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. 2022 Sep 30;36(6):2002–2008. doi: 10.1111/jvim.16552

Effect of inhaled albuterol on whole blood potassium concentrations in dogs

Andrzej Ogrodny 1, Jared A Jaffey 1,✉, Rachael Kreisler 2, Mark Acierno 1, Teela Jones 1, Renata S Costa 1, Anderson da Cunha 1, Emily Westerback 1
PMCID: PMC9708417  PMID: 36178135

Abstract

Background

Albuterol by inhalation (IH) is a common treatment for hyperkalemia in humans but its effect on blood potassium concentrations in dogs is unknown.

Objective

Determine whether albuterol (IH) decreases blood potassium concentrations in healthy normokalemic dogs and if effects are dose‐dependent.

Animals

Ten healthy dogs.

Methods

Prospective, crossover experimental study. Albuterol sulfate was administered at a low‐dose (90 μg) in phase I and, 7 days later, high‐dose (450 μg) in phase II. Blood potassium and glucose concentrations (measured via blood gas analyzer) and heart rates were obtained at baseline and then 3, 5, 10, 15, 30, 60, 90, 120, 180, and 360 minutes after inhaler actuation.

Results

Blood potassium concentrations decreased rapidly after albuterol delivery with a significant reduction compared to baseline within 30 minutes in both phases (P = .05). The potassium nadir concentration of phase I occurred at 60 minutes (mean, SD; 4.07 mmol/L, 0.4) and was significantly decreased from baseline, (4.30 mmol/L, 0.3; t(9) = 2.40, P = .04). The potassium nadir concentration of phase II occurred at 30 minutes (mean, SD; 3.96 mmol/L, 0.39) and was also significantly decreased from baseline, (4.33 mmol/L, 0.4; t(9) = 2.22, P = .05). The potassium nadir concentration decreased by 0.1 mmol/L for each 10 μg/kg increase in dose of albuterol (P = .01). Five dogs had ≥1 hyperglycemic measurement (ie, >112 mg/dL). No median heart rate was tachycardic nor was any mean blood glucose concentration hyperglycemic at any time point.

Conclusion and Clinical Importance

Albuterol IH decreases blood potassium concentrations in a dose‐dependent manner without clinically meaningful alterations to heart rate or blood glucose concentrations in healthy dogs. The mean decrease in potassium concentration at the high‐dose of albuterol was modest (0.38 mmol/L).

Keywords: blood gas, electrolytes, hyperkalemia, β2‐agonist

Abbreviations

ICC

intraclass correlation

IQR

interquartile range

1. INTRODUCTION

Hyperkalemia is a common electrolyte disturbance in dogs evaluated on an emergency basis. Urinary diseases are the most common cause for hyperkalemia in dogs with other etiologies including hypoadrenocorticism, diabetes mellitus, intestinal parasites, acute tumor lysis syndrome, and secondary to several drugs. 1 Hyperkalemia is a risk factor for death in dogs and humans in an emergency setting because of its role in causing potentially life‐threatening arrhythmias. 1 , 2 , 3

Moderate‐to‐severe hyperkalemia requires urgent intervention. 1 The goals of treatment are to mitigate cardiac conduction disturbances, eliminate excess potassium, shift potassium into cells, and resolve the underlying disease process. Therapies used to eliminate excess potassium include IV fluid therapy, loop or thiazide diuretics, hemodialysis, and continuous renal replacement therapy. Fluid diuresis is effective at rapidly lowering blood potassium concentrations but is contraindicated after initial hemodynamic stabilization in some of the most common conditions that cause hyperkalemia in dogs including oliguric or anuric kidney injury, uroabdomen, and complete urinary obstruction until after diversion or resolution. 4 , 5 , 6 , 7 , 8 , 9 , 10 Loop and thiazide diuretics could have adjunctive value to promote renal excretion of potassium but should be avoided in the presence of dehydration or hypovolemia. 11 , 12 Hemodialysis and continuous renal replacement therapy can rapidly decrease blood potassium concentrations but are rarely used for the purpose of treating hyperkalemia alone in dogs. 13 Therapeutic options in veterinary medicine to promote intracellular shifting of potassium are limited and include dextrose with or without insulin or sodium bicarbonate with the latter typically reserved for cases with severe acidosis. 5 , 14 , 15 , 16 The β2‐agonist terbutaline decreases serum potassium concentrations in dogs when administered as a continuous infusion; however, its safety as well as alternative dosing strategies have not been investigated. 17

