ACE 2008 5B Flashcards
1
Q
1. At the outpatient surgicenter, a 66 year old healthy woman had an uneventful laparoscopic cholecystectomy approximately 3 hours ago. The postanesthesia care unit nurses inform you that her SPO2 is 89% on room air. Her preoperative SPO2 was 98%. Which of the following therapies is MOST likely to improve her oxygenation? A. incentive spirometry B. deep breathing exercises C. continuous positive airway pressure D. chest physiotherapy
A
- C Hypoxemia is an extremely common complication; 30%-50% of all patients experience some period of hypoxemia (SPO2>93% at sea level) after uneventful abdominal surgery. The most common etiology of hypoxemia is atelectasis associated with the anesthesia and surgical procedure. A small segment of patients who undergo open upper abdominal surgery have persistent hypoxemia that requires tracheal intubation and mechanical ventilation, leading to prolonged intensive care unit stays and increased morbidity and mortality. The diagnosis of atelectasis is usually one of exclusion. Findings on physical examination include dyspnea and tachypnea, asymmetrical chest movement, or decreased breath sounds. The specificity of this exam is low and frequently the only finding is a persistent decreased SpO2. However, diagnostic tests can rule out other causes such as aspiration pneumonitis, pulmonary edema, or pneumothorax. The most readily available test is a simple chest radiograph, and the diagnostic criteria used for a radiographic diagnosis include- opacification of a lobe or lobar segment, displacement of the interlobar fissure, elevation of the hemidiaphragm and mediastinal shift, compensatory overinflation of aerated segments. With the current emphasis on outpatient procedures, aggressive efforts to prevent or treat pulmonary atelectasis are often used. Most therapies aim to produce a large and sustained increase in transpulmonary pressure to reexpand the collapsed alveoli. The most frequently employed therapies include intermittent positive pressure breathing, deep-breathing exercises, incentive spirometry, and chest physiotherapy. A meta-analysis of the effectiveness of these therapies for improving oxygenation in patients after upper abdominal surgery found that all the methods had equal effect; more precisely, none were found to be clinically or statistically effective. In fact, in the meta-analysis the most effective therapy to reverse atelectasis, particularly in patients who develop severe hypoxemia, is the use of supplemental oxygen and 7.5 cm H2O of nasal continuous positive pressure airway pressure. Patients receiving continuous positive airway pressure (CPAP) had a lower occurrence of pneumonia and reintubation than patients who only received oxygen therapy. Nasal CPAP may be a good, brief, first-line therapy for patients with unacceptable postoperative SpO2 on room air, particularly for patients who normally use CPAP or oxygen at night.
2
Q
- A patient with a cardiac rhythm management device (CRMD) that has both pacemaker and implantable cardioverter-defibrillator functions is scheduled for elective cholecystectomy. Which of the following is the MOST appropriate management prior to inducing anesthesia?
