Hemodynamic and respiratory responses to variable arterial partial pressure of oxygen in halothane-anesthetized horses during spontaneous and controlled ventilation.

Cardiovascular and respiratory responses to variable PaO2 were measured in 6 horses anesthetized only with halothane during spontaneous (SV) and controlled (CV) ventilation. The minimal alveolar concentration (MAC) for halothane in oxygen was determined in each spontaneously breathing horse prior to establishing PaO2 study conditions--mean +/- SEM, 0.95 +/- 0.03 vol%. The PaO2 conditions of > 250, 120, 80, and 50 mm of Hg were studied in each horse anesthetized at 1.2 MAC of halothane and positioned in left lateral recumbency. In response to a decrease in PaO2, total peripheral resistance and systolic and diastolic arterial blood pressure decreased (P < 0.05) during SV. Cardiac output tended to increase because heart rate increased (P < 0.05) during these same conditions. During CV, cardiovascular function was usually less than it was at comparable PaO2 during SV (P < 0.05). Heart rate, cardiac output, and left ventricular work increased (P < 0.05) in response to a decrease in PaO2, whereas total peripheral resistance decreased (P < 0.05). During SV, cardiac output and stroke volume increased and arterial blood pressure and total peripheral resistance decreased with duration of anesthesia at PaO2 > 250 mm of Hg. During SV, minute expired volume increased (P < 0.05) because respiratory frequency tended to increase as PaO2 decreased. Decrease in PaCO2 (P < 0.05) also accompanied these respiratory changes. Although oxygen utilization was nearly constant over all treatment periods, oxygen delivery decreased (P < 0.05) with decrease in PaO2, and was less (P < 0.05) during CV, compared with SV, for comparable PaO2 values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rate of rise of arterial carbon dioxide tension in the halothane-anesthetized horse

The rate of rise of arterial partial pressure of carbon dioxide (PaCO2) was determined in 49 apneic halothane-anesthetized horses following controlled ventilation. Drugs given for induction of anesthesia did not affect the rapid rate of rise of PaCO2 during the first minute after controlled ventilation, the PaCO2 at 1 minute after controlled ventilation, or the PaCO2 at which spontaneous ventilation began. Horses given xylazine-ketamine for induction of anesthesia had a significantly (P less than 0.05) faster rate of rise of PaCO2 after 1 minute following controlled ventilation than did horses receiving xylazine-thiamylal for induction.     

Arterial oxygen and carbon dioxide tensions in conscious laterally recumbent ponies

Six adult ponies were trained calmly to assume and maintain left lateral recumbency without the use of sedative or immobilising agents. During a 30 min recumbent period, pHa, arterial oxygen and carbon dioxide tensions (PaO2 and PaCO2) and heart and respiratory rates were monitored at regular intervals to evaluate ventilatory response. Overall, there were no statistically significant differences found between mean control and recumbent or final standing values. When lightweight ponies were compared to heavyweight ponies, only mean PaO2 at 10 mins recumbency was different. This information supports the hypothesis that ventilation impairment during the first 30 mins of equine general anesthesia is primarily drug-mediated, rather than initiated by recumbency per se.     

Hemodynamic effects of carbon dioxide during intermittent positive-pressure ventilation in horses

The hemodynamic effects of high arterial carbon dioxide pressure (PaCO2) during anesthesia in horses were studied. Eight horses were anesthetized with xylazine, guaifenesin, and thiamylal, and were maintained with halothane in oxygen (end-tidal halothane concentration = 1.15%). Baseline data were collected while the horses were breathing spontaneously; then the horses were subjected to intermittent positive-pressure ventilation, and data were collected during normocapnia (PaCO2, 35 to 45 mm of Hg), moderate hypercapnia (PaCO2, 60 to 70 mm of Hg), and severe hypercapnia (PaCO2, 75 to 85 mm of Hg). Hypercapnia was induced by adding carbon dioxide to the inspired gas mixture. Moderate and severe hypercapnia were associated with significant (P less than 0.05) increases in aortic blood pressure, left ventricular systolic pressure, cardiac output, stroke volume, maximal rate of increase and decrease in left ventricular pressure (positive and negative dP/dtmax, respectively), and median arterial blood flow, and decreased time constant for ventricular relaxation. These hemodynamic changes were accompanied by increased plasma epinephrine and norepinephrine concentrations. Administration of the beta-blocking drug, propranolol hydrochloride, markedly depressed the response to hypercapnia. This study confirmed that in horses, hypercapnia is associated with augmentation of cardiovascular function.     

