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Biomedical subjects

J A Kline

Publications and source records attributed to J A Kline.

At least 37 records · Page 2Linked to original sources
PubMed2000

Alveolar dead space as a predictor of severity of pulmonary embolism.

OBJECTIVE: To determine whether the alveolar dead space volume (V(D)alv), expressed as a percentage of the alveolar tidal volume (V(D)alv/V(T)alv), can predict the degree of vascular occlusion caused by pulmonary embolism (PE). METHODS: Fifty-three subjects with suspected PE were prospectively studied. Pulmonary embolism was diagnosed in 33 by high-probability ventilation/perfusion (V/Q) scan (n = 19) or by pulmonary arteriography (PAG, n = 14). Pulmonary embolism was excluded by PAG in 20 subjects. The V(D)alv/V(T)alv was determined from volumetric capnography and arterial blood gas analysis, which permits measurement of the physiologic dead space, V(D)phys (mL) = [(PaCO2 - PeCO2)/PaCO2]. tidal volume. Airway dead space (V(D)aw) was subtracted to yield the alveolar dead space [(V(D)phys - V(D)aw) = V(D)alv (mL)]; the percentage of alveolar volume occupied by alveolar dead space per breath = V(D)alv/V(T)alv x 100%. Percentage perfusion defect was determined from V/Q scans by a radiologist blinded to other data. Regression analysis was performed to show correlation between V(D)alv/V(T)alv and defect on V/Q scan or systolic pulmonary arterial pressure (SPAP). RESULTS: For subjects with PE, the mean perfusion defect on lung scan was 38 +/- 22%; the mean V(D)alv = 208 +/- 115 mL, V(T)alv = 452 +/- 251 mL, and V(D)alv/V(T)alv = 43 +/- 18%. Regression of V(D)alv/V(T)alv vs perfusion defect yielded r2 = 0.41. Regression of V(D)alv/V(T)alv vs pulmonary artery pressures yielded r2 = 0.59. For subjects without PE, V(D)alv/V(T)alv = 27 +/- 14% and V(D)alv = 89 +/- 66 mL. CONCLUSIONS: The V(D)alv/V(T)alv correlates with the lung perfusion defect and the pulmonary artery pressures in subjects with PE. These findings show the potential for V(D)alv/V(T)alv to quantify the embolic burden of PE.

Adult↗
PubMed2000

Utility of lower extremity venous ultrasound scanning in the diagnosis and exclusion of pulmonary embolism in outpatients.

STUDY OBJECTIVE: Emergency physicians frequently rely on normal findings from a lower extremity venous ultrasound examination as a method to decrease the probability of pulmonary embolism (PE) in outpatients with a nondiagnostic ventilation-perfusion lung scan (V/Q scan). The objective of this study was to evaluate the diagnostic utility of bilateral lower extremity venous ultrasound scanning in the diagnosis of PE in emergency department patients with a low-, moderate-, or indeterminate-probability (nondiagnostic) V/Q scan. METHODS: This prospective, 2-center, descriptive study was conducted at the EDs of 2 large teaching hospitals. From an initial cohort of 570 nonreferred outpatients, a convenience sample of 156 patients who had both a nondiagnostic V/Q scan and a lower extremity venous ultrasound scan performed was selected as the study population. The sensitivity and specificity for a single lower extremity venous ultrasound scan and the posttest probability of PE were determined for the study population. RESULTS: In the study population, the best-case sensitivity of the lower extremity venous ultrasound scan for PE was 54% (95% confidence interval [CI] 37% to 71%) and the specificity was 98% (95% CI 94% to 100%). The likelihood ratio of a positive test result was 27. The likelihood ratio of a negative test result was 0.49, yielding a lowest possible posttest probability of PE of 12% (95% CI 6% to 17%). CONCLUSION: This study demonstrates that the combination of a nondiagnostic (low, moderate, or indeterminate) V/Q scan plus a single negative result from lower extremity venous ultrasound examination, even in a best-case scenario, does not exclude the diagnosis of PE.

Adult↗
PubMed1999

Insulin-glucose as adjunctive therapy for severe calcium channel antagonist poisoning.