A. disabling the anti-tachycardia function
B. maintaining the minute ventilation rate response
C. enabling the artifact filter on the electrocardiographic monitor
D. placing a magnet over the device
A
- A. disabling the antitachycardia function. More patients with cardiac rhythm management device (CRMD) including pacemaker and/or cardioverter-defibrillator functions are presenting for surgical procedures than ever before. Anesthesiologists caring for patients with these devices should become familiar with the anesthetic implications and be able to develop an appropriate management plan for the perioperative period. Patients with both a pacemaker and implantable cardioverter-defibrillator will be subject to the anesthetic implications of both devices. Pacemaker function: Anesthetic management for patients with CRMD with pacemaker function should begin with determining the reason for placement including the degree of pacemaker dependency. Preoperative interrogation of the device should include obtaining information regarding the performance, settings, and remaining battery life of the device. All rate-adaptive functions, including minute ventilation responsiveness, should be programmed to the “off”setting; this will reduce the likelihood of inappropriate tachycardia from the CRMD. Typically the device is reprogrammed to an asynchronous mode during the intraoperative period.The artifact filter on the electrocardiographic monitor should be disabled; this will allow the pacemaker spikes to be displayed within the electrocardiogram. Device interrogation, including resetting the CRMD to the preoperative settings, should be performed following completion of the surgical procedure. Cardioverter-Defibrillator Function: Anesthetic management for patients with a CRMD that includes cardioverter-defibrillator function should include determining the reason for placement and obtaining information regarding the remaining battery life and discharge history of the device. The anti-tachycardia and defibrillator functions of the device should be disabled for the intraoperative period; this will prevent inappropriate discharge from the defibrillator. If correctly applied to a CRMD with cardioverter-defibrillator function, a magnet will generally suspend anti-tachycardia therapy and have no impact on the pacing rate for bradycardia. However some devices may have no response to a magnet and others may be permanently disabled in response to application of a magnet. Because the response to a magnet is unpredictable without knowledge of the specific device, routine prophylactic use of a magnet is generally not warranted. Once defibrillator function of the CRMD has been disabled, an external defibrillator should be immediately available until this function is restored. Device interrogation, including resetting the cardioverter-defibrillator function to the preoperative settings, should be performed following completion of the surgical procedure.
3
Q
- Which statement about ketamine is MOST likely true?
A. It is a potent cerebral vasodilator
B. It increases seizure threshold
C. Its primary site of action is at gamma-aminobutyric acid (GABA) receptors
D. It is contraindicated in patients with a known susceptibility to malignant hyperthermia.
A
- A. A potent cerebral vasodilator. A unique and interesting anesthetic, ketamine is an arylcyclohyxlamine similar in structure to phencyclidine. Its pharmacologic action is to function as an antagonist at the N-methyl-D-aspartate (NMDA) receptor. Preoperations are avilable as an aqueous mixture of two optical isomers; the S (+) ketamine isomer has greater anesthetic and analgesic potency than the R (-) isomer. Ketamine is extensively metabolized by hepatic cytochrome P-450 primarily into the active metabolite norketamine. Norketamine is approximately one third to one fifth as potent as ketamine and is excreted by the kidneys. Ketamine produces profound analgesia and amnesia. It does not directly alter seizure threshold itself but may lower seizure threshold when combined with other agents such as aminophylline. There are effectively two separate dose response relationships- one for analgesia and another for dissociative anesthesia. At lower doses ketamine may produce analgesia without inducing a “dissociative state”. In the dissociative state, patient may maintain airway reflexes intact. This is thought to occur through simultaneous electrophysiologic stimulation of the limbic system as well as inhibition of the thalamocortical pathways. Ketamine rapidly crosses the blood-brain barrier. It is a potent cerebral vasodilator that can increase cerebral blood flow (CBF) by 60%. Ketamine is typically avoided in patients with a potential for elevated intracranial pressure (ICP) secondary to its tendency to increase cerebral metabolic rate, CBF, and ICP. Ketamine has been used safely in both humans and animals with known susceptibility to malignant hyperthermia.
