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Question

Frank Starling:

Answer 1

increase in SV that results from more forceful cardiac contraction in response to increased cardiac filling. Helpful in transplanted heart physiology

Answer 2

increased risk of infection from nasal flora-so no if possible

Answer 3

Slow controlled to avoid drops in SVR-use etomidate | Good med: Isoprterenol: potent beta 1 and beta 2 adrenoreceptor agonist-excellent choice in pts with cardiac transplant

Answer 4

Yes. even though it wont' change the HR< it can help reduce bronchospasm and increase salivation. KIM that neostigmine can cause bradycardia in transplanted hearts, so be ready

Answer 5

If on nephrtoxic immunosuppressive drugs-NO. could exacerbate kidney damage, and also increase risk of gastritis (pts have gastritis with immunosuppressive drugs)

Answer 6

Prior to delivery I would ensure that the appropriate support personnel and equipment were available for neonatal resuscitation (i.e. a self-inflating bag attached to 100% oxygen, a neonatal oxygen mask, wall suction, a radiant warmer or other heat source, warmed linens, appropriately sized laryngoscopy blade and ETTs, resuscitation medications, and blow by oxygen capabilities).

Answer 7

(tracheal suctioning should be performed if the baby does not demonstrate strong respiratory effort, good muscle tone, and a heart rate > 100 beats/minute).

Answer 8

below 100, he remained apneic, or he was gasping, I would provide positive mask ventilation with air, or an air/oxygen mixture, and consider applying a pulse oximeter. If after 30 seconds of positive mask ventilation the HR was less than 60, then I would INTUBATE increase the oxygen concentration to 100%, begin chest compressions (3 compressions to 1 breath for a total of 120 events/minute), and establish venous(umbilical·vein catheterization).~r intraosseous ac~~~~ (risks include tibial fracture and osteomyelitis). If after another 30 seconds there were still no improvement, I would administer 0. 01-0. 03 mg/kg of epinephrine via the umbilical vein or established intraosseous access, and consider volume expansion.

Answer 9

If magnesium toxicity were confirmed, I would administer calcium (100 mg/kg of calcium gluconate or 30 mg/kg of CaCh), recognizing that calcium therapy has been associated with cerebral calcification and decreased survival in stressed newborns (therefore, it should only be administered to reverse the effects of magnesium toxicity). In the case of hypoglycemia (glucose< 35 mg/dL), glucose should be administered (8 mg/kg/minute of 10% solution). While placental transfer of maternally administered narcotics could potentially be exacerbating this neonate's condition, I would not administer naloxone unless all other resuscitative efforts had failed; as this drug is no longer recommended during the initial resuscitation in the delivery room (can worsen the neurologic damage caused by asphyxia). Calcium can cause cerebral calcification and decreased survival in stressed newborns.

Answer 10

Class 1: complete visualization of soft paalte 2: complete visualization of the uvula 3: Visualization of only base of uvula 4: soft palate not visible at all

Answer 11

1: Full view of glottis 2a: partial view of glottis 2b: only arytenoids seen 3: only epiglottis seen 4: neither glottis nor epiglottis seen

Answer 12

determine the severity of his hepatic disease by performing a thorough history and physical, focusing on the onset and etiology of his cirrhosis, and the presence of jaundice, bleeding disorders, ascites, asterixis, and hepatic encephalopathy. Based on my findings, I may consider additional lab work to aid in discerning the severity of liver disease, including bilirubin, transaminases, alkaline phosphatase, albumin, total protein, prothrombin time, INR, and hepatitis serologies

Answer 13

Cirrhosis' effects on the respiratory system include intrapulmonary arteriovenous (AV) shunts, reduced PRC, restrictive lung disease, pleural effusions, and attenuation of hypoxic pulmonary vasoconstriction. Cerebral effects include the accumulation of ammonia and other toxins, which may lead to encephalopathy. Thrombocytopenia and clotting factor deficiencies may result in a coagulopathy. Cardiovascular effects include decreased peripheral vascular resistance, increased cardiac output, and cardiomyopathy. Potential metabolic effects include dilutional hyponatremia, hypokalemia, hypoglycemia, and hypoalbuminemia. Various additional effects of cirrhosis include portal hypertension, esophageal varices, delayed gastric emptying, ascites, and hepatorenal syndrome

Answer 14

I would prefer to use a muscle relaxant that is not dependent on hepatic metabolism, such as Cis-Atracurium. This drug's duration of action should not be affected by liver failure, because it undergoes degradation in the plasma by Hofinann elimination, and is reduced to inactive metabolites. If that choice unavailable-i would recognize potential for increased duration of action and monitor nm fxn with nerve stimulator

Answer 15

(PDPH), I would consider an epidural blood patch. Initially, however, I would review the patient's record and assess him for signs and symptoms of a PDPH, such as frontal-occipital headache, decreased pain with recumbent positioning, nausea, vomiting, neck stiffness, back pain, visual disturbances (photophobia, diplopia, and difficulty in accommodation), and auditory disturbances (tinnitus, hypacusis, and hearing loss). I would also require a coagulation profile, since he may be receiving anticoagulants following his recent knee surgery. If a blood patch were contraindicated for any reason, I would recommend conservative therapy, which consists of hydration, caffeine, and pain control.

Answer 16

The lost CSF, decreased buoyant support for the brain, and cerebral vasodilation (increased cerebral blood flow to compensate for decreased CSF) that accompanies significant dural puncture, can lead to the signs and symptoms of a PDPH, which include a frontal-occipital headache, decreased pain with recumbent positioning, nausea, vomiting, neck stiffness, back pain, photophobia, diplopia, difficulty in accommodation, tinnitus, and hypacusis (hearing loss). Rarely, PDPH is associated with seizures (most likely secondary to cerebral vasospasm), abdominal pain, and diarrhea. Loss of CSF can also lead to cranial nerve stretching with subsequent palsy.

Answer 17

While less effective than blood patch, conservative treatment consisting of hydration (no evidence of therapeutic benefit), caffeine, the placement of an abdominal binder (increases abdominal pressure, possibly leading to an increase in CSF pressure), and pain control provides an alternative when a blood patch is contraindicated.

Answer 18

esophageal pouch communicates with trachea, but is otherwise the same as c (esophageal atresia with blind upper pouch and lower segment tracheal fistula)

Answer 19

Ideally the tip of the ETT should be placed distal to the fistula and proximal to the carina, allowing positive pressure ventilation of both lungs without excessive airflow through the fistula One method of properly positioning the ETT is to advance the ETT into the right main-stem bronchus and then slowly withdraw it until breath sounds are heard through a stethoscope placed in the left axilla. If excessive airflow through fistula occurs surgeon can perform a gastrostomy to decompress the stomach

Answer 20

SUDDEN ONSET, fever, drooling, stridor, substernal retractions. Radiographs should only be done when child is stable and when appropriate people can accompany child. Severe should immediately be transferred to OR with Anesthesiologist and the Surgeon

Answer 21

100% O2 Emergency drugs and airway stuff ready No versed Parents come with me stan ASA monitors, emergency airway cart and surgeon in room-an intramuscular dose of ketamine (2-3 mg/kg) with the goals of providing sedation and maintaining spontaneous ventilation while securing intravenous access. Then deepen anesthesia with IV medications, place tube 1/2 size smaller than normal. Let the surgeon do their thing and then consider switching to nasal intubation as it is typically tolerated better in children.

Answer 22

I would only consider extubation once the child's fever, neutrophilia, and epiglottic swelling had resolved (these patients usually remain intubated for 24- 48 hours following the initiation of treatment). The resolution of airway edema is suspected with the return of swallowing and when a significant leak around the nasotracheal tube is present (10-20 cm. H20 peak inflation pressure). Prior to extubation, I would transfer the patient to the operating room, induce general anesthesia, and confirm the resolution of airway edema by visual inspection with a flexible fiberoptic bronchoscope. I would then extubate the child and continue to monitor her for post-extubation edema.

Answer 23

What kind is it? Cushings, acromegaly, see if there is suprasellar extension (ha, blurry vision, rhinorrhea)

Answer 24

The PVCs are likely to be the result of the injection of epinephrine- containing local anesthetic or the use of cocaine pledgets. With this in mind, I would alert the surgeon to stop the infiltration, ensure adequate ventilation with 100% oxygen, check blood pressure, and examine the EKG for signs of myocardial ischemia. I would then be prepared to treat any hypertension and/or significant arrhythmias that may occur. 4) What do you think was the cause? UBP Answer: As I mentioned, the most likely cause is systemic uptake of epinephrine contained in the local anesthetic. However, other potential causes include, hypoxia, cardiac ischemia, air embolism, electrolyte abnormalities, or anesthetic induced cardiac depression.

Answer 25

The bilateral crackles on exam are suggestive of pulmonary edema, which could be associated with the use of terbutaline, preeclampsia (increased vascular permeability), pulmonary embolism, or a previously unrecognized cardiac condition. Although a rare complication, terbutaline use has been associated with pulmonary edema.

Answer 26

It would depend on identifying and treating the cause. cardiogenic in origin (i.e. myocardial ischemia, cardiomyopathy, or a dysrhythmia), I would consider using diuretics, inotropic agents, beta-blockers, or afterload reducing agents, as indicated.non-cardiogenic in origin, I might simply provide diuretic therapy and fluid restriction. In either. case, I would consider providing ventilatory support with PEEP. While intubation and mechanical ventilation may prove necessary, I would first consider using CPAP.

