Adsorption of desflurane from the scavenging system during high-flow and minimal-flow anaesthesia by zeolites.

Application of high-silica zeolites in a special adsorber allows complete selective adsorption of the inhalation anaesthetic desflurane from the outlet port of the scavenging system of the anaesthesia machine. In comparison with charcoal filters, zeolites allow almost complete desorption at moderate temperatures followed by condensation of the desflurane to the liquid phase. The adsorption of scavenged desflurane by zeolites was measured in 13 patients. The duration of the anaesthesia was between 70 and 130 min. A minimal-flow regime (0.5 L min-1 fresh gas inflow) was used for maintenance in seven patients and a higher-flow regime (3 L min-1 fresh gas flow) was used for maintenance in six patients. In minimal-flow anaesthesia, 62% of the delivered desflurane was adsorbed by the zeolite while 86% of the delivered desflurane was adsorbed in higher-flow anaesthesia. Preliminary results show that about 85% of the adsorbed desflurane could be recovered as liquid with high purity via desorption.

[Ornipressin (POR 8)--effect on coronary blood circulation and the peripheral circulation. An animal experimental study]. / Ornipressin (POR 8)--Wirkung auf die Koronardurchblutung und die periphere Zirkulation. Eine tierexperimentelle Studie.

Ornipressin (POR 8), referred to below as OR, is a synthetic derivative of natural vasopressin. It was introduced into clinical practice to replace epinephrine as a local vasoconstrictor because OR was presumed to produce fewer undesirable side-effects. However, mayor cardiovascular complications following local infiltration of OR have been reported in recent time. Beside increased blood pressure and changes in heart rate, there is evidence that the systemic effects of OR include a distinct vasopressor activity on coronary arteries. This study was planned to investigate the effects of OR in haemodynamics and the coronary vascular system. METHODS. The effects of OR on systemic haemodynamics and coronary circulation were studied in nine anaesthetized closed-chest mongrel dogs. Anaesthesia was administered using N2O/O2 (FiO2:0.33) and enflurane (1.0 vol% endtidal). Saline-filled catheters were used to measure intravascular pressures. Left ventricular pressure change (dP/dt) was monitored with a tip catheter manometer. Cardiac output (CO) was determined using thermodilution and coronary sinus blood flow, using a Pitot catheter. Recording of baseline values was followed by bolus injection of OR (0.03 U/kg) and changes in haemodynamics were measured for 90 min at fixed time intervals. Statistical analysis was performed by analysis of variance for repeated measures. A value of P < or = 0.05 was considered to indicate statistical significance. RESULTS. Significant maximum changes occurred within 3-5 min after administration of OR. Systolic and diastolic arterial pressures increased by 33% and 39%, respectively. With only minor changes in heart rate, cardiac output markedly decreased by 44% and total peripheral resistance increased by 159%. Impaired pump function of the left ventricle became obvious by a decrease in maximum dP/dt, a decrease in ejection fraction by 35%, and a concomitant sharp increase in left ventricular enddiastolic pressure by 68% and in endosystolic volume by 41%. At the same time, OR produced a marked impairment of coronary perfusion. Myocardial blood flow fell by 32%, while coronary vascular resistance rose by 112%. Increased myocardial oxygen demand and reduced oxygen supply resulted in very low values of coronary venous oxygen saturation (< 20%). CONCLUSIONS. Systemic effects of OR are characterized by a sharp rise in arterial blood pressure. Concomitantly a decrease of myocardial contractility leads to a compromised left ventricular function with marked increases in left ventricular enddiastolic pressure. These haemodynamic changes are associated with an imbalance of myocardial oxygen demand and delivery due to the distinct OR-induced coronary constriction. With regard to the deterioration of systemic and cardiac haemodynamics the indications and use of ornipressin in clinical practice need to be reevaluated.

[Signs of a severe myocardial ischemia following peritonsillar infiltration with ornipressin (POR 8)]. / Zeichen einer schweren Myokardischämie nach peritonsillärer Infiltration mit Ornipressin (POR 8).