Cardiovascular and respiratory effects of inspired oxygen fraction in halothane-anesthetized horses

Anesthesia of equids is associated with pulmonary dysfunction. Cardiovascular and respiratory effects of inhalation anesthetic agents and duration of anesthesia have been studied, using oxygen as the carrier gas. To our knowledge, the effects of inspired oxygen have not been determined. We studied the cardiovascular and respiratory effects of 2 inspired oxygen fractions (0.30 and greater than 0.85) in 5 laterally recumbent, halothane-anesthetized horses. Mean systemic arterial blood pressure, cardiac output, central venous pressure, pulmonary arterial pressure, arterial pH, and arterial base excess were similar in horses of the 2 groups during 4 hours of anesthesia at constant end-tidal halothane concentration. End-tidal partial pressure of CO2, arterial partial pressure of CO2 and O2, and alveolar-to-arterial O2 tension difference were greater in horses exposed to the higher oxygen concentration. On the basis of the data obtained, we suggest that greater hypoventilation and ventilation/perfusion mismatch occur when horses are breathing high-oxygen fraction. Arterial partial pressure of O2 was not different between the 2 groups of horses after they were disconnected from the anesthesia circuit and allowed to breathe room air. Horses recovered from anesthesia without complications.     

Partial pressures of oxygen and carbon dioxide, pH, and concentrations of bicarbonate, lactate, and glucose in pleural fluid from horses

Samples of pleural fluid from 20 horses with effusive pleural diseases of various causes were evaluated; samples from 19 horses were used for the study. There were differences for pH (P = 0.001) and partial pressure of oxygen (PO2) between arterial blood and nonseptic pleural fluid (P = 0.0491), but there were no differences for pH, PO2, partial pressure of carbon dioxide (PCO2), and concentrations of bicarbonate (HCO3-), lactate, and glucose between venous blood and nonseptic pleural fluid. Paired comparisons of venous blood and nonseptic pleural fluid from the same horse indicated no differences. There were differences (P = 0.0001, each) for pH, PO2, PCO2, and concentrations of HCO3- between arterial blood and septic pleural fluid. Differences also existed for pH (P = 0.0001), PCO2 (P = 0.0003), and concentrations of HCO3- (P = 0.0001), lactate (P = 0.0051), and glucose (P = 0.0001) between venous blood and septic pleural fluid. Difference was not found for values of PO2 between venous blood and septic pleural fluid, although 4 samples of septic pleural fluid contained virtually no oxygen. Paired comparisons of venous blood and septic pleural fluid from the same horse revealed differences (P less than 0.05) for all values, except those for PO2. These alterations suggested functional and physical compartmentalization that separated septic and healthy tissue. Compartmentalization and microenvironmental factors at the site of infection should be considered when developing therapeutic strategies for horses with septic pleural disease.     

Blood oxygen and carbon dioxide tensions in normal dogs and in dogs with respiratory failure

Arterial blood samples were obtained from thirty normal conscious dogs breathing air. The mean values and standard deviations recorded were PaO₂ 101.3±5.6 mmHg, PaCO₂ 34.0±3.9 mmHg, oxygen saturation 93.8 ±1.2%, oxygen content 19.3 ± 1.8 ml/100 ml. Ten dogs with respiratory problems were also examined and of these animals seven had lower than normal oxygen tensions while three had carbon dioxide levels higher than those found in healthy dogs. It was concluded that, in severe respiratory disease, measurement of arterial oxygen tension gives a useful assessment of respiratory failure in dogs.     