Answer 27

PEEP improves oxygenation and pulmonary function by redistributing alveolar fluid to areas that are less involved in gas exchange, and by recruiting collapsed alveoli that are contributing to pulmonary shunting. KIM that PEEP can worsen cardiac fxn secondary to decreased preload

Answer 28

While PEEP has the potential to hyperin:flate already open alveoli, the goal is to achieve optimum PEEP where collapsed alveoli are recruited

Answer 29

LAST Total spinal (with resp sxs to follow) 1) paralysis of the recurrent laryngeal nerve, which is located near the stellate ganglion (would result in hoarseness); 2) pneumothorax could lead to respiratory distress and hypotension (the latter occurring with a tension pneumothorax); Indications: CPRS. Also angina, phantom limb pain, vascular insufficiency, hyperhidrosis Anatomy: Inferior cervical + T1 sympathetic ganglia @ C7. Lays under the SCM/carotid, above the lung Side Effects: Horner’s (intentional), hoarseness (RLN), eleveated hemidiaphragm (phrenic) Complications: hematoma, brachial plexus injury, pneumothorax, esophageal perforation, intrathecal/epidural/intravascular injection

Answer 30

(1) call for help and a lipid rescue kit; (2) ensure adequate ventilation and oxygenation to correct and/or avoid factors that enhance the systemic toxicity of local anesthetics, such as hypercarbia (increased cerebral blood flow, intra- neuronal ion trapping of the drug, and decreased plasma protein binding of the drug), acidosis (decreased plasma protein binding of the drug), and hypoxemia; (3) administer a benzodiazepine to stop the seizure (seizure activity increases metabolism, which may lead to hypoxemia, hypercarbia, and acidosis); ( 4) administer succinylcholine and intubate her if ventilation were inadequate, the risk of aspiration was significant (history of GERD or hiatal hernia), or if tonic-clonic movements persisted despite benzodiazepine administration (succinylcholine would minimize the metabolic acidosis associated with seizure-induced.muscle activity, it would not, however, affect the acidosis that develops secondary to seizure-induced increases in cerebral metabolism); (5) alert the nearest facility with cardiopulmonary bypass capability; and ( 6) treat hypotension, bradycardia, and dysrhythmias as indicated (avoid procainamide, lidocaine, j3-blockers, vasopressin, and calcium channel blockers when treating bupivacaine-induced cardiac arrhythmias). Moreover, I would (7) initiate lipid emulsion therapy if the signs and symptoms of local anesthetic toxicity appeared to be rapidly progressing, she experienced prolonged seizure activity, or she developed signs of cardiac toxicity (i.e. bradycardia, heart block, hypotension, asystole, or ventricular arrhythmia). Finally, if the patient did not respond adequately to these therapies, I would (8) consider utilizing cardiopulmonary bypass to provide "bridging" therapy until her tissue levels of local anesthetic were no longer toxic.

Answer 31

Bolus 1.5 mL/kg of 20% lipid solution over 1 minute (roughly 100 mL in adults) and start a continuous infusion at 0.25 mL/kg/minute. If cardiovascular instability persists after 5 minutes, repeat the bolus and double the infusion rate. Maintain the infusion for at least lO·minutes after attaining circulatory stability. The recommended upper limit for initial lipid dosing is approximately 10 mL/kg over 30 minutes.

Answer 32

I would immediately: (1) start chest compressions, (2) call for a defibrillator (in case a shockable rhythm developed during resuscitation), (3) secure the airway with an endotracheal tube, and ( 4) provide 100% oxygen. Next, I would (5) attempt to confirm true asystole (make sure all cables are connected properly,ensure adequate monitor gau;, check another lead, 'check for pulse - very fine ventricular fibrillation can look like asystole), (6) initiate lipid emulsion therapy (if not already done), (7) administer a 1 μg/k:g intravenous bolus of epinephrine, recognizing that higher doses of epinephrine have been associated with poorer outcomes in the setting ofbupivacaine-induced asystole (epinephrine is highly arrhythmogenic and may reduce the efficacy of lipid emulsion therapy), and (8) correct any potential contributing factors, such as hypoxia, hypercarbia, and acidosis. I would then (9) continue to monitor the patient for the development of a shockable rhythm, (10) notify the nearest facility with cardiopulmonary bypass capabilities, and (11) consider placing her on bypass if she remained inadequately responsive to these interventions. Continue CPR for at least 60 min

Answer 33

NO!!! No vasopressin in LAST

Answer 34

the amount of blood flow at the site of injection (intravenous> tracheal > intercostal > caudal > paracervical > epidural > brachial plexus > sciatic/femoral> subcutaneous), (2) the dose, (3) the properties of the injected local anesthetic (the higher the lipid solubility and protein binding of a drug, the lower the rate of systemic absorption), and ( 4) the addition of vasoconstrictors to the local anesthetic solution (the vasoconstriction associated with the addition of epinephrine decreases the rate of systemic absorption). The closer to physiologic pH that the pKa is, the more anesthetic exists in the uncharged base form. With the exception of benzocaine, the pKa’s of all local anesthetics are greater than tissue pH (7.4). Lower pKa results in a more rapid onset. Onset is also reduced by increasing the solution pH. Onset can also be shortened by increasing the concentration or dose. Chloroprocaine, despite having a pKa of 9, has a rapid onset because of its use in high (as high as 3%) concentrations. More lipophilic and protein bound a local anesthetic is, less systemic absorption

Answer 35

limit the administered dose of local anesthetic drug,Other preventative measures include the use of ultrasound, aspiration prior to injection, the use of small incremental drug dosing, avoidance of excessive sedation during block

Answer 36

The ECG of patients with a transplanted heart often shows two sets of P-waves, with the origin of one P-wave being the native sinoatrial node, while the origin of the other is the donor's sinoatrial node. While the native sinoatrial node may continue to be affected by autonomic influences, it does not alter cardiac function because the generated impulse is unable to traverse the suture line between the native heart and transplanted heart

Answer 37

The onset of fetal bradycardia following the initiation of spinal analgesia suggests that the (1) rapid onset of analgesia has resulted in an abrupt decrease in circulating epinephrine, with subsequent uterine hypertonus . (tachysystole) and decreased uterine perfusion (spinal anesthesia --> rapid decrease in pain ---> abrupt decrease in plasma epinephrine - decreased stimulation of beta- adrenergic receptors in the uterus ---> increased uterine tone ---> reduced uterine blood flow (most uterine blood flow occurs during uterine relaxation/diastole) ---> diminished fetal oxygen delivery ----> fetal bradycardia). other less likely causes: maternal hypotension secondary to sympathectomy (spinal anesthesia), aortocaval compression (inadequate left uterine displacement), hypovolemia The increase in uterine tone that can occur with the initiation of neuraxial anesthesia to control labor pain is more pronounced when: (1) oxytocin is utilized, (2) spinal anesthesia is employed rather than epidural (more rapid sympathectomy), (3) the height of sensory blockade is relatively higher, and (4) when there is a greater difference between pre and post-analgesia pain scores. • The, fetal bradycardia following neuraxial anesthesia is usually transient and readily treatable. Moreover, it does not increase the incidence of emergency cesarean section or the overall risk for adverse outcome.

Answer 38

In addressing the fetal bradycardia, I would: (1) provide supplemental oxygen, (2) ensure adequate left uterine displacement (especially important in this patient with a transplanted heart, due to the dependence on preload in responding to hypotension), (3) discontinue any intravenous oxytocin administration, (3) treat any maternal hypotension, and ( 4) consider fetal scalp stimulation. If the uterine hypertonus and fetal bradycardia persisted, I would (5) administer a tocolytic (i.e. 50- 100 μg of intravenous nitroglycerine or 125-250 μg of intravenous terbutaline (careful-it can cause pulmonary edema)

Answer 39

In evaluating this patient, I would: (1) talk to the transplant team about the patient's cardiac status, irnrnunosuppression, and the need for antibiotic prophylaxis; (2) review the most recent echocardiography, endomyocardial biopsy, and/or coronary angiography results, and evaluate the patient for signs of rejection such as arrhythmias, fever, malaise, shortness of breath, accelerated coronary atherosclerosis, and myocardial dysfunction (when there are signs of rejection, echocardiography, coronary angiography, and endomyocardial biopsy should be repeated as time permits); (3) identify and evaluate any pacemaker placed to control bradydysrhythrnias (many post-cardiac transplant patients require a pacemaker for this purpose); ( 4) determine whether her hypertension is due to preeclampsia or is chronic in nature, and treat accordingly ( cyclosporine-induced hypertension is common in this patient population); ( 5) evaluate her ECG for signs of myocardial infarction and/or ischemia, recognizing that cardiac denervation masks the usual symptoms associated with these events (i.e. silent ischemia); (6) identify any complications associated with irnrnunosuppressive therapy, such as nephrotoxicity (secondary to cyclosporine therapy), bone marrow suppression, osteoporosis, hepatotoxicity, and opportunistic infection; (7) administer a stress dose of corticosteroid, if not already done (these patients are usually receiving steroids as part of their irnrnunosuppressive therapy); (8) ensure norrnovolemia, recognizing that this preload dependent patient (transplanted heart) is likely hypovolemic (secondary to PET and HTN), obtain platelet level (PET), examine airway.

Answer 40

97% of patients develop hypertension by 10 years post-transplant. This is often attributed to treatment with cyclosporine. Treatment usually involves the use of a calcium channel blocker (i.e. diltiazem) and/or an ACE inhibitor. Nifedipine may be a less desirable choice since it may cause significant vasodilation, which is poorly tolerated by these patients who are preload dependent. !)-blockers should also be avoided, if possible, since cardiac responsiveness during exercise is dependent of circulating catecholamines. • Allograft rejection usually occurs in the first 6 months and presents with fever, malaise, arrhythmias, shortness of breath, accelerated coronary atherosclerosis, and myocardial dysfunction. Hemodynamic compromise is considered a late sign of rejection. Rejection is typically treated with steroids, but may require immunosuppression with IV immunoglobulin or plasmapheresis . • Immunosuppressive therapy usually includes cyclosporine, azathioprine, and prednisone. • Pregnancy is usually well tolerated by post-cardiac transplant patients. • In the setting of renal dysfunction, avoid drugs that may exacerbate renal dysfunction (i.e. NSAIDs) or primarily undergo renal excretion.

