Effects of using the simplified airway risk index vs usual airway assessment on unanticipated difficult tracheal intubation - a cluster randomized trial with 64,273 participants.

BACKGROUND: Unanticipated difficult intubation remains a challenge in anaesthesia. The Simplified Airway Risk Index (SARI) is a multivariable risk model consisting of seven independent risk factors for difficult intubation. Our aim was to compare preoperative airway assessment based on the SARI with usual airway assessment. METHODS: From 01.10.2012 to 31.12.2013, 28 departments were cluster-randomized to apply the SARI model or usual airway assessment. The SARI group implemented the SARI model. The Non-SARI group continued usual airway assessment, thus reflecting a group of anaesthetists' heterogeneous individual airway assessments. Preoperative prediction of difficult intubation and actual intubation difficulties were registered in the Danish Anaesthesia Database for both groups. Patients who were preoperatively scheduled for intubation by advanced techniques (e.g. video laryngoscopy; flexible optic scope) were excluded from the primary analysis. Primary outcomes were the proportions of unanticipated difficult and unanticipated easy intubation. RESULTS: A total of 26 departments (15 SARI and 11 Non-SARI) and 64 273 participants were included. In the primary analyses 29 209 SARI and 30 305 Non-SARI participants were included.In SARI departments 2.4% (696) of the participants had an unanticipated difficult intubation vs 2.4% (723) in Non-SARI departments. Odds ratio (OR) adjusted for design variables was 1.03 (95% CI: 0.77-1.38). The proportion of unanticipated easy intubation was 1.42% (415) in SARI departments vs 1.00% (302) in Non-SARI departments. Adjusted OR was 1.26 (0.68-2.34). CONCLUSIONS: Using the SARI compared with usual airway assessment we detected no statistical significant changes in unanticipated difficult- or easy intubations. CLINICAL TRIAL REGISTRATION: NCT01718561.

Accumulation of hyaluronan and tissue edema in experimental myocardial infarction.

Experimental myocardial infarction was induced in rats. The myocardial accumulation of hyaluronan (HA) and water during the development of infarction was measured. The extractable HA content of the infarcted area increased progressively from day 1 and on day 3 reached a threefold increase compared with the HA amounts in myocardium of sham operated controls. The relative water content of infarcted areas also increased progressively reaching a maximum value by day 3 and was strongly correlated with the HA accumulation. Affinity histochemistry visualized a thin rim of HA in the endoperimysium in healthy myocardium. By day 2 an interstitial edema with inflammatory cells was apparent. The widened endoperimysium stained extensively for HA. By its water-binding ability, interstitial accumulation of HA will contribute to the interstitial edema in infarcted myocardial tissue. An interstitial edema is likely to influence the electromechanical characteristics of the myocardium and facilitate reentry phenomena due to a loss of contact between muscle cells. The edema also induces an increased extracellular pressure and an altered myocardial wall compliance that might impair myocardial microcirculation. The findings are relevant to an understanding of the beneficial effect of hyaluronidase treatment in limiting cellular damage during myocardial ischemia.

Right atrial temperature and electrical activity during cardioplegic cardiac arrest.

In 18 patients undergoing coronary artery bypass surgery the relation between right atrial temperature and right atrial electrical reactivation during cardioplegic cardiac arrest was studied. The administration of cardioplegic solution induced immediate ventricular and atrial arrest in all patients. No recurrence of ventricular activity was observed while right atrial activity subsequently recurred in 11 patients. Activity at the surface ECG was recorded only in one patient with right atrial reactivation. No right atrial electrical activity was found below 19 degrees C. The average atrial temperature was 21.5 degrees C while the average apex temperature was 15 degrees C. The study has confirmed previous observations that during cardioplegic cardiac arrest the right atrium is not as well protected as the ventricular tissue against rewarming. Monitoring of the right atrial electrical activity or right atrial temperature is essential to ensure atrial arrest during the entire period of cardioplegic cardiac arrest.

Ruptured abdominal aortic aneurysm with fistula into the inferior vena cava.