Ornipressin (OR), a synthetic derivative of natural vasopressin, is widely used in combination with local anaesthetics in order to reduce surgical bleeding and systemic absorption of the local anaesthetic. As shown previously in experimental studies, OR causes severe coronary vasoconstriction. The myocardial oxygen balance is compromised by an increase in myocardial oxygen demand due to hypertension and impaired oxygen delivery following coronary vasoconstriction. We describe the case of a 19-year-old male who was admitted to the hospital for elective tonsillectomy. There was no evidence of systemic or cardiovascular disease (ASA I). Following the induction of anaesthesia with thiopentone 4 mg/kg and ventilation with N2O/O2 (FiO2:0.25), vecuronium was administered to facilitate orotracheal intubation. Anaesthesia was maintained with N2O/O2 (FiO2:0.33) and 2 MAC isoflurane. After reaching an anaesthetic steady state with stable haemodynamic conditions, peritonsillar infiltration with a prilocaine solution containing a total of 0.8 IU OR (0.1 IU/ml) produced marked tachycardia and hypertension. Concomitantly, distinct ST-segment-depression was observed in a lead II ECG. Hypertension and tachycardia occurred within 3 min after the local infiltration with prilocaine/OR. Maximum ST-segment depression and haemodynamic changes were recorded 11 min after infiltration, with an increase in heart rate from 58 to 136 min and a rise in blood pressure from 115/50 to 217/130 mmHg. Considering experimental results, the ECG changes in this case show clear evidence that even in healthy humans OR-induced systemic haemodynamic changes may be complicated by severe myocardial ischaemia due to coronary vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Dose-related effects of intracoronary application of nisoldipine on central and peripheral circulatory parameters.

In a randomized study central and peripheral circulatory parameters were determined in 12 anaesthetized mongrel dogs before and after intracoronary injection of nisoldipine and placebo. Administration of 0.2 to 0.8 micrograms/kg nisolpine was followed by a 46% to 62% decrease in coronary vascular resistance and a 109% to 141% increase in myocardial blood flow lasting 10 min. There was no significant change in myocardial contractility or peripheral circulatory parameters. An increase in dosage to 1.6 micrograms/kg did not cause a further increase in myocardial blood flow or decrease in coronary vascular resistance. However, there was a significant decrease in total peripheral resistance of up to 32% and a 36% increase in heart rate attributable to counter-regulation lasting 3 to 5 min. At this dosage level a significant decrease in myocardial contractility and an increase in left ventricular end-diastolic pressure are to be expected. This implies a major dissociation between coronary vascular effects and changes in parameters of myocardial performance and peripheral resistance after intracoronary administration of nisoldipine, an effect which is dose-related. Injection of 0.4 to 0.8 micrograms/kg would seem to be the optimal dosage range for intracoronary administration of nisoldipine producing maximum coronary dilatation without myocardial depression.

[Determination of cardiac output under PEEP-respiration with the "NCCOM 3" non-invasive bioimpedence monitor in comparison with the thermodilution method. A study in anesthetized dogs]. / Die Bestimmung des Herzzeitvolumens unter PEEP-Beatmung mit dem nichtinvasiven Bioimpedanzgerät "NCCOM 3" im Vergleich zur Thermodilutionsmethode. Eine Untersuchung an narkotisierten Hunden.

A new noninvasive cardiac output (CO) computer ("NCCOM 3") based on the bioimpedance principle was compared to a CO computer based on standard thermodilution measurements. Simultaneous measurements were made on dogs who were ventilated with or without positive end expiratory pressure (PEEP). There was no correlation of cardiac output measurements with the two methods (r = 0.10, n = 60). Comparing only measurements without PEEP yielded r = 0.41. Thermodilution measurements showed the well-known decline in cardiac output during PEEP, whereas the bioimpedance device recorded an increase in cardiac output. These differences were statistically significant. We conclude that the NCCOM 3 cannot at present replace the invasive standard methods of CO measurement in ventilated patients. A lack of differentiation of circulatory effects, thoracic gas volume, and intrathoracic fluid content is the most likely cause of the discrepancies seen.