Answer 41

Assuming there were no signs of coagulopathy (increased risk in the setting of preeclampsia ), I would utilize her epidural catheter for the case in order to avoid the instrumenting the airway of this pregnant and preeclamptic patient who is at increased risk for difficult airway management. However, I recognize that immunosuppression therapy increases the risk for infection, and denervation makes the transplanted heart dependent on circulating catecholamines and preload (autonomic influences are absent, but the Starling relationship between diastolic end- diastolic volume and cardiac output is normal). Therefore, I would pay special attention to aseptic technique and raise the levels of epidural analgesia very slowly to avoid a rapid sympathectomy that would potentially reduce preload (the preloaddependence associated with the transplanted heart makes epidural anesthesia preferable to spinal anesthesia). General, spinal and epidural can all be done-just be careful with preload

Answer 42

Due to the increased risk of infection: o Invasive monitoring and lines should only be employed when necessary o Oropharyngeal intubation is preferred to the nasopharyngeal route (the latter is associated with an increased risk of infection due to the organisms typically located in the nasopharynx).

Answer 43

Given the timing of her hypotension, the most likely etiology is (1) an anesthetic-induced drop in systemic vascular resistance, with a subsequent reduction in preload. Since the transplanted heart is initially unable to respond to acute hypotension with an increase in heart rate due to the lack of autonomic innervation, it relies on adequate preload to maintain cardiac output (since a and Beta receptors remain intact on the transplanted heart, there is a delayed increase in heart rate in response to increased circulating catecholamines). other:anaphylaxis, pe, Adrenal suppression (most cardiac pts on steroids)

Answer 44

The response to circulating catecholamines is normal and possibly enhanced due to denervation sensitivity (increased receptor density), even though sympathetic innervation is absent. • The heart rate response to normal respiratory variations (sinus arrhythmia), carotid sinus massage, valsalva maneuvers, and the oculocardiac reflex are absent. • The absence of vagal influences causes a relatively high resting heart rate (90-120 beats/minute)

Answer 45

In treating her hypotension, I would: (1) ensure adequate left uterine displacement; (2) evaluate her ECG for signs of arrhythmia and/or myocardial ischemia; (3) administer fluids to maintain high-normal preload, keeping in mind that overaggressive fluid may lead to pulmonary or cerebral edema in this patient with severe preeclampsia; (4) administer a direct vasoconstrictor, such as phenylephrine (indirect vasopressors, such as ephedrine, are not as effective due to the absence of catecholamine stores in myocardial neurons); and (5) reduce or discontinue any volatile agent. If these interventions are ineffective, I would (6) consider starting an isoproterenol or epinephrine infusion and (7) evaluate the patient for signs of anaphylaxis (i.e. hives, flushing, swelling, and bronchospasm) or pulmonary embolism (thrombotic or amniotic fluid).

Answer 46

I would administer a muscarinic antagonist along with the cholinesterase inhibitor for reversal of muscle relaxation, since some cardiac reinnervation may occur after 6 months post-transplant. In addition to that, it has benefits of decreased saliva

Answer 47

The presence of asymptomatic mitral valve prolapse uncomplicated by other medical conditions is not a sufficient reason for further cardiac testing. However, ifher MVP were associated with significant mitral regurgitation, syncope, chest pain, or symptoms of congestive heart failure, further testing may be warranted. Therefore, I would begin by performing a focused history and physical exam to illicit signs and symptoms of congestive heart failure or myocardial ischemia such as angina, orthopnea, dyspnea on exertion, exercise intolerance, peripheral edema, pulmonary rales, S3 gallop, systolic ejection click, or murmur. If she reported significant symptomatology that was insufficiently evaluated by previous cardiac workup, I would consider pre-operative echocardiographic evaluation. Cardiac echocardiography would be helpful in identifying any mitral regurgitation and the presence or absence of a patent foramen ovale, with the latter being important due to the increased risk of air embolism when undergoing surgery in the sitting position (in the presence of a patent foramen ovale, an air embolism may pass into the coronary or cerebral circulations).

Answer 48

-Induction of anesthesia -Anaphylaxis --the development of acute mitral regurgitation and decreased cardiac output. This may occur because patients with MVP often experience worsening prolapsed and/or mitral regurgitation with increased emptying of the left ventricle. (KEEP THAT LEFT VENTRICLE FULL) Therefore, factors such as tachycardia (THEY DON'T WANT TO BE FAST LIKE MR) (decreased filling time), increased myocardial contractility (sympathetic stimulation and inotrope administration), decreased systemic vascular resistance (decreased afterload), hypovolemia (reduced filling), and assumption of the upright posture (decreased filling) may result in acute mitral regurgitation, decreased cardiac output, and hypotension. I would inform the surgeon, return the patient to the supine position, evaluate the EKG, auscultate the chest for cardiac murmurs and bilateral ventilation, ventilate with 100% oxygen, give a fluid bolus, administer a pure al-agonist such as phenylephrine (the tachycardia associated with the administration of an indirect vasoconstrictor, such as ephedrine, may worsen mitral valve prolapsed and mitral regurgitation), and consider reducing my anesthetic. During treatment, I would avoid agents that would increase cardiac contractility and accentuate mitral regurgitation. If she remained unstable despite these interventions, I would utilize TEE to further evaluate her cardiac condition.

Answer 49

Anaphylaxis is a type I hypersensitivity reaction that occurs with the second exposure to an antigen that previously evoked the production of antigen- specific IgE antibodies. Degranulation of mast cells and basophils results in the release of histamine, leukotrienes, prostaglandins, TNF, and various cytokines, with subsequent increased capillary permeability (histamine, leukotrienes ), peripheral vasodilation (histamine), bronchoconstriction (histamine, leukotrienes, prostaglandins ), negative inotropy (leukotrienes ), and coronary artery vasoconstriction (leukotrienes). The initial manifestations of this life-threatening reaction usually occur within 10 minutes of exposure to the inciting antigen The clinical presentation of an anaphylactoid reaction is indistinguishable from anaphylaxis, with the primary difference being that mast cell and basophil degranulation is triggered by direct interaction with certain allergens, rather than by interaction with antigen-specific IgE antibodies. Anaphylactoid reactions, therefore, do not require prior sensitization and produce anaphylaxis-like symptomatology in a dose-dependent manner. Classic anaphylaxis, by contrast, does not behave in a dose- dependent manner, since the immune system is primed to recognize even minute amounts of the offending allergen and is able to amplify the reaction via IgE mediation.

Answer 50

In managing this situation, I would inform the surgeon and call for help; discontinue all infusions and inhalational agents; ventilate with 100% oxygen; start a 1-2 liter fluid bolus (to replace intravascular volume); infuse intravenous epinephrine (administer subcutaneously when the patient is normotensive ); administer corticosteroids (enhances B-agonist effects of other drugs and inhibits the production of leukotrienes and prostaglandins, but the effects are delayed for 4-6 hours), histamine blockers, an H2-blocker, and an inhaled beta2 agonist; and provide supportive care. Recognizing that early intervention with intravenous epinephrine plays a critical role in reversing the life-threatening events associated with anaphylaxis, I would double the dose of epinephrine every 1-2 minutes until a satisfactory systemic blood pressure response was achieved. If her hypotension proved refractory, I would consider administering bicarbonate to correct any acidemia ( acidemia attenuates the effects of epinephrine on the heart and systemic vasculature ), starting a vasopressin infusion (often used to treat refractory hypotension associated with high cardiac output), and evaluating her cardiac function using echocardiography.

Answer 51

Epinephrine's u-agonist activity leads to vasoconstriction and reversed hypotension, while the drug's B-agonist activity relaxes bronchial smooth muscles and increases intracellular cAMP, with the increase in intracellular cAMP serving to restore membrane permeability and decrease the release of vasoactive mediators. The severity of my patient's condition would determine the dose and route of administration. For this patient in complete cardiovascular collapse, I would start with a 100 μg (range of 100 μg-1 mg) intravenous dose of epinephrine. If, however, my patient were hypotensive, but not in complete cardiovascular collapse, I would start with a 10 μg intravenous dose of epinephrine. Finally, if my patient were normotensive, I would avoid intravenous epinephrine and administer 0.3-0.5 mg subcutaneously. In all cases, I would double and repeat epinephrine dosing every 1-2 minutes until I achieved an adequate cardiovascular response.

Answer 52

Epinephrine's u-agonist activity leads to vasoconstriction and reversed hypotension, while the drug's B-agonist activity relaxes bronchial smooth muscles and increases intracellular cAMP, with the increase in intracellular cAMP serving to restore membrane permeability and decrease the release of vasoactive mediators. The severity of my patient's condition would determine the dose and route of administration. For this patient in complete cardiovascular collapse, I would start with a 100 μg (range of 100 μg-1 mg) intravenous dose of epinephrine. If, however, my patient were hypotensive, but not in complete cardiovascular collapse, I would start with a 10 μg intravenous dose of epinephrine. Finally, if my patient were normotensive, I would avoid intravenous epinephrine and administer 0.3-0.5 mg subcutaneously. In all cases, I would double and repeat epinephrine dosing every 1-2 minutes until I achieved an adequate cardiovascular response.

Answer 53

The risk of latex allergy is highest in children with spina bifida due to repeated latex exposure associated with their increased health care requirements. Other risk factors include congenital urinary tract abnormalities, undergoing multiple surgeries or medical procedures, and working in the health care field or rubber industry. Finally, patients with an allergy to certain foods containing similar allergens to those found in latex, such as avocados, bananas, chestnuts, kiwis and passion fruit, may have antibodies that cross-react with latex.