Aortocaval fistula is an unusual complication of ruptured abdominal aortic aneurysm. A case of coincident rupture of an abdominal aortic aneurysm into both the retroperitoneum and the inferior vena cava is presented. The symptoms and the treatment are discussed.

Myocardial contractile response and IP3, cAMP and cGMP interrelationships.

An experimental study in the perfused working normal and pressure overloaded rat heart. A mini review based on a doctoral thesis.

Supraventricular tachyarrhythmias after coronary bypass surgery--a double blind randomized trial of prophylactic low dose propranolol.

In the present study 75 patients were double blind randomized either to receive 10 mg propranolol orally 4 times a day (35 patients) or a placebo (40 patients). Episodes of clinically important supraventricular tachyarrhythmias were recorded in the first 4 postoperative days. They appeared in 5 of 35 patients receiving propranolol and in 5 of 40 patients receiving placebo (no statistically significant difference). In conclusion this study indicates the need for further evaluation to clarify if low-dose propranolol or any other drug is effective in reducing the frequency of SVT in the early postoperative period after coronary artery bypass surgery.

Effects of adrenergic and muscarinic agonist stimulation on IP3 and cyclic nucleotide levels in the pressure overloaded rat heart.

In this study, the dynamic interrelationships between myocardial functional state and changes in the second messenger content in pressure-overloaded hypertrophied hearts were investigated. Forty-three rat hearts were used after partial clamping of the abdominal aorta. The isolated hearts were perfused with Krebs-Henseleit buffer and allocated to perfusion for 20 s or 40 min as controls (n = 12); or with noradrenaline (10(-6) mol l-1, n = 11); carbachol (3 x 10(-7) mol l-1, n = 9); or noradrenaline plus carbachol (10(-6) mol l-1 + 3 x 10(-7) mol l-1, respectively, n = 11). maxdP/dt increased more than 2-fold already after 20 s on noradrenaline stimulation, followed by a significant increase in cAMP. After 40 min, maxdP/dt was lower than the maximal value, although higher than controls. cAMP was also decreased, but still significantly higher than controls. Perfusion with noradrenaline plus carbachol produced the same changes in maxdP/dt as those seen after noradrenaline stimulation alone, but failed to increase cAMP content after both 20 s and 40 min. The inositol trisphosphate (IP3) content was increased 40 min of control perfusion (p < 0.05). Noradrenaline and carbachol, separately, produced an increase in IP3 content already after 20 s (p < 0.05). The combination of noradrenaline plus carbachol also produced an increase of IP3 (p < 0.05; compared to controls), but to a lesser extent when compared either to noradrenaline or carbachol (p < 0.05). After 40 min of perfusion, IP3 was in the same range regardless of added agonist(s) and still slightly above control level (p < 0.05). The early increase in maxdP/dt induced by noradrenaline or the combination of noradrenaline plus carbachol was not paralleled by a decrease in ATP content. This was also the case upon addition of carbachol alone. However, after 40 min of agonistic perfusion, ATP levels were substantially decreased. In conclusion, myocardial IP3 content in pressure-overloaded hypertrophied hearts was not different from that of sham-operated hearts. After agonistic stimulation, an early increase in IP3 formation was seen. Attenuation of the IP3 response by combined stimulation with noradrenaline and carbachol was initially present in pressure-overloaded hypertrophied hearts. After 40 min no attenuation was found for either IP3 or for cAMP content, suggestive of induction of a desensitization.

Dynamic changes of myocardial inositoltrisphosphate and cyclic nucleotides: relationship to contractile response in the perfused working rat heart after adrenergic and muscarinic agonist stimulation.