4
Q
4. An otherwise healthy 27 year old patient presents for an open repair of an ankle injury under general anesthesia with controlled ventilation. At the time of surgical incision a tourniquet placed on the thigh was inflated. After 90 minutes the tourniquet is deflated. Which of the following is MOST likely to increased immediately after deflation of the tourniquet? A. Core temperature B. End-tidal carbon dioxide (PETCO2) C. Arterial pH D. Systemic arterial pressure
A
- B end tidal carbon dioxide. Orthopedic surgeons commonly use an occlusive pneumatic tourniquet on an extremity in an effort to decrease blood loss and provide a dry surgical field. Typically the extremity is exsanguinated prior to tourniquet inflation, thereby producing an increase in central blood volume. With the tourniquet inflated, the extremity becomes ischemic and cools. Deflation of the tourniquet is associated with the following changes: 1. Increased end-tidal carbon dioxide (PETCO2). Products of metabolism including CO2, accumulate in the cells of the ischemic extremity. With reperfusion there is a transient increase in CO2 elimination. An increase in minute ventilation generally occurs in spontaneously ventilating patients. Assuming there is no increase in respiratory rate or tidal volume in patients whose ventilation is controlled, there will be a transient increase in PETCO2 when the tourniquet is released. 2. Decreased core temperature. During tourniquet inflation the temperature of the ischemic extremity tends to decrease. With tourniquet deflation, reperfusion of the extremity increases the temperature of the extremity, but core temperature tends to decrease. 3. Acidosis. Tourniquet inflation causes ischemic of the limb with conversion to anaerobic metabolism. With release of the tourniquet and reperfusion, venous blood returning from the extremity has mixed metabolic and respiratory acidosis, which results in a decreased arterial pH. 4. Decreased systemic blood pressure. Reperfusion of the previously ischemic extremity results in a decrease in systemic arterial pressure. This change is generally attributed to a combination of decreased SVR and increased venous capacitance (due to mechanical effects of removal of the tourniquet) and decreased myocardial ocntractility (attributed to the release of vasoactive substances from the ischemic extremity). 5. Hypoxemia. Tourniquet deflation has the potential to release emboli (thrombus, fat, marrow, and potentially air) into the central circulation with a resultant pulmonary embolism. (In fact, TEE documents embolization to the central circulation to be a common occurrence with tourniquet release). Depending on the magnitude of the embolism, hypoxemia may occur.
5
Q
- Which statement about the oculocardiac reflex is MOST likely true?
A. It is reliably prevented by prophylactic administration of anticholinergic agents
B. It is reliably prevented by a retrobulbar block
C. Atrioventricular block is the most common associated dysrhythmia
D. It is more likely to occur with sudden rather than gradual traction on an extraocular muscle
A
- D. It is more likely to occur with sudden rather than gradual traction on extraocular muscle. The oculocardiac reflex (OCR) is a reflex that can occur during manipulation of ocular structures in patients of all ages, although it is more common in the pediatric population. The most common sign of the OCR is sinus bradycardia. Other cardiac rhythms that have been reported in association with the OCR include junctional rhythm, atrioventricular block, ventricular bigeminy, and asystole. The reflex can be initiated by pressure on the globe, traction on the extraocular muscles, and manipulation of the conjunctiva. The OCR has also been reported in patients with enucleated orbits and during the performance of the retrobulbar block. The OCR is more likely to occur with sudden rather than gradual traction. THE OCR is described as fatigable; that is, continued traction results in a diminished response. The OCR has afferent and efferent limbs. The afferent limb is mediated by the trigeminal nerve (cranial nerve V). The afferent pathway travels through the ciliary ganglion with the opthalmic branch of the trigeminal nerve to the gasserian ganglion. The efferent limb is mediated by the vagus nerve (cranial nerve X). The OCR may occur during local or general anesthesia irrespective of the anesthetic depth. Hypercapnia and hypoxemia may increase the likelihood of the OCR occuring.The initial treatment of the dysrhythmias due to OCR is to stop stimuli to all ocular structures. This will usually abolish the reflex and return the heart rate to baseline. If this is ineffective, anticholinergic administration or (rarely) cardiac resuscitation may be required. Anticholinergics have been shown to reduce the risk of developing bradycardia due to OCR. Retrobulbar blocks, after the placement, have also been shown to reduce the risk of the OCR. No technique has been demonstrated to consistently prevent the OCR.