Answer 54

The most effective way to prevent health care workers from becoming "latex sensitive" is to reduce work-related exposure by utilizing non-powdered latex gloves or latex-free gloves. A healthcare worker who develops a skin rash and/or is suspected of having a latex allergy, should be referred to an allergist for further evaluation. If a healthcare worker is diagnosed with latex allergy, then strict avoidance of latex is critical to preventing a potential anaphylactic reaction.

Answer 55

I would place the patient in the supine position with the arm abducted and the elbow flexed at 90 degrees. Next, I would prep and drape the axillary area in a sterile fashion, use ultrasound to identify the axillary artery and fascial sheath, insert a 22 gauge short bevel needle into the nerve sheath under ultrasound guidance, aspirate to ensure extravascular needle placement, and inject 15-20cc oflocal anesthetic. I would then identify the musculocutaneous nerve within the coracobrachialis muscle and inject 5cc of local anesthetic next to the nerve. If a tourniquet were required for the surgery, I would perform a subcutaneous field block just distal to the axilla to block the medial brachial cutaneous and intercostobrachial nerves.

Answer 56

While the axillary approach to brachial plexus blocks is associated with a very low complication rate, there are potential complications, including intravascular injection, intraneural injection, hematoma, infection, and block failure.

Answer 57

The musculocutaneous nerve, which provides motor innervation to the biceps muscle and sensory innervation to the lateral aspect of the forearm, has already left the sheath at the level of the axilla and, subsequently, is the most commonly missed. Adequate blockade of the musculocutaneous nerve is achieved by injecting 5cc of local anesthetic into the coracobrachialis muscle.

Answer 58

There are several possibilities, including administration of the wrong medication, an insufficient dose of heparin, infiltration of the IV, inaccurate ACT measurement (machine malfunction), and heparin resistance. Heparin resistance can be due to Antithrombin III deficiency, which may result from inherited defects in production, excessive loss (e.g., nephrotic syndrome), or excess consumption (e.g., sepsis, trauma). If Antithrombin III deficiency was thought to be the problem, then the treatment would be to administer FFP.

Answer 59

It has antithrombin 3

Answer 60

``` UBP Answer: There is no reliable way to prevent this type of reaction, but diluting the protamine (e.g., dilute in 50-100 cc and infuse via micro drip) and administering it slowly (e.g., over at least 5-10 minutes) seems a reasonable approach. ```

Answer 61

UBP Answer: I would not administer it directly into the PAC since it could cause pulmonary HTN, nor would I administer it directly into the bypass circuit because it may result in clot formation in the bypass machine. In general, the route of administration, central vs. peripheral, does not seem to make a difference in the likelihood of adverse reactions. However, there is some evidence that aspirin administered one week prior to CPB may be beneficial.

Answer 62

Since distinct the decelerations are beginning within 10-30 seconds after the beginning of each uterine contraction, and resolving within 10-30 seconds following the end of each contraction, I would conclude that this FHR tracing is showing late decelerations. Moreover, although the baseline heart rate is normal (110-160 bpm), fetal heart rate variability, defined as fluctuations in the FHR of more than 2 cycles per minute, appears to be minimal (<5 bpm).

Answer 63

minimal FHR variability, on the other hand, appears to be the most significant intrapartum sign of fetal compromise. Various factors that may cause or contribute to decreased FHR variability include fetal hypoxia, fetal sleep state, prematurity, fetal neurologic abnormalities, fetal tachycardia, betamethasone administration, congenital anomalies, and/or the administration of central nervous system depressants such as opioids, barbiturates, magnesium sulfate, and benzodiazepines.

Answer 64

(1) inform the obstetrician, provide supplemental oxygen, ensure adequate uterine displacement (or even turn the patient on her side), discontinue the administration of oxytocin (a tocolytic may be considered in the presence of tonic uterine contractions), begin a fluid bolus, and optimize maternal hemodynamics; (2) perform a careful history and physical focusing on her airway (exam, previous anesthetics, etc.), coagulation status (platelet count and trend; signs of a primary hemostatic defect - easy bruising, bleeding at IV sites, etc.), comorbidities, other complications associated with pre-eclampsia (cerebral edema - change in mental status, pulmonary edema, hypovolemia), and prenatal course; (3) discuss the obstetric plan with the obstetrician; and, assuming there were enough time and no contraindications to regional anesthesia (i.e. coagulopathy), ( 4) recommend the early initiation of epidural anesthesia in order to avoid the need for general anesthesia (especially ifher airway was concerning).

Answer 65

AH is also associated with nasal stuffiness, headache, visual changes, dysrhythmias, nausea, confusion, and difficulty breathing. Left untreated, sudden and sustained hypertension may lead to cerebral, retinal, or subarachnoid hemorrhage; loss of consciousness; seizures; myocardial ischemia; dysrhythmias; and pulmonary edema DDX: bladder rupture, myocardial ischemia, inadequate anesthesia

Answer 66

Cutaneous (pain) or visceral (i.e. bladder or rectal distention) stimulus below the level of spinal cord injury results in a reflex sympathetic discharge. Because the area of the body below the transaction is neurologically isolated, the sympathetic activity in this area is not modulated by inhibitory impulses from higher central nervous system centers. This unopposed sympathetic activity leads to vasoconstriction below the level of the lesion, with reflex vasodilation above the level of the lesion. When the lesion is above T7, vasodilation above the lesion is insufficient to prevent systemic hypertension, which then stimulates carotid sinus receptors, leading to reflex bradycardia.

Answer 67

Patients with transections above T 7 are at risk for autonomic hyperreflexia when spinal cord reflexes return following spinal shock (usually 1 to 3 weeks post-injury, but may persist for up to 3 months). It's rare, but not impossible

Answer 68

While adequate general and regional anesthesia affectively prevent AH, topical anesthesia has proven unreliable. When it comes to neuraxial anesthesia, spinal anesthesia is more reliable than epidural anesthesia for labor, perineal surgery, or bladder surgery, presumably due to more reliable and complete blockade of sacral roots.

Answer 69

Given this patient's severe hypertension, I would first remove the inciting stimulus by asking the surgeon to stop operating and by reducing any bladder distention. I would then place an arterial line for continuous blood pressure monitoring; administer a short acting direct vasodilator, such as sodium nitroprusside; and deepen the anesthetic. Finally, I would cancel the case, monitor the patient closely for subsequent complications (myocardial ischemia, intracerebral hemorrhage, seizures, etc.), and allow for complete resolution of the autonomic hyperreflexia.

Answer 70

``` Pseudocholinesterase deficiency Drug error Equipment error electrolyte abnormalities hypothermia myasthenia graves-associated with those who have thyroiditis (as this pt did) ```

Answer 71

Yes, because that therapy may result in reduced plasma cholinesterase

Answer 72

I would provide supportive care (including post-operative ventilation), consult a neurologist, and consider administering an anticholinesterase to prolong the action of acetylcholine at the postsynaptic membrane (these drugs may, themselves, have some limited agonist affect at the acetylcholine receptors), keeping in mind that overaggressive treatment with an anticholinesterase has the potential to induce a cholinergic crisis (excessive muscarinic effects of acetylcholine ), which may also result in weakness. Given her disease process and recent treatment with an anticholinesterase, her weakness could be the result of either a myasthenic or a cholinergic crisis. Both conditions result in muscle weakness, salivation, and sweating. The two conditions may be differentiated by administering lOmg of edrophonium (Tensilon test), with improved strength implying myasthenic crisis and increased weakness suggesting a cholinergic crisis. Additionally, an examination of the patient for other signs of cholinergic crisis, such as ( 1) constricted pupil size (pupils are dilated in a myasthenic crisis, secondary to sympathetic activation), (2) weakness and muscle fasciculations (depolarizing phenomenon occurs at the neuromuscular junction), (3) bradycardia, ( 4) bronchorrhea (an excessive discharge of watery mucous from the lungs),

Answer 73

Assuming pt still has pulse, I would... The timing suggests that local anesthetic injected for the retrobulbar block has spread through the optic nerve sheath and into the central nervous system, resulting in general anesthesia and apnea. However, I would also consider other possibilities, including narcotic or anxiolytic overdose, stroke, and cardiac arrest. Therefore, I would quickly assess the patient; provide supportive care, including intubation and positive pressure ventilation; review all the medications that were given; and order tests and lab work as indicated.

Answer 74

Complications from retrobulbar block are uncommon, but include direct trauma to the optic nerve, retrobulbar hemorrhage, increased intraocular pressure (IOP) secondary to transient globe compression, globe perforation, stimulation of the oculocardiac reflex, intravascular or intraneural injection, and apnea secondary to local anesthetic spread into the CNS.

Answer 75

DDX: While this could simply be an asthmatic attack, the occurrence of the child's respiratory distress shortly after a snack would be consistent with other potential etiologies such as foreign body aspiration and food allergy-induced anaphylaxis. I would perform a careful history to identify any known food allergies or previous diagnosis of asthma; similar episodes of respiratory distress; the type of food ingested during the afternoon snack (peanuts, jellybeans, popcorn, and hotdogs are the foods most commonly associated with foreign body aspiration); and the occurrence of coughing or choking during food ingestion (suggestive of foreign body aspiration). Moreover, assuming the child were stable, I would observe his response to a bronchodilator, recognizing that a lack of response is more consistent with foreign body aspiration; examine him for additional signs of anaphylaxis, such as pulmonary edema, hypotension, urticaria, and pruritus; examine him for other signs of foreign body aspiration such as stridor, hoarseness, aphonia, retractions, and use of accessory muscles of respiration; and consider a chest radiograph to help identify the presence and location of a foreign body. Although most foreign bodies are radiolucent, inspiration/expiration chest x-rays may indirectly identify the location of an aspirated object by demonstrating hyperinflation (air trapping in the affected lung), atelectasis, and/or mediastinal shifting toward the unaffected side.

