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Biomedical subjects

D F Van Riper

Publications and source records attributed to D F Van Riper.

9 recordsLinked to original sources
PubMed1997

Difficult or impossible ventilation after sufentanil-induced anesthesia is caused primarily by vocal cord closure.

INTRODUCTION: Opioid-induced rigidity often makes bag-mask ventilation difficult or impossible during induction of anesthesia. Difficult ventilation may result from chest wall rigidity, upper airway closure, or both. This study further defines the contribution of vocal cord closure to this phenomenon. METHODS: With institutional review board approval, 30 patients undergoing elective cardiac surgery participated in the study. Morphine (0.1 mg/kg) and scopolamine (6 microg/kg) given intramuscularly provided sedation along with intravenous midazolam as needed. Lidocaine 10% spray provided topical anesthesia of the oropharynx. A fiberoptic bronchoscope positioned in the airway photographed the glottis before induction of anesthesia A second photograph was obtained after induction with 3 microg/kg sufentanil administered during a period of 2 min. A mechanical ventilator provided 10 ml/kg breaths at 10/min via mask and oral airway with jaw thrust. A side-stream spirometer captured objective pulmonary compliance data. Subjective airway compliance was scored. Pancuronium (0.1 mg/kg) provided muscle relaxation. One minute after the muscle relaxant was given, a third photograph was taken and compliance measurements and scores were repeated. Photographs were scored in a random, blinded manner by one investigator. Wilcoxon signed rank tests compared groups, with Bonferroni correction. Differences were considered significant at P < 0.05. RESULTS: Twenty-eight of 30 patients exhibited decreased pulmonary compliance and closed vocal cords after opioid induction. Two patients with neither objective nor subjective changes in pulmonary compliance had open vocal cords after opioid administration. Both subjective and objective compliances increased from severely compromised values after narcotic-induced anesthesia to normal values (P = 0.000002) after patients received a relaxant. Photo scores document open cords before induction, progressing to closed cords after the opioid (P = 0.00002), and opening again after a relaxant was administered (P = 0.00005). CONCLUSION: Closure of vocal cords is the major cause of difficult ventilation after opioid-induced anesthesia.

Humans↗
PubMed1996

Upper airway closure: a primary source of difficult ventilation with sufentanil induction of anesthesia.

Large-dose opioid induction of anesthesia can lead to difficult ventilation via a mask. Poor ventilatory compliance (VC) may be secondary to "rigid" chest and abdominal wall musculature, glottic closure, or upper airway obstruction. This double-blind study assessed the contribution of the upper airway to poor VC by inducing sufentanil anesthesia in patients undergoing cardiac surgery who are ventilated via a mask (Group M) or endotracheal tube fiberoptically inserted (Group E). After induction of anesthesia with sufentanil 3 microgram/kg from time (T) = 0 min to T = 2 in Group M (n = 17) or Group E(n = 23), VC and adductor pollicis (AP) twitch tension was measured continuously. Immediately prior to muscle relaxant (pipecuronium or doxacurium) administration at T = 3, Group E demonstrated significantly better VC (46 mL/cm H2O [39-55 interquartile range (IQR)]) than Group M (19 mL/cm H2O [7-24 IQR]). The effect of muscle relaxant administration on VC preceded its effect at the AP. After complete relaxation of the AP at T = 9, both groups had similar VC. Difficult ventilation during sufentanil induction of anesthesia lies at the level of the glottis or above. Bypassing these structures with an endotracheal tube overcomes the usual decreased VC.

Aged↗
PubMed1995

The dose-response relationship of tranexamic acid.

BACKGROUND: Prophylactic administration of the antifibrinolytic drug tranexamic acid decreases bleeding and transfusions after cardiac operations. However, the best dose of tranexamic acid for this purpose remains unknown. This study explored the dose-response relationship of tranexamic acid for hemostatic efficacy after cardiac operation. METHODS: In prospective, randomized, double-blinded fashion, 148 patients undergoing cardiac operation with extracorporeal circulation were divided into six groups: a placebo group and five groups receiving tranexamic acid in loading doses before incision (range 2.5 to 40 mg.kg-1) and one-tenth the loading dose hourly for 12 h. The mass of blood collected by chest tubes over 12 h represented blood loss. Allogeneic transfusions within 12 h and within 5 d of surgery were tallied. RESULTS: The six groups presented similar demographics. Patients receiving placebo had increased postoperative D-dimer concentration compared to groups receiving tranexamic acid. Patients receiving at least 10 mg.kg-1 tranexamic acid followed by 1 mg.kg-1.h-1 bled significantly less (365, 344, and 369 g.12 h-1, respectively, for those three groups) compared with patients who received placebo (552 g, P < 0.05). Tranexamic dose did not affect transfusions. Only initial hematocrit affected whether a patient received an allogeneic transfusion within 5 days of operation (odds ratio 2.08 for each 3% absolute decrease in hematocrit). CONCLUSIONS: Prophylactic tranexamic acid, 10 mg.kg-1 followed by 1 mg.kg-1.h-1, decreases bleeding after extracorporeal circulation. Larger doses do not provide additional hemostatic benefit.

