Intramuscular Doses of Succinylcholine as an Adjunct in Anesthesia

Glowacki, Edward T.; Austin, Shirley; Greifenstein, F. E.

doi:10.1213/00000539-195807000-00013

Cited by 5 publications

(5 citation statements)

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“…This concerns especially the short initial changes, e.g. the decrease in peripheral blood flow, fall in arterial blood pressure, bradycardia, cardiac arrhythmia, and a possible inotropic effect on the heart (2,21,25,36,53,54,61,64,65,68,83,110,120,138,139,149,167,172,188,193,201,202,212,220,222,225,234,243,281,290,300). However, a complete prevention of the circulatory and vagal-stimulatory effects of SCh requires fairly high, preferably intravenous doses of atropine (201,290).…”

Section: M E C H a N I S M S Of Sch A C T I O N O N C I R C U L A mentioning

confidence: 99%

Circulatory Effects of Succinylcholine in Man

Gräf

Ström

Wåhlin

1963

Acta Anaesthesiol Scand

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SUMMARY The effects of intravenous (standard apnoeic) and intra‐arterial doses of succinylcholinc chloride (SCh) on peripheral circulation (forearm, hand, skeletal musculature, skin, mucosa of the sigmoid colon), arterial blood pressure and heart rate were studied in 15 unanaesthetized and 17 anaesthetized subjects. Standard apnoeic doses of SCh injected intravenously in anaesthetized subjects produced circulatory changes usually of a biphasic character, a sudden initial decrease in peripheral blood flow and heart rate followed by an increase throughout The apnoeic period; there was also a rise in arterial blood pressure. The initial decrease occurred synchronously with the preparalytic activity of the skeletal musculature (twitchings), but unlike the latter also after repeated injections of SCh. The magnitude of the initial decrease was, on an average, 16 per cent for the peripheral circulation, and 7 per cent for heart rate. The subsequent average increase amounted to 16 per cent above the initial control value for the peripheral circulation, 8 per cent (5 mm Hg) for the systolic, 21 per cent (6 mm Hg) for the diastolic and 9 per cent (4 mm Hg) for the mean arterial blood pressures. Doses of SCh which caused local muscular relaxation on continuous infusion into the brachial artery of unanaesthetized subjects also caused an average blood flow increase in forearm and hand of 43 per cent. This blood flow response remained only during the first few minutes, and then gradually decreased to the control level during the course of the next 10–15 minutes. After the second or third repeated intravenous injection of SCh, but not after further injections, a sudden and marked bradycardia sometimes occurred, with a duration of up to 3 minutes. With repeated intravenous injections of SCh in a standard apnoeic dose, the size and duration of both the circulatory reactions and the duration of the apnoeic period gradually decreased (‘tachyphylaxis’). The individual sensitivity to SCh was rather variable. This was particularly evident in patients with a labile and hyperkinetic circulation (‘vasoregulatory asthenia’) in whom the average blood flow increase during continuous intra‐arterial infusion of SCh was considerably higher than in the control group. The circulatory changes after an intravenous injection of an apnoeic SCh dose should be evaluated in relation to the various interfering factors, such as anaesthesia, atropine premedication, endotracheal intubation, positive‐pressure ventilation, hypoxia, hypercapnia, hypothermia during anaesthesia, and acidosis. The possible mechanisms by which SCh exerts its circulatory effects are discussed, especially the direct effects on the vessels and heart and the indirect effects via nervous or humoral mediators. It is concluded that SCh seems to be a general vasodilator substance. A review of the literature shows that the vasodilator effect of SCh also exists in circulatory areas of the body not directly studied in the present investigation. The vasodilatation is partially caused by a ...

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Section: M E C H a N I S M S Of Sch A C T I O N O N C I R C U L A mentioning

confidence: 99%

Circulatory Effects of Succinylcholine in Man

Gräf

Ström

Wåhlin

1963

Acta Anaesthesiol Scand

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“…One subject complained of myalgias in both lower extremities for 48 hours after the study, a phenomenon similar to that observed with clinical use of IV succinylcholine, but surprising, in view of the very Serial small dose employed in our study. recordings from ADQ and AH showed no signifi- 7,11,17,19 cant changes at any time point in the subjects as a group after succinylcholine injections, indicating minimal (or probably nil) circulating succinylcholine concentrations overall. One subject developed a transient depression in ADQ CMAP amplitude to 83% of baseline, but experienced no symptoms.…”

Section: Figure 1 Bmentioning

confidence: 82%

Sustained focal effects of low‐dose intramuscular succinylcholine

1993

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We studied low-dose intramuscular succinylcholine in 9 subjects as part as an ongoing investigation of its potential to predict responses to botulinum toxin. We measured compound muscle action potentials (CMAPs) from the extensor digitorum brevis (EDB) muscles in each foot before and after intramuscular injections of 2.5 mg of succinylcholine into the EDB. Succinylcholine reduced mean CMAP amplitudes to 42% of baseline; the maximal reduction occurred at 19 +/- 6 (mean +/- standard deviation) minutes. Recovery to 73% of the baseline CMAP amplitude (approximately 50% recovery from block) occurred at 105 +/- 49 minutes after injection. Repetitive (train-of-four) stimulation at 2 Hz produced mild CMAP decrements (5-25%), but only during the recovery phase. Varying the succinylcholine concentrations (10, 20, or 50 mg/mL) while holding the total drug dose constant did not change the rate of onset or the extent of block. No systemic complications occurred. We conclude that: (1) 2.5 mg intramuscular succinylcholine can safely induce selective muscle weakness with a time course that differs from intravenously administered succinylcholine; and (2) further clinical studies comparing intramuscular succinylcholine and botulinum toxin are warranted.

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“…Work looking at speeding the onset of intramuscular suxamethonium has been generally disappointing. The use of hyaluronidase has thrown up conflicting results [7]; however, there is animal work showing the ‘time to collapse’ in goats to be shorter in the hyaluronidase group by 25%[8]. Using different concentrations of suxamethonium (2% or 5% solutions) made no difference [9].…”

Section: Intramuscular Succinylcholine (Intramuscular Route)mentioning

confidence: 99%