[Dose-dependent effect of amrinone on hemodynamics, myocardial circulation and myocardial energy requirement. An experimental study]. / Die dosisabhängigen Wirkungen von Amrinone auf die Hämodynamik, die Myokarddurchblutung und den myokardialen Energiebedarf--Eine experimentelle Studie.

This study was designed to assess the dose-dependent effects of amrinone (1, 2 and 4 mg/kg i.v.) on hemodynamics, myocardial blood flow and myocardial oxygen consumption in anesthetised closed chest dogs (n = 8). Heart rate (HR), cardiac output, mean aortic pressure (MAP), left ventricular end-diastolic pressure (LVEDP), maximum dp/dt (dp/dtmax), myocardial blood flow (MBF) and aorto-coronary sinus oxygen difference (AVDO2 cor) were measured. Cardiac index (CI), stroke volume index (SVI), ejection fraction (EF), total peripheral resistance (TPR), coronary vascular resistance (CVR) and myocardial oxygen consumption (MVO2) were calculated from standard formulas. Amrinone improved myocardial pump function by a direct positive inotropic effect on the myocardium. EF and SVI increased to a maximal degree with 1 mg/kg amrinone (28% resp. 30%). dp/dtmax increased dose dependent (46, 64, 71%). Following a systemic vasodilation due to amrinone, left ventricular filling pressure and TPR decreased significantly. With 1 and 2 mg/kg amrinone MAP remained unchanged. 4 mg/kg produced a distinct fall in MAP accompanied by an increase in HR. The improvement in myocardial contractility did not cause a comparable increase of myocardial oxygen consumption. Due to an unloading of the heart 1 and 2 mg/kg amrinone induced no significant and prolonged augmentation of the myocardial oxygen demand. In the coronary circulation a non energy dependent vasodilation occurred followed by a marked decrease of AVDO2 cor (10, 18, 28%).

The effects of glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside on haemodynamics, coronary blood flow and myocardial oxygen consumption - an experimental study.

The influences of glyceryl trinitrate, isosorbide dinitrate and sodium nitroprusside intravenously on haemodynamics, coronary circulation and myocardial oxygen consumption were investigated in closed chest dogs (n = 8). In an attempt to simulate heart failure the dogs received blood transfusion (15 ml/kg) in the presence of halothane-induced myocardial depression. All three nitrates reduced the loads for the left ventricle. With isosorbide dinitrate and sodium nitroprusside the preload and pulmonary pressure decreased to a greater extent than with glyceryl trinitrate. The haemodynamic results suggest that sodium nitroprusside is the favourable nitrate in left ventricular failure because it produces a balanced reduction in the ratio of pre- and afterload. Four micrograms/kg X min sodium nitroprusside induced marked coronary dilatation; glyceryl trinitrate had only a slight coronary vasodilating effect. With isosorbide dinitrate the myocardial blood flow remained well adapted to oxygen demand, the coronary vascular resistance did not change. Sodium nitroprusside produced a significant change of the transmural myocardial blood distribution-expressed as the epi/endocardial blood flow ratio. The ratio was increased by sodium nitroprusside, much more than by glyceryl trinitrate or isosorbide dinitrate.

[The influence of pressure loading upon haemodynamics and myocardial metabolism during beta-adrenoreceptor blockade (author's transl)]. / Hëmodynamik und Energiebilanz beta-blockierter Herzen während einer Erhöhung der linksventrikulären Nachlast.

This study compares the effects of a primary increase in afterload (induced by angiotensin) upon haemodynamics, myocardial function and metabolism of anaesthetized, closed chest dogs with (n = 7) and without (n = 7) beta-adrenoreceptor blockade. In both groups cardiac index (-20%) and stroke index (-30 resp. 40%) decreased by afterload increase. Pressure loading and beta-adrenoreceptor blockade were associated with a higher left ventricular enddiastolic pressure (+60%) and a higher heart rate (+35%) than in the control group. The high left ventricular enddiastolic pressure is supposed to be induced by the loss of homoiometric autoregulation. The increase in heart rate is due to the Bainbridge reflex. In the group of dogs with beta-adrenoreceptor blockade the myocardial oxygen consumption rose in proportion more than in the control group. The clinical implications are discussed.

