Hemodynamic and respiratory responses in halothane-anesthetized horses exposed to positive end-expiratory pressure alone and with dobutamine

The influence of positive end-expiratory pressure (PEEP) on the alveolar-arterial O2 tension difference [P(A-a)O2], physiologic right-to-left shunt fraction, physiologic dead space-to-tidal volume ratio, and hemodynamic variables was studied in halothane-anesthetized horses maintained in dorsal recumbency during controlled ventilation. Dobutamine was used to minimize the adverse cardiovascular consequences of PEEP. Six adult horses were anesthetized, using xylazine (2.2 mg/kg of body weight, IM), guaifenesin (50 mg/kg, IV), thiamylal Na (4.4 mg/kg, IV), and halothane (1.5 to 2% inspired) in 100% O2. Mechanical ventilation was controlled to maintain arterial eucapnia for at least 45 minutes during base-line measurements. Hemodynamic and respiratory variables were determined every 15 minutes during equilibration. Each horse was subjected to 4 randomized treatments: 5 cm of H2O PEEP, 10 cm of H2O PEEP, 5 cm of H2O PEEP plus dobutamine (1 microgram/kg/min), and 10 cm of H2O PEEP plus dobutamine (1 microgram/kg/min). Each treatment lasted 15 minutes and immediately followed its predecessor. Although the magnitude of PEEP was randomized with and without dobutamine, PEEP without dobutamine always preceded PEEP with dobutamine. Differences in hemodynamic or respiratory variables among base-line measurements, 5 cm of H2O PEEP, or 10 cm of H2O PEEP were not significant (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Body position and mode of ventilation influences arterial pH, oxygen, and carbon dioxide tensions in halothane-anesthetized horses.

Effects of body position and type of ventilation were determined on arterial blood gases (PaO2, PaCO2) and pH during and immediately following clinical halothane anesthesia in 36 young, physically conditioned horses. Horses in dorsal recumbency had a lower PaO2 than did similarly breathing horses in a lateral position. Predictably controlled positive-pressure ventilation inproved arterial oxygenation and permitted maintenance of a normal PaCO2. Most horses, regardless of type of ventilation and operative body positioning, were hypoxemic in the immediate postanesthetic period.     

Hemodynamic effects of high-frequency oscillatory ventilation in halothane-anesthetized dogs

Hemodynamic effects of spontaneous ventilation, intermittent positive-pressure ventilation (IPPV), and high-frequency oscillatory ventilation (HFOV) were compared in 6 dogs during halothane anesthesia. Anesthesia was induced with IV thiamylal Na and was maintained with halothane (end-tidal concentration, 1.09%). During placement of catheters, dogs breathed spontaneously through a conventional semiclosed anesthesia circuit. Data were collected, and dogs were mechanically ventilated, using IPPV or HFOV in random order. Ventilation was adjusted to maintain PaCO2 between 38 and 43 mm of Hg during IPPV and HFOV. Cardiac index, aortic blood pressure, and maximum rate of increase of left ventricular pressure were significantly (P less than 0.05) less during HFOV than during spontaneous ventilation, whereas right atrial and pulmonary artery pressure were significantly greater during HFOV than during spontaneous ventilation. During IPPV, only the maximum rate of increase of left ventricular pressure was significantly less than that during spontaneous ventilation.     

End-tidal partial pressure of CO2 as an estimate of arterial partial pressure of CO2 during various ventilatory regimens in halothane-anesthetized dogs

The correlation between end-tidal partial pressure of CO2 (PETCO2) and arterial PCO2 (PaCO2) was studied in six halothane-anesthetized dogs maintained under four different ventilatory regimens: (A) spontaneous breathing; (B) assisted positive-pressure ventilation; (C) intermittent manual inflation; and (D) ventilator-controlled breathing. For procedures A, B, and D together, there was a strong correlation between PETCO2 and PaCO2 (r = 0.8) that was highly significant at P less than 0.0001 for PETCO2 values between 31.3 and 61 mm of Hg. In spontaneous and controlled breathing, PETCO2 is representative of PaCO2 and provides a useful noninvasive tool for monitoring the patient maintained under general anesthesia. Furthermore, data suggest that any ventilatory support of the anesthetized patient markedly improves blood gas and acid-base status compared with that of the unsupported, spontaneously breathing animal.     

