Maintenance of blood pressure and CO is of paramount importance in an anesthetized patient so that adequate organ perfusion and Do2 are maintained. A recent study1 in anesthetized human patients revealed that an MABP < 55 mm Hg during noncardiac surgery was associated with a risk of postoperative acute kidney injury and myocardial infarction. Results of other studies2–4 in humans have shown that cerebral perfusion is mostly dependent on MABP and cardiac perfusion is mostly dependent on DABP, whereas renal perfusion is dependent on both MABP and CO. Additional investigation is needed to examine the hemodynamic impact of sedative drugs on anesthetized animals and their role in Do2 and organ perfusion.
Acepromazine and dexmedetomidine are pre-anesthetic sedatives commonly used in healthy dogs. Acepromazine is an α1-adrenergic receptor antagonist that induces a dose-dependent decrease in MABP and CO in dogs when administered at 0.05 to 0.20 mg/kg (0.023 to 0.091 mg/lb), IV.5–7 A low dose of acepromazine (0.05 mg/kg, IV) potentiated isoflurane-induced vasodilation but did not alter CO in dogs,7 suggesting that the predominant cardiovascular effect of acepromazine is systemic hypotension.
Dexmedetomidine is a highly selective α2-adrenergic receptor agonist. Dexmedetomidine induces a higher systemic arterial blood pressure than does acepromazine and also causes reflex bradycardia and CO reduction.8,9 The increase in systemic blood pressure is caused by an α2-adrenergic receptor–mediated constriction of vascular smooth muscles of arterial vessels. The effect on heart rate is mainly due to a baroreceptor reflex as well as an α2-adrenergic receptor agonism that results in centrally mediated bradycardia.9,10
Propofol and isoflurane are used extensively for induction and maintenance of anesthesia in dogs sedated with acepromazine or dexmedetomidine. Propofol and isoflurane are each associated with a degree of cardiovascular depression. In 1 study,11 a constant rate infusion of propofol decreased MABP in dogs owing to reduced heart rate, SV, and CO. Similarly, isoflurane anesthesia has been shown to cause a dose-dependent decrease in CO and SV followed by systemic hypotension and tachycardia.12,13
Combined administration of acepromazine, propofol, and isoflurane in dogs decreases PCV14,15 and therefore oxygen-carrying capacity owing to sequestration of erythrocytes in the spleen as well as in the liver, skeletal muscle, and skin.14 The effect of dexmedetomidine on PCV and oxygen-carrying capacity in propofol- and isoflurane-anesthetized dogs is unclear, and to our knowledge, research comparing the effects of acepromazine and dexmedetomidine premedication on oxygen-carrying capacity in isoflurane-anesthetized dogs has not been performed.
The goals of the study reported here were to characterize the hemodynamic effects of acepromazine and dexmedetomidine premedication in dogs undergoing general anesthesia induced with propofol and maintained with isoflurane in oxygen, and to determine the effects of acepromazine and dexmedetomidine on PCV and oxygen-carrying capacity in these propofol-isoflurane anesthetized dogs. We hypothesized that acepromazine would exacerbate the hypotension induced by propofol and isoflurane, and dexmedetomidine would exacerbate the reduced CO induced by propofol and isoflurane. We also hypothesized that PCV and oxygen-carrying capacity would be higher in anesthetized dogs following dexmedetomidine treatment than following acepromazine treatment.
Materials and Methods
Animals—Six 1-year-old mixed-breed dogs (3 females and 3 males; mean ± SD weight, 22.5 ± 2.2 kg [49.5 ± 4.8 lb]) were included in the study. Each dog was considered healthy on the basis of medical history and the results of a physical examination, CBC, and serum biochemical analysis. The dogs were acclimated for ≥ 21 days prior to the study. Food but not water was withheld from each dog for 12 hours prior to anesthesia. The study was approved by the Purdue University Animal Care and Use Committee.
Instrumentation—Anesthesia was induced with sevofluranea in 100% oxygen administered by a face mask until tracheal intubation could be achieved. Following intubation, each dog was allowed to breathe spontaneously, and anesthesia was maintained by the use of sevoflurane and a circle anesthesia system while instrumentation was performed. Each dog was positioned in right or left lateral recumbency on a warm water circulating blanketb; additionally, a warm forced-air blanketc was used to maintain body temperature within the reference range (37.5° to 38.8°C [99.5° to 101.8°F]). Instrumentation included a 22-gauge catheterd inserted percutaneously into a dorsal pedal artery for continuous monitoring of arterial blood pressure and for collection of arterial blood samples. A 7F thermodilution cathetere was aseptically inserted into the right or left jugular vein and advanced into the lumen of the pulmonary artery; its position was confirmed by a characteristic pressure waveform and pressure values detected via an electronic monitor.f The electronic monitor included a pressure transducer, capnograph, pulse oximeter, and ECG machine such that direct arterial blood pressure, end-tidal sevoflurane and CO2 concentrations, blood hemoglobin saturation for oxygen, and heart rate and rhythm (via limb-lead ECG) were monitored continuously throughout the remainder of the anesthesia session. Each dog was then disconnected from the electronic monitor, the arterial and thermodilution catheters were bandaged in place, and each dog was allowed to recover from anesthesia and rest for 4 hours. The instrumentation for each dog during sevoflurane-induced anesthesia was completed within 60 minutes. The interval between termination of anesthesia for instrumentation and the start of experimental study procedures was 4 hours.
Study design, premedication, and anesthesia procedures—The study had a crossover design, with dogs assigned by a computer-generated randomization table to receive either acepromazineg or dexmedetomidineh premedication prior to induction of general anesthesia. Following a 48-hour interval, each dog received the alternate treatment.
Awake baseline (time 0) cardiorespiratory and hemodynamic measurements were obtained in each dog, and the awake dog was then premedicated with either dexmedetomidine (15.0 μg/kg [6.82 μg/lb], IM) or acepromazine (0.05 mg/kg, IM). Three liters of 100% oxygen/min was provided by a face mask during the premedication phase until after anesthetic induction and intubation. Five and 15 minutes after premedication, the premedication phase hemodynamic measurements were obtained. Propofoli (6.0 mg/kg [2.73 mg/lb]) was drawn into a syringe and administered at 10% increments every 10 seconds over a 90-second period or until endotracheal intubation was achieved. One individual (JCK) administered propofol while another individual (SCG) assessed the anesthetic plane of the dog. Jaw tone and stage of anesthesia were evaluated for suitability of endotracheal intubation during induction with propofol. After endotracheal intubation, anesthesia was maintained for 30 minutes with isofluranej at 1.28% (equivalent to 1 MAC)14 in 100% oxygen via a circle anesthetic breathing circuit (designated as the isoflurane maintenance phase at 20 to 50 minutes after premedication). Body temperature was maintained as described for instrumentation procedures.
