Comparison of venous air embolism monitoring methods in supine dogs.
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Biomedical subjects
Publications and source records attributed to M R Hodges.
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Twelve male mongrel dogs were used for this study; six were untreated (control) and six were given intravenous furosemide (1 mg/kg) daily for seven consecutive days before each study. Each animal received intravenous KCl 0.8, 1.6 or 3.2 mMol/kg/hr for one hour, but only one dose for each study and at least seven days were allowed between studies. The animals were given thiopentone for tracheal intubation and mechanically ventilated, maintaining a PaCO2 of 4.0 to 4.5 kPa (30-35 torr) and anaesthetized with nitrous oxide-oxygen and halothane. Daily administration of furosemide reduced serum potassium from 4.48 to 4.09 mMol/1 with no significant change in serum sodium. A greater number of furosemide-pretreated animals (6 vs 3) developed cardiac dysrhythmias during non-lethal intravenous KCl at 0.8, 1.6 mMol/kg/hr. The furosemide-pretreated group tended to succumb at a lower serum potassium concentration (12.2 vs 13.8 mMol/I, P less than 0.05) and developed earlier onset (44 vs 54 min, P less than 0.05) of cardiac standstill or ventricular fibrillation following intravenous KCl at 3.2 mMol/kg/hr. Cardiac output, heart rate and mean arterial pressure were significantly elevated during serum concentrations of 6.9-9.1 mMol/1, while no statistically significant changes were observed for stroke volume and peripheral resistance. There were no significant differences of urinary potassium excretion between the untreated and treated groups when like doses of KCl were infused. These data suggest that acute infusion of KCl in furosemide-pretreated dogs may not be an effective means of treating hypokalaemia and could be hazardous.
The effects of lithium carbonate on the responses to five neuromuscular blocking agents were evaluated in dogs anesthetized with halothane (1 per cent) and N2O (60 per cent) in O2. Latency (time from first twitch-height depression to maximal blockade), maximal twitch-height depression, and times to return to 50 per cent and 100 per cent control twitch tension were measured before and after intravenous infusion of lithium carbonate (1 mg/kg/min for one hour) during neuromuscular blockades produced by succinylcholine, decamethonium, gallamine, d-tubocurarine, or pancuronium. Lithium prolonged the latencies of neuromuscular blockades produced by 0.1 mg/kg succinylcholine and 0.1 mg/kg decamethonium by 248.1 per cent and 49.0 per cent, respectively, but had no effect on latency produced by 0.02 mg/kg pancuronium. The times for return to 50 per cent of control twitch height were prolonged by 69.5, 40.0, and 120.1 per cent, respectively. Lithium had no effect on latency or duration of blockades produced by 0.15 mg/kg d-tubocurarine and 0.6 mg/kg gallamine, but enhanced maximal twitch-height depressions produced by 0.9 mg/kg gallamine and 0.02 mg/kg pancuronium by 22.9 and 9.9 per cent, respectively. Twitch tensions decreased 5-10 per cent over three hours in three dogs receiving lithium infusion without relaxants. Twitch tension was depressed 0-2 per cent in three dogs after five hours of anesthesia in the absence of lithium or relaxants. Lithium prolonged the time required for neostigmine to reverse neuromuscular blockade produced by pancuronium in two of three dogs from a mean of 60 seconds to 135 seconds.
The effects of continuous positive airway pressure (CPAP) on cardiovascular dynamics and pulmonary shunt (QS/QT) were investigated in 12 dogs before and during sodium nitroprusside infusion that decreased mean arterial blood pressure 40-50 per cent. Before nitroprusside infusion, 5 cm H2O CPAP significantly, P less than .05, decreased arterial blood pressure, but did not significantly alter heart rate, cardiac output, systemic vascular resistance, or QS/QT. Ten cm H2O CPAP before nitroprusside infusion produced a further decrease in arterial blood pressure and significantly increased heart rate and decreased cardiac output and QS/QT. Nitroprusside caused significant decreases in arterial blood pressure and systemic vascular resistance and increases in heart rate, but did not change cardiac output or QS/QT. Five cm H2O CPAP during nitroprusside did not further alter any of the above-mentioned variables. However, 10 cm H2O CPAP decreased arterial blood pressure, cardiac output, and QS/QT. These data indicate that nitroprusside infusion rates that decrease mean arterial blood pressure by 40-50 per cent do not change cardiac output or QS/QT. During nitroprusside infusion low levels of CPAP do not markedly alter cardiovascular dynamics, but high levels of CPAP (10 cm H2O), while decreasing QS/QT, produce marked decreases in arterial blood pressure and cardiac output.
