Henriksson Ba

β-Receptor Blockade and Spinal Anaesthesia. Withdrawal versus Continuation of Long-term Therapy

A prospective study was performed in 43 men scheduled for transurethral resections under spinal anaesthesia. All patients were on chronic β‐receptor blockade because of hypertension and/or ischaemic heart disease. The patients were randomly subjected to either a gradual preoperative withdrawal or a continuation of the β‐receptor blockade. Haemodynamics were measured non‐invasively. Spinal anaesthesia was performed and an i.v. injection of atropine given. The patients were then placed in a lithotomy position. Mean anaesthetic level included T6. After β‐receptor blocker withdrawal consistently elevated heart rates, a high incidence of arhythmias, angina pectoris and postoperative ST‐T changes indicating myocardial ischaemia were seen. These changes were not seen in patients with continued β‐receptor blockade. Withdrawal of β‐receptor blockers was also associated with an increased total peripheral vascular resistance in connection with spinal anaesthesia. These results suggest that patients on long‐term β‐receptor blockade should continue the therapy during and after spinal anaesthesia.

β-Receptor Blockade and Neurolept Anaesthesia. Withdrawal vs Continuation of Long-Term Therapy in Gall-Bladder and Carotid Artery Surgery

Forty‐eight chronically (>3 months) β‐receptor‐blocked patients with ischaemic heart disease and/or hypertension were studied on 49 occasions after random distribution to a 4‐day, gradual preoperative withdrawal (n = 26) or a continuation (n = 23) of β‐receptor blockers. The patients were scheduled for either a cholecystectomy (n = 28) or a carotid thrombendarterectomy (n = 21) under neurolept anaesthesia. Three patients were excluded from the randomized part of the study due to complications (tachycardia, hypertension, severe angina) after therapy withdrawal. In subgroups, central haemodynamics (β‐receptor blockers withdrawn n = 6, continued n = 8) and creatinine‐kinase B (β‐receptor blockers withdrawn n = 9, continued n= 11) were studied. Withdrawal of β‐receptor blockers was associated with high heart rates, supraventricular tachyarrhythmias and a hyperkinetic circulation during pain stimuli. Significantly more postoperative ECG changes (p<0.02) indicative of myocardial ischaemia were found than in β‐receptor blocked patients. These patients had low heart rates but also pronounced increases in pulmonary capillary wedge pressures, which in single patients could be associated with myocardial damage. These results imply that β‐receptor blockers should be continued before surgery and that a concomitant vasodilatatory therapy is likely to avoid the drawbacks of an increased cardiac afterload.

Long‐Term β‐Receptor Blockade ‐ Adrenergic and Metabolic Response to Surgery and Neurolept Anaesthesia

Twenty‐six patients on chronic (>3 months) β‐receptor blocking therapy due to ischaemic heart disease and/or hypertension were randomly distributed to a 4‐day gradual withdrawal (n= 13) or a continuation of ordinary therapy until a planned cholecystectomy under neurolept anaesthesia (n = 13). Plasma‐adrenaline, ‐noradrenaline, ‐potassium, ‐glycerol, ‐FFA, ‐insulin and b‐glucose were determined perioperatively. The metabolic response to surgery was as expected with hyperglycaemia and depressed insulin levels, which did not differ significantly between the two groups of patients. Plasma‐catecholamines showed the highest mean values during emergence from anaesthesia. Plasma‐adrenaline and ‐potassium were constantly highest in the β‐receptor‐blocked patients, who also showed indices of a relatively depressed lipolysis compared to patients in whom β‐receptor blockers had been withdrawn. These discrepancies between withdrawal versus continuation of preoperative β‐receptor blockade seemed to be of small clinical importance and did not oppose the present view that β‐receptor blockers should generally be continued during surgery. However, findings in individual patients suggest that β‐receptor blockade may maintain hypoglycaemia in catabolic patients.