Accuracy of pulse oximetry and capnography in healthy and compromised horses during spontaneous and controlled ventilation

The objective of this prospective clinical study was to evaluate the accuracy of pulse oximetry and capnography in healthy and compromised horses during general anesthesia with spontaneous and controlled ventilation. Horses anesthetized in a dorsal recumbency position for arthroscopy (n = 20) or colic surgery (n = 16) were instrumented with an earlobe probe from the pulse oximeter positioned on the tip of the tongue and a sample line inserted at the Y-piece for capnography. The horses were allowed to breathe spontaneously (SV) for the first 20 min after induction, and thereafter ventilation was controlled (IPPV). Arterial blood, for blood gas analysis, was drawn 20 min after induction and 20 min after IPPV was started. Relationships between oxygen saturation as determined by pulse oximetry (S_pO₂), arterial oxygen saturation (S_aO₂)_, arterial carbon dioxide partial pressure (P_aCO₂), and end tidal carbon dioxide (P_(et)CO₂), several physiological variables, and the accuracy of pulse oximetry and capnography, were evaluated by Bland–Altman or regression analysis. In the present study, both S_pO₂ and P_(et)CO₂ provided a relatively poor indication of S_aO₂ and P_aCO₂, respectively, in both healthy and compromised horses, especially during SV. A difference in heart rate obtained by pulse oximetry, ECG, or palpation is significantly correlated with any pulse oximeter inaccuracy. If blood gas analysis is not available, ventilation to P_(et)CO₂ of 35 to 45 mmHg should maintain the P_aCO₂ within a normal range. However, especially in compromised horses, it should never substitute blood gas analysis.     

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.     

Sevoflurane anaesthesia in chickens during spontaneous and controlled ventilation

A crossover study design was used to investigate the dose-related effects of sevoflurane at end-tidal concentrations of 2.2 to 4.4 per cent on the respiratory rate, blood gases, heart rate, arterial blood pressure and ocular signs of chickens during spontaneous and controlled ventilation. The mean (sd) carbon dioxide partial pressure (PaCO2) increased as the concentration of sevoflurane increased, and was 86 (29) mmHg at an end-tidal concentration of 4.4 per cent during spontaneous ventilation, but was maintained between 29 and 42 mmHg during controlled ventilation. The heart rate increased as the concentration of sevoflurane increased during spontaneous ventilation, but did not change during controlled ventilation. Sevoflurane decreased arterial blood pressure during both spontaneous and controlled ventilation, but a dose-dependent decrease in arterial blood pressure was observed only during controlled ventilation. The mean arterial blood pressure at an end-tidal concentration of 4.4 per cent was significantly higher during spontaneous ventilation than during controlled ventilation. Controlled ventilation prevented the increases in PaCO2 and heart rate that were observed during spontaneous ventilation. The decrease in arterial blood pressure during spontaneous ventilation was less than that during controlled ventilation, possibly owing to the effects of hypercapnia.     

Effects of spontaneous, assisted, and controlled ventilatory modes in halothane-anesthetized geldings

Cardiopulmonary effects of spontaneous, assisted, and controlled ventilatory modes were determined with 6 young, healthy geldings anesthetized with halothane at a constant dose (1.3 minimum alveolar concentration). All horses were in lateral recumbency, and all modes of ventilation were studied at least once during each anesthetic exposure. Cardiac output did not differ between spontaneous and assisted ventilation modes, but both modes were associated with significantly (P less than 0.05) higher cardiac output than that with controlled ventilation. The PaCO2 differed significantly (P less than 0.01) between all modes of ventilation. Although controlled ventilation maintained a normal PaCO2, assisted ventilation reduced PaCO2 as compared with spontaneous ventilation with less cardiovascular depression than that with controlled ventilation. Mixed venous O2 tensions were higher with spontaneous and assisted ventilation modes than with controlled ventilation. Except for shorter inspiratory time and smaller inspiratory/expiratory ratio associated with spontaneous ventilation, there were no ventilatory mode-related effects on ventilatory variables.     