CASE REPORT: This case series documents the clinical courses of 4 patients after verapamil overdose and 1 patient after amlodipine-atenolol overdose. All subjects had hypodynamic circulatory shock (hypotension, bradycardia, and acidosis) that was not adequately responsive to conventional treatment. After initiation of insulin-dextrose infusion, the hemodynamic status of all 5 patients stabilized and all patients survived. Plasma drug concentrations are reported for all cases and verapamil levels were extremely high in 2 patients (3710 ng/mL and 3980 ng/mL). However, because patients were not treated according to a standard protocol, each patient received variable other supportive measures and inotropic agents, and the infusion rates of insulin were variable among patients. This report provides preliminary evidence toward a larger trial of insulin-dextrose to treat hypodynamic shock from calcium channel blocker overdose.

Adolescent↗
PubMed1999

Large-pore hemodialysis in acute endotoxin shock.

OBJECTIVE: This study was undertaken to test the hypothesis that hemodialysis with a large-pore membrane would improve heart function during acute endotoxin shock. SETTING: Large animal laboratory. DESIGN: Eighteen mongrel dogs were instrumented to measure left ventricular maximum end-systolic elastance (left ventricular maximum elastance at end systole), cardiac output, circumflex artery blood flow, and myocardial mechanical efficiency (CO x MAP/MVO2, where CO is cardiac output, MAP is mean arterial pressure, and MVO2 is myocardial oxygen consumption). Plasma catecholamine concentrations were determined by high-performance liquid chromatography. Endotoxin shock was induced by infusing 5.0 microg/kg/min of Escherichia col 0127:B8 endotoxin in the portal vein for 60 mins, followed by 2.0 microg/kg/min of constant infusion. Control dogs (n = 6) received 4.0 mL/kg/min of saline; hemodialysis dogs (n = 6) underwent venovenous hemodialysis in 50-min intervals using a polysulfone filter (1.2 m2; mean pore size, 0.50 nm; blood flow rate, 400 mL/min; ultrafiltrate, "zero-balanced"); shams (n = 5) were treated identically to hemodialysis dogs, except that no convective dialysis was performed. A fourth group (n = 6) was treated with dopamine (5.0-7.0 microg/kg/min, optimal dose for contractile increase based on dose-response studies). MEASUREMENTS AND MAIN RESULTS: After 2 hrs of treatment, left ventricular maximum elastance at end systole increased and was unchanged in controls (30 +/- 5 mm Hg/mm) and shams (24 +/- 6 mm Hg/mm) compared with basal control. Hemodialysis treatment increased contractility (53 +/- 4 mm Hg/mm), as did dopamine treatment (54 +/- 7 mm Hg/mm). Endotoxin shock reduced mechanical efficiency to 45% of basal control; with hemodialysis treatment, left ventricular efficiency returned to 64% of basal control measurement, compared with 49% with dopamine treatment. During treatment, myocardial glucose uptake was increased with hemodialysis compared with other groups. No difference was observed among groups for left ventricular end-diastolic pressures or dimensions, or catecholamine concentrations. CONCLUSIONS: Large-pore hemodialysis increased left ventricular contractility to a similar degree as dopamine and provided a marginal improvement in myocardial glucose uptake and mechanical efficiency.

Acute Disease↗
PubMed1999

Pulmonary gas exchange during intramedullary fixation of femoral shaft fractures.

BACKGROUND: This study was undertaken to determine if the alveolar dead space fraction (Vd/Vt) or the alveolar-arterial oxygen gradient (A-a DO2) increased during intramedullary fixation of femoral shaft fractures. METHODS: Fifty hemodynamically stable patients with femur fractures were prospectively enrolled. Three serial measurements of Vd/Vt and A-a DO2 were obtained immediately before femoral nailing (Pre), 30 minutes after nailing (+30), and 120 minutes after nailing (+120). Vd/Vt was determined by simultaneously measuring PaCO2 and the steady-state end-tidal CO2 (PetCO2), where Vd/Vt = (1 - PetCO2/PaCO2). RESULTS: Vd/Vt before nailing was 0.09 +/- 0.09 (mean +/- SD); at +30 and +120, Vd/Vt was 0.10 +/- 0.06 and 0.08 +/- 0.07, respectively (p > 0.2; paired t test, both time points). A-a DO2 before nailing was 84 +/- 85 mm Hg, and it did not change significantly at +30 (89 +/- 69 mm Hg; p = 0.51 vs. Pre; paired t-test) or at +120 (51 +/- 45 mm Hg). No difference in data was found with analysis by fracture classification or number of reamer passes. Vd/Vt and A-a DO2, however, were both significantly increased in patients with lung contusion (n = 6) before nailing, but neither measurement increased after nailing. One patient developed fat embolism (Vd/Vt of 0.35 at Pre and 0.31 at +120), and another patient experienced postoperative pulmonary thromboembolism (Vd/Vt increased from 0.06 at Pre to 0.17 at +120). CONCLUSION: The process of femoral nailing does not cause enough pulmonary embolization to alter pulmonary gas exchange as measured by Vd/Vt and A-a DO2. If Vd/Vt is increased preoperatively, the likelihood of subsequent pulmonary dysfunction secondary to either preoperative lung injury or fat embolism is increased.