Effects of thoracic epidural anesthesia and adrenoceptor blockade on the cardiovascular response to dopamine in the dog

The cardiovascular effects of dopamine are different before and during thoracic epidural anesthesia (TEA). To evaluate underlying adrenoceptor‐mediated mechanisms, dopamine effects were investigated in nine chloralose‐anesthetized dogs. The circulatory response to dopamine (0–40 μg · kg‐1 · min‐1) was studied before and during TEA, and during TEA after introducing the α1‐antagonist prazosin (0.3 mg · kg‐1), the α2‐antagonist rauwolscine (0.3 mg · kg‐1), and the β1‐antagonist metoprolol (0.5 mg · kg‐1). TEA decreased mean arterial pressure (MAP) by 29%, cardiac output (CO) by 36%, heart rate (HR) by 27%, and the maximum rate of change of left ventricular pressure (LVdP/dt) by 52%. Systemic vascular resistance, pulmonary vascular resistance and mean pulmonary artery pressure (MPAP) remained unaltered by TEA. Dopamine‐induced increases in MAP and HR were augmented by TEA. Both MAP and LVdP/dt increased above pre‐TEA levels at 10 μg · kg‐1 · min‐1. Prazosin attenuated the increases in MAP and MPAP by dopamine. Adding rauwolscine almost abolished the dopamine response in MAP and MPAP. Metoprolol almost eliminated the dopamine effects on CO and LVdP/dt. Only minor alterations in cardiac filling pressures were observed during the study. Plasma norepinephrine (NE) concentration was lower during than before TEA at corresponding dopamine infusion rates. NE was reduced by the β1‐blockade. During TEA, the plasma dopamine levels were generally higher, and they were further increased by adding β1‐blockade. In conclusion, myocardial contractility and arterial pressure were restored to pre‐TEA values by dopamine at 5–10 μg · kg‐1 · min‐1. The circulatory response to dopamine during TEA is mainly mediated by α1‐, α2‐ and β1‐adrenoceptor activation, and may be influenced by altered plasma catecholamine levels.

Successful Vasoconstrictor Therapy of Anaphylactoid Reactions during Induction of Anaesthesia: A Report of Two Cases

Anaphylactoid reactions were evoked during intravenous induction of anaesthesia in two patients on three occasions. In the first patient the reaction occurred during the first anaesthetic on propranolol and hydrochlorthiazide medication due to hypertension. Since the major target organ for the anaphylactoid reaction in this patient was the pulmonary circulation, the cardiovascular collapse at his first anaesthetic was misinterpreted as a nonspecific reaction to anaesthesia reinforced by the beta‐receptor blocking therapy. At the second anaesthetic central haemodynamics, plasma adrenaline (A) and noradrenaline (NA) were measured. Following injection of thiopentone sudden decreases of mean arterial blood pressure (60%), cardiacoutput (60%). and systemic vascular resistance (20%) were observed. Thirty minutes later, still during circulatory shock, the concentration of A had increased whereas that of NA was normal. In the second patient the anaphylactogenic drug was supposed to be thiopentone, suxamethonium or alcuronium. In this patient, the fall in arterial blood pressure was associated with bronchospasm and the sudden appearance of peripheral oedema. In both cases initial resuscitation comprised volume replacement and beta1‐agonist therapy but the cardiovascular state was not normalized until vasoconstricting agents were infused.

Intestinal vascular effects of inhaled and locally administered enflurane in the cat.

The effects of enflurane on intestinal vascular resistance and blood flow in the intestine were studied in cats during basal chloralose anaesthesia. A jejunal segment was prepared and perfused with blood from both femoral arteries, allowing control of intestinal inflow pressure. Mesenteric venous blood flow was measured with an optical drop recorder. During constant intestinal arterial pressure (75 mmHg; 10 kPa), intestinal vascular resistance was calculated during enflurane inhalation at MAC 0.5 and 1.0 before and after post‐ganglionic denervation of the jejunal segment. Inhalation of enflurane reduced intestinal vascular resistance in a dose‐dependent fashion. The decrease in vascular resistance was attenuated but not abolished by post‐ganglionic denervation, indicating both peripheral and central nervous sites of action for enflurane. Furthermore, with the intestinal segment perfused at systemic arterial pressure, the effects of locally intra‐arterially infused enflurane dissolved in a fat emulsion was studied. A vasodilator response was elicited in the intestine when exposed to local arterial enflurane concentrations in the same range as encountered during surgical anaesthesia in man, supporting the hypothesis of a peripheral site of action.

