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Biomedical subjects

P Berthelsen

Publications and source records attributed to P Berthelsen.

At least 19 recordsLinked to original sources

Intramuscular low-dose ketamine versus pethidine for postoperative pain treatment after thoracic surgery.

In a double-blind prospective study the effects of low-dose intramuscular ketamine (1 mg/kg) were compared to pethidine (1 mg/kg) in the treatment of pain after pulmonary surgery. Thirty patients were admitted to the study and postoperatively randomized to either a ketamine or a pethidine group. The analgesic effect was evaluated using a scale ranging from 0 to 10, where 0 denoted no pain and 10 severe pain. We did not find any significant difference between the analgesic effect of ketamine and pethidine; however, the duration of action of ketamine appeared to be slightly longer. Throughout the study PaCO2 was significantly lower in the ketamine group. PaO2 increased through the study in both groups and was significantly higher after 2 h. Heart rates increased significantly only in the pethidine group. Mean arterial pressures remained unchanged and the respiratory frequencies were similar in the two groups. The incidence of adverse reactions was low and not significantly different between the groups. The findings indicate that low-dose intramuscular ketamine is a potent analgesic for postoperative analgesia following thoracic surgery and that it has no respiratory depressive effect.

Adult

Effect of piroxicam in addition to continuous thoracic epidural bupivacaine and morphine on postoperative pain and lung function after thoracotomy.

Twenty-eight patients scheduled for lung resection with lateral thoracotomy and postoperative chest drains during combined thoracic epidural bupivacaine plus morphine and general anaesthesia were studied. Postoperative pain treatment was continuous epidural infusion of bupivacaine 0.25% 5 ml h-1 plus morphine 0.2 mg h-1 for 48 h and, in addition, the patients received rectal piroxicam 40 mg randomly and double-blind 12 h and 1 h before surgery and 20 mg 24 h-1 postoperatively or placebo. Pain was evaluated at rest, during cough and mobilisation, together with pulmonary function (FEV1, FVC, PEFR) and sensory level of analgesia repeatedly for 48 h. The results showed efficient pain relief, but without differences in pain scores or need for supplementary analgesics between the two groups. Pulmonary function decreased similarly in the two groups. Thus we were unable to show enhanced analgesia by supplementing an otherwise effective low-dose epidural bupivacaine and morphine treatment with piroxicam after thoracic surgery with chest drains.

Administration, Rectal

Dissociation of renal and respiratory effects of acetazolamide in the critically ill.

The effects of acetazolamide on renal and erythrocyte carbonic anhydrase were studied in 12 critically ill patients. In the first part of the investigation (n = 6) we examined the renal effects of increasing doses of acetazolamide. The maximal renal excretion of water and bicarbonate was achieved with acetazolamide 2.5-5 mg kg-1 i.v. In the second part (n = 6), the associated respiratory effects of the effective renal dose of acetazolamide 5 mg kg-1 were evaluated. We found a statistically significant 4% decrease in pulmonary carbon dioxide excretion in the 10-min sampling period immediately following the administration of acetazolamide, but thereafter carbon dioxide elimination proceeded at a normal rate. The observed carbon dioxide retention is clinically unimportant, and we recommend acetazolamide as an effective means of eliminating surplus water and bicarbonate in the critically ill.

Acetazolamide

PEEP reverses nitroglycerin-induced hypoxemia following coronary artery bypass surgery.

Intravenous nitroglycerin is increasingly used during and after cardiac surgery to control blood pressure and improve subendocardial and peripheral circulation. A dramatic decrease in arterial oxygenation has, however, been reported in a number of poorly controlled clinical trials. In the present investigation 16 patients were studied 2-4 h after coronary artery bypass procedures. All were treated with a continuous infusion of nitroglycerin (1 microgram X kg-1 X min-1). Utilizing an on-off-on drug design, it was clearly established that nitroglycerin depresses arterial oxygenation by increasing the pulmonary venous admixture. Three possible underlying mechanisms are discussed, but at the present time no firm conclusion can be drawn as to the nature of the changes. Eight patients were ventilated with 1 kPa (10 cmH2O) positive end-expiratory pressure (PEEP) during the nitroglycerin infusion. PEEP-ventilation reversed nitroglycerin-induced changes in arterial oxygenation and pulmonary shunting without adversely affecting hemodynamic stability.

