Effects of Atropine and Glycopyrrolate on Esophageal, Gastric, and Tracheal pH in Anesthetized Dogs

Atropine, glycopyrrolate, or saline solution was administered before anesthesia in a blinded, controlled study of 40 dogs scheduled to undergo surgery. Effects of treatment on esophageal, gastric, and tracheal pH were measured with an intraluminal pH meter. Preanesthetic administration of atropine and glycopyrrolate had no effect on esophageal, gastric, or tracheal pH but did result in increased heart rate. Thoracotomy procedures resulted in decreased intraluminal esophageal pH and increased heart rate. Esophageal pH at the level of the thoracic inlet decreased over the duration of surgery.     

The Effects of Atropine and Glycopyrrolate on Heart Rates in Conscious Mature Goats

The effects of intravenously administered atropine (0.2 mg/kg) and glycopyrrolate (0.01 mg/kg) on heart rate were studied in 10 conscious mature goats. In a drug cross-over fashion, either atropine, glycopyrrolate, or 0.9% saline solution was administered using the same volume (0.05 mL/kg). Atropine and glycopyrrolate caused a significant increase in heart rate ( P <.05), whereas saline solution (0.09%) did not. The mean percent changes in heart rate from baseline were similar for atropine and glycopyrrolate up to 14 minutes after administration. Thereafter, glycopyrrolate had a significantly greater mean change in heart rate than atropine, ie, up to 29 minutes ( P <.05). Within the atropine group, the mean percentage changes in heart rate became significantly lower compared with the initial increase (1 minute) starting at 11 minutes. For the glycopyrrolate group, the mean percent changes became significantly lower starting at 27 minutes. Glycopyrrolate and atropine had a mean percentage change in heart rate of greater than 1.0%, up to 31 and 22 minutes, respectively. At the doses used, glycopyrrolate had longer duration of action than atropine but the magnitude of increase was similar.     

Hemodynamic Effects of Intravenous Midazolam-Xylazine-Butorphanol in Dogs

The hemodynamic effects of a mixture of midazolam (1.0 mg/kg), xylazine (0.44 mg/kg), and butorphanol (0.1 mg/kg) were evaluated in six adult dogs. The dogs were anesthetized with isoflurane for instrumentation. As the dogs returned to consciousness, baseline values were recorded and the midazolam-xylazine-butorphanol mixture and glycopyrrolate (0.01 mg/kg) were administered intravenously (IV). Hemodynamic data were recorded 3, 10, 20, 30, 40, 50, and 60 minutes after injection. Mean arterial pressure (AP), mean pulmonary arterial pressure (PAP), heart rate (HR), rate-pressure product (RPP), mean pulmonary capillary wedge pressure (PCWP), systemic vascular resistance (SVR), and right ventricular stroke work index (RVSWI) were increased significantly above baseline values. Cardiac output (CO), stroke volume (SV), cardiac index (CI), stroke index (SI), mean central venous pressure (CVP), and left ventricular stroke work index (LVSWI) were decreased significantly below baseline values. When administered IV at the dosages used in this study, midazolam-xylazine-butorphanol-glycopyrrolate induced profound acute alterations in several critical hemodynamic variables.     

Hemodynamic Effects of Epidural Ketamine in Isoflurane-Anesthetized Dogs

Objective —The purpose of this study was to determine the hemodynamic effects of epidural ketamine administered during isoflurane anesthesia in dogs. Study Design —Prospective, single-dose trial. Animals —Six healthy dogs (five males, one female) weighing 25.3 ± 3.88 kg. Methods —Once anesthesia was induced, dogs were maintained at 1.5 times the predetermined, individual minimum alveolar concentration (MAC) of isoflurane. Dogs were instrumented and allowed to stabilize for 30 minutes before baseline measurements were recorded. Injection of 2 mg/kg of ketamine in 1 mL saline/4.5 kg body weight was then performed at the lumbosacral epidural space. Hemodynamic data were recorded at 5, 10, 15, 20, 30, 45, 60, and 75 minutes after epidural ketamine injection. Statistical analysis included an analysis of variance (ANOVA) for repeated measures over time. All data were compared with baseline values. A P < .05 was considered significant. Results —Baseline values ±standard error of the mean (X ± SEM) for heart rate, mean arterial pressure, mean pulmonary artery pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, stroke index, systemic vascular resistance, pulmonary vascular resistance, and rate-pressure product were 108 ± 6 beats/min, 85 ± 10 mm Hg, 10 ± 2 mm Hg, 3 ± 1 mm Hg, 5 ± 2 mm Hg, 2.3 ± 0.3 L/min/m², 21.4 ± 1.9 mL/beat/m², 3386 ± 350 dynes/sec/cm⁵, 240 ± 37 dynes/sec/cm⁵, and 12376 ± 1988 beats/min±mm Hg. No significant differences were detected from baseline values at any time after ketamine injection. Conclusions —The epidural injection of 2 mg/kg of ketamine is associated with minimal hemodynamic effects during isoflurane anesthesia. Clinical Relevance —These results suggest that if epidural ketamine is used for analgesia in dogs, it will induce minimal changes in cardiovascular function.     

