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. 2009 Feb;50(2):179–184.

Efficacy of preanesthetic intramuscular administration of ephedrine for prevention of anesthesia-induced hypotension in cats and dogs

Christine Egger 1,✉, Mary-Ann McCrackin 1, Erik Hofmeister 1, Gwenola Touzot-Jourde 1, Bart Rohrbach 1
PMCID: PMC2629422  PMID: 19412398

Abstract

To determine if the preanesthetic administration of ephedrine would prevent anesthesia-induced hypotension in dogs and cats, 10 cats were anesthetized with acepromazine, butorphanol, ketamine, and isoflurane, and 8 dogs were anesthetized with acepromazine, morphine, propofol, and halothane. Cats received ephedrine or saline 10 minutes after premedication. Dogs received ephedrine or saline at the time of premedication. Systolic arterial blood pressure, respiratory rate, heart rate, end-tidal CO2, O2 saturation, cardiac rhythm, and rectal temperature were recorded.

The systolic arterial pressure in cats receiving saline was significantly lower than baseline at 10 minutes after premedication, and systolic arterial pressure was < 80 mmHg for the duration of anesthesia. In cats receiving ephedrine, the systolic arterial pressure was significantly lower than baseline for the duration of anesthesia, but systolic arterial pressure was not < 80 mmHg until 25 min after induction. In dogs, systolic arterial pressure was significantly lower than baseline by 5 and 40 min after pre-medication in dogs receiving saline and ephedrine, respectively. There was no difference in heart rate, respiratory rate, end-tidal CO2, rectal temperature, O2 saturation, or cardiac rhythm among treatment groups. Prophylactic ephedrine delayed, but did not prevent, the onset of hypotension.

Introduction

Volatile anesthetics can produce hypotension in cats and dogs (1–3). Clinically important hypotension is defined as a systolic arterial pressure (SAP) that is < 80 mmHg, a mean arterial pressure (MAP) that is < 60 mmHg, or blood pressure that is > 30 mmHg below baseline normal (4,5). Hypotension can compromise organ perfusion and result in ischemia of organs such as the kidneys, the heart, and the brain (5,6). Untreated severe or prolonged hypotension may result in cardiac arrest during anesthesia, blindness, or renal failure (4,6,7).

Arterial blood pressure monitoring is not routinely performed in many private small animal practices (8–10), and indirect methods of blood pressure measurement vary in their accuracy in dogs and cats (11–14). These factors make it difficult for practitioners to know with confidence whether they are increasing the risk of organ damage in their patients due to undetected hypotension.

Ephedrine is a synthetic, noncatecholamine inotrope and chronotrope that stimulates alpha- and beta-adrenergic receptors directly; it also increases endogenous norepinephrine release (15). The cardiovascular effects of ephedrine resemble those of epinephrine, but its systemic blood pressure-increasing response is less intense and, in humans, lasts approximately 10 times longer (15). In anesthetized human patients, ephedrine is most commonly administered intravenously (IV) or intramuscularly (IM) after the onset of hypotension (15). Prophylactic ephedrine is also administered to prevent or minimize anesthesia-induced hypotension (16–19). Adverse effects are dose-related and, although relatively uncommon, include tachycardia, hypertension, and fetal acidosis (20–22).

There is no information regarding the use of ephedrine in cats. One study in dogs reported that ephedrine [0.1 mg/kg body weight (BW), IV] caused transient, statistically significant increases in MAP, cardiac index (CI), stroke volume (SV), arterial oxygen content (CaO2), and delivery of oxygen (DO2), and statistically significant decreases in heart rate (HR) and systemic vascular resistance (SVR). The observed increase in MAP lasted for < 5 min. In the same study, ephedrine (0.25 mg/kg BW, IV) caused a greater and more prolonged increase in MAP (15 min), as well as increases in CI, SV, and SVR, and a decrease in HR (23). In a more recent study in anesthetized, hypotensive dogs, ephedrine (0.2 mg/kg BW, IV) was found to increase CI and SV, decrease SVR, but only transiently increase MAP (< 5 min) (24).

The objectives of this study were to determine if ephedrine, administered around the time of premedication, would have significant pressor effects throughout anesthesia and provide an effective method of preventing anesthesia-induced hypotension in dogs and cats. It was hypothesized that prophylactic ephedrine (0.1 mg/kg BW, IM) would have sustained pressor effects in dogs and cats.