Effect of body position on the arterial partial pressures of oxygen and carbon dioxide in spontaneously breathing,conscious dogs in an intensive care unit

Objective – To evaluate the effect of body position on the arterial partial pressures of oxygen and carbon dioxide (PaO₂, PaCO₂), and the efficiency of pulmonary oxygen uptake as estimated by alveolar‐arterial oxygen difference (A‐a difference). Design – Prospective, randomized, crossover study. Setting – University teaching hospital, intensive care unit. Animals – Twenty‐one spontaneously breathing, conscious, canine patients with arterial catheters placed as part of their management strategy. Interventions – Patients were placed randomly into lateral or sternal recumbency. PaO₂ and PaCO₂ were measured after 15 minutes in this position. Patients were then repositioned into the opposite position and after 15 minutes the parameters were remeasured. Measurements and Main Results – Results presented as median (interquartile range). PaO₂ was significantly higher (P=0.001) when patients were positioned in sternal, 91.2 mm Hg (86.0–96.1 mm Hg), compared with lateral recumbency, 86.4 mm Hg (73.9–90.9 mm Hg). The median change was 5.4 mm Hg (1.1–17.9 mm Hg). All 7 dogs with a PaO₂<80 mm Hg in lateral recumbency had improved arterial oxygenation in sternal recumbency, median increase 17.4 mm Hg with a range of 3.8–29.7 mm Hg. PaCO₂ levels when patients were in sternal recumbency, 30.5 mm Hg (27.3–32.7 mm Hg) were not significantly different from those in lateral recumbency, 32.2 mm Hg (28.3–36.0 mm Hg) (P=0.07). The median change was ?1.9 mm Hg (?3.6–0.77 mm Hg). A‐a differences were significantly lower (P=0.005) when patients were positioned in sternal recumbency, 21.7 mm Hg (17.3–27.7 mm Hg), compared with lateral recumbency, 24.6 mm Hg (20.4–36.3 mm Hg). The median change was ?3.1 mm Hg (?14.6–0.9 mm Hg). Conclusions – PaO₂ was significantly higher when animals were positioned in sternal recumbency compared with lateral recumbency, predominantly due to improved pulmonary oxygen uptake (decreased A‐a difference) rather than increased alveolar ventilation (decreased PaCO₂). Patients with hypoxemia (defined as PaO₂<80 mm Hg) in lateral recumbency may benefit from being placed in sternal recumbency. Sternal recumbency is recommended to improve oxygenation in hypoxemic patients.     

Pulmonary arterial wedge pressures: blood gas tensions and pH in the resting horse.

Blood pressure recordings were made from right atrium, right ventricle, pulmonary trunk, and pulmonary arterial "wedge" positions in the standing, resting, adult horse. Similarly, comparisons were made of blood samples collected from these vascular positions, as well as from jugular vein and carotid artery. A consistently lower partial pressure of carbon dioxide and a greater partial pressure of oxygen and pH were found in blood samples from pulmonary arterial wedge than from carotid artery. A technique for safe and rapid collection of pulmonary trunk and pulmonary arterial wedge blood gases, pH, and pressure data, using a balloon-tipped flow-directed catheter, is described in the nonsedated, nontranquilized, resting, adult horse.     