Adult↗
PubMed1999

A comparison of resuscitation with packed red blood cells and whole blood following hemorrhagic shock in canines.

Resuscitation with crystalloid and packed red blood cells has for the most part replaced the use of plasma and whole blood in the initial treatment of hemorrhagic shock. The effects of such changes on cardiovascular function following hemorrhagic shock remain largely unexplored. We examined cardiovascular function in anesthetized canines subjected to severe hemorrhagic shock. Mongrel canines of either gender were anesthetized with isoflurane and instrumented for measurement of arterial pressure, cardiac output, coronary flow, and left ventricular pressure and volume for the determination of end systolic elastance (Ees). Following a 30-min stabilization period, blood was rapidly removed to induce fixed pressure (mean arterial pressure = 35 mmHg) hemorrhagic shock for 90 min or until an arterial lactate of 7.0 mM was achieved. Animals were then resuscitated with 2/3 of the shed volume as lactated Ringer's and an equal volume of either whole blood (WB, n = 8) or packed red blood cells (PRBC, n = 10) resuspended in lactated Ringer's (LR) solution to replace expressed plasma volume. PRBC resuscitated dogs showed lower values of mean arterial pressure, cardiac output, rates of ventricular contraction and relaxation and myocardial work. Increasing the maintenance infusion rate of LR (10 mL/kg/h) following PRBC infusion normalized mean arterial pressure, but not other indices of cardiovascular function. Thus, WB, but not PRBC resuscitation restores normal myocardial function during resuscitation from severe hemorrhagic shock.

Animals↗
PubMed1999

Heart function after severe hemorrhagic shock.

OBJECTIVE: Test whether brief deep hemorrhagic hypotension or prolonged moderate hemorrhagic hypotension impairs intrinsic heart function. METHODS: Pentobarbital-anesthetized, non-anticoagulated rats were cannulated via the carotid artery. This study focuses on three main groups: 1) hemorrhage to a mean arterial blood pressure (MAP)=25 mm Hg for 1 h (1 h severe shock), 2) hemorrhage to MAP=40 mm Hg for 3 h (3 h moderate shock), 3) no hemorrhage (control). Hearts were either freeze-clamped in-situ for tissue analysis (n=6 per group) or were removed to study in vitro cardiac function and efficiency using a working heart perfusion (n=12 per group, glucose (11 mM)/palmitate (0.4 mM), 3% BSA buffer). Following perfusion, hearts were freeze-clamped and analyzed for free CoA, acetyl-, succinyl-, and malonyl-CoA, ATP content and for TNF-alpha content. RESULTS: Isolated working hearts obtained following 1 h of severe shock generated 20% less hydraulic work than hearts obtained from control rats or rats subjected to 3 h of moderate shock. The cardiac efficiency (work/O2 consumption) was also significantly reduced with 1 h severe shock (0.76 +/- 0.07 after 15 min perfusion) versus control (0.96 +/- 0.06) or 3 h prolonged shock (1.10 +/- 0.09). Myocardial Co-A ester, ATP and TNF-alpha concentrations were not different between control and shocked hearts, although TNF-alpha concentrations increased significantly in all hearts during ex vivo perfusion. CONCLUSIONS: Depth of hypotension is more important than duration in causing intrinsic cardiac dysfunction. This post-hemorrhagic cardiac dysfunction is not a result of substrate limitation to the heart, nor myocardial TNF-alpha accumulation, but is more likely a result of impaired transfer of energy from molecular oxygen into external cardiac work.