Materials and methods

Animals

Ten purpose-bred, healthy, adult cats, 5 male and 5 female, 1 to 2 years of age and weighing from 3.2 to 4.3 kg, and 8 random source, healthy, adult, mongrel dogs, 4 male and 4 female, of unknown ages, and weighing from 9 to 27 kg, were studied. All animals were handled and housed according to the Institutional Animal Care and Use Guidelines. The animals were considered to be healthy, based on the results of a physical examination and the determination of packed cell volume, total solids, blood glucose, and urine specific gravity.

Cat treatment protocol

Thirty minutes prior to the induction of anesthesia (T−30), cats undergoing anesthesia for ovariohysterectomy or castration were premedicated with acepromazine (Promace; Fort Dodge Animal Health, Fort Dodge, Iowa, USA), 0.1 mg/kg BW and butorphanol (Torbugesic; Fort Dodge Animal Health), 0.4 mg/kg BW, IM. Ten minutes later (T−20), the cats were administered either saline (S), 1.0 mL (Group S), or ephedrine (E) (Ephedrine sulfate injection, USP, Eli Lilly, Indianapolis, Indiana, USA), 0.1 mg/kg BW, diluted to 1 mL with saline (Group E), IM. Twenty minutes after treatment (T0), an IV catheter [22 standard wire gauge (SWG), 11/4 inch, Sovereign Indwelling Catheter; Sherwood Medical Industries, Tullamore, Ireland] was inserted into the cephalic vein, and general anesthesia was induced with ketamine (Ketaset; Fort Dodge Animal Health), 10 mg/kg BW, IV. Cats were intubated per trachea and maintained in a surgical plane with isoflurane (IsoFlo; Abbott Laboratories, Chicago, Illinois, USA) in oxygen (2 L/min), using a nonrebreathing anesthetic circuit. Monitoring equipment was attached and the patient prepared for surgery during a 30-min stabilization period prior to the surgical procedure (T0–30). The cats were spayed or castrated over a 20-min period (T30–50), then monitored for an additional 20 min before termination of anesthesia (T50–70). An additional dose of butorphanol, 0.4 mg/kg BW, IM, was given after extubation. Butorphanol was administered, as needed, for analgesia. Cats were studied once.

Dog treatment protocol

With the use of a randomized crossover design, 8 dogs underwent anesthesia on 2 occasions, with a 2-week washout period between treatments. Thirty minutes prior to anesthetic induction, the dogs were premedicated with acepromazine (Promace; Fort Dodge Animal Health), 0.05 mg/kg BW, morphine (Morphine sulphate; Baxter Healthcare Corporation, Cherry Hill, New Jersey, USA), 0.5 mg/kg BW, and either ephedrine (E), 0.1 mg/kg BW diluted to 1 mL with saline, or 1 mL of saline, IM (T−30). Twenty-five minutes later (T−5), an over the needle catheter (20 SWG, 11/4 inch; Sovereign Indwelling Catheter, Sherwood Medical Industries) was placed into the cephalic vein and anesthesia was induced with propofol (Propoflo; Abbott Laboratories), IV, to effect (T0). The dose of propofol required to intubate the dogs per trachea was recorded. Following intubation, the dogs were maintained in a light plane of anesthesia (ventromedial eye position, slight palpebral reflex), as determined by a blinded observer, for 60 min (T0–60) with halothane (Fluothane; Ayerst Laboratories, Philadelphia, Pennsylvania, USA) in oxygen (2 L/min) by using a rebreathing anesthetic circuit. After 60 min, the halothane was discontinued and the dogs were allowed to recover from general anesthesia.

Measurements

In cats, indirect SAP, HR, RR, and RT were measured before premedication (baseline) (T−30), 10 min after premedication, and immediately prior to treatment with E or S (T−20), 10 min after injection of E or S (T−10), and from 5 min after induction until termination of anesthesia. In dogs, indirect SAP, HR, RR, and RT were measured before premedication and treatment with E or S (baseline) (T−30), 5 min after premedication and treatment (T−25), and from 5 min after induction until termination of anesthesia. From 5 min after induction to termination of anesthesia, indirect SAP, HR, RR, and RT heart rhythm, end-tidal isoflurane (cats) or end-tidal halothane (dogs), ETCO2, and SaO2, were monitored every 5 min in both dogs and cats.

