The In Vivo Skills Laboratory in Anesthesiology Residency Training.

BACKGROUND: Anesthesiologists routinely perform high-risk procedures that are associated with permanent disability or death. Critical perioperative events require that the anesthesiologist perform procedures that are only used intermittently. Teaching these procedures is complicated by their infrequency and pressure to maximize operating room efficiency; therefore we created an annual 1-day anesthesiology skills lab as an innovative method of residency education. METHODS: Anesthetized pigs served as the educational platform for first-year anesthesiology residents to gain hands-on experience performing regional, thoracic, vascular, and difficult airway techniques. A 20-question test was administered pre- and post-lab to assess the effectiveness of our educational intervention. Participants evaluated the quality of the educational experience (1-poor to 5-excellent). RESULTS: First-year anesthesiology residents participated (n=70, 2008-2012). Residents' pre-test scores measured 50.3±2.6% (range 20-80). Following lab participation, their test scores signi ficantly improved to a mean of 84.2±1.9% (range 45-100, p<0.0001). Participants increased their knowledge and skills (mean 4.96±0.02), considered the skills lab to be a worthwhile educational experience (mean 4.99±0.01), and agreed that the lab should be repeated in the future (mean 5.00). CONCLUSIONS: In vivo labs confers educational benefits which are both perceived and self-reported by the participants and objectively demonstrated by marked improvements in their post-test scores. Animal models provide high-fidelity tactile learning, real-time physiological changes, and potential for complications which builds residents' familiarity and confidence with anesthesiology-related procedures and crisis events that would otherwise involve potential patient risk. Our lab is an enriching and well-received educational tool which promotes our goal of improving patient safety.

Right ventricular remodeling in restrictive ventricular septal defect.

Restrictive ventricular septal defect (rVSD) presents with little/no hemodynamic aberrations despite a patent septal defect. Clinically, these patients are observed with the hope that the defect will functionally close over time without the need for surgical repair and development of heart failure. Without evidence supporting a definitive therapeutic strategy, rVSD patients may have increased risk of a poor outcome. We tested the hypothesis that rVSD results in subclinical RV diastolic dysfunction and molecular remodeling. Five pigs underwent surgical rVSD creation. Echocardiography, hemodynamics, myocyte contractility experiments, and proteomics/Western blot were performed 6-weeks post-rVSD and in controls. *p<0.05. LV and RV hemodynamics in rVSD were comparable to controls. The tricuspid valve early/late diastolic inflow velocity ratio (TV E/A ratio) decreased from 1.6+/-0.05 in controls to 1.0+/-0.08* in rVSD, indicating RV diastolic dysfunction. rVSD RV myocytes showed abnormalities in contraction (departure velocity (Vd) -51%*, Vd time +55%*) and relaxation (return velocity (Vr) -50%*, Vr time +62%*). Mitochondrial proteins (fatty acid, TCA cycle) increased 2-fold*, indicating heightened RV work. Desmin protein upregulated 285%* in rVSD RV myocardium, suggesting cytoskeletal remodeling. rVSD causes RV diastolic dysfunction, myocyte functional impairment, and mitochondrial/cytoskeletal protein upregulation in our model. Desmin upregulation may hinder sarcomeric organization/relaxation, representing a key subclinical early marker for future RV dysfunction. TV E/A measurements are a non-invasive modality to assess rVSD patients for diastolic dysfunction. Translational research applications may lead to fundamental changes in the clinical management of rVSD by providing evidence for early repair of the defect.

Cytoskeletal remodeling of desmin is a more accurate measure of cardiac dysfunction than fibrosis or myocyte hypertrophy.