Albuterol, like terbutaline, is a β2‐agonist that promotes an intracellular shift of potassium via stimulation of endogenous insulin release and the induction of extracellular membrane‐bound Na/K‐ATPase pumps in an insulin‐independent fashion. 18 , 19 Albuterol is commonly used alone or with regular insulin and dextrose to treat moderate‐to‐severe hyperkalemia in humans and can be administered via inhalation or as an IV infusion. 20 , 21 , 22 In humans, albuterol IH decreases serum potassium concentrations within 15 to 30 minutes of administration, with duration of effect lasting up to 180 minutes, making it an ideal intervention. 18 , 19 , 20 , 21 , 22 , 23 , 24 Tachycardia and hyperglycemia are reported potential adverse effects to albuterol administration in humans. 25 , 26 , 27 There have been no published studies that have investigated the effect of inhaled albuterol on blood potassium concentrations in dogs.

Our study had 3 objectives: (i) to determine whether inhaled albuterol decreases blood potassium concentrations in dogs; (ii) to determine if nadir blood potassium concentrations are associated with delivered albuterol dose; and (iii) to assess if inhaled albuterol affects heart rate or blood glucose concentrations. We hypothesized that inhaled albuterol would decrease blood potassium concentrations and the nadir potassium concentration would be associated with the delivered dose. Furthermore, we hypothesized that inhaled albuterol would not affect heart rate or blood glucose concentrations.

2. MATERIALS AND METHODS

2.1. Animals

Dogs of any age, breed, or sex owned by faculty, staff, and students at the Midwestern University College of Veterinary Medicine that weighed 5 to 20 kg with whole blood potassium concentrations of 3.5 to 5.5 mmol/L (ie, normokalemic) were eligible for inclusion. Dogs were excluded if there was previously documented history of cardiac disease or if either a heart murmur or an arrhythmia (brady‐ or tachyarrhythmia) were identified on physical examination performed by a board‐certified small animal internist (JAJ). In addition, dogs were excluded if 1 or more of the following medications with potential blood potassium altering effects were administered within 60 days of enrollment, enalapril, benazepril, telmisartan, losartan, diuretics, trilostane, mitotane, potassium gluconate/citrate, fludrocortisone, desoxycorticosterone pivalate, or insulin. Client consent was obtained. This study was approved by the Midwestern University Animal Care and Use Committee (protocol #3010).

2.2. Study design

The study was performed with a prospective, open‐label, 2‐way crossover design.

Pharmaceutical grade albuterol sulfate (metered‐dose inhaler, 90 μg/actuation; Teva Pharmaceuticals Ireland, Waterford, Ireland) was delivered via an AeroDawg spacer (Trudell Animal Health, London, Ontario, Canada) attached to a tightly sealed silicone facemask (Figure 1) at a dose of 90 μg (1 metered actuation) in phase I (ie, low‐dose) and 450 μg (5 metered actuations) in phase II (ie, high‐dose), executed 7 days later.

FIGURE 1.