Heart rate was obtained by auscultation and palpation, RR was obtained by observation, and RT was obtained with a digital thermometer. Systolic blood pressure was measured by placing a Doppler transducer (Model 811; Parks Medical Electronics, Beaverton, Oregon, USA) on the shaved, palmar surface of the forelimb, over the common digital branch of the radial artery to detect blood flow, and placing a blood pressure monitoring cuff (width 40% to 50% of limb circumference) half way between the elbow and the carpus; the leg was positioned with the elbow and carpus in extension. Oxygen saturation, end-tidal isoflurane (cats), end-tidal halothane (dogs), ETCO2, and heart rhythm were monitored with a multiparameter monitor (Patient monitor, model 1100; Criticare Systems, Waukesha, Wisconsin, USA) calibrated at the beginning of each experiment by the use of commercial gas supplied by the manufacturer [1% isoflurane (cats) or 1% halothane (dogs) in 5% CO2 and 60% N2O (Criticare Systems)]. Lactated Ringer’s solution was infused at a rate of 3 mL/kg BW/h throughout the anesthetic period in dogs and cats. All animals were allowed to breathe spontaneously. External heat support was provided to all animals with a circulating warm-water blanket. The same surgeon and anesthetist performed all procedures, and both were blinded to treatment.

Statistical analysis

All statistical procedures were performed by using a commercial software program (SAS V9.1; SAS Institute, Cary, North Carolina, USA). The effect of ephedrine over time, from 30 min before induction to 60 min postinduction, on HR, RR, SAP, RT, ETCO2 and SaO2 in dogs was evaluated with a mixed model, repeated measures, analysis of variance (ANOVA). Treatment, time, week, and weight, together with the interaction between treatment and time, were included as independent variables in the model. Dog and the 3-way interaction between dog, week, and treatment were included as random factors in the model, with time as the repeated measure. Fit of the model to the data was measured by observation of the distribution of residuals to approximate a normal distribution. The model used for the analysis of data from cats was similar to that used for dogs, with the exception that the variable week (used in the crossover design) was excluded. Adjustment for multiple levels of the independent variable included in the ANOVA models was performed according to the method of Bonferroni (25). Data are presented as least-squares means and standard error. Comparisons of age and weight between cats, as well a total propofol dose administered between dogs, were done by using an unpaired t-test. A 2-tailed P-value of ≤ 0.05 was considered significant for all statistical analyses.

Results

In cats, there was no significant difference in mean body weight or age between the treatment groups. At 10 min after premedication, and just prior to administration of E or S (T−20), SAP was significantly below baseline in both treatment groups (P < 0.01) (Figure 1). At 20 min after premedication, and 10 min after injection of E or S (T−10), SAP was not statistically different from baseline in Group E (P = 0.3). In Group S, the SAP remained significantly lower than baseline at all times after premedication P ( = 0.003). Except during the brief surgical period (T30–50), cats receiving S were hypotensive (SAP < 80 mmHg) for the duration of anesthesia. The SAP in cats receiving E was significantly lower than baseline during anesthesia (P = 0.005). However, these cats did not develop hypotension (SAP < 80 mmHg) until 25 min after induction and were only hypotensive at 25 and 30 min after induction (Figure 1). There were no significant differences in HR, RR, RT, end-tidal isoflurane concentration, or ETCO2 between treatment groups. Heart rate and RT decreased similarly over time in both treatment groups. No dysrhythmias were noted in either group. Oxygen saturation was ≥ 97% at all times, and all cats recovered uneventfully.

Figure 1.

Figure 1

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Systolic arterial pressure (SAP) (least-squares means and standard error) in cats receiving ephedrine (E) or saline (S), over time (on the X-axis, −30, −20, 5–30, 35–50, and 55–70 minutes correspond with time of premedication, treatment with S or E, anesthesia without surgery, anesthesia and surgery, and anesthesia without surgery, respectively). # — significant difference from baseline (> 30 mmHg difference); + — statistically significant difference between treatment groups; * — clinically significant hypotension (SAP < 81 mmHg).

In dogs receiving S, the SAP was significantly lower than baseline at 5 min after premedication (T−25) (P = 0.002) and remained significantly lower than baseline for the duration of anesthesia (Figure 2). The SAP in dogs receiving E was significantly lower than baseline at 40 min after premedication, or 10 min after induction of anesthesia (T10) (P = 0.002), and then remained significantly lower than baseline until the termination of anesthesia (Figure 2). Hypotension (SAP < 80 mmHg) was not observed in either group, except transiently at 45 min (T45) after induction in the dogs receiving E. There were no significant differences in HR, RR, RT, end-tidal halothane concentration, or ETCO2 between treatment groups. Heart rate and RT decreased similarly over time in both treatment groups. No dysrhythmias were noted in either group. Oxygen saturation was ≥ 97% at all times, and all dogs recovered uneventfully. There was no difference in the propofol induction dose between treatment groups.