AIMS: Fibrosis and myocyte hypertrophy are classical remodeling parameters in heart failure (HF); however, an intriguing possibility is that myocytes undergo intracellular remodeling which decrease compliance, contributing to diastolic dysfunction. The most obvious candidates are cytoskeletal proteins. The cytoskeletal protein desmin reinforces the sarcomeres, enabling force generation. As a contributor to sarcomere performance, desmin may represent a better appraisal of dysfunction than fibrosis or myocyte hypertrophy. MAIN METHODS: HF was induced in sheep via coronary microembolization. Echocardiography was performed at baseline, 4-, and 12-months in HF. Desmin, fibrosis, and myocyte hypertrophy from infarcted LV posterior and noninfarcted LV anterior walls were measured using Western blot, immunohistochemistry, and digital image analysis. Multivariate regression analysis was performed, providing structure/function mechanisms. *p<0.05. KEY FINDINGS: EF decreased from 55% to 24%*. LV end-diastolic area (LVEDA) increased 123%* at month-12. Fibrosis increased only in posterior LV whereas myocyte hypertrophy increased in both LV posterior and LV anterior regions but only at month-12. Desmin content progressively increased 121% at month-4 and 182%* at month-12 in both LV posterior and anterior walls. Multivariate linear regression (beta coefficient standardization) demonstrated that desmin was a much better predictor of EF (beta=-0.38*) and LVEDA (beta=0.58*) than fibrosis or myocyte hypertrophy. SIGNIFICANCE: Desmin, fibrosis, and myocyte hypertrophy are temporally and spatially heterogeneous in HF. Desmin content more accurately correlated with remodeling than fibrosis or myocyte hypertrophy, suggesting that intra-myocyte responses, likely related to mechanical stretch, are better predictors of LV function and may represent novel targets for therapeutic intervention.

Left ventricular assist device support induces acute changes in myocardial electrolytes in heart failure.

The regulation of myocardial electrolyte concentrations is critical to proper cardiac function. Myocardial ischemia is associated with deranged ion transport. Left ventricular assist device (LVAD) therapy improves myocyte bioenergetics in chronic heart failure (CHF), which may manifest as electrolyte alterations; however, rapid electrolyte shifts may place critically ill patients at risk for arrhythmias upon initiation of LVAD support. We examine the effect of incremental increases in LVAD support on acute changes in myocardial arteriovenous electrolytes in CHF. CHF was induced in sheep via coronary microembolization. Four months later, sheep underwent acute LVAD implantation. LVAD support was incrementally increased (0%, 25%, 50%, 75% support). Paired arterial and coronary sinus blood samples were obtained at each increment and analyzed for K+, Ca2+, and Na+ concentrations. Arteriovenous electrolyte concentrations (mmol/l) were inverted in CHF before LVAD support: K+ (-0.08), Ca2+ (-0.04), and Na+ (0.04). These imbalances were corrected within 20 minutes and with as little as 25% LVAD support: K+ (0.06), Ca2+ (0.012), and Na+ (-0.80). The arteriovenous differences further widened as LVAD support was increased. In conclusion, LVAD support in CHF induces acute alterations in myocardial electrolytes. Rapid shifts myocardial arteriovenous electrolyte balances during LVAD support may in part explain the incidence of post-LVAD arrhythmias observed clinically in humans.

Dexmedetomidine for conscious sedation in difficult awake fiberoptic intubation cases.

Currently used methods of sedation for fiberoptic intubation such as benzodiazepines, propofol, or opioids have their limitations. Dexmedetomidine (DEX) is a selective alpha-2 adrenergic agonist that has been used clinically for its sympatholytic, analgesic, and sedative properties. We report on 4 patients with particularly difficult airways who underwent successful awake fiberoptic intubation with DEX. Dexmedetomidine was used to provide a moderate level of conscious sedation without causing respiratory distress or hemodynamic instability during fiberoptic intubation.

Uvular edema secondary to snoring under deep sedation.

A 57-year-old male with a documented history of obstructive sleep apnea with loud snoring received deep intravenous sedation with midazolam, fentanyl, ketamine, and propofol infusion and a left interscalene brachial plexus nerve block for a left biceps tendon repair. Loud snoring during the case was noted. On the second postoperative day, he was observed to have significant uvular edema. After due consideration of the various elements in the differential diagnosis, it was concluded that negative pressure trauma from deep snoring during the sedation was the most likely etiology.