Initial and late effects by adrenergic and muscarinic agonists on inositol trisphosphate (IP3) and cyclic nucleotide levels were determined and correlated to mechanical response in perfused rat hearts. Forty-three rat hearts were perfused with Krebs-Henseleit buffer in a modified Langendorff apparatus as a working preparation. The hearts were perfused as controls (n = 11), or with noradrenaline (10(-6) mol l-1) (n = 21), or with carbachol (3 x 10(-7) mol l-1) (n = 11) added to the perfusion buffer. The hearts were frozen at 20 s, 30 s and 40 min after addition of noradrenaline and at 20 s and 40 min after addition of carbachol, and after 5 and 45 min of control perfusion. cAMP and cGMP were determined by radioligand methods and IP3 by a combined fast performance liquid chromatography (FPLC)-isotachophoretic method. cAMP increased by 36% within 20 s followed by a decrease (22%) during the 10 s following noradrenaline addition. After 40 min cAMP regained its value near that of 20 s. Noradrenaline perfusion did not influence IP3 levels during the first 30 s although the value at 40 min was significantly higher (59%). IP3 increased (42%) after 20 s of carbachol perfusion followed by a 25% decrease at 40 min. Sustained stimulation of beta-receptors (after 40 min in our model) resulted in a repeated increase in cAMP only, without an increase in contractility.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial inositoltrisphosphate is depressed by dibutyryl cAMP. An experimental study in the isolated working rat heart.

A possible interrelation between IP3 and cAMP was studied in rat myocardium through circumvention of the receptor mediated stimulatory step of adenylyl cyclase by the administration of dibutyryl cAMP (db-cAMP). Changes in IP3 and cyclic nucleotide contents were correlated to changes in contractility after 40 min of beta- and alpha-adrenergic stimulation. Rat hearts (n = 23) were perfused with Krebs-Henseleit buffer in a modified Langendorff apparatus as a working preparation. The hearts were allocated to perfusion as control (n = 6); or with phenylephrine (10(-6) mol L-1, n = 6); (-)-isoproterenol (10(-6) mol L-1, n = 6); db-cAMP (2 x 10(-4) mol L-1, n = 5). All hearts were freeze-clamped after 40 min of perfusion. Phenylephrine produced a slow increase in maxdP/dt reaching a maximal value after 10 min (P < 0.05); thereafter it decreased, reaching the control level at 30 min. Isoproterenol perfusion resulted in an early (20 s) increase in maxdP/dt (P < 0.05). Over the next 10s maxdP/dt decreased markedly reaching an inflection point at 30 s. Thereafter only a slow increase during the rest of the perfusion was seen. Dibutyryl cAMP increased maxdP/dt slowly during the whole perfusion period reaching maximum after 40 min. Cyclic-AMP was increased by 21% after 40 min of phenylephrine perfusion while the corresponding increases by isoproterenol and db-cAMP were 131 and 105%, respectively (P < 0.05). Phenylephrine increased IP3 content to the same extent as isoproterenol perfusion (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Carbachol-induced increase in inositol trisphosphate (IP3) content is attenuated by adrenergic stimulation in the isolated working rat heart.

The interrelated responses of concomitant adrenergic and muscarinic receptor stimulation on second messengers and mechanical activity in the isolated perfused working rat heart were studied. The hearts were perfused with Krebs-Henseleit buffer in a modified Langendorff apparatus. The hearts were perfused with noradrenaline (10(-6) mol L-1, n = 20), with carbachol (3 x 10(-7) mol L-1, n = 11) or with noradrenaline plus carbachol (n = 20) in the above-mentioned concentrations. The hearts were frozen at 20 s, 30 s and 40 min after addition of noradrenaline and noradrenaline plus carbachol and at 20 s and 40 min after addition of carbachol. Five hearts were freeze-clamped directly after preperfusion and another five hearts after 40 min of perfusion and used as controls. Myocardial cAMP increased at 20 s and 40 min after noradrenaline perfusion. In contrast to this cAMP was unchanged at 20 s and decreased at 40 min after perfusion with noradrenaline plus carbachol. IP3 content increased after 20 s of carbachol- and after 40 min of noradrenaline perfusion (P < 0.05). However, noradrenaline plus carbachol did not induced any significant increase in IP3 content after 20 s and 30 s, but after 40 min a decrease below basal level was found (P < 0.05). Noradrenaline stimulation attenuated muscarinic agonist induced IP3 formation. A reciprocity existed in that noradrenaline induced IP3 formation was attenuated by carbachol. No direct relationship was observed between the IP3 response and contractility, also valid for cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Functional and biochemical effects of a K(+)-ionophore on the isolated perfused rat heart.