Adult↗
PubMed1991

Ventilatory compliance after three sufentanil-pancuronium induction sequences.

Poor ventilatory compliance, a predictable side effect of high-dose opioid induction techniques, is purportedly blunted by pretreatment with nondepolarizing muscle relaxant. This study used both total compliance and a subjective compliance score to compare three different sequences of opioid induction using a 2-min infusion of sufentanil 3 micrograms.kg-1. Nineteen patients in each of three groups received a total of 100 micrograms.kg-1 of pancuronium, in the following randomized double-blinded fashion: control, all pancuronium 1 min after sufentanil; pretreated, 1 mg pancuronium 1 min before sufentanil and the balance of pancuronium 1 min after sufentanil; and mixed, all pancuronium mixed with sufentanil. Topical lidocaine prior to induction permitted early oral airway insertion midway through the sufentanil infusion. Immediately at the conclusion of sufentanil infusion, a tightly fitted mask, anterior jaw thrust, and mechanical ventilator permitted measurement of plateau airway pressure and exhaled volume in five replicates. Pressure and volume measurements were repeated 5 min later. Total compliance was calculated as the median plateau airway pressure divided into its associated exhaled volume. Groups did not differ in demographics. In one control patient and two pretreated patients hemoglobin oxygen saturation as measured by pulse oximetry decreased below 90%. Immediately after sufentanil infusion, the total compliance for control patients of 4.1 ml.cmH2O-1 (mean [2.6-6.5, 95% confidence interval] ) did not differ from that of the pretreated group (6.3 [3.5-11.4] ml.cmH2O-1), but the mixed group exhibited higher compliance (40.3 [33.8-47.9] ml.cmH2O-1) than the other groups (P less than 10(-8]. All groups achieved similar total compliances several minutes after a total of 100 micrograms.kg-1 pancuronium had been administered.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗
PubMed1991

Hemostatic effects of tranexamic acid and desmopressin during cardiac surgery.

BACKGROUND: Desmopressin-induced release of tissue plasminogen activator from endothelial cells may explain the absence of its hemostatic effect in patients undergoing cardiac surgery. Prior administration of the antifibrinolytic drug tranexamic acid might unmask such an effect, and combination therapy might thereby improve postoperative hemostasis. METHODS AND RESULTS: A double-blinded design randomly allocated 163 adult patients undergoing coronary revascularization, valve replacement, both procedures, or repair of atrial septal defect to four treatment groups: placebo, tranexamic acid given as 10 mg/kg over 30 minutes followed by 1 mg.kg-1.hr-1 for 12 hours initiated before skin incision, desmopressin given as 0.3 micrograms/kg over 20 minutes after protamine infusion, and both drugs. One surgeon performed all operations. Blood loss consisted of mediastinal tube drainage over 12 hours. Follow-up visits sought evidence of myocardial infarction and stroke. Desmopressin decreased neither the 12-hour blood loss nor the amount of homologous red cells transfused. Tranexamic acid alone significantly reduced 12-hour blood loss, by 30% (mean, 318 versus 453 ml; p less than 0.0001), without enhancement by desmopressin. Tranexamic acid also decreased the proportion of patients receiving homologous blood within 12 hours of operation (8% versus 21%, p = 0.024) and within 5 days of operation (22% versus 41%, p = 0.011). CONCLUSIONS: Desmopressin exerts no hemostatic effect, with or without prior administration of antifibrinolytic drug. Prophylactic tranexamic acid alone appears economical and safe in decreasing blood loss and transfusion requirement after cardiac surgery.

Blood Coagulation Tests↗
PubMed1990

Mixed venous oximetry during automatic implantable cardioverter-defibrillator placement.

Mixed venous oxygen saturation (SvO2) monitoring was used to assess tissue and circulatory recovery following induced ventricular tachycardia or fibrillation in 17 patients undergoing surgery for automatic implantable cardioverter-defibrillator (AICD) placement. Return of systemic arterial pressure conventionally determines adequate recovery. The duration of circulatory arrest during defibrillator threshold (DFT) testing, measured from the moment of absent phasic pressure at the radial artery until its return, was 18 +/- 8 seconds (mean +/- SD, n = 118 episodes). The absolute decrease in SvO2 from baseline to nadir for these 118 episodes was 14% +/- 6% absolute, and correlated well with the duration of circulatory arrest (r = 0.757, P = 0.0001). The time from onset of phasic arterial blood pressure to the nadir of SvO2, available for 46 episodes, was 28 +/- 14 seconds, and did not correlate with the duration of arrest. The time from onset of phasic pressure to the return of SvO2 to within 1% (absolute) of baseline saturation, available for 84 episodes, was 52 +/- 32 seconds and, in the aggregate, correlated poorly (r = 0.401) with duration of arrest. Simultaneous recording of arterial pressure and SvO2 (n = 41) showed that arterial recovery (6 +/- 3 seconds) occurred long before SvO2 recovery (48 +/- 16 seconds, P = 0.0001). The authors interpret these data as showing that mixed venous oximetry, compared to arterial blood pressure, provides a more sensitive indicator of tissue recovery following periods of circulatory arrest during DFT testing of AICDs.

Arrhythmias, Cardiac↗