FIGURE 1

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Illustration of albuterol sulfate delivery via “AeroDawg” AeroDawg spacer attached to a tightly sealed silicone facemask

In both phases, heart rates were recorded followed by blood sample acquisition at baseline (time [t] = 0; before delivery of inhaled albuterol) and at 3, 5, 10, 15, 30, 60, 90, 120, 180, and 360 minutes after the tenth breath following inhaler actuation. Blood was collected by venipuncture and immediately transferred to lithium heparin‐containing tubes. Whole blood was analyzed by a veterinary benchtop blood gas analyzer (Stat Profile Prime Plus Vet, Nova Biomedical, Waltham, Massachusetts) within 5 minutes of collection. 28 Whole blood potassium and glucose concentrations were recorded for each time‐point. Throughout the study period, the blood gas analyzer underwent daily quality control and routine maintenance as instructed by the manufacturer. Dogs were housed in a quiet room under continuous observation by investigators, water was available ad libitum, and food was withheld through the duration of each phase. Hyperglycemia and hypoglycemia were defined as blood glucose concentrations of >112 and <65 mg/dL, respectively. 29 Hypokalemia was defined as blood potassium concentrations of <3.5 mmol/L. 1 Tachycardia was defined as a heart rate of >180 beats/min (bpm). 30

2.3. Statistical analysis

Statistical analyses were performed using proprietary software (Stata Statistical Software version 17, StatCorp LLC, College Station, Texas). Normality was assessed using tests of skewness and kurtosis. Normally distributed values were reported as mean, SD, and range and values at each time point compared to baseline values using T‐tests, with the t statistic (t‐value), an indication of the difference between 2 samples, and degrees of freedom (df) reported as t(df) = t‐value. Non‐normally distributed values were reported as median and range and compared using Wilcoxon rank‐sum tests. In each phase, the nadir value for variables was defined as the time point with the lowest mean or median while similarly the apex value for variables was defined as the time point with the highest mean or median. The effect of inhaled albuterol dose (ie, μg/kg) on nadir potassium concentration was assessed using multilevel mixed‐effects linear regression with patient as a random effect. The model was validated through visual inspection of the residuals. The contribution of interpatient variability to the dose‐effect was assessed using the intraclass correlation (ICC), with values <0.5 considered poor and values ≥0.5 considered moderate or better. 31 A P‐value of ≤.05 was considered significant.

3. RESULTS

3.1. Dogs

Ten dogs fulfilled the inclusion criteria and were enrolled. No dogs were excluded. There were 6 mixed breed dogs. Purebred dogs included were Miniature schnauzer (n = 2), and 1 each of Cattle dog and Australian shepherd. The median age and weight were 5 years (range, 2.5‐9.8) and 15.9 kg (range, 5.6‐19.6). There were 5 castrated males, 4 spayed females, and 1 intact female.

3.2. Effect on potassium concentration

Potassium concentrations decreased rapidly after administration of inhaled albuterol in both phases, before reaching a nadir and slowly increasing toward baseline (Figure 2). There was no difference in baseline potassium concentration (t(18) = 0.22, P = .83) between phases, with mean baseline potassium concentrations of 4.30 mmol/L (SD, range; 0.3, 3.99‐4.87) and 4.33 (SD, range; 0.4, 3.90‐5.14) for phase I and II, respectively. The potassium nadir concentration of phase I occurred at t = 60 minutes (mean, SD, range; 4.07 mmol/L, 0.4, 3.54‐4.53) and was significantly decreased from baseline, t(9) = 2.40, P = .04. The potassium nadir concentration of phase II occurred at t = 30 minutes (mean, SD, range; 3.96 mmol/L, 0.39, 3.36‐4.53) and was also significantly decreased from baseline, (t(9) = 2.22, P = .05). Mean potassium concentrations remained decreased at t = 360 minutes as compared to baseline, although this difference was not statistically significant for either phase I (t(18) = 0.86, P = .4) or phase II (t(18) = 0.93, P = .36).

FIGURE 2.