[Systemic and coronary haemodynamic effects of dobutamine and norepinephrine during metabolic acidosis]. / Wirkungen von Dobutamin und Noradrenalin auf den Systemkreislauf und die Sauerstoffversorgung des Myokards bei metabolischer azidose.

The effects of clinical doses of dobutamine (5 microgram/kg x min) and norepinephrine (0.2 microgram/kg x min) on systemic haemodynamics and coronary circulation were studied during normal pH and during metabolic acidosis (pH 7.0) induced by hydrochloric acid in 9 anaesthetized closed chest dogs. Metabolic acidosis per se failed to show any significant depression of cardiac function, indicating that animals with intact sympathoadrenal system are highly resistant to acidaemia. Our results further demonstrated that a significant circulatory response to clinical doses of dobutamine and norepinephrine was still present during metabolic acidosis. However, the increase in cardiac output, max dp/dt and mean arterial pressure after dobutamine was found to be significantly reduced at low pH-values, whereas the vasopressor response to norepinephrine was not affected. From these results it may be speculated that metabolic acidosis differently influences the responsiveness of alpha- and beta-adrenergic receptors. Finally our results show that metabolic acidosis did not compromise the coronary adjustment to catecholamine-induced increases in myocardial oxygen demand.

Circulatory pattern and duration of action of naloxone in dogs with and without opioid pretreatment.

We investigated the circulatory pattern of naloxone reversal after high-dose fentanyl infusion in dogs. Within 1 min there was a sudden decrease in total peripheral resistance with a concomitant increase in stroke volume index. All other parameters changed back in direction of pre-fentanyl values in various degrees with peak effects in about 3-7 min. The persistency of reversal was different for individual parameters, but 20 min after injection of naloxone almost all changes induced by antagonisation of narcotic activity had returned to pre naloxone levels. In a control series with animals not pretreated with opioid, naloxone was shown to have no specific pharmacologic action of its own.

[The haemodynamic effects of dobutamine and dopamine in patients with coronary artery disease. A study performed under general anaesthesia (author's transl)]. / Hämodynamische Wirkungen von Dobutamin und Dopamin bei Patienten mit koronarer Herzkrankheit. Eine Untersuchung unter den Bedingungen einer Allgemeinanaesthesie.

The haemodynamic effects of dobutamine (2 microgram/kg . min and 4 microgram/kg . min) and dopamine (4 microgram/kg . min and 8 microgram/kg . min) were studied in 17 patients with coronary artery disease prior to coronary bypass surgery. The study was performed under general anaesthesia (modified neurolept analgesia) and controlled ventilation. Dopamine improved cardiac index significantly, increased mean aortic pressure slightly while heart rate and total peripheral resistance remained unchanged. Dobutamine failed to increase cardiac and stroke index significantly, but increased mean aortic pressure distinctly due to an elevated total peripheral resistance. Both catecholamines increased left ventricular filling and mean pulmonary artery pressure. The HR x ASP-product which is closely related to left ventricular oxygen consumption was found to be augmented to a greater extent during dobutamine. For the above reasons dopamine should be favoured for increasing cardiac output in patients undergoing aortocoronary bypass surgery. Our study does not confirm earlier results which have shown dobutamine to be the preferable catecholamine. The possible reasons for this discrepancy are discussed.

[The influence of sodiumnitroprusside on the oxyhaemoglobin dissociation curve in vitro (author's transl)]. / Einfluss von Natriumnitroprussid auf die Sauerstoffaffinität des Hämoglobins.