Adenosine Triphosphate↗
PubMed1999

Research fundamentals: V. The use of laboratory animal models in research.

Animal research has provided important information about many aspects of the pathophysiology of human disease. Well-performed animal studies can determine the potential benefit of many proposed therapeutic interventions, and experimental results from animal studies have served as the basis for many landmark clinical trials. Many animal research models are described in the research literature, and choosing the appropriate model to answer a research question can be a daunting task. Even more challenging is developing a new model when none of the existing systems are relevant to the proposed question. This article was prepared by members of the SAEM Research Committee to provide an overview of animal modeling. Important considerations in choosing, applying, and developing animal research models are outlined. Practical discussions of potential problems with animal models are also provided.

Animals↗
PubMed1999

Neural network analysis of the volumetric capnogram to detect pulmonary embolism.

BACKGROUND: Pulmonary embolism (PE) produces ventilation/perfusion mismatch that may be manifested in various variables of the volume-based capnogram (VBC). We hypothesized that a neural network (NN) system could detect changes in VBC variables that reflect the presence of a PE. METHODS: A commercial VBC system was used to record multiple respiratory variables from consecutive expiratory breaths. Data from 12 subjects (n = 6 PE+ and n = 6 PE-) were used as input to a fully connected back-propagating NN for model development. The derived model was tested in a prospective, observational study at an urban teaching hospital. Volumetric capnograms were then collected on 53 test subjects: 30 subjects with PE confirmed by pulmonary angiography or diagnostic scintillation lung scan, and 23 subjects without PE based on pulmonary angiography. The derived NN model was applied to VBC data from the test population. RESULTS: Seventeen VBC variables were used by the derived NN model to generate a numeric probability of PE. When the derived NN model was applied to VBC data from the 53 test subjects, PE was detected with a sensitivity of 100% (95% CI = 89% to 100%) and a specificity of 48% (95% CI = 27% to 69%). The likelihood ratio positive [LR(+)] for the VBC-NN test was 1.82 and the LR (-) was 0.1. CONCLUSION: This study demonstrates the feasibility of developing a rapid, noninvasive breath test for diagnosing PE using volumetric capnography and NN analysis.

Angiography↗
PubMed1998

Mechanisms of Ca2+ antagonism in imipramine-induced toxicity of isolated adult rat cardiomyocytes.

Classic explanations of cyclic antidepressant toxicity often focus on Na+ channel blockade; however, cyclic antidepressant toxicity often causes decreased myocardial contractile function. The present experiments first examine inhibition of cytosolic Ca2+ signals by imipramine. Second, the experiments test if alkalinization prevents the inhibition of Ca2+ signals. Cardiomyocytes from adult rat hearts were loaded with fura-2 dye, and intracellular calcium, [Ca2+]i, was quantified using ratio fluorescence techniques. Changes in [Ca2+]I were induced by electrical pacing, depolarization with KCl (84 mM), or treatment with caffeine (10 mM). Imipramine (10-30 microM) inhibited [Ca2+]i transients in electrically paced cardiomyocytes. Imipramine (7.5-30 microM) also inhibited Ca2+ signals in KCl depolarized cells. These inhibitory effects were similar to those observed with nisoldipine (100-2000 nM), a selective L-channel blocker. The rise in [Ca2+]i that was triggered with caffeine (10 mM) was not significantly changed by imipramine (30 microM). Inhibition of KCl-induced Ca2+ signals by imipramine was prevented by alkalinization of the medium (tris(hydroxymethyl)aminomethane, pH 7.6), but not by elevation of extracellular sodium to 170 mM. Alkalinization was effective in the presence of HOE642, a selective Na+/H+ (NHE) subtype 1 inhibitor. These data show that imipramine causes Ca2+ antagonism in heart cells which is independent of sarcoplasmic reticulum Ca2+, and that alkaline treatment prevents this Ca2+ antagonism rather than stimulating an alternate source of Ca2+ via Na+/H+ and subsequent Na+/Ca2+ exchange.