Answer 76

While a chest x-ray may prove helpful in identifying the presence and location of a foreign body, I would not delay bronchoscopy in this case where the child may have aspirated an unroasted peanut. Peanut aspiration is not only associated with the absorption of water and increasing friability over time, but UNROASTED peanuts may lead to a peanut oil-induced chemical irritation of the airway with subsequent atelectasis and complete airway obstruction.

Answer 77

In preparing for induction, I would administer metoclopramide to facilitate stomach emptying in this patient with a history of recent food ingestion. I would also consider giving glycopyrrolate to reduce airway secretions and attenuate the reflex bradycardia often associated with airway instrumentation and bronchoscopy. Next, I would apply the appropriate monitors and ensure the presence of emergency airway equipment, the ENT surgeon, and a rigid bronchoscope. Given the potential for distal migration of the foreign body with assisted ventilation, I would perform an inhalational induction using oxygen and Sevoflurane and attempt to maintain spontaneous ventilation; recognizing that this method of induction places him at increased risk for aspiration of gastric contents. After ensuring an adequate depth of anesthesia to prevent coughing, laryngospasm, or bronchospasm, I would obtain intravenous access, allow the ENT surgeon to perform direct laryngoscopy, spray the vocal cords with lidocaine (to reduce the risk of laryngospasm during endoscopy), and insert the rigid bronchoscope. Once the bronchoscope was in place, I would connect the anesthesia circuit to the bronchoscope to allow for ventilation during foreign body removal.

Answer 78

Despite the risk of aspiration, I would not perform a rapid sequence induction in this situation, recognizing that positive-pressure ventilation may place the patient at risk for: (1) distal migration of the foreign body, making extraction more difficult; and (2) hyperinflation and/or pneumothorax, if the foreign body is producing a ball-valve affect. Rather, I would perform an inhalational induction with the goal of maintaining spontaneous respirations. However, I do recognize that there is no evidence that outcomes for this procedure are altered by the chosen method of ventilatory management during induction (i.e. spontaneous vs. controlled ventilation), and would consider altering or modifying my strategy depending on the circumstances (e.g. patient is vomiting preoperatively, further increasing the risk of aspiration).

Answer 79

I would immediately inform the surgeon that ventilation has become impossible and ask him to either quickly remove the foreign body or attempt to push it distally into one of the main bronchi so that one-lung ventilation was possible. If these interventions were unsuccessful, I would attempt to improve ventilation by moving the patient into the lateral or prone position, or by advancing an ETT beyond the obstruction. If these interventions were also unsuccessful and life-threatening hypoxia was imminent, I would consider placing the patient on cardiopulmonary bypass until the obstruction could be cleared.

Answer 80

Complications arising from foreign body aspiration depend on the location and type of foreign body aspirated (organic vs. non-organic, sharp vs. dull), and the duration of time the foreign body remained in the airways. Nuts and certain vegetable materials are highly irritating to the bronchial tree and produce a chemical pneumonitis. If the foreign body is successfully removed within 24 hours of the incident, the complication rate is very low. However, the longer the foreign body remains in the airways, the more likely complications such as bronchial stenosis, bronchiectasis, pneumonia, lung abscess, tissue erosion/perforation, and pneumomediastinum or pneumothorax will occur.

Answer 81

The concern in providing neuraxial anesthesia to a patient with hypertrophic obstructive cardiomyopathy (HOCM) is that a sympathectomy-induced reduction in systemic vascular resistance (SVR) may lead to reduced preload and the subsequent development or exacerbation of left ventricular outflow tract (L VOT) obstruction. However, as long as euvolemia is maintained, epidural anesthesia may be safely employed to achieve levels sufficient for vaginal or surgical delivery.

Answer 82

Hypertrophic obstructive cardiomyopathy (HOCM) is a genetic condition characterized by left ventricular hypertrophy, systolic anterior movement of the mitral valve (SAM), dynamic left ventricular outflow tract (L VOT) obstruction, decreased left ventricular size, diastolic dysfunction, myocardial ischemia (even in the absence of coronary artery disease), and dysrhythmias (these dysrhythmias are responsible for the sudden death that may occur in young adults with HOCM). In patients with HOCM, hyperdynamic left ventricular contraction of the hypertrophied septum results in the rapid movement of blood through the narrowed L VOT creating a Venturi effect on the anterior leaflet of the mitral valve. This Venturi effect leads to SAM, which in turn leads to dynamic LVOT obstruction and mitral regurgitation. Diagnosis: Echo Definitive diagnosis:endomyocardial biopsy and DNA analysis

Answer 83

The dynamic outflow obstruction associated with HOCM is accentuated by any intervention or event that results in a reduction in left ventricular end diastolic volume. Therefore, the obstruction is potentially exacerbated by the following conditions: (1) hypovolemia (reduced preload); (2) sympathectomy and/or vasodilation (decreased SVR/afterload, which facilitates left ventricular emptying); (3) increased myocardial contractility (increased left ventricular emptying); (4) tachycardia (reduced diastolic filling time); (5) sympathetic stimulation (tachycardia and/or increased inotropy); (6) dysrhythmia (inadequate ventricular filling); (7) excessive positive-pressure ventilation and/or PEEP (decreased preload); and, in this case, (8) inadequate left uterine displacement (decreased preload).

Answer 84

Recognizing that the systemic vasodilation and reflex tachycardia often associated with the administration of oxytocin could accentuate L VOT obstruction, I would consider administering an intramuscular injection of methylergonovine (methergine) or intravenous 15-methyl prostaglandin F2a (Hemabate) to induce uterine contraction. I would avoid the intravenous injection of methergine due to the increased risk of acute hypertension, seizures, cerebrovascular accident, retinal detachment, and myocardial arrest associated with this route of administration. If I believed it was necessary to administer oxytocin, I would give it very slowly to reduce the risk of a significant reduction in SVR.

Answer 85

The diastolic dysfunction associated with HOCM places these patients at increased risk of developing pulmonary edema with fluid overload. Therefore, the timing of this event suggests that her pulmonary edema may be secondary to the abrupt autotransfusion of blood into the central circulation that occurs with post-delivery uterine contraction and involution. However, recognizing that patients with HOCM are at increased risk of developing myocardial ischemia, I would also consider the possibility of left heart failure secondary to myocardial ischemia or infarction. Another consideration would be that the "bearing down" (valsalva-induced reduction in preload) and/or pain (sympathetic-induced tachycardia and/or inotropy) occurring during delivery resulted in worsening LVOT obstruction, with subsequent left heart failure. Other considerations would include hypovolemia (excessive blood loss secondary to uterine atony or other cause), a sympathectomy-induced decrease in SVR (due to excessive level of neuraxial anesthesia), cardiac arrhythmia, thrombotic embolism (pregnant patients are hypercoagulable ), and amniotic fluid embolism.

Answer 86

My treatment would be aimed at the correction or elimination of factors that could be accentuating her dynamic L VOT obstruction. Therefore, I would ensure adequate volume replacement and treat any hypotension, tachycardia, and/or dysrhythmia. More specifically, I would administer a ~-blocker to slow her heart rate, prolong diastolic filling time, and decrease myocardial contractility. If she were hypotensive, I would administer phenylephrine (the tachycardia associated with ephedrine administration would be undesirable) and ensure adequate volume replacement. If intubation and positive pressure ventilation became necessary, I would perform a rapid sequence induction (assuming a reassuring airway) and begin positive pressure ventilation with smaller tidal volumes and an appropriately increased ventilatory rate (to avoid the decreased preload associated with excessive intrathoracic pressures). While PEEP and diuretics are often utilized in the treatment of pulmonary edema, these interventions would potentially reduce her cardiac preload, thereby accentuating LVOT obstruction, the primary cause of her pulmonary edema.

Answer 87

When treating a patient with this life-threatening condition, I would: (1) provide supplemental oxygen to maintain the oxygen saturation above 90%; (2) administer B2-agonists (i.e. albuterol), corticosteroids (recognizing that it may take 4- 6 hours to realize a therapeutic benefit), aminophylline (to induce bronchodilation, stimulate the central respiratory cycle, reduce diaphragmatic muscle fatigue, and relax vascular smooth muscles), empirical broad-spectrum antibiotics, and intravenous fluids (although the benefits of this treatment are limited); (3) order pulmonary function tests and arterial blood gasses to monitor the adequacy of oxygenation, ventilation, and the patient's response to treatment; (4) consider the addition of intravenous magnesium sulfate (for bronchodilatory affects), if the patient's response to other bronchodilators is inadequate; and (5) consider mechanical ventilation, if the patient begins to show signs of respiratory fatigue and/or inadequate ventilation and oxygenation (PaC02 > 50 mmHg).

Answer 88

I would consider intubation and the initiation of mechanical ventilation ifthe patient began to show signs of respiratory fatigue and/or inadequate ventilation and oxygenation. Therefore, I would monitor the patient's response to therapy using pulmonary function tests and arterial blood gasses. If pulmonary function testing showed a FEV1 or peak expiratory flow rate :S 25% of normal, or if arterial blood gasses showed a PaC02 > 50 mrnHg, despite aggressive therapy, I would intubate the patient and initiate mechanical ventilation. Therefore, I would employ a pressure control mode of ventilation, recognizing that the decelerating flow pattern associated with this mode of ventilation will more efficiently overcome the high resistance of the asthmatic's airways, minimize the peak pressures required to deliver a given tidal volume, andimprove the distribution of ventilation. Moreover, I would establish a prolonged expiratory phase to allow for complete exhalation and to avoid auto-PEEP (breath stacking), which can result in barotrauma. When the patient's FEV1 or peak expiratory flow rates increased to 2: 50% of normal, I would initiate weaning from mechanical ventilation.