Hemodynamic and Electrocardiographic Effects of Magnesium Sulfate in Healthy Dogs

We investigated the effects of graded dosages of magnesium given i.v. to anesthetized dogs on blood pressure, cardiac output, and electrophysiology. Magnesium was infused at 0.12 mEq/kg/minute until ventricular fibrillation occurred naturally or was provoked by programmed electrical stimulation or until arrest of the sinuatrial node in 8 dogs. Plasma total magnesium concentrations doubled in 1 minute of that infusion rate, and a hemodynamically safe plasma concentration of 12.2 mEq/L was achieved after 16 minutes of infusion. Heart rate, inotropy, lusitropy, and cardiac output increased up to a cumulative infusion dosage of magnesium of 1.0-2.0 mEq/kg, which produced plasma magnesium concentrations of 8.5-12.2 mEq/L (n = 5). Above the cumulative infusion dosage, inotropy decreased and lusitropy increased until death occurred between cumulative infusion dosages of 5.9 mEq/kg and 10.9 mEq/kg. Arterial pressure and vascular resistance decreased, and PQ interval and QRS complex increased, in a dose-dependent fashion. The relationship between ionized and total magnesium was y = 0.624x - 0.542 (r2 = .986), where y is ionized and x is total magnesium in mEq/L in 3 dogs. In conclusion, a cumulative infusion dosage of 0.1-0.2 mEq/kg of magnesium may be given without changing hemodynamic parameters, but with higher cumulative infusion doses heart rate accelerates. Hemodynamic parameters except those related to blood pressure continued to increase to a cumulative infusion dosage of 2.0 mEq/kg. At higher cumulative infusion dosages dogs became hypotensive and the PQ interval was prolonged. However, dangerous arrhythmias were not provoked until a total dosage of 3.9 mEq/kg.     

Evaluation of the Hemodynamic Effects of Interpleural Bupivacaine in Dogs

The hemodynamic effects of interpleural (IP) bupivacaine were studied in six halothane-anesthetized dogs. On four separate occasions, each dog received IP saline (S), or bupivacaine at a low dosage of 1.5 mg/kg (L), high dosage of 3.0 mg/kg (H), or high dosage of 3.0 mg/kg with epinephrine 5 μg/mL (HE). Heart rate, systolic and mean arterial pressures, and base excess were significantly lower in the H dosage group than in the other treatment groups. Cardiac output, expressed as a percentage of change from baseline, was significantly higher in the L group than in the H and S groups. Pulmonary arterial pressure and respiratory rate were significantly higher in the HE group than in the other three groups. Mean plasma concentrations of bupivacaine peaked between 5 and 15 minutes after IP injection. Maximum plasma concentrations in individual dogs were variable; however, mean maximum plasma concentrations in the H and HE groups were not significantly different. Clinically significant hypotension occurred in one dog in the H group and in one dog in the HE group. No pulmonary complications were detected.     

Hemodynamic Effects of Atropine, Dobutamine, Nitroprusside, Phenylephrine, and Propranolol in Conscious Horses

The authors investigated the cardiovascular effects of low doses of nitroprusside, dobutamine, and phenylephrine and a beta-adrenergic blocking dose of propranolol in conscious, healthy horses with and without prior atropine administration. A parasympathetic blocking dose of atropine produced significant increases in heart rate and arterial pressures, and decreased stroke volume, ejection fraction, pulse pressure, and right-ventricular end-diastolic pressure and volume. Cardiac output was not changed by atropine administration. Nitroprusside reduced arterial pressures to a greater extent in atropinized horses but increased heart rate in both atropinized and non-atropinized horses. Dobutamine increased mean arterial pressure in both non-atropinized and atropinized horses but increased heart rate, diastolic arterial pressure, and systemic vascular resistance only in atropinized horses. Propranolol did not affect any of the hemodynamic variables that were measured. Phenylephrine, in the presence of beta-adrenergic blockade, increased mean arterial pressure and reduced cardiac output. This study showed that low doses of nitroprusside, dobutamine, and phenylephrine produce significant hemodynamic effects in conscious, healthy horses and that these effects are modified by prevailing parasympathetic tone.     