End-tidal isoflurane concentration and end-tidal CO2 were measured by use of sidestream capnography with inhalation anesthetic agent monitoring capacity. The sidestream capnometer was connected to a 5F red rubber catheter inserted coaxially through the lumen of the endotracheal tube with the tip of the catheter positioned at the thoracic inlet. The airway gases (CO2, oxygen, and isoflurane) were all calibrated and zeroed at the beginning of each experimental episode. Respiratory rate was determined by observing the excursion of the reservoir bag of the anesthetic breathing circuit as well as that recorded from the capnometer of the multiparameter monitor. Following propofol induction, the isoflurane vaporizer was adjusted as necessary by means of an overpressure technique to reach an end-tidal isoflurane concentration of 1.28%. Once this was achieved, the isoflurane vaporizer was adjusted to maintain the same end-tidal isoflurane concentration during the isoflurane maintenance phase. The dogs were allowed to breathe spontaneously during the entire study.
The timeline for hemodynamic measurements started with administration of premedication. Measurements were obtained at time 0 (awake), 5 and 15 minutes (premedication phase), and 20, 30, 40 and 50 minutes (isoflurane maintenance phase) after premedication. At 50 minutes, isoflurane delivery was terminated and hemodynamic values were measured again at 55, 65, and 75 minutes (isoflurane recovery phase).
The dogs were monitored regularly during recovery after the last hemodynamic variable measurement. Three liters of 100% oxygen/min was provided during the isoflurane recovery phase via the endotracheal tube or by a face mask after the dog was extubated. Investigators were not blinded to treatment group of the dogs because the sedation level and hemodynamic nature of dexmedetomidine and acepromazine were easily distinguishable.
Hemodynamic measurements—For recordings, each dog was positioned in either left or right lateral recumbency and connected to the electronic monitor as described. The position of the thermodilution catheter was validated as described, and measurements were obtained at the predetermined time points. After the final hemodynamic measurements were obtained, the thermodilution and arterial catheters were removed prior to recovery from anesthesia. Direct blood pressures (SABP, DABP, and MABP) were measured via an arterial blood pressure transducerk that was connected to the catheter in the dorsal pedal artery and attached to the electronic monitor; the transducer and monitor were calibrated and zeroed approximately at the level of the heart prior to use for each dog. Heart rate was determined from the arterial pulse through the arterial catheter with the electronic monitor. The CO was determined by use of a thermodilution technique. Briefly, 5 mL of chilled 5% dextrose solution was administered into the right atrium via the thermodilution catheter over a period of 2 seconds, after which CO was determined by use of a CO computer.l At each data collection time, CO was measured 3 to 4 times and the mean of the 3 most similar values was calculated and recorded. Measurements of core body temperature, central venous pressure, mean pulmonary artery pressure, and pulmonary artery wedge pressure were obtained directly by means of the thermodilution catheter connected to the electronic monitor. Core body temperature was taken as the blood temperature recorded from the thermistor located at the tip of the thermodilution catheter, whereas central venous and mean pulmonary artery pressures were recorded from the proximal and distal ports of the thermodilution catheter, respectively. The pulmonary artery wedge pressure was recorded by intermittently inflating the balloon of the thermodilution catheter with air (1 mL) so that the pulmonary artery portion was wedged and the pressure was recorded. All equipment was calibrated and zeroed prior to use for each dog.
At each data collection time, an arterial blood sample (2 mL) was obtained via the catheter in the dorsal pedal artery and anaerobically collected into a polypropylene syringe that had been rinsed with heparin; samples were used for blood gas analysism (Pao2, Paco2, arterial HCO3− concentration, and pH) and calculation of arterial oxygen content. A paired mixed-venous blood sample (2 mL) was anaerobically collected (at the same time as the arterial blood sample) via the thermodilution catheter into a polypropylene syringe that had been rinsed with heparin; these samples were used for blood gas analysis (pH and Po2 and Pco2 in mixed-venous blood), measurement of PCV, calculation of venous oxygen content, and measurement of hemoglobin and l-lactate concentrations. Oxygen hemoglobin concentration was measured via a blood gas analyzer equipped with co-oximetry.m The l-lactate concentration was measured by means of a commercially available metern that has been validated for use in dogs.16 Blood samples were immediately analyzed after collection.
The following hemodynamic variables were calculated from measured values: CI, SV, SV index, SVR, PVR, arterial oxygen content, venous oxygen content, Do2, o2, and OER (Appendix). Oxygen saturation values for arterial and mixed-venous blood samples were obtained via blood gas analyses.17 In this study, hypotension was defined as MABP ≤ 60 mm Hg, hypertension was defined as MABP ≥ 90 mm Hg, bradycardia was defined as heart rate ≤ 60 beats/min, hypoventilation was defined as Paco2 ≥ 45 mm Hg, and acidosis was defined as blood pH ≤ 7.35.
Statistical analysis—Values were log-transformed or ranked when necessary to obtain an approximately normal distribution (as assessed by kurtosis and skewness) and achieve homogeneity of variances before statistical analysis was performed. Data were reported as mean ± SD. A statistical software packageo was used for statistical analysis. Repeated-measures ANOVA was used to detect differences in measured parameters between treatment groups and over time by use of a mixed-models procedure. Values of P < 0.05 were considered significant; Bonferroni-adjusted P values were used when indicated by a significant F test (P < 0.05). Between-group comparisons were conducted at the same time points, and within-group comparisons were made versus the baseline value in awake dogs of the same group. Within-group comparisons were also made among time points after baseline for the variables of interest.
Results
Hemodynamic changes associated with acepromazine and dexmedetomidine premedication and propofol induction followed by isoflurane maintenance were summarized (Tables 1–4). Summarized changes in heart rate and CO following acepromazine-propofol-isoflurane and dexmedetomidine-propofol-isoflurane treatments are shown (Figures 1–6). Mean body temperature of dogs was not significantly or clinically different within or between treatment groups over time during the experiments.
Mean ± SD values for cardiovascular variables of 6 healthy dogs in a crossover-design study to evaluate the hemodynamic effects of acepromazine and dexmedetomidine premedication in dogs undergoing general anesthesia induced with propofol and maintained with isoflurane.