Coronary Artery Bypass

Central venous access via the external jugular vein in cardiovascular surgery.

In 115 consecutive adult patients scheduled for cardiovascular surgery, 150 catheterizations of the innominate or superior caval veins via an external jugular vein were attempted. The Seldinger technique was employed. In 99 (96-100)% of the attempts a straight, J-modified straight or a J-wire could be passed into the central venous system. One hundred and forty-six (97 (93-99)% of the subsequent catheter insertions were successful. Thirty-five patients had bilateral catheter insertions. Both sides proved to be equally suitable. Six anesthetists participated in the study and the longest catheterization time was 16 min. All catheterization procedures were uncomplicated.

Adult

Oxygen uptake and carbon dioxide elimination after acetazolamide in the critically ill.

Acetazolamide, which reversibly inhibits carbonic anhydrase, is a useful diuretic in alkalotic and over-hydrated patients. In two earlier investigations we have consistently found increases in the arterial and venous oxygen saturation and tension when patients were treated with acetazolamide 15 mg . kg-1. A plausible explanation of this phenomenon is that acetazolamide diminishes oxygen consumption. In the present study we measured oxygen uptake in 10 critically ill patients. We found a minor and statistically insignificant decrease in oxygen consumption. Nevertheless SVO2 increased from 0.77 to 0.83 and PVO2 from 5.9 kPa to 6.8 kPa. It is still not possible from this investigation to determine the origin of the improvement in blood oxygenation. The inhibition of carbonic anhydrase caused a CO2 retention of 5.8% of the total CO2 production. An increase in body stores of CO2 of this magnitude is without clinical significance.

Acetazolamide

Hemodynamic effects of alfentanil in verapamil-treated dogs.

The hemodynamic effects of alfentanil were investigated in six dogs receiving verapamil 0.5 mg X kg-1 and six dogs receiving saline in equal volume. Basic measurements were done after 30 min and the dogs were then given alfentanil 160 micrograms X kg-1 with measurements at 5, 15, and 30 min. Significant increases in central venous pressure (CVP), mean pulmonary arterial pressure and pulmonary wedge pressure (PWP) were found 30 min after verapamil. After verapamil-alfentanil, increases were seen in CVP and PWP at 5 and 15 min and in PWP at 30 min. Mean arterial pressure and cardiac index were unchanged, while a decrease in heart rate was fully compensated by an increase in stroke volume. Indices of contractility were unchanged. All values were within the limits of normal hemodynamic function. We conclude that high-dose alfentanil has no adverse effects on hemodynamic parameters during calcium blockade.

Alfentanil

Alfentanil and skeletal muscle circulation, oxygen consumption and P50.

The preservation of blood flow to skeletal muscles has low priority in the intact organism. If cardiovascular function is disturbed, for example by anesthetic drugs, skeletal muscle circulation diminishes or stops. Skeletal muscle surface pH (m-pH) is a sensitive indicator of muscle cell oxygenation and a fall in m-pH therefore provides an early warning of deterioration in overall cardiovascular performance. In the present study we investigated the peripheral effects of a new short-acting fentanyl derivative, alfentanil. Twelve dogs were anesthetized with a bolus injection of alfentanil 0.16 mg . kg-1 i.v. M-pH was recorded continuously, while total body oxygen consumption, oxygen transport and P50 were calculated. No changes were found. In the second part of the study, we pretreated six of the dogs with the "calcium antagonist" verapamil 0.5 mg X kg-1, while the other six dogs served as controls. After a rechallenge dose of alfentanil, we again found the peripheral perfusion sufficient to meet the oxygen demand of the muscles. Side-effects to alfentanil were a decrease in Pao2, due to an increase in pulmonary shunting of venous blood, and an increase in PaCO2. The changes in pulmonary ventilation-perfusion relationships were, however, not of a magnitude that should cause concern when alfentanil is used in normal subjects.

Adjuvants, Anesthesia

Carbon dioxide elimination after acetazolamide in patients with chronic obstructive pulmonary disease and metabolic alkalosis.