A study of cardiovascular function under controlled and spontaneous ventilation in isoflurane–medetomidine anaesthetized horses

Objective To determine, in mildly hypercapnic horses under isoflurane–medetomidine balanced anaesthesia, whether there is a difference in cardiovascular function between spontaneous ventilation (SV) and intermittent positive pressure ventilation (IPPV). Study design Prospective randomized clinical study. Animals Sixty horses, undergoing elective surgical procedures under general anaesthesia: ASA classification I or II. Methods Horses were sedated with medetomidine and anaesthesia was induced with ketamine and diazepam. Anaesthesia was maintained with isoflurane and a constant rate infusion of medetomidine. Horses were assigned to either SV or IPPV for the duration of anaesthesia. Horses in group IPPV were maintained mildly hypercapnic (arterial partial pressure of carbon dioxide (PaCO₂) 50–60 mmHg, 6.7–8 kPa). Mean arterial blood pressure (MAP) was maintained above 70 mmHg by an infusion of dobutamine administered to effect. Heart rate (HR), respiratory rate (f_R), arterial blood pressure and inspiratory and expiratory gases were monitored continuously. A bolus of ketamine was administered when horses showed nystagmus. Cardiac output was measured using lithium dilution. Arterial blood‐gas analysis was performed regularly. Recovery time was noted and recovery quality scored. Results There were no differences between groups concerning age, weight, body position during anaesthesia and anaesthetic duration. Respiratory rate was significantly higher in group IPPV. Significantly more horses in group IPPV received supplemental ketamine. There were no other significant differences between groups. All horses recovered from anaesthesia without complications. Conclusions There was no difference in cardiovascular function in horses undergoing elective surgery during isoflurane–medetomidine anaesthesia with SV in comparison with IPPV, provided the horses are maintained slightly hypercapnic. Clinical relevance In horses with health status ASA I and II, cardiovascular function under general anaesthesia is equal with or without IPPV if the PaCO₂ is maintained at 50–60 mmHg.     

Cardiopulmonary effects of hypercapnia during controlled intermittent positive pressure ventilation in the horse.

The cardiopulmonary effects of eucapnia (arterial CO2 tension [PaCO2] 40.4 +/- 2.9 mm Hg, mean +/- SD), mild hypercapnia (PaCO2, 59.1 +/- 3.5 mm Hg), moderate hypercapnia (PaCO2, 82.6 +/- 4.9 mm Hg), and severe hypercapnia (PaCO2, 110.3 +/- 12.2 mm Hg) were studied in 8 horses during isoflurane anesthesia with volume controlled intermittent positive pressure ventilation (IPPV) and neuromuscular blockade. The sequence of changes in PaCO2 was randomized. Mild hypercapnia produced bradycardia resulting in a significant (P < 0.05) decrease in cardiac index (CI) and oxygen delivery (DO2), while hemoglobin concentration (Hb), the hematocrit (Hct), systolic blood pressure (SBP), mean blood pressure (MBP), systemic vascular resistance (SVR), and venous admixture (QS/QT) increased significantly. Moderate hypercapnia resulted in a significant rise in CI, stroke index (SI), SBP, MBP, mean pulmonary artery pressure (PAP), Hct, Hb, arterial oxygen content (CaO2), mixed venous oxygen content (CvO2), and DO2, with heart rate (HR) staying below eucapnic levels. Severe hypercapnia resulted in a marked rise in HR, CI, SI, SBP, PAP, Hct, Hb, CaO2, CvO2, and DO2. Systemic vascular resistance was significantly decreased, while MBP levels were not different from those during moderate hypercapnia. No cardiac arrhythmias were recorded with any of the ranges of PaCO2. Norepinephrine levels increased progressively with each increase in PaCO2, whereas plasma cortisol levels remained unchanged. It was concluded that hypercapnia in isoflurane-anesthetized horses elicits a biphasic cardiopulmonary response, with mild hypercapnia producing a fall in CI and DO2 despite an increase in MBP, while moderate and severe hypercapnia produce an augmentation of the cardiopulmonary performance and DO2.     