Treatment group | Phase | Time after premedication Injection (min) | SABP (mm Hg) | DABP (mm Hg) | MPAP (mm Hg) | PAWP (mm Hg) |
---|---|---|---|---|---|---|
Acepromazine | Baseline | 0 | 111.5 ± 12 | 70.8 ± 12.4 | 11.2 ± 5.6 | 6.0 ± 3.7 |
Premedication | 5 | 101.2 ± 11† | 57 ± 7.8*† | 6.7 ± 3.1 | 3.0 ± 2.6† | |
15 | 101.4 ± 14.1† | 56 ± 6.9*† | 9.2 ± 2.6 | 4.8 ± 2.6† | ||
Isoflurane maintenance | 20 | 77.7 ± 21.7*†‡§ | 42.2 ± 7.8*†‡§ | 11.5 ± 3.4 | 4.0 ± 2.6† | |
30 | 65.7 ± 16.1*†‡§ | 36.5 ± 5*†‡§ | 10.3 ± 4.1 | 4.8 ± 2.6† | ||
40 | 67.2 ± 9.4*†‡§ | 37.2 ± 4.7*†‡§ | 10.7 ± 4.8 | 3.8 ± 2.7† | ||
50 | 66.5 ± 7.5*†‡§ | 37.5 ± 3*†‡§ | 10.8 ± 3.8 | 4.7 ± 1.6† | ||
Recovery | 55 | 93.3 ± 9.1*†‖ | 51.8 ± 5.1*†‖ | 9.7 ± 2.5 | 4.2 ± 2.8 | |
65 | 100.2 ± 13.6†‖ | 56.8 ± 10.7*†‖ | 9.8 ± 2.3 | 4.0 ± 2.7† | ||
75 | 118.2 ± 12.4‖ | 68 ± 6.8†§‖ | 9.0 ± 3.3 | 5.2 ± 3.1† | ||
Dexmedetomidine | Baseline | 0 | 115 ± 9.9 | 74 ± 7.9 | 12.7 ± 4.0 | 7.8 ± 2.4 |
Premedication | 5 | 145.2 ± 18.9*† | 94.7 ± 15.9*† | 15.0 ± 4.4 | 11.2 ± 4.9*† | |
15 | 144 ± 6.1*† | 99.8 ± 6.4*† | 15.2 ± 2.6 | 11.0 ± 2.3*† | ||
Isoflurane maintenance | 20 | 134 ± 9.9*† | 91.3 ± 13.6*†§ | 15.8 ± 2.1 | 12.2 ± 2.7*† | |
30 | 127.8 ± 11.3†‡§ | 86.7 ± 14.8*†§ | 15.2 ± 2.4 | 10.7 ± 2.2† | ||
40 | 116.8 ± 15.6†‡§ | 76.3 ± 13.7†‡§ | 14.2 ± 2.8 | 9.7 ± 3.9† | ||
50 | 111.7 ± 12.2†‡§ | 70.8 ± 12.1†‡§ | 13.2 ± 2.1 | 8.5 ± 1.9† | ||
Recovery | 55 | 127.5 ± 11.6†‡‖ | 84 ± 8.5†§‖ | 12.5 ± 2.0 | 7.3 ± 2.0 | |
65 | 134.2 ± 4.7*†‖ | 87.3 ± 3.3*†§‖ | 12.7 ± 3.1 | 8.8 ± 2.1† | ||
75 | 130.7 ± 19‖ | 86.3 ± 8.7*†§‖ | 13.5 ± 1.9 | 8.5 ± 1.8† |
Measurements were obtained before and after administration of acepromazine (0.05 mg/kg [0.023 mg/lb]) or dexmedetomidine (15.0 μg/kg [6.82 μg/lb]), followed by propofol (IV to effect) and isoflurane (1.28% in oxygen via endotracheal tube for 30 minutes). After 48 hours, each dog underwent the alternate treatment. Time 0 was the time of baseline measurement in awake dogs; postinjection measurements before anesthetic induction (premedication phase), during isoflurane anesthesia (isoflurane maintenance), and after termination of isoflurane (recovery) are shown.
Within a treatment group, value differs significantly (P < 0.05) from the baseline value.
Within a time point, values differ significantly (P < 0.05) between treatment groups.
Within a treatment group, value differs significantly (P < 0.05) from that at 5 minutes.
Within a treatment group, value differs significantly from that at 15 minutes.
Within a treatment group, value differs significantly from that at 50 minutes.
MPAP = Mean pulmonary arterial pressure. PAWP = Mean pulmonary artery wedge pressure.
Mean ± SD values for hemodynamic variables in the same dogs as in Table 1.
Treatment group | Phase | Time after premedication injection (min) | CI (mL/min/kg) | SV (mL/beat) | SVI (mL/beat/kg) | PVR (dynes•s/cm5) | RR (breaths/min) |
---|---|---|---|---|---|---|---|
Acepromazine | Baseline | 0 | 161 ± 34 | 39.5 ± 11.6 | 1.7 ± 0.6 | 114 ± 41 | 26.3 ± 6.5 |
Premedication | 5 | 146 ± 36† | 32.5 ± 17.6* | 1.4 ± 0.6 | 93 ± 20† | 16.0 ± 3.3* | |
15 | 151 ± 49† | 35.6 ± 14.4* | 1.5 ± 0.5 | 116 ± 60† | 15.6 ± 8.5* | ||
Isoflurane maintenance | 20 | 167 ± 67† | 31.2 ± 13.6* | 1.4 ± 0.5 | 187 ± 78‡§ | 14.3 ± 3.5*† | |
30 | 139 ± 37† | 28.2 ± 10.1* | 1.3 ± 0.4 | 148 ± 80 | 14.5 ± 7.9*† | ||
40 | 141 ± 28† | 28.0 ± 7.1* | 1.2 ± 0.3 | 179 ± 75 | 12.7 ± 8.3* | ||
50 | 137 ± 36 | 25.6 ± 7.2* | 1.1 ± 0.3 | 163 ± 64 | 16.8 ± 17.3*† | ||
Recovery | 55 | 128 ± 26† | 30.5 ± 7.7* | 1.3 ± 0.3 | 161 ± 59† | 23.2 ± 13.8 | |
65 | 126 ± 22† | 32.8 ± 7.1* | 1.5 ± 0.3 | 171 ± 52 | 20.3 ± 13.9 | ||
75 | 126 ± 27† | 32.0 ± 7.8* | 1.4 ± 0.3 | 144 ± 66† | 27.4 ± 23.9 | ||
Dexmedetomidine | Baseline | 0 | 138 ± 26 | 35.5 ± 5.1 | 1.4 ± 0.3 | 123 ± 62 | 27.8 ± 7.7 |
Premedication | 5 | 66 ± 19*† | 29.3 ± 5* | 1.3 ± 0.3 | 215 ± 132*† | 14.3 ± 5.7* | |
15 | 56 ± 9*†‡ | 30.7 ± 7.3* | 1.4 ± 0.3 | 273 ± 122*† | 14.5 ± 3.1* | ||
Isoflurane maintenance | 20 | 76 ± 11*†§ | 20.5 ± 5.7* | 0.9 ± 0.3 | 178 ± 87§ | 5.0 ± 3.0*†‡§ | |
30 | 93 ± 16*†‡§ | 25.7 ± 4.8* | 1.1 ± 0.3 | 175 ± 51§ | 6.8 ± 4.3*†‡§ | ||
40 | 103 ± 14*†‡§ | 23.7 ± 3.4* | 1.1 ± 0.2 | 155 ± 73§ | 7.8 ± 3.2*‡§ | ||
50 | 113 ± 11‡§ | 25.2 ± 5.1* | 1.1 ± 0.2 | 143 ± 53§ | 6.5 ± 3.2*†‡§ | ||
Recovery | 55 | 69 ± 12*†‖ | 22.3 ± 2.9* | 1.0 ± 0.1 | 275 ± 82*†‖ | 14.5 ± 3.7*‖ | |
65 | 68 ± 10*†‖ | 24.5 ± 5.5* | 1.1 ± 0.2 | 198 ± 67* | 15.3 ± 3.9*‖ | ||
75 | 63 ± 10*†‖ | 24.7 ± 5.1* | 1.1 ± 0.2 | 298 ± 111*†‖ | 15.3 ± 4.8*‖ |
RR = Respiratory rate. SVI = SV index.