The Acute Hemodynamic Effects of Milrinone in Dogs With Severe Idiopathic Myocardial Failure

To examine the effects of acute oral milrinone administration (0.75 mg/kg) on dogs with severe idiopathic myocardial failure and the effect of prolonged milrinone administration on survival time, we measured hemodynamics before and 2 hours after drug administration and recorded survival time and cause of death in 13 dogs with dilated cardiomyopathy. Hemodynamics were measured using a Swan-Ganz catheter and femoral artery puncture along with recording an M-mode echocardiogram. Cardiac index increased from 1.92 +/- 0.54 to 3.06 +/- 0.81 L/min/m2, stroke volume index increased from 11.3 +/- 4.3 to 16.7 +/- 6.3 ml/beat/m2, and pulmonary capillary wedge pressure decreased from 23 +/- 8 to 12 +/- 8 mmHg. A clinically significant increase in heart rate was observed in seven dogs, resulting in a statistically significant increase in heart rate for the group from 174 +/- 34 to 194 +/- 44 beats/minute. Mean arterial blood pressure did not change significantly for the group but did decrease more than 20 mmHg in three dogs, suggesting a predominant primary vasodilating effect of milrinone in these dogs. An increase in contractility appeared to be the predominant reason for the improved hemodynamics in seven dogs. Eight dogs died of causes other than worsening heart failure, including four of eight Doberman pinschers that died suddenly, presumably from an acute tachyarrhythmia. Two dogs that had the greatest increase in an index of contractility are alive more than 2 years after the initiation of milrinone administration.     

Hemodynamic and Biochemical Alterations in Dogs with Lymphoma after Induction of Chemotherapy

Background

Doxorubicin is a common antineoplastic agent with dose‐dependent cardiotoxic adverse effects, and pre‐existing myocardial dysfunction is a contraindication to its use.

Objectives

To systematically define the hemodynamic and biochemical alterations in dogs undergoing chemotherapy for newly diagnosed lymphoma and assess the reversibility of these alterations with fluid administration.

Animals

Twenty‐one client‐owned dogs with newly diagnosed lymphoma were evaluated 1 week after induction of chemotherapy. Underlying degenerative valve disease was exclusionary. Eighteen healthy age‐ and weight‐matched dogs were used as controls.

Methods

Physical examination, blood pressure by Doppler, echocardiography, and biochemical evaluation (routine serum biochemistry, plasma renin activity and aldosterone concentrations, plasma and urine osmolalities, and urine electrolyte concentrations) were measured in dogs with lymphoma and compared to controls. Dogs with lymphoma received crystalloids IV at 6 mL/kg/h for 24 hours. All variables were reassessed at 4 and 24 hours. Deuterium oxide dilution and bromide dilution were used to determine total body water and extracellular water space, respectively.

Results

Baseline echocardiograms showed significantly smaller chamber dimensions in dogs with lymphoma compared to controls. These changes were reversed by fluid administration. Systolic blood pressure and urine sodium concentration were significantly increased, and bromide dilution space, PCV, urine specific gravity, and urine potassium concentration were significantly decreased compared to controls.

Conclusion and Clinical Importance

Echocardiographic and biochemical abnormalities in dogs with lymphoma appear consistent with volume depletion, and may be the result of systemic hypertension and subsequent pressure natriuresis.     

