) followed by a 1 mg/min infusion for 6 hours and 0.5 mg/min for 18 hours. max dose is 2.2 g/24 hours.
how would you manage postop pain in this patient?
my goal is to achieve adequate analgesia while minimizing the risk of posts respiratory depression. pts with OSA are extremely sensitive to the respiratory depressant effects of opioids, so i would utilize non-narcotics such as local anesthetics (regional anesthesia and local wound infiltration), NSAIDs, and ice as much as possible. IV narcotics will likely be necessary though, so i would duse a short acting agent, such as fentanyl via PCA without a basal infusion. i would provide supplemental oxygen, head-up positioning, and CPAP or NIPPV to further reduce the risk of respiratory compromise.
patient is extubated and taken to PACU. how would you monitor the patient's respiratory status postop and when would you discharge him home?
in keeping with the 2014 ASA Practice guidelines for the periop management of a patient with OSA, i would:
1. place in non-supine position throughout recovery
2, provide supplemental O2 until he was able to maintain his baseline oxygen sat with room air
3. utilize continuous pulse-oximetry
4. apply CPAP or NIPPV if he used these preop
i would not discharge him to an unmonitored setting (home or unmonitored hospital bed) until his pain was controlled without narcotics, airway swelling had decreased, and I no longer considered him to be at risk for postoperative resp depression (when could maintain baseline oxygen sat at room air while in a quiet environment or asleep)
30 min later you are called stat to PACU. staff are attempting to bag-mask ventilate the patient. he is hypoxic with SpO2 of 78%. what do you do?
1. call for help, emergency airway cart, surgeon
2. ensure patient was head-up (to improve respiratory mechanics)
3. take over mask vent
4. place oral/nasal airway
5. provide two hand jaw thrust
6. attempt to mask vent with 100% oxygen
if ventilation still inadequate
1. place an LMA, consider reintubation
bag mask vent is ineffective, intubation attempts unsuccessful, he becomes bradycardic. what next?
ask ENT surgeon to proceed with emergency teach. if surgeon unavailable, i would place a needle through the cricothyroid membrane and then pass a wire, make an incision and pass a trach or endotracheal tube.
confirm placement with auscultation, chest rise, fog, ETCO2
trach is successful but pt remains slightly hypoxic with SaO2 of 89% while breathing 100% oxygen. what is your ddx?
1. mainstem intubation
5. pulm edema (heart failure or NPPE)
8. heart failure
i would auscultate lungs and confirm tube position. i would check CO, BP, and order a CXR. depending on findings, i would administer a bronchodilator, adjust the tube, place a chest tube, optimize his hemodynamics, adjust vent settings.
exam reveals diffuse pulmonary crackles and CXR shows generalized pulm edema. what could have caused this?
Given his OSA, HTN, recent hypoxic event, this is either negative pressure pulm edema or HF.
in the case of upper airway obstruction, sustained ventilatory effort against a closed glottis could have resulted in high negative intrapleural pressure with subsequent movement of fluid from capillaries to alveoli.
on the other hand, hypoxia-induced ischemia, dysrhythmias, and HTN may lead to left heart failure with subsequent pulm edema.