Effect of high PaCO2 and time on cerebrospinal fluid and intraocular pressure in halothane-anesthetized horses

The effects of different arterial carbon dioxide tensions (PaCO2) on cerebrospinal fluid pressure (CSFP) and intraocular pressure (IOP) were studied in 6 male halothane-anesthetized horses positioned in left lateral recumbency. Steady-state anesthetic conditions (1.06% end-tidal halothane concentration) commenced 60 minutes following anesthetic induction with only halothane in oxygen. During atracurium neuromuscular blockade, horses were ventilated, and respiratory rate and peak inspiratory airway pressure were maintained within narrow limits. The CSFP and IOP were measured at 3 different levels of PaCO2 (approx 40, 60, and 80 mm of Hg). The PaCO2 sequence in each horse was determined from a type of switchback design with the initial PaCO2 (period 1), established 30 minutes after the commencement of steady-state anesthesia, being repeated in the middle (period 3) and again at the end (period 5) of the experiment. Measurements taken from the middle 3 periods (2, 3, and 4) would form a Latin square design replicated twice. The interval between each period was approximately 45 minutes. Data from periods 2, 3, and 4 indicated that CSFP (P less than 0.05) and mean systemic arterial pressure increased significantly (P less than 0.05) with high PaCO2. Mean central venous pressure, heart rate, and IOP did not change significantly during these same conditions. Measurements taken during periods 1, 3, and 5 were compared to assess the time-related responses to anesthesia and showed a significant increase in CSFP, a significant decrease in mean central venous pressure, and a small (but not statistically significant) increase in mean systemic arterial pressure.     

Relationship of pulmonary arterial pressure to pulmonary haemorrhage in exercising horses

Exercise-induced pulmonary haemorrhage (EIPH) is characterised by blood in the airways after strenuous exercise and results from stress failure of the pulmonary capillaries. The purpose of this experiment was to establish a threshold value of transmural pulmonary arterial pressure at which haemorrhage occurs in the exercising horse. Five geldings, age 4-14 years, were run in random order once every 2 weeks at 1 of 4 speeds (9, 11, 13, 15 m/s); one day with no run was used as a control. Heart rate, pulmonary arterial pressure and oesophageal pressure were recorded for the duration of the run. Transmural pulmonary arterial pressure was estimated by electronic subtraction of the oesophageal pressure from the intravascular pulmonary arterial pressure. Within 1 h of the run, bronchoalveolar lavage was performed and the red and white blood cells in the fluid were quantified. Red cell counts in the lavage fluid from horses running at 9, 11 and 13 m/s were not significantly different from the control value, but after runs at 15 m/s, red cell counts were significantly (P<0.05) higher. White cell counts were not different from control values at any speed. Analysis of red cell count vs. transmural pulmonary arterial pressure indicated that haemorrhage occurs at approximately 95 mmHg. Red cell lysis in the lavage fluid was also apparent at transmural pulmonary arterial pressures above 90 mmHg. We conclude that, in the exercising horse, a pulmonary arterial pressure threshold exists above which haemorrhage occurs, and that pressure is often exceeded during high speed sprint exercise.     