Hemodynamic stability during labor and delivery with continuous epidural infusion.

CONTEXT: Epidural anesthesia for labor pain is frequently complicated by maternal hypotension. OBJECTIVE: To test whether continuous epidural infusion (CEI) of local anesthetic, without bolus administration, lowers the incidence of hypotension in parturient patients. METHODS: In a single-blind clinical study, subjects were randomly assigned to CEI-only (10 mL/h of 0.2% ropivacaine hydrochloride without bolus) or control (10 mL of 0.2% ropivacaine hydrochloride per hour with 10-mL bolus) epidural dosing groups. The incidence of hypotension (20% decrease in systolic blood pressure or mean arterial pressure (MAP), systolic blood pressure lower than 100 mm Hg, or MAP lower than 65 mm Hg) was recorded for 2 hours after dosing. Statistical analysis included a 2x2 chi(2) analysis, the Fisher exact test, and paired two-tailed t tests. RESULTS: Fifty subjects were studied, with 25 randomly assigned to each study group (CEI-only vs control). Baseline blood pressure was not different between groups (CEI-only, 127 [11]/77 [8.7] mm Hg; control, 131 [14]/78 [2]). The incidence of hypotension was lower in the CEI-only group than in the control group (5 [20%] vs 15 [60%]; P=.009), with intervention required in 1 (20%) of 5 CEI-only subjects and 7 (47%) of 15 control subjects. Sensory block reached the T10 dermatome in 54.4 (18) minutes in the CEI-only group and 38 (24) minutes in the control group (P=.04). Pain scores and maternal and fetal pulse rates were not different between groups. Analgesic supplementation (250 microg of epidural fentanyl) was used more frequently in the CEI-only group (72% vs 32%; P=.01), without adverse effects. CONCLUSIONS: Continuous epidural infusion of 0.2% ropivacaine hydrochloride without bolus administration reduces the incidence of hypotension by 67% and is safer than traditional bolus dosing for routine labor. This method requires further study in high-risk patients, including those with preeclampsia and cardiovascular disease.

Partial support with a centrifugal left ventricular assist device reduces myocardial oxygen consumption in chronic, ischemic heart failure.

BACKGROUND: Left ventricular assist devices (LVAD) are increasingly used for heart failure (CHF); however, the level of optimal support has not been elucidated. We hypothesize that partial LVAD support in an ovine model of microinfarction-induced CHF significantly reduces left ventricular myocardial oxygen consumption (LVVO2). METHODS AND RESULTS: Microembolization of the circumflex coronary artery was used to induce CHF in 5 sheep (ejection fraction 28 +/- 2%). Four months later, animals underwent implantation of a centrifugal LVAD. LVAD flow was incrementally increased from 0% (baseline) to 25%, 50%, and 75% support of the LV. LVVO2 and stroke work (SW) were calculated at each increment. At baseline, LVVO2 (microL/100 g LV/beat) measured 43.2 +/- 3.4. LVVO2 decreased to 26.5 +/- 8.2,* 20.3 +/- 8.9,* and 12.6 +/- 6.3* at 25%, 50%, and 75% support (*P < .05). SW (mm Hg/mL) measured 1933.0 +/- 275.7 at baseline and decreased to 1588.0 +/- 204.1, 1181.0 +/- 157.2,* and 764.5 +/- 171.7* at 25%, 50%, and 75% support. Cardiac output, heart rate, and left main coronary artery blood flow were unaffected with partial support. CONCLUSION: Complete support with a centrifugal LVAD is not necessary for achieving significant reductions in LVVO2 . Partial support of as little as 25% significantly reduces LVVO2 in CHF through comparatively minor reductions in cardiac work. This is the first study to examine partial LVAD support in a CHF model.

Regional anesthesia techniques for the lower extremity.

This article focuses on regional anesthesia for orthopedic procedures of the lower extremity.

Selective microembolization of the circumflex coronary artery in an ovine model: Dilated, ischemic cardiomyopathy and left ventricular dysfunction.