FIGURE 2

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Scatterplot and LOWESS curves of the potassium concentration at baseline (ie, before administration of inhaled albuterol) and at 3, 5, 10, 15, 30, 60, 90, 120, 180, and 360 minutes after the tenth breath following albuterol inhaler actuation for phase I (1 inhaler actuation, 90 μg) and phase II (5 inhaler actuations, 450 μg). Solid blue vertical line at the potassium nadir concentration of phase II (30‐minutes time point) and dashed vertical red line at nadir concentration of phase I (60‐minutes time point)

A multivariable mixed‐effects linear regression model with potassium nadir as the dependent variable, dose and baseline potassium as independent variables and patient as the random effect found a significant inverse association between the inhaled albuterol dose and potassium nadir concentration (P = .01, Figure 3). The potassium nadir concentration decreased by 0.1 mmol/L (95% CI: −0.12, −0.02) for each 10 μg/kg increase in inhaled albuterol dose, while each 0.1 mmol/L increase in baseline potassium concentration resulted in a 0.04 mmol/L (95% CI: 0.01‐0.08) increase at nadir (P = .03). The ICC for the random effect of patient was 0.5 (95% CI: 0.1‐0.9; Figure 4).

FIGURE 3.

FIGURE 3

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Relationship between nadir potassium concentration and albuterol IH dose (μg/kg) overlaid by linear best fit line and 95% CI. Phase I values as red squares and phase II values as blue diamonds. Nadir potassium concentration was inversely associated with inhaled albuterol dose (P = .01)

FIGURE 4.

FIGURE 4

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Change in blood potassium concentration for individual dog (D) from baseline (open red circle) to nadir (open green triangle) for phase I at time 60 minutes (A) and phase II at 30 minutes (B)

Hypokalemia occurred in 3% (6/200) of time points (phase I, n = 1; phase II, n = 5). The potassium concentration reflective of the single occurrence of hypokalemia in phase I was 3.42 mmol/L. The median potassium concentration of the 5 time points associated with hypokalemia in phase II was 3.41 mmol/L (range, 3.36‐3.44). Hypokalemia resolved without intervention in all cases.

3.3. Effect on glucose concentration

Glucose concentration decreased briefly in both phases, with the nadir (mean, SD, range; 91.7 mg/dL, 16.5, 66‐116) for phase I occurring at t = 10 minutes before rebounding to an apex at t = 180 minutes (109.8 mg/dL, 15.8, 92‐134). Phase II reached the nadir (mean, SD, range; 87.2 mg/dL, 20.2, 65‐122) at t = 5 minutes before subsequently increasing to the apex (106.9 mg/dL, 9.0, 94‐119) at t = 360 minutes (Figure 5). The mean glucose concentration at baseline was 95.8 mg/dL (SD, range; 13.4, 67‐111) for phase I and 100.1 mg/dL (14.3, 77‐127) for phase II, and these were not different (t(18) = 0.69, P = .5). In phase I, the glucose nadir was not different from baseline (t(18) = 0.61, P = .55). The apex mean concentration achieved statistical significance (t(18) = −2.14, P = .05). There was no difference in the glucose nadir (t(18) = 1.65, P = .12) or apex (t(18) = −1.27, P = .22) concentration as compared to baseline in phase II.

FIGURE 5.

FIGURE 5

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Scatterplot and LOWESS curves of the mean glucose concentration at baseline (ie, before administration of inhaled albuterol) and at 3, 5, 10, 15, 30, 60, 90, 120, 180, and 360 minutes after the tenth breath following albuterol inhaler actuation for phase I (1 inhaler actuation, 90 μg) and phase II (5 inhaler actuations, 450 μg). Solid vertical blue line at the glucose apex concentration of phase I (180‐minutes time point) and dashed vertical red line at apex concentration of phase II (360‐minutes time point)

Hyperglycemia occurred in 21% (42/200) of time points (phase I, n = 22; phase II, n = 20). In both phases, there were 5 dogs that had 1 or more hyperglycemic measurements. Three of these dogs had hyperglycemic measurements in both phases, while the remaining 2 in each phase were unique to their phase and did not experience hyperglycemia in the alternate phase. The median glucose concentration for the hyperglycemic values were 117.5 mg/dL (range, 114‐141, n = 22) and 122 mg/dL (114‐134, n = 20) for phase I and phase II, respectively. Hypoglycemia occurred in 0.5% (1/200) of time points (phase II, n = 1). The blood glucose concentration associated with hypoglycemia was 64 mg/dL.

