Francis L. Miller

The laryngeal mask airway reliably provides rescue ventilation in cases of unanticipated difficult tracheal intubation along with difficult mask ventilation.

In 1995, our department of anesthesiology established an airway team to assist in treating unanticipated difficult endotracheal intubations and an airway quality im-provement (QI) form to document the use of emergency airway techniques in airway crises (laryngeal mask airway [LMA], flexible fiberoptic bronchoscopy, retrograde intubation [RI], transtracheal jet ventilation [TTJV], and cricothyrotomy). Over a 2-yr period, team members and staff anesthesiologists completed airway QI forms to document the smallest peripheral SpO2 during an airway crisis, the number of direct laryngoscopies (DL) performed before using an emergency airway technique, and the emergency airway technique that succeeded in rescue ventilation. Team members agreed to use the LMA as the first emergency airway technique to treat the difficult ventilation/difficult intubation scenario. A SpO2 value <or=to90% during mask ventilation defined difficult ventilation. Inability to perform tracheal intubation by DL defined difficult intubation. An increase in the SpO2 value >90% defined rescue ventilation. Review of airway QI forms from October 1, 1995 until October 1, 1997 revealed 25 cases of difficult ventilation/difficult intubation. Before airway rescue, the median SpO2 was 80% (range 50%-90%), and there were four median attempts at DL (range one to nine). The LMA had a success rate of 94% (95% confidence interval [CI] 77-100). Flexible fiberoptic bronchoscopy, TTJV, RI, and surgical cricothyrotomy had success rates of 50% (95% CI 0-100), 33% (95% CI 0-100), 100% (95% CI 37-100), and 100% (95% CI 37-100), respectively. LMA insertion as the first alternative airway technique was useful in dealing with unanticipated instances of simultaneous difficulty with mask ventilation and tracheal intubation. Implications: Twenty-five cases of simultaneous difficulty with mask ventilation and tracheal intubation occurred after the induction of general anesthesia during the study period. The laryngeal mask was used in 17 cases, and it provided rescue ventilation without complication in 94% of these cases (95% confidence interval 77-100). (Anesth Analg 1998;87:661-5)

The Incidence of large venous emboli during total knee arthroplasty without pneumatic tourniquet use

Echogenic venous emboli accompany tourniquet deflation during total knee arthroplasty.Two types of echogenic emboli appear in the central circulation: small venous emboli (miliary emboli) and large venous emboli (masses of echogenic material superimposed on miliary emboli). Presumably, medullary cavity trespass releases small and large echogenic emboli. However, patients undergoing lower extremity procedures with a tourniquet have large echogenic emboli regardless of medullary cavity invasion. Avoiding tourniquet inflation may decrease the release of large venous emboli. Thirteen patients undergoing total knee arthroplasty without pneumatic tourniquet received intramedullary guides and 11 patients received tibial extramedullary guides. Recordings of hemodynamic variables, mixed venous oximetry, end-tidal CO2, and echocardiographic images were made after the induction of anesthesia and for 15 min after femoral prosthesis cementing. Mean arterial pressure did not change during the study, and mean pulmonary arterial pressure increased minimally. Large venous emboli appeared in eight patients, small venous emboli appeared in 12 patients, and no emboli appeared in four patients. Compared with previous investigations of large venous emboli during total knee arthroplasty with a pneumatic tourniquet, multiple logistic regression analysis discloses a 5.33-fold greater risk of large venous embolism accompanied the use of a tourniquet during total knee arthroplasty. Implications: One third of knee replacements performed without a tourniquet demonstrated large emboli. Reducing marrow cavity invasion did not decrease the release of large emboli. Compared with knee replacement without tourniquet, tourniquet use places patients at a 5.33-fold greater risk of having a large emboli. (Anesth Analg 1998;87:439-44)

Mechanical Factors Do Not Influence Blood Flow Distribution in Atelectasis

The contribution of mechanical factors to the vascular resistance of the atelectatic lung has been studied in vivo in the anesthetized open-chest dog. When the left lung was ventilated with an hypoxic gas mixture (while the right lung was ventilated with 100% O2), left lung blood flow decreased from 0.99 +/- 0.11 1.min-1 to 0.40 +/- 0.08 1.min-1 due to hypoxic pulmonary vasoconstriction (hypoxic stimulus PSO2 = 36.1 +/- 0.8 mmHg). When the left lung was made atelectatic, blood flow decreased to 0.65 +/- 0.11 1.min-1, consistent with a weaker hypoxic stimulus (PSO2 = 54.0 +/- 3.2 mmHg). With the addition of sodium nitroprusside infused intravenously, left lung blood flow increased to 1.05 +/- 0.14 1.min-1 during atelectasis, and to 0.61 +/- 0.09 1.min-1 during hypoxic ventilation, while flow remained at 0.94 +/- 0.18 1.min-1 during hyperoxic ventilation. When the results were plotted on pressure-flow diagrams, the hyperoxic, hypoxic, and atelectatic lung points fell on the same pressure-flow line in the presence of nitroprusside. It is concluded that hypoxic pulmonary vasoconstriction is the major (but not necessarily only) determinant of increased vascular resistance in the atelectatic lung, and that passive mechanical factors do not measurably affect blood flow distribution during open-chest atelectasis.