Figure 2.

Figure 2

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Systolic arterial pressure (SAP) (least-squares means and standard error) in dogs receiving ephedrine (E) or saline (S), over time (on the X-axis, −30, −25, and 5–60 minutes correspond with time of premedication and treatment with S or E, 5 minutes after premedication, and the period of halothane anesthesia without surgery, respectively). # — statistically significant difference from baseline; * — hypotension (SAP < 81 mmHg).

Discussion

In cats, the administration of E delayed the onset of hypotension (SAP < 80 mmHg), and in dogs, a significant decrease in SAP was delayed. Although we expected significant, sustained pressor effects, based on evidence in humans (15), neither dogs nor cats receiving E had sustained improvements in SAP under anesthesia.

Several factors may have contributed to the lack of sustained pressor effects. The lack of noxious stimulation in the dogs, and the brief period (20 min) of noxious stimulation in the cats, may have affected the results. In the saline-treated cats, the SAP increased transiently to clinically acceptable values (> 80 mmHg) during surgery. However, the reliance on noxious stimulation to increase SAP is not recommended (26). In dogs and horses, the increase in SAP seen with surgical stimulation has been shown to be due to an increase in systemic vascular resistance (SVR) and did not reflect an improvement in cardiac output (CO) and tissue perfusion (26,27).

In human patients, there is controversy regarding dose, route, timing, and frequency of administration of prophylactic E (16–22). Ephedrine has been administered IM or IV, with pre-medication, prior to induction, or immediately after induction, and as multiple bolus injections and continuous rate infusions (16–22). Doses in human patients vary from 0.08 to 0.9 mg/kg BW, but adverse effects, such as tachycardia and hypertension, increase with increasing dosage (15–22).

The recommended IV dose of E for dogs and cats ranges from 0.02 to 0.25 mg/kg BW (28,29), and no recommended IM doses have been published. Although a dose-response pilot study would have been ideal, this could not be performed because the animals were only available for a short time before being transferred to another study or the teaching laboratory. We chose 0.1 mg/kg BW, IM, anticipating that this dose and route of administration would be safe, effective, and provide sustained effects on arterial pressure. A previous study in dogs showed that E, 0.1 mg/kg BW, IV, decreased SVR and only transiently increased MAP (< 5 min), although CO and tissue delivery of O2 were increased for up to 30 min (23). A 0.25 mg/kg BW dose of E, IV, increased SVR, and resulted in a more prolonged increase in MAP (15 min). An improvement in CO was transient, but delivery of O2 to tissues remained elevated for the 60-minute study period because of splenic contraction and increased circulating red blood cells (23). More recently, in a study in hypotensive dogs, the investigators reported a very transient (5 min) increase in MAP after administration of 0.2 mg/kg BW of E, IV, although CI and DO2 remained elevated for a longer period (24). Although a higher dose of E might have resulted in greater and more sustained pressor effects, it might not have improved cardiac output.

Although the duration of effect of IM E has not been determined in dogs and cats, E was administered IM in this study, assuming that it would result in a more prolonged effect, with less likelihood of tachycardia. In the current study, E was administered 20 and 30 min prior to induction in cats and dogs, respectively, which may account for the slightly better effect seen with the cats. Because the duration of pressor effects was so brief, administration of E immediately prior to or after induction may be more effective in preventing hypotension for the duration of anesthesia.

In humans, there is good bioavailability of IM E after injection deep into the paravertebral muscles (30,31), but the bio-availability of IM E in dogs and cats is not known. All animals were injected deep into the gluteal muscles, assuming that injection into this well perfused area would facilitate uptake of the drug, but, because we did not measure plasma E concentrations, it is impossible to determine uptake and bioavailability or predict plasma concentrations in these animals. There may also be differences in volume of distribution, elimination half-life, clearance, and pharmacodynamic responses among species.

Standard practice for prophylactic blood pressure support in human patients undergoing spinal anesthesia is to administer a fluid bolus of 5–10 mL/kg BW to patients prior to administration of E; even normovolemic patients would benefit from this increase in blood volume because of the vasodilatory effects of volatile and spinal anesthetics (15,19). To avoid the confounding effect of increasing blood volume, animals in this study were not fluid loaded, but administered lactated Ringer’s solution at 3 mL/kg BW/h. Although all animals appeared to have normal hydration on physical examination and normal PCV and total solids, detection of mild dehydration is difficult, with 5% dehydration being considered the lowest percentage that is clinically detectable (32). Since venoconstriction, resulting in improved venous return, is a dose-dependent effect of ephedrine (23), the combination of an SC or IV fluid bolus administered prior to anesthesia and prophylactic E might have been more efficacious in increasing and maintaining SAP.