Effects of warm-up intensity on kinetics of oxygen consumption and carbon dioxide production during high-intensity exercise in horses

OBJECTIVE: To compare effects of low and high intensity warm-up exercise on oxygen consumption (VO2) and carbon dioxide production (VCO2) in horses. ANIMALS: 6 moderately conditioned adult Standard-breds. PROCEDURES: Horses ran for 2 minutes at 115% of maximum oxygen consumption (VO2max), 5 minutes after each of the following periods: no warm-up (NoWU); 10 minutes at 50% of VO2max (LoWU); or 7 minutes at 50% VO2max followed by 45-second intervals at 80, 90, and 100% VO2max (HiWU). Oxygen consumption and VCO2 were measured during exercise, and kinetics of VO2 and VCO2 were calculated. Accumulated O2 deficit was also calculated. RESULTS: For both warm-up trials, the time constant for the rapid exponential increase in VO2 was 30% lower than for NoWU. Similarly, the rate of increase in VCO2 was 23% faster in LoWU and HiWU than in NoWU. Peak values for VO2 achieved during the high-speed test were not significantly different among trials (LoWU, 150.2 +/- 3.2 ml/kg/min; HiWU, 151.2 +/- 4.2 ml/kg/min; NoWU, 145.1 +/- 4.1 ml/kg/min). However, accumulated O2 deficit (ml of O2 equivalents/kg) was significantly lower during LoWU (65.3 +/- 5.1) and HiWU (63.4 +/- 3.9) than during NoWU (82.1 +/- 7.3). CONCLUSIONS AND CLINICAL RELEVANCE: Both the low- and high-intensity warm-up, completed 5 minutes before the start of high-intensity exercise, accelerated the kinetics of VO2 and VCO2 and decreased accumulated O2 deficit during 2 minutes of intense exertion in horses that were moderately conditioned.     

Parasympathetic influence on the arrhythmogenicity of graded dobutamine infusions in halothane-anesthetized horses.

We investigated the influence of parasympathetic tone on the arrhythmogenicity of graded dobutamine infusions in horses anesthetized under clinical conditions. Six horses were used in 9 trials. Two consecutive series of graded dobutamine infusions were given IV; each continuous graded dobutamine infusion was administered for 20 minutes. The dobutamine infusion dosage (5, 10, 15, and 20 micrograms/kg of body weight/min) was increased at 5-minute intervals. Isovolumetric saline solution vehicle (v) or atropine (A; 0.04 mg/kg) was administered IV, or bilateral vagotomy (VG) was performed as a treatment before the second series of dobutamine infusions. Treatment was not administered prior to the first dobutamine infusion. Significant interaction between treatment and dosage of dobutamine infusion existed for differences from baseline for mean arterial pressure, systolic arterial pressure, diastolic arterial pressure, heart rate, and cardiac index at dosages of 5 and 10 micrograms of dobutamine/kg/min, given IV and for heart rate at dosage of 15 micrograms of dobutamine/kg/min, given IV. Results for group-V horses were different from those for group-A and group-VG horses, but were not different between group-A and group-VG horses in all aforementioned cases, except for heart rate and cardiac index at dosage of 5 micrograms of dobutamine/kg/min, given IV. Normal sinus rhythm, second-degree atrioventricular block, and bradyarrhythmias predominated during low dobutamine infusion rates during the first infusion series (nontreated horses) and in group-V horses during the second infusion series. Only tachyarrhythmias were observed during the second infusion series in the horses of the A and VG groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Haematological characteristics predicting susceptibility for ascites. 1. High carbon dioxide tensions in juvenile chickens