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The possible association between acute respiratory failure and disseminated intravascular coagulation was examined in eight patients with severe acute respiratory failure--a condition characterized by tachypnea, right to left intrapulmonary shunting of blood greater than 30 per cent of cardiac output, increased pulmonary artery pressure with low or normal pulmonary artery wedge pressure and roentgenologic interstitial pulmonary edema. Treatment consisted of mechanical ventilation with positive end expiratory pressure sufficient to minimize intrapulmonary shunting. There was no abnormality in platelet concentration fibrin split product concentration, fibrinogen concentration, prothrombin time or activated partial thromboplastin time during the period of most severe respiratory failure in any patient. However, mean platelet concentration fell to 90,000+/-9,000 per cubic millimeter, less than 0.001, and mean fibrin split product levels rose to 60+/-10 micrograms per milliliter, p less than 0.05, the fourth day after the onset of acute respiratory failure. No significant change occurred in other coagulation parameters. Disseminated intravascular coagulation developed in none of the patients nor was there any correlation between coagulation abnormalities and severity of acute respiratory failure that would suggest a cause and effect relationship.
BACKGROUND: Voriconazole has proven efficacy against invasive aspergillosis and oesophageal candidiasis. This multicentre, randomised, non-inferiority study compared voriconazole with a regimen of amphotericin B followed by fluconazole for the treatment of candidaemia in non-neutropenic patients. METHODS: Non-neutropenic patients with a positive blood culture for a species of candida and clinical evidence of infection were enrolled. Patients were randomly assigned, in a 2:1 ratio, either voriconazole (n=283) or amphotericin B followed by fluconazole (n=139). The primary efficacy analysis was based on clinical and mycological response 12 weeks after the end of treatment, assessed by an independent data-review committee unaware of treatment assignment. FINDINGS: Of 422 patients randomised, 370 were included in the modified intention-to-treat population. Voriconazole was non-inferior to amphotericin B/fluconazole in the primary efficacy analysis, with successful outcomes in 41% of patients in both treatment groups (95% CI for difference -10.6% to 10.6%). At the last evaluable assessment, outcome was successful in 162 (65%) patients assigned voriconazole and 87 (71%) assigned amphotericin B/fluconazole (p=0.25). Voriconazole cleared blood cultures as quickly as amphotericin B/fluconazole (median time to negative blood culture, 2.0 days). Treatment discontinuations due to all-cause adverse events were more frequent in the voriconazole group, although most discontinuations were due to non-drug-related events and there were significantly fewer serious adverse events and cases of renal toxicity than in the amphotericin B/fluconazole group. INTERPRETATION: Voriconazole was as effective as the regimen of amphotericin B followed by fluconazole in the treatment of candidaemia in non-neutropenic patients, and with fewer toxic effects. RELEVANCE TO PRACTICE: There are several options for treatment of candidaemia in non-neutropenic patients, including amphotericin B, fluconazole, voriconazole, and echinocandins. Voriconazole can be given both as initial intravenous treatment and as an oral stepdown agent.