See Table 1 for remainder of key.
Mean ± SD arterial blood gas analysis results for the same dogs as in Table 1.
Treatment | Phase | Time after premedication injection (min) | Arterial pH (mmol/L) | Paco2 (mm Hg) | Pao2 (mm Hg) | Sao2 (%) | HCO3− (mEq/L) |
---|---|---|---|---|---|---|---|
Acepromazine | Baseline | 0 | 7.395 ± 0.011 | 35.5 ± 2 | 93.7 ± 5.9 | 99.2 ± 0.7† | 21.1 ± 1.1 |
Premedication | 5 | 7.377 ± 0.021 | 37.2 ± 3.1 | 369.6 ± 115.5 | 99.9 ± 0.1* | 21.6 ± 1.4 | |
15 | 7.377 ± 0.021† | 38.1 ± 2.8 | 377.1 ± 128.1 | 99.9 ± 0.1* | 21.3 ± 1.7 | ||
Isoflurane maintenance | 20 | 7.324 ± 0.019*†‡§ | 44.1 ± 4.6*† | 484.0 ± 28.1 | 100 ± 0.0* | 22.2 ± 1.5 | |
30 | 7.296 ± 0.019*†‡§ | 47.7 ± 3.5*† | 508.7 ± 24.2 | 99.9 ± 0.1* | 22.6 ± 1.3 | ||
40 | 7.300 ± 0.026*†‡§ | 46.7 ± 3.3*† | 508.1 ± 30.8 | 99.9 ± 0.1* | 22.4 ± 1.7 | ||
50 | 7.291 ± 0.031*†‡§ | 47.8 ± 3.7*† | 503.0 ± 34 | 100 ± 0.0* | 22.4 ± 1.4 | ||
Recovery | 55 | 7.348 ± 0.012*†‡§‖ | 40.3 ± 3.6‖ | 486.5 ± 39.7 | 100 ± 0.0* | 21.6 ± 1.5 | |
65 | 7.359 ± 0.013*†‖ | 36.3 ± 6.7†‖ | 509.3 ± 33.3 | 100 ± 0.0* | 21.3 ± 1.5 | ||
75 | 7.371 ± 0.019†‖ | 38.1 ± 3.4‖ | 454.2 ± 128.5 | 99.9 ± 0.1* | 21.5 ± 1.5 | ||
Dexmedetomidine | Baseline | 0 | 7.397 ± 0.023 | 34.0 ± 2.7 | 97.1 ± 7.4 | 98.8 ± 0.7† | 20.2 ± 1.1 |
Premedication | 5 | 7.359 ± 0.031* | 37.4 ± 3.3 | 334.5 ± 168.2 | 99.9 ± 0.1* | 20.3 ± 1.1 | |
15 | 7.337 ± 0.027*†‡ | 37.8 ± 3.5* | 483.2 ± 25.9 | 100 ± 0.0* | 19.5 ± 1.2 | ||
Isoflurane maintenance | 20 | 7.236 ± 0.049*†‡§ | 52.3 ± 8.8*†‡§ | 472.6 ± 37.8 | 99.9 ± 0.1* | 21.2 ± 1.5 | |
30 | 7.224 ± 0.031*†‡§ | 54.3 ± 6.2*†‡§ | 480.5 ± 40.8 | 100 ± 0.0* | 21.6 ± 1.6 | ||
40 | 7.226 ± 0.032*†‡§ | 55.3 ± 7.9*†‡§ | 484.0 ± 23 | 99.9 ± 0.1* | 21.1 ± 1.9 | ||
50 | 7.220 ± 0.032*†‡§ | 57 ± 7.6*†‡§ | 486.0 ± 20.6 | 100 ± 0.0* | 22.4 ± 1.6 | ||
Recovery | 55 | 7.301 ± 0.027*†‡§‖ | 43.1 ± 4.6*‡§‖ | 501.2 ± 32.8 | 100 ± 0.0* | 20.6 ± 1.2 | |
65 | 7.305 ± 0.018*†‡§‖ | 42.2 ± 5.5*†‖ | 502.6 ± 33.5 | 100 ± 0.0* | 20.3 ± 2.4 | ||
75 | 7.314 ± 0.011*†‡‖ | 40.6 ± 2.6*‖ | 497.8 ± 38.5 | 100 ± 0.0* | 20.0 ± 1.2 |
Sao2 = Arterial oxygen saturation.
See Table 1 for remainder of key.
Mean ± SD values for PCV, plasma protein concentration, mixed-venous oxygen content (Cvo2), o2, OER, and blood l-lactate concentration in the same dogs as in Table 1.