Answer 89

I would first perform a careful history, focusing on the severity and characteristics of her pulmonary disease, along with the effectiveness of her current therapy. To this end, I would attempt to elicit information concerning the age of onset, triggering events, allergies, recent respiratory infection, changes in symptomatology (cough, sputum, wheezing, etc.), current medications, anesthetic history, and her recent hospital course. Next, I would perform a physical exam to identify any pulmonary wheezing or crepitations and/or the use of accessory muscle of respiration. Considering the severity of her disease, I would order: (1) pulmonary function tests, before and after bronchodilator therapy, to more accurately assess the severity of obstruction and her response to therapy; (2) arterial blood gasses, to evaluate the adequacy of ventilation/oxygenation and to establish baseline levels (helpful in the event of subsequent respiratory dysfunction); and (3) chest x-rays, to identify or rule out pulmonary infection.

Answer 90

My goals in preparing this patient for surgery are to optimize her asthma, control her pain, reduce her anxiety, and minimize the risk of aspiration. Therefore, I would reassure the patient and family, continue her current medications, and consider chest physiotherapy. Moreover, I would administer fentanyl, to avoid the pulmonary splinting, decreased ability to cough, and bronchospasm potentially associated with pain (avoid narcotics that release histamine and carefully titrate to avoid respiratory depression); diphenhydramine (an H1-receptor blocker), to inhibit histamine-induced bronchoconstriction and reduce the potential for anxiety-induced bronchospasm; a stress dose of hydrocortisone (100 mg), given the potential for hypothalamic-pituitary-adrenal suppression with chronic steroid treatment (she is being treated with dexamethasone ); metoclopramide, to facilitate stomach emptying; and ondansetron, to treat her nausea. Just prior to induction, I would administer a short acting B2-agonist (i.e. albuterol), to minimize the risk of bronchoconstriction during intubation.

Answer 91

Anticholinergic medications may be beneficial for asthmatic patients secondary to reduced mucous gland secretions (possibly improving inflammation) and airway hyperreactivity (secondary to reduced vagal tone and inhibition of muscarinic cholinergic receptors). However, their preoperative administration is controversial, since they could result in increased inspissation (increased viscosity and thickening of airway secretions), potentially leading to airway plugging and the initiation of an asthmatic attack. Therefore, considering these potential complications, and recognizing that the intramuscular doses of anticholinergic medications typically used for pre-anesthetic medication are unlikely to significantly decrease her airway resistance (they would be sufficient to reduce airway secretions), I would not administer this medication pre-operatively. If I wanted to administer an anticholinergic, preoperatively, to optimize his asthmatic condition, I would consider providing an inhaled medication, such as ipratropium.

Answer 92

My goals when inducing this severely asthmatic patient with a full stomach and nausea, are to achieve an adequate plane of anesthesia to avoid bronchoconstriction in response to mechanical stimulation while, at the same time, minimizing the risk of aspiration. Therefore, assuming her airway exam were reassuring, I would: (1) administer a short acting B2-agonist; (2) denitrogenate with 100% oxygen; (3) ensure that she had received metoclopramide and ondansetron to facilitate gastric emptying and treat her nausea, respectively; (4) administer 2μ/kg of fentanyl, 2-3 minutes prior to induction, to avoid light anesthesia during laryngoscopy; (5) give 1-2 mg/kg of intravenous lidocaine, 1-2 minutes prior to induction, to prevent reflex-induced bronchoconstriction (Topical lidocaine may also be used, but the application may provoke bronchospasm if the depth of anesthesia is insufficient. Since there is significant risk for light anesthesia during a RSI, I would not employ this technique.); (6) apply cricoid pressure; and (7) perform a RSI using ketamine (induces bronchodilation), propofol (produces bronchodilation and a more reliable depth of anesthesia as compared to thiopental), and succinylcholine. While succinylcholine could potentially result in significant histamine release (risk for histamine-induced bronchospasm), I believe that its ability to facilitate the rapid placement of an endotracheal tube is important to reduce the risk of aspiration in this patient presenting for emergent surgery (inadequate fasting), an acute abdominal process (delayed gastric emptying), and active nausea.

Answer 93

While I would consider several potential causes of these symptoms, such as hypoxia, acidosis, myocardial ischemia, alcohol withdrawal, and a seizure disorder, the timing of the event and the progression of his symptomatology are most consistent with local anesthetic toxicity. Recognizing that the presentation of local anesthetic toxicity is extremely variable in onset and initial symptomatology, I would consider this possibility in any situation where a patient experienced an altered mental state, neurologic symptoms, or cardiovascular instability following the administration of local anesthetic for regional anesthesia.

Answer 94

Initially, the patient developing local anesthetic toxicity may experience nonspecific neurologic symptoms such as metallic taste, circumoral paresthesias, tongue numbness, visual disturbances (i.e. blurred vision and difficulty focusin), auditory disturbances (i.e. tinnitus), lightheadedness, dizziness, and a feeling of "impending doom". When administering local anesthetics, it is important to keep in mind that patients may progress rapidly to seizure activity and cardiac toxicity without experiencing any of the initial nonspecific neurologic symptoms, as may occur following a direct arterial injection. Likewise, the onset of symptoms may be significantly delayed, as may be the case following tumescent procedures (delayed for over 15 minutes in some reports).

Answer 95

In the case of ropivacaine, the reduced cardiac depression of its propyl side chain, as compared to the butyl side chain of bupivacaine, may also play a role. Another potential advantage of ropivacaine is the provision of similar sensory blockade in association with less extensive motor blockade, as compared to an equal dose ofbupivacaine.

Answer 96

The addition of epinephrine may reduce the risk of local anesthetic toxicity by reducing systemic absorption (secondary to vasoconstriction) and/or helping to identify unintended intravascular injection (i.e. an increase in heart rate of IO beats/minute or an increase in systolic pressure of> 15 mmHg).

Answer 97

The inhibition of voltage-gated sodium channels results in the following direct cardiac effects: (1) slowed cardiac conduction (increased PR-interval and widened QRS complex), (2) decreased rate of depolarization (secondary to a reduction in availability of the fast sodium channels that allow the rapid sodium influx required for membrane depolarization), (3) a dose-dependent reduction in cardiac contractility (potentially contributing to hypotension, metabolic acidosis, and reduced clearance oflocal anesthetic), and (4) depressed spontaneous pacemaker activity in the sinus node (potentially leading to bradycardia and cardiac arrest). Peripheral vascular effects vary depending on the amount of local anesthetics in the plasma, with low concentrations resulting in (5) vasoconstriction and high concentrations causing (6) vasodilation.

Answer 98

In treating this complication, I would: (1) stop injecting local anesthetic; (2) call for help and a lipid rescue kit; (3) ensure adequate ventilation and oxygenation to correct and/or avoid factors that enhance the systemic toxicity of local anesthetics, such as hypercarbia (increased cerebral blood flow, intra-neuronal ion trapping of the drug, and decreased plasma protein binding of local anesthetics), acidosis (reduces the seizure threshold and decreases plasma protein binding of local anesthetics), and hypoxemia; (4) administer a benzodiazepine to treat his seizure (seizure activity increases metabolism, which may lead to hypoxemia, hypercarbia, and acidosis); (5) administer succinylcholine and intubate the patient if ventilation were inadequate, the risk of aspiration was significant (history of GERD or hiatal hernia), or if tonic-clonic movements persisted despite benzodiazepine administration (while succinylcholine would minimize the metabolic acidosis associated with seizure-induced muscle activity, it would not affect the acidosis that develops secondary to seizure-induced increases in cerebral metabolism); (6) initiate lipid emulsion therapy with a bolus of 1.5 mL/kg of 20% lipid solution (roughly 100 mL in adults) and a continuous infusion at 0.25 mL/kg/minute, with plans to discontinue the infusion only after establishing hemodynamic stability for at least 10 minutes (repeat bolus and double infusion rate every 5 minutes as necessary, keeping in mind that the recommended upper limit for initial dosing is 10 mL/kg for 30 minutes); (7) administer adenosine and/or amiodarone for additional treatment of his ventricular dysrhythmia (procainamide, lidocaine, ~-blockers, calcium channel blockers, and vasopressin should be avoided when treating bupivacaine-induced ventricular arrhythmias); (8) perform immediate synchronized cardioversion if the patient became unstable (assuming he remained in monomorphic VT- polymorphic VT usually requires unsynchronized shock); and (9) consider cardiopulmonary bypass if the patient's response to these therapies was inadequate (cardiopulmonary bypass may serve as "bridging therapy" until tissue levels of local anesthetic have diminished).

Answer 99

Epinephrine - Standard resuscitation doses of epinephrine (1 mg) are not recommended during resuscitation of a patient experiencing local anesthetic toxicity because epinephrine is highly arrhythmogenic and can reduce the efficacy of lipid rescue. Therefore, it is recommended utilize smaller doses in this setting (<1 μg/kg or 10-100 μg boluses). No vaso No beta blockers No calcium channel blockers No lidocaine or procainaide (local anesthetics)

Answer 100

Given the potential for cardiovascular instability in this situation, I would not administer propofol. While propofol and thiopental are acceptable alternatives to quickly stop seizure activity, they should be avoided in the setting of cardiovascular instability because of their direct cardiodepressant effects. Furthermore, the low lipid content of propofol makes it an inappropriate substitute for lipid emulsion therapy.

Answer 101

The appropriate time to initiate lipid emulsion therapy is controversial. Since early treatment may prevent cardiovascular collapse, many practitioners believe. that waiting until standard therapy has failed to initiate lipid emulsion therapy is unreasonable. On the other hand, administering lipids at the first sign of local anesthetic toxicity would result in unnecessary treatment, since only a fraction of patients progress from the initial premonitory symptoms to severe toxicity. Therefore, I would initiate therapy when the signs and symptoms of local anesthetic toxicity appeared to be rapidly progressing or when a patient experienced prolonged seizure activity or signs of cardiac toxicity (i.e. bradycardia, heart block, hypotension, asystole, or ventricular arrhythmia).