Blood from 16 donors was incubated with 3 microgram sodiumnitroprusside (SNP)/ml blood and the PO2 for halfsaturation of haemoglobin at standard pH and temperature was measured. There was no significant shift of the oxygen dissociation curve. Erythrocyte 2, 3 DPG and met-Hb concentrations did not show significant differences between SNP-treated and control blood. Although the red cells and the haemoglobin are involved in the metabolism of SNP, in clinical doses SNP does not alter the oxygen affinity.

[A comparison of cardiovascular effects of dobutamine and dopamine (author's transl)]. / Ein Vergleich der kardiovaskulären Wirkungen von Dobutamin und Dopamin.

The influences of dobutamine and dopamine 5-40 microgram/kg-min intravenously on hemodynamics and myocardial oxygen consumption were investigated in closed chest dogs (n=9). Heart rate (HR), cardiac index (CI), stroke volume (SVI), mean aortic pressure (MAP), pulmonary artery pressure (PAP), central venous pressure (CVP), left ventricular enddiastolic pressure (LVEDP), myocardial blood flow (MBF) and maximum dp/dt (dp/dtmax) were measured. Total peripheral resistance (TPR), coronary vascular resistance (CVR), myocardial oxygen consumption (MVO2), efficiency of heart work (EME), the ventricular volumes (EDV, ESV) and the ejection fraction (EF) were calculated. When dopamine was infused, the cardiac output rose mainly by an increase of heart rate. During dobutamine an increase of stroke volume and ejection fraction was involved in the improvement of cardiac output. Heart rate and mean aortic pressure increased to a greater extent by dopamine. Dobutamine and dopamine increase myocardial blood flow and oxygen consumption. The comparatively slight effects of dobutamine on afterload and heart rate resulted in smaller increases in myocardial oxygen consumption. The efficiency of external heart work was increased by dobutamine at the doses of 5 microgram and 10 microgram/kg-min. In the higher dose range external myocardial efficiency decreased under dopamine and dobutamine. Load data and heart rate indicate that a greater inotropic effect of dobutamine compared with equal doses of dopamine is involved in the increase of dp/dtmax. The results are discussed in relation to a clinical use of dobutamine and dopamine.

[Pathophysiological mechanisms in stagnant hypoxia with special reference to myocardial ischaemia (author's transl)]. / Stagnationshypoxie Pathophysiologische Mechanismen am Beispiel der myokardialen Ischämie.

The extent of biochemical changes arising from hypoxia due to slowed circulation and the rate at which they occur are closely related to the degree of functional and morphological impairment of the affected organ. The pathophysiological mechanisms operating in stagnant-type hypoxia are reviewed with special reference, on account of its practical importance, to myocardiac ischaemia. Differences between regional hypoxia and damage to the whole organ, and also the additional damage caused by stoppage of the circulation are discussed in detail. The importance of adjusting the therapeutic measures to the pathophysiological regulatory mechanisms when treating ischaemic cardiac arrest or myocardiac infarction is stressed.

[The effects of the vasodilator nitroprusside on haemodynamics and myocardial oxygen consumption during drug induced myocardial depression (author's transl)]. / Kardiovaskuläre Wirkungen von Natriumnitroprussid während einer Myokarddepression.

The effect of the vasodilator nitroprusside (NP) on haemodynamics and myocardial oxygen consumption during drug induced myocardial oepression was examined in dogs (n = 7). The investigations were performed on closed chest dogs lightly anaesthetized with piritramide and N2O/O2 (ratio 2:1) under controlled ventilation and after beta-adrenergic blockade (1.5 mg/kg propranolol). After a loading dose and a continuous infusion of 0.3 mg/kg X min of pentobarbitone left ventricular maximum dp/dt was reduced to 50% of the control level, which was taken for granted as a standardized myocardial depression. Using an infusion of NP at a mean rate of 7 microgram/kg X min mean arterial pressure was then lowered to 80 mmHg for 20 min. The vasodilator therapy led to an increase in cardiac output and in stroke volume by 16%. Since the calculated endsystolic volume of the left ventricle decreased simultaneously (19%), the ejection fraction increased from 38% to 46%. There was also a significant reduction in left ventricular enddiastolic pressure (46%), which is supposed to result from the combined effects of an improved myocardial performance, a pooling of blood in peripheral vessels (indicated by decreases in enddiastolic volume by 6%, in mean pulmonary arterial pressure by 25% and in central venous pressure by 45%) and an increased ventricular compliance. Since the myocardial wall tension, a major determinant of myocardial energy demand, was lowered by increased ventricular compliance and reduced pre- and afterload, the oxygen consumption of the heart decreased by 22%. The smaller demand was supplied by an unchanged coronary blood flow. The narrowing of the a-v oxygen difference of the heart indicated a coronary dilatation (10%). The results obtained from this study support the clinical observations that NNP may improve an imbalanced ratio between myocardial oxygen supply and demand, in patients with impaired cardiac performance.