Treatment group | Phase | Time after premedication injection (min) | PCV (%) | Plasma protein (g/dL) | Cvo2 (mL/dL) | o2 (mL/min) | OER (%) | Blood l-lactate (mmol/L) |
---|---|---|---|---|---|---|---|---|
Acepromazine | Baseline | 0 | 40.5 ± 2.8 | 5.3 ± 0.4 | 14.2 ± 1.6 | 116.5 ± 33.6 | 19.1 ± 5.5 | 1.0 ± 0.4 |
Premedication | 5 | 41.5 ± 9.1 | 5.1 ± 0.3 | 15.2 ± 0.4*† | 88.6 ± 38.7* | 15.3 ± 2.4*† | 1.1 ± 0.6 | |
15 | 37.4 ± 6.8*‡ | 5.2 ± 0.4 | 15 ± 1.1† | 79.9 ± 44.7* | 13.8 ± 4.7*† | 1.1 ± 0.5 | ||
Isoflurane maintenance | 20 | 34.5 ± 8*†‡§ | 5.0 ± 0.3 | 15.3 ± 1.4 | 71.0 ± 23.2* | 12.0 ± 4.5*† | 1.0 ± 0.3 | |
30 | 38.2 ± 6.4*†‡ | 4.9 ± 0.2 | 15.1 ± 1.3† | 76.1 ± 25.9* | 14.1 ± 3* | 1.0 ± 0.3 | ||
40 | 34.4 ± 6.4*†‡ | 4.9 ± 0.4 | 14.9 ± 1.1† | 68.8 ± 23.7* | 13.9 ± 3.2* | 0.9 ± 0.2 | ||
50 | 37.6 ± 4.4* | 4.8 ± 0.3 | 14.5 ± 0.9† | 67.3 ± 16.8* | 12.8 ± 5.1* | 0.9 ± 0.2 | ||
Recovery | 55 | 35.1 ± 5.2*†‡ | 4.7 ± 0.3 | 13.3 ± 1.8†‡§II | 64.8 ± 26.9* | 14.8 ± 4.5 | 0.8 ± 0.1 | |
65 | 33.5 ± 2.8*‡ | 4.7 ± 0.4 | 14.1 ± 1.1‡ | 64.5 ± 20.5* | 14.4 ± 4.5† | 0.8 ± 0.2 | ||
75 | 33.5 ± 1.3*†‡ | 4.8 ± 0.5 | 13.3 ± 0.8†‡§ | 95.8 ± 40.4 | 20.0 ± 2.7‡§‖ | 0.8 ± 0.1 | ||
Dexmedetomidine | Baseline | 0 | 38.6 ± 4.3 | 5.2 ± 0.4 | 14.0 ± 1.7 | 126.1 ± 62 | 21.8 ± 6.1 | 0.8 ± 0.2 |
Premedication | 5 | 39.7 ± 3.7 | 5.0 ± 0.4 | 12.1 ± 1*† | 88.3 ± 27.5* | 33.0 ± 5.9*† | 0.9 ± 0.2 | |
15 | 41.8 ± 2.8 | 5.1 ± 0.5 | 13.2 ± 1†‡§ | 81.9 ± 13.7* | 33.4 ± 5.3*† | 0.9 ± 0.2 | ||
Isoflurane | 20 | 42.3 ± 4.3† | 5.1 ± 0.5 | 15.9 ± 0.8*‡§ | 78.6 ± 18.8* | 22.5 ± 4.3†‡§ | 0.9 ± 0.2 | |
maintenance | 30 | 42.1 ± 4.6† | 5.1 ± 0.5 | 17.7 ± 2.4*†‡§ | 73.1 ± 13.9* | 16.9 ± 3.7‡§ | 0.9 ± 0.2 | |
40 | 40.6 ± 4.4† | 5.1 ± 0.5 | 17.6 ± 1.8*†‡§ | 62.5 ± 18* | 13.2 ± 2.9*‡§ | 0.8 ± 0.1 | ||
50 | 42.3 ± 4.5 | 5.2 ± 0.5 | 18.1 ± 1.9*†‡§ | 61.9 ± 22.3* | 11.9 ± 3.5*‡§ | 0.9 ± 0.2 | ||
Recovery | 55 | 40.6 ± 3.3† | 5.0 ± 0.6 | 16.1 ± 1.6*†‡§‖ | 55.6 ± 16.3* | 18.5 ± 5.1‡§‖ | 0.9 ± 0.2 | |
65 | 39.7 ± 4.5 | 5.0 ± 0.6 | 15.6 ± 1.5‡§‖ | 67.9 ± 15.2* | 22.4 ± 3.9†‡§‖ | 1.0 ± 0.2 | ||
75 | 40.7 ± 4.2† | 5.0 ± 0.6 | 15.3 ± 1.6†‡§‖ | 68.7 ± 16.4* | 24.2 ± 4§‖ | 1.0 ± 0.2 |
See Table 1 for key.
Hemodynamic effects of acepromazine and dexmedetomidine during the premedication phase—After acepromazine administration, heart rate was increased significantly at 5 minutes, but not at 15 minutes, compared with the baseline value in awake dogs (Figure 1). In contrast, heart rate decreased significantly at 5 and 15 minutes after dexmedetomidine premedication. The MABP and DABP, but not SABP, decreased significantly from the baseline values at 5 and 15 minutes after acepromazine administration (Table 1; Figure 2). The CO and Do2 did not change significantly from baseline after acepromazine premedication but were significantly reduced during this interval after dexmedetomidine premedication (Figures 3 and 4).
The SABP, DABP, and MABP were significantly higher and heart rate, Do2, and CI were lower at 5 and 15 minutes after premedication in the dexmedetomidine group, compared with the acepromazine group (Tables 1 and 2; Figures 1 and 4). The PVR and pulmonary wedge pressure were significantly higher in the dexmedetomidine group than in the acepromazine group at all time points during this phase. Dexmedetomidine significantly increased the SVR at 5 and 15 minutes after premedication, whereas there was no change in SVR in the acepromazine-treated dogs during the same time period (Figure 5). Both acepromazine and dexmedetomidine resulted in decreased respiratory rate in both groups at 5 and 15 minutes after premedication; however, there was no hypoventilation as evidenced by Paco2 within the reference range (Tables 2 and 3).
Hemodynamic effects during isoflurane maintenance phase—There was no significant (P = 0.18) difference in induction dose of propofol between the acepromazine and dexmedetomidine groups. The mean propofol induction dose for the acepromazine group was 3.0 ± 0.1 mg/kg (1.36 ± 0.05 mg/lb) and 2.3 ± 0.9 mg/kg (1.05 ± 0.41 mg/lb) for the dexmedetomidine group.
During the isoflurane maintenance phase, heart rate was increased to values similar to the baseline, and CI increased gradually during the isoflurane maintenance period to approximate the baseline value at 50 minutes in the dexmedetomidine group (Figure 1; Table 2). Dogs in this group had a significant increase in CO between 5 minutes of the premedication phase and 30, 40, and 50 minutes of the isoflurane phase. There was also a significant increase of this variable from the 15-minute time point of the premedication phase at 20, 30, 40, and 50 minutes of the isoflurane maintenance phase. The SABP, DABP, and MABP decreased from the values at 5 and 15 minutes after dexmedetomidine premedication during the isoflurane phase (Table 1; Figure 2). The MABP remained above 60 mm Hg throughout the 30-minute isoflurane maintenance phase for this group.
In contrast to the dexmedetomidine group, the acepromazine group developed hypotension, with MABP as low as 46 ± 8 mm Hg during the isoflurane maintenance phase while maintaining CI, when compared with the values at 5 and 15 minutes after premedication (Figure 2; Table 2). The CI was higher for the acepromazine group than for the dexmedetomidine group during the isoflurane maintenance phase, except at 50 minutes after premedication.