6
Q
6. Which of the following is MOST likely to be present in a patient with myotonic dystrophy? A. Atrioventricular block B. Aortic insufficiency C. Hypercortisolism (Cushing syndrome) D. Myalgias
A
- A. AV block. Myotonic dystrophy, a neuromuscular disorder inherited in an autosomal dominant pattern, is characterized by normal muscle contraction followed by inability to achieve muscle relaxation in a normal time frame. The estimated prevalence of myotonic dystrophy is from 2 to 5 per 100,000. Weakness, with wasting of distal muscles, is the most common initial presentation; myotonic dystrophy is an exception to the generalization that neuropathies present with distal manifestations and myopathies present with proximal manifestation. Myotonia is not painful, and patients with myotonic dystrophy do not report myalgias. The genetic defect of myotonic dystrophy has been located on chromosome 19; the pathophysiology is distinguished by abnormal chloride conductance and reduced sodium channel inactivation of muscle fibers. Cardiovascular manifestation of myotonic dystrophy are common. Preferential involvement of the conduction tissues with fibrosis and fatty degeneration results in rhythm disturbances as the primary cardiovascular manifestation. An abnormal ECG is reported in more than 60% of patients diagnosed with myotonic dystrophy. Progression of abnormalities is cause to recommend that these patients undergo an annual ECG. Q waves without evidence of myocardial infarction are commonly reported. Recent guidelines have recommended that asymptomatic conduction abnormalities in patients with neuromuscular diseases, including myotonic dystrophy, receive special consideration for prophylactic pacemaker implantation. In france, where this is common practice, up to 50% of patients with myotonic dystrophy have pacemakers placed. Although the exact mechanism of sudden death related to dysrhythmia is unknown, the leading theory is that asystole or ventricular fibrillation results from disease in hte distal conducting system that prevents an appropriate escape rhythm when AV block occurs. The most common cause of death is pneumonia; dysrhythmias are the second leading cause of death in this patient population. It has been reported that general anesthesia is associated with an increased risk for the development of dysrhthmias, including AV block. Consideration should be given to placement of a temporary pacemaker in patients with myotonic dystrophy who have a high degree AV block. Other cardiac problems associated with myotonic dystrophy include cardiomyopathy ( with associated lefet and right ventricular dysfunction) and mitral valve prolapse; there is no known associated between myotonic dystrophy and aortic insufficiency. Endocrine abnormalities are common in patients with myotonic dystrophy. Adrenocortical insufficiency, not Cushing syndrome, is associated with myotonic dystrophy. Addisonian crisis has been reported in infants with myotonic dystrophy. Diabetes is also commonly associated with myotonic dystrophy.
7
Q
7. In which of the following conditions is the mixed venous oxygen saturation (SvO2) MOST likely to increase? A. Fever B. Cyanide toxicity C. Cardiogenic shock D. Anemia
A
- B. Cyanide toxicity. Mixed venous blood is the term given to blood in the distal pulmonary artery. The oxygen saturation of mixed venous blood (SvO2) may be monitored by means of an “oximetric” pulmonary artery catheter or by analysis of a sample. A sample of mixed venous blood may be obtained by aspirating blood from the distal port of the pulmonary artery catheter. Blood must be aspirated slowly to minimize mixing of the oxygenated blood, which would artificially increase the mixed venous oxygen saturation. The normal value for SvO2 is between 68% and 75%. The mixed venous oxygen saturation is determined by the arterial oxygen saturation, oxygen consumption, cardiac output, and hemoglobin in the following equation:
SvO2 = (SaO2 - VO2)/ (CO x Hgb).
VO2 = oxygen consumption. The question of what most likely increases SvO2 may be answered by fitting the proposed change into the relationship with the following results: Cyanide toxicity will decrease the VO2 (because oxygen cannot be used in the mitochondrial electron transport chain), leading to an increase in SvO2. A low cardiac output in the setting of cardiogenic shock will result in a decrease in SvO2. In the abscence of compensatory increase in cardiac output, anemia will produce a reduction in SvO2. Increased temperature will result in an increased oxygen consumption, which will cause a decrease in SvO2.
8
Q
- A 52 year old man is intubated and ventilated in the ICU after repair of a thoracoabdominal aortic aneurysm. Which of the following will MOST effectively decrease his risk of VAP?