The authors determined the effects of short-term, vigorous intermittent positive-pressure breathing (IPPB) on arterial blood O2 tension (Pao2) in 10 unmedicated preoperative adult patients (ASA class I). Arterial blood was analyzed before and 0.5, 5, 15, and 40 minutes after 12 minutes of IPPB with nebulized 0.9% HaCl and room air. Pao2 increased from 89.1 +/- 11 torr (mean +/- SD) to 102.1 +/- 13.9 torr, and arterial CO2 tension decreased from 29.5 +/- 4 torr to 18.4 +/- 3 torr, causing significant respiratory alkalosis (pHa 7.62 +/- 0.05). Five minutes after IPPB, Pao2 decreased to 69.2 +/- 8 torr; alveolar-arterial Po2 difference, breathing 21% O2, increased significantly; and serum K+ concentration decreased significantly. All these values returned to baseline levels within 40 minutes. The authors, acknowledging the value of IPPB when specifically indicated, counsel caution in patients with borderline pulmonary reserve and arterial oxygenation.
Pulmonary venous admixture (Qsp/Qt) was analyzed as a function of fractional concentration of inspired O2 (FIO2) in 30 patients who required postoperative mechanical ventilation. Pulmonary and radial artery blood-gas tensions and pH were measured and Qsp/Qt was calculated with FIO2 ranging from 0.21 to 1. In all patients, Qsp/Qt decreased when FIO2 was increased from 0.21 to 0.4 and then stabilized to an FIO2 of approximately 0.6. As the FIO2 was increased to 1, Qsp/Qt increased. Since the inhalation of gas mixture with FIO2 greater than or equal to 0.6 increased right-to-left intrapulmonary shunting of blood, we recommend respiratory function be evaluated during inhalation of a clinically useful concentration of O2 rather than at an FIO2 of 1.
Continuous positive-pressure ventilation may decrease cardiac output. However, a few reports have separated the effects of positive and end-expiratory pressure (PEEP) from those of mechanical ventilation. Ten surgical patients requiring mechanical ventilatory support had catheters inserted for measurement of right atrial pressure (RAP), pulmonary artery occlusion pressure (PAOP), intrapleural, radial artery, airway, and atrial filling pressures, and cardiac output. All patients breathed spontaneously between mechanical breaths delivered every 30 seconds by intermittent mandatory ventilation (IMV). Measurements were made with 0, 5, and 10 cm H2O PEEP, and during intermittent positive-pressure ventilation (IPPV) with 12 breaths/min without PEEP. Airway pressure (Paw), intrapleural pressure, RAP, and PAOP were increased by PEEP and IPPV. Intrapleural pressure increased most during IPPV (p less than 0.001). Atrial filling pressures and cardiac output were unaffected by PEEP but decreased during IPPV (p less than 0.001). Patients receiving IMV maintained negative intrapleural pressure, atrial filling pressure, cardiac output and, therefore, O2 delivery, regardless of PEEP level. The authors conclude that patients requiring mechanical respiratory support, with or without PEEP, may maintain better cardiopulmonary function when allowed some spontaneous ventilatory activity.
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The relationship between changes in wholebody O2 consumption (VO2) and cardiovascular dynamics during changing levels of N2O-fentanyl and N2O-thiopental anesthesia was determined in 24 dogs. Dose-dependent reductions in VO2, mean blood pressure, and cardiac output occurred with infusion of fentanyl and thiopental. Painful stimuli increased VO2 during light anesthesia but not during deeper levels of anesthesia. Deep levels of N2O-fentanyl and N2O-thiopental anesthesia may protect the patient with limited cardiac reserve by reducing VO2 and preventing increases in VO2 caused by painful stimuli.
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In summary, the United States Tort System, with malpractice actions based upon the law of negligence, remains a driving force in affecting health care delivery costs. The reforms and attempted reforms under consideration by legislative branches nationwide also play a key role in this endeavor. Yet, tort reform alone is not the answer. Reducing the initial occurrence of medical injury remains the ultimate method of easing the current liability crisis. Health care providers must assure the delivery of quality care to their patients or face consequences in areas of licensure qualifications, license renewal, professional discipline, suspensions, probations and fines. An effective quality assurance program that provides measurable results should be a priority for all health care providers. Administration, medical staffs and all departments within a health provider's facility must work together to achieve quality patient care. Proven risk management programs, combined with similar cooperative efforts by health care companies, physicians, attorneys, insurance companies, state regulatory agencies and the federal government, will prove extremely effective in controlling future health care delivery costs.
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