1. Male broilers of two different genetic stocks, a pure broiler sire line (A) and commercially available Ross broilers (B), were used to study the effect of haematological characteristics in juvenile chickens on the development of clinical ascitic signs. Production performance (body weight gain (BWG), feed intake (FI), feed conversion ratio (FCR)) from 448 birds per stock was measured from 2 to 5 weeks of age. Mortality was recorded from 2 to 6 weeks of age. The birds were housed at a low ambient temperature to stimulate the incidence of ascites. 2. From each stock, 32 birds with the highest (high risk: HRc) and 32 birds with the lowest (low risk: LRc) carbon dioxide tensions (pCO2) in venous blood were selected at 11 d of age. These birds were marked for future blood sampling to determine changes in pCO2 with age to relate these values to ascites susceptibility. 3. At 2 weeks of age all birds (including HRc and LRc birds) were allotted to 32 floor pens (one HRc and one LRc in each pen) per stock. Venous blood samples were collected weekly from HRc and LRc birds for blood gas analysis and haematocrit, and at week 5 also for thyroid hormone (T3, T4) concentrations in plasma. At 5 weeks of age all HRc and LRc birds were examined post-mortem, relative heart, lung, and liver weights and arterial pressure index (API) values were recorded. 4. Birds from stock A showed a lower BWG and FCR and notably higher ascites mortality compared with stock B. An effect of pCO2 tensions at d 11 was found on the incidence of ascitic signs in selected birds of both stocks up to week 5. From the HRc groups 30% of the birds showed ascitic signs, whereas this was only 8% in the LRc group. LRc birds of stock B in particular showed constant low API values (20 +/- 3%) and none of these birds showed signs of ascites. 5. Our results suggest that the ascites problem in Ross birds can be eliminated by selection for low pCO2 tensions in venous blood. Stock effects on API, liver weight, lung weight, and plasma thyroid hormone independent of pCO2 showed a more complex picture of the ascitic signs in stock A compared with B. 6. We concluded that in this experiment a high pCO2 tension in venous blood measured at d 11 was a reliable predictor for ascites susceptibility observed at 5 weeks of age. A low pCO2 tension provides an appropriate criterion for genetic selection, whereas a high pCO2 tension emphasises the necessity for intensive management in poultry houses.     

Arterial hypotension and the development of postanesthetic myopathy in halothane-anesthetized horses

The effect of halothane-induced hypotension on the development of postanesthetic myopathy was studied, using 6 healthy adult horses. Horses were anesthetized with halothane in oxygen for 3.5 hours on each of 2 occasions. Intermittent positive-pressure ventilation was used to maintain PaCO2 of 45 to 55 mm of Hg throughout both anesthetic exposures. By regulating the inspired halothane concentration, a mean arterial blood pressure of 85 to 95 mm of Hg (normotension) was maintained throughout the 1st anesthetic exposure, and a mean arterial blood pressure of 55 to 65 mm of Hg (hypotension) was maintained during the 2nd anesthetic exposure. All horses recovered uneventfully from normotensive anesthesia, but all had some muscle dysfunction after prolonged hypotensive anesthesia. Because of apparent animal discomfort and lameness involving more than 1 limb, 3 horses were euthanatized soon after they recovered from hypotensive anesthesia. The 3 other horses showed a degree of lameness. In addition, 1 horse had raised, swollen plaques over the hip, rib, and facial areas which were in contact with the surgical table, and another had evidence of facial nerve paralysis. One hour after the 6 horses stood after hypotensive anesthesia was completed, values obtained for aspartate transaminase and creatinine were significantly (P less than 0.05) greater than those obtained after normotensive anesthesia was completed. Aspartate transaminase, total bilirubin, and creatinine values were significantly (P less than 0.05) increased when compared with those obtained before horses were anesthetized. A large increase was measured in creatine kinase. Twenty-four hours after hypotensive anesthesia was completed, creatine kinase and lactate dehydrogenase in the 3 surviving horses were significantly (P less than 0.05) greater than those values after normotensive anesthesia was completed.     