Animals↗
PubMed1998

Preliminary study of the capnogram waveform area to screen for pulmonary embolism.

STUDY OBJECTIVE: Acute pulmonary embolism (PE) increases alveolar dead space, which can dilute carbon dioxide content in exhaled breath. This study was undertaken to determine whether the capnogram waveform area from patients with PE is decreased compared with that from patients without PE and to examine the potential role of the capnogram waveform area as a screening test for PE. METHODS: Studies were conducted on patients from a large, urban emergency department. Steady-state capnograms were collected from subjects breathing room air, and data were electronically stored for later analysis; arterial blood was collected for blood gas analysis. PE was diagnosed or excluded on the basis of appropriate combinations of isotopic ventilation-perfusion lung scanning, lower-extremity venous Doppler ultrasound studies, and pulmonary angiography. Capnogram areas were measured by tracing waveforms on printed copies with an electronic digitizing tablet. RESULTS: The mean capnogram area from patients with PE (n=19) was 28+/-10 mm Hg x sec, significantly less than for patients without PE (n=120), 53+/-17 mm Hg x sec (95% confidence interval [CI] for a difference of 25 mm Hg x sec, 17 to 33 mm Hg x sec). At a cutoff of 50 mm Hg x sec, the test sensitivity was 100% (95% CI, 82% to 100%), with a negative likelihood ratio (LR-) of .17, and the specificity was 53% (95% CI, 44% to 62%), with a positive likelihood ratio (LR+) of 2.1. At a cutoff of 25 mm Hg x sec, the test sensitivity was 42% (95% CI, 20% to 67%; LR-, .6) and the specificity was 97% (95% CI, 92% to 99%; LR+, 12.3). The area under the smoothed receiver operating characteristic curve for the capnogram area was .896 (95% Cl, .80 to .99). CONCLUSION: The capnogram waveform area may be useful in screening for PE in the ED.

Adolescent↗
PubMed1998

A multicenter study to improve emergency medicine residents' recognition of intracranial emergencies on computed tomography.

STUDY OBJECTIVE: Cranial computed tomography (CT) has assumed a critical role in the practice of emergency medicine for the evaluation of intracranial emergencies. Several recent studies have documented a deficiency in the emergency physician's ability to interpret these studies. The purpose of this study was to quantify the baseline ability of emergency medicine residents to interpret cranial CTs, and to test a novel method of cranial CT interpretation designed for the emergency physician in training. METHODS: A standardized pretest was administered to assess baseline ability to interpret CT scans. A standardized posttest was given 3 months after the course. Each test consisted of 12 CT scans with a short accompanying history. All scans were validated by 3 expert reviewers for difficulty and diagnosis. A 2-hour course based on the mnemonic "Blood Can Be Very Bad" was then administered. "Blood" reminds the examiner to search for blood, "Can" prompts the examiner to identify 4 key cisterns, "Be" denotes the need to examine the brain, "Very" prompts a review of the 4 ventricles, and finally "Bad" reminds the examiner to evaluate the bones of the cranium. RESULTS: Eighty-three residents at 5 institutions were initially examined. The mean percentage correct before the course was 60% (95% confidence interval [CI] 58%-64%) on the standardized pretest. At retesting 3 months after the course, the accuracy rate increased to 78% (n=61, 95% CI 75%-81%, P<.001 paired t test). CONCLUSION: Emergency medicine residents are deficient in their ability to interpret cranial CT scans. A novel educational course was demonstrated to significantly improve this ability.

Adolescent↗
PubMed1997

Activation of pyruvate dehydrogenase improves heart function and metabolism after hemorrhagic shock.