Acetazolamide, an inhibitor of carbonic anhydrase, which catalyzes hydration/dehydration of carbon dioxide, has been used for correction of metabolic alkalosis in patients with chronic obstructive pulmonary disease (COPD). Animal experiments have shown that the gradient between tissue and the alveolar CO2 tension increases after inhibition of carbonic anhydrase, suggesting retention of CO2. In order to determine the true degree of carbon dioxide retention after total inhibition of carbonic anhydrase, 10 patients with COPD and pronounced metabolic alkalosis (base excess above 6) under controlled mechanical ventilation were studied. The study showed that there was a statistically significant increase in tissue PCO2 and a temporary decrease in pulmonary carbon dioxide excretion. Furthermore, it was found that PaO2 and PVO2 increased significantly after inhibition of carbonic anhydrase, which could, at least partly, explain the improvement seen in patients with COPD and metabolic alkalosis after treatment with acetazolamide.

Acetazolamide

Fructose, xylitol and glucose in total parenteral nutrition.

A comparison was made between isocaloric amounts of 24% glucose and 24% Triofusin (composed of 120 g fructose, 60 g glucose and 60 g xylitol per liter) during the course of a 6-day, 3-phase crossover study of 15 patients undergoing total parenteral nutrition. The patients received a total of 0.5 g carbohydrate per kg per day. Plasma glucose as significantly higher during glucose infusion (7-22 mmol/l, median: 9 mmol/l,) than during Triofusin infusion (5-16 mmol/l, median: 6 mmol/l). A moderate to severe glucosuria was detected in three patients during infusion of 24% glucose, and this declined considerably during the Triofusin period. The total renal carbohydrate loss during the glucose period was 0-143 g, median: 6 g per day, and during the Triofusin period was 6-68 g, median: 10 g per day. The nitrogen balance and carbamide production rate were the same in the two infusion regimes. Changes in biochemical liver parameters were observed in most of the patients, but these could not be attributed to parenteral nutrition. None of the patients developed symptoms of metabolic acidosis. There was a slightly but significantly higher urinary excretion of oxalate in the Triofusin period (0.1-1.1 mmol per day, median: 0.5 mmol per day) than in the glucose period (0.1-1.0 mmol per day, median: 0.4 mmol per day). Most of the patients exhibited a slightly increased urinary excretion of urate, irrespective of the infusion regimen. Serum urate remained normal. It was concluded that Triofusin infused in the described dosage is a suitable calorie source for parenteral nutrition, but that it does not present a distinct advantage over the use of pure glucose solution. In patients suffering from reduced glucose tolerance, however, Triofusin represents a more easily manageable calorie course.

Adult

Cardiovascular performance and oxyhemoglobin dissociation after acetazolamide in metabolic alkalosis.

In patients with metabolic alkalosis, compensatory alveolar hypoventilation may induce hypercapnia and hypoxemia. In edematous or normally-hydrated patients without electrolyte deficiencies, acetazolamide--a carbonic anhydrase inhibitor--has been advocated to correct the primary acid-base disturbance, thereby preventing hypoxemia. The hemodynamic consequences and the effect on oxyhemoglobin dissociation of acetazolamide, were studied. Twelve critically ill patients with metabolic alkalosis were given 15 mg/kg body wt. acetazolamide intravenously. Cardiovascular performance was completely unchanged. The P50 was 26.6 mm Hg at the beginning and the end of the study, indicating that hemoglobin-oxygen affinity is unaffected by acetazolamide. In six patients, investigated after open-heart surgery, the arterial oxygen tension increased by 10-45%. This was probably related to the combined effects of slight reductions in total body oxygen consumption or shunting of venous blood through the lungs. Eight of the 12 patients were on controlled ventilation. After acetazolamide there was a mean increase in mixed venous carbon dioxide tension (PvCO2) of 4.5 mm Hg, with no increase in arterial carbon dioxide tension (PaCO2), indicating only a limited interference with carbon dioxide uptake and release of the carbonic anhydrase inhibition. No other adverse reactions were observed.

Acetazolamide

Allen's test and systolic arterial pressure in the thumb.

The result of Allen's test for arterial patency was compared with systolic arterial pressure in the thumb following manual occlusion of the radial artery in 8 patients aged 11-72 yr undergoing cardiovascular surgery. In 19 of 235 hands (8.1%), manual compression of the radial artery reduced the systolic arterial pressure in the thumb to less than 40 mm Hg, indicating inadequacy of the collateral ulnar arterial supply. The predictive value of a negative Allen's test was 0.992. Thus, in only 0.8% of cases would a negative Allen's test falsely indicate adequacy of the collateral ulnar supply. These results justify general application of Allen's test before radial artery cannulation.