Valinomycin, a K(+)-specific ionophore, influenced function and metabolism of isolated perfused rat hearts in a dose-dependent fashion. At a concentration of 0.05 micrograms ml-1 in perfusion fluid a 50% reduction of heart rate (HR) and a 90% reduction in max dP/dt were observed. These effects were paralleled by a substantial decrease of myocardial energy charge from about 0.80 to 0.20. A 2.5 fold increase in tissue lactate concentration indicated an increased rate of glycolytic activity. Low ATP combined with high ADP and AMP levels as found in these valinomycin-treated hearts is known to promote phosphofructokinase activity and may explain the elevated lactate levels. A significant increase in the concentrations of adenosine, IMP and inosine was observed as well.

Double-contrast enhanced MR imaging of myocardial infarction in the pig.

Myocardial infarction was induced by ligating a diagonal branch of the left anterior descending artery in 18 pigs. All pigs were sacrificed 6 h after the occlusion. Dysprosium diethylenetriamine-pentaacetic acid bismethylamide (Dy-DTPA-BMA, 1.0 mmol/kg) was administered i.v. to 6 pigs, starting 3 min before sacrifice (injection time approximately 1 min). In a second group of 6 pigs, a double-contrast technique was used, consisting of an i.v. injection of gadolinium-DTPA-BMA (0.4 mmol/kg) 2 h before sacrifice, followed by an i.v. injection of Dy-DTPA-BMA (1.0 mmol/kg) 3 min before sacrifice. Six additional pigs, subjected to 6 h of coronary artery occlusion without administration of contrast medium, served as controls. The hearts were excised and imaged with MR. In the control animals, the infarctions demonstrated an increased signal intensity in the proton density- and T2-weighted images. Administration of Dy-DTPA-BMA primarily improved infarct visualization in the proton density- and T2-weighted images, due to reduction of signal intensity in nonischemic myocardium. The double-contrast technique further improved infarct visualization in all sequences.

Parasympathetic muscarinic stimulation limits noradrenaline induced myocardial creatine kinase release: a study in the isolated perfused working rat heart.

It has long been known that high concentrations of catecholamines may induce myocardial damage, and aggravate ischaemic injury. It has also been shown that beta-blockade may protect the myocardium from ischaemic damage. Stimulation of muscarinic receptors modulates beta-adrenergic receptor affinity for isoproterenol and attenuates isoproterenol induced adenylyl cyclase activation. Effects of muscarinic receptor stimulation were therefore investigated in isolated anterogradely perfused rat hearts under different experimental conditions. One group of hearts was perfused with noradrenaline, 10(-6) mol l-1 for 45 min, and another group was perfused with different carbachol concentrations (3 x 10(-7)-10(-5) mol l-1) with or without noradrenaline 10(-6) mol l-1, for 45 min. Release of creatine kinase to the perfusion buffer was taken as a sign of cell damage. Heart rate, left ventricular maxdP/dt and left ventricular pressure were measured throughout the perfusion time by insertion of a 20 gauge cannula through the left ventricular wall near the base. Carbachol (3 x 10(-7) mol l-1) alone induced a decrease of heart rate by 25% and maxdP/dt by 13%. Noradrenaline produced a 20% increase in heart rate, whereas the combination of noradrenaline plus carbachol induced a minor decrease in heart rate. Muscarinic receptor stimulation alone decreased myocardial contractility. However, when combined with noradrenaline no decrease in contractility was seen. Also, the release of creatine kinase to the perfusion buffer containing the combination of carbachol plus noradrenaline was reduced. Thus, muscarinic receptor stimulation protected the myocardium from catecholamine induced damage at concentrations where no change in contractility was seen.(ABSTRACT TRUNCATED AT 250 WORDS)

Dy-DTPA-BMA as an indicator of tissue viability in MR imaging. An experimental study in the pig.