This study was designed to test the hypothesis that activation of myocardial pyruvate dehydrogenase (PDH) would improve recovery of heart function after brief, severe hemorrhagic shock. Pentobarbital-anesthetized rats were instrumented to monitor arterial blood pressure and right ventricular pressures. Rats were hemorrhaged via femoral artery to 25-30 mmHg mean arterial pressure (MAP) for 60 min, followed by retransfusion of shed blood with either 1.0 cc saline with no dichloroacetate (-DCA) or 1.0 cc saline containing 150 mg/kg sodium dichloroacetate (+DCA). Rats were observed for 3 h after retransfusion. Hearts were freeze-clamped in situ for analysis of adenosine triphosphate (ATP), creatine phosphate (CrP), lactate and pyruvate content as well as PDH activity (PDHa) and total PDH activity (PDHt). Three h after retransfusion, the rate pressure product (RPP=HRxPSP) was 23 000+/-2733 with no DCA treatment v 36 2769 mmHg/min with DCA treatment (P<0.05, ANOVA). Treatment with DCA also increased myocardial tissue content of high energy phosphates (ATP=10.1+/-1.1 and CrP=5.8+/-1.0 micromol/g weight-DCA, v 15.1+/-0.9 and 14.7+/-1.0 micromol/g dry weight+DCA, P<0.05, both measurements). DCA administration also significantly reduced myocardial lactate contents (14.6+/-2.7 micromol/g dry weight-DCA v 5.9+/-1.0+DCA). Hemorrhagic shock did not change PDHa or PDHt compared to hearts obtained during the pre-hemorrhage period. Retransfusion with DCA significantly increased PDHa activity (6.8+/-1.1 micromol/g dry weight/min-DCA v 29.7+/-2.0 micromol/g dry weight/min+DCA). PDHt was not different between controls and DCA-treated groups. These data indicate that activation of myocardial PDH by adding DCA to retransfused blood improved heart function and metabolism after severe hemorrhagic shock.

Adenosine Triphosphate↗
PubMed1997

The diabetogenic effects of acute verapamil poisoning.

Verapamil poisoning is known to produce hyperglycemia and metabolic acidosis in humans. The purpose of this study was to elucidate mechanisms of verapamil-induced hyperglycemia in awake dogs. Mongrel canines were chronically instrumented to permit studies in the conscious state. In six healthy dogs, steady-state glucose infusion requirement after 1 hr of insulin infusion at 1000 mU/min was 19 +/- 1 mg/kg/min. In six separate dogs, verapamil toxicity was induced via verapamil infusion in the portal vein; during verapamil toxicity, the glucose infusion requirement with an insulin infusion rate of 1000 mU/min was significantly decreased (3 +/- 1 mg/kg/min; p < 0.05, unpaired t test). Eleven other verapamil-toxic dogs were also treated with either saline (n = 6, 3.0 ml/kg/hr) or glucagon (n = 5, 10 microg/kg/min). Insulin concentrations were not changed vs basal concentrations in either group. Catecholamine concentrations increased at least 15-fold in all groups (from 458 +/- 169 to 6973 +/- 480 pg/L in the saline-treated group). Glucose concentrations increased in saline-treated animals from 3.7 +/- 0.3 to 11.2 +/- 1.0 micromol/L, and with glucagon treatment, increased from 3.3 +/- 0.3 to 16.1 +/- 1.6 micromol/L (p < 0.05 vs saline, ANOVA). Verapamil poisoning appears to produce hyperglycemia by inducing systemic insulin resistance, blocking insulin release, together with an intact stress hormone response and glucogenic capacity.

Animals↗
PubMed1997

Insulin improves heart function and metabolism during non-ischemic cardiogenic shock in awake canines.

OBJECTIVES: This study was undertaken to examine in-situ heart function and metabolism during insulin treatment of verapamil-induced cardiogenic shock in awake canines. METHODS: Twenty mongrel canines were instrumented to monitor myocardial substrate uptakes (glucose, lactate, free fatty acids, oxygen [MVO2]), as well as ventricular (LV) end-systolic elastance (Emax), LV efficiency (LV minute work/MVO2), and Tau. Shock was induced by graded intraportal verapamil infusion followed by randomized assignment to one of 4 treatment groups: saline control (3.0 ml/kg/min, n = 5), epinephrine (5 micrograms/kg/min, n = 5), glucagon (10 micrograms/kg/min, n = 5) or insulin (1000 mU/min, n = 5) with dextrose to clamp arterial [glucose] +/- 10% of basal concentrations. RESULTS: Insulin treatment significantly increased Emax (34 +/- 3 vs. 17 +/- 3 mmHg/mm, saline control), and shortened Tau (9 +/- 3 ms) compared to saline control (42 +/- 5 ms), epinephrine (20 +/- 4 ms) and glucagon (35 +/- 8 ms). With insulin treatment, mechanical efficiency increased to 20,097 +/- 2070 vs. 12,424 +/- 1615 mmHg.mm/ml/O2/100 g in controls. Simultaneously, insulin increased myocardial lactate uptake (35 +/- 2 vs. 17 +/- 4 mumol/min/100 g. saline control), but did not increase glucose uptake. Epinephrine and glucagon decreased mechanical efficiency compared to saline controls, coincident with increased myocardial fatty acid consumption, but without increasing lactate uptake. One dog died early with glucagon treatment before the first death in the saline-treated group. CONCLUSIONS: Insulin improves systolic and diastolic heart function during aerobic shock and accelerates in-vivo myocardial lactate oxidation.