[Doxapram-induced changes in circulation and myocardial efficiency (author's transl)]. / Kreislaufstimulation durch Doxapram

The effects of Doxapram 2.0 mg/kg intravenously on circulation and myocardial oxygen supply were studied in 9 anaesthetized closed chest dogs. Immediately after Doxapram increases in heart rate (maximum+40.5%, 1st min), mean aortic pressure (+49%, 3rd min), cardiac index (+18%, 3rd min), total peripheral resistance (+32%, 3rd min), pulmonary arterial pressure (+48%, 1st min), left ventricular end-diastolic pressure (+79%, 1st min), myocardial blood flow (+38%, 3rd min), myocardial oxygen consumption (+74%, 1st min) and left ventricular work (+76%, 1st min) were observed. The changes in heart rate, mean aortic pressure, myocardial blood flow, myocardial oxygen consumption and heart work were persistent up to 20 min after Doxapram 2.0 mg/kg intravenously. Max dp/dt, coronary vascular resistance and the myocardial efficiency were not influenced after Doxapram.

Effects of althesin, etomidate and fentanyl on haemodynamics and myocardial oxygen consumption in man.

The acute effects of althesin, etomidate and fentanyl upon haemodynamics, myocardial contractility and oxygen comsumption of the heart were studied in healthy premedicated patients (n = 15) lightly anaesthetized with N2O-O2 (ratio 2:1), 0.3 volumes per cent of halothane and isoflurane respectively. All individuals were ventilated at a normal level. The patients (n = 9) in the halothane group received etomidate 0.3 mg/kg and 20 minutes later althesin 0.075 ml/kg intravenously. In a second group of 6 patients on isoflurane fentanyl 0.01 mg/kg was given. Etomidate did not affect the cardiovascular system significantly. While the decrease in blood pressure after althesin (24 per cent) was the result of a reduction in total peripheral resistance (32 per cent), hypotension associated with fentanyl (23 per cent) was caused by diminished output due to bradycardia (18 per cent). Load data,heart rate, and maximum dp/dt indicated moderate negative inotropic properties only of althesin. Using the complex haemodynamic parameter developed by Bretschneider the myocardial oxygen consumption was calculated. The energy demand of the heart decreased with etomidate, althesin and fentanyl by 14 per cent, 16 per cent and 32 per cent respectively. It is concluded that the risk of cardiovascular depression at induction in patients with impaired myocardial performance and coronary insufficiency can be minimized with etomidate and/or fentanyl.

Dopamine effects on circulation and myocardial oxygen supply.

We measured the action of dopamine given intravenously at dosage ranging from 2.5 to 320 micrograms/kg per min in closed chest anaesthetized dogs. Dopamine produced a dose-dependent increase in heart rate, cardiac index, mean arterial pressure, total peripheral resistance, pulmonary artery pressure, left ventricular end diastolic pressure, coronary flow and myocardial oxygen consumption. At dopamine dosage of 80-320 micrograms/kg per min, the coronary vascular resistance, the stroke volume index, the efficiency of heart work and the central venous pressure are all decreased. The maximum effect of dopamine on the circulation was seen at a dose between 40 and 80 micrograms/kg per min.