Transoesophageal echocardiography for the detection and quantification of pleural fluid in cardiac surgical patients.

BACKGROUND: Transoesophageal echocardiography (TOE) can image pleural fluid. Left pleural collections may be easier to detect than right, as the thoracic aorta serves as an acoustic window. Attempts to quantify pleural fluid using TOE are restricted to a case report in which volume was predicted by multiplying maximal cross-sectional area (CSA(max)) by axial length (AL). A computed tomography (CT) derived formula for quantifying pleural effusions is maximal effusion depth squared (d2) multiplied by maximal effusion length. METHODS: Eight patients were studied before chest closure following coronary bypass surgery. Fifty millilitre saline aliquots were instilled into the pleural space until detected by TOE. Saline was then instilled up to the next 200 ml increment and further 200 ml aliquots added until it spilled from the pleural space. CSA(max), d and AL were measured for each stage and used to calculate pleural fluid volume. RESULTS: Median detection volume (range) was 125 ml (50-200) on the left and 225 ml (150-300) on the right (P = 0.016). Volume calculated by CSA(max) x AL correlated strongly with actual volume (r2 = 0.93 left and 0.92 right) as did volume calculated by d2 x AL (r2 = 0.86 left and 0.89 right). Mean difference between volume calculated by CSA(max) x AL and actual volume was - 51 ml on the left and 45 ml on the right vs - 253 ml on the left and - 212 ml on the right for volume calculated by d2 x AL. CONCLUSIONS: TOE detects small volumes of pleural fluid on both sides of the chest. CSA(max) x AL provides a reasonably accurate measure of pleural fluid volume.

Performance of breathing filters under wet conditions: a laboratory evaluation.

INTRODUCTION: Heat and moisture exchangers in combination with a bacterial and viral filter (HMEF) are widely used during general anaesthesia. Excess patient secretions occluding the HMEF have been responsible for previous case reports of airway obstruction. A previous study suggested that differences in HMEF design might contribute to filter obstruction under wet conditions. METHODS: We tested 14 types of HMEF under wet conditions to establish which design features contributed to HMEF obstruction. Incremental amounts of saline were added to each filter. The pressure across the filter was measured with an air flow of 60 litre min(-1). RESULTS: We observed that saline added to the filter was often not easily visible to the casual observer. This concealment volume varied between filters. Ceramic hydrophobic pleated-membrane filters did not absorb saline and their resistance did not change. The composite filter where the moisture exchange component was either polyurethane foam or cellulose absorbed saline and contributed to a rise in resistance of 70-480% with the higher value more typical of the cellulose-paper-based HMEF. CONCLUSION: The ideal HMEF for use during general anaesthesia should prevent the passage of viral, bacterial and prion material, should provide this filtration performance even under wet conditions, should supplement humidification of the inspired air and anaesthetic gases and should not increase respiratory work. We have identified large variations in HMEF performance under wet conditions. Users should be aware of performance variation in HMEFs and use a filter suited to the intended application.

Air flow resistance of three heat and moisture exchanging filter designs under wet conditions: implications for patient safety.

Heat and moisture exchanging filters (HMEFs) can be blocked by secretions. We have studied HMEF performance under wet conditions to see which particular design features predispose to this complication. Dar Hygrobac-S (composite felt filter and cellulose exchanger), Dar Hygroster (composite pleated ceramic membrane and cellulose exchanger) and Pall BB22-15 (pleated ceramic membrane) HMEFs were tested. Saline retention, saline concealment, and changes in air flow resistance when wet were assessed. The cellulose exchanger in the composite Hygrobac-S and Hygroster retained saline, producing a 'tampon' effect, associated with bi-directional air flow resistances in excess of the international standard of a 5 cm H(2)O pressure drop at 60 litre min(-1) air flow. Furthermore, high air flow resistances occurred before free saline was apparent within the transparent filter housing. The pleat only BB22-15 showed a significant increase in expiratory air flow resistance, but only after the presence of saline was apparent. These data imply that composite HMEFs with cellulose exchangers are more likely to block or cause excessive work of breathing as a result of occult accumulation of patient secretions than pleat only HMEFs.

Effect of anaesthesia on the cardiac response to intravenous adenosine.

The cardiac response to intravenous adenosine 112 micrograms kg-1 was studied in 16 patients scheduled for coronary artery bypass surgery before and during anaesthesia with 1% end-tidal isoflurane and fentanyl 10 micrograms kg-1. Mean time from injection to onset of adenosine-induced PR prolongation was significantly greater during anaesthesia (12.8 (SD 5) vs 9.9 (3) s, P = 0.032). Atrioventricular block (assessed by the total number of non-conducted P waves) was significantly less during anaesthesia (12 vs 27, P = 0.016). We conclude that anaesthesia including 1% isoflurane and fentanyl 10 micrograms kg-1 delays the onset and reduces the magnitude of adenosine-induced atrioventricular block.