The Do2 and OER were not significantly different between the acepromazine and dexmedetomidine treatment groups during the isoflurane maintenance phase except at 20 minutes after premedication (Table 3; Figure 4). The SVR significantly decreased during the isoflurane maintenance phase from the values of the premedication phase in both treatment groups (Figure 5). No differences in PVR were detected between the treatment groups in this phase (Table 2). However, a significant difference in PVR was detected between 15 minutes and 20 minutes within the acepromazine group, and between 15 minutes and all time points of the isoflurane maintenance phase within the dexmedetomidine group. The pulmonary wedge pressure was significantly higher in the dexmedetomidine group than in the acepromazine group during isoflurane maintenance (Table 1).
In both groups, the respiratory rate was decreased from baseline at most time points (Table 2). Hypoventilation occurred in both treatment groups as indicated by Paco2 greater than the reference range (Table 3).
Hemodynamic effects during recovery phase—After termination of isoflurane delivery, the SABP, DABP, and MABP increased and the heart rate decreased from the values of the 50-minute time point of the isoflurane maintenance phase in both treatment groups. However, these effects were more pronounced for the dexmedetomidine group, with lower heart rate and higher DABP, MABP, and SABP (except for the 75-minute SABP), compared with those for the acepromazine group (Table 1; Figures 1 and 2). Second-degree atrioventricular blocks (Mobitz type I) developed in 2 dogs in the dexmedetomidine group at the 55-minute time point (5 minutes after termination of isoflurane delivery), and these resolved spontaneously ≤ 10 minutes after detection. In 1 dog, the atrioventricular block was accompanied by pronounced sinus arrhythmia.
The CI and Do2 in the dexmedetomidine group were significantly decreased from 50-minute isoflurane maintenance phase values in the recovery phase, and these values were significantly lower than those of the acepromazine group (Table 2; Figure 4). The OER was also increased significantly from the value of the 50-minute time point of the isoflurane phase at 75 minutes in the acepromazine group and throughout recovery phase in the dexmedetomidine group (Table 4).
In the dexmedetomidine group, SVR and PVR increased during the recovery phase from isoflurane phase values and returned to approximate values of the premedication phase, whereas in the acepromazine group, SVR returned to approximate baseline value (Table 2, Figure 5). The respiratory rates increased in the dexmedetomidine group and were similar to the values of the premedication phase (eucapnia).
Recovery quality, although not specifically quantitated for comparative purposes, was considered smooth and quiet for both treatment groups and could be characterized by rapid extubation with minimal struggling or vocalization. Subjectively, dogs treated with acepromazine remained in lateral recumbency following extubation, whereas dexmedetomidine-treated dogs assumed sternal recumbency more quickly (approx 10 to 20 minutes faster). Dogs in both groups were able to stand and walk with minimal ataxia within 2 hours after termination of isoflurane delivery.
Effects on PCV, total protein concentration, and oxygen carrying capacity—In the acepromazine group, PCV decreased significantly from the baseline value of awake dogs at 15 minutes after premedication and remained at this lower concentration throughout the study (Table 4). In contrast, the PCV remained unchanged throughout the study in the dexmedetomidine group. The PCV was significantly higher in the dexmedetomidine group than in the acepromazine group at 20, 30, 40, 55, and 75 minutes after premedication. Minimal changes were detected in total protein concentration for both treatment groups over time, compared with the respective baseline value.
Arterial oxygen content was significantly increased from the baseline value at 15 minutes after premedication in the dexmedetomidine group and remained significantly increased throughout the study (Figure 6). Oxygen content was significantly higher in the dexmedetomidine group than in the acepromazine group between 15 and 75 minutes. The l-lactate concentration in mixed-venous blood was < 2 mmol/L in both treatment groups throughout the study (Table 4).
Discussion
Results of the present study showed that acepromazine premedication (0.05 mg/kg, IM) in healthy dogs reduced MABP and DABP at 5 and 15 minutes and increased heart rate at 5 minutes after administration, compared with baseline values (measured in awake dogs). The reduction in blood pressures in acepromazine-treated dogs was likely due to decreases in SVR and SV. Studies5,6 have shown that acepromazine given at 0.1 to 0.2 mg/kg IV resulted in hypotension (MABP < 60 mm Hg) with reduced CO and SV compared with baseline values for unsedated dogs. Collectively, these results suggest that acepromazine at dosages between 0.05 to 0.2 mg/kg can induce negative hemodynamic changes. In contrast to acepromazine-induced hypotension, dexmedetomidine premedication induced hypertension, bradycardia, and an increase in SVR with a reduction in CO. This finding is consistent with previous studies,9,18 which reported the same negative hemodynamic changes associated with dexmedetomidine administration in dogs.
The induction dose of propofol following acepromazine and dexmedetomidine administration (3.0 ± 0.1 mg/kg and 2.3 ± 0.9 mg/kg, respectively) was not significantly different between groups. The magnitude of the hemodynamic impacts of propofol to each of these treatment groups was likely to be similar, considering the similar induction dose requirement. The results of the present study also showed several important hemodynamic impacts of acepromazine and dexmedetomidine premedication in dogs under anesthesia induced with propofol and maintained with isoflurane. First, acepromazine premedication augmented the hypotensive effects of propofol and isoflurane while maintaining CO in these dogs. The MABP of acepromazine-treated dogs decreased from 70.6 ± 8.9 mm Hg at 15 minutes after premedication to 47.0 ± 3.6 mm Hg at the end of the 30-minute isoflurane maintenance phase (50 minutes after acepromazine premedication). These enhanced hypotensive effects were associated with significant reductions in SVR and SV during this time. Our results were similar to those reported by Sinclair and Dyson,7 who showed that acepromazine (0.05 mg/kg, IV) enhances isoflurane-induced hypotension (MABP, 45 to 50 mm Hg) through the reduction of SVR while maintaining CO. In the present study, the CO of acepromazine-premedicated dogs was maintained fairly well during the isoflurane maintenance phase, despite the reduction in SVR and SV from the baseline value in awake dogs. The reason CO was maintained under these circumstances is likely attributable to the consistent maintenance of heart rate similar to the awake baseline values in these dogs after the administration of acepromazine and propofol and during isoflurane delivery.
