Comparative effects of etomidate, ketamine, propofol, and fentanyl on myocardial contractility in dogs

Kawakubo, Atsushi; Fujigaki, Toru; Uresino, Hiroyuki; Zang, Shiping; Sumikawa, Koji

doi:10.1007/s005400050030

Cited by 18 publications

(4 citation statements)

References 20 publications

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“…23 Ketamine has sympathomimetic effects but it can also have direct negative inotropic effects, particularly in patients with catecholamine depletion. 24 Administration of propofol in this case may have exacerbated the pre-existing haemodynamic instability in this dog and contributed to ventricular standstill.…”

Section: Discussionmentioning

confidence: 83%

Successful transcutaneous pacing following ventricular standstill during anaesthetic induction in a dog with third‐degree atrioventricular block

Miller¹,

Gozalo-Marcilla²,

Culshaw³

et al. 2020

Vet Record Case Reports

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Third-degree atrioventricular block is a haemodynamically unstable bradycardia frequently resulting in signs of lethargy, weakness and collapse. In this reported case, a four year-four month-old male neutered Cavalier King Charles spaniel diagnosed with third-degree atrioventricular block was referred for transvenous permanent pacemaker implantation. During induction of general anaesthesia, the dog suffered cardiac arrest consistent with ventricular standstill, as indicated by cessation of ventricular electrical activity on the ECG monitor and the absence of a peripheral pulse. The prior placement of transthoracic pacing pads under sedation allowed for rapid commencement of temporary transcutaneous pacing and proved effective in achieving ventricular capture with re-establishment of cardiac output. The subsequent general anaesthesia for implantation of a permanent pacemaker was uneventful. This report considers the possible causes of ventricular escape rhythm suppression and highlights the importance of ensuring availability of a temporary pacing method from the outset when anaesthetising animals with unstable and symptomatic bradycardias.

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Section: Discussionmentioning

confidence: 83%

Successful transcutaneous pacing following ventricular standstill during anaesthetic induction in a dog with third‐degree atrioventricular block

Miller¹,

Gozalo-Marcilla²,

Culshaw³

et al. 2020

Vet Record Case Reports

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“…Previous studies have shown that fentanyl has no effect on myocardial contractility at a clinical dose and increases myocardial contractile force at supraclinical doses 28,29. According to the findings described above, the net hemodynamic effect of fentanyl in vivo is a composite of the effect of fentanyl on blood vessel, central sympathetic activity and the heart 26-29.…”

Section: Discussionmentioning

confidence: 84%

Inhibitory Effect of Fentanyl on Phenylephrine-Induced Contraction of the Rat Aorta

et al. 2009

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PurposeFentanyl was reported to inhibit the α1-adrenoceptor agonist-induced contraction. The goal of this in vitro study was to identify the α1-adrenoceptor subtype primarily involved in the fentanyl-induced attenuation of phenylephrine-induced contraction in isolated endothelium-denuded rat aorta.Materials and MethodsAortic rings were suspended in order to record isometric tension. Concentration-response curves for phenylephrine (10-9 to 10-5 M) were generated in the presence or absence of one of the following drugs: fentanyl (3×10-7, 10-6, 3×10-6 M), 5-methylurapidil (3×10-8, 10-7, 3×10-7 M), chloroethylclonidine (10-5 M) and BMY 7378 (3×10-9, 10-8, 3×10-8 M). Phenylephrine concentration-response curves were generated in the presence or absence of fentanyl in rings pretreated with either 3×10-9 M prazosin, 10-9 M 5-methylurapidil or 3×10-9 M BMY 7378.ResultsFentanyl (10-6, 3×10-6 M) attenuated phenylephrine-induced contraction in the rat aorta. 5-Methylurapidil and BMY 7378 produced a parallel rightward shift in the phenylephrine concentration-response curve. The pA2 values for 5-methylurapidil and BMY 7378 were estimated to be 7.71 ± 0.15 and 8.99 ± 0.24, respectively. Fentanyl (10-6 M) attenuated phenylephrine-induced contraction in rings pretreated with 10-9 M 5-methylurapidil, but did not alter the rings when pretreated with 3×10-9 M BMY 7378. Pretreatment of the rings with chloroethylclonidine showed a 72.9 ± 2.3% reduction in phenylephrine-induced maximal contraction.ConclusionThe results suggest that fentanyl attenuates phenylephrine-induced contraction by inhibiting the pathway involved in the α1D-adrenoceptor-mediated contraction of the rat aorta.