Calculation of bovine haemoglobin oxygen saturation by algorithms integrating age,haemoglobin content,blood pH,partial pressures of oxygen and carbon dioxide in the blood,and temperature

In human and veterinary medicine, arterial and venous haemoglobin oxygen saturations are often used to estimate the severity of a disease and to guide therapeutic decisions. In veterinary medicine, haemoglobin oxygen saturation (SO(2)) is usually calculated using a blood gas analyser and algorithms developed for humans. It is possible, therefore, that the values obtained in animals may be distorted, particularly in animals with a high haemoglobin oxygen affinity, like young calves. In order to verify this hypothesis, we compared the arterial (SaO(2)) and venous (SvO(2)) haemoglobin oxygen saturations calculated using three different algorithms, and the oxygen exchange fraction (OEF) at the tissue level, which is the degree of haemoglobin desaturation between arterial and venous blood (SaO(2)-SvO(2)), with the values obtained from the whole bovine oxygen equilibrium curve (OEC) determined by a reference method. The blood gas analysers underestimated SvO(2) values; consequently, the OEF was overestimated (by about 10%). Two methods of reducing these errors were assessed. As the haemoglobin oxygen affinity decreases during the first month of life in calves a relationship between PO(2) at 50% haemoglobin saturation (P50) and age was established in order to correct the calculated values of venous and arterial SO(2), taking into account the estimated position of the OEC. This method markedly reduced the error for SvO(2) and OEF. Secondly, the SO(2) was calculated using a mathematical model taking into account the age of the animal and the specific effects of pH, PCO(2), and temperature on the bovine OEC. Using this method, the mean difference between the OEF values calculated using the mathematical model and those calculated by the reference method was close to zero. The errors produced by blood gas analysers can thus be minimised in two ways: firstly, by simply introducing a P50 estimated from the age of the calf into the analyser before the measurement; and secondly, by calculating the SO(2) using a mathematical model applied to the bovine OEC.     

Effect of pre-operative starvation on intra-operative arterial oxygen tension in horses

This study assessed the effect of pre-operative starvation on intramperative arteriaI oxygen tension (PaO₂) by examination of anaesthetic records from starved and non-starved horses undergoing general anaesthesia. PaO₂ data from 69 horses were included, 33 of which were starved pre-operatively and 36 were not. Thirty minutes after induction of anaesthesia the mean PaO₂ in the non-starved group was higher than in the starved group (non-starved 40 [2649] kPa vs starved 30 [15–46] kPa. median and 25–75 percentile) but at 60 and 90 min the values for PaO₂ for the non-starvcd group were lower than those for the starved group (60 min: starved 31 [15–49] kPa vs non-starved 27 [11–38] kPa; 90 min: starved 31 [1244] kPa vs non-starved 22 [12–38] kPa) None of the differences between these values was statistically significant. Pre-operative starvation did not significantly increase intra-operativc PaO₂ under the conditions of this study.     

Effect of xylazine on the arrhythmogenic dose of epinephrine in thiamylal/halothane-anesthetized horses.

The effect of xylazine on the arrhythmogenic dose of epinephrine (ADE) was studied in 9 horses. Anesthesia was induced by administration of guaifenesin (50 mg/kg of body weight, IV) followed by thiamylal (4 to 6 mg/kg, IV) and was maintained at 1 minimal alveolar concentration (MAC) of halothane (0.89%). Base apex ECG and facial artery pressure were recorded. Epinephrine was infused in a sequence of arithmetically spaced increasing rates (initial rate 0.25 micrograms/kg/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate to the nearest 0.25 micrograms/kg/min at which at least 4 premature ventricular depolarizations occurred in a 15-second period. Xylazine (1.1 mg/kg, IV) was administered after the control ADE was determined. Xylazine did not significantly alter the ADE (control, 1.12 +/- 0.38 micrograms/kg/min; xylazine, 1.21 +/- 0.46 micrograms/kg/min). Blood pressure increased transiently for 8 minutes after xylazine administration. Baseline systolic and diastolic arterial pressures and heart rate were not significantly different from control baseline pressures and heart rate 15 minutes after xylazine administration. Blood pressure and heart rate increased significantly during control and xylazine ADE determinations. Significant differences in pH, PaO2, PaCO2, or base excess were not observed between baseline and ADE in the control or xylazine groups. One horse developed atrial fibrillation, and 2 horses developed ventricular fibrillation during ADE determinations.