Animals↗
PubMed1997

Use of the alveolar dead space fraction (Vd/Vt) and plasma D-dimers to exclude acute pulmonary embolism in ambulatory patients.

OBJECTIVE: To evaluate the utility of a modified calculation of the alveolar dead space fraction (Vd/Vt), combined with plasma D-dimers, to aid in the exclusion of acute pulmonary embolism (PE). METHODS: A prospective comparison of screening modalities was performed in a metropolitan teaching ED. Ambulatory patients evaluated for PE underwent simultaneous end-tidal CO2 and arterial blood gas determinations, as well as venous latex-agglutination D-dimer quantification. The modified Bohr equation was used to calculate Vd/Vt as an index of alveolar dead space. Acute PE was diagnosed or excluded using appropriate combinations of clinical suspicion, ventilation-perfusion lung scanning, lower-extremity venous Doppler ultrasonography, pulmonary angiography, and comprehensive follow-up. RESULTS: Of 170 subjects studied, PE was confirmed (PE+) in 26 (15%) and excluded (PE-) in 144 (85%). In the PE+ group, Vd/Vt was 0.31 +/- 0.13 (mean +/- SD), and in the PE- group, Vd/Vt was 0.06 +/- 0.10 (p < 0.05, t-test). Regarding false-negative rates, Vd/Vt was normal (i.e., < 0.2) in 3/26 PE+ patients and D-dimer concentrations were normal (< 0.5 microgram/L) in 4/26 patients in the PE+ group. The combination of a normal Vd/Vt and D-dimer concentration was 100% sensitive (95% CI = 88-100%) in excluding PE. False-positive testing (either test positive) occurred in 49/144 subjects (specificity 65%, 95% CI = 52-73%). The age-adjusted alveolar-arterial O2 gradient was 33 +/- 38 torr in the PE+ group vs 13 +/- 37 torr in the PE- group (p = 0.11). CONCLUSIONS: In ambulatory patients, the finding of Vd/Vt < 0.2 and D-dimers < 0.5 microgram/L lowers the probability of acute PE.

Acute Disease↗
PubMed1997

The clinical features of acute pulmonary embolism in ambulatory patients.

OBJECTIVE: To identify clinical findings and predisposing conditions associated with acute pulmonary embolism (PE) in ambulatory patients being evaluated for PE. METHODS: A prospective observational study was conducted. A standardized multicomponent data collection form was administered to ambulatory subjects being evaluated for PE. The diagnosis of PE was confirmed or excluded using a combination of scintillation lung scanning, lower-extremity venous Doppler ultrasonography, and selective use of pulmonary angiography. RESULTS: Data collection was completed for 170 subjects, with 26 (15%) cases of PE. Subjects with PE were significantly older (56 vs 41 years, 99% CI for difference of 15 years [6 to 25 years]), were more likely to report unexplained dyspnea (92% vs 69%, 99% CI for difference of 23% [7% to 40%]), and waited longer after symptom onset to seek medical evaluation (73 vs 36 hours, 99% CI for difference of 37 hours [11 to 63 hours]). No difference was found for multiple variables commonly associated with PE. Assignment to risk categories was of limited diagnostic utility. For example, low-risk assignment yielded 85% sensitivity, 20% specificity; high-risk assignment: 31% sensitivity, 85% specificity, with diagnostic accuracy below 80% in both categories. CONCLUSIONS: Among outpatients selected for evaluation for PE, further risk stratification demonstrated poor diagnostic utility. Clinical features alone cannot be used to differentiate presence or absence of PE in at-risk ambulatory patients.

Adult↗