A. elevation of the head of the bed more than 30 degrees
B. Administration of prophylactic antibiotics
C. nasal intubation
D. changing of the ventilator circuit daily
A
- A. elevation of the head of bed 30%. VAP is a parenchymal lung infection manifesting more than 48 hours after initiation of mechanical ventilation. It occurs in 10-25% of patients intubated for longer than 48 hours and is one of the most commonly acquired infections in the ICU patients. Prevention of VAP has been a focus of quality initiatives in the ICU. The mechanisms of VAP include: antibiotic therapy and antacid therapy alter the milieu of the mouth and stomach. Oropharyngeal and gastric colonization by pathogenic, gram negative organisms, development of subglottic secretion pool, aspiration of pooled secretions around the cuff of the tracheal tube, aerosolization of the aspirated secretion during the inspiratory phase of the ventilator cycle, dispersion of the aerosolized bacteria into the lung, development of VAP. Methods to decrease the risk of VAP include: use of semirecumbent position (elevation of the head of bed greater than 30 degrees). This decreases the chance of aspiration associated with nursing a ventilated patient in the supine position. Use of noninvasive ventilation, thus avoiding tracheal intubation, which is associated with bypassing the usual oropharyngeal protective mechanisms. Less frequent change of ventilator circuitry. (It has been demonstrated that ventilator circuit changes more often than every 7 days are associated with a higher risk of VAP.) staff hand washing, regular patient oral hygiene and teeth cleaning. decrease in length of mechanical ventilation (eg by means of sedation holidays). oral (versus nasal) intubation. nasal intubation increases the risk of sinusitis and VAP.
9
Q
9. A 63 year old man developed postoperative acute renal failure and required placement of a large-bore dialysis catheter in the jugular vein. The renal function improved and dialysis is no longer required. Which of the following tis the MOST appropriate maneuver to use during removal of the catheter? A. Reverse Trendelenburg position B. Valsalva maneuver C. Deep inspiration D. Diuresis
A
- B. Valsalva maneuver. Vascular air embolism (VAE) may occur during insertion or removal of a central venous catheter. Certain situations may increase the risk of VAE during these procedures and should be avoided. These include: failure to occlude the end of the catheter, deep inspiration, hypovolemia, upright or reverse Trendelenburg position. The increased risk associated with some of these maneuvers results from either a reduction in CVP or an increase in negative intrathoracic pressure. Both of these conditions promote air entrainment. For instance, deep inspiration during CVP removal will increase the negative intrathoracic pressure. Hypovolemia, which would result from diuresis, and the reverse Trendelenburg position will both lead to a decrease in CVP. Adhering to certain recommendations for the removal of central venous catheters may help decrease the risk of VAE associated with this procedure. Many of these maneuvers are aimed at increasing the CVP. These include use of the Valsava maneuver as well as the Trendelenburg position. Synchronization of catheter removal with active exhalation might also be beneficial by allowing the procedure to take place during a period of positive intrathroacic pressure. Air entrainment via a persistent catheter tract is another concern, especially with large bore catheters. Therefore, occlusion of the catheter site after removal is also important to minimize the risk of VAE.
10
Q
- Which statement comparing the use of drug-eluting coronary artery stents with use of bare-metal stents is MOST likely true?