High-dose almitrine bismesylate inhibits hypoxic pulmonary vasoconstriction in closed-chest dogs

The effect of almitrine bismesylate on the hypoxic pulmonary vasoconstrictor (HPV) response was studied in seven closed-chest dogs anesthetized with pentobarbital and paralyzed with pancuronium. The right lung was ventilated continuously with 100% O2, while the left lung was ventilated with either 100% O2 (“hyperoxia”) or with an hypoxic gas mixture (“hypoxia”: end-tidal Po2 = 50.1 ± 0.1 mmHg). Cardiac output (CO) was altered from a “normal” value of 3.10 ± 0.18 1 · min-1 to a “high” value of 3.92 ± 0.16 1 · min-1 by opening arteriovenous fistulae which allowed measurements of two points along a pressure-flow line. These four phases of left lung hypoxia or hyperoxia with normal and high cardiac output were repeated in the presence and absence of almitrine. Almitrine bismesylate was administered as a constant infusion of 14.3 μg · kg-1 · min-1 for a mean plasma concentration of 219.5 ± 26.4 ng · ml-1. Relative blood (low to each lung was measured with a differential CO2 excretion (VCO2) method corrected for the Haldane effect. With both lungs hyperoxic, the percent left lung blood flow (%QL-VCO2) was 44 ± 1%. When the left lung was exposed to hypoxia, the %QL-VCO2 decreased significantly to 22 ±1%- However, with the administration of almitrine, the %QL-VCO2 during left lung hypoxia increased significantly to 36 ± 2%. The arterial oxygen tension decreased significantly between hyperoxia (Pao2 = 633 ± 6 mmHg) and hypoxia (271 ± 31 mmHg). With the addition of almitrine, there was no change during hyperoxia; however, during hypoxia, the Pao2 decreased significantly to 124 ± 15 mmHg. Cardiac output did not influence these findings. The pulmonary vascular conductance (G) is the slope of the pressure-flow line. The pulmonary vascular conductance of the right lung (GR × 103) (1.6 ± 0.1 dyn-1 8 cm5 · s-1) did not change significantly during hyperoxia or hypoxia when no drug was given. With the administration of almitrine, GR decreased significantly to 1.0±0.1 dyn-1 · cm5 · s-1 during both hyperoxia and hypoxia. The same was true at normal and high cardiac output. The pulmonary vascular conductance of the left lung (GL) decreased significantly between hyperoxia (1.24 ± 0.1 dyn-1 · cm5 · s-1) and hypoxia (0.7 ± 0.1 dyn-1 · cm5 · s-1). However, with the addition of almitrine, GL decreased significantly during hyperoxia (0.8 ± 0.1 dyn-1 · cm-1 · s-1), but not during hypoxia (0.8 ± 0.1 dyn-1 · cm5 · s-1). The same was true at normal and high cardiac output. It is concluded that almitrine bismesylate caused nonspecific pulmonary vasoconstriction that was greater in the 100% O2 ventilated lung than in the hypoxic lung regions. Therefore, blood flow was diverted from the hyperoxic back to the hypoxic lung causing a reduction of the HPV response.

Low-dose Almitrine Bismesylate Enhances Hypoxic Pulmonary Vasoconstriction in Closed-chest Dogs

The effect of almitrine bismesylate on the hypoxic pulmonary vasoconstrictor response was studied in six closed-chest dogs anesthetized with pentobarbital and paralyzed with pancuronium. The right lung was ventilated continuously with 100% O2; the left lung was ventilated either with 100% O2 (“hyperoxia”) or with an hypoxic gas mixture (“hypoxia”: end-tidal oxygen tension = 60.3 ± 0.6 mm Hg). On two consecutive days, each dog received either almitrine (Vectarion, Servier Lab) or malic acid. Consecutive almitrine doses of 0.003, 0.03, 0.3, and 3.0 μg·kg−1·min−1, or the equivalent volumes of malic acid without almitrine, were administered intravenously as a constant peripheral infusion for 15 min. Percent blood flow to each lung was calculated based on a variation of the traditional shunt equation. The change in percent left lung blood flow (Δ%QL-VA) increased significantly between the hypoxia-no drug and the hypoxia-almitrine (3.0μg·kg−1·min−1) phase. No significant changes occurred during the other almitrine doses or the respective malic acid control phases. The change in arterial oxygen tension (ΔPaO2) also increased significantly between the hypoxia-no drug and the hypoxia-almitrine (3.0 μg·kg−1·min−1) phase. No significant changes occurred during the other almitrine doses or the respective malic acid control phases. It is concluded that in dogs low-dose almitrine enhances hypoxic pulmonary vasoconstriction and that this enhancement is dose-related.

Hypoxic Pulmonary Vasoconstriction Is Not Potentiated by Repeated Intermittent Hypoxia in Closed Chest Dogs

Hypoxic pulmonary vasoconstrictor (HPV) responses were measured with repeated intermittent hypoxic challenges in eight non-traumatized closed chest dogs anesthetized with pentobarbital. The right lung was ventilated continuously with 100% O2 while the left lung was either ventilated with 100% O2 (control) or ventilated with a gas mixture containing 3–4% O2 (hypoxia). Mean per cent left lung blood flow for all four normoxic periods was 43.1 ± 1.5% (mean ± SE) of the total blood flow by the SF6 excretion method and 40.8 ± 1.1% by the differential CO2 excretion method, corrected for the Haldane effect. With hypoxic ventilation, flow diversion from the hypoxic lung was maximal with the first exposure and did not change subsequently with a total of four alternating exposures to normoxia and hypoxia. Flow diversion during hypoxia was approximately 50.5 ± 2.4% by the SF6 method and 50.3 ± 3.5% by the Vco2 method. This result contrasts with the increasing flow diversion response with intermittant hypoxic exposure that has been reported in animals exposed first to thoracotomy and surgical dissection. It is concluded that in the absence of surgical trauma the initial response to hypoxia is maximal and is not potentiated by repeated hypoxic stimulation.