Hemodynamic Changes During Laparoscopic Radiofrequency Ablation of Normal Adrenal Tissue in Dogs

Objective— To determine the hemodynamic response to radiofrequency ablation (RFA) of normal adrenal tissue in dogs.
Study Design— Experimental study.
Animals— Healthy adult mixed-breed dogs (n=6).
Methods— During general anesthesia a Swan–Ganz thermodilution catheter was flow directed into the pulmonary artery and used to quantify cardiac output. An arterial catheter was used for direct blood pressure measurements. An RFA device was introduced into the left adrenal gland under observation through laparoscopic instrumentation. Blood samples were collected and hemodynamic variables studied after a stable surgical anesthetic depth was achieved (time 1), during CO₂ insufflation of the abdomen (time 2), during adrenal RFA (time 3), and after completed RFA (time 4). Catecholamine determinations were performed with a human enzyme immunoassay. Histopathology was performed to verify medullary necrosis.
Results— Arterial, pulmonary arterial and central venous pressure, and plasma norepinephrine increased more during RFA than during abdominal insufflation. Heart rate and cardiac index did not differ between time points. High baseline epinephrine was present and significant differences between time points were not detected. Systemic vascular resistance had very high individual variation and differences were not detected.
Conclusions— RFA of normal adrenal tissues is associated with severe hemodynamic alterations. Further studies of the optimal blockage of catecholamine-induced hypertension in dogs are warranted.
Clinical Relevance— Clinicians should prepare for potential hypertensive crisis during RFA of adrenal masses, especially if treating a margin of normal tissue.     

Captopril Provides Sustained Hemodynamic Benefits in Dogs with Experimentally Induced Mitral Regurgitation

Mitral regurgitation was created surgically in 10 dogs. After measurement of baseline hemodynamic parameters on day 2, treatment with captopril (2 mg/kg orally 3 times daily) was begun in five dogs. Five control dogs received no therapy during the study. The hemodynamic parameters were measured again at weeks 6 and 22. In the treated dogs, the forward ejection fraction (FEF) increased slightly and the total peripheral resistance index (TPRI) decreased. In the controls, the FEF decreased and the TPRI increased. Changes in FEF and TPRI were significantly different between the two groups. The change in FEF correlated significantly with the change in TPRI in both groups. Although the most dramatic changes were observed at week 6, the differences persisted throughout the study. Captopril administration resulted in sustained hemodynamic improvement and may, therefore, delay the onset of congestive heart failure in dogs with mitral regurgitation.     

Short-Term Hemodynamic Evaluation of Circumferential Mitral Annuloplasty for Correction of Mitral Valve Regurgitation in Dogs

Objective —To determine the short-term hemodynamic effects associated with circumferential mitral annuloplasty (CMA) in dogs with mitral regurgitation.
Study Design —Prospective experimental study.
Animals —Seven healthy adult mongrel dogs.
Methods —Mitral regurgitation was surgically induced, and annular dilation occurred. Echocardiography and cardiac catheterization were used to determine forward ejection fraction (FEF), regurgitant fraction (RF), pulmonary capillary wedge pressure (PCWP), and annular diameter before and immediately after CMA in five dogs. FEF and RF were also evaluated 7 days after annuloplasty.
Results —Mean annular diameter and PCWP were significantly reduced immediately after CMA. Significant increases in FEF of 19% and 22% were shown immediately and 7 days after CMA. Significant reductions in RF of 19% and 22% were also shown immediately and 7 days after annuloplasty.
Conclusions —Sustained hemodynamic benefits and a reduction in annular diameter were achieved by CMA in a canine model of mitral regurgitation.
Clinical Implications—CMA may be a suitable treatment for heart failure because of mitral regurgitation when early signs of cardiovascular decompensation persist despite appropriate medical management.     

Echocardiographic Assessment of Hemodynamic Changes Produced by Two Methods of Inducing Fluid Deficit in Dogs

Background: Hydration status is important to the cardiovascular system because of its effects on preload. Decreased preload can alter echocardiographic measurements of systolic and diastolic function, potentially confounding interpretation of results. Hypothesis/Objectives: Mild fluid deficits are associated with measurable echocardiographic changes that are validated by physical and biochemical markers of decreased intravascular volume. Animals: Twenty‐five healthy staff/student‐owned dogs with no evidence of cardiac or renal disease. Methods: Prospective, interventional laboratory study. Dogs were randomly assigned to water deprivation (WD) alone for 8 hours (n = 13) or to furosemide treatment (FTx, 2.5 mg/kg IV) followed by WD for 8 hours (n = 12). Echocardiograms, biochemical sampling, and physical parameters were measured at baseline, and after 4 and 8 hours. Results: Both protocols induced fluid deficit as indicated by significant (P < .00001) decreases in weight at 4 hours (WD, 1.1%; FTx, 3.7%) and 8 hours (WD, 2.7%; FTx, 4.5%). Furosemide significantly decreased left ventricular end‐diastolic volume (54.3 ± 19.3–42.1 ± 17.3 mL, P < .0001), cardiac index (4.2 ± 1.1–2.9 ± 0.9 L/min/M², P < .0001), and mitral valve E wave velocity (0.79 ± 0.2–0.66 ± 0.2 m/s, P= .0004). These changes were accompanied by significant increases in blood urea nitrogen concentration (13.8 ± 2.6–14.8 ± 2.7 mg/dL, P= .04), vasopressin concentration (1.4 ± 1.2–3.3 ± 1.9 pg/mL, P= .045), and PCV (49.8 ± 4.5–53.2 ± 6.5%, P= .006). Effects of water deprivation alone were similar, but less pronounced. Conclusions and Clinical Importance: Mild fluid deficits have measurable hemodynamic effects in dogs. Hydration status should be considered when evaluating cardiac function by echocardiogram.     