Vasodepressor reactions after orthotopic cardiac transplantation: relationship to reinnervation status.

Ventricular vagal nerve endings are thought to trigger vasodepressor syncope. Reports of vasodepressor reactions associated with donor bradycardia after cardiac transplantation have led to speculation that vagal reinnervation occurs. We assessed reinnervation status in seven patients 23-36 months (median 24 months) post-transplantation. Heart rate responses to vagal manoeuvres (respiration, Valsalva) and sympathetic stimuli (exercise and injection of tyramine into the coronary artery supplying the sinus node) were measured. All patients underwent 60 min of 60 degrees head-up tilt with foot plate support. During tilt four of the seven had vasodepressor reactions with a fall in mean arterial pressure of 20-90 mmHg. During vasodepression two patients had falls in donor heart rate of 13 and 40% relative to peak heart rate during tilt. These two patients had evidence of functional sympathetic reinnervation. By contrast the two patients without donor bradycardia during vasodepression had only limited or no evidence of sympathetic reinnervation. No patient had consistent evidence of parasympathetic reinnervation as judged by the heart rate response to vagal manoeuvres. Head-up tilt can thus produce vasodepressor reactions with donor bradycardia after cardiac transplantation in the absence of consistent evidence of vagal reinnervation. Left ventricular nerve endings may not be the only mediators of tilt-induced vasodepressor reactions in man. Donor bradycardia during vasodepression may reflect sympathetic withdrawal and not vagal reinnervation.

Cardiovascular and respiratory effects of adenosine in humans after pulmonary denervation.

Adenosine infusion causes tachycardia in normal subjects. A proposed mechanism is secondary pulmonary stretch receptor activation due to hyperventilation, induced by direct stimulation of carotid body chemoreceptors by adenosine. We examined responses to adenosine (incremental doses given by intravenous infusion, 5 min each rate) in six normal volunteers and six lung-transplant recipients with pulmonary denervation. Adenosine caused chemoreceptor stimulation in both groups with minute ventilation increasing from 5.8 +/- 0.4 to 10.7 +/- 1.3 l/min (P < 0.05) in the volunteers and from 4.8 +/- 0.4 to 9.2 +/- 0.8 l/min (P < 0.001) in the lung-transplant recipients. There was no difference in the magnitude of the ventilatory increase between the two groups (P = NS at all infusion rates). Adenosine produced tachycardia in both groups, with heart rate increasing from 66 +/- 5 to 84 +/- 3 beats/min (P < 0.01) in the volunteers and from 82 +/- 6 to 110 +/- 6 beats/min (P < 0.05) in the lung-transplant recipients. There was no difference in the magnitude of the heart rate response between the two groups (P = NS at all infusion rates). These data suggest, contrary to previous thinking, that pulmonary stretch receptor activation does not contribute to adenosine-induced tachycardia in humans.

Intravenous adenosine reveals intermittent preexcitation by direct and indirect effects on accessory pathway conduction.

In some patients with accessory pathways preexcitation occurs intermittently during sinus rhythm. In these patients the antegrade refractory period of the accessory pathway may either exceed the sinus cycle length under some circumstances, or conduction block in the accessory pathway may be variable. The ability of intravenous adenosine to unmask intermittent preexcitation was determined in patients with intermittent preexcitation but absent preexcitation at the time of study. Six patients undergoing assessment of the Wolff-Parkinson-White syndrome received incremental doses of intravenous adenosine (3, 6, and 12 mg). Adenosine administration was repeated in three patients after intravenous beta blockade (propranolol 0.2 mg/kg). Adenosine unmasked preexcitation in all patients. P delta intervals with preexcited beats were substantially shorter than resting PR intervals in all cases (range 40-80 msec shorter). In 4/6 patients preexcitation was seen early, coincident with the onset of atrioventricular nodal block. In 4/6 patients preexcitation was seen late during the secondary sinus tachycardia that follows the direct cardiac effects of adenosine. Two patients exhibited early preexcitation and late preexcitation. Beta blockade failed to prevent early preexcitation (2/2 patients) but abolished preexcitation related to sinus tachycardia (3/3 patients). Early preexcitation, coincident with the onset of AV nodal block, suggests a direct effect of adenosine on accessory pathway conduction. Late preexcitation, occurring during secondary sinus tachycardia, and abolished by beta blockade, suggests enhanced accessory pathway conduction due to sympathetic activation.