3.4. Effect on heart rate

Heart rate decreased briefly in both phases (Figure 6). The median heart rate nadir in phase I was 108 bpm (range, 94‐150) and occurred at t = 30 minutes. The median heart rate nadir in phase II was 104 bpm (range, 100‐140) and occurred at t = 15 minutes. The median heart rate apex in phase I was 122 bpm (range, 94‐156) and occurred at t = 360 minutes, while the median heart rate apex in phase II was 120 bpm (90‐132) at t = 180 minutes. The median heart rate at baseline was 116 bpm (range, 100‐124) for phase I and 114 bpm (100‐160) for phase II, of which there was no difference between phases (T = 171, z = −0.54, P = .61). Neither the heart rate nadir (T = 171, z = 0.12, P = .93) nor apex (T = 171, z = −1.26, P = .22) was significantly different from baseline for phase I. Nor was the heart rate nadir (T = 167, z = 1.12, P = .28) or apex (T = 169, z = 0.15, P = .89) for phase II. Tachycardia did not occur at any time point in the study.

FIGURE 6.

FIGURE 6

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Scatterplot and LOWESS curves of the median heart rate (beats per min, bpm) at baseline (ie, before administration of inhaled albuterol) and at 3, 5, 10, 15, 30, 60, 90, 120, 180, and 360 minutes after the tenth breath following albuterol inhaler actuation for phase I (1 inhaler actuation, 90 μg) and phase II (5 inhaler actuations, 450 μg). Dashed vertical red line at the heart rate apex of phase I (60‐minute time point) and solid vertical blue line at heart rate apex of phase II (60 and 360‐minutes time points). Note that the vertical lines overlap for the 60‐minute timepoints

4. DISCUSSION

This prospective, open‐label, 2‐way crossover, experimental study investigates the effect of inhaled albuterol on whole blood potassium, glucose concentration and heart rate in dogs. Whole blood potassium concentration decreased rapidly after delivery of inhaled albuterol with significant effects occurring within 30 minutes. There was a dose‐dependent relationship in maximum potassium reduction. Lastly, there were no clinically relevant changes in blood glucose concentration or heart rate, nor were there any observed adverse events, after delivery of inhaled albuterol in either phase of the study.

Albuterol IH significantly decreased whole blood potassium concentration in a dose‐dependent manner within 30 minutes in both phases and the peak effect occurred at t = 60 minutes in phase I (low‐dose) and t = 30 minutes in phase II (high‐dose). These results support our hypothesis and are similar to findings in humans. Inhaled or nebulized albuterol significantly decreases serum potassium concentration in humans with hyperkalemia within 5 to 30 minutes of delivery. 18 , 20 , 32 , 33 , 34 , 35 In addition, similar to results from our study, a dose‐response relationship in maximum serum potassium reduction is observed in humans. 20 The mean maximal decrease in blood potassium concentration in our study was 0.38 mmol/L, and occurred in phase II with delivery of high‐dose albuterol. These results are similar to findings in humans after inhaled or nebulized albuterol in which the mean maximum decrease in serum potassium ranges from 0.3 to 0.9 mmol/L. 18 , 24 , 32 , 33 , 34 , 35 , 36 , 37 The potassium lowering effects of inhaled albuterol in normokalemic dogs reported in the current study might underestimate the expected magnitude of reduction in dogs with hyperkalemia. There have been no studies comparing the potassium lowering effects of albuterol in normokalemic and hyperkalemic human patients. However, 2 studies have shown a more modest decrease in serum potassium concentrations in normokalemic humans after nebulized albuterol administration (0.5 mmol/L) 35 , 36 compared to what is generally reported in hyperkalemic patients (0.61‐0.9 mmol/L). 24 , 32 , 33 , 34 , 37

The interindividual variation in the potassium lowering effect of albuterol IH observed in our study, as measured by ICC for the random effect of dog, was on the very low end of moderate and with a wide confidence interval due to the small number of subjects. Human literature has found interindividual variation, with some patients appearing relatively resistant to the potassium lowering effect of albuterol. 20 , 24 , 34 The cause for this lack of expected potassium lowering effect of albuterol in a subset of patients is unknown although 1 theory suggests it could be related to elevated circulating concentrations of endogenous catecholamines. 21 One potential explanation for the variability in our study could be related to the reluctance of some dogs to breathe normally with the silicone facemask placed onto their muzzle. Therefore, shallow breaths might have affected the amount of delivered albuterol, even after 10 breaths.