Mandibular Condylectomy Effects in Normal Dogs

Mandibular condylectomy and meniscectomy were performed unilaterally on six dogs and bilaterally on six dogs. All six dogs that underwent unilateral condylectomy functioned normally. Bilateral condylectomy caused temporary malocclusion in five of six dogs. At necropsy one to six months following surgery, a fibrous pseudoarthrosis had formed. One dog that underwent bilateral condylectomy had significant loss of maximal mouth opening three months after surgery. Good functional use of the mandible was obtained with unilateral and bilateral condylectomy.     

Coagulopathic Effects and Therapy of Brodifacoum Toxicosis in Dogs

The clinical signs and laboratory changes of brodifacoum (BDF) intoxicated dogs and their response to vitamin K1 treatment were examined. Brodifacoum, a second-generation anticoagulant rodenticide, was fed to four dogs for 3 consecutive days producing a cumulative dose of 1.1 mg BDF/kg body weight. Clinical observations of the animals were made daily throughout the study. Monitored laboratory parameters included: one-stage prothrombin time (OSPT), activated partial thromboplastin time (APTT), activated coagulation time (ACT), complete blood counts, thrombocyte counts, and serum chemistry values. Response to vitamin K1 therapy was evaluated clinically and by laboratory tests. Serum BDF concentrations were monitored. Inappetence and hemorrhagic tendencies were exhibited by day 5 postrodenticide exposure. One-stage prothrombin time, APTT, and ACT were 25% greater than time zero values at 24, 24, and 72 hours postdosing, respectively. All laboratory parameters returned to normal within 48 hours of initiating vitamin K1 therapy (0.83 mg/kg orally, TID for 5 days). Serum brodifacoum concentrations were highest (1065-1215 ng/mL) during the 3 days after BDF dosing and were detectable (3.0-7.5 ng/mL) until day 24 postexposure. A mean BDF elimination half-life of 6 +/- 4 days was observed.     

The Cardiopulmonary Effects of Oxymorphone in Hypovolemic Dogs

Blood was withdrawn from 15 dogs over the course of about 1 hour until the mean arterial blood pressure was reduced to 60 mm Hg. Small aliquots of additional blood were withdrawn in order to maintain the mean arterial blood pressure near 60 mm Hg for an additional hour. Oxymorphone (0.4 mg/kg) was then administered intravenously to ten dogs, and all measurements were repeated in 5, 15, 30, and 60 minutes. Five dogs served as controls.
Heart rate, tidal volume, arterial oxygen, oxygen extraction, and pH significantly decreased after oxymorphone administration, while systemic and pulmonary arterial blood pressures, systemic vascular resistance (transiently), breathing rate, minute ventilation, physiologic dead space, venous admixture, venous oxygen, arterial and venous carbon dioxide, and bicarbonate concentration increased significantly. Cardiac output was also increased, but the change was not statistically significant. Oxymorphone was associated with significantly lower heart rate, tidal volume, arterial oxygen, and pH, and higher systemic and pulmonary arterial pressure, cardiac output, venous oxygen, and arterial and venous carbon dioxide, compared to the control group, which did not receive oxymorphone.
Oxymorphone significantly improved cardiovascular performance and tissue perfusion in these hypovolemic dogs. Oxymorphone did cause a significant increase in arterial carbon dioxide and a decrease in arterial oxygenation. Oxymorphone is an opioid agonist that may represent a reasonable alternative for the induction of anesthesia in patients who are candidates for induction hypotension.