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“…Thus, conclusions involving these endpoints should be made cautiously. The anesthetic agent used to sedate the monkeys prior to echocardiography, ketamine HCl, is known to reduce myocardial contractility thus it likely affected heart function in this study (60). However, all animals were subject to the same dose of ketamine on a per kg BW basis, so effects should be uniform across groups.…”

Section: Discussionmentioning

confidence: 99%

Effect of Depression and Sertraline Treatment on Cardiac Function in Female Nonhuman Primates

Groban

Kitzman²,

et al. 2014

Psychosomatic Medicine

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Objective Depression is a proposed risk factor for heart failure based largely on epidemiological data; little experimental data is available addressing this hypothesis. Methods Depression was evaluated in relation to cardiac structural and functional phenotypes assessed by transthoracic echocardiography in 42 adult female cynomolgus monkeys that consumed a Western-like diet for 3 years. Half of the monkeys were treated with the SSRI sertraline HCl for 18 months and depressive behavior was assessed for 12 months prior to echocardiography. Results Depressed monkeys (the 19/42 with depressive behavior rates above the mean rate) had higher HRs (171±4.1 vs 152±6.1), and smaller BSA (0.13±0.003 vs 0.15±0.004). Cardiac measures showed lower LV end systolic dimension (0.75±0.05 vs 0.89±0.04), LV systolic (0.76±0.08 vs 1.2±0.11) and diastolic (2.4±0.23 vs 3.4±0.26) volumes, and left atrial volumes (1.15±0.14 vs 1.75±0.12) in depressed versus nondepressed monkeys (p’s <0.05). Doppler profiles of depressed monkeys indicated greater myocardial relaxation (higher e′ and higher e′/a′ ratio) and lower filling pressures (lower E/e′) compared to nondepressed monkeys (p’s<0.05). Although treatment with sertraline reduced HR (150±5.8 vs 171±4.8) and modestly increased chamber dimensions (left ventricular end systolic dimension: 0.91±0.05 vs 0.74±0.03; left ventricular end diastolic dimension, BSA adjusted 1.69±0.05 vs 1.47±0.06) (p’s<0.05), it did not overtly affect systolic or diastolic function (p’s >0.10). Conclusions These data suggest that behavioral depression in female primates is accompanied by differences in cardiac function, although not in ways classically associated with subclinical heart failure. SSRIs show promise in supporting heart function by reducing HR and perhaps improving LV filling, however further investigation is needed to confirm this hypothesis.

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Comparative effects of etomidate, ketamine, propofol, and fentanyl on myocardial contractility in dogs

Abstract: On the basis of clinical doses, the direct myocardial depressant effect of ketamine is more than twice as potent as that of etomidate and slightly more than that of propofol. Fentanyl has no inotropic effect and does not enhance the direct myocardial depressant effect of propofol.

Cited by 18 publications

References 20 publications

Successful transcutaneous pacing following ventricular standstill during anaesthetic induction in a dog with third‐degree atrioventricular block

Successful transcutaneous pacing following ventricular standstill during anaesthetic induction in a dog with third‐degree atrioventricular block

Inhibitory Effect of Fentanyl on Phenylephrine-Induced Contraction of the Rat Aorta

Effect of Depression and Sertraline Treatment on Cardiac Function in Female Nonhuman Primates

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