The anesthetic protocols used were chosen to represent typical protocols used in clinical practice. Acepromazine, butorphanol, and morphine are common premedications used in dogs and cats. Atropine or glycopyrrolate are also commonly used, but they were excluded from this study’s protocol to remove the confounding effects of an anticholinergic on blood pressure. The cats were induced to anesthesia with ketamine alone, although ketamine and diazepam inductions are more common. Premedication with acepromazine provides adequate sedation and muscle relaxation, and induction with ketamine alone is also common (33). Diazepam has very little effect on heart rate or blood pressure, so its absence from the protocol likely did not affect the results (33). Halothane, rather than isoflurane, was used for maintenance of anesthesia in dogs. Halothane is not frequently used as an anesthetic in North America, although it was in common usage at the time this study was performed (10). The use of isoflurane, because of its different effects on HR, BP, and cardiac output, could have provided different results.

Both dogs and cats were premedicated with acepromazine, an alpha-adrenergic receptor antagonist (28,34). Blockade of the alpha-adrenergic receptor with acepromazine might have interfered with the agonist activity of E at the same receptors, preventing vasoconstriction and mitigating the increase in arterial pressure. In a previous clinical study, ephedrine (0.2 mg/kg BW, IV) was found to have less of a pressor effect than dopamine in dogs premedicated with acepromazine (24), and acepromazine has recently been found to blunt the alpha-adrenergic receptor activity of dopamine (34). Exclusion of acepromazine from the protocol might have resulted in more significant changes in arterial pressure with E, but acepromazine is a very common preanesthetic used in clinical practice. A higher dose of E might have resulted in more significant pressor effects in the face of alpha-receptor blockade with acepromazine.

Monitoring HR and BP during anesthesia only allows predictions of CO, tissue perfusion, and DO2. Variations in blood volume, preload, SVR, myocardial contractility, and HR can affect blood pressure (5). In addition, as indirect arterial pressure monitoring can be inaccurate in dogs and cats, these results should be interpreted with caution (11–14). The placement of direct arterial catheters was not possible in this study, so the Doppler method was chosen, although this is a weakness of the study. The Doppler probe and cuff method to measure BP lacks accuracy and precision, and, is best used for showing “trends” in blood pressure (11,14). It is, however, more likely to be used in clinical practice than a direct measurement technique. Variations in cuff placement, cuff size, and operator technique also contribute to variability; these were minimized by using a standard technique for choosing cuff size and cuff placement, and by having the same individual perform all BP measurements. It is also possible that some transient increases in BP were not observed, because measurements were made only every 5 min. Again, the use of direct arterial BP monitoring would have allowed continuous monitoring of BP and transient changes would have been observed.

Systolic arterial pressure was chosen for measurement in this study, as it is the parameter, other than HR, most likely to be monitored in private clinical practice. Several studies have shown that CO and tissue delivery of O2 is increased with E, without a concurrent increase in arterial pressure (23,24). Future studies should include measurement and calculation of direct SAP, MAP, central venous pressure, CO, SV, SVR, DO2, and tissue lactate concentrations in order to more accurately assess adequacy of tissue perfusion and DO2 with the prophylactic use of E.

When compared with saline, the prophylactic IM administration of E, at the dose studied, delayed but did not prevent the onset of clinically significant hypotension in healthy dogs and cats. Although there were no adverse effects observed in these healthy animals, further study is required to determine the optimal dose, timing of administration, and safety of prophylactic E, as it may prove useful in healthy patients undergoing short, elective surgical procedures.

Footnotes

Reprints will not be available from the authors.

Authors’ contributions

Dr. Egger conceived and designed the study, assisted with data acquisition, analyzed and interpreted the data, and drafted the manuscript. Dr. McCrackin performed all the surgeries and assisted with the analyses and the writing of the manuscript. Dr. Hofmeister and Touzor-Jourde contributed to the planning of the study, the collection of the data, and the writing of the manuscript. Dr. Rohrbach assisted with the statistical analysis, the interpretation of the data and the writing of the manuscript. CVJ

Dr. Egger’s current address is the Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee 37996 USA.

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