There were no clinically relevant changes to mean blood glucose concentration, with the single statistically significant mean apex reading found in phase I below the pre‐determined cutoff for hyperglycemia and the highest blood glucose value recorded for any dog at any time point was 141 mg/dL. There were no statistically significant changes to median heart rate after delivery of inhaled albuterol in either phase of this study. Mild transient increases in heart rate and blood glucose concentration can occur after inhaled/nebulized albuterol in humans. 18 , 32 , 33 Tachycardia can occur with high doses of albuterol because of direct stimulation of atrial β2‐receptors, myocardial β1‐receptors, as well as from reflex cardiac stimulation from peripheral vasodilation. 38 , 39 The reason relevant changes in heart rate and blood glucose were not identified in our study could be related to the dose of delivered albuterol. The majority of studies in humans that have investigated the hypokalemic effects of inhaled/nebulized albuterol have used high doses ranging from 10 to 20 mg. 18 , 20 , 32 , 33 It is possible the incidence of adverse effects could increase with higher doses of albuterol IH in dogs. This theory is supported by the results from 2 recent retrospective studies that revealed tachycardia (81%‐94%), hypokalemia (21%‐69%), and hyperglycemia (67%) were common sequela to intoxication by high‐dose salbutamol (albuterol) exposure in dogs. 40 , 41

This study had several limitations that require further elucidation. The dogs in this study were healthy and normokalemic. The safety and potassium lowering effect of inhaled albuterol could vary in critically ill dogs and in those that are stable with various comorbid disorders. Therefore, our results should not be extrapolated for use in clinical situations until future studies investigating the safety and effectiveness in unhealthy hyperkalemic dogs are performed. Ours, was an exploratory study aimed at determining whether inhaled albuterol lowered blood potassium concentrations in dogs; therefore, optimal dose and frequency of administration were not determined. In addition, we did not pre‐specify whether our cutoff for significance would be P < or ≤.05. Lastly, randomized order of treatment protocols was not utilized in the design of this study. The lack of randomization could have had unknown effects on results. However, the wash out period was sufficient to minimize carry over biologic effects between phases and all dogs readily accepted the AeroDawg chamber and facemask in both phases.

5. CONCLUSION

Our findings revealed that inhaled albuterol caused a rapid decrease in blood potassium concentrations in healthy normokalemic dogs. The potassium lowering effect of inhaled albuterol was dose‐dependent, and caused no adverse effects. Additional studies with larger sample populations are needed to better understand the safety and efficacy of inhaled albuterol in unhealthy hyperkalemic dogs.

CONFLICT OF INTEREST DECLARATION

Authors declare no conflict of interest.

OFF‐LABEL ANTIMICROBIAL DECLARATION

Authors declare no off‐label use of antimicrobials.

INSTITUTIONAL ANIMAL CARE AND USE COMMITTEE (IACUC) OR OTHER APPROVAL DECLARATION

This study was conducted in accordance with guidelines for clinical studies and approved by the Midwestern University Animal Care and Use Committee (protocol# 3010).

HUMAN ETHICS APPROVAL DECLARATION

Authors declare human ethics approval was not needed for this study.

ACKNOWLEDGMENT

No funding was received for this study. The authors thank Paige Hunsinger for her technical assistance.

Ogrodny A, Jaffey JA, Kreisler R, et al. Effect of inhaled albuterol on whole blood potassium concentrations in dogs. J Vet Intern Med. 2022;36(6):2002‐2008. doi: 10.1111/jvim.16552

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