The aim of this study was to investigate whether dysprosium (Dy) induced signal intensity (SI) loss in infarcted tissue in MR imaging. Myocardial infarction was induced in 12 pigs and Dy-DTPA-BMA (1.0 mmol/kg b.w.) was administered i.v. to 6 pigs 4 hours after occlusion and allowed to accumulate in the infarctions for 2 hours. Dy was analysed by inductively coupled plasma atomic emission spectrometry in infarcted and non-ischaemic tissue samples. The remaining 6 pigs, not administered contrast medium, served as controls. The infarctions demonstrated a high SI in the proton density- and T2-weighted sequences in both groups (ex vivo), although the Dy-DTPA-BMA group demonstrated a 3-fold greater concentration of Dy in infarcted compared with non-ischaemic myocardium. The lack of SI loss after Dy accumulation indicates that susceptibility effects are minor or absent in infarcted myocardium.

Magnetic resonance imaging of acute myocardial infarction in pigs using Gd-DTPA.

Six pigs with coronary artery occlusion were investigated with MR imaging before and subsequently for about 2.5 hours at repeated intervals after the intravenous administration of Gd-DTPA (0.4 mmol/kg). The animals were sacrificed after a total occlusion time of 6 hours and the hearts were excised. The excised hearts were then reexamined in the MR equipment and stained with TTC (triphenyl tetrazolium) in order to define areas of infarction. Four control hearts with 6-hour-old infarctions were only imaged ex vivo without any previous administration of contrast media. In vivo, there was no clear demarcation of infarction with or without Gd-DTPA. Ex vivo, without any contrast media, the infarctions were poorly discriminated with a discretely increased signal intensity relative to normal myocardium in the T2 weighted images. Gd-DTPA was found to accumulate in the infarctions, which caused an elevated signal intensity most pronounced in the T1 weighted images. This considerably improved the delineation of the infarcted area.

MR imaging of acute myocardial infarction in pigs using Gd-DTPA-labeled dextran.

Myocardial infarctions were induced in 12 pigs. In 6 pigs, dextran-(Gd-DTPA)15 (approximately 0.1 mmol Gd/kg b.w.) was injected i.v. 4 to 4.5 hours after coronary artery occlusion. ECG gated MR images were obtained repeatedly before (n = 4) and after (n = 6) contrast medium injection. Relaxation times in blood samples were measured repeatedly. The animals were sacrificed 2 hours after contrast medium administration. The hearts were excised, reexamined in the MR equipment and stained with triphenyltetrazolium chloride (TTC) in order to define areas of infarction. The remaining 6 pigs were sacrificed 6 hours after occlusion without administration of contrast medium. These hearts were only imaged ex vivo. In vivo, the infarctions could not be identified with or without dextran-(Gd-DTPA)15. Ex vivo, without contrast medium, the infarctions had an increased signal intensity, most pronounced in the T2-weighted images. Dextran-(Gd-DTPA)15 caused a prolonged, pronounced shortening of T1 and T2 in blood samples. The infarct demarcation improved in the T1-weighted images after injection of dextran-(Gd-DTPA)15, due to a moderate enhancement in normal myocardium and a stronger enhancement at the periphery of the infarctions, while the central parts of the infarctions were only weakly enhanced.

The diabetic heart: a porcine model evaluated with positron emission tomography using 1-11C-palmitate and 3-11C-pyruvate.

The potential value of positron emission tomography (PET) in evaluating the myocardial energy metabolism was studied in two previously healthy mini-pigs before, during and after the induction of non-insulin dependent diabetes with alloxan. The distribution and kinetics of radioactivity derived from trace amounts of 11C-pyruvate and 1-11C-palmitate were followed in different sections of the myocardium. The early distribution of both tracers was similar even after the development of diabetes. The elimination of 11C-pyruvate derived radioactivity was slower in the diabetic heart. The rate of beta-oxidation was also decreased as suggested by the elimination curve of 11C-palmitate and the incorporation of 11C-palmitate into the triglyceride and phospholipid pool of the myocardium was increased in the diabetic animals. The results are consistent with previous observations using other techniques. Positron emission tomography offers the opportunity to characterize regional tissue metabolism quantitatively in vivo. This method may become a powerful tool in studying myocardial metabolism and the metabolic basis for the cardiac dysfunction in diabetes mellitus.