The second vital hemodynamic influence associated with premedication was that dexmedetomidine premedication attenuated the vasodilatory effects of propofol and isoflurane. This evidence was demonstrated by the significant reduction in SVR after propofol and isoflurane delivery and the abrupt resumption of SVR values significantly greater than baseline within 5 minutes after the termination of isoflurane delivery. Alleviation of the dexmedetomidine-induced high SVR at 15 minutes after premedication (from 6,893.7 ± 1,389.9 dynes•s/cm5 to 2,521.0 ± 529.2 dynes•s/cm5) resulted in an increase in heart rate (from 40.5 ± 4.2 beats/min to 96.0 ± 12.3 beats/min) and CO (from 1.2 ± 0.2 L/min to 2.5 ± 0.3 L/min) at the end of the isoflurane maintenance phase (at 50 minutes). The dexmedetomidine premedication also prevented hypotension during the isoflurane maintenance phase. This is evident by the fact that the MABP in the dexmedetomidine-premedicated dogs was maintained between 84.5 ± 11.4 mm Hg and 105.3 ± 11.3 mm Hg and there was a significant difference in MABP between dexmedetomidine-premedicated dogs (84.5 ± 11.4 mm Hg) and acepromazine-premedicated dogs (47.0 ± 3.6 mm Hg) at 30 minutes after isoflurane maintenance (50 minutes after premedication). In the present study, we hypothesized that the vasoconstriction caused by dexmedetomidine premedication would counteract propofol-isoflurane–induced hypotension during the 30 minutes of the isoflurane maintenance phase. The study results confirmed this prediction. Similar results have been reported for dogs treated with other α2-adrenergic receptor agonists, including xylazine and medetomidine, and subsequently anesthetized with isoflurane.19,20
The hemodynamic interactions between α-adrenergic receptor agonist (nonsedative or sedative)–mediated vasoconstriction and isoflurane-induced vasodilation have been previously reported.19–22 Kenny et al21 showed that isoflurane (2%) attenuates the vasoconstrictive effect of bolus administration of α1- (phenylephrine) and α2-(azepexol) adrenergic receptor agonists. The mechanism by which isoflurane attenuated the vasopressor effect induced by the α-adrenergic receptor agonists was considered to be nonselective and was not enhanced by the calcium channel blockers.22 It is recognized that the administration of xylazine19 or medetomidine20 as a premedication in dogs increases vascular tone, thereby attenuating isoflurane-induced vasodilation and reducing the isoflurane requirement.
There are several reports regarding dexmedetomidine and its hemodynamic interactions with propofol and inhalation anesthetics in dogs. Kuusela et al8 reported that dogs premedicated with dexmedetomidine at 0.2, 2.0, and 20 μg/kg (0.09, 0.9, and 9.1 μg/lb), IV, that subsequently had anesthesia induced with propofol (0.8 to 6.0 mg/kg [0.36 to 2.73 mg/lb], IV) and maintained with isoflurane (0.2% to 1.4%) had an increase in heart rate and reduction in MABP after induction. Kersten et al23 reported that dogs given dexmedetomidine PO followed by isoflurane had decreased MABP and SVR, increased heart rate, and no change in CO. Similar cardiovascular effects were reported by Gomez-Villamandoz et al24 In that study,24 dogs were premedicated with 1.0 or 2.0 μg of dexmedetomidine/kg (0.45 to 0.9 μg/lb), IV, and anesthesia was induced with propofol (2.3 to 3.3 mg/kg [1.05 to 1.5 mg/lb], IV) and maintained with desflurane. The results of our study are similar to those reports. Furthermore, our results not only indicated that CO significantly improved when propofol and isoflurane were administered in the dexmedetomidine-treated dogs, but also showed that when isoflurane administration was terminated, the CO in these dogs reverted back to values similar to those of the premedication phase.
Another important finding of this study was that Do2, o2 and OER were not significantly different between the 2 treatment groups during the isoflurane maintenance phase, with the exception of the 20-minute time point, despite the significantly lower MABP and higher CO of the acepromazine premedication group than those of the dexmedetomidine premedication group throughout most of the study. During the premedication phase, acepromazine and dexmedetomidine induced opposite hemodynamic effects that resulted in a significant difference in Do2 and OER between treatment groups. The greatest Do2 reduction induced by dexmedetomidine was a significant 56% difference (from 561.1 ± 140 to 246.8 ± 39.5 mL/min) between the baseline value in awake dogs and the measurement obtained 15 minutes after premedication, whereas acepromazine premedication was associated with a nonsignificant change (3.6% reduction [from 633 ± 164.3 mL/min to 610.4 ± 255.7 mL/min]) in Do2 at the same time point. This difference was mainly attributable to the marked reduction in CO following dexmedetomidine administration. A similar reduction of CO and Do2 following dexmedetomidine administration has been recently reported by Keating et al,25 who found that as little as 2.5 μg of dexmedetomidine/kg (1.14 mg/lb), IV, reduced CO and Do2 at extubation in dogs receiving a constant rate infusion of fentanyl at 5.0 μg/kg/h (2.27 μg/lb/h) IV.
Studies18,26 have shown that when tissues experience hypotension or severe CO reduction, one of the first responses is an increase in OER. When increasing OER cannot meet the demand of o2, especially when Do2 decreases to below the critical level (9.0 to 11.0 mL/kg/min [4.1 to 5.0 mL/lb/h]), hyperlactatemia occurs as an alternative way of producing energy.26,27 In the present study, the OER initially increased from the baseline value during the premedication phase in dogs that received dexmedetomidine, mainly owing to the reduction of CO and Do2, indicating an increased need for tissue extraction of oxygen from the blood supply during this time. Later, the OER significantly decreased, compared with baseline, during the isoflurane maintenance phase (at 40 to 50 minutes after premedication [20 and 30 minutes of isoflurane maintenance]). This decrease in OER corresponded to increases in CO and Do2 and a decrease in o2. In contrast to the dexmedetomidine group, the OER was significantly reduced in the acepromazine group during both the premedication and isoflurane maintenance phases. This was attributable to a relatively well-maintained CO and Do2 and a reduction of o2 in the acepromazine group.
Collectively, Do2 was maintained above the critical level (9.0 to 11.0 mL/kg/min)27 and the blood l-lactate concentration remained within the normal range (< 2 mmol/L)26 in both treatment groups, despite hypotension and significantly decreased CO detected in the acepromazine and dexmedetomidine treatment groups, respectively. It is, however, important to remember that these animals were healthy dogs, and their cardiorespiratory systems were able to accommodate hemodynamic changes associated with these anesthetics. The same premedication and anesthetic protocols may induce a very different hemodynamic response in diseased or debilitated dogs.
Sedative premedications such as acepromazine and dexmedetomidine induce CNS depression and lead to decreased respiratory function. Dose-dependent reduction in respiratory rate has been reported in dogs sedated with acepromazine5,6 and dexmedetomidine.8 In the present study, both acepromazine and dexmedetomidine treatment significantly decreased the respiratory rate during the premedication phase, compared with the baseline values. However, respiratory depression did not lead to the development of hypoventilation because dogs in both treatment groups maintained Paco2 within the reference range. When propofol and isoflurane were administered in the acepromazine- and dexmedetomidine-treated dogs, hypoventilation did occur. The hypoventilation was indicated by further reduction of respiratory rate and a significant increase in Paco2, which led to respiratory acidosis during the isoflurane maintenance phase in both treatment groups. In addition, the hypoventilation and respiratory acidosis were more profound in the dexmedetomidine group than in the acepromazine group. These results are in agreement with those reported by Kuusela et al,8 who indicated that hypercapnia occurs when propofol and isoflurane are administered to dogs premedicated with dexmedetomidine.