A. Patients receiving a drug-eluting stent have a lower risk of MI at 12 months
B. Patients receiving a drug-eluting stent have a higher risk of late thrombosis
C. The purchase prices for drug eluting and bare-metal stents are comparable.
D. Patients receiving a drug-eluting stent have a 50% lower risk of death in the first five years following stent placement
A
- B. drug eluting stent has a higher risk of late thrombosis. It is important from a perioperative standpoint to understand the differences involved in the ongoing controversy surrounding coronary artery stenting. There are two commonly used types of stents: bare metal stents and drug-eluting stents. Drug eluting stents have a potent antiproliferative drug embedded into the nonresorbable polymer matrix covering the stent struts. These stents slowly extrude the drug in high concentrations to local tissue and inhibit neointimal hyperplasia that commonly occurs with vessel injury and is the most common cause of restenosis in patients with bare-metal stents. However, recently it has been reported that these drug-eluting stents markedly inhibit or delay endotheliazation of the stent struts. Patients with drug eluting stents are therefore at risk for thrombosis for longer time periods than those with bare metal stents and are particularly at risk if the dual antiplatelet therapy (commonly ASA and clopidogrel) is prematurely interrupted. Analysis of initial randomized studies comparing theh two types of stents indicated that a drug eluting stent resulted in a 3 to 4 fold reduction in restenosis at 12 months, but the risk of MI and death was not reduced. With the analysis of four year follow up data, stent manufacturers are now reporting higher rates of late thrombosis in patients receiving drug eluting stents than in pts receiving baremetal stents. According to these manufacturers, the late stent thrombosis is not associated with increased rates of MI or cardiac related death. In addition, this risk of late thrombosis may be counterbalanced by the reductions seen inn restenosis. There is also concern over the fact that initial studies of drug eluting stents involved uncomplicated coronary lesions and now these stents are being used in more complex coronary disease. Lastly a drug eluting stent costs approximately 3300 compared to $800 for a bare metal stent, andrecently the major cardiovascular societies have recommended that dual antiplatelet therapy be extended for at least one year; adding additional overall cost. Therefore the costs of a drug eluting stent are substantial compared with those of a bare metal stent. .
11
Q
11. Which of the following is the MOST likely contributor to development of a fire in the CO2 absorber when sevoflurane is administered? A. Desiccated absorbent B. Presence of Ca(OH)2 in the absorbent C. Low sevoflurane concentration D. Low fresh gas flows
A
- A. dessicated absorbent. Interactions of the anesthetics with CO2 absorbent can produce degradation of the anesthetic agent, which may ultimately lead to serious complications, including fire or carbon monoxide toxicity. Sevoflurane may interact with a strong base (KOH or NaOH) in the absorbent to produce an exothermic chemical reaction. Dessication of the CO2 absorbent makes the reaction more exothermic, producing temperatures within the CO2 canister as high as 400C. Melting of the CO2 canister, contained explosions, and fire within the breathing circuit have been reported. KOH causes significantly more degradation than NaOH, while Ca(OH)2 is not associated with degradation of sevoflurane. Most of these fires have occurred with the use of Baralyme, which contains more KOH than any other absorbent, although fire has also been reported with the use of soda lime. Fires associated with sevoflurane use can be prevented by using absorbents that contain no strong base. Baralyme which contains the most KOH has been removed from the market in the US. In addition, some soda lime formations have removed KOH although they still contain NaOH. If an absorbent containing a strong base is used, it is important that measures be taken to prevent use of desiccated absorbent. These include: turning off the fresh gas flow at the end of the day, changing the absorbent at regular intervals (eg, once a week), replacing absorbent if there is any suspicion of desiccation. Some commercially available absorbents are now available with color indicators that detect dessication, similar to the color indicator that designates depletion of the CO2 absorbing capacity. Low fresh gas flow rate has been associated with sevoflurane degredation to compound A but it is not associated with CO2 absorber fires. In fact, use of lower flows can help prevent absorbent desiccation. Low sevoflurane concentrations have not been implicated in sevoflurane-absorbent fires.