BACKGROUND: Ventricular remodeling often occurs after myocardial infarction, yet the natural history remains unpredictable because of the chronicity of the process and therapeutic interventions involved. We induced cardiac dysfunction in an ovine model via selective microembolization of the circumflex coronary artery (LCx) to test the hypothesis that ventricular remodeling progresses following coronary microembolization for up to 24 months. Methods and results Sheep underwent weekly selective microembolization of the LCx until left ventricular ejection fraction stabilized <35% for 2 consecutive weeks. In a subgroup carried out to 4 months, the end-systolic pressure-volume relationship slope decreased from 2.3+/-0.6 (baseline) to 1.3+/-0.5 at month 4 (P<.05). In a second group, echocardiography at 24 months, the ejection fraction decreased from 51+/-3% (baseline) to 25+/-2% (month 5) (P<.05) and stabilized through month 24 (23+/-5%, P<.05), whereas left ventricular end-systolic area and left ventricular end-diastolic area increased by 222% and 98%, respectively, through month 24. CONCLUSIONS: Selective microembolization of the LCx induces left ventricular dysfunction followed by dilated, ischemic cardiomyopathy, which continues to progress for up to 2 years despite stabilization of left ventricular ejection fraction. This model of ventricular remodeling secondary to microinfarction may be a useful experimental platform for large animal heart failure investigations.

Neuroprotection is associated with beta-adrenergic receptor antagonists during cardiac surgery: evidence from 2,575 patients.

OBJECTIVE: To determine the impact of perioperative beta-adrenergic receptor (betaAR) antagonist administration on neurologic complications. DESIGN: Observational database analysis. SETTING: A clinical investigation at a single tertiary academic medical center. PARTICIPANTS: Elective coronary artery bypass graft surgical patients operated on in the period 1994-1996. INTERVENTIONS: Patients were divided into 2 groups: (1) patients given betaAR antagonist-blocking drugs in the perioperative period, including during operation, and (2) patients not given betaAR antagonists. MEASUREMENTS AND MAIN RESULTS: betaAR antagonist use in 2,575 consecutive patients undergoing coronary artery bypass graft surgery (1994-1996) was determined using the Cardiovascular Database and Anesthesia Information System Database. Outcome variables were postoperative stroke, coma, and transient ischemic attack. Of patients, 113 (4.4%) had postoperative neurologic complications, including stroke (n = 44), coma (n = 12), and transient ischemic attack (n = 3). Of patients, 2,296 (89%) received perioperative betaAR antagonist therapy, and 279 (11%) did not. Adverse neurologic events occurred in 3.9% (n = 90) of patients who received perioperative betaAR antagonists and 8.2% (n = 23) of patients who did not receive betaAR antagonists (odds ratio, 0.45; 95% confidence interval, 0.28 to 0.73; p = 0.003, unadjusted.) Severe neurologic outcomes (stroke and coma) occurred in 1.9% (n = 44) of patients who received betaAR antagonists and 4.3% (n = 12) of patients who did not receive betaAR antagonists (odds ratio, 0.43; 95% confidence interval, 0.23 to 0.83; p = 0.016). CONCLUSION: Use of beta-adrenergic antagonists was associated with a substantial reduction in the incidence of postoperative neurologic complications. A prospective randomized trial is needed to verify this potentially important neuroprotective strategy in cardiac surgery.

Anesthesia for foot and ankle surgery.

Regional anesthesia (RA) is the anesthetic of choice for all foot and ankle surgery. Advances in anesthetic equipment and techniques have made peripheral nerve blocks the perfect anesthetic technique for these patients, who should be educated about them in their surgeon's office. The anesthetic alternative of choice is, in the authors' opinion, a neuraxial (i.e. spinal or subarachnoid) technique, rather than a general anesthesia (GA). GA has a higher morbidity and complication rate compared to RA. Performance of a peripheral nerve block, or PNB, requires proper training, equipment, and support personnel in order to handle any and all complications, including general anesthesia.