Use of end-tidal partial pressure of carbon dioxide to predict arterial partial pressure of carbon dioxide in harp seals during isoflurane-induced anesthesia

OBJECTIVE: To evaluate the relationship between end-tidal partial pressure of CO(2) (ETCO(2)) and PaCO(2) in isoflurane-anesthetized harp seals. ANIMALS: Three 5-month-old 25- to 47-kg harp seals (Phoca groenlandica). PROCEDURES: PaCO(2) was determined in serial arterial samples from isoflurane-anesthetized seals and compared with concomitant ETCO(2) measured with a side-stream microstream capnograph. Twenty-four paired samples were subjected to linear regression analysis and the Bland-Altman method for assessment of clinical suitability of the 2 methods (ie, PaCO(2) and ETCO(2) determinations). The influence of ventilation rate per minute (VR) on the ETCO(2) to PaCO(2) difference (P[ET-a] CO(2)) was examined graphically. RESULTS: The correlation coefficient between the 2 measurements was 0.94. The level of agreement between ETCO(2) and PaCO(2) varied considerably. Values of ETCO(2) obtained with a VR of < 5 underestimated PaCO(2) to a greater degree (mean bias, -4.01 mm Hg) and had wider limits of agreement of -13.10 to 5.07 mm Hg (-4.01 mm Hg +/- 1.96 SD), compared with a VR of > or = 5 (mean bias, -2.24 mm Hg; limits of agreement, -7.79 to 3.30 mm Hg). CONCLUSIONS AND CLINICAL RELEVANCE: These results indicate that a microstream sidestream capnograph provides a noninvasive, sufficiently accurate estimation of PaCO(2) with intermittent positive ventilation at a VR > or = 5 in anesthetized harp seals.     

Effect of pressure support ventilation during weaning on ventilation and oxygenation indices in healthy horses recovering from general anesthesia

ObjectiveTo determine if pressure support ventilation (PSV) weaning from general anesthesia affects ventilation or oxygenation in horses.Study designProspective randomized clinical study.AnimalsTwenty client‐owned healthy horses aged 5 ± 2 years, weighing 456 ± 90 kg.MethodsIn the control group (CG; n = 10) weaning was performed by a gradual decrease in respiratory rate (f_R) and in the PSV group (PSVG; n = 10) by a gradual decrease in f_R with PSV. The effect of weaning was considered suboptimal if PaCO₂ > 50 mmHg, arterial pH < 7.35 plus PaCO₂ > 50 mmHg or PaO₂ < 60 mmHg were observed at any time after disconnection from the ventilator until 30 minutes after the horse stood. Threshold values for each index were established and the predictive power of these values was tested.ResultsPressure support ventilation group (PSVG) had (mean ± SD) pH 7.36 ± 0.02 and PaCO₂ 41 ± 3 mmHg at weaning and the average lowest PaO₂ 69 ± 6 mmHg was observed 15 minutes post weaning. The CG had pH 7.32 ± 0.02 and PaCO₂ 57 ± 6 mmHg at weaning and the average lowest PaO₂ 48 ± 5 mmHg at 15 minutes post weaning. No accuracy in predicting weaning effect was observed for f_R (p = 0.3474), minute volume (p = 0.1153), SaO₂ (p = 0.1737) and PaO₂/PAO₂ (p = 0.1529). A high accuracy in predicting an optimal effect of weaning was observed for V_T > 10 L (p = 0.0001), f_R/V_T ratio ≤ 0.60 breaths minute^?1 L^?1 (p = 0.0001), V_T/bodyweight > 18.5 mL kg^?1 (p = 0.0001) and PaO₂/FiO₂ > 298 (p = 0.0002) at weaning. A high accuracy in predicting a suboptimal effect of weaning was observed for V_T < 10 L (p = 0.0001), f_R/V_T ratio ≥ 0.60 breaths minute^?1 L^?1 (p = 0.0001) and Pe′CO₂ ≥ 38 mmHg (p = 0.0001) at weaning.Conclusions and clinical relevancePressure support ventilation (PSV) weaning had a better respiratory outcome. A higher V_T, V_T/body weight, PaO₂/FiO₂ ratio and a lower f_R/V_T ratio and Pe′CO₂ were accurate in predicting the effect of weaning in healthy horses recovering from general anesthesia.     

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)