12
Q
12. Following massive red cell transfusion, the BEST initial therapy in treating trauma-associated coagulopathy is the early use of A. recombinant factor VIIa B. Fresh frozen plasma C. Desmopressin (DDAVP) D. Cryoprecipitate
A
- B. fresh frozen plasma. Red blood cell administration should be started early in the hypotensive bleeding patient. In massive transfusion all coagulation factors, including calcium and fibrinogen, as well as platelets are lost, consumed, or are less effective if the patient is hypothermic or acidotic. There are several cohort studies suggesting that outcome is improved with early administration of FFP and platelets. Administering 1 unit of FFP for every 1-2 units of PRBCs and 1 pooled, platelet apheresis pack (analogous to a six pack of platelets in earlier terminology) to ever 7.5 units of PRBCs may improve survival. Factor VIIa is approved by the FDA only for patients with hemophilia or factor VII deficiency. Off-label use of this factor in trauma has been successful in several case reports and case series in treating uncontrolled hemorrhage unresponsive to conventional blood component therapy. It augments thrombin generation and clot formation at the site of injury. In the only randomized, placebo-controlled, double blind study of blunt and penetrating trauma, patients were assigned to receive three injection of factor VIIa (200mcg/kg after 8 units of PRBCs, 100mcg/kg after 1 hour, and 100mcg/kg 3 hours later) or placebo. After 48 hours, the treatment group had received almost 4 fewer units of PRBCs, half the amount of FFP, and 1/3rd fewer units of platelets. In general, massive transfusion of blood products of 20 units or more was required in over 20% of placebo-treated patients compared to 6% of the pts treated with factor VIIa. Other benefits were a reduced incidence of ARDS (2% vs 12%) and multiple organ failure (3% vs 13%). The incidence of thromboembolic events was no different between the 2 groups (3% vs 4%). However, the Cochrane review on recombinant factor VIIa for its therapeutic use in uncontrolled hemorrhage found no difference in outcomes and complications except a trend toward reduced mortality. The main problem in evaluating the efficacy of this medication is that patient populations studied, the timing, and amount of factor VIIa use were heterogenous. Desmopressin may be used in the treatment of von Willebrand disease and uremic platelet dysfunction but is not the best initial therapy for coagulopathy associated with massive transfusion. Cryoprecipitate only contains factor VIII, factor XIII, fibronectin, and fibrinogen. In massive hemorrhage all coagulation factors are depleted.
13
Q
13. Mortality from preeclampsia is MOST commonly due to A. hepatic rupture B. intracerebral hemorrhage C. coagulopathy D. cardiomyopathy
A
- B. Intracerebral hemorrhage. Intracerebral hemorrhage is the most common cause of mortality from preeclampsia. HTN associated with preeclampsia can lead to ischemic or hemorrhagic strokes. Pts with preexisting cerebral aneurysms and AV malformations are at increased risk of rupture during pregnancy due to changes in blood volume, increases in cardiac output, vasodilation, and straining during labor. Although mortality associated with hepatic rupture is very high, it is an extremely rare complication in patients with preeclampsia. Isolated thrombocytopenia or HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) occur in certain subsets of patients with preeclampsia but are not the leading cause of mortality in this patient group. Disseminated intravascular coagulation is a very rare complication of preeclampsia. The prevalence of cardiomyopathy in parturients appears to be increasing and is becoming a more common cause of mortality in the pregnant population. However the majority of parturients who develop cardiomyopathy are not preeclamptic. Cardiomyopathy is not the most common cause of death in preeclamptic patients.
14
Q
- Which statement about characteristics common to all Mapleson circuits is MOST likely true?
A. Rebreathing is possible
B. Unidirectional valves direct gas flow
C. A carbon dioxide absorber is incorporated into the circuit
D. They can only be used for controlled ventilation
A
- A. Rebreathing is possible. Anesthetic circuits capable of permitting rebreathing have been classified as Mapleson types A through F, all of which can be used for either spontaneous or controlled ventilation. When describing the characteristics of each circuit, they are sometimes grouped as A;B;C; and D;E;F. Each circuit includes, at a minimum, a reservoir bag, reservoir tubing, a fresh gas inlet, and a mask. Most, but not all, include an adjustable pressure limiting (APL) valve. The circuits differ in the relationship of one component to the others. The performance (eg. efficiency) of each of these circuits with spontaneous or controlled ventilation is determined by these relationships. None of the Mapleson circuits incorporates either a carbon dioxide absorber or unidirectional valves to