Answer 102

Patients should be monitored for at least 30 minutes following the administration of potentially toxic doses of local anesthetic because toxicity has been reported to present longer than 15 minutes after injection (this recommendation refers to patients who have yet to develop any signs or symptoms of toxicity). • Patients should be monitored very closely for at least 12 hours following significant local anesthetic toxicity because local anesthetic can continue to redistribute to the circulation from tissue depots, potentially resulting in delayed recurrence of severe toxicity.

Answer 103

The acoustic impedance of water and body tissues is similar, the shock wave travels through body tissues without a significant dissipation of energy, causing minimal tissue damage.

Answer 104

While intravenous analgesia and sedation are usually adequate for procedures performed with second and third generation lithotripters, the increased discomfort associated with the more powerful first-generation lithotripters often requires general anesthesia, neuraxial anesthesia, or flank infiltration with/without intercostal blocks. If I was concerned about airway, I could do a spinal or epidural of course after looking at CBC and coags and assuming the pt not on AC

Answer 105

While this technique is a viable option for the procedure, I believe that neuraxial anesthesia would more reliably provide adequate analgesia (as compared to flank infiltration combined with intercostal nerve blocks), thus reducing the potential necessity for additional sedation. Since one of my principal goals in managing this patient with a potentially difficult airway is to maintain spontaneous ventilation and avoid the necessity for airway manipulation, I would prefer to proceed with the technique that most reliably avoids the need for supplemental intravenous sedation.

Answer 106

While the overall risk is low, there is some risk that patients with a cardiac rhythm management device (CRMD), such as a pacemaker or automatic implantable cardioverter-defibrillator (AICD), will experience shock wave-induced intraoperative arrhythmias during ESWL (as are those with a history of arrhythmias). Moreover, lithotripter-induced shock waves can lead to CRMD malfunction, such as switching to magnet mode, pacing suppression, oversensing of asynchronous shocks,However, as long as the CRMD generator is not located in the abdomen (usually located in the pectoral region), ESWL is not contraindicated in patients with these devices.

Answer 107

(1) ascertain the indication for placement, the patient's underlying rhythm and rate, and the degree of pacemaker dependency; (2) determine the type, manufacturer, programmability, and functionality of the device (i.e. battery life, lead integrity, the presence of any alert status, and sensing/pacing thresholds); (3) verify the behavior of the device when exposed to a magnet (usually disables tachydysrhythmia detection and therapy); (4) ensure the availability of a programming device, trained pacemaker programmer, and alternative pacing modality in the operating room; (5) make sure that the patient's CRMD is not in the shock wave path (the focal point of the lithotripter should be kept at least six inches away from the pacemaker); (6) employ continuous telemetry; (7) begin lithotripsy with low energy shock waves followed by gradually increasing energy levels, while closely monitoring pacemaker function; (8) terminate lithotripsy if the patient developed an arrhythmia; and (9) use a magnet only if there were inhibition of the device's pacemaker function. I would not require preoperative interrogation as long as his device had been checked within the last 6 months (Recommendation: implantable cardioverter-defibrillators should ideally be checked within last 6 months, and pacemakers within the last 12 months).

Answer 108

Tell surgeon!!! Always communicate with them!!!!! A drop of 3.6 mg/dL in the hemoglobin concentration is significant, and would elevate my suspicion of intra-abdominal or retroperitoneal hemorrhage. In evaluating his progressive anemia, I would examine the patient's abdomen, stabilize his hemodynamics, look for other sources of bleeding, and consider radiographs or CT to identify any hematoma formation. During this evaluation, I would also consider other potential causes of his postoperative anemia, such as hemodilution from excessive fluid administration and/or shock wave-induced damage to the gastrointestinal, pulmonary, or urinary systems.

Answer 109

Given the potential for difficult intubation and ventilation, I would: ( 1) perform a standard airway exam, including mouth opening, neck range of motion, thyromental distance, etc.; (2) review the surgeons notes from the most recent fiberoptic and mirror inspection, to help identify the extent of the mass; (3) look at the most recent CT scan of his neck to identify and assess the extent of airway compromise; ( 4) palpate the patient's neck to identify any masses and/or tracheal deviation, and to assess tissue plasticity (the latter may be affected by mass affect and/or radiation therapy); and (5) further examine the patient for signs of airway obstruction, such as stridor, hoarseness, dyspnea, sternal retraction, and the use of accessory muscles of respiration.

Answer 110

While an awake fiberoptic intubation is often utilized in the management of a known or anticipated difficult airway, it may not be the best approach in the setting of advanced obstructive laryngeal disease due to: (1) the risk of complete obstruction as the fiberscope passes through the mass; (2) the difficulty of achieving adequate airway analgesia in the setting of advanced laryngeal pathology; and (3) the technical difficulty of performing fiberoptic intubation through a large vascular friable tumor (i.e. tortuous route, bleeding, and/or edema). Therefore, I would consider one of the following options: (1) an inhalational induction with the goal of maintaining spontaneous ventilation until the airway was secured; (2) placement of a transtracheal catheter under local anesthesia, followed by intravenous induction and jet ventilation through the catheter; or (3) an awake elective tracheostomy under local anesthesia.

Answer 111

Recognizing that there is no longer a communication between the oropharynx and the lower trachea in a patient who has undergone total laryngectomy, I would have someone call for a surgeon capable of obtaining emergency airway access. In the meantime, I would attempt to oxygenate and ventilate the patient via a partially inflated LMA applied over the stoma site, or jet ventilation through a catheter inserted into the stoma.

Answer 112

Assuming she were hemodynamically stable and that I believed this to be ``` supraventricular tachycardia (i.e. heart rate > 180 bpm in a child, absent or abnormal P- waves, and/or a history of abrupt rate changes), I would first apply supplemental oxygen and ``` attempt to convert her arrhythmia with a vagal maneuver, such as applying ice to her face. If this were ineffective, I would establish intravenous access and administer 0.1 mg/kg of adenosine in an attempt to interrupt any reentry circuit involving the atrioventricular node (the usual cause of SVT in children) by temporarily blocking conduction through the atrioventricular node. If her SVT persisted or reoccurred, I would give successive doses of 0.2 and 0.4 mg/kg every 1-2 minutes, as necessary. At the same time, I would ensure adequate monitoring (i.e. ECG, blood pressure cuff, pulse oximeter), secure her airway (preferably an ETT), prepare for cardioversion in case the patient became unstable, and treat any possible contributing factors, especially hypoxia.

Answer 113

Assuming she remained hemodynamically stable, I would make a quick attempt at obtaining peripheral intravenous access. If I were unable to quickly achieve this, I would immediately insert an interosseous needle into the anterior surface of her tibia (1-2 cm below and 1 cm medial to the tibial tuberosity). While an interosseous line provides good access for the administration of all fluids and medications routinely given duringcardiopulmonary resuscitation, it is also associated with several complications, such as osteomyelitis, fat and bone marrow embolism, and compartment syndrome. Therefore, I would view this as a temporary solution until a more definitive intravenous line could be placed.

Answer 114

While central line access may be preferable due to the rapid metabolism of adenosine by red blood cell adenosine deaminase (half-life= 10 seconds), I would administer it through a peripheral line if necessary. However, given its rapid metabolism, I would quickly flush the peripheral line with 10 mL of saline following drug administration.

Answer 115

In the setting of supraventricular tachycardia and hemodynamic instability, I would prepare for immediate synchronized cardioversion, beginning at 0.5 J/kg and doubling the energy dose as required up to 2 J/kg. While cardioversion was being prepared, I would secure her airway, apply 100% oxygen, and attempt to place an interosseous line (in the setting ofhemodynamic instability, time should not be wasted attempting to obtain intravenous access, which may prove more difficult secondary to poor peripheral perfusion). However, given the urgency of converting her arrhythmia, I would not delay cardioversion for intravenous access.

Answer 116

While I understand that the true cross-reactivity between penicillin and cephalosporins is about 0.5% for first-generation cephalosporins and near zero for both second and third-generation cephalosporins, I would not administer a cephalosporin to a patient who had experienced anaphylaxis following penicillin administration due to the potentially serious consequences of this type ofreaction. Therefore, since this patient's history of difficulty breathing is consistent with an anaphylactic response, I would suggest utilizing vancomycin rather than a cephalosporin for antibiotic prophylaxis.

Answer 117

The timing of his hypotension, along with flushing ("very red") and upper body erythema, is consistent with "red man's syndrome", which results when rapid administration of vancomycin leads to histamine release. While the most common manifestation of rapid administration ( 10-15 mg/kg should be administered over 60 minutes) is isolated hypotension, other symptoms such as pruritus, flushing, upper body erythema, and even cardiac arrest may occur. Giving antihistamines, such as diphenhydramine (H1-receptor antagonist) and cimetidine (H2-receptor antagonist), one hour before vancomycin administration may attenuate the drop in systemic vascular resistance associated with histamine release.

Answer 118

There are several potential causes of arachnoiditis (inflammation of the meninges and subarachnoid space), such as: (I) direct injury to the spine, as may occur with trauma, spinal surgery, and multiple lumbar punctures (especially when bleeding into the spinal fluid occurs); (2) infections, such as tuberculosis or viral and fungal meningitis; (3) chemicals, such as contrast dye, disinfectants, and preservatives found in local anesthetic and epidural steroid preparations; and ( 4) chronic compression of spinal nerves, as may occur with degenerative disc disease and/or severe spinal stenosis. Symptoms associated with arachnoiditis include: (1) back pain that increases with activity; (2) various sensory and motor abnormalities, such as tingling, numbness, weakness, cramps, spasms, and severe shooting leg pain; and (3) bowel, bladder, and/or sexual dysfunction. Computerized axial tomography and magnetic resonance imaging are often used to help establish the diagnosis.