Adolescent

Skeletal muscle circulation during sufentanyl and morphine anesthesia in propranolol treated dogs.

Sufentanyl is a new, potent, short-acting, fentanyl-like morphinomimetic. In the present study we compared the effects of high doses of sufentanyl and morphine on the peripheral circulation in beta-blocked dogs. Skeletal muscle surface pH (m-pH) was recorded continuously as an index of the microcirculation. Sufentanyl (0.01 mg/kg) had no adverse effects on the peripheral perfusion. Morphine (4 mg/kg) caused a severe and rapid fall in m-pH from 7.34 to 7.14 during the 30-min experimental period. At the same time calculated blood volume decreased by 20%. This hypovolemic deterioration of the circulation was probably caused by a histamine-mediated increase in capillary pressure and filtration of plasma from the intravascular space to the interstitial space. As sufentanyl could be safely administered to beta-blocked dogs, we recommend human studies. On the other hand, we discourage the use of high-dose morphine anesthesia until human studies have proved that the collapse of the peripheral perfusion seen in this study is species specific.

Adrenergic beta-Antagonists

Early response in central hemodynamics to high doses of sufentanil or morphine in dogs.

The hemodynamic effects of high doses of sufentanil, a newly synthetized highly potent analgesic, were investigated in dogs. This study compared the early (30 min) cardiovascular effects of sufentanil 0.01 mg . kg-1 and morphine 4 mg . kg-1. Sufentanil caused a moderate and insignificant decrease in mean arterial pressure (MAP). A 30% decrease in cardiac index (CI) was almost outbalanced by an increased systemic vascular resistance (SVRI). The lowering of CI was due to a more than 50% decrease in heart rate (HR) which was partly compensated for by a greater stroke volume index (SVI). In the first 5 min after morphine injection, MAP fell significantly to about 50 mmHg (below 50% of the control value). CI was reduced to about 50% of the control value because of significant decreases in both SVI and HR. The calculated SVRI was unchanged after morphine. Within 30 min some of the initially changed parameters had returned to control levels. Central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) increased immediately after sufentanil, but decreased after morphine. With time, both parameters returned towards control values. Peak left ventricular dP/dt decreased by about 25-50% after both analgesics. The rate-pressure products (RPP) were significantly decreased to less than one half of the control values after both analgesics. Mixed venous oxygen tension (PVO2), oxygen transport and oxygen consumption were significantly lowered in the sufentanil group, whereas immediate decreases after morphine were followed by gradual increases towards control values. We conclude that the use of high doses of sufentanil in dogs is safe. Apart from initial, transient changes, a stable cardiovascular state characterizes the high-dose sufentanil anesthesia, while morphine causes fluctuations in several hemodynamic parameters. Compared to morphine anesthesia, sufentanil anesthesia appears to be an attractive alternative which deserves further evaluation in humans.

Analgesics, Opioid

High-dose analgesic anesthesia with morphine or sufentanil in propranolol-treated dogs.

In propranolol-pretreated dogs (2 mg . kg -1) the immediate cardiovascular effects of sufentanil (0.01 mg . kg -1) or morphine (4 mg . kg -1) were compared. Besides a 40% decrease in cardiac index (CI), sufentanil and morphine initiated quite different hemodynamic changes. Sufentanil did not significantly change mean arterial pressure (MAP), central venous pressure (CVP) and mean pulmonary artery pressure (MPAP), while the pulmonary capillary wedge pressure (PCWP) increased by 50%. After morphine, MAP declined significantly by about 65%, and significant decreases in MPAP (14%) and PCWP (33%) were also observed. Propranolol reduced heart rate by 16%, and morphine caused no further reduction in HR. A significant decrease of about 30% was seen in HR after sufentanil. Sufentanil significantly raised systemic vascular resistance index (SVRI) by 15%, whereas morphine decreased it by 32%. Pulmonary vascular resistance index (PVRI) was unchanged after sufentanil, but significantly increased after morphine. Right ventricular stroke work index (RVSWI) was unaffected by both analgesics, and morphine decreased left ventricular work index (LVSWI) significantly by 80%. Oxygen transport index declined significantly after both analgesics. Sufentanil reduced oxygen consumption by 20%, while morphine left this parameter unaffected. We conclude that the administration of high-dose sufentanil leads to a stable circulation, even when a total beta-blockade exists.

Analgesics, Opioid