Effects of desflurane on systemic, preportal and renal circulatory responses to infra‐renal aortic cross‐clamping in the pig

Background: Different pharmacological approaches have been used in the control of cardiovascular responses to surgical infra‐renal aortic occlusion (AXC). The aim of the present study was to explore the modulatory effects of desflurane (DES) on these responses.

Vasodilator Responses to Enflurane in the Small Intestine

Local effects of enflurane on intestinal vascular resistance were studied in vivo in cats. A jejunal segment was prepared and perfused at constant flow with blood from the femoral arteries. The intestine was either: (1) left with intact sympathetic innervation, (2) denervated and exposed to electrical post‐ganglionic vasoconstrictor nerve stimulation, or (3) excluded from neurogenic remote control by post‐ganglionic denervation. Enflurane dissolved in lipid and intra‐arterially administered to the jejunal segment in doses comparable to those clinically encountered, decreased intestinal vascular resistance in relation to the intra‐arterial concentration of the drug. The vasodilator response was, at the highest enflurane doses studied (blood concentration: 400 and 800 mg · l‐1), most pronounced in the intestine with intact sympathetic innervation. Otherwise, no differences were observed in vasodilator responses between the three different investigated modes of neurogenic influence on the intestine. In vitro enflurane (‐in‐lipid) did not affect the vasoconstrictor response to electrical field stimulation in the rat mesenteric arterioles. Enflurane, however, dose‐dependently reduced spontaneous contractile activity in the rat portal veins.

Cardiovascular Studies during Controlled Baroreflex Activation in the Dog: I. Effects of Enflurane

In chloralose‐anaesthetized dogs the carotid sinuses were bilaterally perfused with blood from a femoral artery, either at systemic arterial pressure through a direct by‐pass or with a pump in order to control the sinus pressure. Influences from cardiac receptors and aortic baroreceptors were eliminated by denervation. Administration of enflurane (1.6% end‐tidal concentration) with the presence of barostatic modulation, i. e. the carotid sinuses were perfused at prevailing systemic arterial pressure, reduced cardiac performance (cardiac output, cardiac contractility, heart rate and left ventricular stroke work) and mean arterial pressure. When barostatic compensation of enflurane‐induced circulatory changes was prevented by maintaining sinus perfusion pressure constant at the pre‐enflurane level, these haemodynamic alterations, with the exception of cardiac output, were significantly more pronounced. Furthermore, systemic vascular resistance decreased. We conclude that barostatic reflexes significantly modify cardiovascular depressive effects of enflurane.

Bupivacaine for Intercostal Nerve Blockade in Patients on Long‐term β‐Receptor Blocking Therapy

Possible cardiovascular side effects of a local anaesthetic in patients on long‐term β‐receptor blocking therapy were studied in 26 patients given postoperative intercostal nerve blockades (ICB) with 18–28 ml of plain bupivacaine 0.5% (1.30‐1.82 mg kg‐1). The patients had a history of hypertension and/or ischaemic heart disease and were scheduled for gall bladder surgery. Thirteen patients were randomized to a gradual preoperative withdrawal of the β‐receptor blockers and the other 13 continued the β‐receptor blockade until surgery. Cardiovascular changes were measured noninvasively and 11 patients were also monitored with pulmonary artery catheters. Blood pressure and heart rate (HR) were stable in all patients although those in whom the β‐receptor blockade was withdrawn had the highest HR and most frequent arrhythmias both before and after ICB. The ICB was associated with a decrease in the overall postoperative arrhythmia incidence, but seemed most efficient (P<0.02) concerning the ventricular arrhythmias in the β‐receptor‐blocked patients (even including idionodal rhythm). The bupivacaine blood levels did not modify other cardiovascular changes except in one β‐receptor‐blocked patient with cardiac failure in whom signs of a slight transient cardiodepression were observed. It is concluded that bupivacaine does not negatively affect cardiovascular stability in long‐term β‐receptor‐blocked patients. In the presence of cardiac failure, however, an additive cardiodepression may be elicited.