Various studies have shown that sedative and anesthetic administration can affect PCV in dogs. Acepromazine administered at 0.044 mg/kg (0.02 mg/lb), IM, decreased PCV by 22%.14 More recently, Baldo et al15 reported a reduction of PCV in dogs after acepromazine (0.03 mg/kg [0.014 mg/lb]) and propofol (5.0 mg/kg) administration IV. Steffey et al28 reported a 15% to 30% reduction, and Merin et al29 reported a 13% reduction of PCV in dogs that received halothane. Reported effects of α2 adrenergic receptor agonists on PCV are more controversial and not as clear as those associated with acepromazine, propofol, or inhalation anesthesia. It has been shown that PCV decreased in horses sedated with α2-adrenergic receptor agonists. In dogs, results of 1 study29 indicated that dexmedetomidine reduced PCV concentration, whereas other results28 showed that PCV was unchanged by this drug. Several mechanisms have been proposed for changes in PCV after sedative or anesthetic administration, including splenic, muscle, skin, or liver sequestration of RBCs14,30–32; RBC lysis33; fluid shift among body compartments30,31; and decreased sympathetic tone associated with sedation.30
The results of our study clearly showed that PCV significantly decreased from the baseline value 15 minutes after acepromazine administration and remained decreased in treated dogs during and after propofol and isoflurane administration, with the lowest value corresponding to the last measurement obtained. Such a reduction in PCV from the baseline could have been induced by acepromazine alone or in combination with propofol and isoflurane because both propofol and isoflurane have been shown to decrease PCV in dogs.15,34 In contrast to the acepromazine group, the PCV did not decrease from baseline in the dexmedetomidine group but remained fairly consistent throughout the study and was significantly higher than the PCV of the acepromazine-treated dogs for most of the time points evaluated. We speculate that the steady and significantly higher PCV of the dexmedetomidine group was attributable to either the vasoconstrictive nature of dexmedetomidine, which prevented drastic splenic sequestration of blood, or a lack of propofol- and isoflurane-induced changes in PCV substantial enough to override the dexmedetomidine effect on PCV. We measured the plasma protein concentration simultaneously with PCV, and the values of plasma protein concentration did not change over time in either group, indicating the changes of PCV were unlikely to have been caused by bodily fluid shifts.
There were several limitations of the present study. The use of high-end doses of acepromazine and dexmedetomidine may not represent some of the current clinical practices in which lower doses of these drugs are combined with an opioid in dogs. Furthermore, comparison of the clinical equipotent doses of acepromazine (a tranquilizer) and dexmedetomidine (a sedative-analgesic) was not feasible. Therefore, we compared doses in a common clinical range rather than trying to achieve similar levels of sedation with 2 very different drugs. The washout period between drug treatments in this study was 48 hours, and a potential residual effect may have carried over. A longer drug washout period would have been ideal; however, maintaining a thermodilution catheter in place for a longer period of time would potentially have increased the risk of complications in these dogs. In addition, the elimination half-life of acepromazine and dexmedetomidine have been reported to be 7.1 hours and < 1 hour, respectively,35,36 and a 48-hour washout period should have provided sufficient time for the elimination of acepromazine and dexmedetomidine (approx 3 to 5 half-lives) in these dogs.
ABBREVIATIONS
CI | Cardiac index |
CO | Cardiac output |
DABP | Diastolic arterial blood pressure |
Do2 | Oxygen delivery |
MABP | Mean arterial blood pressure |
MAC | Minimum alveolar concentration |
OER | Oxygen extraction ratio |
PVR | Pulmonary vascular resistance |
SABP | Systolic arterial blood pressure |
SV | Stroke volume |
SVR | Systemic vascular resistance |
o2 | Oxygen consumption |
SevoFlo, Abbott Animal Health, Abbott Park, Ill.
Gaymar TP Professional, Gaymar Industries Inc, Orchard Park, NY.
Gaymar Hot Air Hugger, Gaymar Industries Inc, Orchard Park, NY.
Seruflo Teflon I.V. Catheter 22 gauge, 1 inch, Terumo Medical Corp, Somerset, NJ.
Swan-Ganz, Edwards Lifesciences Corp, Irvine, Calif.
Datascope DPM7, Mindray, Mahwah, NJ.
Acepromazine, Boehringer Ingelheim Vetmedica Inc, Fort Dodge, Iowa.
Dexdomitor, Zoetis Animal Health, Florham Park, NJ.
Propoflo, Abbott Laboratories, North Chicago, Ill.
IsoFlo, Abbott Animal Health, Abbott Park, Ill.
PX260 Pressure Monitoring Kit with TruWave Transducer, Edwards Lifesciences Corp, Irvine, Calif.
COM-1 CO computer, Edwards Lifesciences Corp, Irvine, Calif.
Rapidlab 855 Blood Gas Analyzer, Bayer Corp, New York, NY.
Lactate Pro Meter, FaCT Canada Consulting Ltd, Quesnel, BC, Canada.
Version 9.3, SAS Institute Inc, Cary, NC.
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Appendix
Hemodynamic calculations used in a crossover-design study to evaluate the hemodynamic effects of acepromazine and dexmedetomidine premedication in healthy dogs undergoing general anesthesia induced with propofol and maintained with isoflurane.
Variable | Equation |
---|---|
CI (mL/min/kg) | CI = CO/body weight |
SV (mL/beat) | SV = CO/HR |
SVI (mL/beat/kg) | SVI = SV/body weight |
SVR (dynes•s/cm5) | SVR = 80 × (MABP – CVP)/CO |
PVR (dynes•s/cm5) | PVR = 80 × (MPAP – PAWP)/CO |
Cao2 (mL/dL) | Cao2 = (1.34 × Sao2 × Hb) + (0.003 × Pao2) |
Cvo2 (mL/dL) | Cvo2 = (1.34 × Svo2 × Hb) + (0.003 × Pvo2) |
Do2 (mL/min) | Do2 = 10 × Cao2 × CO |
o2 (mL/min) | o2 = CO × (Cao2 – Cvo2) |
OER (%) | OER = (Cao2 – Cvo2) × 100%/Cao2 |
Cao2 = Arterial oxygen content. Cvo2 = Venous oxygen content. CVP = Central venous pressure. HR = Heart rate. MPAP = Mean pulmonary arterial pressure. PAWP = Mean pulmonary arterial wedge pressure. Pvo2 = Venous Po2. Sao2 = Arterial oxygen saturation. SVI = SV index.