direct gas flow. In considering the performance of each type of Mapleson circuit, it is convenient to consider ventilation as consisting of an inspiratory phase, an expiratory phase, and an end-expiratory pause. Mapleson A: Spontaneous ventilation: exhaled gas, initially anatomic dead space gas (devoid of carbon dioxide) and then alveolar gas (containing carbon dioxide), enters the corrugated tubing and flows toward the reservoir bag where it mixes with fresh gas (which is continuously flowing into the reservoir bag). After the reservoir bag is full, subsequent exhaled (alveolar) gases exit through the APL valve. During inspiration the gas initially inspired will be alveolar gas from the volume between the patient and the APL valve. Subsequent inspired gas will come from the corrugated tubing and then the reservoir bag. As initially described, the volume of the corrugated tubing is approximately equal to the tidal volume. In this circumstance, the degree to which the reservoir bag contains exhaled gas (dead space or alveolar) is determined by the fresh gas flow rate - if the fresh gas flow rate is high, all exhaled gas will exit via the APL valve; if the fresh gas flow rate is low, some alveolar gas will be retained in the reservoir bag and rebreathing of carbon dioxide will occur. Controlled ventilation: no fresh gas flow enters the circuit during exhalation. Accordingly if the volume of exhaled gas exceeds the capacity of the corrugated tubing the reservoir bag will contain a mixture of dead space and alveolar gas. In most circumstances, the corrugated tubing will contain primarily or perhaps exclusively alveolar gas. With the onset of inspiration the first gas to enter the patient will be the alveolar gas contained in the corrugated tubing. When the pressure in the circuit exceeds the threshold of the APL valve, gas (both exhaled and fresh gas) will be exhausted from the circuit and the patient will receive a mixture of fresh and alveolar gases. Accordingly it is possible to use a Mapleson A circuit for controlled ventilation, this would not be a logical choice. Mapleson B and C: The mapleson B and C circuits differ from A circuit in having the fresh gas inflow located closer to the patient. The B and C circuits differ from one another by the length of the tubing between the patient and the reservoir bag. Neither one is used with any regularity in contemporary anesthesia practice. Mapleson D,E, and F: All of these circuits include a T piece (a 3 way connection between the fresh gas flow, the patient, and the corrugated tubing). Spontaneous ventilation: During exhalation fresh gas mixes with exhaled gas and flows through the corrugated tubing to the reservoir bag. During the expiratory pause, fresh gas flow continues to enter the circuit, displacing the fresh/exhaled gas toward the reservoir bag and APL valve. A combination of fresh gas and gas from the corrugated tubing will initially be inspired. With an adequate fresh gas flow rate, it is possible to prevent rebreathing. Controlled ventilation: essentially the same as spontaneous ventilation.
15
Q
15. Which of the following BEST describes the cycle (termination) trigger for pressure support ventilation (PSV)? A. Tidal volume B. Minimum flow rate C. Maximum pressure D. Inspiratory time
A
- B. Minimum flow rate. Pressure support ventilation is a mode of ventilation that is available on all modern ICU ventilators and becoming available on new generation gas machines. During pressure support ventilation, the ventilator cycles from inspiration to exhalation based on an operator defined minimum flow (usually a % of the pt’s peak inspiratory flow rate). During this type of ventilation, maximum flow occurs shortly after breath initiation and decreases throughout the inspiratory phase. Cycling to exhalation then occurs when this flow decreases to a preset minimum flow (commonly a % of the maximum flow). In pressure support ventilation, the tidal volume varies with each breath related to the compliance and resistance of the respiratory system and is not used to cycle the ventilator to exhalation. Like tidal volume, the inspiratory time also varies with each breath and does not cause the ventilator to cycle to exhalation. Although the maximum pressure limit is operator defined, it does not cause the ventilator to cycle to exhalation during a pressure-supported breath. Although ventilator manufacturers do not always strictly follow the traditional nomenclature, modes of ventilation are generally defined based on 4 characteristics (control, trigger, limit, and cycle variables). The control (or target) variable is the independent factor that is held constant during inspiration at the expense of the other factors. The trigger variable is the factor used to begin inspiration, usually when some preset value is reached and its sensitivity is set to determine the patient effort required to trigger inspiration. The limit variable is used to restrict the effect of inspiration. The cycle variable is used to end inspiration.
