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Does dexmedetomidine affect cardiac function based on echocardiography in dogs? | VETgirl Veterinary Continuing Education Podcasts

In today’s VETgirl veterinary continuing education podcast, we review the use of certain sedatives such as dexmedetomidine on cardiac function (based on echocardiography) in dogs. We know that alpha-2 agonist sedatives provide dose-dependent sedation by reducing the central nervous system’s sympathetic outflow. The alpha agonist properties of these drugs also have significant cardiovascular effects – specifically vasoconstriction – which results in an increase in vascular resistance and potential for reflex bradycardia. Dexmedetomidine, a readily available alpha-2 agonist in veterinary medicine, has been documented to cause bradycardia, systemic hypertension, hypothermia, and reduced cardiac output with administration. Given these cardiovascular effects, it is possible that these drugs may significantly alter echocardiographic parameters of cardiac function if used for sedation for echocardiography (thus resulting in artifactual results). So, Kellihan et al out of University of Wisconsin wanted to evaluate this by assessing dexmedetomidine’s effect – in other words, how well it results in level of sedation and whether it effects echocardiographic parameters of cardiac function. They looked at two doses – the labeled dose at 10 ug/kg and a lower dose of 5 ug/kg.

This was a double-blinded, randomized clinical trial that enrolled 14 healthy dogs that had presented to the orthopedic service for lameness. All dogs received auscultation, temperature, sedation score, electrocardiogram, oscillometric blood pressure, and echocardiogram at baseline prior to sedation. Then, dogs were randomized to receive either 10 ug/kg dexmedetomidine hydrochloride (defined as the regular dose group) or 5 ug/kg medetomidine (defined as the lower dose group) in addition to 0.4 mg/kg butorphanol tartate, intramuscularly. This butorphanol dose has been previously established to be hemodynamically insignificant in dogs, by the way. 20 and 60 minutes after sedation, baseline measurements were repeated. In the 10 ug/kg group, dogs achieved greater maximal sedation scores compared with the lower dose group (5 ug/kg). The regular dosed group of dogs had a lower median heart rate and respiratory rate at both 20 and 60 minutes. There was no change in rectal temperature or blood pressure in this group. In the lower dose group, a lower median heart rate and respiratory rate was only observed at the 60 minute mark; lower rectal temperatures were observed at this time also as compared to at the 20 minute time. Also, a lower systolic and mean blood pressure was observed at the 20 minute mark. Overall, there were no significant differences in heart rate, respiratory rate, or temperature between the regular and lower dose groups. A higher mean arterial pressure was seen at the 20 minute mark in the regular dose group versus the lower dose group.

Dexdomitor

As for echocardiography results, there was a significantly decreased left ventricular internal diameter and end-systole, fractional shortening, and ejection fraction at the 20 and 60 minute mark in the regular dose group versus baseline. NOTE: All of these parameters are echocardiographic measures of systolic function. At the 60 minute mark, there was decreased fractional shortening observed in the lower dose group. Also, there was increased left atrial diameter at the 20 and 60 minute mark for the lower dose group versus baseline. In the regular dose group, there was decreased aortic/pulmonic ejection velocities at the 20 and 60 minute time mark, but no significant changes in the lower dose group. The regular dose group also had decreased heart rate and cardiac output at the 20 and 60 minute time mark. Heart rate and cardiac output was significantly decreased at the 60 minute mark in the lower dose group. Lastly, mitral and tricuspid regurgitation and “smoke” (e.g., echocardiographic spontaneous contrast within a cardiac chamber that is suggestive of blood flow stasis) were noted in the majority of dogs at the 20 minute time mark in the regular dose group.

As for the level of sedation observed in this study, sedation was adequate in all dogs, but dose-dependent among groups in terms of degree. Significant cardiovascular effects including bradycardia, reduced cardiac output, and decreased echocardiographic indices of systolic function were observed with both dose groups, but these effects were not observed to a significant degree at the 20 minute mark in the lower dose group (as opposed to both time points in the regular dose group and at the 60 minute mark in the lower dose group). This suggests that for relatively short procedures/diagnostics, the 5 ug/kg dose is likely to provide adequate sedation without significant cardiovascular effects to the patient (provided that a reversal agent is administered upon completion of the procedure and sedation not continued to 60 minutes). Effects of dexmedetomidine on blood pressure are difficult to interpret in this study, as systemic vascular resistance (SVR, an invasive measurement) would be the ideal way to evaluate these effects and was not measured in the study. For example, dexmedetomidine may increase a patient’s SVR, causing a reflex bradycardia, and the resultant combination may be an unchanged or normal noninvasive blood pressure measurement. With regards to sedation specifically for the purpose of performing an echocardiogram, the cardiovascular effects of either dose group on systolic function, blood flow, and induction of valvular regurgitation have the potential to significantly artifactually alter a clinical diagnosis of the presence/type of heart disease. Dexmedetomidine (and potentially any alpha-2 agonist) would therefore not be ideal as a sedative agent for echocardiography.

So, what do we take from this VETgirl podcast? Overall, this was a nice, concise study to officially document what is generally discussed and accepted as the cardiovascular sequelae for alpha-2 agonists as sedatives, and particularly how this can affect echocardiography. To echo (no pun intended) the sentiments on the discussion section further, although fractional shortening was not “statistically significantly lower” for the lower dose group at the 20 minute mark (but was at 60 minute mark and for the regular dose group at the 20 and 60 minute mark), if you examine the actual numbers themselves in Table 3 in this paper, the median fractional shortening went from 28% at baseline to 22.5% at the 20 minute mark in the lower dose group. Whether that is statistically significant or not is almost irrelevant, given that the generally accepted value for low end of normal fractional shortening in dogs is 25%. Even this “non-statistically significant” effect would have a major impact on how that patient’s echocardiogram might be interpreted! (And for the record, the lowest fractional shortening value reported at the 20 minute mark in an lower dose group patient was 12%…. that would be consistent with severe systolic dysfunction!).

So, in conclusion, significant effects on heart rate and systolic cardiac function occur with both 5 ug/kg and 10 ug/kg doses of dexmedetomidine in dogs, though the effects were less prominent at 20 minutes post-administration (compared with 60 minutes) in the low dose group, despite adequate sedation in both dose groups at both time periods. The jist of it all? The significant effects on cardiac function make dexmedetomidine a particularly poor choice for sedation when specifically used for the purpose of performing an echocardiogram.

References:
1. Kellihan HB, Stepien RL, Hassen KM, et al. Sedative and echocardiographic effects of dexmedetomidine combined with butorphanol in healthy dogs. J Vet Cardiol 2015;17:282-292.

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