Answer 119

Since there is no cure for arachnoiditis, the treatment is similar to that utilized for other chronic pain conditions. Treatment modalities include physical therapy, pain medications (i.e. NSAIDs, narcotics, corticosteroids, anti-spasm drugs, anti-convulsants (help with burning pain), intrathecal pump placement, transcutaneous electrical nerve stimulation, and/or a spinal cord stimulator.

Answer 120

Assuming this patient who was recently in a bar fight would tolerate undergoing the procedure under regional anesthesia (i.e. not intoxicated or combative), and that his long-term tobacco use had not resulted in significant pulmonary disease (may not tolerate hemidiaphragmatic paralysis), I would consider an interscalene block for this procedure. However, since the surgical procedure involves the forearm, an axillary block or supraclavicular block may be more appropriate considering the ulnar nerve sparing that is often associated with an interscalene block (the C8-Tl nerve roots, which form the ulnar nerve, are spared with an interscalene block up to 50% of the time). Therefore, ifthe surgeon and patient preferred an interscalene block for this procedure, I would let them know that the ulnar nerve may need to be blocked with a separate injection.

Answer 121

There are a number of complications associated with prolonged tourniquet use, dull achy pain, tachycardia, and hypertension; (2) muscle damage, occurring beneath the tourniquet at 2 hours (direct pressure), and distal to the tourniquet at 4 hours (muscular ischemia, edema, and microvascular congestion); (3) nerve injury, occurring secondary to direct pressure under the cuff (some sources say ischemia contributes) ; ( 4) thrombotic embolism, occurring with tourniquet release; (5) vascular injury, most commonly in patients with peripheral vascular disease; (6) undesirable drug effects (inadequate antibiotic tissue concentrations when given after tourniquet inflation; tissue sequestration of drugs administered prior to inflation, followed by release and subsequent affect following deflation; and reduced volume of distribution for drugs administered following inflation); (7) transient metabolic acidosis, occurring with deflation and the washout of accumulated metabolic waste products in the ischemic extremity; and (8) skin damage, such as pressure necrosis, friction bums, and chemical bums (the latter resulting from antiseptic skin preparation solutions becoming trapped under the cuff and compressed against the skin).

Answer 122

While the exact mechanism of tourniquet pain is unknown, it is believed that pain transmission through unmyelinated C-fibers occurs with the recession oflocal anesthetic blockade. The pain, which occurs despite adequate surgical analgesia, is often described as a dull ache or burning sensation, begins around 45-60 minutes following tourniquet inflation, and is associated with tachycardia and hypertension. This patient, however, may be experiencing pain secondary to inadequate analgesia of the medial brachial cutaneous and intercostobrachial nerves supplying cutaneous innervation to the medial aspect of the upper arm, since these nerves are spared with an interscalene block. Recognizing that the definitive treatment for tourniquet pain is to release the tourniquet, I would ask the surgeon to allow deflation as soon as possible. In the meantime, I would provide small doses of an opioid and midazolam to ease his discomfort, with the goal of maintain adequate airway reflexes in this patient who was recently at a bar and is likely at risk for aspiration (i.e. alcohol, food, etc.). If this was inadequate and tourniquet deflation was still required, I would consider employing general anesthesia by performing a rapid sequence induction with cricoid pressure.

Answer 123

I would explain to him that, while it is possible that the residual numbness in his pinky finger is due to nerve damage incurred during the interscalene block (or separate ulnar nerve block), it is more likely the result of multiple contributing factors, such as positioning, inadequate padding at the elbow, and direct pressure on the ulnar nerve from the pneumatic tourniquet. I would also reassure him that this type of injury usually resolves quickly(< 1 week). However, I would let him know that if his symptoms persisted beyond a week, he should ask his surgeon or a primary care physician to arrange for an appointment with a neurologist.

Answer 124

moderate sedation/analgesia ("Conscious Sedation") is a drug-induced depression of consciousness during which patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation. No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate.

Answer 125

At minimum I would require 2 sources of oxygen, ASA standard monitors, airway equipment, emergency medications, crash cart, a battery powered flashlight, and personnel trained in cardiopulmonary resuscitation.

Answer 126

The ASA standards for post anesthetic care apply to all locations and all patients who have received general anesthesia, regional anesthesia, or monitored anesthesia care. In general, the standards include transfer of the patient to a designated P ACU or equivalent area by a member of the anesthesia team, a verbal report of the patient given to the P ACU nurse, continual evaluation, and monitoring in the immediate post-operative period. General medical supervision, coordination of patient care, and discharge from the P ACU should be the responsibility of an anesthesiologist.

Answer 127

I would set his initial tidal volumes at 6 mL/kg (ideal body weight should be used rather than actual body weight, since lung volumes more closely correlate with height than weight). Given the risk of auto-PEEP (air trapping) associated with COPD secondary to limited expiratory flow (auto-PEEP increases the risk ofbarotrauma, pneumothorax, cardiovascular compromise, and V ALI), and recognizing the increased morbidity and mortality associated with the development of auto-PEEP in COPD patients, I would provide adequate sedation and attempt to prolong the expiratory time by employing low tidal volumes, a low rate of ventilation (8-12 breaths/minute), and a reduced inspiratory time.

Answer 128

A reduced inspiratory time does result in increased inspiratory flow rate and, subsequently, increased peak airway pressures. However, most of the peak pressure is dissipated as gas flows through the endotracheal tube and large airways, making this an acceptable trade for an increased expiratory time, which can significantly reduce ventilator-associated complications in COPD patients. Moreover, the increased expiratory time leads to a reduction in end-expiratory, static or plateau, and mean airway pressures, despite the increased inspiratory flow rate. Finally, while hypercapnia and respiratory acidosis are not desirable, the benefits of avoiding significant auto-PEEP most likely outweigh the potential detrimental effects of respirator acidosis in this patient.

Answer 129

There are several options for weaning a patient from mechanically supported ventilation such as: 1) a progressive reduction in the number of mandatory breaths/minute while employing synchronized intermittent mandatory ventilation, 2) the incremental reduction of pressure-support ventilation, and 3) trials of total separation of the patient from mechanical ventilation ("T-piece trials"). However, the most important component of separating the patient from mechanical ventilation is the resolution of the underlying condition responsible for the needed respiratory support. I would consider extubation when he was awake and alert, demonstrating active laryngeal reflexes, generating an effective cough and clearing secretions, and when he was able to comfortably breathe without ventilatory support for 2 hours without experiencing a deterioration of his cardiac function, mental status, or arterial blood gasses. Moreover, I would take into consideration other proposed extubation criteria such as: 1) a Pao2 above 60 mmHg with a Fi02 < 50%, 2) a PaC02 less than 50 mmHg, 3) an arterial pH> 7.30, 4) a vital capacity> 15 mL/kg, and 5) required< 5 cm H20.

Answer 130

``` Volume-cycled ventilation includes assist-control (A/C), Continuous mandatory ventilation (CMV), and synchronized intermittent mandatory ventilation (SIMV). This mode of ventilation delivers a set tidal volume, with airway pressures varying according to lung compliance and the selected flow rate. ``` • o A/C- This mode is the simplest and most effective means of providing full mechanical ventilation. In this mode, each inspiratory effort beyond the set sensitivity threshold triggers delivery of a fixed tidal volume. In order to ensure a desired minimum respiratory rate, a mandatory respiratory rate is established. o CMV-In this mode the ventilator provides mechanical breaths according to a preset rate and volume, ignoring any patient respiratory effort. This mode of ventilation is uncomfortable, usually requiring patient sedation. o SIMV-Like CMV, this mode of ventilation delivers breaths at a preset rate and volume. However, in this mode, the breaths are synchronized to the patient's efforts. Moreover, in contrast to A/C ventilation,patient efforts above the set respiratory rate are unassisted.

Answer 131

continuous positive airway pressure (CP AP), pressure control ventilation (PCV), pressure support ventilation (PSV),airway pressure-release v~ntilation (APRV), a~d several noninvasive modalities. With all of these modes, the ventilator delivers a set inspiratory pressure, with tidal volume varying according to lung compliance. Unfortunately, changes in respiratory system mechanics can result in unrecognized changes in minute ventilation. CP AP- provides a continuous level of elevated pressure to maintain adequate oxygenation, and decrease the work of breathing. No cycling of ventilator pressures occurs and the patient must initiate all breaths. CP AP may be used invasively through an endotracheal tube or tracheostomy or non-invasively with a face mask or nasal prongs. o Pressure control ventilation- is similar to A/Cventilation, except that each inspiratory effort beyond the set sensitivity threshold delivers a set amount of pressure support rather than a set tidal volume. This mode of ventilation is set to maintain a minimum respiratory rate and the preset pressure is maintained for a fixed inspiratory time. o Pressure support ventilation- provides ventilation support only when triggered by the patient. Pressure is typically cut off when backpressure causes flow to drop below a certain point. Thus, a longer or deeper inspiratory effort by the patient results in a larger tidal volume. This mode is commonly used to liberate patients from mechanical ventilation by letting them assume more of the work of breathing. However, there is not sufficient evidence to indicate that this approach is more successful. ARPV: APRV-This mode of ventilation cycles between two different levels of CP AP - an upper pressure level (inspiratory) and a lower pressure level (expiratory). The bi-level positive airway pressure allows gas movement in and out of the lung, while maintaining continuous positive pressure. It is · important to understand that the baseline airway pressure is the upper CP AP level, and that this baseline pressure is intermittently "released" (decreased) to a lower level in order to eliminate waste gas.